Acute Myocardial Infarction With Normal Coronary Arteries

1650Cardiovascular disease is the leading cause of death in the United States. Coronary artery disease, which is responsible for more than 50% of all cardiovascular disease–related deaths, was expected to account for more than $80 billion in direct costs in 2010. In the United States, approximately 1 million people sustain an acute myocardial infarction (MI) every year because of atherosclerotic coronary disease. Although recent advances in percutaneous intervention have reduced the number of referrals for surgical intervention, coronary artery bypass grafting (CABG) still remains one of the most effective treatments for coronary artery disease and is the most commonly performed open cardiac procedure in the United States.CORONARY ARTERY ANATOMY AND PHYSIOLOGY Anatomic ConsiderationsThe coronary arteries are the predominant blood supply con-duits to the heart. The coronary arteries arise from the sinuses of Valsalva, which are elastic saccular bulges of the aortic root. The coronary arteries are the first arterial branches of the aorta and usually two are present. They are designated as right and left according to the embryologic chamber that they predomi-nantly supply. The left coronary artery (LCA) arises from the left coronary sinus, which is located posteromedially, whereas the right coronary artery (RCA) arises from the right coronary sinus, which is located anteromedially. The LCA, also called the left main coronary artery , averages approximately 2 to 3 cm in length and courses in a left posterolateral direction, winding behind the main pulmonary artery trunk and then splitting into the left anterior descending (LAD) and left circumflex arteries. The LAD courses in an anterolateral direction to the left of the pulmonary trunk and runs anteriorly over the interventricular septum. The diagonal branches of the LAD supply the antero-lateral wall of the left ventricle. The LAD is considered the most important surgical vessel because it supplies more than 50% of the left ventricular mass and most of the interventricular septum. The LAD has several septal perforating branches that supply the interventricular septum from the anterior aspect. The LAD extends over the interventricular septum up to the apex of the heart, where it may form an anastomosis with the posterior descending artery (PDA), which is typically a branch of the right coronary system (Fig. 60-1).The circumflex artery passes through the atrioventricular groove (AV) and follows a clockwise course. Where the circum-flex artery courses through the AV groove, it gives off branches in a perpendicular fashion that extend toward, but do not quite reach, the apex of the heart. These branches are designated the obtuse marginal braches and are designated numerically from proximal to distal. The circumflex coronary artery usually ter-minates as the left posterolateral branch after taking a perpen-dicular turn toward the apex.The term ramus intermedius is used to designate a dominant epicardial coronary vessel that arises from the occasional trifurca-tion of the left main coronary artery. The ramus typically emerges from under the left atrial appendage, which is used as a landmark for identifying this branch and courses over the anterolateral wall of the left ventricle. This branch can be intramyocardial and difficult to locate at times.The RCA supplies most of the right ventricle, as well as the posterior part of the left ventricle. The RCA emerges from its ostium in the right coronary sinus, passes deep in the right AV groove, and then proceeds over the anterior surface of the heart. At the superior end of the acute margin of the heart, the RCA turns posteriorly toward the crux and usually bifurcates into the PDA over the posterior interventricular sulcus and right postero-lateral artery. The RCA also supplies multiple right ventricular branches (acute marginal branches). Occasionally, the PDA arises from both the RCA and LCA and the circulation is con-sidered to be codominant. The AV node artery arises from the RCA in approximately 90% of patients. The sinoatrial node artery arises from the proximal RCA in 50% of patients. Other prominent branches arising from the RCA include the acute marginal artery and anterior ventricular branches. Although thesource of the PDA is often used clinically to define dominanceACQUIRED HEART DISEASE: CORONARY INSUFFICIENCYRaja R. Gopaldas, Danny Chu, and Faisal G. BakaeenAcquired HeArt diseAse: coronAry insufficiency Chapter 60 1651systems—the coronary sinus and its tributaries, the anterior right ventricular veins, and the thebesian veins. The coronary sinus predominantly drains the left ventricle and receives 85% of coronary venous blood. It lies within the posterior AV groove and empties into the right atrium. The anterior right ventricular veins travel across the right ventricular surface to the right AV groove, where they enter directly into the right atrium or form the small cardiac vein, which enters into the right atrium directly or joins the coronary sinus just proximal to its orifice. The the-besian veins are small venous tributaries that drain directly into the cardiac chambers and exit primarily into the right atrium and right ventricle. Understanding the anatomy of the coronary sinus is essential for placing the retrograde cardioplegia cannula during cardiopulmonary bypass.Physiology and Regulation of Coronary Blood FlowAortic pressure is a driving force in the maintenance of myocar-dial perfusion. During resting conditions, coronary blood flow is maintained at a fairly constant level over a wide range of aortic perfusion pressures (70 to 180 mm Hg) through the process of autoregulation.Because the myocardium has a high rate of energy use, normal coronary blood flow