Effects of cardiac hypertrophy secondary to hypertension on the coronary circulation

Marcus, Melvin L.; Mueller, Timothy I.; Gascho, Joseph; Kerber, Richard E.

doi:10.1016/0002-9149(79)90239-x

Cited by 146 publications

(40 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The association with HPPT is largely justified by the influence of increased arterial stiffness on coronary flow at rest: more rigid the arterial wall, higher the workload required to keep an adequate coronary flow 5. Coronary flow velocity at rest was also associated with LV mass, which can increase the extravascular resistance of coronary microvessels by the compressive force of myocardial fibrosis 39, 45, 47, 49. Choudhury et al47 observed that in patients with hypertensive LV hypertrophy, CFR impairment, measured with positron emission tomography, was mainly due to an increased baseline myocardial blood flow, whereas the blunted response to dipyridamole did not achieve statistical significance.…”

Section: Discussionmentioning

confidence: 99%

Association Between Elevated Pulse Pressure and High Resting Coronary Blood Flow Velocity in Patients With Angiographically Normal Epicardial Coronary Arteries

Lembo

Sicari

Esposito

et al. 2017

JAHA

View full text Add to dashboard Cite

BackgroundThe aim of our study was to evaluate the relationship of pulse pressure (PP), a raw index of arterial stiffness, with noninvasively determined coronary flow reserve (CFR) and its components, in patients with angiographically normal epicardial coronary arteries.Methods and ResultsThe study population included 398 patients without angiographic evidence of coronary stenosis, who underwent high‐dose dipyridamole stress echocardiography with transthoracic‐derived CFR evaluation on the left anterior descending artery. CFR was calculated as the ratio between high‐dose dipyridamole and resting coronary diastolic peak velocities. Patients were divided into 2 groups: the first group included the first and second PP tertiles (n=298, PP ≤60 mm Hg) and the second group included the highest PP tertile (n=100, PP >60 mm Hg). Mean blood pressure, systolic blood pressure (both P<0.0001), age (P<0.002), and left ventricular mass index (P=0.013) were higher in the highest PP tertile, which also showed higher resting coronary flow velocity (31.6±9.6 cm/s versus 27.7±6.4 cm/s, P<0.0001) and marginally lower CFR (2.5±0.6 versus 2.6±0.6, P=0.044). Hyperemic coronary flow velocity did not differ between the 2 groups. By separate multiple linear regression analyses, after adjusting for sex, age, the highest systolic blood pressure tertile (≥140 mm Hg), left ventricular mass index, and cardiovascular risk factors, the highest PP tertile was associated with resting coronary flow velocity (P=0.003) and only marginally with hyperemic coronary flow velocity (P<0.02), whereas its association with CFR was not significant.ConclusionsIn patients without epicardial coronary artery stenosis, the highest PP tertile is associated with an increased coronary flow velocity at rest.

show abstract

Section: Discussionmentioning

confidence: 99%

Association Between Elevated Pulse Pressure and High Resting Coronary Blood Flow Velocity in Patients With Angiographically Normal Epicardial Coronary Arteries

Lembo

Sicari

Esposito

et al. 2017

JAHA

View full text Add to dashboard Cite

show abstract

“…For example, coronary vasodilator reserve was found to be reduced in hypertensive patients as well as in experimental hypertension. [25][26][27] However, the underlying mechanisms for the functional abnormalities of coronary arterioles in arterial hypertension remain incompletely understood. Interestingly, in vivo studies indicate that coronary flow regulation in hypertensive animals under resting conditions is near normal, but the flow supply is significantly reduced during metabolic stress.…”

Section: Discussionmentioning

confidence: 99%

“…Interestingly, in vivo studies indicate that coronary flow regulation in hypertensive animals under resting conditions is near normal, but the flow supply is significantly reduced during metabolic stress. 26,27 Because adenosine is involved in the metabolic regulation of coronary blood flow, it is reasonable to speculate that the coronary response to adenosine might be impaired in hypertension. In vivo studies support this view, showing that coronary vasodilatory reserve for adenosine is significantly reduced in humans and animals with chronic hypertension.…”

