Effect of Angiotensin-Converting Enzyme Inhibitors on Energy Metabolism in Chronic Heart Failure - Enzymatic Studies of Myocardial Biopsies
Severe chronic heart failure is characterized by poor systolic function with low cardiac output, increased systolic and diastolic volumes, augmented diastolic pressures and ventricular hypertrophy secondary to cavity dilatation [10, 22, 23]. The myocardial oxygen demand is heightened due to wall stress, myocardial contractility and heart rate [21, 24]. However, the oxygen supply, at least to the subendocardium, is inadequate, which is caused by decreased coronary blood flow, an increased intramyocardial vascular resistance by elevated filling pressures and a shortened diastolic perfusion time [17, 24]. There is evidence that progressive deterioration of the heart is due to the inadequate coronary blood flow to the subendocardium, leading to decreased oxygen delivery to this area with a resultant loss of its ability to contribute to the work of the heart. Thus the imbalance between myocardial oxygen supply and demand might initiate a vicious cycle that worsens heart failure and further decreases coronary blood flow [1, 22].
KeywordsChronic Heart Failure Angiotensin Converting Enzyme Inhibitor Coronary Blood Flow Rate Pressure Product Severe Chronic Heart Failure
Unable to display preview. Download preview PDF.
- 1.Bishop SP, Altschuld RA (1971) Evidence for increased glycolytic metabolism in cardiac hypertrophy and congestive heart failure. In: Alpert NA (ed) Cardiac hypertrophy. Academic, New York, pp 567–585Google Scholar
- 2.Captopril Multicenter Research Group (1983) A placebo-controlled trial of captopril in refractory chronic congestive heart failure. J Am Coll Cardiol 2: 755–763Google Scholar
- 3.Cleland JGF, Dargie HJ, Ball SG, Gillen G, Hodsman GP, Morton JJ, East BW, Robertson I, Ford I, Robertson JIS (1985) Effects of enalapril in heart failure: a double blind study of effects on exercise performance, renal function, hormones, and metabolic state. Br Heart J 54: 305–312PubMedCrossRefGoogle Scholar
- 4.CONSENSUS Trial Study Group (1987) Effects of enalapril on mortality on severe congestive heart failure. Results of the Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS). N Engl J Med 316: 1429–1435Google Scholar
- 5.Ertl G (1986) The effect of angiotensin I and II at normal and reduced coronary perfusion. Pflugers Arch 406 [Suppl]: R49Google Scholar
- 6.Everse J, Kaplan NO (1975) Mechanisms of action and biological functions of various dehydrogenase isoenzymes. In: Markert CL (ed) Isoenzymes. II. Physiological functions. Academic, New York, pp 29–43Google Scholar
- 8.Foult JM, Nitenberg A, Tovolaro O, Antony I (1987) Selective coronary vasodilator effect of enalaprilat in patients with dilated cardiomyopathy: demonstration by a bilateral intracoronary infusion technique. J Am Coll Cardiol 9: 192 AGoogle Scholar
- 14.Magrini F, Shimizu M, Roberts N, Fouad FM, Tarazi RC, Zanchetti A (1987) Convertingenzyme inhibition and coronary blood flow. Circulation 75 [Suppl I]: 168–174Google Scholar
- 16.Nadal-Ginard B, Markert CL (1975) Use of affinity chromatography for purification of lactate dehydrogenase and for assessing the homology and function of the A and B subunits. In: Markert CL (ed) Isoenzymes. II. Physiological functions. Academic, New York, pp 45–67Google Scholar
- 20.Schultheiss H-P, Zähringer J, v. Scheidt W, Ulrich G (1986) Myocardial lactate dehydrogenase (LDH) isoenzyme distribution in chronic heart failure (CHF) before and after treatment with enalapril. Circulation 74 [Suppl II]: 508Google Scholar
- 21.Strauer BE (1987) Cardiac energetics in clinical heart disease. In: Jacob R, Just HJ, Holubarsch C (eds) Cardiac energetics. Steinkopff, Darmstadt; Springer, New YorkGoogle Scholar