Regulation of myocardial blood flow by oxygen consumption is maintained inthe failing heart during exercise

Citation
Jh. Traverse et al., Regulation of myocardial blood flow by oxygen consumption is maintained inthe failing heart during exercise, CIRCUL RES, 84(4), 1999, pp. 401-408
Citations number
32
Categorie Soggetti
Cardiovascular & Hematology Research
Journal title
CIRCULATION RESEARCH
ISSN journal
00097330 → ACNP
Volume
84
Issue
4
Year of publication
1999
Pages
401 - 408
Database
ISI
SICI code
0009-7330(19990305)84:4<401:ROMBFB>2.0.ZU;2-B
Abstract
The hemodynamic abnormalities and neurohumoral activation that accompany co ngestive heart failure (CHF) might be expected to impair the increase in co ronary blood flow that occurs during exercise. This study was performed to determine the effects of CHF on myocardial oxygen consumption and coronary blood flow during exercise. Coronary blood flow was measured in chronically instrumented dogs at rest, during 2 stages of graded treadmill exercise un der control conditions (n=10), and after the development of CHF produced by 3 weeks of rapid ventricular pacing (n=9). In the normal dogs, coronary bl ood flow increased during exercise in proportion to the increase in the hea rt rateXthe left ventricular systolic blood pressure product (RPP). After t he development of CHF, resting myocardial blood flow was 25% lower than nor mal (P<0.05). Myocardial blood flow increased during the first stage of exe rcise, but then failed to increase further during the second stage of exerc ise despite an additional increase in the RPP. Myocardial oxygen consumptio n during exercise was significantly lower in animals with CHF and parallele d coronary flow. Despite the lower values for coronary blood flow in animal s with CHF, there was no evidence for myocardial ischemia. Thus, even durin g the second level of exercise when coronary flow failed to increase, myoca rdial lactate consumption continued and coronary venous pH did not fall. In addition, the failure of coronary flow to increase as the exercise level w as increased from stage 1 to stage 2 was not associated with a further incr ease in myocardial oxygen extraction. Thus, cardiac failure was associated with decreased myocardial oxygen consumption and failure of oxygen consumpt ion to increase with an increase in the level of exercise. This abnormality did not appear to result from inadequate oxygen availability, but more lik ely represented a reduction of myocardial oxygen usage with a secondary dec rease in metabolic coronary vasodilation.