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Biomedical subjects

G Gerstenblith

Publications and source records attributed to G Gerstenblith.

At least 55 records · Page 3Linked to original sources
PubMed1987

Silent ischemia predicts infarction and death during 2 year follow-up of unstable angina.

Silent myocardial ischemia as detected on Holter electrocardiographic (ECG) monitoring is present in greater than 50% of patients with unstable angina despite intensive medical therapy. The presence and the extent of silent ischemia have been correlated with an increased risk of early (1 month) unfavorable outcome including myocardial infarction and need for coronary revascularization for persistent symptoms. Seventy patients with unstable angina who had undergone continuous ECG monitoring for silent ischemia were followed up for 2 years; 37 patients (Group I) had Holter ECG evidence of silent ischemia at bed rest in the coronary care unit during medical treatment with nitrates, beta-receptor blockers and calcium channel antagonists; the other 33 patients (Group II) had no ischemic ST segment changes (symptomatic or silent) on Holter monitoring. Over a 2 year follow-up period, myocardial infarction occurred in 10 patients in Group I (in 2 it was fatal) compared with one nonfatal infarction in Group II (p less than 0.01 by Kaplan-Meier analysis); revascularization with either coronary bypass surgery or angioplasty for symptomatic ischemia was performed in 11 Group I and 5 Group II patients (p less than 0.05). Multivariate Cox's hazard analysis demonstrated that the presence of silent ischemia was the best predictor of 2 year outcome. Therefore, persistent silent myocardial ischemia despite medical therapy in patients with unstable angina carries adverse prognostic implications that persist over a 2 year period.

Angina Pectoris↗
PubMed1987

Negative inotropic effects of furosemide in the isolated rabbit heart: a prostaglandin-mediated event.

Furosemide is an effective diuretic that initiates a rapid diuresis and peripheral vasodilatation through renal adenylate cyclase inhibition and prostaglandin synthesis. Recently, it has been shown to be associated with activation of the neurohumoral vasoconstrictor mechanism and a further compromise of left ventricular function in patients with heart failure. The present study was performed to investigate the direct effects of furosemide on myocardial performance in the isolated perfused rabbit heart. Furosemide (10(-3) M) caused a significant decrease in developed pressure as well as a similar fall in coronary perfusion pressure. Furosemide also decreased myocardial contractility when the coronary perfusion pressure was kept constant. The change in developed pressure but not the decrease in coronary perfusion pressure could be blocked by treatment with indomethacin. Furosemide did not antagonize rabbit cardiac membrane adenylate cyclase. Therefore, furosemide has a direct inhibitory effect on cardiac contractility that is related to prostaglandin synthesis.

Adenylyl Cyclases↗
PubMed1987

Prolonged decrease in cardiac volumes after maximal upright bicycle exercise.

Sequential exercise-gated cardiac blood pool scintigrams provide a noninvasive technique for evaluating the effect of therapeutic interventions on cardiac volumes and function only if both exercise periods are equivalent in the absence of an intervention. To assess whether they are indeed equivalent, 14 healthy subjects underwent gated blood pool scintigraphy during two maximal upright exercise periods separated by 60 min without changing position. Although resting cardiac output and blood pressure returned to base-line values 60 min after the first exercise period, mean resting heart rate was markedly higher (89.4 +/- 2.7 vs. 66.5 +/- 2.5 beats/min, P less than 0.001) and upright cardiac volumes lower [39.1 +/- 4.9 vs. 56.3 +/- 6.0 ml, P less than 0.001, for end-systolic volume (ESV) and 112.6 +/- 8.0 vs. 144.9 +/- 9.0 ml, P less than 0.001, for end-diastolic volume (EDV)] than before the first exercise period. These differences persisted during low levels of the subsequent exercise but not at high and maximum work loads. Cardiac volumes and heart rate 60 min after an identical exercise protocol in a second group of 22 subjects who received propranolol, 0.15 mg/kg iv, after their initial exercise, however, were the same as those preexercise. Thus higher sympathetic tone may be responsible for the persistently higher heart rate and decreased cardiac volumes after exercise, and the assumption that cardiac volumes and function are similar during two closely spaced sequential exercise studies is not always valid.

Adult↗
PubMed1987

Prophylactic antiarrhythmic therapy of high-risk survivors of myocardial infarction: lower mortality at 1 month but not at 1 year.

