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Biomedical subjects

G Gerstenblith

Publications and source records attributed to G Gerstenblith.

At least 91 records · Page 5Linked to original sources
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↗
PubMed1985

Safety of acute calcium antagonist withdrawal: studies in patients with unstable angina withdrawn from nifedipine.

The acute effects of nifedipine withdrawal were studied in 81 patients with angina at rest who had completed a prospective, double-blind, randomized trial of nifedipine versus placebo. Thirty-nine of the 81 patients (group 1) were withdrawn from nifedipine or placebo at the time of coronary artery bypass surgery for uncontrolled angina or left main coronary artery disease. When the patients withdrawn from nifedipine were compared with those withdrawn from placebo, no significant differences were seen in the incidence of hypotension, myocardial infarction, significant arrhythmias or vasopressor or vasodilator requirements during the perioperative period. Forty-two patients (group 2) completed 2 years on a protocol consisting of nitrates and propranolol, in addition to nifedipine or placebo. These patients were hospitalized for a controlled withdrawal of the study drug (nifedipine or placebo), and no significant difference was noted in either exercise performance on serial treadmill testing or the number or duration of episodes of ischemic ST-segment changes during continuous electrocardiographic monitoring. Eight patients continued to experience occasional episodes of angina at rest. Angina at rest recurred during the withdrawal period in 5 of these 8 patients. Four of these 5 patients were withdrawn from nifedipine. Of the 34 stable patients in group 2 who were not experiencing angina at rest before withdrawal, none had angina at rest during the withdrawal study period. Thus, there were no early untoward effects of acute nifedipine withdrawal either in patients undergoing coronary bypass surgery or in stable patients on long-term medical therapy. However, patients with persistent symptoms of angina at rest may experience early recurrent ischemia upon withdrawal from nifedipine.

Angina Pectoris↗
PubMed1985

Regional wall motion improvement after coronary thrombolysis with recombinant tissue plasminogen activator: importance of coronary angioplasty.

To evaluate functional recovery in 20 consecutive patients with acute myocardial infarction who received recombinant tissue-type plasminogen activator, serial two-dimensional echocardiograms were performed before and immediately after tissue plasminogen activator administration and at 1 and 10 days postinfarction. Tissue plasminogen activator was administered intravenously (17 patients) or by intracoronary infusion (3 patients) after angiographic confirmation of total occlusion. Reperfusion, documented by angiography, occurred in 13 of the 20 patients. The mean time from onset of chest pain to thrombolysis was 5.1 +/- 1.1 hours. Echocardiograms were evaluated for regional function with a visual semiquantitative scoring system by two independent observers who had no knowledge of patient identity, temporal sequence, therapy or effect of therapy. There was no immediate or 24 hour improvement in wall motion. At day 10 compared with pretreatment, 28 of 33 reperfused infarct zone segments versus 6 of 20 nonreperfused infarct segments demonstrated improved wall motion (p = 0.01). This improvement did not relate to time from onset of chest pain to successful thrombolysis. Of reperfused infarct zone segments in the distribution of coronary artery balloon dilation, 19 of 23 segments exhibited improvement versus 7 of 17 (reperfused, no angioplasty) and 6 of 20 (nonreperfused, no angioplasty) segments (p = 0.001). Infarct zone segments reperfused at the time of ongoing chest pain demonstrated functional recovery compared with segments reperfused in the absence of chest pain (18 of 23 versus 10 of 20, respectively; p = 0.05). Thus, in this uncontrolled series, there was echocardiographically detectable improvement in function of reperfused infarct segments 10 days after coronary thrombolysis with recombinant tissue plasminogen activator.

Adult↗
PubMed1985

Results of a randomized prospective trial of intraaortic balloon counterpulsation and intravenous nitroglycerin in patients with acute myocardial infarction.