Section: Discussionmentioning

confidence: 99%

Upregulation of Vascular Arginase in Hypertension Decreases Nitric Oxide–Mediated Dilation of Coronary Arterioles

et al. 2004

View full text Add to dashboard Cite

Abstract-One characteristic of hypertension is a decreased endothelium-dependent nitric oxide (NO)-mediated vasodilation; however, the underlying mechanism is complex. In endothelial cells (ECs), L-arginine is the substrate for both NO synthase (NOS) and arginase. Because arginase has recently been shown to modulate NO-mediated dilation of coronary arterioles by reducing L-arginine availability, we hypothesized that upregulation of vascular arginase in hypertension contributes to decreased NO-mediated vasodilation. To test this hypothesis, hypertension (mean arterial blood pressure Ͼ150 mm Hg) was maintained for 8 weeks in pigs by aortic coarctation. Coronary arterioles from normotensive (NT) and hypertensive (HT) pigs were isolated and pressurized for in vitro study. NT vessels dilated dose-dependently to adenosine (partially mediated by endothelial release of NO) and sodium nitroprusside (endothelium-independent vasodilator). Conversely, HT vessels exhibited reduced dilation to adenosine but dilated normally to sodium nitroprusside. Adenosine-stimulated NO release was increased Ϸ3-fold in NT vessels but was reduced in HT vessels. Moreover, arginase activity was 2-fold higher in HT vessels. Inhibition of arginase activity by N -hydroxynor-L-arginine or incubation with L-arginine partially restored NO release and dilation to adenosine in HT vessels. Immunohistochemistry showed that arginase expression was increased but NOS expression was decreased in arteriolar ECs of HT vessels. These results suggest that NO-mediated dilation of coronary arterioles is inhibited in hypertension by an increase in arginase activity in EC, which limits L-arginine availability to NOS for NO production. The inability of arginase blockade or L-arginine supplementation to completely restore vasodilation may be related to downregulation of endothelial NOS expression. Key Words: arginine Ⅲ hypertension Ⅲ microcirculation Ⅲ nitric oxide synthase Ⅲ vasodilation H ypertension is a major risk factor for coronary artery disease. One characteristic of hypertension that appears to be critical in the development of vascular disease is the impairment of endothelial function. For example, there is a markedly reduced endothelium-dependent vasodilation in both large and small coronary arteries from hypertensive humans and animal models of hypertension. 1 Mounting evidence suggests that this vascular impairment may be related to a diminished production and bioavailability of the potent vasodilator nitric oxide (NO), which may result from an increased vascular production of superoxide anion 2 or decreased endothelial levels of tetrahydrobiopterin 3,4 or L-arginine. 5 Interestingly, administration of NO precursor L-arginine restores endothelium-mediated vasodilatory function in patients with essential hypertension, 5 improves coronary hemodynamics in spontaneously hypertensive rats, 6 and increases NO production and reduces blood pressure in hypertensive rats with 7 or without 8 renal failure. These results suggest the possible reduction of L-arginine ...

show abstract

“…[1][2][3] Cannon et al 4 showed that even in the absence of atherosclerotic coronary artery disease, patients with nonobstructive HCM might demonstrate abnormal lactate metabolism during atrial pacing, suggesting that the presence of ischemia is the result of abnormalities of the coronary microcirculation. 5,6 Recent studies have shown that possible mechanisms for this ischemia include intramyocardial small vessel disease, [6][7][8] septal perforator artery compression, 9 coronary artery spasm, inadequate capillary density in relation to the increased myocardial mass, 10 an increase in systolic perivascular resistance, 11,12 and a limitation to the increase in myocardial blood flow caused by abnormal diastolic relaxation in HCM. 13,14 Furthermore, small vessel coronary artery disease [6][7][8] with intimal hyperplasia, medial hypertrophy, and impaired coronary flow reserve 9,15,16 may correlate closely with the myocardial ischemia and fibrosis seen in HCM.…”

