Endothelial and Non-Endothelial Coronary Blood Flow Reserve and Left Ventricular Dysfunction in Systemic Hypertension

Abstract

Rocha AM, Salemi VMC, Neto PAL, Matsumoto AY, Pereira VFA, Fernandes F, Nastari L, Mady C. Endothelial and non-endothelial coronary blood flow reserve and left ventricular dysfunction in systemic hypertension. Clinics. 2009;64(4):327-35 OBJECTIVES: We evaluated the impairment of endothelium-dependent and endothelium-independent coronary blood flow reserve after administration of intracoronary acetylcholine and adenosine, and its association with hypertensive cardiac disease. INTRODUCTION: Coronary blood flow reserve reduction has been proposed as a mechanism for the progression of compensated left ventricular hypertrophy to ventricular dysfunction. METHODS: Eighteen hypertensive patients with normal epicardial coronary arteries on angiography were divided into two groups according to left ventricular fractional shortening (FS). Group 1 (FS ≥0.25): n=8, FS=0.29 ± 0.03; Group 2 (FS <0.25): n=10, FS= 0.17 ± 0.03. RESULTS: Baseline coronary blood flow was similar in both groups (Group 1: 80.15 ± 26.41 mL/min, Group 2: 100.09 ± 21.51 mL/min, p=NS). In response to adenosine, coronary blood flow increased to 265.1 ± 100.2 mL/min in Group 1 and to 300.8 ± 113.6 mL/min (p <0.05) in Group 2. Endothelium-independent coronary blood flow reserve was similar in both groups (Group 1: 3.31 ± 0.68 and Group 2: 2.97 ± 0.80, p=NS). In response to acetylcholine, coronary blood flow increased to 156.08 ± 36.79 mL/min in Group 1 and to 177.8 ± 83.6 mL/min in Group 2 (p <0.05). Endothelium-dependent coronary blood flow reserve was similar in the two groups (Group 1: 2.08 ± 0.74 and group Group 2: 1.76 ± 0.61, p=NS). Peak acetylcholine/peak adenosine coronary blood flow response (Group 1: 0.65 ± 0.27 and Group 2: 0.60 ± 0.17) and minimal coronary vascular resistance (Group 1: 0.48 ± 0.21 mmHg/mL/min and Group 2: 0.34 ± 0.12 mmHg/mL/min) were similar in both groups (p= NS). Casual diastolic blood pressure and end-systolic left ventricular stress were independently associated with FS. CONCLUSIONS: In our hypertensive patients, endothelium-dependent and endothelium-independent coronary blood flow reserve vasodilator administrations had similar effects in patients with either normal or decreased left ventricular systolic function.

Comparison between adenosine and isoflurane for assessing the coronary flow reserve in mouse models of left ventricular pressure and volume overload

“…At the same time, cardiac function was significantly suppressed during 2.5% isoflurane inhalation compared with during 1% isoflurane inhalation or adenosine infusion in those mice, especially in the AR mice. We also found that CFR was closely related to cardiac function, which was in accord with previous studies in humans (20) and mice (10). All of the evidence suggests that high-concentration isoflurane-induced cardiac dysfunction may lead to underestimation of CFR.…”

“…Nevertheless, CFR is closely related with cardiac function (10,20). Given that isoflurane can depress cardiac function through myofilament desensitization (5), the findings in mice without significant cardiac overloading could not be simply extrapolated to mice with loading changes (e.g., pressure or volume overload) or cardiac remodeling (concentric or eccentric hypertrophy).…”

Anti-Hypertensive Drugs Have Different Effects on Ventricular Hypertrophy Regression

“…Hemodynamic overload promotes myocyte stretch, the release of intracellular calcium, the activation of calcineurin and the induction of gene expression reprogramming 1. In athletes, left ventricular hypertrophy (LVH) is regarded as a physiological response that results from a hemodynamic overload; this physiological response does not result in the harmful effects of hypertension development or other heart diseases 10–12. The literature explains physiological LVH as the result of a volume and pressure overload that results from intense physical training (the hemodynamic stimulus), which is not necessarily accompanied by neural and humoral changes 13…”

Endothelial‐Mediated Coronary Flow Reserve and Its Relation to Mitral Annular Tissue Doppler Velocities in Offspring of Hypertensive Parents

“…1 Endothelial dysfunction is an important, early and reversible feature of atherogenesis. 6 Noninvasive transthoracic ultrasound imaging of coronary blood flow is increasingly being used to identify derangements of coronary microcirculation at the level of coronary flow in the absence of epicardial coronary stenosis. 4,5 Impairment of endothelium-dependent coronary vasodilatation capacity is one of the mechanisms responsible for inadequate myocardial flow early in hypertensive patients before the development of morphological alterations.…”