Acute myocardial infarct and left ventricular dysfunction. Morphologic bases, clinical aspects and pharmacologic prevention

The morphological bases which condition left ventricular disfunction after acute myocardial infarction as well as the concepts of expansion and remodelling of the myocardium are reviewed. The clinical aspects indicating ventricular disfunction are presented and several pharmacological effects which have been proposed for the prevention of this situation. Particular emphasis is given to the role of angiotensin-converting enzyme inhibitors in the prevention of left ventricular disfunction after acute myocardial infarctions, based on the most recent clinical trials.     

Clinical and metabolic aspects of juvenile myocardial infarct

A clinical and metabolic study of 61 patients with myoocardial infarct before the age of 40 yr showed a high frequency of familial involvement, particularly in subjects with type IIA and IIB hyperbetalipoproteinaemia. Excess weight and arterial hypertension were rare, while premonitory angina was absent in 59%. Four subjects were diabetic. Oral glucose tolerance was normal in 14 and of diabetic type in 26 of 40 patients examined; the insulin response pointed to insulin-resistance. Dyslipidaemia was noted in 45%, including type IIA and IIB hyperbetalipoproteinaemia in 27%. Distribution of the frequency of infarct in function of cholesterolaemia classes gave a bimodal curve indicative of distinct normo- and hypercholesterolaemic groups within the series. Reduced glucose tolerance was more frequent in patients with low blood cholesterol. This suggests that reduced tolerance and high blood cholesterol are independent risk factors in coronary disease. No relation between the clinical and metabolic data could be ascertained.     

Right ventricular radiofrequency ablation of ventricular tachycardia after myocardial infarction

Radiofrequency transcatheter ablation of ventricular tachycardia in the setting of a prior myocardial infarction is typically performed with application of energy to the left ventricular endocardium. In this article, two cases are described in which successful radiofrequency transcatheter ablation of ventricular tachycardia occurred with energy delivery to the right ventricular septum after failed ablation attempts from the left ventricle. Both patients had tachycardias with a left bundle branch block morphology and markedly presystolic activity recorded from the right ventricular septum. Right ventricular septal activation mapping during ventricular tachycardia should be performed in patients with left bundle branch block tachycardia morphology and coronary artery disease to maximize efficacy of the catheter ablation procedure.     

Thrombolytic treatment of acute myocardial infarct. 3]

In a population of close to 2.5 million infants born from 1983 to 1993 registered in the California Birth Defects Monitoring Program, we compared the prevalence of structural birth defects among 2,894 infants with Down syndrome (DS) with that of infants without DS. Among 61 defects uniformly ascertained in affected and unaffected infants, 45 were significantly more common in DS, with atrioventricular canal (risk ratio = 1,009), duodenal atresia (risk ratio = 265), and annular pancreas (risk ratio = 430) being the most common. Most defects of blastogenesis and most midline defects were either nonsignificantly associated or not observed in infants with DS. Theories on the pathogenesis of defects in trisomies must account for the lack of and for the presence of specific defects.     

Secondary prevention of myocardial infarct

Preventive measures are the most powerful measures to treat manifestations of ischemic cardiopathy. Secondary prevention of myocardial infarction involves the following intervention areas: a) Limitation of adverse physiological and emotional consequences of the acute illness; b) Identification of the patients particularly exposed to the risk of new episodes of ischemic cardiopathy or to their consequences, namely reinfarction and sudden death; c) Institution of therapeutic attitudes, surgical or medical, that can prolong life and can oppose functional deterioration and prevent symptoms; d) Institution of measures that can oppose the progression of the initial disease that is, in almost all cases, atherosclerosis. Measures that can oppose the progression of cardiac disease and its consequences after an episode of myocardial infarction, and measures that can oppose the evolution of atherosclerosis are described in this article. The measures that can influence the risk factors after an episode of myocardial infarction are briefly commented: characteristics related to life style and physical exercise; smoking habits; plasmatic lipid levels; high blood pressure; and therapeutic substitution with estrogens after menopause. Pharmacological interventions in secondary prevention of myocardial infarction are described, namely with the following groups of substances: beta-adrenergic blocking agents; platelet active agents; anticoagulants; and angiotensin-converting enzyme inhibitors.     