mentioning

confidence: 99%

Abnormal Coronary Flow Profiles at Rest and During Rapid Atrial Pacing in Patients With Hypertrophic Cardiomyopathy

et al. 1999

View full text Add to dashboard Cite

ypertrophic cardiomyopathy (HCM) comprises several different syndromes with varying clinical presentations, natural histories, and pathologic findings. Myocardial ischemia may play a critical role in the symptomatic presentation and the natural history of HCM. [1][2][3] Cannon et al 4 showed that even in the absence of atherosclerotic coronary artery disease, patients with nonobstructive HCM might demonstrate abnormal lactate metabolism during atrial pacing, suggesting that the presence of ischemia is the result of abnormalities of the coronary microcirculation. 5,6 Recent studies have shown that possible mechanisms for this ischemia include intramyocardial small vessel disease, 6-8 septal perforator artery compression, 9 coronary artery spasm, inadequate capillary density in relation to the increased myocardial mass, 10 an increase in systolic perivascular resistance, 11,12 and a limitation to the increase in myocardial blood flow caused by abnormal diastolic relaxation in HCM. 13,14 Furthermore, small vessel coronary artery disease 6-8 with intimal hyperplasia, medial hypertrophy, and impaired coronary flow reserve 9,15,16 may correlate closely with the myocardial ischemia and fibrosis seen in HCM. 15 Cannon et al demonstrated that patients with HCM showed an initial rise in great cardiac vein flow, measured by a thermodilution catheter at an intermediate heart rate of 130 beats/min, but with continued pacing to a heart rate of 150 beats/min, mean coronary flow fell. However, phase analysis of systolic and diastolic coronary flow during tachycardia has not been performed in patients with HCM and the precise mechanism of exercise-induced ischemia remains obscure.The present study was designed to evaluate the mechanisms responsible for myocardial ischemia in patients with nonobstructive HCM by phase analysis of coronary blood flow using a Doppler flow wire at rest and during rapid atrial pacing. Methods Study PatientsWe studied 11 consecutive patients with clinical and echocardiographic evidense of HCM and angiographically normal coronary arteries. The patients underwent transthoracic echocardiographic examinations within 10 days of a diagnostic cardiac catheterization that included coronary arteriography. The patient group included 5 men and 6 women, 24-77 year old (mean, 57±16): 9 patients with asymmetric septal hypertrophy (Maron's classification 17 : type 1, 3 patients; type 2, 4; type 3, 2) with a ventricular septal thickness greater than 15 mm and a ratio of interventricular septum to posterior wall thickness greater than 1.3, and 2 patients with symmetric hypertrophy determined by transthoracic echocardiography. Eight patients presenting with atypical chest pain (5 men and 3 women), 55-67 year old (mean, 63±5) served as control subjects. They did not have significant coronary stenosis or left ventricular hypertrophy, as revealed by selective coronary angiography and echocardiography, respectively. Informed consent was obtained from all patients.Jpn Circ J 1999; 63: 350 -356 (Received October 19, 1998; r...

show abstract

Effects of cardiac hypertrophy secondary to hypertension on the coronary circulation

Cited by 146 publications

References 19 publications

Association Between Elevated Pulse Pressure and High Resting Coronary Blood Flow Velocity in Patients With Angiographically Normal Epicardial Coronary Arteries

Association Between Elevated Pulse Pressure and High Resting Coronary Blood Flow Velocity in Patients With Angiographically Normal Epicardial Coronary Arteries

Upregulation of Vascular Arginase in Hypertension Decreases Nitric Oxide–Mediated Dilation of Coronary Arterioles

Abnormal Coronary Flow Profiles at Rest and During Rapid Atrial Pacing in Patients With Hypertrophic Cardiomyopathy

Contact Info

Product

Resources

About