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Biomedical subjects

G A Hermann

Publications and source records attributed to G A Hermann.

11 recordsLinked to original sources

Progressive transmural electrographic, myocardial potassium ion/sodium ion ratio and ultrastructural changes as a function of time after acute coronary occlusion.

The progressive transmural electrographic, biochemical and ultrastructural changes as a function of time after acute coronary occlusion were systematically assessed in eight dogs. Transmural plunge electrodes with poles 1 mm apart were placed in the ischemic and nonischemic zones, and coronary occlusion was maintained for 4 hours. Transmural full thickness biopsy specimens were obtained from each zone for electron microscopy before, and 1 and 4 hours after occlusion. Endocardial and epicardial layers were also obtained for assessment of myocardial potassium ion (K+) and sodium ion (Na+) concentrations. Before coronary occlusion, local Q waves were recorded an average depth of 1.0 +/- 0.34 mm from the endocardial surface. After 1 hour of occlusion, Q waves appeared at an average depth of 3.8 +/- 0.67 mm and progressed to a depth of 5.2 +/- 0.7 mm at 2 hours, 6.2 +/- 0.5 mm at 3 hours and 7.0 +/- 0.5 mm at 4 hours. After 1 hour, ultrastructural changes of early ischemia, including a decrease in glycogen and mild mitochondrial swelling, were seen in the endocardial layer; the epicardial layer showed normal morphologic features. After 4 hours, the endocardial layer showed well developed ischemic changes marked by the loss of mitochondrial cristae, vacuolization, the appearance of amorhopous mitochondrial cristae, vacuolization, the appearance of amorphous mitochondrial densities, an increase in interfibrillary space and the appearance of I bands. In contrast, the epicardial layer at this time showed only early ischemic changes. At the end of 4 hours, the endocardial layer showed a marked decrease in myocardial K+ concentration and an increase in Na+ concentration leading to complete reversal of K+/Na+ ratio (0.7 +/- 1.0; P less than 0.001). In the epicardial layer, a smaller decrease in K+ concentration and an increase in Na+ concentration occurred, resulting in a diminution but not a reversal of K+/Na+ ratio (1.4 +/- 0.2; P less than 0.005). Thus, the dynamic evolution of an acute myocardal infarction involves a sequential progression from endocardium to epicardium as a function of time, resulting in an epicardial "border zone" in the early stages after acute coronary occlusion.

Animals

Pathophysiologic significance of S-T and T wave abnormalities in patients with the intermediate coronary syndrome.

The frequent association of new ST-T wave changes without Q waves in the surface electrocardiogram of patients with the intermediate coronary syndrome necessitates a better understanding of the pathophysiologic significance of this finding. A previous study in patients with stable coronary artery disease indicated that the surface electrocardiogram is insensitive in detecting epicardial Q waves. This relation was evaluated in 21 patients with the intermediate syndrome, characterized by recurrent chest pain at rest associated with significant new S-T or T wave abnormalities, or both, and no new Q waves in the surface electrocardiogram at the time of open heart coronary bypass surgery. Unipolar electrograms were recorded from the epicardial surface of the left ventricle before the bypass procedure. In 19 patients, epicardial electrograms revealed initial R waves over areas of the left ventricle in which the acute S-T and T wave abnormalities were evident in the surface electrocardiogram. Two patients had epicardial Q waves (one laterally and one inferiorly). In seven patients, a transmural biopsy specimen was also obtained from the ischemic area. All showed histologically normal myocardium without evidence of early inflammatory or necrotic tissue. Of the 19 patients discharged, only one demonstrated new postoperative Q waves that had been detected by epicardial recordings before bypass. In summary, patients with the intermediate syndrome exhibiting S-T or T wave abnormalities, or both without new Q waves in the surface electrocardiogram generally do not have Q waves either in the intraoperative epicardial or postoperative surface electrocardiogram. In addition, no histopathologic abnormalities are apparent in biopsy specimens taken from the ischemic area.

Adult

Local characteristics of the normal and asynergic left ventricle in man.

The significance of ventricular asynergy in determining medical prognosis and surgical risk in patients with coronary artery disease and its delineation by ventriculography have been of increasing interest. To determine the underlying histopathologic and electrographic features of left ventricular asynergy, 39 patients undergoing open heart surgery were studied. Thirty-six histopathologic specimens were obtained in 31 patients (26 as transmural needle biopsies and 10 as aneurysm resections). In four normally contracting areas and 12 hypokinetic areas, neither fibrosis nor early changes of myocardial damage was evident. In contrast, of eight akinetic areas there was more than 50 per cent muscle loss in four and from 30 to 35 per cent muscle loss in three, in only one area was there less than 10 per cent muscle loss. Of 12 dyskinetic zones there was more than 75 per cent muscle loss in 10 zones, 35 per cent in one and no pathologic abnormalities in one. Epicardial electrograms were obtained from 35 areas in 29 patients. Of 10 normally contracting ventricles, in one, pathologic Q waves were demonstrated only over the inferior area. Progressive increases in the severity of asynergy were associated with a progressive increase in frequency of initial abnormal Q waves. In only one of nine hypokinetic areas were epicardial Q waves exhibited, but they were present in six of 10 akinetic and five of six dyskinetic areas. Both histopathologic and electrographic data were available from 20 asynergic areas in 16 patients. Initial epicardial R waves were associated with normal biopsy specimens in seven of eight hypokinetic areas. Of seven akinetic areas, initial R waves were associated with 30 to 35 per cent muscle loss in three; of four areas with initial Q waves, there was a 35 per cent muscle loss in one and more than 50 per cent muscle loss in three. Similarly, of five dyskinetic segments, a QS pattern was associated with more than 75 per cent fibrosis in four. In one dyskinetic area there was an intial R wave in association with a normal appearing biopsy specimen. In summary, a good correlation exists between the severity of asynergy by ventriculography, the degree of muscle loss and the presence of epicardial Q waves. However, a significant amount of histologically and electrographically normal myocardium may be present even in severely asynergic areas.

Cardiac Catheterization

Reversible asynergy. Histopathologic and electrographic correlations in patients with coronary artery disease.

Histopathologic-electrographic studies of ventriculography depicted nitroglycerin responsive and unresponsive asynergic areas were performed in 25 patients. Of 29 areas, 12 improved with nitroglycerin, showing less than 10% muscle loss. Seventeen unimproved zones demonstrated significant fibrosis. Epicardial electrograms showed R waves in eight of nine improved zones. Of 11 unimproved zones, eight had Q waves. Histopathologic-electrographic data from five responders showed less than 10% muscle loss, of whom four had epicardial R waves. Six unresponsive areas had significant fibrosis, with a QS over four. Thus, nitroglycerin responsive asynergic areas are generally comprised of histologically intact myocardium and are associated with epicardial R waves.

Adult