ESH AND ESC GUIDELINES
2013ESH/ESC Guidelines for the management of arterial hypertension
The Task Force for the management of arterial hypertension of the European Society of Hypertension (ESH)and of the European Society of Cardiology (ESC)
Authors/Task Force Members:Giuseppe Mancia (Chairperson)(Italy)*,Robert Fagard (Chairperson)(Belgium)*,Krzysztof Narkiewicz (Section co-ordinator)(Poland),Josep Redon (Section co-ordinator)(Spain),Alberto Zanchetti (Section co-ordinator)
(Italy),Michael Bo
¨hm (Germany),Thierry Christiaens (Belgium),Renata Cifkova (Czech Republic),Guy De Backer (Belgium),Anna Dominiczak (UK),
Maurizio Galderisi (Italy),Diederick E.Grobbee (Netherlands),Tiny Jaarsma (Sweden),Paulus Kirchhof (Germany/UK),Sverre E.Kjeldsen (Norway),
Ste
′phane Laurent (France),Athanasios J.Manolis (Greece),Peter M.Nilsson (Sweden),Luis Miguel Ruilope (Spain),Roland E.Schmieder (Germany),Per Anton Sirnes (Norway),Peter Sleight (UK),Margus Viigimaa (Estonia),Bernard Waeber (Switzerland),Faiez Zannad (France)
ESH Scienti?c Council:Josep Redon (President)(Spain),Anna Dominiczak (UK),Krzysztof Narkiewicz (Poland),Peter M.Nilsson (Sweden),Michel Burnier (Switzerland),Margus Viigimaa (Estonia),Ettore Ambrosioni (Italy),Mark Cau?eld (UK),Antonio Coca (Spain),Michael Hecht Olsen (Denmark),Roland E.Schmieder (Germany),Costas Tsiou?s (Greece),Philippe van de Borne (Belgium).
ESC Committee for Practice Guidelines (CPG):Jose Luis Zamorano (Chairperson)(Spain),Stephan Achenbach
(Germany),Helmut Baumgartner (Germany),Jeroen J.Bax (Netherlands),He
′ctor Bueno (Spain),Veronica Dean (France),Christi Deaton (UK),Cetin Erol (Turkey),Robert Fagard (Belgium),Roberto Ferrari (Italy),David Hasdai (Israel),Arno W.Hoes (Netherlands),Paulus Kirchhof (Germany/UK),Juhani Knuuti (Finland),Philippe Kolh (Belgium),Patrizio Lancellotti (Belgium),Ales Linhart (Czech Republic),Petros Nihoyannopoulos (UK),
Massimo F.Piepoli (Italy),Piotr Ponikowski (Poland),Per Anton Sirnes (Norway),Juan Luis Tamargo (Spain),Michal Tendera (Poland),Adam Torbicki (Poland),William Wijns (Belgium),Stephan Windecker
(Switzerland).
*Corresponding authors:The two chairmen equally contributed to the document.Chairperson ESH:Professor Giuseppe Mancia,Centro di Fisiologia Clinica e Ipertensione,Via F.Sforza,
35,20121Milano,Italy.Tel:+390392333357,Fax:+39039322274.Email:giuseppe.mancia@unimib.it .Chairperson ESC:Professor Robert Fagard,Hypertension &Cardiovascular Rehab.Unit,KU Leuven University,Herestraat 49,3000Leuven,Belgium.Tel:+3216348707,Fax:+3216343766,Email:robert.fagard@uzleuven.be
These guidelines also appear in the Journal of Hypertension ,doi:10.1097/https://www.doczj.com/doc/cf16698591.html, and in Blood Pressure ,doi:10.3109/08037051.2013.812549.With special thanks to Mrs Clara Sincich and Mrs Donatella Mihalich for their contribution.Other ESC entities having participated in the development of this document:
ESC Associations:Heart Failure Association (HFA),European Association of Cardiovascular Imaging (EACVI),European Association for Cardiovascular Prevention &Rehabilitation (EACPR),European Heart Rhythm Association (EHRA)
ESC Working Groups:Hypertension and the Heart,Cardiovascular Pharmacology and Drug Therapy
ESC Councils:Cardiovascular Primary Care,Cardiovascular Nursing and Allied Professions,Cardiology Practice
The content of these European Society of Cardiology (ESC)and European Society of Hypertension (ESH)Guidelines has been published for personal and educational use only.No com-mercial use is authorized.No part of the ESC Guidelines may be translated or reproduced in any form without written permission from the ESC.Permission can be obtained upon sub-mission of a written request to Oxford University Press,the publisher of the European Heart Journal and the party authorized to handle such permissions on behalf of the ESC.
Disclaimer.The ESH/ESC Guidelines represent the views of the ESH and ESC and were arrived at after careful consideration of the available evidence at the time they were written.Health professionals are encouraged to take them fully into account when exercising their clinical judgement.The guidelines do not,however,override the individual responsibility of health professionals to make appropriate decisions in the circumstances of the individual patients,in consultation with that patient,and where appropriate and necessary the patient’s guardian or carer.It is also the health professional’s responsibility to verify the rules and regulations applicable to drugs and devices at the time of prescription.
&The European Society of Hypertension (ESH)and European Society of Cardiology (ESC)2013.All rights reserved.For permissions please email:journals.permissions@https://www.doczj.com/doc/cf16698591.html,.
European Heart Journal (2013)34,2159–2219doi:10.1093/eurheartj/eht151
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Document Reviewers:Denis L.Clement (ESH Review Co-ordinator)(Belgium),Antonio Coca (ESH Review Co-ordinator)(Spain),Thierry C.Gillebert (ESC Review Co-ordinator)(Belgium),Michal Tendera (ESC Review Co-ordinator)(Poland),Enrico Agabiti Rosei (Italy),Ettore Ambrosioni (Italy),Stefan D.Anker (Germany),Johann Bauersachs (Germany),Jana Brguljan Hitij (Slovenia),Mark Caul?eld (UK),Marc De Buyzere (Belgium),
Sabina De Geest (Switzerland),Genevie
`ve Anne Derumeaux (France),Serap Erdine (Turkey),Csaba Farsang (Hungary),Christian Funck-Brentano (France),Vjekoslav Gerc (Bosnia &Herzegovina),Giuseppe Germano (Italy),Stephan Gielen (Germany),Herman Haller (Germany),Arno W.Hoes (Netherlands),Jens Jordan (Germany),Thomas Kahan (Sweden),Michel Komajda (France),Dragan Lovic (Serbia),Heiko Mahrholdt (Germany),
Michael Hecht Olsen (Denmark),Jan Ostergren (Sweden),Gianfranco Parati (Italy),Joep Perk (Sweden),Jorge Polonia
(Portugal),Bogdan A.Popescu (Romania),Z
ˇeljko Reiner (Croatia),Lars Ryde ′n (Sweden),Yuriy Sirenko (Ukraine),Alice Stanton (Ireland),Harry Struijker-Boudier (Netherlands),Costas Tsiou?s (Greece),Philippe van de Borne (Belgium),Charalambos Vlachopoulos (Greece),Massimo Volpe (Italy),David A.Wood (UK).
The af?liations of the Task Force Members are listed in the Appendix.The disclosure forms of the authors and reviewers are available on the respective society websites https://www.doczj.com/doc/cf16698591.html, and https://www.doczj.com/doc/cf16698591.html,/guidelines
Online publish-ahead-of-print 14June 2013
------------------------------------------------------------------------------------------------------------------------------------------------------Keywords
Hypertension ?Guidelines ?Antihypertensive treatment ?Blood pressure ?Blood pressure
measurement ?Cardiovascular risk ?Cardiovascular complications ?Device therapy ?Follow-up ?Lifestyle ?Organ damage
Table of Contents
Abbreviations and acronyms ........................21621Introduction (2163)
1.1Principles ...............................21631.2New aspects .............................21632Epidemiological aspects .. (2164)
2.1Relationship of blood pressure to cardiovascular and renal
damage ...................................21642.2De?nition and classi?cation of hypertension .........21652.3Prevalence of hypertension ....................21652.4Hypertension and total cardiovascular risk ..........21652.4.1Assessment of total cardiovascular risk .........21652.4.2Limitations ...........................21662.4.3Summary of recommendations on total cardiovascular risk assessment ............................21673Diagnostic evaluation (2167)
3.1Bood pressure measurement...................21683.1.1Of?ce or clinic blood pressure ...............21683.1.2Out-of-of?ce blood pressure................21683.1.3White-coat (or isolated of?ce)hypertension
and masked (or isolated ambulatory)hypertension ......21703.1.4Clinical indications for out-of-of?ce blood pressure ..21703.1.5Blood pressure during exercise and laboratory stress .21713.1.6Central blood pressure ...................21723.2Medical history............................21723.3Physical examination ........................21733.4Summary of recommendations on blood pressure
measurement,history,and physical examination .........21733.5Laboratory investigations .....................21733.6Genetics .. (2173)
3.7Searching for asymptomatic organ damage ..........21743.7.1Heart ...............................21743.7.2Blood vessels ..........................21763.7.3Kidney ..............................21763.7.4Fundoscopy ...........................21773.7.5Brain ...............................21773.7.6Clinical value and limitations . (2177)
3.7.7Summary of recommendations on the search for asymptomatic organ damage,cardiovascular disease,and chronic kidney disease ........................21783.8Searching for secondary forms of hypertension .......21784Treatment approach ...........................
.21784.1Evidence favouring therapeutic reduction of high blood pressure...................................21784.2When to initiate antihypertensive drug treatment .....21784.2.1Recommendations of previous Guidelines .......21784.2.2Grade 2and 3hypertension and high-risk grade 1hypertension ..............................21794.2.3Low-to-moderate risk,grade 1hypertension ......21794.2.4Isolated systolic hypertension in youth ..........21814.2.5Grade 1hypertension in the elderly ...........21814.2.6High normal blood pressure ................21814.2.7Summary of recommendations on initiation
of antihypertensive drug treatment ................21814.3Blood pressure treatment targets ................21824.3.1Recommendations of previous Guidelines .......21824.3.2Low-to-moderate risk hypertensive patients ......21824.3.3Hypertension in the elderly .................21824.3.4High-risk patients ......................
.2182
ESH and ESC Guidelines
2160
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targets (2184)
4.3.8Summary of recommendations on blood pressure
targets in hypertensive patients (2184)
5Treatment strategies (2185)
5.1Lifestyle changes (2185)
5.1.1Salt restriction (2185)
5.1.2Moderation of alcohol consumption (2185)
5.1.3Other dietary changes (2185)
5.1.4Weight reduction (2185)
5.1.5Regular physical exercise (2186)
5.1.6Smoking cessation (2186)
5.1.7Summary of recommendations on adoption of lifestyle
changes (2186)
5.2Pharmacological therapy (2187)
5.2.1Choice of antihypertensive drugs (2187)
5.2.2Monotherapy and combination therapy (2189)
5.2.3Summary of recommendations on treatment
strategies and choice of drugs (2193)
6Treatment strategies in special conditions (2194)
6.1White-coat hypertension (2194)
6.2Masked hypertension (2194)
6.2.1Summary of recommendations on treatment
strategies in white-coat and masked hypertension (2194)
6.3Elderly (2194)
6.3.1Summary of recommendations on antihypertensive
treatment strategies in the elderly (2195)
6.4Young adults (2195)
6.5Women (2195)
6.5.1Oral contraceptives (2195)
6.5.2Hormone replacement therapy (2196)
6.5.3Pregnancy (2196)
6.5.4Long-term cardiovascular consequences in gestational
hypertension (2196)
6.5.5Summary of recommendations on treatment
strategies in hypertensive women (2197)
6.6Diabetes mellitus (2197)
6.6.1Summary of recommendations on treatment
strategies in patients with diabetes (2198)
6.7Metabolic syndrome (2198)
6.7.1Summary of recommendations on treatment
strategies in hypertensive patients with metabolic syndrome2198
6.8Obstructive sleep apnoea (2199)
6.9Diabetic and non-diabetic nephropathy (2199)
6.9.1Summary of recommendations on therapeutic
strategies in hypertensive patients with nephropathy (2200)
6.9.2Chronic kidney disease stage5D (2200)
6.10Cerebrovascular disease (2200)
6.10.1Acute stroke (2200)
6.10.2Previous stroke or transient ischaemic attack (2200)
6.11.1Coronary heart disease (2201)
6.11.2Heart failure (2201)
6.11.3Atrial?brillation (2201)
6.11.4Left ventricular hypertrophy (2202)
6.11.5Summary of recommendations on therapeutic
strategies in hypertensive patients with heart disease (2202)
6.12Atherosclerosis,arteriosclerosis,and peripheral artery
disease (2203)
6.12.1Carotid atherosclerosis (2203)
6.12.2Increased arterial stiffness (2203)
6.12.3Peripheral artery disease (2203)
6.12.4Summary of recommendations on therapeutic
strategies in hypertensive patients with atherosclerosis,
arteriosclerosis,and peripheral artery disease (2203)
6.13Sexual dysfunction (2203)
6.14Resistant hypertension (2204)
6.14.1Carotid baroreceptor stimulation (2204)
6.14.2Renal denervation (2205)
6.14.3Other invasive approaches (2205)
6.14.4Follow-up in resistant hypertension (2205)
6.14.5Summary of recommendations on therapeutic
strategies in patients with resistant hypertension (2205)
6.15Malignant hypertension (2206)
6.16Hypertensive emergencies and urgencies (2206)
6.17Perioperative management of hypertension (2206)
6.18Renovascular hypertension (2206)
6.19Primary aldosteronism (2206)
7Treatment of associated risk factors (2207)
7.1Lipid-lowering agents (2207)
7.2Antiplatelet therapy (2207)
7.3Treatment of hyperglycaemia (2207)
7.4Summary of recommendations on treatment of risk factors
associated with hypertension (2208)
8Follow-up (2208)
8.1Follow-up of hypertensive patients (2208)
8.2Follow-up of subjects with high normal blood pressure and
white-coat hypertension (2208)
8.3Elevated blood pressure at control visits (2208)
8.4Continued search for asymptomatic organ damage (2209)
8.5Can antihypertensive medications be reduced or stopped?2209
9Improvement of blood pressure control in hypertension (2209)
10Hypertension disease management (2210)
10.1Team approach in disease management (2211)
10.2Mode of care delivery (2211)
10.3The role of information and communication technologies2211
11Gaps in evidence and need for future trials (2212)
APPENDIX:Task Force members af?liations (2212)
References (2213)
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ABCD Appropriate Blood pressure Control in Diabetes ABI ankle–brachial index
ABPM ambulatory blood pressure monitoring ACCESS Acute Candesartan Cilexetil Therapy in Stroke Sur-
vival
ACCOMPLISH Avoiding Cardiovascular Events in Combination
Therapy in Patients Living with Systolic Hyperten-
sion
ACCORD Action to Control Cardiovascular Risk in Diabetes ACE angiotensin-converting enzyme
ACTIVE I Atrial Fibrillation Clopidogrel Trial with Irbesartan
for Prevention of Vascular Events
ADVANCE Action in Diabetes and Vascular Disease:Preterax
and Diamicron-MR Controlled Evaluation AHEAD Action for HEAlth in Diabetes
ALLHAT Antihypertensive and Lipid-Lowering Treatment to
Prevent Heart ATtack
ALTITUDE ALiskiren Trial In Type2Diabetes Using
Cardio-renal Endpoints
ANTIPAF ANgioTensin II Antagonist In Paroxysmal Atrial Fib-
rillation
APOLLO A Randomized Controlled Trial of Aliskiren in the
Prevention of Major Cardiovascular Events in
Elderly People
ARB angiotensin receptor blocker
