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Biomedical subjects

G Gerstenblith

Publications and source records attributed to G Gerstenblith.

87 records · Page 5Linked to original sources
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↗
PubMedDate not supplied

Initial and late results of coronary angioplasty for early postinfarction unstable angina.

Unstable angina that occurs in the early postinfarction period is associated with an increased incidence of unfavorable cardiac events despite aggressive medical therapy. We examined the results of coronary angioplasty in 47 consecutive patients with postinfarction unstable angina who were referred for the procedure 12.9 +/- 7 days following myocardial infarction, 14 of which were Q wave and 33 of which were non-Q-wave. Coronary angioplasty was performed on a total of 55 arteries with a mean predilatation stenosis of 95 +/- 8%. These included 46 infarct-related arteries and nine noninfarct arteries. Double-vessel angioplasty was performed in eight patients. Successful coronary angioplasty (greater than 30% reduction of predilatation stenosis) was achieved in 43 patients (91%), with a mean residual stenosis of 33 +/- 28%. There was one in-hospital death, one patient required emergency bypass surgery, and two patients had early reocclusion resulting in myocardial infarctions. The 39 patients who had successful angioplasty procedures and who were discharged from the hospital without an unfavorable outcome were followed for 16.3 +/- 7 months, and repeat coronary angioplasty was required in five patients from 45 to 105 days after the initial procedure. Two patients had subsequent elective bypass surgery, one had a recurrent myocardial infarction, and one patient had a noncardiac death. For selected patients with suitable coronary anatomy, coronary angioplasty appears to offer an efficacious therapeutic option for early postinfarction unstable angina.

Adult↗
PubMedDate not supplied

Acute doxorubicin cardiotoxicity: functional, metabolic, and morphologic alterations in the isolated, perfused rat heart.

The acute effects of doxorubicin on coronary perfusion and left ventricular pressures and intracellular phosphate metabolite levels, the latter obtained by 31P nuclear magnetic resonance, were measured simultaneously in isolated, isovolumic rat hearts (Langendorf preparation) perfused at constant flow. Nineteen experimental hearts were perfused for 70 min with oxygenated HEPES-buffered solution containing 6 mg/L doxorubicin. These were compared with 18 control hearts (C), perfused under identical conditions but without doxorubicin, by repeated measures analysis of variance. In the experimental group, coronary perfusion pressure steadily increased to 226.3 +/- 13.8% (mean +/- SEM) of initial levels (p less than 0.0001 vs. C). Because flow was constant, the increase in coronary perfusion pressure in experimental hearts indicates a greater than twofold increase in coronary resistance. Intracellular phosphocreatine and ATP decreased to 80.3 +/- 3.9% (p less than 0.005 vs. C) and 82.1 +/- 6.4% (p less than 0.05 vs. C), whereas inorganic phosphate increased to 149.7 +/- 19.1% (p less than 0.05 vs. C) of initial levels, respectively. Accompanying these changes, diastolic pressure steadily increased to 521.7 +/- 91.4% of initial levels (p less than 0.0001 vs. C). Developed pressure initially increased to 107.1 +/- 4.5% at 30 min, and thereafter decreased to 76.2 +/- 6.3% at 70 min (p less than 0.05 vs. C). Typical structural alterations in myocyte nuclei were noted. Cellular calcium was not increased in doxorubicin-exposed hearts. Thus, acute doxorubicin cardiotoxicity is characterized by an increase in coronary resistance and is closely correlated with alterations in ventricular function and a decrease in intracellular high-energy phosphate content.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