averages 225 mL/min (0.7 to 0.9 mL/g of myocardium/min) and delivers 0.1 mL/g/min of oxygen to the myocardium. Under normal conditions, more than 75% of the delivered oxygen is extracted in the coronary capillary bed, so any additional oxygen demand can only be met by increasing the flow rate. This highlights the importance of unobstructed coronary blood flow for proper myocardial func-tion. Box 60-1 summarizes the unique features of coronary blood flow.In response to increased load, such as that caused by strenu-ous exercise, the healthy heart can increase myocardial blood flow fourfold to sevenfold. Increased blood flow occurs through several mechanisms. Local metabolic neurohumoral factors cause coronary vasodilation when stress and metabolic demand increase, thereby lowering the coronary vascular resistance. This results in increased delivery of oxygen-rich blood, mimicking the phenomenon of reactive hyperemia. When a transient occlu-sion to the coronary artery is released (e.g., during the perfor-mance of a beating heart operation), blood flow immediately rises to exceed the normal baseline flow and then gradually returns to its baseline level. The autoregulatory mechanism responsible is guided by several metabolic factors, including CO 2, O 2 tension, hydrogen ions, lactate, potassium ions, and adenosine. Of these, adenosine is one of the leading candidates in the autoregulatory mechanism. Adenosine, a potent vasodila-tor and a degradation product of adenosine triphosphate (ATP),of circulation in the heart, anatomists define it according to where the sinoatrial node artery arises. Table 60-1 summarizes the hierarchy of the coronary artery anatomy.All the epicardial conductance vessels and septal perforators from the LAD give rise to a multitude of branches, termed resistance vessels, which traverse perpendicularly into the ven-tricular wall. These vessels play a crucial role in oxygen and nutrient exchange with the myocardium by forming a rich plexus capillary network. The rich capillary plexus offers a low-resistance sink to allow for unimpeded increase of arterial blood flow when oxygen demand rises. This is important because the myocardial vascular bed extracts oxygen at its full capacity, even in low-demand circumstances, thereby allowing no margin for further oxygen extraction when demand is high.An intricate network of veins drains the coronary circula-tion and the venous circulation can be divided into threeFIGURE 60-1 Anatomy of normal coronary artery vasculature.RCPDAcuteLM CALAD Diag.OM1652 SeCtION XI cHestEpidemiologic evidence suggests that coronary artery ath-erosclerosis is closely linked to the metabolism of lipids, specifi-cally LDLc. The development of lipid-lowering drugs has resulted in a significant reduction in mortality. In one observa-tional study of patients who received statin therapy and were known to have coronary artery disease (CAD), statin treatment was associated with improved survival in all age groups.1 The greatest survival benefit was found in those patients in the highest quartile of plasma levels of high-sensitivity C-reactive protein (hs-CRP), a biomarker of inflammation and CAD.2 Animal and human studies have demonstrated that statin therapy also modifies the lipid composition within plaques by lowering the amount of LDLc and stabilizing the plaque through various mechanisms, including reduction in macro-phage accumulation, collagen degradation, reduction in smooth muscle cell protease expression, and decrease in tissue factor expression.PathogenesisThe primary cause of atherosclerotic coronary disease is endo-thelial injury induced by an inflammatory wall response and lipid deposition. There is evidence that an inflammatory response is involved in all stages of the disease, from early lipid deposition to plaque formation, plaque rupture, and coronary artery throm-bosis. Vulnerable or high-risk plaques that are prone to rupture are characterized by the following:1. A large, eccentric, soft lipid core 2. A thin fibrous cap3. Inflammation within the cap and adventitia4. Increased plaque neovascularity5. Evidence of outward or positive vessel remodelingThinner fibrous caps are at a higher risk for rupture, prob-ably because of an imbalance between the synthesis and degrada-tion of the extracellular matrix in the fibrous cap that results in an overall decrease in the collagen and matrix components (Fig. 60-2). Increased matrix breakdown caused by matrix degrada-tion by an inflammatory cell-mediated metalloproteinase oraccumulates in the interstitial space and relaxes vascular smooth muscle. This results in vasomotor relaxation, coronary vasodila-tion, and increased blood flow. Another substance that plays an important role is nitric oxide (NO), which is produced by the endothelium. Without the endothelium, coronary arteries do not autoregulate, suggesting that the mechanism for vasodilation and reactive hyperemia is endothelium-dependent.Extravascular compression of the coronaries during systole also plays an important role in the regulation of blood flow. During systole, the intracavitary pressures generated in the left ventricular wall exceed intracoronary pressure and blood flow is impeded. Hence, approximately 60% of the coronary blood flow occurs during diastole. During exercise. increased heart rate and reduced diastolic time can compromise flow time but this can be offset by vasodilatory mechanisms of the coronary vessels. Buildup of atherosclerotic plaques and fixed coronary occlusion significantly impair coronary blood compensatory mechanisms during increased heart rates. This forms the basis for exercise-induced stress tests, in which increased activity or exercise unmasks underlying coronary disease.HISTORY OF CORONARY ARTERY BYPASS SURGERYOne of the first attempts at myocardial