ARIC Atherosclerosis Risk In Communities
ARR aldosterone renin ratio
ASCOT Anglo-Scandinavian Cardiac Outcomes Trial ASCOT-LLA Anglo-Scandinavian Cardiac Outcomes Trial—
Lipid Lowering Arm
ASTRAL Angioplasty and STenting for Renal Artery Lesions A-V atrioventricular
BB beta-blocker
BMI body mass index
BP blood pressure
BSA body surface area
CA calcium antagonist
CABG coronary artery bypass graft
CAPPP CAPtopril Prevention Project
CAPRAF CAndesartan in the Prevention of Relapsing Atrial
Fibrillation
CHD coronary heart disease
CHHIPS Controlling Hypertension and Hypertension Im-
mediately Post-Stroke
CKD chronic kidney disease
CKD-EPI Chronic Kidney Disease—EPIdemiology collabor-
ation
CONVINCE Controlled ONset Verapamil INvestigation of CV
Endpoints
CT computed tomography
CV cardiovascular
CVD cardiovascular disease
D diuretic DBP diastolic blood pressure
DCCT Diabetes Control and Complications Study
DIRECT DIabetic REtinopathy Candesartan Trials
DM diabetes mellitus
DPP-4dipeptidyl peptidase4
EAS European Atherosclerosis Society
EASD European Association for the Study of Diabetes
ECG electrocardiogram
EF ejection fraction
eGFR estimated glomerular?ltration rate
ELSA European Lacidipine Study on Atherosclerosis
ESC European Society of Cardiology
ESH European Society of Hypertension
ESRD end-stage renal disease
EXPLOR Amlodipine–Valsartan Combination Decreases
Central Systolic Blood Pressure more Effectively
than the Amlodipine–Atenolol Combination
FDA U.S.Food and Drug Administration
FEVER Felodipine EVent Reduction study
GISSI-AF Gruppo Italiano per lo Studio della Sopravvivenza
nell’Infarto Miocardico-Atrial Fibrillation
HbA1c glycated haemoglobin
HBPM home blood pressure monitoring
HOPE Heart Outcomes Prevention Evaluation
HOT Hypertension Optimal Treatment
HRT hormone replacement therapy
HT hypertension
HYVET HYpertension in the Very Elderly Trial
IMT intima-media thickness
I-PRESERVE Irbesartan in Heart Failure with Preserved Systolic
Function
INTERHEART Effect of Potentially Modi?able Risk Factors asso-
ciated with Myocardial Infarction in52Countries
INVEST INternational VErapamil SR/T Trandolapril
ISH Isolated systolic hypertension
JNC Joint National Committee
JUPITER Justi?cation for the Use of Statins in Primary Preven-
tion:an Intervention Trial Evaluating Rosuvastatin
LAVi left atrial volume index
LIFE Losartan Intervention For Endpoint Reduction in
Hypertensives
LV left ventricle/left ventricular
LVH left ventricular hypertrophy
LVM left ventricular mass
MDRD Modi?cation of Diet in Renal Disease
MRFIT Multiple Risk Factor Intervention Trial
MRI magnetic resonance imaging
NORDIL The Nordic Diltiazem Intervention study
OC oral contraceptive
OD organ damage
ONTARGET ONgoing Telmisartan Alone and in Combination
with Ramipril Global Endpoint Trial
PAD peripheral artery disease
PATHS Prevention And Treatment of Hypertension Study
PCI percutaneous coronary intervention
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PREVEND Prevention of REnal and Vascular ENdstage Disease PROFESS Prevention Regimen for Effectively Avoiding Sec-
ondary Strokes
PROGRESS Perindopril Protection Against Recurrent Stroke
Study
PWV pulse wave velocity
QALY Quality adjusted life years
RAA renin-angiotensin-aldosterone
RAS renin-angiotensin system
RCT randomized controlled trials
RF risk factor
ROADMAP Randomized Olmesartan And Diabetes MicroAl-
buminuria Prevention
SBP systolic blood pressure
SCAST Angiotensin-Receptor Blocker Candesartan for
Treatment of Acute STroke
SCOPE Study on COgnition and Prognosis in the Elderly SCORE Systematic COronary Risk Evaluation
SHEP Systolic Hypertension in the Elderly Program STOP Swedish Trials in Old Patients with Hypertension STOP-2The second Swedish Trial in Old Patients with
Hypertension
SYSTCHINA SYSTolic Hypertension in the Elderly:Chinese trial SYSTEUR SYSTolic Hypertension in Europe
TIA transient ischaemic attack
TOHP Trials Of Hypertension Prevention TRANSCEND Telmisartan Randomised AssessmeNt Study in
ACE iNtolerant subjects with cardiovascular
Disease
UKPDS United Kingdom Prospective Diabetes Study VADT Veterans’Affairs Diabetes Trial
VALUE Valsartan Antihypertensive Long-term Use
Evaluation
WHO World Health Organization
1Introduction
1.1Principles
The2013guidelines on hypertension of the European Society of Hypertension(ESH)and the European Society of Cardiology(ESC) follow the guidelines jointly issued by the two societies in2003and 2007.1,2Publication of a new document6years after the previous one was felt to be timely because,over this period,important studies have been conducted and many new results have been pub-lished on both the diagnosis and treatment of individuals with an ele-vated blood pressure(BP),making re?nements,modi?cations and expansion of the previous recommendations necessary.
The2013ESH/ESC guidelines continue to adhere to some funda-mental principles that inspired the2003and2007guidelines,namely (i)to base recommendations on properly conducted studies identi-?ed from an extensive review of the literature,(ii)to consider,as the highest priority,data from randomized,controlled trials(RCTs) and their meta-analyses,but not to disregard—particularly when dealing with diagnostic aspects—the results of observational the level of scienti?c evidence and the strength of recommendations
on major diagnostic and treatment issues as in European guidelines on
other diseases,according to ESC recommendations(Tables1and2).
While it was not done in the2003and2007guidelines,providing the recommendation class and the level of evidence is now regarded as important for providing interested readers with a standard approach,
by which to compare the state of knowledge across different?elds of medicine.It was also thought that this could more effectively alert physicians on recommendations that are based on the opinions of
the experts rather than on evidence.This is not uncommon in medi-
cine because,for a great part of daily medical practice,no good science is available and recommendations must therefore stem
from common sense and personal clinical experience,both of
which can be fallible.When appropriately recognized,this can
avoid guidelines being perceived as prescriptive and favour the per-formance of studies where opinion prevails and evidence is lacking.
A fourth principle,in line with its educational purpose,is to provide
a large number of tables and a set of concise recommendations
that could be easily and rapidly consulted by physicians in their routine practice.
The European members of the Task Force in charge of the2013 guidelines on hypertension have been appointed by the ESH and
ESC,based on their recognized expertise and absence of major con-
?icts of interest[their declaration of interest forms can be found on
the ESC website(https://www.doczj.com/doc/cf16698591.html,/guidelines)and ESH website (https://www.doczj.com/doc/cf16698591.html,)].Each member was assigned a speci?c
writing task,which was reviewed by three co-ordinators and then
by two chairmen,one appointed by ESH and another by ESC.The
text was?nalized over approximately18months,during which the
Task Force members met collectively several times and corre-sponded intensively with one another between meetings.Before publication,the document was also assessed twice by42European reviewers,half selected by ESH and half by ESC.It can thus be con?-
dently stated that the recommendations issued by the2013ESH/ESC guidelines on hypertension largely re?ect the state of the art on hypertension,as viewed by scientists and physicians in Europe. Expenses for meetings and the remaining work have been shared
by ESH and ESC.
1.2New aspects
Because of new evidence on several diagnostic and therapeutic aspects of hypertension,the present guidelines differ in many respects from the previous ones.2Some of the most important differ-
ences are listed below:
(1)Epidemiological data on hypertension and BP control in Europe.
(2)Strengthening of the prognostic value of home blood pressure
monitoring(HBPM)and of its role for diagnosis and manage-
ment of hypertension,next to ambulatory blood pressure mon-
itoring(ABPM).
(3)Update of the prognostic signi?cance of night-time BP,white-
coat hypertension and masked hypertension.
(4)Re-emphasis on integration of BP,cardiovascular(CV)risk
factors,asymptomatic organ damage(OD)and clinical compli-
cations for total CV risk assessment.
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(5)Update of the prognostic signi?cance of asymptomatic OD,
including heart,blood vessels,kidney,eye and brain.
(6)Reconsideration of the risk of overweight and target body mass
index (BMI)in hypertension.(7)Hypertension in young people.
(8)Initiation of antihypertensive treatment.More evidence-based
criteria and no drug treatment of high normal BP.
(9)Target BP for treatment.More evidence-based criteria and
uni?ed target systolic blood pressure (SBP)(,140mmHg)in both higher and lower CV risk patients.
(10)Liberal approach to initial monotherapy,without any all-ranking
purpose.
(11)Revised schema for priorital two-drug combinations.(12)New therapeutic algorithms for achieving target BP.
(13)Extended section on therapeutic strategies in special conditions.(14)Revised recommendations on treatment of hypertension in the
elderly.
(15)Drug treatment of octogenarians.
(16)Special attention to resistant hypertension and new treatment
approaches.
(17)Increased attention to OD-guided therapy.
(18)New approaches to chronic management of hypertensive
disease.
2Epidemiological aspects
2.1Relationship of blood pressure to cardiovascular and renal damage
The relationship between BP values and CV and renal morbid-and fatal events has been addressed in a large number of observational studies.3The results,reported in detail in the 2003and 2007ESH/ESC guidelines,1,2can be summarized as follows:
(1)Of?ce BP bears an independent continuous relationship with the
incidence of several CV events [stroke,myocardial infarction,sudden death,heart failure and peripheral artery disease (PAD)]as well as of end-stage renal disease (ESRD).3–5This is true at all ages and in all ethnic groups.6,7
(2)The relationship with BP extends from high BP levels to rela-tively low values of 110–115mmHg for SBP and 70–75mmHg for diastolic BP (DBP).SBP appears to be a better predictor of events than DBP after the age of 50years,8,9and in elderly individuals pulse pressure (the difference between SBP and DBP values)has been reported to have a possible additional prognostic role.10This is indicated also by the par-ticularly high CV risk exhibited by patients with an elevated SBP and a normal or low DBP [isolated systolic hypertension (ISH)].11
(3)A continuous relationship with events is also exhibited by
out-of-of?ce BP values,such as those obtained by ABPM and HBPM (see Section 3.1.2).
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modi?ed by the concomitance of other CV risk factors.
Metabolic risk factors are more common when BP is high than when it is low.12,13
2.2De?nition and classi?cation
of hypertension
The continuous relationship between BP and CV and renal events makes the distinction between normotension and hypertension dif-?cult when based on cut-off BP values.This is even more so because,in the general population,SBP and DBP values have a uni-modal distribution.14In practice,however,cut-off BP values are uni-versally used,both to simplify the diagnostic approach and to facilitate the decision about treatment.The recommended classi?cation is un-changed from the2003and2007ESH/ESC guidelines(Table3). Hypertension is de?ned as values≥140mmHg SBP and/or ≥90mmHg DBP,based on the evidence from RCTs that in patients with these BP values treatment-induced BP reductions are bene?cial (see Sections4.1and4.2).The same classi?cation is used in young, middle-aged and elderly subjects,whereas different criteria,based on percentiles,are adopted in children and teenagers for whom data from interventional trials are not available.Details on BP classi-?cation in boys and girls according to their age and height can be found in the ESH’s report on the diagnosis,evaluation and treatment of high BP in children and adolescents.15
2.3Prevalence of hypertension
Limited comparable data are available on the prevalence of hyperten-sion and the temporal trends of BP values in different European coun-tries.16Overall the prevalence of hypertension appears to be around 30–45%of the general population,with a steep increase with ageing. There also appear to be noticeable differences in the average BP levels across countries,with no systematic trends towards BP changes in the past decade.17–37
Owing to the dif?culty of obtaining comparable results among countries and over time,the use of a surrogate of hypertension status has been suggested.38Stroke mortality is a good candidate, because hypertension is by far the most important cause of this and mortality for stroke has been reported.39The incidence
and trends of stroke mortality in Europe have been analysed by
use of World Health Organization(WHO)statistics.Western Euro-
pean countries exhibit a downward trend,in contrast to eastern European countries,which show a clear-cut increase in death rates
from stroke.40
2.4Hypertension and total cardiovascular
risk
For a long time,hypertension guidelines focused on BP values as the
only-or main variables determining the need for—and the type of—treatment.In1994,the ESC,ESH and European Atherosclerosis Society(EAS)developed joint recommendations on prevention of coronary heart disease(CHD)in clinical practice,41and emphasized
that prevention of CHD should be related to quanti?cation of total
(or global)CV risk.This approach is now generally accepted and
had already been integrated into the2003and2007ESH/ESC guide-
lines for the management of arterial hypertension.1,2The concept is
based on the fact that only a small fraction of the hypertensive popu-
lation has an elevation of BP alone,with the majority exhibiting add-
itional CV risk factors.Furthermore,when concomitantly present,BP
and other CV risk factors may potentiate each other,leading to a total
CV risk that is greater than the sum of its individual components. Finally,in high-risk individuals,antihypertensive treatment strategies (initiation and intensity of treatment,use of drug combinations,etc.:
see Sections4,5,6and7),as well as other treatments,may be differ-
ent from those to be implemented in lower-risk individuals.There is evidence that,in high-risk individuals,BP control is more dif?cult and
more frequently requires the combination of antihypertensive drugs
with other therapies,such as aggressive lipid-lowering treatments.
The therapeutic approach should consider total CV risk in addition
to BP levels in order to maximize cost-effectiveness of the manage-
ment of hypertension.
