Circulation. 2013; 127: 322-330
Effect of Valsartan on Systemic Right Ventricular Function
A Double-Blind, Randomized, Placebo-Controlled Pilot Trial
Teun van der Bom, MD et al. Netherland.
Methods and Results—Multicenter, double-blind, parallel, randomized controlled trial of angiotensin II receptor blocker valsartan 160 mg twice daily compared with placebo in patients with a systemic right ventricle caused by congenitally or surgically corrected transposition of the great arteries.
The primary end point was change in right ventricular ejection fraction during 3-year follow-up, determined by MRI or CT. Secondary end points were change in right ventricular volumes and mass, peak, and quality of life. Primary analyses were performed on an intention-to-treat basis.
A total of 88 patients (valsartan, n=44; placebo, n=44) were enrolled in the trial. No serious adverse effects occurred in either group. There was no significant effect of 3-year valsartan therapy on systemic right ventricular ejection fraction (treatment effect, 1.3%; 95% confidence interval, −1.3% to 3.9%; P=0.34), maximum exercise capacity, or quality of life. There was a larger increase in right ventricular end-diastolic volume (15 mL; 95% confidence interval, 3–28 mL; P<0 .01="" 2="" 95="" and="" confidence="" g="" group.="" group="" in="" interval="" mass="" p="0.01)" placebo="" than="" the="" valsartan="">
Conclusions—There was no significant treatment effect of valsartan on right ventricular ejection fraction, exercise capacity, or quality of life. Small but significant differences between valsartan and placebo were present for change in right ventricular volumes and mass.
Wednesday, January 23, 2013
Saturday, December 15, 2012
IVC Development - Alexander Barry's hypothesis
Clin Anat. 2010 Apr;23(3):297-303. doi: 10.1002/ca.20930.
Fetal development of the retrohepatic inferior vena cava and accessory hepatic veins: Re-evaluation of the Alexander Barry's hypothesis.
Jin ZW, Cho BH, Murakami G, Fujimiya M, Kimura W, Yu HC.
Dept. of Surgery, Chonbuk National University Medical School, Jeonju, South Korea.
Abstract
The retrohepatic inferior vena cava (IVC) is commonly considered to originate from the right vitelline or omphalomesenteric vein. In contrast, Alexander Barry hypothesized that one of the hepatic veins grows to merge with the subcardinal vein and develops into the retrohepatic IVC. We re-examined fetal development of the retrohepatic IVC and other related veins using serial histological sections of 20 human fetuses between 6 and 16 weeks of gestation. At 6-7 weeks, when a basic configuration of the portal-hepatic vein systems had just been established, one of hepatic veins (i.e., the posterocaudal vein in the present study) had grown caudally to reach the posterocaudal surface of the liver, and notably, extended into the primitive right adrenal gland (five of the eight early-staged fetuses). Because the inferior right hepatic vein (IRHV) and retrohepatic IVC appeared at the same developmental stage, it is likely that any peripheral remnants of the posterocaudal vein would continue to function as primary drainage territory for the IRHV. The caudate vein developed rapidly in accordance with marked caudal and leftward extension of Spiegel's lobe at 12-16 weeks. Thin accessory hepatic veins developed later than the caudate vein and IRHV. The present results supported Barry's hypothesis.
Fetal development of the retrohepatic inferior vena cava and accessory hepatic veins: Re-evaluation of the Alexander Barry's hypothesis.
Jin ZW, Cho BH, Murakami G, Fujimiya M, Kimura W, Yu HC.
Dept. of Surgery, Chonbuk National University Medical School, Jeonju, South Korea.
Abstract
The retrohepatic inferior vena cava (IVC) is commonly considered to originate from the right vitelline or omphalomesenteric vein. In contrast, Alexander Barry hypothesized that one of the hepatic veins grows to merge with the subcardinal vein and develops into the retrohepatic IVC. We re-examined fetal development of the retrohepatic IVC and other related veins using serial histological sections of 20 human fetuses between 6 and 16 weeks of gestation. At 6-7 weeks, when a basic configuration of the portal-hepatic vein systems had just been established, one of hepatic veins (i.e., the posterocaudal vein in the present study) had grown caudally to reach the posterocaudal surface of the liver, and notably, extended into the primitive right adrenal gland (five of the eight early-staged fetuses). Because the inferior right hepatic vein (IRHV) and retrohepatic IVC appeared at the same developmental stage, it is likely that any peripheral remnants of the posterocaudal vein would continue to function as primary drainage territory for the IRHV. The caudate vein developed rapidly in accordance with marked caudal and leftward extension of Spiegel's lobe at 12-16 weeks. Thin accessory hepatic veins developed later than the caudate vein and IRHV. The present results supported Barry's hypothesis.
