Decreased Coronary Reserve

Marcus, Melvin L.; Doty, Donald B.; Hiratzka, Loren F.; Wright, Creighton B.; Eastham, Charles L.

doi:10.1056/nejm198211253072202

Cited by 525 publications

(42 citation statements)

References 24 publications

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“…[1][2][3][4] They include impaired cardiac performance and coronary hemodynamics and ventricular fibrosis. [5][6][7][8][9] In a recent study involving normotensive and spontaneously hypertensive rats (SHRs), aged 22,35 and 65 weeks, we demonstrated that associated with aging per se there were progressive impairments in coronary hemodynamics with increased myocardial collagen deposition in both strains. 9 These changes were more pronounced in hypertensive rats at any age, as if hypertension might have induced premature aging alterations of cardiovascular system.…”

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confidence: 99%

Prolonged L-Arginine on Cardiovascular Mass and Myocardial Hemodynamics and Collagen in Aged Spontaneously Hypertensive Rats and Normal Rats

1999

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Abstract-This study was designed to examine whether L-arginine could prevent hypertension-and age-related impairment of coronary hemodynamics and cardiac fibrosis in aged (80-week-old) rats. To differentiate between hypertension-and age-related changes, the study was performed in both normotensive Wistar-Kyoto rats (WKYs) and spontaneously hypertensive rats (SHR). Male 1-year-old rats of both strains were divided into 2 groups and given either placebo or L-arginine (1.2 g/L) in drinking water. After 6 months, systemic and coronary hemodynamics (radionuclide-labeled microspheres), right and left ventricular and aortic mass indexes, and ventricular hydroxyproline (an estimate of collagen) concentrations were determined. In the aged WKYs, L-arginine did not affect any of the examined variables except slightly reducing total peripheral resistance. In contrast, L-arginine diminished arterial pressure, total peripheral resistance, and left ventricular and aortic mass indexes in the SHRs; it also increased coronary flow reserve and reduced minimal coronary flow resistance and myocardial hydroxyproline concentration. Key Words: hypertension Ⅲ aging Ⅲ mass, ventricular Ⅲ mass, aortic Ⅲ hemodynamics, coronary Ⅲ myocardial collagen concentration Ⅲ L-arginine M orphological and functional changes that occur in the cardiovascular system with hypertension and aging are similar in many respects. 1-4 They include impaired cardiac performance and coronary hemodynamics and ventricular fibrosis. [5][6][7][8][9] In a recent study involving normotensive and spontaneously hypertensive rats (SHRs), aged 22, 35 and 65 weeks, we demonstrated that associated with aging per se there were progressive impairments in coronary hemodynamics with increased myocardial collagen deposition in both strains. 9 These changes were more pronounced in hypertensive rats at any age, as if hypertension might have induced premature aging alterations of cardiovascular system.Much evidence exists that suggests that the endothelium, in autocrine/paracrine and endocrine manners, participates in regulating cardiovascular structure and function. 10 The endothelial cells produce and release a variety of vasoactive substances, including nitric oxide (NO). 10 NO is a powerful vasodilator which is derived from L-arginine by the action of NO synthase. 11 Many reports have demonstrated that endothelial dysfunction of NO synthesis and release is present, or even precedes cardiovascular changes associated with hypertension and aging. [12][13][14][15][16][17][18][19] Thus, endothelial dysfunction may participate the development of hypertension and age-related changes in the coronary vasculature and myocardium. Therefore, the purpose of this study was to examine whether prolonged L-arginine administration, the initiator of NO production, could modulate cardiac fibrosis and deterioration of coronary hemodynamics in both old and hypertensive rats. To differentiate between hypertension-and age-induced changes, the results obtained in aging normotensive WistarKyoto rats (WKYs)...

