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Biomedical subjects

G Gerstenblith

Publications and source records attributed to G Gerstenblith.

At least 109 records · Page 6Linked to original sources
PubMed1984

Perfusate sodium during ischemia modifies post-ischemic functional and metabolic recovery in the rabbit heart.

Metabolic and functional recovery following 60 minutes of low flow (0.1 ml/min) ischemia were compared in rabbit hearts perfused with normal sodium and potassium, low sodium (120 mM NaCl replaced by 120 mM LiCl), or zero potassium perfusate during ischemia. During the control, pre-ischemic, and reperfusion periods, all hearts were perfused identically with normal sodium and potassium. 31P NMR was used to monitor intracellular pH (pHi), ATP, and phosphocreatine (PGr). Developed pressure, end diastolic pressure, pHi, and the integrated areas of ATP and PCr were equivalent in the three groups in the pre-ischemic period. The fall in pHi, PCr, ATP, and developed pressure and the rise in end diastolic pressure during 60 min ischemia also did not differ among the three groups. In contrast to the lack of an effect of perfusate sodium and potassium on the decline in parameters of metabolism and function during ischemia, there was a marked difference in the recovery of these indices during reperfusion. Hearts perfused with low sodium during ischemia exhibited the best recovery (expressed as percent of control) of developed pressure (95 +/- 4%), PCr (106 +/- 6%), and ATP (51 +/- 2%) and the smallest rise in end diastolic pressure (229 +/- 50%); hearts perfused with normal sodium and potassium during ischemia had intermediate recovery values for developed pressure (53 +/- 10%), PCr (78 +/- 9%), ATP (45 +/- 4%) and end diastolic pressure (487 +/- 73%) and the hearts perfused with zero potassium solution during ischemia exhibited the poorest recovery of developed pressure (23 +/- 6%), PCr (49 +/- 6%), ATP (39 +/- 5%) and end diastolic pressure (968 +/- 185%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1984

Acute nifedipine withdrawal: consequences of preoperative and late cessation of therapy in patients with prior unstable angina.

Reports of acute ischemic events after withdrawal of calcium antagonist therapy in outpatients and during bypass surgery in patients with prior angina at rest prompted the examination of the effect of nifedipine withdrawal in 81 patients who had completed a prospective, double-blind randomized trial of nifedipine versus placebo for rest angina. Thirty-nine patients underwent bypass surgery for uncontrolled angina or left main coronary artery disease. No significant difference between patients withdrawn from nifedipine or placebo was seen in the incidence of perioperative myocardial infarction, hypotension requiring intraaortic balloon counterpulsation, vasopressor or vasodilator requirements or incidence of significant arrhythmias. An additional 42 patients had completed 2 years on a protocol consisting of nitrates and propranolol in addition to nifedipine or placebo. During a mean of 66 hours of continuous monitoring after withdrawal of nifedipine or placebo, heart rate and blood pressure were unchanged. A worsening of previously present angina at rest occurred in five patients who had continued to experience rest angina before drug withdrawal, four of whom were withdrawn from nifedipine. No patient with class I to III angina experienced new onset of rest angina during drug withdrawal. No patient experienced myocardial infarction. There was no significant difference between patients withdrawn from nifedipine or placebo in the duration or frequency of ischemic ST changes on continuous electrocardiographic monitoring, or in duration or positive results of serial exercise treadmill testing. Thus, no early adverse effects of acute nifedipine withdrawal were found in patients with prior rest angina at the time of bypass surgery or in stable patients receiving long-term medical therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris↗
PubMed1984

Effect of sodium on calcium-dependent force in unstimulated rat cardiac muscle.

