Arterial hemodynamics in human hypertension.

Ting, Chih Tai; Brin, Kenneth P.; Lin, Shing Jong; Wang, S P; Chang, Mau Song; Chiang, B N; Yin, F. C. P.

doi:10.1172/jci112737

Cited by 130 publications

(82 citation statements)

References 37 publications

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“…3,21,22 Furthermore, distal arterial reflection sites are shifted closer to the heart while using nonvasodilating b-blockers, which results in premature return of the arterial wave to the aorta. 23 The directional changes in augmentation pressure and augmentation index in the carvedilol and atenolol arms observed in this study reflect carvedilol's peripheral vasodilatory action compared with atenolol, the latter of which either does not affect peripheral arteries or could paradoxically cause vasoconstriction. At higher doses, atenolol might block vasodilatory b 2 receptors, causing constriction and increased peripheral resistance.…”

Section: Discussionmentioning

confidence: 53%

Carvedilol Reduces Aortic Wave Reflection and Improves Left Ventricular/Vascular Coupling: A Comparison With Atenolol (CENTRAL Study)

Shah¹,

Smith

Nichols

et al. 2011

The Journal of Clinical Hypertension

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Blood pressure (BP) characteristics, such as central aortic pressure and arterial stiffness, independently predict cardiovascular events. The effects of pharmacologically dissimilar b-blockers on these properties have not been fully elucidated. Patients with essential hypertension and without significant concomitant cardiovascular disease were randomly assigned to controlled-release carvedilol, forcetitrated to 80 mg (n=22), or atenolol, force-titrated to 100 mg (n=19); each was given once daily for 4 weeks. Baseline characteristics were similar. At the end of week 4, atenolol and carvedilol reduced central and brachial systolic and diastolic BP to a similar extent. Central augmentation index was increased in atenolol-treated patients but not carvedilol-treated patients (atenolol 4.47% vs carvedilol )0.68%; P=.04). Mean augmented central aortic pressure increased slightly during atenolol treatment (+1.1 mm Hg) but decreased slightly during carvedilol treatment ()1.1 mm Hg), although the difference in these changes was not statistically significant (P=.23). Pulse pressure amplification was reduced more with atenolol at week 4 (atenolol )10.7% vs carvedilol )1.8%; P=.02). Therefore, we conclude that carvedilol results in more favorable pulse pressure amplification and augmentation index by increasing arterial compliance and reducing the magnitude of wave reflection, respectively, compared with atenolol. J Clin Hypertens (Greenwich). 2011;13:917-924. Ó2011 Wiley Periodicals, Inc.For many years, b-blockers were advocated as first-line therapy for most patients with hypertension. This class flourished during the past 50 years as the mainstay for the prevention and treatment of various cardiovascular disorders such as cardiac arrhythmias, myocardial infarction, and hypertension. Recently, the role of bblockers in uncomplicated hypertension has been questioned. Indeed, several recently updated guidelines have deemphasized their place in therapy.2,3 The reasons for this evolution are multifactorial, including publication of several clinical trials and meta-analyses which concluded that b-blockers are less effective than contemporary antihypertensives. [4][5][6][7] These observations could be ascribed to multiple factors including the fact that b-blockers exhibit an adverse metabolic profile, are poorly tolerated relative to newer antihypertensives, and have mismatched mechanisms of action with the pathophysiology of hypertension in elderly hypertensive patients. [8][9][10][11] Multiple recent studies suggest that blood pressure (BP) characteristics beyond the brachial cuff, such as central aortic pressure, wave reflection, and arterial stiffness, independently predict cardiovascular events, including all-cause and cardiovascular mortality, fatal and nonfatal coronary events, and fatal strokes in uncomplicated essential hypertension.12-15 These characteristics cannot be appreciated with conventional clinic BP measurements at the brachial artery. Radial artery tonometry and synthesis of the central aortic pressure wavefor...

