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Biomedical subjects

A E Raizner

Publications and source records attributed to A E Raizner.

At least 91 records · Page 5Linked to original sources

Surgery in active infective endocarditis.

Controversy persists concerning the role of early surgical intervention in severe infective endocarditis (IE). We therefore reviewed 163 episodes of well-documented IE in which 32 cardiac operations were performed during the active phase of IE. Congestive heart failure (CHF) was the principal indication for surgery in 88% (28/32); systemic emboli, 1/32; and persisting sepsis, 3/32. Staphylococcus and enterococcus were the most common infecting organisms in the operative group (44% and 16% respectively). Surgical mortality (11/32,37%) did not differ (p greater than 0.05) from medical mortality (26/131,20%). All 11 operative deaths occurred in patients moribund prior to surgery, including three with preoperative cardiac arrest. Surgical patients undergoing preoperative cardiac catheterization demonstrated marked CHF: a mean left ventricular end-diastolic pressure of 25.3 mm Hg. The mean cardiac index in 8/11 surgical deaths was lower (p less than 0.05) vs surgical survivors: 2.21/min/m2 vs. 3.21/min/m2. Postoperative complications were rare in the 21 surgical survivors. There were no episodes of continued infection, prosthetic dehiscence, or advanced heart block; only one paravalvular leak; and one systemic embolus. These findings emphasize the high medical and surgical mortality in patients with IE, suggest that delayed operative intervention may be a major causative factor resulting in a high surgical mortality, and justify an aggressive surgical approach in patients with valve dysfunction and heart failure. These data indicate that survivors of surgical intervention during active IE have eradication of infection and few postoperative complications.

Adult↗

Coronary artery spasm.

Coronary artery spasm is an important pathogenetic mechanism in some forms of myocardial ischemic disease. Factors that may be important in the genesis of spasm include the autonomic nervous system, prostaglandins, endoperoxides, thromboxanes, and the calcium availability to the contractile apparatus. Spasm results in myocardial ischemia with attendant chest pain and electrocardiographic and hemodynamic changes; it is the primary pathogenetic mechanism in Prinzmetal's variant angina and has been found in association with classic angina pectoris and acute myocardial infarction. Diagnosis of coronary artery spasm is firmly made only by coronary angiography. Treatment includes the use of both short- and long-acting nitrates and the slow-channel blocking agents such as verapamil, nifedipine, and perhexiline.

Angina Pectoris↗

Diastolic mitral regurgitation in patients with hypertrophic cardiomyopathy.

An analysis of the left ventricular angiograms of 31 patients with hypertrophic cardiomyopathy revealed diastolic mitral regurgitation in 4, a prevalence of 12.9%. The clinical, echocardiographic, angiographic, and hemodynamic data of these patients were reviewed. Diastolic mitral regurgitation could not be attributed to arrhythmia, PR interval prolongation, atrioventricular dissociation, aortic insufficiency, or aortic stenosis. Reduced left ventricular compliance was evidenced by elevated end-diastolic pressure following angiography and reduced diastolic E-F slope on echocardiography. It is speculated that the rapid inflow of blood into a poorly compliant ventricle established a turbulent flow pattern that resulted in the "floating" of blood back into the left atrium.

Angiocardiography↗

Myocardial bridges in man: clinical correlations and angiographic accentuation with nitroglycerin.

Little is known of the clinical significance of myocardial bridges, which may be recognized angiographically as systolic coronary artery narrowing (SCAN). A retrospective review of a 1 year's experience (313 consecutive coronary arteriograms) revealed 5 patients with SCAN, an incidence of 1.6%. SCAN involved the proximal and/or middle segments of the left anterior descending coronary artery in all patients. It is of particular note that the administration of nitroglycerin noticeably accentuated the SCAN phenomenon in each of 3 patients to whom it was administered. Four of the 5 patients had left ventricular hypertrophy due to hypertrophic cardiomyopathy (2), aortic stenosis (1), and hypertension (1). All 5 patients with the SCAN phenomenon had anginal chest pains, and critical obstructive coronary atherosclerosis was observed in only 2 cases. The other 3 patients showed, otherwise normal coronary arteriograms. Thus, myocardial bridges appear to be angiographically manifest predominantly in patients with cardiac hypertrophy. Nitroglycerin, which accentuates SCAN, might be useful as a provocative test to enhance the angiographic recognition of this phenomenon. The possible role of myocardial bridges in the production of myocardial ischemia warrants further investigation.

Adult↗

Recurrent catheter-induced coronary artery spasm.