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confidence: 99%

Prolonged L-Arginine on Cardiovascular Mass and Myocardial Hemodynamics and Collagen in Aged Spontaneously Hypertensive Rats and Normal Rats

1999

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“…This was also the case in Park's study, 11 as well as in other studies using quantitative coronary angiography. [13][14][15] It is important to recognize that myocardial blood flow is dependent on many other factors besides proximal coronary stenosis, such as aortic pressure, 12 diffuse coronary atherosclerosis, 16 microvascular function, 17 and collateral blood flow. 12 All these factors are more difficult to measure by coronary CTA.…”

Section: See Article By Dey Et Almentioning

confidence: 99%

Quantifying Plaque Burden and Morphology Using Coronary Computed Tomography Angiography to Predict Coronary Physiology

Carli

Blankstein

2015

Circ: Cardiovascular Imaging

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C oronary computed tomography angiography (CTA) is a powerful noninvasive technique that can be used to visualize the presence, extent, and severity of both noncalcified and calcified plaque. When compared with other noninvasive imaging approaches, coronary CTA has the highest sensitivity to detect anatomic stenosis and, consequently, the highest negative predictive value to exclude obstructive coronary artery disease (CAD).1 However, once a coronary stenosis is identified, a limitation of CTA-which is equally problematic for invasive coronary angiography-is that the physiological consequences associated with those stenoses cannot be determined with any degree of accuracy.2,3 On the other hand, the presence and severity of ischemia are essential for understanding the pathophysiology of patient's symptoms and determining the potential role of coronary revascularization. Consequently, multiple techniques have been introduced to harness physiological data from CTA and infer whether a stenosis is hemodynamically significant. Some investigators have applied computational fluid dynamic modeling to estimate coronary pressure gradients and calculation of the fractional flow reserve across stenosis. 4 Others have relied on the use of iodinated contrast at rest and during pharmacological stress to assess myocardial perfusion (computed tomography [CT] perfusion) 5 in a similar manner to radionuclide scintigraphy and magnetic resonance imaging-based myocardial perfusion techniques. Recent clinical trials have demonstrated that in carefully selected patients, these techniques can provide useful information to understand the physiological significance of stenoses.6-9 So, it is clear that the paradigm of isolated stenosis quantification with angiography (noninvasive or invasive) has provided insufficient and, sometimes, misleading information for diagnosis and management of CAD. However, there is limited data addressing the question of whether a more complete quantification of the atherosclerotic burden with coronary CTA, including all stenosis dimensions and other plaque characteristics, can improve discrimination of flow-limiting lesions. See Article by Dey et alIn this issue of Circulation: Cardiovascular Imaging, Dey et al 10 evaluated the quantitative relationship between stenosis dimensions and x-ray-based characteristics of coronary plaques and myocardial blood flow and coronary flow reserve (CFR)-a validated measure of the functional severity of coronary stenosis. The study included 51 symptomatic patients with known or suspected CAD undergoing vasodilator stress positron emission tomography (PET) myocardial perfusion imaging followed by coronary CTA on an integrated PET/CT system. Coronary flow reserve was calculated as the ratio of myocardial blood flow (in mL/min/g) during vasodilator stress over that at rest. Total coronary plaque volume and burden (plaque volume index by vessel volume), percent stenosis, plaque length, vessel remodeling, and x-ray-based plaque characteristics (calcified and noncalcified) were also...

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“…On the other hand, the increase in the diastolic pressure will result in increased endocardial compression of the coronary arteries and decease in coronary perfusion. Those two factors (decrease the myocardial perfusion time and decrease coronary blood flow) in addition to the increased oxygen demand of the hypertrophied ventricle will result in subendocardial ischemia, which may result in symptoms similar to angina pectoris and LV dysfunction (Marcus, Doty, Hiratzka, Wright, & Eastham, 1982).…”

Section: Pathophysiology and Hemodynamicsmentioning

confidence: 99%

015 * Propensity Score Analysis of Outcomes Following Minimally Invasive Versus Conventional Aortic Valve Replacement

Shehada

Voß

Elhmidi

et al. 2014

Interactive CardioVascular and Thoracic Surgery

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Decreased Coronary Reserve

Cited by 525 publications

References 24 publications

Prolonged L-Arginine on Cardiovascular Mass and Myocardial Hemodynamics and Collagen in Aged Spontaneously Hypertensive Rats and Normal Rats

Prolonged L-Arginine on Cardiovascular Mass and Myocardial Hemodynamics and Collagen in Aged Spontaneously Hypertensive Rats and Normal Rats

Quantifying Plaque Burden and Morphology Using Coronary Computed Tomography Angiography to Predict Coronary Physiology

015 * Propensity Score Analysis of Outcomes Following Minimally Invasive Versus Conventional Aortic Valve Replacement

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