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The effects of pressure-induced cardiac hypertrophy on the functional capacity of the coronary circulation

  • Kevin C Dellsperger
    ,
  • Melvin L. Marcus
Scholary Output:
Contribution to journal
Article
Peer-review

Abstract

Pressure-induced cardiac hypertrophy has many effects on the functional capacity of the coronary circulation. Many studies have been performed in both animal and humans and the major findings are as follows: Most types of myocardial hypertrophy are associated with the decrement in coronary vasodilator reserve; The magnitude of the decrement in coronary reserve in myocardial hypertrophy is usually much more prominent in patients with myocardial hypertrophy than in animal models; Left ventricular hypertrophy secondary to systemic hypertension is associated with altered autoregulation of myocardial perfusion; The perfusion abnormalities associated with hypertension and left ventricular hypertrophy are affected by various factors such as age of onset, ventricular involvement, and the stimulus for hypertrophy; Left ventricular hypertrophy secondary to renal hypertension markedly augments the adverse effects of coronary occlusion. In this setting, coronary occlusion is associated with a three-fold increase in the incidence of lethal ventricular arrhythmias and a 35% increase in infarct size. Thus, pressure-induced hypertrophy profoundly alters the coronary circulation. Am J Hypertens 1988; 1:200-207.

Publication Information

Output type

Scholary Output:
Contribution to journal
Article
Peer-review

Original language

English (US)

Pages from-to (Number of pages)

Pages 200-207 (8 pages)

Journal (Volume, Issue Number)

American journal of hypertension (Volume 1, Issue 2)

Publication milestones

  • Published - 04/1988

Publication status

Published - 04/1988

ISSN

0895-7061

Publication IDs

  • Scopus: 0023877550
  • PubMed: 2969742

Publication metrics

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Fractional count
1
Fractional count
0.50
Fractional count
1
Fractional count
0.50
Fractional count
1
Fractional count
1
Scopus
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Citation count
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Funding Details

The original studies reviewed in this manuscript were supported by the following grants: NIH HL27121, NIH HL32295, NIH HL33967. Dr Dellsperger was recipient of a National Research Service Award IF 32HLO7347-01 from the National Institutes of Health.
FundersFunding numbers
NIH
IF 32HLO7347-01
NHLBI
P50HL032295, R01HL027121, R01HL033967