To determine whether prophylactic antiarrhythmic therapy influences mortality in high-risk patients after acute myocardial infarction, 143 such patients were randomized in a double-blind individually dose-adjusted, placebo-controlled trial an average of 14 +/- 7 days after myocardial infarction and followed for 1 year. Patients were judged to be at high risk on the basis of (1) ejection fraction less than 40% (n = 60), (2) arrhythmias of Lown class 3 or higher (n = 26), or (3) both (n = 57). Aprindine was chosen because of its long half-life, few side effects, and antiarrhythmic efficacy. Baseline characteristics in the treatment arms did not differ. Holter-detected arrhythmias were reduced in aprindine-treated patients at 3 months (p less than .001) and at 1 year (p less than .001). One patient was lost to follow-up; in the remaining patients 1 year mortality was 20% (28/142; 12 aprindine and 16 placebo). There was no significant difference between the two study arms in overall mortality and sudden death. However, among those who died, median duration of survival was longer in aprindine-treated patients (86 vs 21.5 days) (p = .04). Although antiarrhythmic treatment with aprindine of high-risk patients after myocardial infarction does not affect 1 year survival, mortality appears to be delayed; thus there may be a role for short-term treatment before more definitive therapy such as surgery.

Aprindine↗
PubMed1987

Functional and metabolic consequences of vitamin B-6 deficiency in the rat heart.

The cardiac functional and metabolic consequences of pyridoxine deficiency were studied in rats maintained on a pyridoxine-deficient diet for 10 weeks. Because food intake was diminished in the pyridoxine-deficient rats, a second group of animals was fed a diet restricted to the intake of the pyridoxine-deficient animals. The inotropic response (developed pressure) to an isoproterenol or Ca2+ concentration response curve was measured simultaneously with high energy phosphate levels using a modified Langendorf apparatus and 31P nuclear magnetic resonance spectroscopy. The inotropic response to Ca2+ and isoproterenol was significantly decreased relative to controls in both the food-deprived and the pyridoxine-deficient groups. Developed pressure after adrenergic stimulation was significantly less in the pyridoxine-deficient than in the food-deprived animals. Phosphocreatine and ATP levels were maintained and did not differ among the control, pyridoxine-deficient, and food-deprived groups during isoproterenol and Ca2+ stress, implying that the diminished inotropy was not due to an abnormality in generation of high energy phosphate levels.

Adenosine Triphosphate↗
PubMed1987

Exercise and the aging heart.

Studies of the effect of age on cardiac function during exercise are confounded by the increasing prevalence of disease and sedentary lifestyle that accompany aging and by the lack of techniques to clearly distinguish between the contribution of changes in central circulatory and peripheral factors to the age-related alterations in cardiovascular physiology. Although diastolic filling is delayed at rest, end diastolic volume is not compromised either at rest or during exercise. Exercise heart rate is invariably reported to decrease with increasing age, whereas stroke volume has been reported to be both increased and decreased in studies of different populations. Most investigators report an increase in end systolic volume and a diminished ejection fraction in older individuals as well. These changes are mediated, in part, by an age-associated diminished responsiveness to beta-adrenergic stimulation.

Aging↗
PubMed1987

Cardiovascular response to exercise in younger and older men.

Measurements of cardiac performance for humans at various ages is influenced by the variable examined, the population and techniques employed, and the factors that co-vary with age, including the presence of disease and physical conditioning. Interstudy differences in the extent to which occult coronary disease is present in older subjects and in the level of physical conditioning among subjects may underlie the variable perspectives contained in the literature of how aging affects cardiovascular function. In carefully screened, highly motivated but not athletically trained community-dwelling subjects, resting cardiovascular parameters are not age related except for systolic blood pressure, which increases with age. During vigorous exercise the mechanisms used to achieve a high level of cardiac output shift from a dependence on a catecholamine-mediated increase in heart rate and inotropy to a dependence on the Frank Starling mechanism. One reason for the age difference in cardiovascular response to exercise may be a diminished responsiveness to beta-adrenergic stimulation in these subjects. In other elderly subjects who cannot exercise to high work loads, a decline in stroke volume as well as heart rate at peak exercise has been observed. Whether the inability of these individuals to augment stroke volume is caused by a decrease in the ability of the heart to increase diastolic filling, by a decrease in systolic pump function caused by an increased afterload, by intrinsic myocardial contractile defects, or by a greater diminution of the cardiovascular response to beta-adrenergic stimuli is presently unknown.