2.4.1Assessment of total cardiovascular risk
Estimation of total CV risk is easy in particular subgroups of patients,
such as those with antecedents of established cardiovascular disease (CVD),diabetes,CHD or with severely elevated single risk factors.In
all of these conditions,the total CV risk is high or very high,calling for intensive CV risk-reducing measures.However,a large number of patients with hypertension do not belong to any of the above cat-egories and the identi?cation of those at low,moderate,high or
very high risk requires the use of models to estimate total CV risk,
so as to be able to adjust the therapeutic approach accordingly.
Several computerized methods have been developed for estimat-
ing total CV risk.41–48Their values and limitations have been reviewed recently.49The Systematic COronary Risk Evaluation (SCORE)model has been developed based on large European
cohort studies.The model estimates the risk of dying from CV(not
just coronary)disease over10years based on age,gender,smoking habits,total cholesterol and SBP.43The SCORE model allows calibra-
tion of the charts for individual countries,which has been done for numerous European countries.At the international level,two sets
of charts are provided:one for high-risk and one for low-risk coun-
tries.The electronic,interactive version of SCORE,known as Heart-
Score(available through https://www.doczj.com/doc/cf16698591.html,),is adapted to also
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allow adjustment for the impact of high-density lipoprotein choles-terol on total CV risk.
The charts and their electronic versions can assist in risk assess-ment and management but must be interpreted in the light of the phy-sician’s knowledge and experience,especially with regard to local conditions.Furthermore,the implication that total CV risk estimation is associated with improved clinical outcomes when compared with other strategies has not been adequately tested.Risk may be higher than indicated in the charts in:?Sedentary subjects and those with central obesity;the increased relative risk associated with overweight is greater in younger sub-jects than in older subjects.
?Socially deprived individuals and those from ethnic minorities.?Subjects with elevated fasting glucose and/or an abnormal glucose tolerance test,who do not meet the diagnostic criteria for dia-betes.
?Individuals with increased triglycerides,?brinogen,apolipoprotein B,lipoprotein(a)levels and high-sensitivity C-reactive protein.?Individuals with a family history of premature CVD (before the age of 55years in men and 65years in women).In SCORE,total CV risk is expressed as the absolute risk of dying from CVD within 10years.Because of its heavy dependence on age,in young patients,absolute total CV risk can be loweven in the presence of high BP with additional risk factors.If insuf?ciently treated,however,this condition may lead to a partly irreversible high-risk condition years later.In younger subjects,treatment decisions should better be guided by quanti?cation of relative risk or by esti-mating heart and vascular age.A relative-risk chart is available in the Joint European Societies’Guidelines on CVD Prevention in Clinical Practice,50which is helpful when advising young persons.
Further emphasis has been given to identi?cation of asymptomatic OD,since hypertension-related asymptomatic alterations in several organs indicate progression in the CVD continuum,which markedly increases the risk beyond that caused by the simple presence of risk factors.A separate section (Section 3.7)is devoted to searching for asymptomatic OD,51–53where evidence for the additional risk of each subclinical alteration is discussed.
For more than a decade,international guidelines for the manage-ment of hypertension (the 1999and 2003WHO/International Society of Hypertension Guidelines and the 2003and 2007ESH/ESC Guidelines)1,2,54,55have strati?ed CV risk in different categor-ies,based on BP category,CV risk factors,asymptomatic OD and presence of diabetes,symptomatic CVD or chronic kidney disease (CKD),as also done by the 2012ESC prevention guidelines.50The classi?cation in low,moderate,high and very high risk is retained in the current guidelines and refers to the 10-year risk of CV mortality as de?ned by the 2012ESC prevention guidelines (Figure 1).50The factors on which the strati?cation is based are summarized in Table 4.
2.4.2Limitations
All currently available models for CV risk assessment have limitations that must be appreciated.The signi?cance of OD in determining calculation of overall risk is dependent on how carefully the damage is assessed,based on available facilities.Conceptual limita-tions should also be mentioned.One should never forget that the ra-tionale of estimating total CV risk is to govern the best use of limited resources to prevent CVD;that is,to grade preventive measures in relation to the increased risk.Yet,strati?cation of absolute risk is often used by private or public healthcare providers to establish a barrier,below which treatment is discouraged.It should be kept in
BP = blood pressure; CKD = chronic kidney disease; CV = cardiovascular; CVD = cardiovascular disease; DBP = diastolic blood pressure; HT = hypertension; OD = organ damage; RF = risk factor; SBP = systolic blood pressure.
Other risk factors,
asymptomatic organ damage or disease Blood Pressure (mmHg)
High normal SBP 130–139or DBP 85–89
Grade 1 HT SBP 140–159or DBP 90–99Grade 2 HT SBP 160–179or DBP 100–109Grade 3 HT SBP ≥180or DBP ≥110No other RF Low risk Moderate risk High risk 1–2 RF Low risk Moderate risk Moderate to high risk High risk ≥3 RF
Low to Moderate risk Moderate to high risk High Risk High risk OD, CKD stage 3 or diabetes Moderate to high risk High risk High risk High to very high risk Symptomatic CVD, CKD stage ≥4 or diabetes with OD/RFs
Very high risk Very high risk
Very high risk
Very high risk
Figure 1Strati?cation of total CV risk in categories of low,moderate,high and very high risk according to SBP and DBP and prevalence of asymptomatic OD,diabetes,CKD stage or symptomatic CVD.Subjects with a high normal of?ce but a raised out-of-of?ce BP (masked hypertension)a CV risk in the hypertension range.Subjects with a high of?ce BP but normal out-of-of?ce BP (white-coat hypertension),particularly if there diabetes,OD,CVD or CKD,have lower risk than sustained hypertension for the same of?ce BP.
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3.1.2Out-of-of?ce blood pressure
The major advantage of out-of-of?ce BP monitoring is that it provides a large number of BP measurements away from the medical environ-ment,which represents a more reliable assessment of actual BP than of?ce BP.Out-of-of?ce BP is commonly assessed by ABPM or HBPM, usually by self-measurement.A few general principles and remarks hold for the two types of monitoring,in addition to recommenda-tions for of?ce BP measurement:64–67
?The procedure should be adequately explained to the patient,with verbal and written instructions;in addition,self-measurement of BP requires appropriate training under medical supervision.
?Interpretation of the results should take into account that the re-producibility of out-of-of?ce BP measurements is reasonably good for24-h,day and night BP averages but less for shorter periods within the24hs and for more complex and derived indices.68
?ABPM and HBPM provide somewhat different information on the subject’s BP status and risk and the two methods should thus be regarded as complementary,rather than competitive or alterna-tive.The correspondence between measurements with ABPM and HBPM is fair to moderate.
?Of?ce BP is usually higher than ambulatory and home BP and the difference increases as of?ce BP increases.Cut-off values for the de?nition of hypertension for home and ambulatory BP,according
Table6.64–67
?Devices should have been evaluated and validated according to international standardized protocols and should be properly
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Pressure Monitoring.64,65ABPM is performed with the patient wearing a portable BP measuring device,usually on the non-dominant arm,for a24–25h period,so that it gives information on BP during daily activities and at night during sleep.At the time of?tting of the portable device,the difference between the initial values and those from BP measurement by the operator should not be greater than 5mmHg.In the event of a larger difference,the ABPM cuff should be removed and?tted again.The patient is instructed to engage in normal activities but to refrain from strenuous exercise and,at the time of cuff in?ation,to stop moving and talking and keep the arm still with the cuff at heart level.The patient is asked to provide infor-mation in a diary on symptoms and events that may in?uence BP,in addition to the times of drug ingestion,meals and going to-and rising from bed.In clinical practice,measurements are often made at15min intervals during the day and every30min overnight;exces-sive intervals between BP readings should be avoided because they reduce the accuracy of24-h BP estimates.69It may be recommended that measurements be made at the same frequency during the dayand night—for example every20min throughout.The measurements are downloaded to a computer and a range of analyses can be performed.At least70%of BPs during daytime and night-time periods should be satisfactory,or else the monitoring should be repeated.The detection of artifactual readings and the handling of outlying values have been subject to debate but,if there are suf-?cient measurements,editing is not considered necessary and only grossly incorrect readings should be deleted.It is noteworthy that readings may not be accurate when the cardiac rhythm is marked-ly irregular.70
3.1.2.1.2Daytime,night-time and24-hour blood pressure In addition to the visual plot,average daytime,night-time and24-h BP are the most commonly used variables in clinical practice.Average daytime and night-time BP can be calculated from the diary on the basis of the times of getting up and going to bed.An alternative method is to use short,?xed time periods,in which the rising and retiring periods—which differ from patient to patient—are eliminated.It has,for example,been shown that average BPs from10am to8pm and from midnight to6am correspond well with the actual waking and sleeping BPs,71but other short,?xed time periods have been pro-posed,such as from9am to9pm and from1am to6am.In the event of different measurement intervals during the day and the night,and to account for missing values,it is recommended that average24-h BP be weighted for the intervals between successive readings or to cal-culate the mean of the24hourly averages to avoid overestimation of average24-h BP.72
The night-to-day BP ratio represents the ratio between average night-time and daytime BP.BP normally decreases during the night—de?ned as‘dipping’.Although the degree of night-time dipping has a normal distribution in a population setting,it is generally agreed that the?nding of a nocturnal BP fall of.10%of daytime values(night–day BP ratio,0.9)will be accepted as an arbitrary cut-off to de?ne subjects as‘dippers’.Recently,more dipping categories have been proposed:absence of dipping,i.e.nocturnal BP increase(ratio.1.0);mild dipping(0.9,ratio≤1.0);dipping (0.8,ratio≤0.9);and extreme dipping(ratio≤0.8).One should bear in mind that the reproducibility of the dipping pattern is limited.73,74Possible reasons for absence of dipping are sleep 3.1.2.1.3Additional analyses A number of additional indices may be derived from ABPM recordings.75–81They include:BP variability,75 morning BP surge,76,77,81blood pressure load,78and the ambulatory arterial stiffness index.79,80However,their added predictive value is
not yet clear and they should thus be regarded as experimental,
with no routine clinical use.Several of these indices are discussed
in detail in ESH position papers and guidelines,64,65including informa-
tion on facilities recommended for ABPM software in clinical prac-
tice,which include the need for a standardized clinical report,an interpretative report,a trend report to compare recordings obtained
over time and a research report,offering a series of additional para-meters such as those listed above.
3.1.2.1.4Prognostic signi?cance of ambulatory blood pressure Several studies have shown that hypertensive patients’left ventricular hyper-
trophy(LVH),increased carotid intima-media thickness(IMT)and
other markers of OD correlate with ambulatory BP more closely
than with of?ce BP.82,83Furthermore,24-h average BP has been con-sistently shown to have a stronger relationship with morbid or fatal
events than of?ce BP.84–87There are studies in which accurately measured of?ce BP had a predictive value similar to ambulatory
BP.87Evidence from meta-analyses of published observational studies and pooled individual data,88–90however,has shown that ambulatory BP in general is a more sensitive risk predictor of clinical
CV outcomes,such as coronary morbid or fatal events and stroke,
than of?ce BP.The superiority of ambulatory BP has been shown
in the general population,in young and old,in men and women,in untreated and treated hypertensive patients,in patients at high risk
and in patients with CV or renal disease.89–93Studies that accounted
for daytime and night-time BP in the same statistical model found
that night-time BP is a stronger predictor than daytime BP.90,94
The night–day ratio is a signi?cant predictor of clinical CV outcomes
but adds little prognostic information over and above24-h BP.94,95
With regard to the dipping pattern,the most consistent?nding is
that the incidence of CV events is higher in patients with a lesser
or no drop in nocturnal BP than in those with greater
drop,89,91,92,95,96although the limited reproducibility of this phe-nomenon limits the reliability of the results for small between-
group differences.89,91,92,95Extreme dippers may have an increased
risk for stroke.97However,data on the increased CV risk in extreme dippers are inconsistent and thus the clinical signi?cance of this phe-nomenon is uncertain.89,95
3.1.2.2Home blood pressure monitoring
3.1.2.2.1Methodological aspects The ESH Working Group on Blood Pressure Monitoring has proposed a number of recommendations
for HBPM.66,67The technique usually involves self-measurement of
BP but,in some patients,the support of a trained health provider
or family member may be needed.Devices worn on the wrist are cur-
rently not recommended but their use might be justi?ed in obese sub-
jects with extremely large arm circumference.For diagnostic evaluation,BP should be measured daily on at least3–4days and pref-
erably on7consecutive days;in the mornings as well as in the eve-nings.BP is measured in a quiet room,with the patient in the
seated position,back and arm supported,after5min of rest and
with two measurements per occasion taken1–2min apart:the
results are reported in a standardized logbook immediately after
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not always be reliable,which can be overcome by storage in a memory-equipped device.Home BP is the average of these readings, with exclusion of the?rst monitoring https://www.doczj.com/doc/cf16698591.html,e of telemonitoring and smartphone applications for HBPM may be of further advantage.98,99 Interpretation of the results should always be under the close guid-ance of the physician.
When compared with of?ce BP,HBPM yields multiple measure-ments over several days,or even longer periods,taken in the indivi-dual’s usual https://www.doczj.com/doc/cf16698591.html,pared with ambulatory BP,it provides measurements over extended periods and day-to-day BP variability,is cheaper,100more widely available and more easily re-peatable.However,unlike ABPM,it does not provide BP data during routine,day-to-day activities and during sleep,or the quanti?-cation of short-term BP variability.101
3.1.2.2.2Prognostic signi?cance of home BP Home BP is more closely related to hypertension-induced OD than of?ce BP,particularly LVH,82,83and recent meta-analyses of the few prospective studies in the general population,in primary care and in hypertensive patients,indicate that the prediction of CV morbidity and mortality is signi?cantly better with home BP than with of?ce BP.102,103 Studies in which both ABPM and HBPM were performed show that home BP is at least as well correlated with OD as is the ambulatory BP,82,83and that the prognostic signi?cance of home BP is similar to that of ambulatory BP after adjustment for age and gender.104,105
3.1.3White-coat(or isolated of?ce)hypertension
and masked(or isolated ambulatory)hypertension
Of?ce BP is usually higher than BP measured out of the of?ce,which has been ascribed to the alerting response,anxiety and/or a condi-tional response to the unusual situation,106and in which regression to the mean may play a role.Although several factors involved in of?ce or out-of-of?ce BP modulation may be involved,107the differ-ence between the two is usually referred to—although somewhat improperly—as the‘white-coat effect’,107,108whereas‘white-coat-’or‘isolated of?ce-’or‘isolated clinic hypertension’refers to the con-dition in which BP is elevated in the of?ce at repeated visits and normal out of the of?ce,either on ABPM or HBPM.Conversely,BP may be normal in the of?ce and abnormally high out of the medical environment,which is termed‘masked-’or‘isolated ambulatory hypertension’.The terms‘true-’or‘consistent normotension’and ‘sustained hypertension’are used when both types of BP measure-ment are,respectively,normal or abnormal.Whereas the cut-off value for of?ce BP is the conventional140/90mmHg,most studies in white-coat or masked hypertension have used a cut-off value of 135/85mmHg for out-of-of?ce daytime or home BP and130/ 80mmHg for24-h BP.Notably,there is only moderate agreement between the de?nition of white-coat or masked hypertension diag-nosed by ABPM or HBPM.101It is recommended that the terms ‘white-coat hypertension’and‘masked hypertension’be reserved to de?ne untreated individuals.
