Coronary artery disease in patients dying from cardiogenic shock or congestive heart failure in the setting of acute myocardial infarction.

Pathological findings in the heart and particularly in the coronary arteries are reported from 70 patients dying from pump failure after acute myocardial infarction. Fifty of the patients had died in cardiogenic shock, the remainder from refractory congestive heart failure. Three-vessel disease (greater than or equal to 75% occlusion) was present in 68 per cent of the group with cardiogenic shock but in only 35 per cent of those with fatal congestive heart failure (P less than 0-02). In both groups there was an almost equal incidence (84% for cardiogenic shock and 80% for congestive heart failure) of severe disease (greater than or equal to 75% occlusion) over a long segment of the left anterior descending artery. However, there were differences between the two groups regarding the involvement of the other coronary arteries. Whereas patients with cardiogenic shock generally showed severe disease over a long segment in all coronary arteries, in 60 per cent of those with congestive heart failure there was only local severe narrowing of the right coronary artery with little or no narrowing of the peripheral part. Similarly, 60 per cent of those with congestive heart failure had less than 75 per cent narrowing in the left circumflex artery. These anatomical findings may be of relevance with regard to desirability of acute coronary bypass surgery in patients with pump failure after acute myocardial infarction.     

Amounts of coronary arterial narrowing by atherosclerotic plaque at necropsy in patients with lower extremity amputation.

In 26 patients (mean age at death 68 +/- 9 years) who had undergone amputation (at mean age 63 +/- 12 years) of 1 or both lower extremities due to severe peripheral arterial atherosclerosis, the amounts of narrowing at necropsy in the 4 major (left main, left anterior descending, left circumflex, and right) epicardial coronary arteries were determined. During life, 15 of the 26 patients (58%) had symptoms of myocardial ischemia: angina pectoris alone in 1, acute myocardial infarction alone in 5, and angina and/or infarction plus congestive heart failure or sudden coronary death in 9. Twelve of the 26 patients (42%) died from consequences of myocardial ischemia: acute myocardial infarction in 5, sudden coronary death in 3, chronic congestive heart failure in 3, and shortly after coronary bypass surgery in 1. Grossly visible left ventricular necrosis or fibrosis, or both, was present in 21 patients (81%). Of the 26 patients, 24 (92%) had narrowing 76 to 100% in cross-sectional area of 1 or more major coronary arteries by atherosclerotic plaque. The mean number of coronary arteries per patient severely (> 75%) narrowed was 2.3 +/- 1.0/4.0. Of the 104 major coronary arteries in the 26 patients, 60 (58%) were narrowed > 75% in cross-sectional area by plaque. The 4 major coronary arteries in the 26 patients were divided into 5-mm segments and a histologic section, stained by the Movat method, was prepared from each segment.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cardiac failure in coronary heart disease

Cardiac failure, which used to be rare in coronary heart disease, is now its most common complication. Coronary heart disease can cause or appear as cardiac failure through one or more of 12 mechanisms: acute myocardial infarction, acute reversible ischemia, right ventricular dysfunction, cardiogenic shock, acute mitral regurgitation, ventricular septal perforation, cardiac free wall rupture, ischemic cardiomyopathy, ventricular aneurysm, coexisting diseases, iatrogenesis, and pseudoheart failure. An understanding of the responsible mechanism or mechanisms is essential not only for appropriate treatment but also for prognostication. Various therapeutic modalities, both medical and surgical, should be able to improve not only symptoms but also survival. Current efforts in the management of patients with cardiac failure as a result of coronary heart disease should be aimed at prevention, both primary and secondary.     

Echocardiography in ischemic heart disease.