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Section: Discussionmentioning

confidence: 53%

Carvedilol Reduces Aortic Wave Reflection and Improves Left Ventricular/Vascular Coupling: A Comparison With Atenolol (CENTRAL Study)

Shah¹,

Smith

Nichols

et al. 2011

The Journal of Clinical Hypertension

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“…It is unlikely that hypertension will result in a much wider range since abnormal hemodynamic parameters in these hypertensive patients could be brought within normal ranges with small doses of vasodilators. 24 This small range for b implies that the pressure-volume relations of large arteries retain their basic exponential shape since the b coefficient relates primarily to the shape of the exponential pressure-volume rela- tion. Whether the same holds for smaller arteries and arterioles is, of course, not known.…”

Section: Resultsmentioning

confidence: 99%

“…The aortic impedance data for these subjects were described earlier. 24 The study was approved by a clinical research review committee and informed consent was obtained from each subject. Criteria for categorization into normotensive and hypertensive groups as well as details on the methodology for catheterization, data acquisition, and the experimental protocols can be found in this earlier publication.…”

Section: Methodsmentioning

confidence: 99%

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Aortic compliance in human hypertension.

et al. 1989

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Aortic compliance in normotensive and hypertensive Chinese subjects undergoing diagnostic cardiac catheterization was compared by using a newly described method that allows for determination of the pressure dependence of compliance if one assumes a value for the exponential coefficient of the pressure-volume relation of the large arteries. Under baseline conditions in the normotensive and hypertensive groups at mean aortic pressures of 963 and 128.6 mm Hg, aortic compliance averaged 1.47 and 0.80 ml/mm Hg, respectively. Compliance in the hypertensive group at a diastolic pressure of 99.4 mm Hg (which was nearly equal to the mean normotensive pressure) was 1.072 ml/mm Hg-still significantly lower than in the normotensive group. During nitroprusside infusion, however, the compliances in the hypertensive group increased to levels equal to or greater than those in the normotensive group. Thus, these data confirm that aortic compliance is lower in hypertensive than in normotensive humans. They further demonstrate that the lower compliance cannot be attributed entirely to the elevated blood pressure, suggesting that excess smooth muscle tone may be partly responsible. (Hypertension 1989;14:129-136) C ompliance is an important property of the arterial system. It is one measure of the properties of the walls of the vasculature, is a component of the load faced by the ventricle, and is a determinant of the configurations of the pressure and flow waves. Abnormalities in compliance can greatly affect cardiovascular function. For example, decreased compliance results in an increase in systolic and a decrease in diastolic aortic pressure-both of which are deleterious to the heart. The increased systolic pressure is an extra load during cardiac ejection and the decreased diastolic pressure can diminish coronary flow under certain conditions.There has been great interest in quantifying total arterial compliance.1 - 13 The accuracy of the values of compliance quoted in these studies is, however, questionable and has not been validated because it is extremely difficult to accurately measure the total arterial blood volume. In addition, compliance is a nonlinear function of pressure.

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“…35,36 Conversely, vasoconstriction is accompanied by the increase of resistive component of impedance without further noteworthy modification of modulus and phase components. 35,36 Aortic input impedance is a well established index of left ventricular afterload in both animals 37,38 and humans, 39,40 and it is used to assess ventricular-arterial coupling.…”

Section: Narrative Papermentioning

confidence: 99%

Ventricular–vascular coupling in hypertension

Saba

Cameli

Casalnuovo

et al. 2014

Journal of Cardiovascular Medicine

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The present review is addressed to analyse the complex interplay between left ventricle and arterial tree in hypertension. The different methodological approaches to the analysis of ventricular-vascular coupling in the time and frequency domain are discussed. Moreover, the role of hypertension-related changes of arterial structure and function (stiffness and wave reflection) on arterial load and how ventricular-vascular coupling modulates the process of left ventricular adaptation to hypertension are analysed.The different interplay between vascular bed and left ventricle emerges as the pathophysiological basis for the development of the multiple patterns of ventricular structural adaptation in hypertension and provides a pathway for the interpretation of systolic and diastolic functional abnormalities observed in hypertensive patients. Targeting the therapeutic approach to improve ventricularvascular coupling may have relevant impact on reversing left ventricular hypertrophy and improving systolic and diastolic dysfunction. J Cardiovasc Med 2014, 15:773-787

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Arterial hemodynamics in human hypertension.

Cited by 130 publications

References 37 publications

Carvedilol Reduces Aortic Wave Reflection and Improves Left Ventricular/Vascular Coupling: A Comparison With Atenolol (CENTRAL Study)

Carvedilol Reduces Aortic Wave Reflection and Improves Left Ventricular/Vascular Coupling: A Comparison With Atenolol (CENTRAL Study)

Aortic compliance in human hypertension.

Ventricular–vascular coupling in hypertension

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