3.1.3.1White-coat hypertension
Based on four population studies,the overall prevalence of white-coat hypertension averaged13%(range9–16%)and it amounted to about32%(range25–46%)among hypertensive subjects in these surveys.109Factors related to increased prevalence of white-is lower in the case of target OD or when of?ce BP is based on repeated measurements or when measured by a nurse or another healthcare provider.110,111The prevalence is also related to the
level of of?ce BP:for example,the percentage of white-coat hyper-
tension amounts to about55%in grade1hypertension and to only
about10%in grade3hypertension.110OD is less prevalent in white-
coat hypertension than in sustained hypertension and prospective
studies have consistently shown this to be the case also for CV events.105,109,112,113Whether subjects with white-coat hypertension
can be equalled to true normotensive individuals is an issue still under
debate because,in some studies,the long-term CV risk of this condi-
tion was found to be intermediate between sustained hypertension
and true normotension,105whereas in meta-analyses it was not sig-
ni?cantly different from true normotension when adjusted for
age,gender and other covariates.109,112,113The possibility exists
that,because white-coat hypertensive patients are frequently treated,the reduction of clinic BP leads to a reduced incidence
of CV events.112Other factors to consider are that,compared
with true normotensive subjects,in white-coat hypertensive patients,(i)out-of-of?ce BP is higher,105,109(ii)asymptomatic OD
such as LVH may be more frequent,114and(iii)this is the case also
for metabolic risk factors and long-term risk of new-onset diabetes
and progression to sustained hypertension.115,116It is recommended
that the diagnosis of white-coat hypertension be con?rmed within
3–6months and these patients be investigated and followed-up closely,including repeated out-of-of?ce BP measurements(see
Section6.1).
3.1.3.2Masked hypertension
The prevalence of masked hypertension averages about13% (range10–17%)in population-based studies.109Several factors
may raise out-of-of?ce BP relative to of?ce BP,such as younger
age,male gender,smoking,alcohol consumption,physical activity, exercise-induced hypertension,anxiety,job stress,obesity,diabetes,
CKD and family history of hypertension and the prevalence is higher
when of?ce BP is in the high normal range.117Masked hypertension is frequently associated with other risk factors,asymptomatic OD and increased risk of diabetes and sustained hypertension.114–119
Meta-analyses of prospective studies indicate that the incidence of
CV events is about two times higher than in true normotension
and is similar to the incidence in sustained hypertension.109,112,117
The fact that masked hypertension is largely undetected and untreated may have contributed to this?nding.In diabetic patients masked hypertension is associated with an increased risk of nephro-
pathy,especially when the BP elevation occurs mainly during the
night.120,121
3.1.4Clinical indications for out-of-of?ce blood pressure
It is now generally accepted that out-of-of?ce BP is an important
adjunct to conventional of?ce BP measurement,but the latter cur-
rently remains the‘gold standard’for screening,diagnosis and man-agement of hypertension.The time-honoured value of of?ce BP, however,has to be balanced against its important limitations,which
have led to the increasingly frequent suggestion that out-of-of?ce
BP measurements play an important role in hypertension manage-
ment.Although there are important differences between ABPM
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indication,availability,ease,cost of use and,if appropriate,patient preference.For initial assessment of the patient,HBPM may be more suitable in primary care and ABPM in specialist care. However,it is advisable to con?rm borderline or abnormal?ndings on HBPM with ABPM,122which is currently considered the reference for out-of-of?ce BP,with the additional advantage of providing night-time BP values.Furthermore,most—if not all—patients should be familiarized with self-measurement of BP in order to optimize follow-up,for which HBPM is more suitable than ABPM.However, (self-measured)HBPM may not be feasible because of cognitive im-pairment or physical limitations,or may be contra-indicated because of anxiety or obsessive patient behaviour,in which case ABPM may be more suitable.Conditions considered as clinical indi-cations for out-of-of?ce BP measurement for diagnostic purposes are listed in Table7.
3.1.5Blood pressure during exercise and laboratory stress BP increases during dynamic and static exercise,whereby the in-crease is more pronounced for systolic than for diastolic BP.123Exer-cise testing usually involves dynamic exercise,either on a bicycle ergometer or a treadmill.Notably,only SBP can be measured reliably with non-invasive methods.There is currently no consensus on normal BP response during dynamic exercise testing.A SBP of ≥210mmHg for men and≥190mmHg for women has been nitions of an exaggerated BP response to exercise have also been used.124,125Furthermore,the increase of SBP at?xed submaximal exercise is related to pre-exercise BP,age,arterial stiffness and ab-dominal obesity and is somewhat greater in women than in men
and less in?t than in un?t individuals.123–127Most—but not all—studies have shown that an excessive rise of BP during exercise pre-
dicts the development of hypertension in normotensive subjects,in-dependently from BP at rest.123,124,128However,exercise testing to
predict future hypertension is not recommended because of a number of limitations,such as lack of standardization of methodology
and de?nitions.Furthermore,there is no unanimity on the associ-
ation of exercise BP with OD,such as LVH,after adjustment for
resting BP and other covariates,as well in normotensives as in hyper-tensive patients.123,124Also the results on the prognostic signi?cance
of exercise BP are not consistent,125which may be due to the fact that
the two haemodynamic components of BP change in opposite direc-
tions during dynamic exercise:systemic vascular resistance decreases whereas cardiac output increases.It is likely that the decisive prog-
nostic factor is a blunted reduction of systemic vascular resistance
during exercise,compatible with structural pathophysiological changes in arteries and arterioles.123,129Whether or not the impaired arterial dilatation is translated into an excessive rise of BP
may at least partly depend on cardiac output.In normotensive sub-
jects and in mild hypertensive patients with adequate increase of cardiac output,an exaggerated BP response predicts a poorer long-
term outcome.125,130In the case of normal resting BP,exercise-induced hypertension can be considered an indication for ABPM because of its association with masked hypertension.131On the
other hand,when hypertension is associated with cardiac dysfunction
and blunted exercise-induced increase of cardiac output,the prog-
nostic signi?cance of exercise BP may be lost.129Finally,a higher BP
during exercise may even carry a better prognosis,such as in
75-year-old individuals,132in patients with suspected cardiac disease,133or with heart failure,134in whom a higher exercise BP implies relatively preserved systolic cardiac function.125In conclu-
sion,the overall results question the clinical utility of BP measure-
ments during exercise testing for diagnostic and prognostic purposes in patients with hypertension.However,exercise testing
is useful as a general prognostic indicator using exercise capacity
and electrocardiogram(ECG)data and an abnormal BP response
may warrant ABPM.
A number of mental stress tests have been applied to evoke stress
and increase BP via a problem of mathematical,technical,or decisio-
nal nature.123However,these laboratory stress tests in general do
not re?ect real-life stress and are not well standardized,have
limited reproducibility,and correlations between BP responses to
the various stressors are limited.In addition,results on the independ-
ent relationships of the BP response to mental stressors with future hypertension are not unanimous and,if signi?cant,the additional explained variance is usually small.123,135A recent meta-analysis sug-
gested that greater responsiveness to acute mental stress has an adverse effect on future CV risk status—a composite of elevated
BP,hypertension,left ventricular mass(LVM),subclinical atheroscler-
osis and clinical cardiac events.136The overall results suggest that BP measurements during mental stress tests are currently not clinically useful.
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3.1.6Central blood pressure
The measurement of central BP in hypertensive patients raises in-creasing interest because of both its predictive value for CV events and the differential effect of antihypertensive drugs,compared with brachial BP.The arterial pressure waveform is a composite of the forward pressure wave created by ventricular contraction and a re?ected wave.137It should be analysed at the central level,i.e.in the ascending aorta,since it represents the true load imposed on heart,brain,kidney and large arteries.The phenomenon of wave re-?ection can be quanti?ed through the augmentation index—de?ned as the difference between the second and ?rst systolic peaks,expressed as a percentage of the pulse pressure,preferably adjusted for heart rate.Owing to the variable superimposition of incoming and re?ected pressure waves along the arterial tree,aortic systolic and pulse pressures may be different from the conventionally measured brachial pressure.In recent years several methods,including applana-tion tonometry and transfer function,have been developed to esti-mate central systolic BP or pulse pressure from brachial pressure wave.They have been critically reviewed in an expert consensus document.138
Early epidemiological studies in the 2000s showed that central aug-mentation index and pulse pressure,directly measured by carotid tonometry,were independent predictors of all-cause and CV mortal-ity in patients with ESRD.139A recent meta-analysis con?rmed these ?ndings in several populations.140However,the additive predictive value of central BP beyond brachial BP was either marginal or not stat-istically signi?cant in most studies.140
Thus the current guidelines,like previous ones,2,141consider that,although the measurement of central BP and augmentation index is of great interest for mechanistic analyses in pathophysiology,pharma-cology and therapeutics,more investigation is needed before recom-mending their routine clinical use.The only exception may be ISH in the young:in some of these individuals increased SBP at the brachial level may be due to high ampli?cation of the central pressure wave,while central BP is normal.142
3.2Medical history
The medical history should address the time of the ?rst diagnosis of arterial hypertension,current and past BP measurements and current and past antihypertensive medications.Particular attention should be paid to indications of secondary causes of hypertension.Women should be questioned about pregnancy-related hyperten-sion.Hypertension translates into an increased risk of renal and CV complications (CHD;heart failure;stroke;PAD;CV death),es-pecially when concomitant diseases are present.Therefore,a careful history of CVDs should be taken in all patients,to allow assessment of global CV risk,including concomitant diseases such as diabetes,clinical signs or a history of heart failure,CHD or PAD,valvular heart disease,palpitations,syncopal episodes,neurological disorders with an emphasis on stroke and transient ischaemic attack (TIA).A history of CKD should include the type and duration of kidney disease.Nicotine abuse and evidence for dyslipidaemia should be sought.A family history of premature hypertension and/or premature CVD is an important ?rst indica-tor of familial (genetic)predisposition to hypertension and CVD
and may trigger clinically indicated genetic tests.Details on family and medical history are summarized in Table 8.
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3.3Physical examination
Physical examination aims to establish or verify the diagnosis of hypertension,establish current BP,screen for secondary causes of hypertension and re?ne global CV risk estimation.BP should be measured as summarized in Section 3.1.1and should be repeated to con?rm the diagnosis of hypertension.On at least one occasion,BP needs to be measured at both arms and differences between the two arms in SBP .20mmHg and/or in DBP .10mmHg—if con?rmed—should trigger further investigations of vascular abnormalities.All patients should undergo auscultation of the carotid arteries,heart and renal arteries.Murmurs should suggest further investigation (carotid ultrasound,echocardiography,renal vascular ultrasound,depending on the location of the murmur).Height,weight,and waist circumference should be measured with the patient standing,and BMI calculated.Pulse palpation and cardiac auscultation may reveal arrhythmias.In all patients,heart rate should be measured while the patient is at rest.An increased heart rate indicates an increased risk of heart disease.An irregular pulse should raise the suspicion of atrial ?brillation,including silent atrial ?brillation.Details on physical examination are summar-ized in Table 9.
3.4Summary of recommendations on blood pressure measurement,history,and physical examination
3.5Laboratory investigations
Laboratory investigations are directed at providing evidence for the presence of additional risk factors,searching for secondary hyperten-sion and looking for the absence or presence of OD.Investigations should progress from the most simple to the more complicated ones.Details on laboratory investigations are summarized in Table 10.
3.6Genetics
A positive family history is a frequent feature in hypertensive patients,143,144with the heritability estimated to vary between 35%and 50%in the majority of studies,145and heritability has been con-?rmed for ambulatory BP.146Several rare,monogenic forms of hyper-tension have been described,such as glucocorticoid-remediable
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aldosteronism,Liddle’s syndrome and others,where a single gene mu-tation fully explains the pathogenesis of hypertension and dictates the best treatment modality.147Essential hypertension is a highly hetero-geneous disorder with a multifactorial aetiology.Several genome-wide association studies and their meta-analyses point to a total of 29single nucleotide polymorphisms,which are associated with systolic and/or diastolic BP.148These ?ndings might become useful contributors to risk scores for OD.
3.7Searching for asymptomatic organ damage
Owing to the importance of asymptomatic OD as an intermediate stage in the continuum of vascular disease,and as a determinant of overall CV risk,signs of organ involvement should be sought carefully by appropriate techniques if indicated (Table 10).It should
sive patients includes linear measurements of interventricular septal and posterior wall thickness and internal end-diastolic diam-eter.While LVM measurements indexed for body size identify LVH,relative wall thickness or the wall-to-radius ratio (2×posterior wall thickness/end-diastolic diameter)categorizes geometry (con-centric or eccentric).Calculation of LVM is currently performed according to the American Society of Echocardiography formula.159Although the relation between LVM and CV risk is con-tinuous,thresholds of 95g/m 2for women and 115g/m 2(body surface area [BSA])for men are widely used for estimates of clear-cut LVH.159Indexation of LVM for height,in which height to the allo-metric power of 1.7or 2.7has been used,160,161can be considered in overweight and obese patients in order to scale LVM to body size and avoid under-diagnosis of LVH.159It has recently been shown that the optimal method is to scale allometrically by body height to the exponent 1.7(g/m 1.7)and that different cut-offs for men
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itional information and is a prerequisite for the diagnosis of diastolic dysfunction.Left atrial size is best assessed by its indexed volume or LAVi.159LAVi≥34mL/m2has been shown to be an independent predictor of death,heart failure,atrial?brillation and ischaemic stroke.172
Normal ranges and cut-off values for hypertensive heart disease for key echocardiographic parameters are summarized in Table11. The most used scaling for evaluating LVH in hypertension is to divide LVM by BSA,so that the effects on LVM of body size and obesity are largely eliminated.Despite largely derived from control study populations with the obvious possibility for bias,these para-meters recommended by the American Society of Echocardiography and the European Association of Echocardiography are used in the majority of laboratories for echocardiography.Data from large general populations in different ethnicities will be available soon. To assess subclinical systolic dysfunction,speckle tracking echo-cardiography can quantify longitudinal contractile function(longitu-dinal strain)and help to unmask early subclinical systolic dysfunction of newly diagnosed hypertensive patients without LVH.173,174However,assessment of LV systolic function in hyperten-sive heart disease does not add prognostic information to LVM,at least in the context of a normal EF.the initial evaluation.However,a wider or more restricted
use will depend on availability and cost.