revascularization was made by Dr. Arthur Vineberg from Canada. He operated on a series of patients who presented with symptoms of myocardial ischemia and implanted the left internal mammary artery into the myocardium by creating a pocket. The operation did not entail a direct anastomosis to any coronary vessel and was performed on a beating heart through a left anterolateral thora-cotomy. Dr. Michael DeBakey performed a successful aortocoro-nary saphenous vein graft in 1964. Dr. Mason Sones, who is credited with inventing cardiac catheterization, helped establish coronary artery bypass surgery as a planned and consistent therapy in patients with angiographically documented coronary artery disease.The development of the heart-lung machine and demon-stration of successful clinical use by Dr. John Heysham Gibbon in the 1950s and the advancement of cardioplegia techniques in later years by Dr. Gerald Buckberg allowed surgeons to perform coronary anastomosis on an arrested (nonbeating) heart with a relatively bloodless field, thus increasing the safety and accuracy of the coronary bypass. In the 1990s, the advent of devices that could atraumatically stabilize the heart provided another pathway for the development of off-pump techniques of myocardial revascularization. T oday, an armamentarium of techniques, ranging from conventional on-pump CABG to minimally inva-sive robotic and percutaneous approaches, is available to manage coronary artery disease. Table 60-2 summarizes the timeline of major historical events in the development of surgery for myo-cardial revascularization.ATHEROSCLEROTIC CORONARY ARTERY DISEASE Coronary atherosclerosis is a process that begins early in the patient’s life. Epicardial conductance vessels are the most suscep-tible and intramyocardial arteries, the least. Risk factors for atherosclerosis include elevated plasma levels of total cholesterol and low-density lipoprotein cholesterol (LDLc), cigarette smoking, hypertension, diabetes mellitus, advanced age, low plasma levels of high-density lipoprotein cholesterol (HDLc), and a family history of premature coronary artery disease.Acquired HeArt diseAse: coronAry insufficiency Chapter 60 1653CLINICAL MANIFESTATIONS AND DIAGNOSIS OF CORONARY ARTERY DISEASEClinical PresentationThe most common presenting symptom of CAD is angina. It may be accompanied by dyspnea or mistaken for a gastrointes-tinal disturbance. The symptoms typically are exacerbated or incited by effort but subsequently resolve with rest. Unstable angina encompasses resting angina, new-onset angina, and accel-erated angina and is usually indicative of severe ischemia and impending MI. However, not all cases of angina are necessarily indicative of CAD, because disease processes from other systems can closely mimic those of angina. Approximately 15% of patients with CAD do not present with angina.The term acute coronary syndrome (ACS) has evolved to refer to a constellation of clinical symptoms that represent myo-cardial ischemia. It encompasses both ST-segment elevation MI (STEMI) and non–ST-segment elevation MI (NSTEMI). MI often presents as crushing chest pain that may be associated with nausea, diaphoresis, anxiety, and dyspnea. Symptoms of hypo-perfusion may also include dizziness, fatigue, and vomiting. Heart rate and blood pressure may be initially normal, but both increase in response to the duration and severity of pain. Loss of blood pressure is indicative of cardiogenic shock and indicates a poorer prognosis. At least 40% of the ventricular mass mustreduced production of extracellular matrix results in thinner fibrous caps. Not all plaque ruptures are symptomatic; whether they are is dependent on the thrombogenicity of the plaque’s components. Tissue factor within the lipid core of the plaque, secreted by activated macrophages, is one of the most potent thrombogenic stimuli. Rupture of a vulnerable plaque may be spontaneous or caused by extreme physical activity, severe emotional distress, exposure to drugs, cold exposure, or acute infection.Fixed Coronary ObstructionsMore than 90% of patients with symptomatic ischemic heart disease have advanced coronary atherosclerosis caused by a fixed obstruction. Atherosclerotic plaques of the coronary arteries are concentric (25%) or eccentric (75%). Eccentric lesions compro-mise only a portion of the lumen; through vascular remodeling, the arterial lumen may remain patent until late in the disease process. The impact of an arterial stenosis on coronary blood flow can be appreciated in the context of Poiseuille’s law. Reduc-tions in luminal diameter up to 60% have minimal impact on flow but when the cross-sectional area of the vessel has decreased by 75% or more, coronary blood flow is significantly compro-mised. Clinically, this loss of flow often coincides with the onset of exertional angina. A 90% reduction in luminal diameter results in resting angina.FIGURE 60-2 components of atherosclerotic plaque. thinning of the fibrous cap eventually results in plaque rupture with extrusion of highly thrombogenic lipid laden material into the coronary artery. this causes an acute occlusion of the coronary artery resulting in myocardial infarc-tion. (Adapted from choudhury rP, fuster V, fayad ZA. Molecular, cellular and functional imaging of atherothrombosis. nature rev drug discov 3:913–925, 2004.)Modality TargetProcess MRIUltrasound PET ++––++++Flow-mediated vasodilation Endothelial dysfunctionAdhesion molecules Endothelial activation++++MacrophagesInflammation +–++++++++++MMPs Cathepsin +±––Lipid core Fibrous capαv β3 integrinFibrinPlatelets αIIb β3 integrin Tissue factor Proteolysis ApoptosisAngiogenesisThrombosis ThrombusFibrous capLipid-rich necrotic coreMonocyte recruitment↓NO productionAngiogenesisInternal elasticlaminaLDLFoam cell Fibrin