DIABETES, VOLUME 45, SUPPLEMENT 1, JANUARY 1996, PAGES S59-S65
Substrate Metabolism, Hormone Interaction, and
Angiotensin-Converting Enzyme Inhibitors in Left Ventricular
Hypertrophy
Yi-chun Zhu, Yi-zhun Zhu, Heidi Spitznagel, Peter Gohlke, and Thomas Unger
Left ventricular hypertrophy is considered to be an independent risk factor giving rise to ischemia, arrhythmias,
and left ventricular dysfunction. Slow movement of intracellular calcium contributes to the impaired contraction
and relaxation function of hypertrophied myocardium. Myofibril content may also be shifted to fetal-type
isoforms with decreased contraction and relaxation properties in left ventricular hypertrophy. Myocyte
hypertrophy and interstitial fibrosis are regulated independently by mechanical and neurohumoral mechanisms. In
severely hypertrophied myocardium, capillary density is reduced, the diffusion distance for oxygen, nutrients, and
metabolites is increased, and the ratio of energy-production sites to energy-consumption sites is decreased. The
metabolic state of severely hypertrophied myocardium is anaerobic, as indicated by the shift of lactate
dehydrogenase marker enzymes. Therefore, the hypertrophied myocardium is more vulnerable to ischemic events.
As a compensatory response to severe cardiac hypertrophy and congestive heart failure, the ADP/ATP carrier is
activated and atrial natriuretic peptide is released to increase high-energy phosphate production and reduce
cardiac energy consumption by vasodilation and sodium and fluid elimination. However, in severely
hypertrophied and failing myocardium, vasoconstrictor and sodium- and fluid-retaining factors, such as the
renin-angiotensin system, aldosterone, and sympathetic nerve activity, play an overwhelming role.
Angiotensin-converting enzyme inhibitors (ACEIs) are able to prevent cardiac hypertrophy and improve cardiac
function and metabolism. Under experimental conditions, these beneficial effects can be ascribed mainly to
bradykinin potentiation, although a contribution of the ACEI-induced angiotensin II reduction cannot be excluded.
Diabetes 45 (Suppl. 1):S59-S65, 1996
Copyright © 1996 American Diabetes Association
Last updated: 5/30/96
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