It has previously been demonstrated that 1) changes in superfusate calcium concentration [Ca2+]o within the low millimolar range result in changes in "resting" force and in the light-scattering properties of unstimulated rat cardiac muscle, and 2) if [Ca2+]o is increased from zero to millimolar concentrations, i.e., reperfusion with Ca2+ after a Ca2+-free period, a large influx of Ca2+ occurs and is associated with a substantial increase in resting force. The present study determined whether the Ca2+ influx in either case was influenced by intracellular sodium (Na+i). In unstimulated isometric rat right ventricular papillary muscles equilibrated at 29 degrees C, [Ca2+]o was increased from 1 to 4 mM or from 0 to 2 mM under conditions that vary Na+i, and the resulting change in intracellular calcium concentration [( Ca2+]i) was monitored by changes in both resting force and the frequency of intensity fluctuations in laser light scattered by the muscle. In each case, lowering Na+i by equilibration in lowered extracellular sodium concentration [( Na+]o) or enhancing [Na+]i by equilibration in the absence of extracellular potassium or in the presence of ouabain markedly lowered and enhanced respectively the apparent Ca2+ influx in response to the step increase in [Ca2+]o. Thus, in unstimulated rat cardiac muscle, Na+i modulates the Ca2+ influx resulting from a step increase in [Ca2+]o both under physiological conditions and following a period of Ca2+-free superfusion, i.e., the "Ca2+ paradox." A passive influx of Ca2+ down its electrochemical gradient would not depend on Na+i, and the voltage-time dependent slow Ca2+o channel is inactivated under the experimental conditions employed. The results are best explained by a sarcolemmal Na+-Ca2+ exchange mechanism and suggest that the reversal potential of this electrogenic exchanger is exceeded during a step increase in [Ca2+]o even at the transmembrane potential of resting muscle.

Animals↗
PubMed1984

Exercise cardiac output is maintained with advancing age in healthy human subjects: cardiac dilatation and increased stroke volume compensate for a diminished heart rate.

To assess the effect of age on cardiac volumes and function in the absence of overt or occult coronary disease, we performed serial gated blood pool scans at rest and during progressive upright bicycle exercise to exhaustion in 61 participants in the Baltimore Longitudinal Study of Aging. The subjects ranged in age from 25 to 79 years and were free of cardiac disease according to their histories and results of physical, resting and stress electrocardiographic, and stress thallium scintigraphic examinations. Absolute left ventricular volumes were obtained at each workload. There were no age-related changes in cardiac output, end-diastolic or end-systolic volumes, or ejection fraction at rest. During vigorous exercise (125 W), cardiac output was not related to age (cardiac output [1/min] = 16.02 + 0.03 [age]; r = .12, p = .46). However, there was an age-related increase in end-diastolic volume (end-diastolic volume [ml] = 86.30 + 1.48 [age]; r = .47, p = .003) and stroke volume (stroke volume [ml] = 85.52 + 0.80 [age]; r = .37, p = .02), and an age-related decrease in heart rate (heart rate [beats/min] = 184.66 - 0.70 [age]; r = -.50, p = .002). The dependence of the age-related increase in stroke volume on diastolic filling was emphasized by the fact that at this high workload end-systolic volume was higher (end-systolic volume [ml] = 3.09 + 0.65 [age]; r = .45, p = .003) and ejection fraction lower (ejection fraction = 88.48 - 0.18 [age]; r = -.33, p = .04) with increasing age. These findings indicate that although aging does not limit cardiac output per se in healthy community-dwelling subjects, the hemodynamic profile accompanying exercise is altered by age and can be explained by an age-related diminution in the cardiovascular response to beta-adrenergic stimulation.

Adult↗
PubMed1984

Variables predictive of successful medical therapy in patients with unstable angina: selection by multivariate analysis from clinical, electrocardiographic, and angiographic evaluations.

