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.     

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.     

Medial medullary infarct

Medial medullary infarct is a rare type of brain stem infarction first described in 1908. It was only since the broad use of MRI that an accurate clinical topographical correlation could be documented in survivors. We observed two patients; one of them had an anteromedial unilateral infarction in the upper medulla, and the clinical picture was characterized by contralateral hemiparesis, facial weakness, dysarthria and palatal weakness. The outcome was good. The second patient however showed a severe tetraparesis with only minor brain stem signs, secondary to bilateral anteromedian infarction with a large craniocaudal extension. He survived with severe residual impairment. The most likely cause of infarction was arteriosclerosis of the A. vertebralis and A. spinalis anterior, respectively. These two different cases suggest that the medial medullary syndrome is heterogeneous comprising small unilateral infarctions with mild clinical signs as well as large bilateral infarctions with a poor outcome.     

Modification of infarct size

The persistent high mortality from power failure resulting from myocardial infarction has stimulated an intensive search for methods of reducing infarct size, which has been shown to relate directly to the occurrence of power failure. By analyzing the time course of myocardial injury during ischemia, the reversibility of lesions with reperfusion, and the characteristics of reversibly injured tissues along the border zone of ischemic areas, concepts have been formulated regarding the possibility of salvaging marginally injured cells. Measures designed to diminish myocardial oxygen consumption, to increase blood flow or oxygen supply to ischemic areas, to increase substrate availability, or to change the degree of swelling and autolysis of injured cells have all been tested in experimental animals with some success. These methods are just beginning to be tested in the clinical setting, and, if successful, will no doubt usher in a new era in medical therapy for acute myocardial infarction.     

Perfusion-MRI in cerebral infarct

PURPOSE: To investigate the hemodynamic changes in patients with acute cerebral stroke by perfusion MRI. MATERIAL AND METHODS: In 12 patients with acute stroke in the territory of the middle cerebral artery, perfusion MRI was performed. Peak time, mean transit time, regional cerebral blood volume and regional cerebral blood flow were calculated in the infarction, the peri-infarction area and the contralateral hemisphere. RESULTS: In the infarction the mean blood flow was 29 ml/100 g/min, compared to about 40 ml/100 g/min in the peri-infarction area and the contralateral hemisphere. In two patients increased cortical blood flow was found in the infarction due to luxury perfusion. The cerebral blood volume was reduced in the infarction, but significantly increased, to 7.3 ml/100 g, in the peri-infarction tissue. CONCLUSION: Perfusion MRI allows one to differentiate various patterns of perfusion disorders in patients with acute cerebral stroke. The resulting data may be helpful in describing the pathophysiologic mechanisms of compensation.     

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.     

Myocardial infarct in the puerperium

Two women of 34 and 31 years suffered an acute myocardial infarction in the puerperium. One of them had many risk factors for atherosclerosis: hypercholesterolaemia, hypertriglyceridaemia, diabetes mellitus, hypertension, obesity, nicotine abuse and a positive family history for cardiovascular disease. She had an occluded right coronary artery and was successfully treated with percutaneous transluminal coronary angioplasty. The other patient had an acute myocardial infarction after her first delivery. She was known with hypercholesterolaemia, obesity and nicotine abuse. During her latest pregnancy she was treated with acetylsalicylic acid. Again she developed an acute myocardial infarction in the puerperium, probably due to coronary dissection. Although the incidence of acute myocardial infarction is low in the peripartal period (less than 1 in 10,000) the diagnosis should be considered when a woman presents with chest pain or dyspnoea.     

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.     

Stress echocardiography in myocardial infarct

For patients with recent myocardial infarction, the main determinants of prognosis are: extent of transmural necrosis, state of the infarct-related artery and the presence and extent of myocardium at risk. The basic principle underlying the use of stress echocardiography states that myocardial ischaemia produces abnormalities of regional wall motion which are by themselves early, sensitive and specific markers of decreased perfusion. Dobutamine infusion allows for evaluation of myocardial contractile reserve by increasing inotropism. In low doses it gives us information on regional viability. In high doses, wall motion under increased oxygen demand, it becomes dependent on the ability of the coronary arteries to increase blood flow. Dipyridamole induces coronary vasodilation. In low doses it produces an increase in the blood flow. In high doses the steal effect deviates blood from the regions dependent on stenosed arteries. Ischaemia and regional wall motion abnormalities ensue. A negative stress echocardiogram, either under dobutamine or dipyridamole, has an excellent negative predictive value while a positive stress echocardiogram is predictive of an increased rate of events in the follow-up.