3.7.1.3Cardiac magnetic resonance imaging
Cardiac magnetic resonance imaging(MRI)should be considered for assessment of LV size and mass when echocardiography is technically
not feasible and when imaging of delayed enhancement would have therapeutic consequences.175,176
3.7.1.4Myocardial ischaemia
Speci?c procedures are reserved for diagnosis of myocardial is-chaemia in hypertensive patients with LVH.177This is particular-
ly challenging because hypertension lowers the speci?city of exercise electrocardiography and perfusion scintigraphy.178An exercise test,demonstrating a normal aerobic capacity and without signi?cant ECG changes,has an acceptable negative pre-
dictive value in patients without strong symptoms indicative of obstructive CHD.When the exercise ECG is positive or unin-terpretable/ambiguous,an imaging test of inducible ischaemia,
such as stress cardiac MRI,perfusion scintigraphy,or stress echocardiography is warranted for a reliable identi?cation of myocardial ischaemia.178–180Stress-induced wall motion abnor-malities are highly speci?c for angiographically assessed
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sion abnormalities are frequently found with angiographically normal coronary arteries associated with LVH and/or coronary microvascular disease.177The use of dual echocardiographic imaging of regional wall motion and transthoracic,Doppler-derived coronary?ow reserve on the left anterior descending artery has recently been suggested to distinguish obstructive CHD(reduced coronary reserve plus inducible wall motion abnormalities)from isolated coronary microcirculatory damage(reduced coronary reserve without wall motion abnormalities).180A coronary?ow reserve≤1.91has been shown to have an independent prognostic value in hypertension.181,182
3.7.2Blood vessels
3.7.2.1Carotid arteries
Ultrasound examination of the carotid arteries with measurement of intima media thickness(IMT)and/or the presence of plaques has been shown to predict the occurrence of both stroke and myocardial infarction,independently of traditional CV risk factors.51,183–186This holds true,both for the IMT value at the carotid bifurcations(re?ect-ing primarily atherosclerosis)and for the IMT value at the level of the common carotid artery(re?ecting primarily vascular hypertrophy). The relationship between carotid IMT and CV events is a continuous one and determining a threshold for high CV risk is rather arbitrary. Although a carotid IMT.0.9mm has been taken as a conservative estimate of existingabnormalities in the2007Guidelines,2the thresh-old value for high CV risk was higher in the elderly patients of the Car-diovascular Health Study and in the middle-aged patients of the European Lacidipine Study on Atherosclerosis(ELSA)study(1.06 and1.16mm,respectively).184,186Presence of a plaque can be iden-ti?ed by an IMT≥1.5mm or by a focal increase in thickness of0.5mm or50%of the surrounding carotid IMT value.187Although plaque has a strong independent predictive value for CV events,51,183–185,188 presence of a plaque and increased carotid IMT added little to each other for predicting CV events and re-classifying patients into another risk category in the Atherosclerosis Risk In Commu-nities(ARIC)study.185A recent systematic review concluded that the added predictive value of additional carotid screening may be primarily found in asymptomatic individuals at intermediate CV risk.189
3.7.2.2Pulse wave velocity
Large artery stiffening and the wave-re?ection phenomenon have been identi?ed as being the most important pathophysiological determinants of ISH and pulse pressure increase with ageing.190 Carotid-femoral PWV is the‘gold standard’for measuring aortic stiff-ness.138Although the relationship between aortic stiffness and events is continuous,a threshold of.12m/s has been suggested by the2007ESH/ESC Guidelines as a conservative estimate of signi?-cant alterations of aortic function in middle-aged hypertensive patients.2A recent expert consensus statement adjusted this thresh-old value to10m/s,191by using the direct carotid-to-femoral distance and taking into account the20%shorter true anatomical distance travelled by the pressure wave(i.e.0.8×12m/s or10m/s).Aortic stiffness has independent predictive value for fatal and non-fatal CV events in hypertensive patients.192,193The additive value of PWV mingham risk score,has been quanti?ed in a number of studies.51,52,194,195In addition,a substantial proportion of patients
at intermediate risk could be reclassi?ed into a higher or lower CV
risk,when arterial stiffness is measured.51,195,196
3.7.2.3Ankle–brachial index
Ankle–brachial index(ABI)can be measured either with automated devices,or with a continuous-wave Doppler unit and a BP sphygmo-manometer.A low ABI(i.e.,0.9)signals PAD and,in general, advanced atherosclerosis,197has predictive value for CV events,198and was associated with approximately twice the
10-year CV mortality and major coronary event rate,compared
with the overall rate in each Framingham category.198Furthermore,
even asymptomatic PAD,as detected by a low ABI,has prospective-
ly been found to be associated in men with an incidence of CV
morbid and fatal events approaching20%in10years.198,199 However,ABI is more useful for detecting PAD in individuals with
a high likelihood of PAD.
3.7.2.4Other methods
Although measurements of carotid IMT,aortic stiffness or ABI
are reasonable for detecting hypertensive patients at high CV
risk,several other methods,used in the research setting for detecting vascular OD,cannot be supported for clinical use.
An increase in the wall–lumen ratio of small arteries can be measured in subcutaneous tissues obtained through gluteal biopsies.
These measurements can demonstrate early alterations in diabetes
and hypertension and have a predictive value for CV morbidity and mortality,199–202but the invasiveness of the method makes this ap-
proach unsuitable for general use.Increase in coronary calcium,as
quanti?ed by high-resolution cardiac computed tomography,has
also been prospectively validated as a predictor of CVD and is highly effective in re-stratifying asymptomatic adults into either a moderate
or a high CVD risk group,203,204but the limited availability and high
cost of the necessary instrumentations present serious problems. Endothelial dysfunction predicts outcome in patients with a variety
of CVDs,205although data on hypertension are still rather scant.206 Furthermore,the techniques available for investigating endothelial re-sponsiveness to various stimuli are laborious,time consuming and
often invasive.
3.7.3Kidney
The diagnosis of hypertension-induced renal damage is based on
the?nding of a reduced renal function and/or the detection of elevated urinary excretion of albumin.207Once detected,CKD
is classi?ed according to estimated glomerular?ltration rate (eGFR),calculated by the abbreviated‘modi?cation of diet in
renal disease’(MDRD)formula,208the Cockcroft-Gault formula
or,more recently,through the Chronic Kidney Disease EPIdemi-
ology Collaboration(CKD-EPI)formula,209which require age, gender,ethnicity and serum creatinine.When eGFR is below
60mL/min/1.73m2,three different stages of CKD are recognized:
stage3with values between30–60mL/min/1.73m2;and stages4
and5with values below30and15mL/min/1.73m2,respective-
ly.210These formulae help to detect mild impairment of renal
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range.211A reduction in renal function and an increase in CV risk can be inferred from the?nding of increased serum levels of cystatin C.212A slight increase(up to20%)in serum creatinine may sometimes occur when antihypertensive therapy—particular-ly by renin-angiotensin system(RAS)blockers—is instituted or in-tensi?ed but this should not be taken as a sign of progressive renal deterioration.Hyperuricaemia is frequently seen in untreat-ed hypertensive patients(particularly in pre-eclampsia)and has been shown to correlate with a reduced renal blood?ow and nephrosclerosis.213
While an elevated serum creatinine concentration or a low eGFR point to diminished renal function,the?nding of an increased rate of urinary albumin or protein excretion points,in general,to a de-rangement in glomerular?ltration barrier.Microalbuminuria has been shown to predict the development of overt diabetic nephro-pathy in both type1and type2diabetic patients,214while the pres-ence of overt proteinuria generally indicates the existence of established renal parenchymatous disease.215In both diabetic and non-diabetic hypertensive patients,microalbuminuria,even below the threshold values usually considered,216has been shown to predict CV events,217–225and continuous relationships between CV,as well as non-CV mortality and urinary albumin/creatinine ratios.3.9mg/g in men and.7.5mg/g in women,have been reported in several studies.224,226Both in the general population and in diabetic patients,the concomitance of an increased urinary protein excretion and a reduced eGFR indicates a greater risk of CV and renal events than either abnormality alone,making these risk factors independent and cumulative.227,228An arbitrary thresh-old for the de?nition of microalbuminuria has been established as 30mg/g of creatinine.228
In conclusion,the?nding of an impaired renal function in a hypertensive patient,expressed as any of the abnormalities mentioned above,constitutes a very potent and frequent pre-dictor of future CV events and death.218,229–233Therefore it is recommended,in all hypertensive patients,that eGFR be esti-mated and that a test for microalbuminuria be made on a spot urine sample.
3.7.4Fundoscopy
The traditional classi?cation system of hypertensive retinopathy by fundoscopy is based on the pioneering work by Keith, Wagener and Barker in1939and its prognostic signi?cance has been documented in hypertensive patients.234Grade III (retinal haemorrhages,microaneurysms,hard exudates,cotton wool spots)and grade IV retinopathy(grade III signs and papil-loedema and/or macular oedema)are indicative of severe hypertensive retinopathy,with a high predictive value for mor-tality.234,235Grade I(arteriolar narrowing either focal or general in nature)and grade II(arteriovenous nicking)point to early stage of hypertensive retinopathy and the predictive value of CV mortality is controversially reported and,overall, less stringent.236,237Most of these analyses have been done by retinal photography with interpretation by ophthalmologists, which is more sensitive than direct ophthalmoscopy/fundoscopy cibility of grade I and grade II retinopathy has been raised,since
even experienced investigators displayed high inter-observer and
intra-observer variability(in contrast to advanced hypertensive retinopathy).239,240
The relationship of retinal vessel calibre to future stroke
events has been analysed in a systematic review and individual participant meta-analysis:wider retinal venular calibre predicted stroke,whereas the calibre of retinal arterioles was not asso-
ciated with stroke.241Retinal arteriolar and venular narrowing, similarly to capillary rarefaction in other vascular beds,242,243
may be an early structural abnormality of hypertension but its additive value to identify patients at risk for other types of
OD needs to be de?ned.243–244The arteriovenous ratio of
retinal arterioles and venules predicted incident stroke and
CV morbidity,but criticism that concomitant changes of the
venule diameters may affect this ratio and the methodology (digitized photographs,need of core reading centre)prohibited
its widespread clinical use.245–248New technologies to assess
the wall–lumen ratio of retinal arterioles that directly measure the vascular remodelling in early and later stages of hypertensive disease are currently being investigated.249
3.7.5Brain
Hypertension,beyond its well-known effect on the occurrence of
clinical stroke,is also associated with the risk of asymptomatic
brain damage noticed on cerebral MRI,in particular in elderly individuals.250,251The most common types of brain lesions are
white matter hyperintensities,which can be seen in almost all
elderly individuals with hypertension250–although with variable severity–and silent infarcts,the large majority of which are
small and deep(lacunar infarctions)and the frequency of
which varies between10%and30%.252Another type of lesion,
more recently identi?ed,are microbleeds,seen in about5%of individuals.White matter hyperintensities and silent infarcts are associated with an increased risk of stroke,cognitive decline and dementia.250,252–254In hypertensive patients without overt CVD,
MRI showed that silent cerebrovascular lesions are even more prevalent(44%)than cardiac(21%)and renal(26%)subclinical damage and do frequently occur in the absence of other signs of
organ damage.255Availability and cost considerations do not
allow the widespread use of MRI in the evaluation of elderly hypertensives,but white matter hyperintensity and silent brain infarcts should be sought in all hypertensive patients with neural disturbance and,in particular,memory loss.255–257As cognitive dis-turbances in the elderly are,at least in part,hypertension related,258,259suitable cognitive evaluation tests may be used in
the clinical assessment of the elderly hypertensive patient.
3.7.6Clinical value and limitations
Table12summarizes the CV predictive value,availability,reproduci-
bility and cost-effectiveness of procedures for detection of OD.The recommended strategies for the search for OD are summarized in
the Table.
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3.7.7Summary of recommendations on the search for asymptomatic organ damage,cardiovascular disease,and chronic kidney disease
See ‘Search for asymptomatic organ damage,cardiovascular disease,and chronic kidney disease’on page 21.
3.8Searching for secondary forms of hypertension
A speci?c,potentiallyreversiblecauseofBPelevationcanbeidenti?edin a relatively small proportion of adult patients with hypertension.However,because of the overall high prevalence of hypertension,sec-ondary forms can affect millions of patients worldwide.If appropriately diagnosed and treated,patients with a secondary form of hypertension might be cured,or at least show an improvement in BP control and a re-duction of CV risk.Consequently,as a wise precaution,all patients should undergo simple screening for secondary forms of hypertension.This screening can be based on clinical history,physical examination and routine laboratory investigations (Tables 9,10,13).Furthermore,a sec-ondaryformofhypertensioncanbeindicatedbyasevereelevationinBP,sudden onset or worsening of hypertension,poor BP response to drug therapyand OD disproportionate to the duration of hypertension.If the basal work-up leads to the suspicion that the patient is suffering from a secondary form of hypertension,speci?c diagnostic procedures may become necessary,as outlined in Table 13.Diagnostics of secondary forms of hypertension,especially in cases with a suspicion of endocrine hypertension,should preferably be performed in referral centres.
4Treatment approach
4.1Evidence favouring therapeutic reduction of high blood pressure
Evidence favouring the administration of BP-lowering drugs to reduce the risk of major clinical CV outcomes (fatal and non-fatal
stroke,myocardial infarction,heart failure and other CV deaths)in hypertensive individuals results from a number of RCTs—mostly placebo-controlled—carried out between 1965and 1995.Their meta-analysis 260was referred to in the 2003edition of ESH/ESC Guidelines.1Supportive evidence also comes from ?nding that a BP-induced regression of OD,such as LVH and urinary protein excre-tion,may be accompanied by a reduction of fatal and non-fatal out-comes,261,262although this evidence is obviously indirect,being derived from post-hoc correlative analyses of randomized data.
Randomizedtrials based onhard clinicalCVoutcomes do,however,alsohave limitations,which have beenconsidered inprevious ESH/ESC Guidelines:2(i)to limit thenumberofpatients needed,trials commonly enrol high-risk patients (old age,concomitant or previous disease)and (ii)for practical reasons,the duration of controlled trials is necessarily short (in best cases between 3and 6years,with an average time to an endpoint of only half of this)—so that recommendations for life-long intervention are based on considerable extrapolation from data obtained over periods much shorter than the life expectancy of most patients.Support for the belief that the bene?ts measured during the ?rst few years will continue over a much longer term comes from observational studies of a few decades duration.263
The recommendations that now follow are based on available evi-dence from randomized trials and focus on important issues for medical practice:(i)when drug therapy should be initiated,(ii)the target BP to be achieved by treatment in hypertensive patients at dif-ferent CV risk levels,and (iii)therapeutic strategies and choice of drugs in hypertensive patients with different clinical characteristics.