Although unstable angina can be initially controlled with medical therapy in most patients, there is a high incidence of subsequent death, myocardial infarction, or need for coronary bypass surgery to control symptoms. Identification at the time of presentation of the patient likely to do poorly on continued medical therapy would be useful in advising consideration of surgical therapy. Since coronary arterial spasm may have a significant role in the pathophysiology of unstable angina in some patients, the recently developed calcium channel antagonists may therefore be of particular benefit in the medical therapy of unstable angina. One hundred thirty-eight patients were entered into a randomized double-blind study of the efficacy of adding nifedipine to conventional treatment of unstable angina (nitrates and beta-blockers) and were followed for 18 months. Of these patients, 104 underwent coronary arteriography. A multivariate Cox's hazard function analysis was applied to variables selected from the history, electrocardiographic (ECG) changes during chest pain, and from scintigraphic and coronary arteriographic data to determine those variables most predictive of response to medical therapy. The percentage of the left ventricular myocardium supplied by vessels with 70% or greater luminal stenosis was the most significant variable in influencing failure of medical therapy defined as sudden death, myocardial infarction, or need for bypass surgery. Whether or not the patient received nifedipine was the second most powerful variable, with the use of nifedipine reducing by half the relative risk of failing medical therapy. These were followed by cigarette smoking and presence of global ST segment changes during ischemia. After 18 months the nifedipine group had fewer patients failing medical therapy (p = .02), with fewer patients undergoing coronary bypass surgery (p less than .01). However, nifedipine did not appear to have a preventive effect against myocardial infarction or death. Kaplan-Meier actuarial curves confirmed that medical therapy was significantly less successful in the presence of increasing numbers of significantly stenotic vessels (p = .03). However, nifedipine provided a significant beneficial effect in patients with two or more stenotic vessels (p less than .01) and in whom 50% or more of the myocardium was supplied by vessels with 70% or greater stenosis (p = .01). Thus, although patients with advanced obstructive coronary disease have the greatest likelihood of unfavorable outcomes, the addition of nifedipine is of significant benefit.(ABSTRACT TRUNCATED AT 400 WORDS)

Angina Pectoris↗
PubMed1983

A randomized clinical trial of intravenous nitroglycerin in patients with acute myocardial infarction: benefits of early treatment.

A prospective randomized clinical trial of intravenous nitroglycerin administered for 48 hours following acute infarction was undertaken to determine whether clinical improvement and/or preservation of ischemic myocardium could be demonstrated. One hundred four patients were randomized to receive either nitroglycerin or placebo infusion. Nitroglycerin infusion was titrated to lower mean arterial pressure 10% using non-invasive monitoring. Early nitroglycerin treatment, defined as treatment initiated less than 10 hours after symptom onset, resulted in a lower incidence of new congestive heart failure, myocardial infarct extension, and/or early death from pump failure (15%) compared to late nitroglycerin treatment (50%, p = 0.008) or early placebo treatment (48%, p = 0.01). Improvement in ejection fraction of greater than or equal to 10% was demonstrated in 7 of 20 (35%) early nitroglycerin treated patients compared to 6, 11 and 0% of patients in the three other subgroups, respectively (p = 0.004). Similarly, thallium-201 perfusion scintigrams showed a greater than 75% improvement in defect score in 23 (48%) patients receiving nitroglycerin within 10 hours compared to 14%, 33% and 0% respectively, in the remaining subgroups (p = 0.035). However, before routine administration of nitroglycerin can be recommended for all patients with acute infarction, larger clinical trials will be required.

Clinical Trials as Topic↗
PubMed1982

Nifedipine in unstable angina: a double-blind, randomized trial.

We assessed the efficacy of adding nifedipine to the conventional treatment of unstable angina in 138 patients in a prospective, double-blind, randomized, placebo-controlled trial. There was no difference between the two groups in the dose of conventional antianginal medication or in age, prior myocardial infarction, ejection fraction, or other risk factors. Failure of medical treatment (defined as sudden death, myocardial infarction, or bypass surgery within four months) occurred in 43 of 70 patients given placebo and in 30 of 68 given nifedipine. Kaplan-Meier survival-curve analysis of the number and time dependence of treatment failures demonstrated a benefit of nifedipine over placebo (P = 0.03). The benefit was particularly marked in patients with ST-segment elevation during angina (P = 0.02). Side effects (transient hypotension or diarrhea) required withdrawal of the drug from four patients given nifedipine and from one given placebo. We conclude that the addition of nifedipine to conventional therapy is safe and effective in unstable angina.

