Biomedical subjects
M J Frank
Publications and source records attributed to M J Frank.
Uterine tumor mimicking Meigs's syndrome (intractable heart failure).
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Pulseless disease producing abdominal angina and simulating anorexia nervosa.
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Cardiomyopathy without cardiomegaly in alcoholics.
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Effects of lidocaine on potassium, sodium, and water in ischaemic myocardium.
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Hemodynamics at rest and during exercise in combined aortic stenosis and insufficiency.
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Exercise stress testing in the evaluation of the cardiac patient.
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Elevated diaphragm from hematoma.
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Effects of cardiac tamponade on myocardial performance, blood flow, and metabolism.
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Comparison of left ventricular volumes by single-plane cineangiography and by indicator dilution.
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The effect of rest and physical effort on the left ventricular burden in mitral and aortic regurgitation.
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Left ventricular coronary flow, metabolism, and performance in mild congenital heart disease with increased left ventricular flow or pressure.
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Effect of angiotensin on myocardial function.
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Ball variance: potentially lethal degeneration of the Starr-Edwards aortic valve poppet.
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Ventricular function in noncardiacs with alcoholic fatty liver: role of ethanol in the production of cardiomyopathy.
Since many patients with cardiomyopathy have a history of chronic ethanolism often associated with malnutrition, we have evaluated left ventricular (LV) function in alcoholics with fatty liver, who had no clinical evidence of cardiac or nutritional disease. During an afterload test of LV function the pressor response to angiotensin evoked a threefold rise of enddiastolic pressure in the alcoholic group which was substantially greater than the 4 mm Hg rise in control subjects. The stroke volume and stroke work response in the noncardiac alcoholic was significantly less than in controls. Diminished LV function was corroborated in the noncardiac alcoholic at rest, using a contractility index. To evaluate the dose-response relationship of ethanol in the production of cardiac malfunction, two groups of noncardiac alcoholic subjects were studied acutely at low and moderate dose levels. After 6 oz, ventricular function, myocardial blood flow, and metabolism were not significantly affected. After 12 oz, there was a progressive rise of end-diastolic pressure and decrease of stroke output at a mean blood alcohol level of 150 mg/100 ml, reverting toward control by 4 hr. The coronary effluent transiently evidenced leakage of cell constituents, despite an increase of coronary blood flow, suggesting a direct but reversible cardiac injury. Myocardial extraction of triglyceride was enhanced, whereas FFA uptake was reduced. A possible role of myocardial triglyceride accumulation in heart muscle was considered in pathogenesis. Chronic ingestion of 16 oz of Scotch daily by an alcoholic subject while on a normal diet produced, after 12 wk, a progressive increase of heart rate and size, circulation time, and venous pressure, and a ventricular diastolic gallop. Normal values were restored within 7 wk after interrupting alcohol. These several studies suggest that the cumulative effects of repeated ingestion of ethanol in intoxicating doses can produce diminished LV function before clinical evidence of cardiac abnormality, or heart disease not necessarily related to malnutrition.
Equilibrium phenomena in solid dosage forms.
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An index of the contractile state of the myocardium in man.
There is a profound need, on both clinical and physiologic grounds, for a measure of the contractile state of the intact ventricle. Such a measure can be obtained by evaluating the force-velocity relationship with a correction for myocardial fiber length. The force-velocity relation can be expressed as the ratio of maximum rate of pressure rise to maximum isovolumetric pressure, a quantity which was described by Hill as the maximum rate of proportional rise of pressure and which is similar to the velocity constant of a chemical reaction. Division of this ratio by an estimate of ventricular circumference corrects for variations due to differences in initial fiber length. This index was evaluated in 11 normal subjects and 46 patients with cardiac disease during left heart catheterization. Maximum rate of pressure rise was obtained by electronic differentiation of the ventricular pressure pulse, and ventricular circumference, assuming a spherical ventricle, was calculated from volumes measured by indicator washout. The contractility index of normal subjects did not differ from that of patients with mitral stenosis, atrial septal defect, or chronic pulmonary disease (patients without left ventricular overloading). In contrast, in patients with left ventricular failure, the indices were more than two standard deviations below the mean value for normal subjects. Such a reduction was not noted in patients with pressure or volume overloading of the left ventricle before the onset of myocardial failure. During exercise, the index rose uniformly in patients without left ventricular disease, responded variably in compensated patients with volume or pressure overloading, and was virtually unchanged in patients with left ventricular decompensation. The administration of isoproterenol or digitalis resulted in increased contractility regardless of the patient's status. It is concluded that the use of this index in physiologic studies of the ventricle and in diagnostic and therapeutic decisions is justified.
Measurement of mitral regurgitation in man by the upstream sampling method using continuous indicator infusions.
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