Prognostic Impact of Coronary Vasodilator Dysfunction on Adverse Long-Term Outcome of Coronary Heart Disease

Schächinger, Volker; Britten, Martina; Zeiher, Andreas M.

doi:10.1161/01.cir.101.16.1899

Cited by 2,360 publications

(1,625 citation statements)

References 37 publications

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“…[7][8][9] Since the noninvasive measurement of endothelial function with ultrasound was established by Celermajer et al, 10 endothelial function has been evaluated for prognosis and response to treatment as an independent predictor of future cardiovascular events. 11,12 Thus, we designed the study to evaluate endothelial function in patients with exaggerated blood pressure response during treadmill tests.…”

Section: Introductionmentioning

confidence: 99%

Endothelial dysfunction in patients with exaggerated blood pressure response during treadmill test

Chang

Chung

Choi

et al. 2004

Clinical Cardiology

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SummaryBackground: The diagnostic and prognostic importance of exaggerated blood pressure response to exercise is controversial. Endothelial dysfunction has been demonstrated in patients with atherosclerosis and risk factors for coronary artery disease, but there is a paucity of information on patients with exercise-induced hypertension.Hypothesis: We designed the study to evaluate endothelial function in patients with exaggerated blood pressure response during exercise.Methods: Exercise-induced hypertension was defined as systolic blood pressure ≥ 210 mmHg in men and ≥ 190 mmHg in women during the treadmill test. Using a high-resolution ultrasound technique, endothelial function of the brachial artery in patients with exercise-induced hypertension (n = 25) and control subjects (n = 25) was investigated.Results: Endothelium-dependent vasodilation was impaired in patients with exercise-induced hypertension compared with controls (7.77 ± 5.14 vs. 2.81 ± 2.29%, p < 0.05). On univariate analysis, the extent of vasodilation correlated negatively with age (r = Ϫ0.43, p < 0.05) and ∆ systolic blood pressure (r = Ϫ0.39, p < 0.05). Even after adjustment for factors known to affect endothelial function, endothelium-dependent vasodila-

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Section: Introductionmentioning

confidence: 99%

Endothelial dysfunction in patients with exaggerated blood pressure response during treadmill test

Chang

Chung

Choi

et al. 2004

Clinical Cardiology

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“…In short, increased vascular superoxide both decreases NO bioactivity and allows vascular oxidative stress to continue. 24,25 Other atherogenic activities have been noted for angiotensin. Increases in plasminogen activator inhibitor-1 (PAI-1), the primary inhibitor of tissue-type plasminogen activator and a critical regulator of fibrinolysis, have been demonstrated in human coronary arteries.…”

Section: Oxidative Stressmentioning

confidence: 95%

“…1). 25,36 Angiotensin-converting enzyme inhibition has also been shown to prevent the rapid tachyphylaxis of the B 2 receptor. 37 Angiotensin II affects oxidative signaling and vascular inflammatory gene expression through its effects on NADPH oxidase and lipoxygenase and subsequent generation of ROS.…”

Section: The Role Of Angiotensin-converting Enzyme Inhibition and Angmentioning

confidence: 99%

Modulating atherosclerosis through inhibition or blockade of angiotensin

Rosenson¹

2003

Clinical Cardiology

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Summary: Angiotensin-converting enzyme (ACE) inhibitors are well recognized for their benefits in treating hypertension and congestive heart failure and preventing postmyocardial infarction heart failure or left ventricular (LV) dysfunction. Recently, blockade of the angiotensin II type 1 (AT 1 ) receptor was shown to reduce cardiovascular events in hypertensive subjects with LV hypertrophy. Several lines of evidence are now converging to show that ACE inhibitors may affect the atherosclerotic process itself. Emerging clinical data indicate that angiotensin-receptor blockers (ARBs) may possibly modulate atherosclerosis as well. The antiatherogenic properties of ACE inhibitors and ARBs may derive from inhibition or blockade of angiotensin II, now recognized as an agent that increases oxidative stress. Angiotensin-converting enzyme inhibition and angiotensin-receptor blockade also increase endothelial nitric oxide formation, which improves endothelial function. In contrast to the effects of ARBs, the vascular effects of ACE inhibitors may, in part, be mediated by an increase in bradykinin. This article reviews some of the biologic mechanisms whereby ACE inhibitors and ARBs may modulate atherosclerosis.

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“…Furthermore, both invasive techniques interrogating the coronary arteries and noninvasive FMD appear to be associated with the risk of future cardiovascular events. 25,26 Obesity and atherosclerosis…”

Section: Vascular Endothelial Functionmentioning

confidence: 99%