4.2When to initiate antihypertensive drug treatment
4.2.1Recommendations of previous Guidelines
The 2007ESH/ESC Guidelines,2like many other scienti?c guide-lines,54,55,264recommended the use of antihypertensive drugs in
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自然辩证法复习题及答案 一、填空题 1、科学的三种类别。3′ 自然科学，社会科学，人文科学 2、科学技术的三种哲学反思。3′ 对科学进行辩护-捍卫科学；对科学进行批判-质疑科学；对科学进行审度-必要的转换 3、《自然辩证法》的学科内容和知识体系。4′ （1）自然观是人们对自然界的总体看法。它是从整体上研究自然界的本质及其发展规律的根本观点。 （2）科学技术观是人们对科学技术的总体看法。它是从整体上概括科学技术及其发展规律的根本观点。 （3）科学技术方法论是人们对科学技术所运用的认识和实践方法的哲学概括。它是关于科学技术研究中常用的一般方法的规律性理论。 （4）科学技术社会论是人们对科学技术的哲学反思。它是关于科学技术性质、作用（正、负）及其发展规律以及科学技术与社会的关系的总观点。 4、《自然辩证法》的学科由来和学科性质。2′ （1）由来：自然辩证法的历史源远流长，其萌芽形态可以上溯到古希腊的自然哲学，但作为一门独立学科则是由马克思和恩格斯在19世纪下半叶共同创立的。自然辩证法是近代自然科学的历史发展及其基本成就的科学总结，特别是十九世纪中后期自然科学最新发展和最新成就的科学总结，同时也是恩格斯本人多年刻苦学习和精心研究自然科学的科学总结。有关《自然辩证法》的材料是恩格斯1873─1886年这一时期写成的。整部著作没有写完，并且在恩格斯生前没有发表过。 （2）性质：自然科学、社会科学和思维科学相交叉的哲学性质的马克思主义理论学科 5、马克思主义自然观的三种类型。3′ 系统层次观，进化历史观，持续发展观 6、系统的基本特点。4′
整体性；层次性；有序性；动态性 7、“可持续发展”的概念。 既满足当代人的需求，又不对后代人满足其自身需求的能力构成危害的发展。 8、科学和技术的本质特征。2′ 科学：人对自然的理论关系、一般生产力。 技术：人对自然的实践关系、直接生产力。 9、四大产业体系的分类。4′ （1）第一产业体系（农、林、牧、畜、渔）； （2）第二产业体系（制造、采掘、建筑、运输）； （3）第三产业体系（通信、商业、金融、医疗、饮食、公共服务）； （4）第四产业体系（科学、文化、教育、咨询） 10、科学的五大解释。5′ （1）知识体系：发展着的认识 （2）认识活动：科学研究活动 （3）社会建制：科学家共同体 （4）思维方式：科学方法 （5）精神气质：科学精神 11、作为知识体系的科学的内容。4′ 科学事实、科学定律、科学假说、科学理论 12、科研选题的四个原则。4′ 需要性原则，创造性原则，科学性原则，可行性原则 13、获取科学事实的主要方法。2′ 科学观察方法；科学实验方法 14、科学实验的主要方法。4′ （1）纯化和简化研究对象（减法实验）：与隔离有关。 （2）强化和激化研究对象（加法实验）。 （3）再现和重演自然过程（过程模拟实验，乘法实验1）。 （4）替代物理过程和数学关系（结构模拟实验，乘法实验2） 15、整理科学事实的主要方法。4′
晋灵公不君（宣公二年） 原文： 晋灵公不君。厚敛以雕墙。从台上弹人，而观其辟丸也。宰夫胹熊蹯不熟，杀之，寘诸畚，使妇人载以过朝。赵盾、士季见其手，问其故而患之。将谏，士季曰：“谏而不入，则莫之继也。会请先，不入，则子继之。”三进及溜，而后视之，曰：“吾知所过矣，将改之。”稽首而对曰：“人谁无过？过而能改，善莫大焉。诗曰：‘靡不有初，鲜克有终。’夫如是，则能补过者鲜矣。君能有终，则社稷之固也，岂惟群臣赖之。又曰：‘衮职有阙，惟仲山甫补之。’能补过也。君能补过，衮不废矣。” 犹不改。宣子骤谏，公患之，使鉏麑贼之。晨往，寝门辟矣，盛服将朝。尚早，坐而假寐。麑退，叹而言曰：“不忘恭敬，民之主也。贼民之主，不忠；弃君之命，不信。有一于此，不如死也！”触槐而死。 秋九月，晋侯饮赵盾酒，伏甲将攻之。其右提弥明知之，趋登曰：“臣侍君宴，过三爵，非礼也。”遂扶以下。公嗾夫獒焉。明搏而杀之。盾曰：“弃人用犬，虽猛何为！”斗且出。提弥明死之。 初，宣子田于首山，舍于翳桑。见灵辄饿，问其病。曰：“不食三日矣！”食之，舍其半。问之，曰：“宦三年矣，未知母之存否。今近焉，请以遗之。”使尽之，而为之箪食与肉，寘诸橐以与之。既而与为公介，倒戟以御公徒，而免之。问何故，对曰：“翳桑之饿人也。”问其名居，不告而退。——遂自亡也。 乙丑，赵穿①攻灵公于桃园。宣子未出山而复。大史书曰：“赵盾弑其君。”以示于朝。宣子曰：“不然。”对曰：“子为正卿，亡不越竟，反不讨贼，非子而谁？”宣子曰：“呜呼!‘我之怀矣，自诒伊戚。’其我之谓矣。” 孔子曰：“董狐，古之良史也，书法不隐。赵宣子，古之良大夫也，为法受恶。惜也，越竞乃免。” 译文： 晋灵公不行君王之道。他向人民收取沉重的税赋以雕饰宫墙。他从高台上用弹弓弹人，然后观赏他们躲避弹丸的样子。他的厨子做熊掌，没有炖熟，晋灵公就把他杀了，把他的尸体装在草筐中，让宫女用车载着经过朝廷。赵盾和士季看到露出来的手臂，询问原由后感到很忧虑。他们准备向晋灵公进谏，士季说：“如果您去进谏而君王不听，那就没有人能够再接着进谏了。还请让我先来吧，不行的话，您再接着来。”士季往前走了三回，行了三回礼，一直到屋檐下，晋灵公才抬头看他。晋灵公说：“我知道我的过错了，我会改过的。”士季叩头回答道：“谁能没有过错呢？有过错而能改掉，这就是最大的善事了。《诗经》说：‘没有人向善没有一个开始的，但却很少有坚持到底的。’如果是这样，那么能弥补过失的人是很少的。您如能坚持向善，那么江山就稳固了，不只是大臣们有所依靠啊。
自然辩证法 1.自然辩证法的性质、内容与方法 性质：自然辩证法是马克思主义的重要组成部分。 它的研究对象与研究范围：自然界-科学-技术-社会。 主要内容：自然观-科学观-技术观-科学技术与社会 研究方法： （1）科学问题的提出 （2）（2）科学事实的获取—观察与实验 （3）科学假说的形成 （4）科学理论的创立 科学思维方法—非演绎方法 ①分析与综合②归纳与概括③类比与联想④思想模型 2.近代唯物主义自然观的特点 (1)直观性：从某种有形的、直观的东西去寻求自然现象多样性的统一。用猜测和想象去说明自然现象； （2）辩证性：把自然界看成一幅由种种联系和过程交织起来的画面。 3.系统自然观、生态自然观的基本思想 系统自然观的基本思想 （1）自然界是一个系统.系统是由若干具有特定属性的组成元素经过特定联系而构成的、与周围环境相互联系的、具有特定的结构和功能的整体. （2）系统整体与部分的关系 系统的整体与部分之间的关系可以概括为两个方面： ①整体与部分相互依赖.整体是由部分组成的,整体不能脱离部分而独立存在. ②整体不等于部分之和.其具体表现在：整体大于部分之和（即所谓“三个臭皮匠,赛过一个诸葛亮”）；整体小于部分之和（即所谓“一个和尚挑水喝,两个和尚抬水喝,三个和尚没水喝”）. 生态自然观的基本思想 1）自然界是人类生存与发展的前提和基础,人是自然界发展的产物,人是自然界的一部分,人类的生存与发展依赖于自然界. 2）自然环境创造人,人也创造环境.人类的创造必须把改造自然与美化自然有机地结合起来,这样才是合乎人性的行为. 3）人要与自然和谐相处,自然环境与社会环境相统一.人要按自然规律办事,自然才会朝着有利于人类社会的方向发展否则,人类就会遭到自然的报复. 4）改革不合理的社会制度,是实现人与自然协调发展的重要途径,只有在共产主义社会才能真正实现人与自然的和谐统一.马克思主义关于“自然主义、人道主义、共产主义”相统一的生态思想揭示了生态自然观的本质. 5）可持续发展是既满足当代人的需要,又不对后代人满足其需要的能力构成危害的发展.它具有整体性、公平性和正义性等特点.人类是一个整体,可持续发展要求超越不同国家的文化和意识形态的差异,并采取联合的共同行动.生态文明所
1、 Blindness is a very serious disability. 失明是非常严重的残疾。 2、 Though he is disabled, he is a gifted artist. 尽管身残疾 (的 )，他是一个有天赋的艺术家。 3、 person with a hearing and eyesight disability misses many things. 一位听力和视力残疾的人会错过很多东西。 4、 Beware of the love syndrome.当心恋爱综合症。 5、 Rosalyn had been there frequently in past years for treatment for infantile paralysis. 罗莎琳在过去的几年中频频来这里治疗小儿麻痹。 6、 Harris went on top in the last lap. 哈里斯在最后一圈跑到了最前面。 7、 He had a high ambition to be a headmaster. 他的抱负是想成为一名校长。 8、 I will love the ambitious for they can inspire me!我爱雄心壮志的人，因为他们能激励我！ 9、 We will have dictation today.我们今天要听写了。 10、 I wrote the letter at Sally's dictation . 我照萨利的口述写信。 11、 The campus is noisy today.今天校园里很吵。 12、 Do believe there is no best man, only much suitable one. 要相信没有最好男人，只有更适合的。 13、 Trees hid the entry of the cave. 洞穴的入口被树丛遮掩。 14、 Fresh air is beneficial to people's health. 新鲜空气对人的健康有好处。 15、 In other words, a classic fudge. 总之一句话，一派胡言。 16、 Mother reproached me for being too clumsy. 母亲责备我笨手笨脚。 17、 He used to be quiet, but now he is very outgoing. 他以前性格沉默少言，但现在很外向。 18、 How do you adapt to this new environment? 你要怎样适应这种新环境呢?。 19、 The bench often does duty for a table. 这条长凳经常当桌子用。 20、 The doctor told me to cut out meat for my fat. 由于肥胖，大夫叫我停止吃肉 21、 He applied his eye to the microscope. 他把眼睛贴近显微镜。 22、 She was out of breath from climbing the stairs. 爬楼梯使她上气不接下气的。 23、 A servant is known by his master's absence.主人不在就可以看出仆人的品行来。 24、 You are a milk-livered fellow!你真是一个胆小的家伙！ 25、 Thank you, my fellow colleagues. 谢谢，同事们。 26、 No joy without annoy. 没有无烦恼之快乐。 27、 I am really very annoyed about it. 我对此事真是很生气。 28、 I felt annoyance at being teased.我恼恨“别人”取笑我。 29、 I let go of all annoyance. 我放下所有烦恼。 30、 He has his faults, but all in all , he is a good guy. 他有缺点，但总的来说，他是不错的人。 单词拼读举例:Di sa bi li ty di sa bled syn drome in fan tile pa ra ly sis am bi tion am bi tious
1.什么是技术创新？它有哪些机制？ 技术创新 技术创新不同于技术发明，它主要是指技术成果在商业上的首次成功应用。技术创新包含技术成果的商业化和产业化，它是技术进步的基本形式。原始创新和集成创新是当前我国科技界和产业界关注的焦点所在，国家创新系统是市场经济架构下企业从事技术创新活动的环境。 技术创新的机制 技术创新的机制分为两个层次：国家层次是指国家创新体系，它主要是从国家竞争力考虑；企业层次主要是指，企业在其内部和外部各种因素的影响下，通过创新建立相应的组织结构，并对社会经济发挥作用的机理和原理，它主要是从企业竞争力考虑。 2.怎样正确地理解人与自然之间的矛盾和关系，谈谈你对中国可持续发展之路 的想法。 （1）人与自然的三重矛盾关系 自然资源和生态环境承载力的有限性与人民日益增长的物质文化需要的矛盾关系；尊重自然的价值与尊重人类发展权利的矛盾关系；技术开发与自然保护的矛盾关系。 （2）人与自然的关系 世界上的任何事物都是矛盾的统一体。我们面对的现实世界，就是由人类社会和自然界双方组成的矛盾统一体，两者之间是辩证统一的关系。一方面，人与自然是相互联系、相互依存、相互渗透的，人类的存在和发展，一刻也离不开自然，必然要通过生产劳动同自然进行物质、能量的交换。与此同时，人与自然之间又是相互对立的。人类为了更好地生存和发展，总是要不断地否定自然界的自然状态，并改变它；而自然界又竭力地否定人，力求恢复到自然状态。人与自然之间这种否定与反否定，改变与反改变的关系，实际上就是作用与反作用的关系，如果对这两种″作用″的关系处理得不好，极易造成人与自然之间失衡。 中国和世界正处在关键的十字路口。随着中国经济的快速发展，资源消耗以及随之产生的废物也大幅度增长，为了取得长期的经济增长，中国必须找到一条可持续发展之路。中国的环境恶化很严重，加上庞大的人口和前所未有的经济发展，这些都对中国走向可持续发展形成了重大障碍。这些都导致中国可持续发展的必然性：（一）人口方面的挑战（二）资源方面的挑战（三）生态环境方面的1、自然生态环境破坏日趋严峻2、自然生态环境污染日趋严峻：（1）水污染严重2)大气污染严重(3)土地污染严重(4)固体废物问题严重(5)噪声污染(6)电磁污染(7)光污染(8)热污染 在我国实施可持续发展必须做好以下几方面工作：首先要改变观念，科学认识自然，掌握自然规律，顺应自然发展，科学地协调、改造自然，善待自然，改变过去那种“先发展，后治理”的老路；其次要珍惜资源，节约资源；最后要唤起公众可持续发展意识，帮助人们树立正确的自然观。 中国走可持续发展道路是中国的必然选择，但这条道路同时是十分艰难的，首先经济实力薄弱是一大障碍，其次实现可持续发展需要科学技术特别是高新科学技术的支持，要达到这一点尚需长期努力，最后是地区发展的不平衡，尤其是西部地区水土流失等生态恶化现象更加严重。虽然有上述不足，但我们同时要看到，只要中国政府坚持发挥主导作用，充分运用科技力量，最广泛地动员公众参与，再加上国际社会的有力支持，随着经济体制改革、增长方式转变和科技进步的支持，中国可持续发展的前景是光明的 3.什么是科学精神？举例说明它的重要性。 科学精神是指从科学研究的过程和成果中所显示出来的科学本身所独有的一种精神气质，以及与之相应的科学思想、科学方法。它是科学价值的核心。科学精神有广泛而深刻的涵义，主要包括以下几个方面内容：
