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Clinical Hypertension (clinical + hypertension)
Selected AbstractsA Dramatic Addition to The Journal of Clinical HypertensionJOURNAL OF CLINICAL HYPERTENSION, Issue 9 2009Michael A. Weber MD No abstract is available for this article. [source] Ten Years and Counting: The Journal of Clinical HypertensionJOURNAL OF CLINICAL HYPERTENSION, Issue 5 2008Marvin Moser MD Editor in Chief First page of article [source] Should You Become a Specialist in Clinical Hypertension?JOURNAL OF CLINICAL HYPERTENSION, Issue 3 2007Article first published online: 20 MAR 200 No abstract is available for this article. [source] Blood Pressure Components in Clinical HypertensionJOURNAL OF CLINICAL HYPERTENSION, Issue 9 2006Michel E. Safar MD This review offers a critical evaluation of the remarkable progress in antihypertensive therapy since its inception. Despite the introduction of newer, more sophisticated drugs, treatment results have remained stable. Problems impeding further improvement include limited patient compliance, clinical inertia, incomplete adherence to guidelines, and dependence on brachial artery cuff pressures for diagnosis, risk assessment, and treatment response. Brachial artery systolic and pulse pressures do not reliably represent aortic or carotid artery pressures, which are better risk predictors for the heart and brain. Mean pressure, which is the same throughout the arterial tree, is directly measurable by cuff oscillometry, and might become the best single risk predictor. Available drugs have limited ability to decrease the aortic stiffness that is responsible for the elevated systolic blood pressure of aging. Therefore, to improve risk assessment and therapeutic benefit, we might include mean blood pressure and pulse pressure into blood pressure measurements, pursue efforts to measure central blood pressure, and search for new drugs to reduce arterial stiffness. [source] Plasma renin and the antihypertensive effect of the orally active renin inhibitor aliskiren in clinical hypertensionINTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 9 2007J. Nussberger Summary Background:, Aliskiren is the first in a new class of orally effective renin inhibitors for the treatment of hypertension. Methods:, In 569 patients with mild-to-moderate hypertension, blood pressure (BP), plasma renin activity (PRA) and plasma renin concentration (PRC) were measured before and after 8 weeks of double-blind treatment with once-daily oral doses of aliskiren (150, 300 or 600 mg), irbesartan 150 mg or placebo. Results:, Aliskiren 150, 300 and 600 mg and irbesartan 150 mg significantly reduced mean cuff sitting systolic BP (SBP) from baseline (p < 0.001 vs. placebo). Aliskiren 150, 300 and 600 mg significantly reduced geometric mean PRA by 69%, 71% and 75% from baseline respectively (p < 0.05 vs. placebo). Irbesartan 150 mg significantly increased PRA by 109% (p < 0.05 vs. placebo). Aliskiren dose-dependently increased PRC from baseline by 157%, 246% and 497%, at 150, 300 and 600 mg respectively, compared with a 9% decrease with placebo (p < 0.05). PRC increased significantly more with aliskiren 300 and 600 mg compared with irbesartan 150 mg (105%; p < 0.05). Regression analysis showed no significant correlations between baseline PRA and changes in SBP in any of the treatment groups, but interestingly, the slopes of the regression lines between changes in SBP and log-transformed baseline PRA were +2.0 for placebo and ,1.5, ,1.8 and ,2.3 for aliskiren 150, 300 and 600 mg respectively. The slope for irbesartan 150 mg (,1.4) was similar to that for aliskiren 150 mg. Conclusions:, Aliskiren reduces SBP and PRA and increases PRC dose-dependently. In contrast, irbesartan reduces SBP but increases both PRC and PRA. As PRA is a measurement of angiotensin I-generating capacity, PRA can be used for measuring the ability of an antihypertensive agent to prevent the generation or action of Ang II, either directly (renin inhibitors, beta-blockers, central ,2 -agonists) or indirectly (AT1 -receptor blockers, ACE inhibitors). [source] | ||||||||||