Adult↗
PubMed1981

The predictive value of a strongly positive stress test in patients with minimal symptoms.

The ability of a strongly positive stress test to predict left main coronary artery disease in people with suspected coronary artery disease but with minimal or no angina was investigated in 40 such patients. Nine had a history of myocardial infarction but no angina. Thirty-one had mild angina or a history of mild angina. The stress electrocardiograms were analyzed according to criteria known to be associated with left main coronary artery disease in moderately or severely symptomatic patients; (1) early S-T segment changes (stage I or II of exercise), (2) 2 mm or more S-T segment depression, (3) downsloping S-T segments, (4) associated exercise-induced hypotension, (5) prolonged S-T segment changes after the test (greater than or equal to 8 minutes) and (6) anterior and inferior S-T segment depression. The prevalence of left main coronary artery disease was 35 percent and that of any severe coronary artery disease 75 percent. The criterion of anterior and inferior electrocardiographic changes with exercise was most predictive of left main coronary artery disease (P less than 0.01 by chi 2). Exercise electrocardiography is useful in the prediction of left main or other severe coronary artery disease even when performed in patients who have minimal angina or in those who are asymptomatic after myocardial infarction.

Adult↗
PubMed1981

Congestive heart failure.

The prevalence of congestive heart failure increases as the population ages. Conventional treatment of congestive heart failure is usually applied to persons over 60 with heart failure; yet very little is known concerning the cardiovascular alterations induced by aging. Animal experiments have indicated that presbycardia as a distinctive entity does exist but that it does not, in and of itself, cause heart failure in large numbers of individuals. The main causes remain the same as those in the younger population (i.e. ischemic and hypertensive disease). Diagnosis is altered in aged individuals because symptoms and signs may not be those classically described and taught. Pharmacologic treatment is hampered by a decreased responsiveness to inotropic agents, while toxicity levels are probably not altered. Although vasodilators may theoretically promote more satisfactory results, their clinical effectiveness and potential toxicities in elderly patients have not been evaluated.

Aged↗
PubMed1978

Effect of lidocaine on conduction in the ischemic His-Purkinje system of dogs.

The effect of lidocaine on His-Purkinje conduction in dogs with ischemic damage to the His bundle was compared with the effect of lidocaine in normal dogs. The anterior septal artery was ligated in 14 dogs, and 30 minutes later atrial pacing was performed to increase residual ischemic damage. Four to 6 days later, His bundle recordings were obtained during sinus rhythm and atrial pacing before and after the administration of lidocaine in a dose of 2 mg/kg and a total dose of 4 mg/kg. His bundle recordings were also obtained in nine control animals beofre and after the administration of lidocaine. Lidocaine significantly increased the H-V time in the animals with ischemic damage during sinus rhythm and at all packing rates. It also resulted in advanced His-Purkinje conduction defects including His bundle block and right bundle branch block in these animals. In contrast, the effect of lidocaine in the normal animals was negligible. It is concluded that lidocaine significantly depresses His-Purkinje conduction in the setting of preexisting ischemic damage. These results suggest that lidocaine may be used as a diagnostic tool to unmask latent His-Purkinje conduction defects due to ischemia.

Animals↗
PubMed1977

Ventricular ectopic activity after premature atrial beats in acute myocardial infarction.

Ventricular ectopic activity occurred only after premature atrial beats in a patient with an acute inferior wall myocardial infarction. The ventricular ectopic activity occurred only when the coupling interval between the premature atrial beats and preceding sinus beat was less than or equal to 0-44 s. The sinus cycle length, however, appeared to influence the form of expression of ventricular ectopic activity independent of coupling intervals, with single premature ventricular contractions occurring at cycle lengths greater than or equal to 0-72 s, couplets at cycle lengths of 0-68 to 0-71 s, and ventricular tachycardia at cycle lengths less than or equal to 0-67 s.