Echocardiographic findings in patients with ischemic heart disease are described; their correlations with clinical, hemodynamic and angiographic data are presented and discussed. Regional abnormalities of left ventricular wall motion and/or thickening during systole are detected in 84 per cent of patients with acute myocardial infarction and in a high percentage of patients with larger than or equal to 75 per cent narrowing of a major coronary artery. These abnormalities may occur with stress and may be reversible. Left ventricular wall thinning during systole indicates acute ischemia or infarction and thin, dense myocardial echoes indicate scar. Echocardiographic evidence of left ventricular dysfunction is useful in predicting heart failure and mortality in patients with acute myocardial infarction and in predicting surgical mortality for patients undergoing aneurysmectomy and/or coronary artery bypass surgery. Echocardiography has not proved useful in determining graft patency following coronary artery bypass surgery. Technical difficulties and limitations of echocardiography in patients with coronary artery disease are discussed.     

Possibilities of early surgical correction of postinfarction remodeling of the heart

Postinfarction remodeling of the heart (PIRH) has unfavorable prognostic value because is associated with elevated risk of fatal arrhythmias, emergence and progression of heart failure. Reversibility of PIRH in early period after myocardial infarction causes interest. We followed dynamics of echocardiographical parameters in a patient who had undergone myocardial infarction with subsequent aorto-coronary bypass operation. Values of left ventricular end diastolic and end-systolic volumes were as follows: baseline - 147 and 70, in the process of infarction - 281 and 141, in 1 month after infarction - 298 and 194, in 10 days after surgery - 194 and 88, in 1 year after surgery - 194 and 83 ml, respectively. Thus PIRH is substantially reversible in the early period after myocardial infarction followed by adequate cardiac muscle revascularization. In can be supposed that at the moment of infarction an abrupt progression of stenotic atherosclerosis of the coronary arteries occurs due to complete or subtotal occlusion of vessels, what aggravates myocardial ischemia and predominantly determines course of subsequent PIRH.     

Animal models of heart failure recent developments and perspectives

Heart failure is a complex syndrome characterized by inability of the heart to supply sufficient cardiac output to meet the metabolic needs of the body. Over the past few decades, a number of animal models of heart failure have been developed to study questions that cannot be readily studied in the clinical setting. Because the syndrome of heart failure in humans has many underlying causes, ranging from primary myocardial disease (often of unknown etiology) to myocardial failure consequent to ventricular overload with secondary cardiac hypertrophy (as in hypertension, valvular heart disease, or myocardial infarction), no single animal model can successfully mimic the pathophysiology of these clinical settings. Regardless of the original cardiac abnormality, however, the end-stage heart failure syndrome generally presents a picture of cardiac dilation and circulatory congestion associated with maladaptive neurohumoral responses affecting the heart and peripheral circulation, which provide prime targets for new treatment strategies. An ideal animal model of heart failure should mimic the clinical setting as closely as possible, be accessible and reproducible, relatively stable under chronic conditions, and sufficiently economical to permit experiments in a large number of animals. In this review, we discuss the advantages and disadvantages of naturally occurring models of heart failure and models in which heart failure is induced in normal animals, focusing in particular on models that are useful for exploring disease mechanisms and interventions to prevent or treat heart failure. Much is being learned from large animals such as the dog and pig, although small animal models (rat and hamster) have many favorable features, and as genetic methods and miniaturized physiologic techniques mature, the mouse is beginning to provide gene-based models of cardiac failure aimed at better understanding of molecular mechanisms. (Trends Cardiovasc Med 1997;7:161-167). ? 1997, Elsevier Science Inc.     

Treatment of cardiac insufficiency in ischemic heart disease

Over 30 per cent of coronary patients die of cardiac failure excluding the acute phase of myocardial infarction. With the exception of preexisting hypertension, there is no compensatory hypertrophy in ischemic heart disease. However, hypertrophy is a costly adaptation in terms of myocardial oxygen demand and, therefore, coronary flow. Fibrous zones are unresponsive to inotropic drugs and so the treatment of cardiac failure due to ischemic heart disease consists in limiting or preventing episodes of ischemia. Each mechanism of ischemia has an appropriate treatment: the preload is reduced by trinitrin and its derivatives and by molsidomine; the after-load by calcium antagonists and angiotensin converting enzyme inhibitors; tachycardia and hypercontractile states by betablockers. The risk of arrhythmia, aggravated by many inotropic therapies, constitutes the major danger to ischemic heart failure; amiodarone, betablockers and preventive nitrate therapy are the most effective and least dangerous antiarrhythmics. Revascularisation is effective for permanently ischemic segments or for ischemia on effort but does not improve large plaques of fibrosis which sometimes require surgical ablation or plastic procedures. But these measures are incomplete if all aspects of the disease are not taken in consideration: loss of excessive body weight, exercise rehabilitation by modern techniques, limitation of bed rest at the ultimate stage of the disease allowing patients with ischemic cardiac failure a better quality of life without aggravating the prognosis.     

