[Pathophysiologic views on the coronary circulation].
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Biomedical subjects
Publications and source records attributed to L R Erhardt.
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ST segment elevations in leads CR4R or V4R indicating right ventricular (RV) involvement are sometimes seen in patients with acute inferior transmural infarction. Whether the RV lesion per se or the concomitant infarction of the posterior septum causes this ECG pattern is unknown. We describe a patient with anteroseptal transmural infarction who developed unusually marked ST segment elevations in lead V4R. At autopsy, extensive old fibrotic infarction was found, involving the anterior and lateral RV walls, as well as recent necrosis of the interventricular septum. These findings suggest that the ST segment elevation in V4R in patients with RV infarction may not be caused by the RV necrosis per se but rather by visualization of the posterior septum through the necrotic RV myocardium.
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3 patients with chronic complete AV block were found at autopsy to have granulomatous giant cell myocarditis (GGCM). In 1 patient an unusual clinical course led to more extensive investigation including echocardiography which revealed ventricular septal abnormalities. A review of the literature is presented. Although GGCM is a rare disease echocardiography may be a useful screening procedure in patient with AV block especially in the presence of immunological disorders.
The ST segment in a single right-sided chest lead, CR4R, has been studied in 92 consecutive patients with acute inferior transmural left ventricular myocardial infarction. A transient ST- segment rise of more than 1 mm. was recorded in 35 patients, and strongly indicated a significant extension of the infarction to the posterior free right ventricular wall according to autopsy findings. This ECG pattern was furthermore associated with right-sided heart failure, hypotension and oliguria. Left heart failure was also common. The short-term prognosis of patients with ST-segment elevation in CR4R was poor.
The presence of radioactivity in coronary arterial thrombi was studied at necropsy by autoradiography in 12 patients with acute myocardial infarction. Seven patients had been given 125I-and five patients 131I-labeled fibrinogen. With a short interval (less than 10 hours) between onset of symptoms and injection of fibrinogen the entire thrombus was radioactive in four of five patients, whereas with longer time intervals only parts or none of the thrombus contained detectable radioactivity. The findings give further evidence that thrombus formation in acute myocardial infarction probably is a slow process and that the major part of the thrombus may form after the onset of necrosis.
The present study on 55 consecutive patients with acute myocardial infarction (AMI) draws attention to the relationship between different enzyme maxima in AMI, with special reference to serum gamma-glutamyl transpeptidase (S-GT). In more than 60% of the patients the S-GT was increased during the hospital stay. The S-GT rise nearly always began during the first days, reached a maximum within 5--8 days and normalized with 2--3 weeks. We failed to find the late increase in S-GT reported by others. The rise of S-GT is particularly common in patients with inferior infarction, with or without right ventricular involvement. We conclude that S-GT activity is not a useful early or late indicator of AMI but a very sensitive test for hepatic dysfunction in patients with AMI.
In an attempt to diagnose ventricular mural thrombi complicating acute myocardial infarction (AMI), 80 patients have been given 100 muCi 125I-labelled fibrinogen after admission to a CCU. Precordial radioactivity was recorded for the following 6 days over four sites corresponding to chest leads CR1-CR4. A sustained rise in radioactivity of at least 15% of initial recordings was classed as type A pattern, a minor rise or flattened response as type B pattern and a rapid decrease as type C pattern; 28% showed a type A, 19% a type B and 54% a type C pattern. There was no significant difference between the groups in incidence of pericardial friction rub but when patients with suspected pericarditis (as evidenced by characteristic pains) were added, pericarditis was significantly overrepresented in the type A group. Smaller infarctions (SGOT less than 100 U/1) were significantly more common in patients with a type C decay pattern. No differences were noted between the groups as regards type and site of the infarction. A sustained rise in precordial radioactivity after an AMI may be an indication of mural thrombosis but the influence of other factors secondary to an infarction, e.g. pericarditis, cannot be determined at present.
Involvement of the RV in AMI is not as rare as previously thought and may lead to a particular clinical and hemodynamic syndrome with raised RV filling pressures, hypotension and oliguria. Major extension to the RV from inferior LV infarctions can be recognized by ST segment elevations iead CR4R or V4R. The significance of anterior RV extension and of RV papillary muscle infarction is still largerly unknown. It has been suggested from autopsy studies that the prognosis of patients with RV involvement might be poor healed extensive RV infarction is rarely seen. Indeed, ST segment elevation in lead CR4R indicating RV involvement has been found to carry a poor short-term prognosis. An increased awareness of the possibility of impaired RV function and of the special therapeutic considerations in some of these patients may increase survival.
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Sixty-one first admissions to a coronary care unit have been analysed regarding "delay period" from onset of chest pain to admission to the CCU in relation to psychosocial information, collected from the closest relative. On the whole, psychosocial variables seemed to play a modest role in the determination of the delay period. However, one "type A behavior" variable, inability to relax during leisure time, was related to a shorter delay period. Young subjects tended to have a relatively short delay.
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