Aged↗
PubMed1977

Echocardiographic assessment of a normal adult aging population.

Echocardiograms were performed on 105 male participants in the National Institutes on Aging's volunteer Longitudinal Study Program. All subjects (25--84 years of age) were physically active and had no evidence of hypertension or cardiovascular disease. Measurements were made of the initial diastolic (E-F) slope of the anterior mitral valve leaflet, the aortic and left ventricular cavity dimensions, and the thickness of the posterior left ventricular wall. Fractional shortening of the minor semi-axis of the left ventricle and the velocity of circumferential fiber shortening were also determined. It was found that increasing age correlated with a decrease mitral valve E-F slope and increased aortic root diameter and left ventricular wall thickness. Aging did not affect left ventricular cavity dimension, fractional shortening of the minor semi-axis, and velocity of circumferential fiber shortening. These findings suggest that aging in the normal male is associated with altered left ventricular diastolic filling, increased aortic root diameter and left ventricle hypertrophy but little change in contractile ability in the resting state.

Adult↗
PubMed1975

Diminished inotropic response of aged myocardium to catecholamines.

The effect of advanced age on the response of active tension, maximal rate of tension development (dT/dt), and contraction duration to catecholamines and to calcium was evaluated in isometric trabeculae carneae from young adult (6-month-old), middle-aged (12-month-old), and aged (25-month-old) rats. Control values were not age dependent except for that for contraction duration which was prolonged in the aged group. At a norepinephrine concentration of 8 times 10-5M, dT/dt increased to 163.8 plus or minus 5.3% of control in the young adult group and to 125.9 plus or minus 6.3% of control in the aged group (P smaller than 0.001). Active tension increased to 121.3 plus or minus 4.0% of control in the young adult muscles but did not increase in the aged muscles (P smaller than 0.01). Contraction duration shortened proportionately in both age groups. Similar results were obtained with isoproterenol. In contrast to the response to catecholamines, there was no age difference in the response of active tension and dT/dt to increasing concentrations of calcium. It is concluded that the intrinsic inotropic response to catecholamines is diminished in the aged myocardium. This finding does not appear to result from differences in tachyphylaxis, tissue uptake of catecholamines, or the ability of the contractile proteins to respond to increasing concentrations of calcium but instead may result from a decreased ability of catecholamines to increase the intracellular calcium available for contraction.

Aging↗
PubMed1975

Prolonged contraction duration in aged myocardium.

Isometric performance at 29degreesC was measured in left ventricular trabeculae carneae from young adult (6-mo) and aged (25-mo) rats (n equals 18 in each group). Active tension and maximal rate of tension development did not differ with age, but contraction duration was 255plus or minus6 ms in the young adult and 283plus or minus6 ms in the aged group (P less than0.001). Although catecholamine content per gram heart weight was less in the aged myocardium, additional experiments showed that neither 1 times 10-6 M propranolol nor pretreatment with 6-hydroxydopamine eliminated the age difference in contraction duration. To determine if this age difference resulted from a prolonged active state, electromechanical dissociation and the overshoot of contraction duration during recovery from hypoxia were measured. During paired stimulation greater mechanical refractoriness was found in aged muscles (P less than0.01), but intracellular action potential recordings showed no age difference in the electrical refractory period. On recovery from hypoxia, contraction duration overshoot was 117plus or minus 4percent of control in the young and 138plus or minus 4percent of control in the aged muscles (P less than0.01). The greater electromechanical dissociation and greater overshoot in contraction duration following hypoxia in aged myocardium suggests that prolonged contraction duration in aged myocardium results from a prolonged active state rather than changes in passive properties or myocardial catecholamine content.

Action Potentials↗