Magnesium orotate in severe congestive heart failure (MACH)

Among many cardiac diseases related to cerebral stroke, left ventricular thrombus formation due to silent myocardial infarction with normal coronary arteries represents a rare cause of cerebral ischemia. We describe an unusual case of cerebral ischemia due to cardiac thrombus formation in a young patient with silent myocardial infarction and normal coronary arteries in which echocardiography and cardiac MR imaging clearly showed the embolic source.     

The heart in fatal unstable angina pectoris

Compared to patients with sudden coronary death and acute myocardial infarction, relatively little morphologic data has been reported in patients with unstable angina pectoris. This article reviews necropsy data collected from one laboratory on unstable angina pectoris. From these data, several observations are appropriate: (1) Patients with unstable angina as a group have more coronary narrowing by atherosclerotic plaque than do patients with sudden coronary death or acute or healed myocardial infarction. (2) Patients with unstable angina have a much higher frequency of severe narrowing of the left main coronary artery than do patients in other coronary subsets. (3) The coronary atherosclerotic plaques in unstable angina consist primarily of fibrous tissue, and they are more similar to those found in patients with sudden coronary death than in patients with acute myocardial infarction. (4) The frequency of acute coronary lesions (thrombi, plaque rupture, and plaque hemorrhage) is similar to that observed in patients with sudden coronary death and significantly less than that observed in acute myocardial infarction. (5) The frequency of multiluminal channels throughout the major coronary arteries is significantly higher in unstable angina compared to sudden coronary death or acute myocardial infarction. (6) The major epicardial arteries and the heart are smaller in patients with unstable angina than in patients with sudden coronary death or acute myocardial infarction. (7) The left ventricular cavity is usually of normal size in patients with unstable angina and therefore left ventricular function is usually normal.     

Effects of cocaine on the coronary arteries

BACKGROUND: A number of studies have documented myocardial ischemia and infarction associated with cocaine use. Mismatch between myocardial oxygen supply and demand from cocaine-induced vasoconstriction and increased myocardial workload are often invoked as the major postulated mechanism by which cocaine induces myocardial ischemia. This article reviews the literature studying the effects produced by cocaine on the coronary arteries to provide insight into the various pathophysiologic mechanisms by which cocaine triggers acute cardiac ischemia or infarction. METHODS: We reviewed the published literature describing the effects of cocaine on the coronary arteries. A MEDLINE search of English language articles published between 1985 and 2000 was performed. Key words included coronary arteries, coronary vasoconstriction, vasospasm, coronary vasodilation, cardiac vasculature, myocardial ischemia, platelets, thrombosis, and cocaine. Both animal and human studies were included. The bibliographies of identified articles were also explored for additional sources of information. RESULTS: A recreational dose of cocaine increases the heart rate by approximately 30 beats/min. It also increases the blood pressure by 20/10 mm Hg. These increases are modest, are equivalent to mild exercise, and are not believed to be sufficient to result in myocardial ischemia in the majority of cases. Animal and human studies have documented cocaine-induced early coronary artery vasodilation as shown by a decrease in coronary perfusion pressure ranging from 13% to 68%. This was followed by a more sustained vasoconstriction demonstrated by a decrease in epicardial coronary artery diameter ranging from 5% to 30% with various doses of cocaine by various methods of administration. These changes alone are also an unlikely explanation for cocaine-induced myocardial ischemia. Therefore neither increases in myocardial workload nor hemodynamic changes are sufficient to explain cocaine-induced myocardial ischemia. However, evidence also exists that cocaine activates platelets and promotes thrombosis, resulting in intracoronary thrombus formation. Cocaine may also promote premature and more severe coronary atherosclerosis. CONCLUSION: The etiology of cocaine-induced myocardial ischemia is complex and is likely to be multifactorial. It appears to be the result of coronary artery vasoconstriction, intracoronary thrombosis, and accelerated atherosclerosis.     

