Upward shift of the lower range of coronary flow autoregulation in hypertensive patients with hypertrophy of the left ventricle.

Abstract

Background. At any given perfusion pressure, coronary reserve is expressed by the difference between autoregulated and maximally vasodilated flow. In hypertension the raised coronary resistance reduces the steepness of the pressure-flow relationship at maximal vasodilatation. In the presence of cardiac hypertrophy the line of autoregulated flow becomes higher. For these reasons coronary reserve is reduced and the point at which baseline flow approaches the maximal achievable flow might be shifted to a higher perfusion pressure. Thus, any reduction below this elevated and critical value of pressure would lower the coronary flow.Methods and Results. The investigated patients were normotensive (controls, nine) and hypertensive with normal (group I, seven) or augmented LV mass index because of concentric LV hypertrophy (group II, eight). All had effort-induced angina and angiographically normal left epicardial branches. Flow in the great cardiac vein was measured by thermodilution in the baseline and during stepwise (5 mm Hg every 5 minutes) decrease of the coronary perfusion pressure with a titrated nitroprusside i.v. infusion; perfusion pressures of 60 mm Hg in the controls and 70 mm Hg in the hypertensives were taken as end points. Baseline flow averaged 102 ml/min in normotensives, 104 ml/min in hypertensive group I and 148 ml/min in hypertensive group II. At the end points flow was similar to baseline in the controls and group I. In group II coronary flow started to decline and myocardial 02 extraction started to slightly but significantly rise at perfusion pressures of 90-80 mm Hg; at the end point flow was reduced by 26% (p<0.01 from baseline). The perfusion patterns did not seem to be related to the changes in tension-time index and heart rate.Conclusions. The association of high blood pressure (reduced ability of the coronary arterioles to dilate) and hypertrophy of the myocardium (augmented baseline coronary flow) may shift the point of exhaustion of coronary reserve to a higher perfusion pressure and make the myocardium vulnerable to treatment-induced relative hypertension. (Circulation 1991;83:845-853)

Coronary flow velocity reserve in hypertensive patients with left ventricular systolic dysfunction

“…However, the increased standard deviation shown for E-wave and E/A values in the HP2 group points to the fact that some heterogeneity remained and could, at least in part, justify the reduction in coronary reserve found in this group. The influence of coronary perfusion pressure 37 seems to be unlikely, since diastolic blood pressures taken during either baseline or maximal coronary flow measurements were comparable between both hypertensive groups. The alleged interference of the type of antihypertensive therapy with CFVR, particularly angiotensin-converting enzyme inhibitor drugs, 38,39 seems unlikely as well.…”

ACE-inhibitor therapy with spirapril increases nocturnal hypotensive episodes in elderly hypertensive patients

“…Moreover, in hypertensive patients also coronary autoregulation in the subendocardium is shifted toward higher pressure, probably owing to Journal of Human Hypertension left ventricular hypertrophy and functional and structural alterations in the small coronary vessels. 3,5,18,19 The relationship between CBF and MAP has been established by invasive BP measurements. 1,20 In general, the non-invasive approach tends, when compared with the invasive approach, to underestimate SBP and overestimate DBP, 21 but the differences are small.…”

Significance of blood pressure levels achieved with felodipine anti-hypertensive treatment on cardiovascular structure and function changes

“…28 Although the mechanisms responsible for the increased danger are not completely defined, they include the modified response to adrenergic stimulation, sodium and calcium intracellular metabolism changes, coronary flow and reserve reduction, increased arrhythmiogenesis and decrease of the ventricular fibrillation threshold, development of congestive heart failure in parallel to the progressive degeneration of myocytes and their replacement by connective tissue. 29 So, a basic target of anti-hypertensive therapy is the regression of LV hypertrophy. This is achieved by the use of different anti-hypertensive drugs and, at least on a short-term basis, it seems to be independent of BP levels and the degree of cardiac wall hypertrophy.…”