Positron emission tomography, echo-doppler, and exercise studies of functional capacity in hypertensive heart disease

Akinboboye, Olakunle O.; Idris, Olajide; Goldsmith, Rochelle L.; Berekashvili, Kati; Chou, Ru-Ling; Bergman, Steven R

doi:10.1016/s0895-7061(02)02985-0

Cited by 10 publications

(8 citation statements)

References 13 publications

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“…In our CCHD patients, hyperemic perfusion was preserved and comparable to that of controls. This differs significantly from observations made previously in patients with acquired hypertrophy due to hypertensive or valvular heart disease (1,9,18,48), in which basal perfusion measurements were normal and hyperemic myocardial perfusion and perfusion reserves were decreased relative to controls. Our observations regarding hyperemic perfusion in the CCHD patients more closely parallel those made in those with the hypertrophy of the "athlete's" heart, in which hyperemic perfusion and perfusion reserves are preserved (21,26).…”

Section: Discussioncontrasting

confidence: 99%

Myocardial perfusion reserve in adults with cyanotic congenital heart disease

Brunken

Perloff

Czernin

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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In patients with cyanotic congenital heart disease (CCHD), a right-to-left shunt results in systemic hypoxemia. Systemic hypoxemia incites a compensatory erythrocytosis, which increases whole blood viscosity. We considered that these changes might adversely influence myocardial perfusion in CCHD patients. Basal [LV, 55 (SD 25) vs. 48 mmHg ⅐ ml Ϫ1 ⅐ g ⅐ min (SD 16); septum, 67 (SD 35) vs. 50 mmHg ⅐ ml Ϫ1 ⅐ g ⅐ min (SD 21); RV, 59 (SD 26) vs. 61 mmHg ⅐ ml Ϫ1 ⅐ g ⅐ min (SD 27), P ϭ not significant]. These findings suggest that adult CCHD patients have remodeling of the coronary circulation to compensate for the rheologic changes attending chronic hypoxemia. heart defects congenital; myocardial perfusion; positron emission tomography; myocardial perfusion reserve IN PATIENTS with cyanotic congenital heart disease (CCHD), infusion of poorly oxygenated blood into the systemic circulation via a right-to-left shunt results in sustained arterial hypoxemia. Arterial hypoxemia accelerates the release of erythropoetin from specialized sensor cells in the renal cortex, which in turn increases the number of circulating red blood cells (erythrocytosis) and the arterial hemoglobin concentration (17,25). This adaptive response helps to sustain tissue oxygen delivery, with equilibrium conditions typically being reached at elevated hematocrit levels (42). Oxygen delivery might also be augmented in the peripheral tissues of CCHD patients by an increase in oxygen extraction (3). However, this mechanism appears to be of limited utility for the coronary microcirculation, because resting oxygen extraction in the healthy human myocardium is already high and approaches 70% under basal conditions (23). This suggests that increases in myocardial oxygen demand need to be accompanied by nearly parallel increases in perfusion to sustain aerobic metabolism. Measurements of myocardial perfusion have previously been made in a small number of CCHD patients during cardiac catheterization, using clearance rates of inert gases or iodine-131 iodoantipyrine (51, 53). These early studies were limited by the methodology used to measure the tracer clearance rates and were further confounded by the need to normalize blood flows to derived estimates of ventricular mass. Moreover, these studies provided information only about global, and not regional, myocardial perfusion.Erythrocytosis increases whole blood viscosity in a nonlinear fashion (30,46). In vivo measurements made with intravital microscopy, for example, indicate that a change in hematocrit from 45% to 65% increases whole blood viscosity by about 60% and nearly doubles microvascular resistance (46). Because prior clinical reports suggest that marked increases in red blood cell mass might impair myocardial perfusion (27,61), it has been proposed that the erythrocytosis in CCHD may be more detrimental than beneficial for some patients. On the other hand, more recent studies indicate that increases in perfusate viscosity are associated with increases in shear stress, which could serve to stimula...

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Section: Discussioncontrasting

confidence: 99%

Myocardial perfusion reserve in adults with cyanotic congenital heart disease

Brunken

Perloff

Czernin

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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“…Furthermore, increased systemic resistance leads to a reduction in cardiac output, which could be an additional cause of decreased oxygen uptake and reduced functional capacity in the hypertensive population. 29 Cornelissen and Fagard 30 in a meta-analysis found that endurance training (!4 weeks) in arterial hypertensive patients results in decreased systemic vascular resistance by 7.1%, plasma norepinephrine by 29%, and plasma renin activity by 20%. Moreover, the authors showed that this regimen, regardless of drug usage, significantly decreased insulin resistance.…”