Myocardial infarction with normal coronary arteries: the pathologic and clinical perspectives

Myocardial infarction with normal coronary arteries is a syndrome resulting from numerous conditions but the exact cause in a majority of the patients remains unknown. Cigarette smokers and cocaine users are more prone to develop this condition. The possible mechanisms causing myocardial infarction with normal coronary arteries are hypercoagulable states, coronary embolism, an imbalance between oxygen demand and supply, intense sympathetic stimulation, non-atherosclerotic coronary diseases, coronary trauma, coronary vasospasm, coronary thrombosis, and endothelial dysfunction. It primarily affects younger individuals, and the clinical presentation is similar to that of myocardial infarction with coronary atherosclerosis. Thrombolytics, aspirin, nitrates, and beta blockers should be instituted as a standard therapy for acute myocardial infarction. Once normal coronary arteries are identified on subsequent angiography, the calcium channel blockers could be added since coronary vasospasm appears to play a major role in the pathophysiology of this condition. The beta blockers should be avoided in cocaine-induced myocardial infarction because the coronary spasm may worsen. In myocardial infarction with normal coronary arteries, complications such as malignant arrhythmia, heart failure, and hypotension are generally less common, and prognosis is usually good. Recurrent infarction, postinfarction angina, heart failure, and sudden cardiac death are rare. Stress electrocardiography and imaging studies are not useful prognostic tests and long-term survival mainly depends on the residual left ventricular function, which is usually good.     

Ischemic ventricular arrhythmias during heart failure: A canine model to replicate clinical events

BACKGROUND: Development of experimental animal models has played an invaluable role in understanding the mechanisms of ventricular arrhythmias. OBJECTIVES: The purpose of this study was to evaluate a new canine model of myocardial infarction (MI), heart failure, and ischemic ventricular arrhythmias in an attempt to replicate clinical conditions. METHODS: Thirty-six mongrel dogs underwent placement of a permanent ventricular pacemaker and induction of an anterior MI by percutaneous transcatheter embolization of polyvinyl foam particles into the left anterior descending coronary artery (just distal to the first septal branch). After a 2-week recovery period, heart failure was induced by continuous rapid ventricular pacing at 200 to 240 ppm for 3 weeks. Transient (4-minute) myocardial ischemia was induced via balloon occlusion of the proximal left circumflex coronary artery. Echocardiographic and electrophysiologic testing was performed before MI creation and repeated prior to acute ischemia induction. RESULTS: Seven dogs (19%) died within several hours of MI creation. All surviving dogs developed severe left ventricular systolic dysfunction. Significant increases in the intraatrial and intraventricular conduction intervals were observed following MI creation and heart failure induction compared with baseline values, as evidenced by increases in the duration of the P wave and QRS complex. Significant increases in corrected QT interval and ventricular refractoriness were observed. Acute transient ischemia induced sustained ventricular tachycardia or ventricular fibrillation in 21 of 29 dogs (72%). CONCLUSION: This canine model can serve as a useful tool for studying ventricular arrhythmias during the interactions of healed infarction, heart failure, increased sympathetic tone, and myocardial ischemia.     

Disorders of heart rhythm during bicycle ergometry in ischemic heart disease]

During a test on a bicycle ergometer disorders of cardiac rhythm were revealed in 41 (20.5%) out of 240 patients with ischemic heart disease who underwent coronary arteriography. It is concluded that disorders of cardiac rhythm are mostly encountered in patients with ischemic heart disease attended by stenosing changes of the coronary arteries and disorders of left ventricular contractile function as demonstrated by ventriculography. In a few cases ventricular extrasystole may be the only sign of myocardial ischemia in patients with ischemic heart disease.     

