Guest guest Posted January 24, 2008 Report Share Posted January 24, 2008 Would Diovan be a good treatment for PA? http://www.circ.ahajournals.org/cgi/content/abstract/108/11/1306 (Circulation. 2003;108:1306.) © 2003 American Heart Association, Inc. Clinical Investigation and Reports Sustained Reduction of Aldosterone in Response to the Angiotensin Receptor Blocker Valsartan in Patients With Chronic Heart Failure Results From the Valsartan Heart Failure Trial Jay N. Cohn, MD; Inder S. Anand, MD; o Latini, MD; Serge Masson, PhD; Yann-Tong Chiang, PhD; Glazer, MD, for the Valsartan Heart Failure Trial Investigators From the Cardiovascular Division (J.N.C.), Department of Medicine, University of Minnesota Medical School, Minneapolis, Minn; VA Medical Center (I.S.A.), Minneapolis, Minn; Istituto " Negri " (R.L., S.M.), Milan, Italy; and Novartis Pharmaceuticals Corporation (Y.-T.C., R.G.), East Hanover, NJ. Correspondence to Jay N. Cohn, MD, Cardiovascular Division, Mayo Mail Code 508, University of Minnesota Medical School, 420 Delaware St SE, Minneapolis, MN 55455. E-mail <mailto:cohnx001@...> cohnx001@... Received May 29, 2003; de novo received July 8, 2003; accepted July 28, 2003. Background— Aldosterone has been implicated in the progression of heart failure. The Valsartan Heart Failure Trial (Val-HeFT) provided the first opportunity to examine the long-term effects of an angiotensin receptor blocker on plasma aldosterone levels in patients with NYHA class II through IV heart failure. Methods and Results— Plasma aldosterone was measured by radioimmunoassay in core laboratories at baseline and during follow-up in patients assigned to valsartan at a target dose of 160 mg twice daily or placebo. In the placebo group, aldosterone (baseline, 150±160 pg/mL, mean±SD; n=2025) increased at 4, 12, and 24 months. In the valsartan group, aldosterone (baseline, 137±124 pg/mL, mean±SD; n=2023) decreased at 4 months and remained suppressed for up to 2 years. At end point (last measurement in each patient), mean aldosterone increased by 17.8±3.0 pg/mL (SEM) (11.9%) in the placebo group and decreased by 23.8±3.0 pg/mL (SEM) (-17.4%) in the valsartan group (P<0.00001). The effect of valsartan was similar in all subgroups, including those receiving neither ACE inhibitors (ACE-I) nor ß-blockers (BB) at baseline and those receiving concomitant ACE-I or BB. In contrast, outcome effects varied in the 4 subgroups, with a statistically significant reduction in the combined mortality/morbidity end point in those receiving neither neurohormonal inhibitor and an adverse trend in those treated with both drugs. Conclusions— Valsartan added to background therapy for heart failure produces sustained reduction in plasma aldosterone, consistent with the observed significant reduction in the combined mortality/morbidity end point. A similar reduction in all subgroups based on ACE-I or BB therapy, despite differing clinical outcomes in these subgroups, suggests that aldosterone plasma levels may not be a critical marker of the progression of heart failure. Val Quote Link to comment Share on other sites More sharing options...
Guest guest Posted January 24, 2008 Report Share Posted January 24, 2008 No it should be worthless as there is not renin to block. Duh!!! CE Grim MS, MD High Blood Pressure Consulting Clnical Professor of Medicine Medical Colege of Wisconsin Board certified in Internal Med, Geritrics and Hypertension. Interests: The effect of recent evolutionary forces on high blood pressure in human populations. On Jan 24, 2008, at 4:25 PM, Valarie wrote: > Would Diovan be a good treatment for PA? > > http://www.circ.ahajournals.org/cgi/content/abstract/108/11/1306 > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > (Circulation. 2003;108:1306.) > © 2003 American Heart Association, Inc. > Clinical Investigation and Reports > Sustained Reduction of Aldosterone in Response to the Angiotensin > Receptor > Blocker Valsartan in Patients With Chronic Heart Failure > Results From the Valsartan Heart Failure Trial > Jay N. Cohn, MD; Inder S. Anand, MD; o Latini, MD; Serge > Masson, PhD; > Yann-Tong Chiang, PhD; Glazer, MD, for the Valsartan Heart > Failure > Trial Investigators > From the Cardiovascular Division (J.N.C.), Department of Medicine, > University of Minnesota Medical School, Minneapolis, Minn; VA > Medical Center > (I.S.A.), Minneapolis, Minn; Istituto " Negri " (R.L., S.M.), > Milan, > Italy; and Novartis Pharmaceuticals Corporation (Y.-T.C., R.G.), East > Hanover, NJ. > Correspondence to Jay N. Cohn, MD, Cardiovascular Division, Mayo > Mail Code > 508, University of Minnesota Medical School, 420 Delaware St SE, > Minneapolis, MN 55455. E-mail <mailto:cohnx001@...> > cohnx001@... > Received May 29, 2003; de novo received July 8, 2003; accepted July > 28, > 2003. > Background— Aldosterone has been implicated in the progression of > heart > failure. The Valsartan Heart Failure Trial (Val-HeFT) provided the > first > opportunity to examine the long-term effects of an angiotensin > receptor > blocker on plasma aldosterone levels in patients with NYHA class II > through > IV heart failure. > Methods and Results— Plasma aldosterone was measured by > radioimmunoassay in > core laboratories at baseline and during follow-up in patients > assigned to > valsartan at a target dose of 160 mg twice daily or placebo. In the > placebo > group, aldosterone (baseline, 150±160 pg/mL, mean±SD; n=2025) > increased at > 4, 12, and 24 months. In the valsartan group, aldosterone > (baseline, 137±124 > pg/mL, mean±SD; n=2023) decreased at 4 months and remained > suppressed for up > to 2 years. At end point (last measurement in each patient), mean > aldosterone increased by 17.8±3.0 pg/mL (SEM) (11.9%) in the > placebo group > and decreased by 23.8±3.0 pg/mL (SEM) (-17.4%) in the valsartan group > (P<0.00001). The effect of valsartan was similar in all subgroups, > including > those receiving neither ACE inhibitors (ACE-I) nor ß-blockers (BB) at > baseline and those receiving concomitant ACE-I or BB. In contrast, > outcome > effects varied in the 4 subgroups, with a statistically significant > reduction in the combined mortality/morbidity end point in those > receiving > neither neurohormonal inhibitor and an adverse trend in those > treated with > both drugs. > Conclusions— Valsartan added to background therapy for heart failure > produces sustained reduction in plasma aldosterone, consistent with > the > observed significant reduction in the combined mortality/morbidity end > point. A similar reduction in all subgroups based on ACE-I or BB > therapy, > despite differing clinical outcomes in these subgroups, suggests that > aldosterone plasma levels may not be a critical marker of the > progression of > heart failure. > Val > > Quote Link to comment Share on other sites More sharing options...
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