Morphogenesis of atypical myocardial infarct

Morphology of atypical myocardial infarctions and their morphogenesis were studied in 120 cases. The importance of atherosclerosis as the background process, the secondary development of coronary thrombosis and the leading role of metabolic factors (hypoxy, acidosis, etc) in the origin of atypical myocardial infarctions were established.     

Heart muscle after heart infarct. Function of surviving heart muscle following acute myocardial infarct

In the initial phase of the infarction, there is a decrease of ventricular function due to loss of contractile activity. In addition, a negative effect of the paradoxical movement of the infarcted area on the hemodynamics of the ventricle is noted. The stiffening of the infarcted area in the early stage has a favorable influence on ventricular function, leading to a change in the elastic properties of the ventricle. The loss of ventricular compliance persists after the infarction, and its severity depends on the extent of myocardial destruction. In the non-compliant ventricle, the end-diastolic pressure rises without a proportionate increase in volume. Consequently, the ventricular function curve shows a shift downward and to the right, making it difficult to distinguish between the loss of contractile function or compliance in the heart in situ. Evaluation of the contractile properties of the surviving cardiac muscle in situ is, however, hardly possible due to the changed geometry and the additonal elastic elements functioning in series with the surviving muscle. To exclude these factors, a study of the contractile properties of the surviving cardiac muscle in the isolated state was carried out following experimental myocardial infarction in cats. By ligating several coronary branches, infarctions in the area of the left ventricle were caused; to avoid the ischaemic border zone of the infarction, right ventricular papillary muscles were studied. Haemodynamic investigations showed an increase in right ventricular end-diastolic pressure which persisted 6 weeks after infarction. As early as 48 hours but, more significantly 1 week after infarction, there was a decrease of actively developed force in the surviving cardiac muscle due to a lower rate of force development. The resting length tension curve of the surviving cardiac muscle after infarction showed no alterations; and 6 weeks following infarction, almost normal contractility parameters were observed. As a result of the infarction, a decrease in contractility in the surviving cardiac muscle is observed during the early stage, which regresses after complete recuperation.     

Thrombolysis following myocardial infarct. European Secondary Prevention Study

For evaluation of the management of patients with acute myocardial infarction, all cases of ten Zurich hospitals (278, 184 men and 94 women) in the period from 1 January to 31 March 1993 were analyzed retrospectively. 223 patients were released from hospital, 55 died. A follow-up was done 6 months after the patient's discharge by means of a questionnaires to the family doctor (return rate: 65.9%). 48.5% of patients were referred to hospital within the first 6 h. after onset of symptoms, 64% within the first 12 h. 28% (n = 76) of the patients received a thrombolytic therapy, of which 91% (n = 69) got streptokinase and 9% (n = 7) got tissue plasminogen activator. In 81% of the cases the thrombolytic therapy was done within the first hour in hospital, in accumulated 97% of the cases within two hours. In the age group under 65 years (39% of the patients, n = 109), 48 patients received thrombolysis (odds ratio [OR] = 1.0). In the age group between 65 and 74 years (24.5 % of the patients, n = 68), 19 patients received thrombolysis (OR: 0.49; 95% CI: 0.42-0.99; p < 0.05), and in the age group over 74 years (36.5% of the patients, n = 101), 9 patients were received thrombolysis (OR: 0.12; 95% CI: 0.05-0.28; p < 0.0001). 31% of the patients (n = 46) received a coronary angiography, 15% (n = 22) had coronary angioplasty, and 11% (n = 1) received coronary bypass surgery. There is evidence that there should be more importance attached to early hospitalization, if acute myocardial infarction is suspected. Thereby age alone should be considered as a contraindication for thrombolytic therapy. The issue of assumed underuse of thrombolytic therapy should be investigated all over Switzerland.