大动脉炎累及冠状动脉7例临床分析

目的 :分析大动脉炎累及冠状动脉的患者的发病率、临床特点、冠状动脉病变性质及治疗效果 ,为临床提供参考。方法 :1990～ 2 0 0 2年 5 2例大动脉炎住院患者中 7例 (女 5例、男 2例 )患者 ,根据其临床表现、辅助检查、大血管造影及冠状动脉造影 ,证实为大动脉炎累及冠状动脉 ,予以激素、扩管等对症治疗 ,随访观察患者症状、心功能、炎症指标等病情变化。结果 :7例患者中 6例有不同程度的心肌缺血症状 ,2例出现心肌梗死 ,3例出现心力衰竭症状。 1例冠状动脉造影显示为左旋支中段中度狭窄 ,1例为左冠状动脉前降支开口处重度狭窄 ,另1例MRI和磁共振血管造影示广泛前壁心肌梗死。经对症治疗后 ,患者血沉、C反应蛋白均能回复正常 ,而症状与心功能无明显改善。结论 :多发性大动脉炎累及冠状动脉并不少见 ,可发生于冠状动脉开口与近端 ,亦可累及中段 ,随病程延长 ,患者心脏情况恶化 ,临床上应对有心肌缺血症状的大动脉炎患者积极行冠状动脉造影 ,早期诊断 ,积极治疗。     

Electrocardiographic evidence suggestive of myocardial infarction without significant organic heart disease

One hundred nineteen catheterized patients had ECG evidence of myocardial infarction in the absence of significant narrowing of coronary arteries or localized contractile abnormalities of the left ventricle. Eighty-seven had organic heart disease, but 32 had no demonstrable abnormality. ECG alterations in the latter group were almost equally divided between those in lead aVF and in the right precordial leads. Although certain depolarization defects are highly suggestive of myocardial infarction, similar changes may rarely be seen in normal people.     

Clinicopathologic correlates of acute ischemic heart disease syndromes

To better define the relations among acute and chronic coronary arterial lesions and different syndromes of acute ischemic heart disease, the clinicopathologic findings in 100 recent myocardial infarcts in 83 patients were reviewed and the results correlated with those of previous studies. Severe atherosclerosis (greater than 75 percent narrowing of luminal cross-sectional area) involved three or more major coronary arteries in 65 percent; two arteries in 16 percent, one artery in 15 percent, and no arteries in 4 percent of cases. The incidence rate of recent occlusive coronary arterial lesions was 61 percent, including 50 (90.2 percent) of 55 grossly apparent transmural infarcts, 9 (34.6 percent) of 26 grossly evident subendocardial infarcts and 2 (10.5 percent) of 19 multifocal microinfarcts associated with clinical episodes of acute coronary insufficiency (p <0.001). The 61 recent occlusive lesions consisted of two thromboemboli, two isolated plaque hemorrhages and 57 in situ thrombi that were associated with a high incidence rate of plaque erosion, rupture and hemorrhage. Clinical conditions predisposing to reduced coronary perfusion were identified before the onset of 26.2 percent of infarcts with recent occlusions and 61.5 percent of infarcts without recent occlusions (p <0.001). Clinical onset of infarction was followed by severe cardiac pump failure or congestive heart failure in 63.9 percent of infarcts with and 41.0 percent of infarcts without recent occlusions (p = 0.04).From this and previous studies, it is concluded that (1) acute ischemic heart disease does not have a constant relation with the severity of chronic atherosclerosis; (2) myocardial necrosis commonly occurs in the absence of acute permanent coronary occlusion, but in this setting is usually limited to subendocardial involvement of variable extent; (3) acute coronary thrombosis frequently acts as a major factor in determining the extent and distribution of an evolving infarct, as indicated by the large incidence of occlusive coronary thrombi with regional transmural infarcts; and (4) coronary thrombus formation is not dependent on a generalized impairment of coronary perfusion, either before or after the onset of infarction.     