Endothelial cell VCAM1, ICAM, selectinsCollagen fibril Smooth muscle cellApoptotic cell PlateletMMPApproximate American HeartAssociation lesion stage I II III IV V VIαv β3 integrin1654 SeCtION XI cHestChest RadiographyThe chest radiograph is helpful in identifying causes of chest discomfort or pain other than CAD. Chest radiography does not detect CAD directly; it only identifies sequelae, such as cardiomegaly, pulmonary edema, and pleural effusions, that are indicative of heart failure. Evidence of calcification in the coro-nary arteries, although suggestive of CAD, is not reflective of the severity of the disease.Resting ElectrocardiographyA 12-lead resting electrocardiogram (ECG) should be obtained in patients suspected of having CAD or its sequelae. The ECG is evaluated for evidence of left ventricular hypertrophy, ST-segment depression or elevation, ectopic beats, or Q waves. In addition, arrhythmias (atrial fibrillation or ventricular tachy-cardia) and conduction defects (left anterior fascicular block, right bundle branch block, left bundle branch block) are sug-gestive of CAD and MI. Persistent ST-segment elevation or an evolving Q wave is consistent with myocardial injury and ongoing ischemia. Fifty percent of patients have normal electro-cardiographic results despite having significant CAD, and 50% of ECGs obtained during chest pain at rest will be normal, indicating the inaccurate nature of the test.Risk Stratification and Further TestingBased on age, clinical history, symptomatology, physical signs, and diagnostic tests, CAD patients are classified as low, interme-diate, or high risk. Such stratification enables the clinician to determine the intensity of medical therapy and timing of coro-nary angiography.Low- to intermediate-risk patients treated early and with a conservative strategy may undergo stress testing for further risk stratification. The choice to conduct stress testing depends on the patient’s resting ECG and ability to perform exercise.An exercise stress ECG is helpful in unmasking underlying CAD and is a more reliable screening test than a resting ECG in patients older than 40 years. The Bruce protocol is the most commonly used standardized treadmill exercise protocol. The protocol involves five 3-minute bouts of treadmill exercise, each designed to elicit greater myocardial oxygen demand than the last, to determine the patient’s ischemic threshold. A typical protocol requires the patient to expend about 12 metabolic equivalents (METs) of energy to ensure a complete test. A posi-tive exercise ECG may show progressive flattening of the ST segment or ST-segment depression as exercise progresses. During the recovery phase, ST depression may persist, with downslop-ing segments and T wave inversion. Additional findings associ-ated with an adverse prognosis and the presence of multivessel occlusive disease include a duration of symptom-limited exercise of less than 6 METs, the failure of systolic blood pressure to increase to more than 120 mm Hg, and the appearance of ven-tricular arrhythmias. For detection of CAD, the sensitivity and specificity of an exercise ECG approach 70% and 80%, respec-tively (Box 60-3).Conditions that preclude accurate interpretation of the stress ECG include digoxin therapy, widespread resting ST- segment depression (≥1 mm), left ventricular hypertrophy, left bundle branch block, and other conduction abnormalities. For patients with these conditions and those unable to exercise, a pharmacologic stress test with an imaging modality using a radionuclide agent such as thallium or sestamibi, multiple-gatedbe involved for cardiogenic shock to occur. The first manifesta-tion of CAD in 40% of patients is sudden onset of a nonper-fusing ventricular rhythm, such as ventricular tachycardia or fibrillation.The prehospital mortality rate for an acute MI (AMI) is approximately 50%. Of those patients who reach the hospital, another 25% die during the hospital stay and another 25% die in the first year afterward.3,4 Mechanical complications of MI include acute ventricular septal defect (VSD), papillary muscle rupture, and free ventricular rupture. They usually occur approx-imately 7 to 10 days after the initial MI.Physical ExaminationSome clinical findings are generic and are related to the systemic manifestations of atherosclerosis. Eye examination may reveal a copper wire sign, retinal hematoma or thrombosis secondary to vascular occlusive disease, and hypertension. Corneal arcus and xanthelasma are features noticed in cases of hypercholesterol-emia. Other clinical manifestations are caused by sequelae of CAD, as noted in Box 60-2.A thorough vascular evaluation is essential for any patient who presents with coronary disease because atherosclerosis is a systemic process. In addition, if surgery is being planned, the extremities should be evaluated for any previous surgical scars or fractures that could potentially preclude vein harvest.Diagnostic TestingBiochemical StudiesPatients suspected of having an ACS should undergo appropri-ate blood testing. Levels of creatinine kinase muscle and brain subunits (CK-MB) and troponin T or I should be assessed at least 6 to 12 hours apart. Additional laboratory tests include a complete blood count (CBC), comprehensive metabolic panel, and lipid profile (total cholesterol, triglycerides, LDLc, HDLc). Elevated brain natriuretic peptide (BNP) and CRP levels suggest a worse outcome.Acquired HeArt diseAse: coronAry insufficiency Chapter 60 1655Multidetector Computed TomographyMultidetector computed tomography (MDCT), one of the most recent imaging modalities, allows imaging of the coronary arter-ies, especially of coronary artery bypass grafts. Studies have indicated that the sensitivity and specificity MDCT approach or exceed those of other noninvasive methods