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G Gerstenblith

Publications and source records attributed to G Gerstenblith.

114 records · Page 7Linked to original sources
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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

Database Conference January 27-30, 2000, Washington D.C.--Do existing databases answer clinical questions about geriatric cardiovascular disease and stroke?

EXECUTIVE SUMMARY: Most randomized, controlled trials evaluating the effectiveness of pharmaceutical, surgical, and device interventions for the prevention and treatment of cardiovascular disease have excluded patients over 75 years of age. Consequently, the use of these therapies in the older population is based on extrapolation of safety and effectiveness data obtained from younger patients. However, there are many registries and observational databases that contain large amounts of data on patients 75 years of age and older, as well as on younger patients. Although conclusions from such data are limited, it is possible to define the characteristics of patients who did well and those who did poorly. The goal of this conference was to convene the principal investigators of these databases, and others in the field of geriatric cardiology, to address questions relating to the safety and effectiveness of treatment interventions for several cardiovascular conditions in the elderly. Seven committees discussed the following topics: (I) Risk Factor Modification in the Elderly; (II) Chronic Heart Failure; (III) Chronic Coronary Artery Disease: Role of Revascularization; (IV) Acute Myocardial Infarction; (V) Valve Surgery in the Elderly; (VI) Electrophysiology, Pacemaker, and Automatic Internal Cardioverter Defibrillators Databases; (VII) Carotid Endarterectomy in the Elderly. The chairs of these committees were asked to invite principal investigators of key databases in each of these areas to discuss and prepare a written statement concerning the available safety and efficacy data regarding interventions for these conditions and to identify and prioritize areas for future study. The ultimate goal is to stimulate further collaborative outcomes research in the elderly so as to place the treatment of cardiovascular disease on a more scientific basis.

Aged↗
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↗
PubMedDate not supplied

Repeated, transient lactate exposure does not "precondition" rat myocardium.

The precise mechanism of the cardioprotective effect of ischemic preconditioning (IPC) is still unclear, although various mechanisms have been suggested, including activation of ATP-dependent potassium (KATP) channels by adenosine and protein kinase C as well as increased expression of heat shock protein (HSP). Increasing evidence suggests that lactate, which accumulates during IPC periods, can activate several of these "triggers" of preconditioning. We tested whether repeated exposure to lactate, producing tissue lactate concentrations similar to those during brief ischemic periods, could contribute to IPC benefits. Five isolated rat hearts were subjected to a previously reported IPC protocol composed of two 5-min ischemia-reperfusion cycles; another five hearts served as controls; and six hearts underwent a "lactate-preconditioning" protocol, consisting of two 5-min exposures to 15 mM lactate and two 5-min periods of reflow with a lactate-free buffer. Subsequently all hearts underwent 30 min of normothermic, total ischemia followed by 30 min of reflow at a constant perfusion pressure of 80 mmHg (1 mmHg = 133.3 Pa). Lactate exposure resulted in tissue lactate levels similar to those during ischemia in ischemia-preconditioned hearts (10.5 +/- 0.6 versus 10.5 +/- 1.2 mumol/g wet weight, mean +/- SEM). However, the recovery of left ventricular developed pressure (DevP) following 30 min of total ischemia was significantly higher in the IPC hearts than in either the control or lactate-exposed hearts, reaching 56.8 +/- 3.4, 14.2 +/- 6.8, and 9.5 +/- 3.6%, respectively, of the baseline values. There was no significant difference between lactate-preconditioned and control hearts. End-diastolic pressure (EDP) was significantly lower during reperfusion in IPC hearts than in lactate-exposed and control hearts, with no significant differences between the latter two groups (36.2 +/- 3.5, 82.0 +/- 2.9, and 81.2 +/- 8.5 mmHg, respectively). In contrast with the proposed hypothesis, repeated, transient lactate exposure resulting in tissue lactate levels similar to ischemic preconditioning did not improve contractile recovery after a prolonged ischemic period in this model.

Animals↗