Catheter-induced spasm has generally been considered to represent an iatrogenic phenomenon without important clinical significance. This report describes two patients who developed catheter-induced spasm in the proximal segment of the right coronary artery in separate studies performed in different laboratories by means of different catheter techniques. One of these patients developed right coronary spasm on three occasions and, in addition, developed catheter-induced spasm of the left main trunk during two different studies. These observations would add support to the hypothesis that a predisposition to coronary artery spasm may exist in certain individiuals. Catheter-induced spasm deserves attention, since it may provide a means of identifying spasm-prone individuals.

Arteries↗

The clinical significance of atrial pacing-induced Mobitz I atrioventricular block in patients with coronary artery disease.

Two hundred consecutive patients with a history of chest pain undergoing cardiac catheterization, coronary angiography and atrial pacing have been analyzed to assess the clinical significance of Mobitz I atrioventricular (A-V) block developing with the stress of atrial pacing. Of 160 patients with coronary artery disease, 26 (16%) developed Mobitz I A-V block at rates below 140 beats/min. Eighteen of these 26 patients (69%) had electrocardiographic evidence of old inferior wall myocardial infarction, compared to only 34 of the remaining 134 patients (29%) (P = less than 0.01). During the mean follow-up of 29.5 months (range 18-50 months) none of the 26 patients has developed spontaneous second or third degree A-V block. Twenty-three of the 26 patients had an exercise test within one week of the pacing study. No A-V block was noticed during or immediately following exercise, although the mean heart rate attained during exercise was higher than the mean pacing rate at which the A-V block occurred (136 +/- 5 vs 122 +/- 3, P = less than 0.01). Eighteen of these 23 achieved heart rates equal to or higher than the pacing rate at which A-V block developed. Nineteen (83%) shortened their P-R interval during exercise and 4 (17%) did not change the P-R length. Although atrial pacing-induced Mobitz I A-V block may indicate a latent A-V nodal conduction abnormality in some cases, its demonstration does not necessarily predict the occurrence of spontaneous advanced A-V block. Exercise should not be restricted in these patients on the basis of such a finding during a pacing study.

Atrioventricular Node↗

Another look at Prinzmetal's variant angina.

Prinzmetal's variant angina is commonly referred to as a syndrome apart from the usual spectrum of atherosclerotic disease. 2 well-studied patients with this form of angina gave past histories compatible with classical angina. They were found to have, in addition to severe atheromatous lesions, coronary artery spasm resulting in complete obstruction of the vessel during Prinzmetal attacks. The concomitant electrocardiographic ST segment elevations are probably the reflection of transmural ischemia injury resulting from the transient complete occlusion of the corresponding coronary artery. Electrocardiograms taken during milder resting anginal attacks showed minimal nonspecific changes of the electrocardiogram or T wave inversions which may possibly reflect less severe ischemia, secondary to milder coronary spasm. These observations support the possibility that at least in some cases, Prinzmetal's angina may just be a phase in the life history of patients with atherosclerotic disease, during which recurrent severe coronary spasms may occur.

Angina Pectoris↗

Congenital absence of the left pericardium: an unusual palpation finding and echocardiographic demonstration of the defect.

A patient with classical clinical and roentgenographic features of congenital absence of the left pericardium is described. On physical examination in the supine position, the precordial apical impluse was markedly displaced laterally. In the left lateral decubitus position, however, the apical impulse was felt in a mor medial location. This apparently paradoxical movement of the apical impulse was not found in persons with normal hearts or with left ventricular enlargement of hypertrophy, and may be characteristic of the pericardial defect. Further, with echocardiography we were able to demonstrate the absence of a pericardial echo on the lateral surface of the heart. Thus, echocardiography may be a useful noninvasive tool in the diagnosis of this defect.

Adult↗

Effect of routine treadmill testing on the serum enzymes.

A number of serum enzymes increase after strenuous exercise. However, there is no information concerning these enzymes after routine treadmill testing, SGOT, CPK and LDH were determined before, immediately after, at 4 and 24 h postexercise in 100 subjects undergoing this test. When the group was considered as a whole, only the SGOT showed a slight but statistically significant elevation immediately after exercise. The mean values of the SGOT at 4 and 24 h, as well as the mean values for the CPK and LDH at all times after exercise, were not significantly increased. SGOT increased more significantly immediately after exercise in those patients who exercised more than 6 min. This group of patients also showed modest but statistically significant elevations of their CPK immediately after completion of the exercise test. Analyses of the data in relation to the presence or absence of ischemic ST shifts and presence or absence of documented coronary obstruction, failed to show any significant correlation. The effect of conditioning on the serum enzyme changes postexercise was not demonstrable.

Aspartate Aminotransferases↗