of visualizing the coronary artery anatomy.5 MDCT is especially useful for imaging proximal CAD and coronary artery bypass grafts. More recent technology improves on conventional MDCT by adding more arrays to the imaging process; 128-slice MDCT arrays are cur-rently available. These scanners can acquire myocardial images within 1 second while exposing the patient to less radiation than traditional scanners. Although it is still preferable that patients have relatively low heart rates during imaging (to reduce arti-fact), the technology has significantly advanced and produces images on par with those generated by the gold standard, con-ventional angiography.6Magnetic Resonance Imaging and Gadolinium Magnetic Resonance ImagingMyocardial first-pass perfusion magnetic resonance imaging (MRI) has been considered a good alternative to nuclear cardiac ischemia and viability testing. However, the procedure has not gained widespread popularity because special training and exper-tise are required to perform this type of imaging and interpret the results.Cardiac Catheterization and InterventionCardiac catheterization remains the gold standard for evaluating the anatomy of the coronary arteries. High-quality coronary angiography is essential for identifying CAD and assessing its extent and severity.Cardiac catheterization is commonly performed by insert-ing a short, self-sealing vascular sheath into either femoral artery. Vascular access may also be obtained via a brachial or radial artery. Angiography is done by using hollow preshaped catheters (5 or 6 Fr), which are placed under fluoroscopic guidance ret-rograde through the aorta into the ostia of the coronary arteries and coronary bypass grafts. A solution of radiographic contrast material is injected through the catheter to opacify the lumen. Images are recorded in rapid succession onto film or in a digital format. The surgeon typically uses the coronary angiography images to determine the number and location of coronary targets where bypass anastomoses are to be constructed (Figs. 60-3, 60-4, and 60-5).Other information obtained from cardiac catheterization includes coronary and aortic calcification, ventricular function, and, if ventriculography is performed, mitral regurgitation. Injection of contrast into the aortic root provides useful root and ascending aortic images when indicated.Right heart catheterization is used to measure central venous, right atrial, right ventricular, pulmonary artery, and pulmonary wedge pressures, as well as cardiac output. It can also be used to identify intracardiac shunts, assess arrhythmias, and initiate temporary cardiac pacing. Preoperative right heart catheterization is used selectively and is generally not necessary unless right ventricular dysfunction or pulmonary vascular disease is suspected.Percutaneous coronary intervention (PCI) techniques in current use include balloon dilation, stent-supported dilation, atherectomy, and plaque ablation with a variety of devices,acquisition [MUGA] scanning, or positron emission tomogra-phy (PET) should be considered. Echocardiography may be considered as an alternative. Pharmacologic stress agents include adenosine, dobutamine, and dipyridamole.EchocardiographyMany patients undergoing CABG also undergo transthoracic echocardiography by the evaluating cardiology team to estimate ventricular wall abnormalities and the ejection fraction. Common indications for a resting echocardiogram include heart murmurs and a suspicion of a structural problem, such as aortic stenosis or insufficiency, hypertrophic cardiomyopathy, mitral valve stenosis or regurgitation, and congestive heart failure. Ven-tricular dilation and wall thinning are other features noted on the echocardiogram in patients with chronic ischemic CAD or prior infarcts.1656 SeCtION XI cHestinsignificant problems, the greatest cause of lumen loss in stented coronary arteries is neointimal hyperplasia. This is the principal mechanism of in-stent stenosis and results from inappropriate cell proliferation—hence, the advent of cytotoxic drug-eluting stents.INDICATIONS FOR CORONARY ARTERY REVASCULARIZATIONBox 60-4 summarizes the indications for myocardial revascular-ization. The first four indications are managed preferably by PCI, whereas indications 5 through 7 are managed preferably by surgical revascularization. The last two indications constitute surgical emergency. Although this stratification is broad and provides a bird’s eye view of the management approach, each patient should be risk-stratified before an appropriate strategy is initiated. When possible, proper risk stratification is absolutely essential to determine the balance of risks and benefits of medical management, PCI, and CABG.Chronic Stable AnginaCardiovascular risk reduction strategy is essential to treating patients with chronic stable angina. In the 2007 focused update of the 2002 American Heart Association (AHA)/American College of Cardiology (ACC) guidelines 7 for managing chronic stable angina, cardiovascular risk reduction strategies includedFIGURE 60-3 Left coronary angiogram demonstrating hemodynami-cally severe lesions in the left anterior descending artery (small arrow) and the circumflex artery (large arrow).FIGURE 60-4 right coronary angiogram demonstrating hemodynam-ically significant lesions (arrow). the right coronary artery terminatesas a posterior descending artery in the right dominant system.thrombectomy with aspiration devices, specialized imaging, and physiologic assessment with intracoronary devices.Coronary artery stents were the first substantial break-through in the prevention of restenosis after angioplasty. Although stent recoil or compression are not completelyFIGURE 60-5 coronary angiogram demonstrating critical left main coronary artery stenosis (arrow).。

