Enhancement of metabolism of jeopardized myocardium by nifedipine

Allan S Jaffe, Daniel R. Biello, Burton E. Sobel, Edward M. Geltman

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

To define effects of nifedipine on regional metabolism in jeopardized myocardium we quantified accummulation of carbon-11 labeled palmitate ([11C]palmitate) in patients with acute myocardial infarction by positron emission tomography in a randomized, double-blind, placebo controlled study. Tomographic studies were performed prior to treatment as soon as possible after hospital admission. Subsequent studies were performed seven days later. Twenty-two patients with acute myocardial infarction were randomized to treatment with nifedipine (n = 13) or placebo (n = 9). The dosage of active medication was guided by a "third party observer" to avoid iatrogenic hypotension. Treatment was initiated within 9.6 ± 1 hours after the onset of symptoms of infarction. The extent of the zone of abnormal accumulation of [11C]palmitate was similar in pre-treatment positron emission tomograms from patients subsequently given nifedipine compared with those given placebo. In subsequent positron emission tomography studies, patients treated with nifedipine exhibited improved metabolism of [11C]palmitate (by 16 ± 10%, SE, P < 0.05) compared with no change in patients given placebo. Neither enzymatic estimates of infarct size nor scintigraphic estimates of left ventricular ejection fraction differed in the two groups. Patients given nifedipine and manifesting substantial improvement in accumulation of [11C]palmitate had a high incidence of chest pain and recurrent infarction compared with those given placebo in whom no improvement was evident. These observations suggest that some regions of myocardium were benefited transiently by nifedipine but that they remained at high risk for recurrent injury. Thus, patients benefited transiently by drugs early after the onset of infarction may require aggressive intervention such as angioplasty or early coronary bypass surgery. Accordingly, they should be evaluated angiographically early for identification of lesions with unusually high risk.

Original languageEnglish (US)
Pages (from-to)77-89
Number of pages13
JournalInternational Journal of Cardiology
Volume15
Issue number1
DOIs
StatePublished - 1987
Externally publishedYes

Fingerprint

Nifedipine
Myocardium
Palmitates
Placebos
Infarction
Positron-Emission Tomography
Myocardial Infarction
Therapeutics
Chest Pain
Angioplasty
Stroke Volume
Hypotension
Carbon
Electrons
Incidence
Wounds and Injuries
Pharmaceutical Preparations

Keywords

  • Calcium entry blocker
  • Myocardial infarction
  • Myocardial protection
  • Myocardial salvage
  • Pharmacology
  • Positron emission tomography

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Enhancement of metabolism of jeopardized myocardium by nifedipine. / Jaffe, Allan S; Biello, Daniel R.; Sobel, Burton E.; Geltman, Edward M.

In: International Journal of Cardiology, Vol. 15, No. 1, 1987, p. 77-89.

Research output: Contribution to journalArticle

Jaffe, Allan S ; Biello, Daniel R. ; Sobel, Burton E. ; Geltman, Edward M. / Enhancement of metabolism of jeopardized myocardium by nifedipine. In: International Journal of Cardiology. 1987 ; Vol. 15, No. 1. pp. 77-89.
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abstract = "To define effects of nifedipine on regional metabolism in jeopardized myocardium we quantified accummulation of carbon-11 labeled palmitate ([11C]palmitate) in patients with acute myocardial infarction by positron emission tomography in a randomized, double-blind, placebo controlled study. Tomographic studies were performed prior to treatment as soon as possible after hospital admission. Subsequent studies were performed seven days later. Twenty-two patients with acute myocardial infarction were randomized to treatment with nifedipine (n = 13) or placebo (n = 9). The dosage of active medication was guided by a {"}third party observer{"} to avoid iatrogenic hypotension. Treatment was initiated within 9.6 ± 1 hours after the onset of symptoms of infarction. The extent of the zone of abnormal accumulation of [11C]palmitate was similar in pre-treatment positron emission tomograms from patients subsequently given nifedipine compared with those given placebo. In subsequent positron emission tomography studies, patients treated with nifedipine exhibited improved metabolism of [11C]palmitate (by 16 ± 10{\%}, SE, P < 0.05) compared with no change in patients given placebo. Neither enzymatic estimates of infarct size nor scintigraphic estimates of left ventricular ejection fraction differed in the two groups. Patients given nifedipine and manifesting substantial improvement in accumulation of [11C]palmitate had a high incidence of chest pain and recurrent infarction compared with those given placebo in whom no improvement was evident. These observations suggest that some regions of myocardium were benefited transiently by nifedipine but that they remained at high risk for recurrent injury. Thus, patients benefited transiently by drugs early after the onset of infarction may require aggressive intervention such as angioplasty or early coronary bypass surgery. Accordingly, they should be evaluated angiographically early for identification of lesions with unusually high risk.",
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