Section: Systemic Circulation and Exercise In Arterial Hypertensionmentioning

confidence: 99%

“…3,4,20,33,36 The cornerstone of the relationship between the left ventricle and functional capacity is myocardial perfusion reserve, which is significantly reduced in arterial hypertension patients. 29 On the other hand, some authors have claimed that myocardial oxygen consumption is even increased in arterial hypertension patients without left ventricular hypertrophy, but normal in arterial hypertension patients with hypertrophy. 37 This normalization of oxygen consumption through hypertrophy happens at the expense of efficiency, which is reduced in arterial hypertension patients with left ventricular hypertrophy.…”

Section: Impact Of Left Ventricle On Exercise Capacity In Arterial Hymentioning

confidence: 99%

“…The vast majority of studies with a large number of arterial hypertensive participants used standard exercise testing, which could provide only approximate results of exercise capacity, 1,6-9,33,35,86-90 whereas cardiopulmonary exercise testing was used in a significantly lower number of investigations. [2][3][4][5]29,32,36 Because of the inconsistency in methodology, it is far more complicated to analyze the relationship between exercise capacity and arterial hypertension, and make a final conclusion.…”

Section: Clinical Studies About Exercise Capacity In Arterial Hypertementioning

confidence: 99%

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Why is functional capacity decreased in hypertensive patients? From mechanisms to clinical studies

Tadić

Ivanović²

2014

Journal of Cardiovascular Medicine

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The influence of arterial hypertension on functional capacity is poorly understood. Studies have shown that peak oxygen consumption has been reduced in hypertensive patients, but the mechanisms are unclear. Left ventricular systolic and diastolic dysfunction, as well as left ventricular hypertrophy, are associated with lower functional capacity in patients with arterial hypertension. Furthermore, some investigations found a significant relationship between right ventricular systolic function and functional capacity in the general population. The aim of this review was to summarize current knowledge about the mechanisms of reduced functional capacity in hypertensive patients, including the impact of systemic and pulmonary circulations, as well as the influence of the left and right ventricle on oxygen consumption. Additionally, we reviewed all clinical studies regarding functional capacity in the population with arterial hypertension.

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“…Thyroid hormone action markedly stimulates the cardiac protein synthesis and leads to concentric cardiac hypertrophy and neo-angiogenesis [72]. When hyperthyroidism is of a limited duration, a "physiological" As a consequence CFR is reduced [6, [80][81][82] and minimal coronary resistance is increased significantly [78]. The reduction of CFR in hypertrophied hypertensive hearts is caused both by a concomitant increase of resting MBF [78], due to higher workload and oxygen consumption, and a reduction of hyperemic response [83] to endothelial dependent [78,84] and independent [78] stressors.…”

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confidence: 99%

The coronary circulation and blood flow in left ventricular hypertrophy

Camici

Olivotto

Rimoldi

2012

Journal of Molecular and Cellular Cardiology

151

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Two distinct types of left ventricular hypertrophy (LVH) have been described: the so called "physiologic" hypertrophy, which is normally found in professional athletes, and "pathologic" LVH which is found in patients with inherited heart muscle disease such as hypertrophic cardiomyopathy (HCM) or patients with cardiac and systemic diseases characterized by pressure or volume overload. Patients with pathologic LVH have often symptoms and signs suggestive of myocardial ischemia despite normal coronary angiograms. Under these circumstances ischemia is due to coronary microvascular dysfunction (CMD). The abnormalities of the coronary microcirculation may be unrelated to the degree of LVH and cause a reduction in maximum myocardial blood flow which, in the absence of epicardial stenoses, is suggestive of CMD. There is no technique that enables direct visualization of coronary microcirculation in vivo in humans. Therefore, its assessment relies on the measurement of parameters which reflect its functional status, such as myocardial blood flow and coronary flow reserve which is an integrated measure of flow through both the large epicardial coronary arteries and the microcirculation. In this review article we discuss the pathophysiological mechanisms responsible for CMD in patients with primary and secondary LVH and how the recognition of this phenomenon is providing new important information on patient stratification and prognosis. Finally, we discuss how assessment of CMD may be used as a valuable surrogate marker to test the efficacy of old and new drugs. This article is part of a Special Issue entitled "Coronary Blood Flow".

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Positron emission tomography, echo-doppler, and exercise studies of functional capacity in hypertensive heart disease

Abstract: Diminished functional capacity in patients with hypertension-induced LVH is related to the impairment in MPR and left ventricular diastolic function.

Cited by 10 publications

References 13 publications

Myocardial perfusion reserve in adults with cyanotic congenital heart disease

Myocardial perfusion reserve in adults with cyanotic congenital heart disease

Why is functional capacity decreased in hypertensive patients? From mechanisms to clinical studies

The coronary circulation and blood flow in left ventricular hypertrophy

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