心梗后室间隔穿孔的治疗进展张亮;刘东海;罗宏;谌启辉;乔晨辉【期刊名称】《河南医学研究》【年(卷),期】2013(022)001【总页数】3页(P144-146)【作者】张亮;刘东海;罗宏;谌启辉;乔晨辉【作者单位】郑州大学第一附属医院心血管外科河南郑州450052;郑州大学第一附属医院心血管外科河南郑州450052;郑州大学第一附属医院心血管外科河南郑州450052;郑州大学第一附属医院心血管外科河南郑州450052;郑州大学第一附属医院心血管外科河南郑州450052【正文语种】中文室间隔穿孔是急性心梗后少见的严重并发症，在急性心梗病人中继发室间隔穿孔的发病率大约为1%～2%［1］，从心梗发生到发生穿孔平均时间为2～4 d，最早可发生于心梗后几小时，最迟见于心梗后2周［2，3］。

但随着积极的药物治疗、迅速有效的控制患者血压和急诊溶栓技术、介入治疗技术的临床应用，心梗后室间隔穿孔的总体发病率降低至0.24%［4］，但值得注意的是，在开展溶栓治疗之后室间隔穿孔平均发生时间提前到心肌梗死后的1 d左右［5］。

一旦发病，短时间内会导致心功能衰竭、心源性休克而致死，预后极差。

及时闭合穿孔是改善这类患者预后的唯一有效方法。

本文就近些年急性心梗后室间隔穿孔的治疗方法及时机进行综述。

1 自然病程在保守治疗的心梗后室间隔穿孔的病人中，将近24%的患者死于发病后的24 h内，46%死于1周内，67%～82%死于2月内，只有5%～7%的患者能够存活超过 1 a［6］。

据 Lemery 等［7］人报道，25 例心梗后室间隔穿孔病人经内科保守治疗，其中19人在1月内死亡。

有报道称极少数的室间隔穿孔患者未经治疗存活14 a［8］。

一项多中心的研究跟踪了55例由于心梗后室间隔穿孔伴发心源性休克的患者。

其中24例患者行内科保守治疗，剩下的31例患者构成了高危手术组。

最终只有7例患者存活，其中6例为手术修复了缺损的病人［9］。

心肌梗塞的英语English:A myocardial infarction, commonly known as a heart attack, occurs when the blood flow to a part of the heart is blocked, leading to damage or death of the heart muscle cells. This blockage is typically caused by a buildup of plaque in the coronary arteries, which restricts the flow of oxygen-rich blood to the heart. The symptoms of a heart attack can vary but often include chest pain or discomfort, shortness of breath, nausea, and lightheadedness. Immediate medical treatment is crucial to prevent further damage to the heart, and may include medications to dissolve the clot, angioplasty to open the blocked artery, or coronary bypass surgery to restore blood flow to the heart muscle. Long-term management may involve lifestyle changes, such as diet modification and exercise, as well as medications to control blood pressure and cholesterol levels.中文翻译:心肌梗塞，通常称为心脏病发作，是指心脏部分区域的血流被阻塞导致心肌细胞受损或死亡。