A randomized prospective clinical trial compared combined treatment with intraaortic balloon pumping and intravenous nitroglycerin for 4 to 5 days with routine clinical management in 20 patients with extensive myocardium at risk for infarction as evidenced by a thallium defect score of 7.0 units or greater. No significant differences in mortality or clinical outcome were observed between the 10 patients receiving the combined treatment and the 10 receiving routine management. In 14 patients two-dimensional echocardiograms obtained 6 to 24 hours after the onset of symptoms and at follow-up 6 to 16 days later (after completion of combined intraaortic balloon pumping plus nitroglycerin therapy) were analyzed to determine whether infarct segment or noninfarct segment lengths were affected by therapy. Among these 14 patients, 5 (3 receiving the combined therapy and 2 receiving routine management) demonstrated an increase in infarct segment length of greater than 1.0 cm. Mean infarct segment length increased 0.30 +/- 0.44 cm in patients receiving the combined therapy and 0.29 +/- 0.36 cm in patients on routine management (p = NS). In contrast, noninfarct segment length increased greater than 1.0 cm (mean increase 1.20 +/- 0.39) in five of seven patients on routine management but in none of 7 patients receiving intraaortic balloon pumping plus nitroglycerin therapy (mean decrease 0.22 +/- 0.20 cm) (p less than 0.05). No significant differences were noted in left ventricular ejection fraction, as measured by gated blood pool scintigraphy, or thallium perfusion defect score in a comparison of day 1 (pretreatment) with day 4 thallium or day 7 to 14 gated blood pool scintigrams. Thus, in patients with extensive myocardium at risk, it is unlikely that a reduction in mortality or a significant improvement in myocardial perfusion or ventricular function can be obtained by early intervention with intraaortic balloon pumping in combination with nitroglycerin. Although this combined therapy failed to prevent infarct segment lengthening (infarct expansion), the combined afterload-lowering effects of intraaortic balloon pumping and nitroglycerin did appear to prevent dilation or remodeling of noninfarcted segments during the first 2 weeks after acute myocardial infarction.

Adult↗
PubMed1985

Calcium-dependent enhancement of myocardial diastolic tone and energy utilization dissociates systolic work and oxygen consumption during low sodium perfusion.

The relationships and correlations among functional, metabolic, and ionic consequences of low sodium perfusion were studied in isovolumic, retrograde-aortic perfused working rat hearts by 31P nuclear magnetic resonance, oxygen consumption, and atomic absorption spectrometry. Reduction of perfusate sodium from 144 to 74, 51, 39, and 25 mM in four separate groups of hearts via lithium substitution for 15 minutes decreased cell sodium to mean values of 62, 51, 43, and 36 mumol/g dry weight, respectively (P less than 0.001 vs. control of 107). There was a transient rise and then a fall in developed pressure and a decline in phosphocreatine and adenosine triphosphate, all of which were graded and correlated with perfusate sodium (P less than 0.01 for all parameters vs. perfusate sodium). This was accompanied by a 2- to 7-fold elevation of diastolic pressure while oxygen consumption remained near control levels. All parameters except adenosine triphosphate returned toward baseline values when normal perfusate sodium was reintroduced. Although cell calcium as measured by atomic absorption spectrometry did not differ among the groups, the functional and metabolic changes did not occur if the sodium steps were performed in reduced perfusate calcium (0.08 mM). In hearts in which systolic function was obliterated by verapamil, exposure to zero sodium caused a 4-fold increase in oxygen consumption, an increase in diastolic pressure, and a reduction of high energy phosphates. In the presence of ryanodine, a specific inhibitor of sarcoplasmic reticulum calcium release, the metabolic changes did not occur, and the excess oxygen consumption in zero sodium was substantially reduced. Thus, the effect of lowered perfusate sodium in beating hearts, i.e., to dissociate oxygen consumption and systolic function, and to increase diastolic pressure and its effect in arrested hearts to increase oxygen consumption, are calcium dependent, energy consuming, and modulated by sarcoplasmic reticulum calcium cycling.

Adenosine Triphosphate↗
PubMed1984

'Calcium paradox' in the heart is modulated by cell sodium during the calcium-free period.

We hypothesized that after a Ca2+-free period the magnitude of the Na+ gradient at the onset of Ca2+ reperfusion would grade the ensuing cell Ca2+ gain. Rabbit interventricular septa perfused with Hepes buffered solution (pH 7.4, [Ca2+] = 1.0 mM) and stimulated to contract isometrically at 60 min-1 at 30 degrees C were exposed to a 30-min Ca2+-free period followed by 30-min of Ca2+ re-introduction. Cell Na without Ca2+-free perfusion was 137 +/- 5 mumol/g dry wt. During the Ca2+-free period, the perfusate was manipulated to result in three groups of septa in which cell Na just prior to Ca2+ re-introduction was 64 +/- 9 (perfusate [Na+] reduced to 47 mM), 170 +/- 12 (perfusate unaltered), and 293 +/- 16 mumol/g dry wt (addition of 5 X 10(-5) M ouabain). Following Ca2+ re-introduction, cell Ca2+ content was 3.4 +/- 0.5, 6.5 +/- 1.0, and 10.6 +/- 0.7 mumol/g dry wt in the low, intermediate, and high cell Na+ groups, respectively. Similar marked and highly significant gradations among the three groups were observed in the extent of cell K+ loss and recovery of contractile function during Ca2+ reintroduction. These results indicate that (1) myocardial cell Na+ increases during Ca2+ free perfusion and (2) the magnitude of the Na+ gradient at the end of the Ca2+ free period is an important determinant of the extent of cell Ca2+ gain, cell K+ loss, and reduction of contractile function with Ca2+ re-introduction, which collectively have been referred to as the 'calcium paradox' in the heart.

Animals↗