如何翻译古文 学习古代汉语，需要经常把古文译成现代汉语。因为古文今译的过程是加深理解和全面运用古汉语知识解决实际问题的过程，也是综合考察古代汉语水平的过程。学习古代汉语，应该重视古文翻译的训练。 古文翻译的要求一般归纳为信、达、雅三项。“信”是指译文要准确地反映原作的含义，避免曲解原文内容。“达”是指译文应该通顺、晓畅，符合现代汉语语法规范。“信”和“达”是紧密相关的。脱离了“信”而求“达”，不能称为翻译；只求“信”而不顾“达”，也不是好的译文。因此“信”和“达”是文言文翻译的基本要求。“雅”是指译文不仅准确、通顺，而且生动、优美，能再现原作的风格神韵。这是很高的要求，在目前学习阶段，我们只要能做到“信”和“达”就可以了。 做好古文翻译，重要的问题是准确地理解古文，这是翻译的基础。但翻译方法也很重要。这里主要谈谈翻译方法方面的问题。 一、直译和意译 直译和意译是古文今译的两大类型，也是两种不同的今译方法。 1．关于直译。所谓直译，是指紧扣原文，按原文的字词和句子进行对等翻译的今译方法。它要求忠实于原文，一丝不苟，确切表达原意，保持原文的本来面貌。例如： 原文：樊迟请学稼，子曰：“吾不如老农。”请学为圃。子曰：“吾不如老圃。”（《论语?子路》） 译文：樊迟请求学种庄稼。孔子道：“我不如老农民。”又请求学种菜蔬。孔子道：“我不如老菜农。”（杨伯峻《论语译注》） 原文：齐宣王问曰：“汤放桀，武王伐纣，有诸？”（《孟子?梁惠王下》） 译文：齐宣王问道：“商汤流放夏桀，武王讨伐殷纣，真有这回事吗？（杨伯峻《孟子译注》） 上面两段译文紧扣原文，字词落实，句法结构基本上与原文对等，属于直译。 但对直译又不能作简单化理解。由于古今汉语在文字、词汇、语法等方面的差异，今译时对原文作一些适当的调整，是必要的，并不破坏直译。例如： 原文：逐之，三周华不注。（《齐晋鞌之战》） 译文：〔晋军〕追赶齐军，围着华不注山绕了三圈。
自然辩证法题库 1.谈谈你对生态文明社会建设的具体设想 21世纪初是中国社会主义生态文明建设的关键阶段。改革开放以来，中国的社会主义生态文明建设取得了巨大成就，但社会主义生态文明建设的任务依然沉重。基于中国社会主义生态文明建设面临的困境与挑战，中国们必须继续坚持以人为本，以人与自然和谐共存为主线，以经济发展为核心，以提高人民生活质量为根本出发点，以体制创新为突破口，推动整个社会走上生产发展、生活富裕、生态良好的文明发展道路。 一是加强生态教育，提高全民族的生态道德素质。生态道德意识是建设社会主义生态文明的精神依托和道德基础。只有大力培育全民族的生态道德意识，使人们对生态环境的保护转化为自觉的行动，才能解决生态保护的根本问题，才能为社会主义生态文明的发展奠定坚实的基础。因此，建设社会主义生态文明，必须把道德关怀引入到人与自然的关系中，树立起人对于自然的道德义务感，养成良好的“生态德性”。尤其要抓好学校教育的环节，特别要重视青少年生态道德意识的培育和提高，帮助学生树立环境生态观念、环境资源观念、环境道德观念。 二是改革生产方式，做强生态产业。对现行的生产方式进行生态化改造是推进社会主义生态文明建设的重要手段。现阶段发展生态产业的重点，是要建立起资源节约、环境少污染型的国民经济体系，走生态农业、生态工业的发展道路。要下决心关停并转那些能源消耗大、经济效益差、环境污染重的企业。发展生态农业，主要包括绿色农业食品和绿色食品原料，生态林业、草业、花卉业，生态渔业，观光农业，生态畜牧产品，生态农业手工业等方面。为此，要研究开发生态技术，防止土壤肥力退化，进行植物病虫害综合防治，实现生活用能替代和多能互补、废弃地复垦利用和陡坡地退耕还林，发展山地综合开发复合型生态经济、以庭院为主的院落生态经济，以及农村绿色产业和绿色产品，提高农业产业化水平，促进农村生态经济的发展。另外，还要重视生态旅游业和环保产业的发展。 三是实施生态工程，全面推进生态环境的保护和治理。生态工程是社会主义生态文明建设的重要组成部分。结合中国的自然、经济和社会特点，“十五”期间，应重点解决危害人民群众身体健康、社会最为关心的环境问题：一要加强城乡饮用水水源地保护，加强工业废水和城市污水的生态处理，抓好重点流域、区域、海域的污染防治工作；二要抓好退耕还林还草和植树造林工程，特别是北京地区风沙源治理、天然林保护和沿海防护林等生态工程建设；三要防治大中城市空气污染、危险废物污染，防止生态破坏； 四要加快自然保护区、环境优美城市和生态省（市、自治区）的创建工程；五要继续推进计划生育的基本国策，提高全社会的计划生育意识，确保控制人口数量，确保提高人口质量；六要在鼓励使用可再生资源的同时，控制可再生资源的利用率不能超过其再生和自然增长的限度，提倡少用或不用不可再生资源，防止资源骤减，力争全面推进生态环境的保护和治理。 四是完善社会主义生态文明建设的政策体系和法律体系。社会主义生态文明建设不仅需要道德力量的推动，也需要政府和权力机关出台必要的政策、制定相关法律法规来进行硬约束。要建立综合决策制度，用政府的权威保证生态环境免遭破坏。特别是在制定规划、计划及重大经济行为的拟议过程中，充分发挥政府综合决策的作用，把生态环境目标和经济发展目标结合起来、统筹考虑，以从源头上解决对生态的危害问题。要适时出台相关政策，用宏观调控手段引导生态建设的积极性。包括：引导生态型项目开发的扶
鞌之战选自《左传》又名《鞍之战》原文：楚癸酉，师陈于鞌(1)。邴夏御侯，逢丑父为右②。晋解张御克，郑丘缓为右(3)。侯日：“余姑翦灭此而朝食(4)”。不介马而驰之⑤。克伤于矢，流血及屦2 未尽∧6)，曰：“余病矣(7)！”张侯曰：“自始合(8)，而矢贯余手及肘(9)，余折以御，左轮朱殷(10)，岂敢言病吾子忍之！”缓曰：“自始合，苟有险，余必下推车，子岂＿识之(11)然子病矣！”张侯曰：“师之耳目，在吾旗鼓，进退从之。此车一人殿之(12)，可以集事(13)，若之何其以病败君之大事也擐甲执兵(14)，固即死也(15)；病未及死，吾子勉之(16)！”左并辔(17) ，右援拐鼓(18)。马逸不能止(19)，师从之，师败绩。逐之，三周华不注(20) 韩厥梦子舆谓己曰：“旦辟左右！”故中御而从齐侯。邴夏曰：“射其御者，君子也。”公曰：“谓之君子而射之，非礼也。”射其左，越于车下；射其右，毙于车中。綦毋张丧车，从韩厥，曰：“请寓乘。”从左右，皆肘之，使立于后。韩厥俛，定其右。逢丑父与公易位。将及华泉，骖絓于木而止。丑父寝于轏中，蛇出于其下，以肱击之，伤而匿之，故不能推车而及。韩厥执絷马前，再拜稽首，奉觞加璧以进，曰：“寡君使群臣为鲁、卫请，曰：‘无令舆师陷入君地。’下臣不幸，属当戎行，无所逃隐。且惧奔辟而忝两君，臣辱戎士，敢告不敏，摄官承乏。” 丑父使公下，如华泉取饮。郑周父御佐车，宛茷为右，载齐侯以免。韩厥献丑父，郤献子将戮之。呼曰：“自今无有代其君任患者，有一于此，将为戮乎”郤子曰：“人不难以死免其君，我戮之不祥。赦之，以劝事君者。”乃免之。译文1：在癸酉这天，双方的军队在鞌这个地方摆开了阵势。齐国一方是邴夏为齐侯赶车，逢丑父当车右。晋军一方是解张为主帅郤克赶车，郑丘缓当车右。齐侯说:“我姑且消灭了这些人再吃早饭。”不给马披甲就冲向了晋军。郤克被箭射伤，血流到了鞋上，但是仍不停止擂鼓继续指挥战斗。他说:“我受重伤了。”解张说:“从一开始接战，一只箭就射穿了我的手和肘，左边的车轮都被我的血染成了黑红色，我哪敢说受伤您忍着点吧！”郑丘缓说:“从一开始接战，如果遇到道路不平的地方，我必定（冒着生命危险）下去推车，您难道了解这些吗不过，您真是受重伤了。”daier 解张说:“军队的耳朵和眼睛，都集中在我们的战旗和鼓声，前进后退都要听从它。这辆车上还有一个人镇守住它，战事就可以成功。为什么为了伤痛而败坏国君的大事呢身披盔甲，手执武器，本来就是去走向死亡，伤痛还没到死的地步，您还是尽力而为吧。”一边说，一边用左手把右手的缰绳攥在一起，用空出的右手抓过郤克手中的鼓棰就擂起鼓来。（由于一手控马，）马飞快奔跑而不能停止，晋军队伍跟着指挥车冲上去，把齐军打得打败。晋军随即追赶齐军，三次围绕着华不注山奔跑。韩厥梦见他去世的父亲对他说:“明天早晨作战时要避开战车左边和右边的位置。”因此韩厥就站在中间担任赶车的来追赶齐侯的战车。邴夏说:“射那个赶车的，他是个君子。”齐侯说: “称他为君子却又去射他，这不合于礼。”daier 于是射车左，车左中箭掉下了车。又射右边的，车右也中箭倒在了车里。（晋军的）将军綦毋张损坏了自己的战车，跟在韩厥的车后说: “请允许我搭乗你的战车。”他上车后，无论是站在车的左边，还是站在车的右边，韩厥都用肘推他，让他站在自己身后——战车的中间。韩厥又低下头安定了一下受伤倒在车中的那位自己的车右。于是逢丑父和齐侯（乘韩厥低头之机）互相调换了位置。将要到达华泉时，齐侯战车的骖马被树木绊住而不能继续逃跑而停了下来。（头天晚上）逢丑父睡在栈车里，有一条蛇从他身子底下爬出来，他用小臂去打蛇，小臂受伤，但他（为了能当车右）隐瞒了这件事。由于这样，他不能用臂推车前进，因而被韩厥追上了。韩厥拿着拴马绳走到齐侯的马前，两次下拜并行稽首礼，捧着一杯酒并加上一块玉璧给齐侯送上去，
自然辩证法概论复习题 1、论技术创新：科学技术与经济的有效结合。 科技与经济相结合，就是强调科技发展要与经济发展相结合。“科学技术是第一生产力”是邓小平科技思想的核心，这一论断说明了科学技术决定着生产力发展的方向、规模和速度，要发展生产力就必须依靠科学技术。只有经济发展了，才可能有生产力的飞速发展。因此，科学技术进步和经济发展成为推动生产力发展的两大重要支柱，发展生产力需要科技与经济的有机结合。 自邓小平提出科技与经济结合这一论断开始，中国就在推进结合的过程中不断发展，几十年来也取得了一些成就，但是不能忽视结合的不彻底，以及存在的种种问题。如今，中国发展进入创新驱动的新阶段，科技与经济结合的问题再次成为焦点，要做好这项工作，必须以更符合创新规律的方式来推动。在对结合的认识上，不仅要加深对其重要性的理解，增强全民科技意识，将结合问题看作科技界的问题，也要看作经济界的问题，切实转变经济工作的根本理念，体现创新的重要性。我们更应该明确技术创新的经济属性，从产业链的高端位置入手，获得高价值。此外，现阶段我国的新产品主要应用者不能依赖于国外市场，应该发挥本国市场对自主创新活动的牵引作用，将市场应用作为自主创新实践不可或缺的环节。另外，资本市场对推动科技与经济结合也至关重要。硅谷的成功不仅仅因为有一流的技术，更是因为有一流的技术与资本对接的机制。从中国的现实来看，尽管开办了创业板，但真正对技术创新的支持还远远不够，短期利益导向严重阻碍了科技与经济结合。当前，在政府资金越来越充裕的条件下，应该下大力气引导投资市场关注科技与经济结合，关注创新型企业培育，形成鼓励创新的投资市场。 或者 社会经济对科学技术发展的影响？ 答：A社会的经济需求是科学技术发展的最重要的推动力量； B社会的经济支持是科学技术发展的最重要的物质基础； C社会的经济竞争是科学技术发展的最重要的刺激因素； D经济对科学技术的影响还集中体现在生产的影响上。 技术创新：技术创新是一个从产生新产品或新工艺的设想到市场应用的完整过程，它包括新设想的产生、研究、开发、商业化生产到扩散这样一系列活动，本质上是一个科技、经济一体化过程，是技术进步与应用创新共同作用催生的产物，它包括技术开发和技术应用这两大环节。 技术创新的主要原则： 1、技术上的新颖性或创造性。技术创新特征在技术上的体现就是“新颖”，它是指在一定时期和市场范围内，相对于原有技术的改进或创造。2、经济上的高风险性和高收益性。技术创新是一项充满风险的事业，但这并不妨碍人们去创新，这是因为创新存在极高的回报。3、技术创新的中介性或过渡性。作为科技发展与经济增长中间环节的创新具有中介性，是技术与经济。 2、从生态自然观的产生说明这种自然观是对辩证唯物主义自然观的丰富的发展？ （1）马克思、恩格斯的生态思想是现代生态自然观的直接的理论来源。马克思、恩格斯的生态思想：①自然界是人类生存和发展的前提和基础；②环境创造人，人也创造环境；③自然生产力是社会生产力的基础；④人要与自然和谐一致。⑤改革不合理的社会制度，是实现人与自然协调发展的重要途径。 （2）以生态科学为基础的生态自然观是当代人类对“生态危机”进行反思和对生态科学进行概括与总结的结晶。“生态危机”是指由于人类不合理的活动，在全球规模或局部区域导致生态过程即生态系统的结构和功能的损害、生命维持系统瓦解，从而危害人的利益、威胁人类生存和发展的现象。其表现为：人口激增、自然资源消耗、短缺、环境污染。 （3）生态自然观的基本思想： ①生态系统是生命系统；②生态系统具有显著的整体性；③生态系统是自组织的开放系统； ④生态系统是动态平衡系统；⑤生态系统是稳定性与变化性相统一的平衡。 生态自然观是对马克思、恩格斯生态思想的继承与发展，是在人类反思全球性“生态危机”的过程中和总结现代生态科学的最新思想成果的基础上形成的。 3、根据选题的基本原理，在你的专业上选一个题，并简述选题的过程和注意事项。 所谓科研选题,从狭义上来讲,是指选择和确定所要研究解决的课题,从广义上来说, 它包括确定研究方向和选择研究课题两个方面。研究课题是指科学技术领域中尚未解决的科学问题。—而研究方向是指研究者在一个较长时期内从事研究活动的领域。 选题的过程 (一)课题调研和实际考察。
《鞌之战》阅读答案（附翻译）原文及翻 译 鞌之战[1] 选自《左传成公二年（即公元前589年）》 【原文】 癸酉，师陈于鞌[2]。邴夏御齐侯[3]，逢丑父为右[4]。晋解张御郤克，郑丘缓为右[5]。齐侯曰：余姑翦灭此而朝食[6]。不介马而驰之[7]。郤克伤于矢，流血及屦，未绝鼓音[8]，曰：余病[9]矣！张侯[10]曰：自始合，而矢贯余手及肘[11]，余折以御，左轮朱殷[12]，岂敢言病。吾子[13]忍之！缓曰：自始合，苟有险[14]，余必下推车，子岂识之[15]？然子病矣！张侯曰：师之耳目，在吾旗鼓，进退从之[16]。此车一人殿之[17]，可以集事[18]，若之何其以病败君之大事也[19]？擐甲执兵，固即死也[20]。病未及死，吾子勉之[21]！左并辔[22]，右援枹而鼓[23]，马逸不能止[24]，师从之。齐师败绩[25]。逐之，三周华不注[26]。 【注释】 [1]鞌之战：春秋时期的著名战役之一。战争的实质是齐、晋争霸。由于齐侯骄傲轻敌，而晋军同仇敌忾、士气旺盛，战役以齐败晋胜而告终。鞌：通鞍，齐国地名，在今山东济南西北。 [2]癸酉：成公二年的六月十七日。师，指齐晋两国军队。陈，