Cardiac transplantation of skeletal myoblasts for heart failure

Heart failure has become the most prevalent cardiovascular syndrome, and its incidence continues to increase. Most cases of heart failure develop as a result of myocardial infarction. Although current treatment modalities have brought us the opportunity to reduce mortality and morbidity after myocardial infarction, our progress has plateaued due to our inability to treat the underlying problem, death of cardiomyocytes. Recently, a new option has emerged. Transplantation of undifferentiated cells into the damaged heart is a promising new treatment modality. These cells may have the capability of adapting to the cardiac environment, regenerating the damaged muscle, restoring cardiac function and preventing transition to heart failure. During the last few years many cell types have been proposed for cardiac repair and promising pre-clinical studies have moved some of these into the clinic. The most widely studied cell type is the progenitor cell of adult muscle, or the myoblast. When transplanted into the heart myoblasts are able to engraft and to a large degree regenerate the infarcted area. Although the feasibility of myoblast transplantation has been proven in animal models of infarction, many questions remain unanswered. In this review we will try to present an overview of where intracardiac myoblast transplantation stands and where it is heading. We also provide our insight into the future potential for myoblast transplantation clinically.     

An autopsy case of rheumatoid arthritis with aortic steno-insufficiency, angina pectoris and severe heart failure

Although nonspecific pericarditis, myocarditis, valvulitis, and coronary arteritis are known as cardiac lesions that accompany rheumatoid arthritis (RA), there have been few reports of the occurrence of clinically severe valvular disease. We report here the case of 69-year-old man with a 25-year history of RA who died of acute left-sided heart failure complicating to aortic steno-insufficiency and angina pectoris. Autopsy findings revealed the coincidence of a congenital bicuspid aortic valve with chronic inflammation, fibrosis and calcification; eccentric hypertrophy and myocardial fibrosis of the left ventricle; 75% luminal narrowing of the proximal portion of the coronary artery due to atherosclerosis, and narrowing of the small arteries of the cardiac muscle due to angitis. It is deduced that the coronary artery lesions, aortic valve lesions and myocardial lesions were aggravated by the bicuspid aortic valve, changes with ageing and corticosteroid therapy.     

Interrelations between obstructive changes in the coronary arteries and clinical manifestations of heart failure in patients after myocardial infarction]

The study was undertaken to examine clinical and angiographic signs in 154 patients with prior myocardial infarction. There was a relationship between the left ventricular performance and heart failure stages and the number of diseased left ventricular segments and heart failure stages. With an increase in the number of diseased left ventricular segments, cardiac contractility decreased. Severe stages of heart failure were observed in the diseased channel of the infarct-related anterior interventricular branch and in its occlusion. The stages of heart failure were unassociated with the number of diseased coronary arteries, and the presence or absence of collaterals. There were more frequently eccentric stenoses of type II and/or irregular shape in severe heart failure groups.     

Myocardial bridge - congenital anomaly of coronary vasculature.

Coronary artery lumen compression during systole by a myocardial bridge can cause myocardial ischemia and even necrosis. Myocardial bridges represent a variant of norm or congenital anomaly of coronary vasculature. They belong to relatively frequent autopsy findings (5.4-85.7%) and are most often located over left anterior descending artery. Main angiographic sign of myocardial bridging is effect of contrast medium pushing out during narrowing of intramural part of a coronary artery during systole. In most cases systolic coronary artery narrowing not associated with any symptoms and bridging is just accidentally found at angiography. However some bridges produce clinical manifestations such as angina pectoris or myocardial infarction which require drug treatment. Therapy failures are managed by stenting or surgery. Under certain conditions systolic coronary artery narrowing can cause sudden death therefore all patients with clinically overt myocardial bridges should be under continuous medical surveillance. A case of clinically successful open heart supracoronary myotomy in a patient with myocardial ischemia due to a bridge causing 80% systolic narrowing of the left anterior descending coronary artery is presented.