血浆脑钠肽在急性冠状动脉综合征的诊断及预后评估中的作用观察陈军;徐任璇【摘要】Objective: To study the roles of brain natriuretic peptide (BNP) in diagnosis and prognostic evaluation of patients with acute coronary syndrome(ACS). Methods:The levels of BNP were detected in 54 patients with acute myocardial infarction(AMI),35 patients with unstable angina pectoris(UAP) ,20 patients with stable angina pectoris(SAP) and 20 healthy volunteers as controls.The correlations were compared between the number of impaired coronary arteries, the lesions of left main coronary artery, the Gensini scores of coronary artery and the levels of BNP respectively. The mortality of the patients with ACS in hospital at 30 days and 3 months,and the major adverse cardiac events ( MACE ), cardiogenic death, re - myocardial infarction, recurrent angina, consequential heart failure and the composite endpoint rates of readmission were analyzed. Results:The levels of BNP in group AMI and group UAP were significantly higher than those in group SAP and controls(P ＜0. 01 ) ,and the level of BNP in group AMI was significantly higher than it in group UAP( P ＜ 0. 01 ). Multivariate logistic regression analysis showed that, the level of plasma BNP was independent with the risk factors of coronary heart disease, such as age, gender, family history, smoking, hyperlipidemia, high blood pressure, diabetes, and so on,but it was associated with mortality and rates MACE ( P ＜ 0. 05 - P ＜ 0.01 ). Conclusions: The levels of BNP inpatients with ACS increase significantly and are associated with degrees of coronary artery disease and myocardial ischemia. The change of plasma BNP is an independent predictor for mortality and incidence of MACE in hospital at 30 days and 3 months among ACS patients.%目的:探讨血浆脑钠肽(BNP)水平变化在急性冠状动脉综合征(ACS)诊断及预后评估中的作用.方法:检测54例急性心肌梗死(AMI组)患者、35例不稳定型心绞痛(UAP组)患者、20例稳定型心绞痛(SAP组)患者以及20名健康体检者(对照组)血浆BNP水平;比较冠状动脉病变支数、左主干病变及冠状动脉Gensini评分与BNP的相关性,并随访患者住院期间及出院后30天、3个月病死率,以及主要心脏不良事件(MACE)、心源性死亡、再次心肌梗死、再发心绞痛、继发心力衰竭和再入院的复合终点发生率.结果:AMI组、UAP组的BNP水平显著高于SAP组和对照组(P<0.01),AMI组BNP 水平显著高于UAP组(P<0.01);冠状动脉3支或左主干病变患者BNP水平均显著高于1支和2支病变(P<0.01),2支病变与3支或左主干病变差异亦有统计学意义(P<0.01).血浆BNP水平独立于年龄、性别、家族史、吸烟、高脂血症、高血压、糖尿病等冠心病危险因素,与出院后30天、3个月病死率独立相关(P<0.01).结论:ACS患者BNP水平明显升高,并与其冠状动脉病变及心肌缺血程度密切相关.血浆BNP水平变化可能独立于各因素预测ACS患者30天和3个月病死率及MACE 发生率.【期刊名称】《蚌埠医学院学报》【年(卷),期】2011(036)006【总页数】4页(P621-624)【关键词】急性冠状动脉综合征;脑钠肽;诊断;预后评估【作者】陈军;徐任璇【作者单位】上海市杨浦区安图医院,心内科,200093;上海市杨浦区安图医院,心内科,200093【正文语种】中文【中图分类】R541.4急性冠状动脉综合征(acute coronary syndrome，ACS)是严重威胁人类健康的一类急性心血管事件，包括不稳定性心绞痛(unstable angina pectoris，UA)、非ST段抬高性心肌梗死(non-ST segment elevationmyocardial infarction，NSTEMI)和ST段抬高性心肌梗死(ST segment elevationmyocardial infarction，STEMI)，以及以上各病症导致的猝死。

急性冠脉综合征患者血清降钙素原、D-二聚体水平测定张晋东;杨海波;赵晓燕;赵荫涛;王小芳;李凌【期刊名称】《郑州大学学报（医学版）》【年(卷),期】2015(000)002【摘要】目的：检测急性冠脉综合征（ACS）患者血清降钙素原、D-二聚体水平，探讨二者与ACS患者冠状动脉病变程度的关系。

方法：根据病情严重程度将因ACS入院的患者分为不稳定型心绞痛组（ UAP组，72例）、急性心肌梗死组（ AMI组，30例），另选取同期行冠状动脉造影、结果正常的20例患者作为对照组。

采用ELISA法测定血清降钙素原、D-二聚体水平。

分析血清降钙素原、D-二聚体水平与病变支数、Gensini积分的关系。

结果：AMI组血清降钙素原、D-二聚体水平高于UAP组及对照组（F＝3．298、5．082，P＜0．05），UAP组与对照组血清降钙素原、D-二聚体水平差异无统计学意义（P＞0．05）。

UAP组血清降钙素原、D-二聚体水平与Gensini积分无关（P＞0．05），AMI组血清D-二聚体水平与Gensini积分呈正相关（r＝0．523，P＜0．05）。

