Reduced vascular compliance is associated with impaired endothelium-dependent dilatation in the brachial artery of patients with congestive heart failure
“…This effect of NTG on BA diameter and distensibility has been additionally examined in both CHF patients and controls although characteristic impedance was not calculated (Nakamura et al 2004).…”
This examination of brachial artery (BA) differential characteristic impedance, DeltaZ (c), illustrates that changes in Z (c) can occur from changes in either BA wall stiffness (Young's modulus, E) and/or its diameter, D. Furthermore, we assessed how changes in both E and D combine in either an isolated, synergistic, or antagonistic manner to yield the net change in BA Z (c). The basis of this analysis is a partial differential equation which approximates DeltaZ (c) as a total differential. The effects on BA DeltaZ (c) of acetylcholine, atenolol, fenoldapine, nitroglycerin, hydrochlorothiazide and other medications are examined using data from previously published studies. Clinical situations which alter BA Z (c), such as congestive heart failure, hypertension, and hyperemia, are also analyzed. Results illustrate the usefulness of the present approach in differentiating how medications, hyperemia, and pathological conditions affect BA DeltaZ (c) by causing independent changes to E and/or D.
“…This effect of NTG on BA diameter and distensibility has been additionally examined in both CHF patients and controls although characteristic impedance was not calculated (Nakamura et al 2004).…”
This examination of brachial artery (BA) differential characteristic impedance, DeltaZ (c), illustrates that changes in Z (c) can occur from changes in either BA wall stiffness (Young's modulus, E) and/or its diameter, D. Furthermore, we assessed how changes in both E and D combine in either an isolated, synergistic, or antagonistic manner to yield the net change in BA Z (c). The basis of this analysis is a partial differential equation which approximates DeltaZ (c) as a total differential. The effects on BA DeltaZ (c) of acetylcholine, atenolol, fenoldapine, nitroglycerin, hydrochlorothiazide and other medications are examined using data from previously published studies. Clinical situations which alter BA Z (c), such as congestive heart failure, hypertension, and hyperemia, are also analyzed. Results illustrate the usefulness of the present approach in differentiating how medications, hyperemia, and pathological conditions affect BA DeltaZ (c) by causing independent changes to E and/or D.
“…Important components of the link between arterial stiffness and heart failure may be impaired NO bioavailability and endothelial dysfunction. Coexisting arterial stiffness or reduced vascular compliance and endothelial dysfunction have been observed in patients with heart failure [50,51] and in patients with β-thalassemia major, a risk factor for LV dysfunction [52]. In addition, impairment of endothelium-dependent LV relaxation has been correlated with moderate pressure-overload LV hypertrophy [53] and is an independent predictor of cardiac death and hospitalization in patients with heart failure [54].…”
Section: Endothelial Function and Arterial Stiffnessmentioning
beta-Blockers have generally demonstrated smaller reductions in cardiovascular events, compared with other antihypertensive classes, despite similar reductions in blood pressure. This may be due to the ineffectiveness of traditional beta-blockers, such as atenolol, in reducing central aortic pressure, a strong, independent predictor of cardiovascular outcome. However, the beta-blocker class is heterogeneous, and some newer beta-blockers, which exhibit vasodilatory effects independent of beta-blockade, provide beneficial effects on arterial stiffness and endothelial dysfunction, which may lead to reductions in central aortic pressure and improvements in clinical outcomes. For example, the vasodilating beta-blocker nebivolol was shown to improve forearm blood flow and arterial stiffness and, in a large clinical study, to significantly reduce morbidity and mortality, independent of left ventricular ejection fraction, among patients with chronic heart failure. Further research is warranted to investigate any potential differences between traditional and newer vasodilating beta-blockers on cardiovascular outcomes.
“…In postmenopausal women with metabolic syndrome, fasting plasma glucose and systolic blood pressure, well-known contributors to endothelial dysfunction, were highly predictable to the increase in arterial stiffness [3]. In patients with congestive heart failure, reduced vascular compliance is associated with impaired endothelium-dependent dilatation in the brachial artery [45]. In patients with coronary artery disease, flow-mediated vasodilation showed statistically significant correlation with several measurements of vascular stiffness, including proximal aortic compliance [1].…”
Section: Do Measures Of Vascular Compliance Correlate With Endotheliamentioning
Accumulating evidence demonstrates that measures of vascular compliance correlate with endothelial function in animal models and patients with cardiovascular, metabolic, and kidney diseases. Nitric oxide modulates not only endothelial function, but also vascular compliance. Disruption of normal endothelial function may, at least partially, be responsible for reduced vascular compliance. Thus, nitric oxide may play a pivotal role as a mechanistic link between impaired vascular compliance and endothelial dysfunction.
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