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.