结论：ACS患者血清降钙素原水平与冠状动脉内的炎症反应及斑块的稳定性有关，而D-二聚体水平与冠状动脉狭窄的严重程度有关。

%Aim:To determine the serum levels of procalcitonin and D-dimer in patients with acute coronary syndrome (ACS) and investigate the association between ACS and the 2 parameters.Methods:All patients with ACS were classified into unstable angina pectoris(UAP)group(n=72) and acute myocardial infarction(AMI) group(n=30),and individuals without coronary heart disease were chosenas the control group ( n =20 ) .Serum procalcitonin and D-dimer levelswere measured by ELISA .The correlations between serum procalcitonin , D-dimer levels and the numbers of impaired coronary arteries,Gensini scores of coronary stenosis were analyzed respectively .Results:The levels of serum procalcitonin and D-dimer in AMI group were significantly higher than those in UAP group and control group (F=3.298 and 5.082,P<0.05), and there was no significant difference between UAP group and control group .There was positive correlation between the D-dimer level and Gensini scores in the AMI group (r=0.523,P<0.05),while there were no correlations between the levels of procalcitonin or D-dimer with Gensini scores in the UAP group (P>0.05).Conclusion:In patients with ACS, the lev-el of serum procalcitonin correlates with the inflammatory response of coronary artery and the stability of plaques , and serum D-dimer level relates to the stenosis severity of coronary artery .【总页数】4页(P267-270)【作者】张晋东;杨海波;赵晓燕;赵荫涛;王小芳;李凌【作者单位】郑州大学第一附属医院心内科郑州450052;郑州大学第一附属医院心内科郑州450052;郑州大学第一附属医院心内科郑州450052;郑州大学第一附属医院心内科郑州450052;郑州大学第一附属医院心内科郑州450052;郑州大学第一附属医院心内科郑州450052【正文语种】中文【中图分类】R543.3【相关文献】1.慢性阻塞性肺疾病合并不成比例肺动脉高压患者血浆D-二聚体水平测定及分析[J], 李晶;孙俊生;卓宋明;申严2.急性早幼粒细胞白血病患者血浆D-二聚体水平测定 [J], 杨艳辉3.胃癌患者手术前后外周血D-二聚体与CA724水平测定及意义 [J], 彭方兴;袁三英;吴宸;陈进;罗亮;陈汇4.急性生理学与慢性健康状况评分Ⅱ联合血清D-二聚体、肌钙蛋白Ⅰ及脑钠肽水平测定对慢性阻塞性肺疾病患者预后评估价值 [J], 罗玉爱;王捷;李贤英5.类风湿关节炎患者血浆D-二聚体水平测定及其临床意义 [J], 付利然;杜转敏;杨毛吉因版权原因，仅展示原文概要，查看原文内容请购买。

出现心绞痛，但冠脉没阻塞？3步搞定这种临床常见难点！冠脉造影发现无明显阻塞的胸痛该做哪些检查？如何治疗？看国际大咖发言。

出现胸痛、心绞痛，但到医院做冠脉造影检查发现没有出现明显阻塞，之后又反复出现这些症状，该怎么办？是不是得考虑去看其他科室。

未必，这时你可能有必要做进一步检查。

近日，Udo Sechtem教授在2020年欧洲心脏病学会（ESC）年会上提出了胸痛伴非阻塞性冠状动脉疾病的诊断、治疗与预后。

这个病很常见，发病占比超过阻塞性冠脉疾病在2019年ESC慢性冠状动脉综合征指南中提到，根据常见症状如胸痛和/或呼吸困难的发生，可以预测阻塞性冠状动脉疾病的发生率。

但是，我们看到即便有典型的胸痛，其实大部分年龄段人群出现冠状动脉疾病的发生率都不到50%，因此，Udo Sechtem教授表示非阻塞性冠状动脉疾病引起的胸痛占了更主要的原因。

表1 不同年龄阶段心绞痛、呼吸困难与冠状动脉疾病发生的关系这该如何解释？首先来了解一下冠状动脉微血管的概念。

它是直径在10-300 μm 的血管，是内皮细胞调节冠脉血流和心肌细胞营养交换的部位，是心脏行使正常生理功能的基本保证。

不过，由于目前冠脉造影只能检测到约500 μm直径的血管，所以不同于大中型冠状动脉，这些冠状动脉微小血管不能被冠脉造影所检测。

这些微小血管出现功能障碍而导致胸痛，现有的冠脉造影无法发现时，就是我们今天要谈的“非阻塞性冠脉疾病”。

图1 冠状动脉微血管的结构图微血管功能障碍和/或心外膜冠状动脉痉挛导致心肌需氧量和血液供应不匹配，是非阻塞性冠状动脉疾病的主要病理机制。

冠脉造影都无法发现，我们要如何诊断？根据今年7月欧洲经皮心血管介入协会（EAPCI）联合欧洲心脏病学会（ESC）发布首部关于缺血伴非阻塞性冠状动脉疾病（INOCA）的专家共识，目前评估缺血的无创技术为心肌单光子发射CT或多巴胺负荷超声心动图，但如果缺血影响到整个心室则以上方法无效。

因此，Udo Sechtem教授推荐使用有创评估法，分为以下三步：①冠状动脉造影；②基于导丝的诊断及腺苷测试。

血引起传导障碍也可使QRS波轻微增宽及QT间期相应延长，David等在犬实验性超急性期心肌缺血模型中，从 Frank导联记录R波振幅及心室内传导时间，在结扎冠状动脉后开始 2～3min内缺血区传导速度呈同步双相反应，初始30s缺血区心室传导加速，R波振幅之和(∑RWA)降低，于第二相时缺血区心室传导减慢，∑RWA增大，提示急性心肌缺血时，R波振幅取决于心室内的传导速度，而不单是血流动力学改变。

Barnhil等对5例变异型心绞痛患者于心绞痛发作时记录正交导联心电图，同时对7只实验性急性心肌缺血模型犬进行电生理检查，观察缺血区R波振幅变化。

结果发现，QRS波振幅变化与心肌内传导速度密切相关，强烈提示变异型心绞痛发作时，缺血区心肌传导速度减慢，引起心室终末除极延迟，最终导致QRS波终末 40ms电压增高。

图 1 急性心肌梗死超急性期，心电图表现缺血周围传导阻滞。