CORONARY HEMODYNAMICS IN LEFT-VENTRICULAR HYPERTROPHY

Citation
Dr. Wallbridge et Sm. Cobbe, CORONARY HEMODYNAMICS IN LEFT-VENTRICULAR HYPERTROPHY, HEART, 75(4), 1996, pp. 369-376
Citations number
42
Categorie Soggetti
Cardiac & Cardiovascular System
Journal title
HEARTACNP
ISSN journal
13556037
Volume
75
Issue
4
Year of publication
1996
Pages
369 - 376
Database
ISI
SICI code
1355-6037(1996)75:4<369:CHILH>2.0.ZU;2-1
Abstract
Background-Left ventricular hypertrophy is associated with an increase d risk of cardiovascular morbidity and mortality. Previous studies hav e shown that patients with left ventricular hypertrophy develop electr ocardiographic changes and left ventricular dysfunction during acute h ypotension, and suggest that the lower end of autoregulation may be sh ifted upwards. Aim-To measure coronary blood flow (velocity) and flow reserve during acute hypotension in patients with left ventricular hyp ertrophy. Patients-Fight patients with atypical chest pain and seven w ith hypertensive left ventricular hypertrophy; all with angiographical ly normal epicardial vessels. Setting-Tertiary referral centre. Method s-The physiological range of blood pressure was determined by previous ambulatory monitoring. Left ventricular mass was determined by echoca rdiography. At cardiac catheterisation, left coronary blood flow veloc ity was measured using a Judkins style Doppler tipped catheter. During acute hypotension with sodium nitroprusside, coronary blood flow velo city was recorded at rest and during maximal hyperaemia induced by int racoronary injection of adenosine. Quantitative coronary angiography w as performed manually. Results-For both groups coronary blood flow vel ocity remained relatively constant over a range of physiological diast olic blood pressures and showed a steep relation with diastolic blood pressure during maximal hyperaemia with intracoronary adenosine. Absol ute coronary blood flow (calculated from quantitative angiographic dat a), standardised for left ventricular mass, showed reduced flow in the hypertensive group at rest and during maximal vasodilatation. Conclus ion-The results are consistent with an inadequate blood supply to the hypertrophied heart, but no upward shift of the lower end of the autor egulatory range was observed.