Adult↗
PubMed1986

Assessing the total ischemic burden in the management of unstable angina. A review.

Unstable angina is a common ischemic syndrome that is characterized by chest pain occurring at rest often with transient ischemic electrocardiographic changes. Although most patients with unstable angina experience relief of pain with intensive medical therapy while in the coronary care unit, they subsequently have a high incidence of unfavorable cardiac events usually occurring within several months. Continuous electrocardiographic monitoring for ischemia has demonstrated a relatively high incidence of ischemic episodes both in patients with stable and unstable angina pectoris. The prognostic importance of such findings has been previously uncertain. The prognostic significance of silent myocardial ischemia in patients with unstable angina receiving intensive medical therapy has been addressed in a study of hospitalized patients in a coronary care unit. All patients were treated with nitrates, nifedipine, and propranolol. Continuous two-channel electrocardiographic monitoring was performed during the first two days of medical therapy. The electrocardiographic recordings were interpreted blindly for frequency and duration of ischemic changes, and these episodes were determined to be either symptomatic or silent. The prevalence of silent ischemic episodes, their prognostic significance, their contribution to the total ischemic burden, and the effects of different medical regimens on these variables are discussed.

Adrenergic beta-Antagonists↗
PubMed1986

Silent ischemia as a marker for early unfavorable outcomes in patients with unstable angina.

We examined the prevalence and prognostic importance of silent myocardial ischemia detected by continuous electrocardiographic monitoring in 70 patients with unstable angina. All the patients received intensive medical treatment with nitrates, beta-blockers, and calcium-channel blockers. Continuous electrocardiographic recordings were made during the first two days in the coronary care unit to quantify the frequency and duration of asymptomatic ischemic episodes, defined as a transient ST-segment shift of 1 mm or more. Thirty-seven patients (Group 1) had at least one episode of silent ischemia, and the other 33 patients had no silent ischemia (Group 2). Over the subsequent month, myocardial infarction occurred in 6 patients in Group 1 and in only 1 in Group 2 (P less than 0.01); bypass surgery or angioplasty was required for recurrent symptomatic angina in 10 patients in Group 1 and only 3 in Group 2 (P = 0.02). Survival-curve analysis demonstrated that silent ischemia was associated with these outcomes (P less than 0.002), and multivariate analysis showed that silent ischemia was the best predictor of these outcomes among the 15 variables tested (P less than 0.002). Patients in Group 1 with 60 minutes or more of silent ischemia per 24 hours had a worse prognosis than those with under 60 minutes per 24 hours (P = 0.04). Silent ischemia occurred in more than 50 percent of our patients with unstable angina, despite intensive medical therapy, and it identified a subset who were at high risk for early unfavorable outcomes.

Adrenergic beta-Antagonists↗
PubMed1986

Therapeutic choices in unstable angina.

Unstable angina pectoris is a high-risk ischemic syndrome with complex, interacting pathophysiologic mechanisms that include coronary atherosclerosis, coronary vasoconstriction, and thrombosis. The roles of various medical strategies, including nitrates, beta blockers, calcium antagonists, and antiplatelet, anticoagulant, and thrombolytic agents, are discussed in conjunction with revascularization procedures such as coronary angioplasty and bypass surgery.

Adrenergic beta-Antagonists↗
PubMed1986

Postural changes in cardiac volumes in men in relation to adult age.

Cardiac volumes by equilibrium gated cardiac blood pool scans and heart rate were measured in the supine and sitting positions in 64 male volunteer subjects (age 25-80 yrs) who had been rigorously screened to exclude cardiovascular disease. After the upright position was assumed, the average cardiac output of all subjects was unchanged but heart rate increased and stroke volume decreased due to a decrease in end diastolic volume. Neither the supine or sitting cardiac output nor the average postural change in cardiac output, cardiac volumes or heart rate was age-related. While the average cardiac output among the subjects was unaltered with a change in posture, in some individuals it increased slightly while in others it decreased. The postural change in cardiac output among the individuals correlated by linear regression analysis with a change in heart rate only in younger subjects and with a change in stroke volume in all age groups, but the slope of this relationship was greater in older than in younger subjects. The postural change in stroke volume was strongly correlated with a change in end diastolic volume and this relationship did not vary with age. Thus, although the average postural change in cardiac output among healthy subjects is not age-related, a given change in cardiac output with posture in an older individual depends more on a change in stroke volume and less on a heart rate change than in a younger one. This result, like the response to vigorous upright exercise previously demonstrated to occur with aging, indicates a greater reliance in the elderly on the Frank-Starling mechanism than on heart rate for a given change in cardiac output in response to perturbations from the basal supine state.