列阵，摆开阵势。 [3]邴夏：齐国大夫。御，动词，驾车。御齐侯，给齐侯驾车。齐侯，齐国国君，指齐顷公。 [4]逢丑父：齐国大夫。右：车右。 [5]解张、郑丘缓：都是晋臣，郑丘是复姓。郤（x ）克，晋国大夫，是这次战争中晋军的主帅。又称郤献子、郤子等。 [6]姑：副词，姑且。翦灭：消灭，灭掉。朝食：早饭。这里是吃早饭的意思。这句话是成语灭此朝食的出处。 [7]不介马：不给马披甲。介：甲。这里用作动词，披甲。驰之：驱马追击敌人。之：代词，指晋军。 [8] 未绝鼓音：鼓声不断。古代车战，主帅居中，亲掌旗鼓，指挥军队。兵以鼓进，击鼓是进军的号令。 [9] 病：负伤。 [10]张侯，即解张。张是字，侯是名，人名、字连用，先字后名。 [11]合：交战。贯：穿。肘：胳膊。 [12]朱：大红色。殷：深红色、黑红色。 [13]吾子：您，尊敬。比说子更亲切。 [14]苟：连词，表示假设。险：险阻，指难走的路。 [15]识：知道。之，代词，代苟有险，余必下推车这件事，可不译。 [16]师之耳目：军队的耳、目（指注意力）。在吾旗鼓：在我们
1、什么是自然辩证法？你认为学习自然辩证法有什么意义？ 2、如何理解自然界的辩证运动？ 3、试述辩证唯物主义自然观的基本内容？ 4、系统自然观的主要内容是什么？举例说明学习系统自然观的意义？ 5、生态自然观的基本观点是什么？依据生态自然观的基本观点如何认识人与自然的关系？ 6、试述现代科学的本质与特征？ 7、科学研究的一般环节是什么？学习科学研究方法对你的研究工作有什么指导意义？ 8、试述技术的本质、特征与发展的动力什么？ 9、试述工程、产业的本质与特征？ 10、你如何理解科学技术是一把双刃剑？ 11、如何理解创新型国家建设？ 12、根据创新型人才的素质特点并结合个人专业谈谈如何才能成为创新型人才？ 1.什么是自然辩证法？你认为学习自然辩证法有什么意义？ 1、自然辩证法是马克思主义学说的一个分支，是马克思主义学说的组成部分，自然辩证法也是关于自然界辩证运动的整体认识。 2、自然辩证法强调的是对自然界总的认识而不是对细节的认识，所谓的自然界是广义的自然界，包括天然自然和人化自然（被科学所认识的自然）、人工自然（被技术改造的自然）、社会自然（被产业产出的自然）。自然界的辩证运动包括天然自然转化为人化自然地运动、天然自然（包括人化自然）转化为人工自然的运动、人工自然向社会自然的转化运动。 3、在转化过程中对科学、技术、工程、产业有了认识即科学指把天然自然转化成人化自然的手段；技术指把天然自然（包括人化自然）转化成人工自然的手段；工程指把天然自然（包括人化自然）转化成人工自然的另一种手段；产业指把人工自然转化成社会自然的手段。 学习自然辩证法的意义： ①学习自然辨证法对人的全面发展起到了很重要的作用。拓展了分析问题的视角，让我从以前的单面思 考问题转变成有了总观全局的意识。 ②有助于培养研究生的创新精神和创新能力； ③有助于培养研究生的科学素养和科学态度； ④有助于提高研究生的马克思主义理论水平； ⑤有助于研究生树立科学发展观 如何理解自然界的辩证运动？ 3个 试述辩证唯物主义自然观的基本内容？ 辩证唯物主义自然观分为运动自然观、系统自然观和生态自然观。 1、运动自然观的内容有以下3点： 自然界存在辩证运动，自然界指广义的自然界包括三大运动：天然自然向人化自然的转化，天然自然（包括人化自然）向人工自然的转化，人工自然向社会自然的转化。辩证运动是多维的。 自然界不仅是事物集合体也是过程集合体。要从天然自然向人化自然的转化中理解科学，从天然自然（包括人化自然）向人工自然转化中理解技术工程，从人工自然向社会自然转化中理解产业。 任何变化都在一定的社会制度下进行。共产主义建立在人工自然和天然自然统一的基础上，共产主义等于人道主义也等于自然主义。 2、系统自然观的内容: 1）自然界本身是一个系统。系统是由若干具有特定属性的组成元素经过特定联系而构成的、与周围环境相互联系的、具有特定的结构和功能的整体。系统与外界之间有物质、能量和信息的交流。 2）系统整体与部分的关系 系统的整体与部分之间的关系可以概括为两个方面：
《鞌之战》阅读答案（附翻译） 《鞌之战》阅读答案（附翻译） 鞌之战[1] 选自《左传·成公二年（即公元前589年）》 【原文】 癸酉，师陈于鞌[2]。邴夏御齐侯[3]，逢丑父为右[4]。晋解张御郤克，郑丘缓为右[5]。齐侯曰：“余姑 翦灭此而朝食[6]。”不介马而驰之[7]。郤克伤于矢， 流血及屦，未绝鼓音[8]，曰：“余病[9]矣！”张侯[10]曰：“自始合，而矢贯余手及肘[11]，余折以御，左轮 朱殷[12]，岂敢言病。吾子[13]忍之！”缓曰：“自始合，苟有险[14]，余必下推车，子岂识之[15]？——然 子病矣！”张侯曰：“师之耳目，在吾旗鼓，进退从之[16]。此车一人殿之[17]，可以集事[18]，若之何其以 病败君之大事也[19]？擐甲执兵，固即死也[20]。病未 及死，吾子勉之[21]！”左并辔[22]，右援枹而鼓[23]，马逸不能止[24]，师从之。齐师败绩[25]。逐之，三周 华不注[26]。 【注释】 [1]鞌之战：春秋时期的著名战役之一。战争的实质是齐、晋争霸。由于齐侯骄傲轻敌，而晋军同仇敌忾、 士气旺盛，战役以齐败晋胜而告终。鞌：通“鞍”，齐
国地名，在今山东济南西北。 [2]癸酉：成公二年的六月十七日。师，指齐晋两国军队。陈，列阵，摆开阵势。 [3]邴夏：齐国大夫。御，动词，驾车。御齐侯，给齐侯驾车。齐侯，齐国国君，指齐顷公。 [4]逢丑父：齐国大夫。右：车右。 [5]解张、郑丘缓：都是晋臣，“郑丘”是复姓。郤（xì）克，晋国大夫，是这次战争中晋军的主帅。又称郤献子、郤子等。 [6]姑：副词，姑且。翦灭：消灭，灭掉。朝食：早饭。这里是“吃早饭”的意思。这句话是成语“灭此朝食”的出处。 [7]不介马：不给马披甲。介：甲。这里用作动词，披甲。驰之：驱马追击敌人。之：代词，指晋军。 [8]未绝鼓音：鼓声不断。古代车战，主帅居中，亲掌旗鼓，指挥军队。“兵以鼓进”，击鼓是进军的号令。 [9]病：负伤。 [10]张侯，即解张。“张”是字，“侯”是名，人名、字连用，先字后名。 [11]合：交战。贯：穿。肘：胳膊。 [12]朱：大红色。殷：深红色、黑红色。 [13]吾子：您，尊敬。比说“子”更亲切。
1 DDT案例简介 二次世界大战期间，DDT的使用范围迅速得到了扩大，而且在疟疾、痢疾等疾病的治疗方面大显身手，救治了很多生命，而且还带来了农作物的增产。 但在上个世纪60年代科学家们发现滴滴涕在环境中非常难降解，并可在动物脂肪内蓄积，甚至在南极企鹅的血液中也检测出滴滴涕，鸟类体内含滴滴涕会导致产软壳蛋而不能孵化，尤其是处于食物链顶极的食肉鸟如美国国鸟白头海雕几乎因此而灭绝。1962年，美国科学家蕾切尔·卡逊（Rachel Carson）在其著作《寂静的春天》中怀疑，DDT进入食物链，是导致一些食肉和食鱼的鸟接近灭绝的主要原因。因此从70年代后滴滴涕逐渐被世界各国明令禁止生产和使用。滴滴涕还成为中国环境保护事业的催生婆。DDT的有毒人造有机物是一种易溶于人体脂肪，并能在其中长期积累的污染物。DDT已被证实会扰乱生物的荷尔蒙分泌，2001年的《流行病学》杂志提到，科学家通过抽查24名16到28岁墨西哥男子的血样，首次证实了人体内DDT水平升高会导致精子数目减少。除此以外，新生儿的早产和初生时体重的增加也和DDT有某种联系，已有的医学研究还表明了它对人类的肝脏功能和形态有影响，并有明显的致癌性能。 由于具有较低的急毒性和较长的持久性，也降低了有机氯杀虫剂的使用次数。然而，却也因此使此类的杀虫剂具有较长的持久性，长期累积下来造，成了生态环境的许多问题。 2 案例分析 历史上，DDT的使用，不仅能很好地治疗疟疾、痢疾等疾病，而且还能极大地提高农作物单位面积的产量。DDT的使用极大地促进了农业的发展，人类在自然面前取得了成功，但是自然反过来又开始报复人类，随着DDT进入生态链，它对人类的健康和生态系统造成严重破坏。类似DDT使用的现代生产活动从根本上改变了原始的自然生态环境系统，引起了人与自然的尖锐对立，时今至日，才认识到人既不是自然的奴隶也不是自然的主人，二是共存共荣的合作伙伴关系。人与自然的关系应该进入一个崭新的阶段——协调发展阶段。 首先，人类应该牢固树立人与自然是相互依存的有机统一体的观念。这是因为，人类为了生存和发展，不可避免地要与自然界进行物质和信息的交换，而这种交换又势必带来自然平衡的改变。人类使用DDT，就是为了从自然界得到更多的农作物，促进农业的发展，当初就是为了追求这种短期的效果而不顾可能造成的长远影响，造成了现在生态环境破坏、物种种类减少。因此人和自然应该建立一种建设性的、尽可能完善的、和谐的关系。 再次，要通过高度发展的科学技术来完善人类自身的认识能力和实践能力。人和自然矛盾的解决，与生产力的水平有很大的关系，低下的生产力水平根本无法协调人与自然的关系，只有高度发展的生产力，才能为人和自然关系的协调发
模块7各单元词汇和短语复习 Unit 1 Living Well Part One 根据首字母或汉语提示写出完整的单词: 1. An unexpected accident made Sang Lan a girl with a physical d____________, but she never gave up. 2. We often observe the tiny cells with m______________ in our biology classes. 3. The production of iron and steel is the most important i______________ of the city. 4. Taiwan is part of China and not an i_______________ state. 5. I have passed all the exams and I am waiting to get the graduation c_______________. 6. A place is a______________ if it is possible to reach it. 7. I was not alone on the journey. Instead, I had so many c________________. 8. You can refer to old people in general as the _______________. 9. When something can help people or improve their lives, we say it is ______________ to people. 10. When the disabled meet with difficulty, we should do what we can to give them a___________. 11. One of his ________________ (志向) is to become a world-wide famous pop singer. 12. He was _____________(笨拙的) with a tool. 13. The patient’s _______________(呼吸) grew stronger and stronger. 14. Who took his place and controlled the company during his ________________ (不在) ? 15. I’m going to give some suggestions to this famous ________________(建筑师). 16. A man’s _______________（尊严）doesn’t depends on his wealth but on his character. Part Two 一、词形变换（用所给词的适当形式填空） 1. The ______________ is good at ______________ TV plays from the stories he reads about or hears. (adapt) 2. The country used to be _____________ on Britain in many ways, but now it has become absolutely_______________. (depend) 3. We have ___________ a lot from the co-operation and I’m sure it will continue to be ________ to both of us. (benefit) 4. Her _____________ lecture ____________ all of us. We won’t forget her ____________. (encourage) 5. ______________ people should be treated equally in spite of their ______________. (disability) 6. You were _____________ yesterday, Tom. Can you tell me the reason for you _____________? (absent) 7. The ______________ serving the passengers on the train is of good_______________. (conduct) 8. ________________ countries pay much attention to the development of ________________. (industry) 二、翻译句子 1. 应该给残疾人尽可能多的鼓励和援助。 ______________________________________________________________________________ 2. 换句话说，这些措施对我们的工业发展是有益的。 ______________________________________________________________________________ 3. 总之，在学校寄宿(board)能帮助学生学会独立。 ______________________________________________________________________________