Adult↗
PubMed1986

Use of the Frank-Starling mechanism during submaximal versus maximal upright exercise.

To evaluate the extent to which the Frank-Starling mechanism is utilized during successive stages of vigorous upright exercise, absolute left ventricular end-diastolic volume and ejection fraction were determined by gated blood pool scintigraphy at rest and during multilevel maximal upright bicycle exercise in 30 normal males aged 26-50 yr, who were able to exercise to 125 W or greater. Left ventricular end-systolic volume, stroke volume, and cardiac output were calculated at rest and during each successive 3-min stage of exercise [25, 50, 75, 100, and 125-225 W (peak)]. During early exercise (25 W), end-diastolic and stroke volumes increased (+17 +/- 1 and +31 +/- 4%, respectively), with no change in end-systolic volume. With further exercise (50-75 W) end-diastolic volume remained unchanged as end-systolic volume decreased (-12 +/- 4 and -24 + 5%, respectively). At peak exercise end-diastolic volume decreased to resting level, stroke volume remained at a plateau, and end-systolic volume further decreased (-48 +/- 7%). Thus the Frank-Starling mechanism is used early in exercise, perhaps because of a delay in sympathetic mobilization, and does not appear to play a role in the later stages of vigorous exercise.

Adult↗
PubMed1986

A phosphorus-31 nuclear magnetic resonance study of the metabolic, contractile, and ionic consequences of induced calcium alterations in the isovolumic rat heart.

Isolated adult rat hearts perfused in an isovolumic mode were used to study the effects of sodium-potassium pump inhibition and sodium-calcium exchange alterations on the tissue content of adenosine triphosphate, phosphocreatine, inorganic phosphate, and intracellular pH, all measured by phosphorus-31 nuclear magnetic resonance spectroscopy. Rates of oxygen consumption, contractile function, and the cell contents of calcium, sodium, and potassium also were determined. The inhibition of sodium-potassium adenosine triphosphatase, either by the reduction in perfusate potassium from 5.9 to 1 millimolar or less, or by the addition of 10(-4) molar ouabain, transiently increased systolic pressure. This was followed by a decrease in systolic pressure, an increase in diastolic pressure, and eventual inexcitability. This contractile profile was accompanied by a persistent increase in oxygen consumption, a monotonic decline in cellular adenosine triphosphate and phosphocreatine content, the development of marked intracellular acidosis, a gain in cell sodium and calcium content, and a reduction in cell potassium. Quite similar metabolic changes were also observed when cell calcium was increased after a reduction in perfusate sodium. These metabolic and contractile effects could be prevented or reversed by decreasing perfusate calcium. The results emphasize the profound role of calcium in modulating cell oxygen consumption, energy balance, pH, excitability, and force production. These data are discussed in light of changes in the myocardial energy supply/demand balance, as well as from the viewpoint of the known competition between mechanisms for mitochondrial calcium transport vs. high-energy phosphate production.

Animals↗
PubMed1986

Angina: current approaches to diagnosis, drug therapy, and surgical referral.

An abnormal resting ST segment renders the stress ECG impossible to interpret. Therefore, one must substitute a radionuclide stress evaluation in the presence of digitalis, left bundle-branch block, left ventricular hypertrophy, a paced rhythm, or any other condition that would cause abnormal baseline ST segments. All these are more common in the elderly. Beta-blocker therapy is useful in patients with demand-related ischemia because it decreases two of the major determinants of myocardial oxygen demand: heart rate and contractility. Propranolol, timolol, and metoprolol have been shown to decrease the reinfarction and mortality rates in patients who have had an infarction.

Adrenergic beta-Antagonists↗
PubMed1986

Hypertension in the elderly: treatment.

Hypertension in the elderly is a common problem confronting the practitioner today. The rationale for treating hypertensive elderly patients is presented in this article. Guidelines for the use of specific agents for the treatment of older patients are also discussed.

Adrenergic beta-Antagonists↗