Tuesday, December 4, 2012
Angiotensin Receptor Blocker for Marfan Syndrome
NEJM 2008;358:2787-95
(Click on image to enlarge)
18 pediatric patients were treated (17 received Lorsartan, 1 received Ibesartan).
Age range:1 -16 yrs (median age 6.5 yrs)
Duration of study: Median 6 yrs (~4 yrs before starting ARB & ~ 2 yrs after starting ARB)
Dose:
Losartan - started at 0.6 mg/kg/day x 3 wks. Then, gradually increased to 1.4 mg/kg/day.
Ibesartan - started at 1.4 mg/kg/day. Then, gradually increased to 2.0 mg/kg/day.
Check BUN, Creatinine, Electrolytes after 3 months.
Monday, November 19, 2012
Wednesday, November 7, 2012
Ultrafiltration vs. Diuretics for Cardiorenal Syndrome
Ultrafiltration in Decompensated Heart Failure with Cardiorenal Syndrome
Bradley Bart et al. NEJM Online (Nov 7, 2012)
Editorial on this article NEJM Online (Nov 7, 2012)
Background
Ultrafiltration is an alternative strategy to diuretic therapy for the treatment of patients with acute decompensated heart failure. Little is known about the efficacy and safety of ultrafiltration in patients with acute decompensated heart failure complicated by persistent congestion and worsened renal function.
Methods
We randomly assigned a total of 188 patients with acute decompensated heart failure, worsened renal function, and persistent congestion to a strategy of stepped pharmacologic therapy (94 patients) or ultrafiltration (94 patients). The primary end point was the bivariate change from baseline in the serum creatinine level and body weight, as assessed 96 hours after random assignment. Patients were followed for 60 days.
Results
Ultrafiltration was inferior to pharmacologic therapy with respect to the bivariate end point of the change in the serum creatinine level and body weight 96 hours after enrollment (P=0.003), owing primarily to an increase in the creatinine level in the ultrafiltration group. At 96 hours, the mean change in the creatinine level was −0.04±0.53 mg per deciliter (−3.5±46.9 μmol per liter) in the pharmacologic-therapy group, as compared with +0.23±0.70 mg per deciliter (20.3±61.9 μmol per liter) in the ultrafiltration group (P=0.003). There was no significant difference in weight loss 96 hours after enrollment between patients in the pharmacologic-therapy group and those in the ultrafiltration group (a loss of 5.5±5.1 kg [12.1±11.3 lb] and 5.7±3.9 kg [12.6±8.5 lb], respectively; P=0.58). A higher percentage of patients in the ultrafiltration group than in the pharmacologic-therapy group had a serious adverse event (72% vs. 57%, P=0.03).
Conclusions
In a randomized trial involving patients hospitalized for acute decompensated heart failure, worsened renal function, and persistent congestion, the use of a stepped pharmacologic-therapy algorithm was superior to a strategy of ultrafiltration for the preservation of renal function at 96 hours, with a similar amount of weight loss with the two approaches. Ultrafiltration was associated with a higher rate of adverse events. (Funded by the National Heart, Lung, and Blood Institute; ClinicalTrials.gov number, NCT00608491.)
Bradley Bart et al. NEJM Online (Nov 7, 2012)
Editorial on this article NEJM Online (Nov 7, 2012)
Background
Ultrafiltration is an alternative strategy to diuretic therapy for the treatment of patients with acute decompensated heart failure. Little is known about the efficacy and safety of ultrafiltration in patients with acute decompensated heart failure complicated by persistent congestion and worsened renal function.
Methods
We randomly assigned a total of 188 patients with acute decompensated heart failure, worsened renal function, and persistent congestion to a strategy of stepped pharmacologic therapy (94 patients) or ultrafiltration (94 patients). The primary end point was the bivariate change from baseline in the serum creatinine level and body weight, as assessed 96 hours after random assignment. Patients were followed for 60 days.
Results
Ultrafiltration was inferior to pharmacologic therapy with respect to the bivariate end point of the change in the serum creatinine level and body weight 96 hours after enrollment (P=0.003), owing primarily to an increase in the creatinine level in the ultrafiltration group. At 96 hours, the mean change in the creatinine level was −0.04±0.53 mg per deciliter (−3.5±46.9 μmol per liter) in the pharmacologic-therapy group, as compared with +0.23±0.70 mg per deciliter (20.3±61.9 μmol per liter) in the ultrafiltration group (P=0.003). There was no significant difference in weight loss 96 hours after enrollment between patients in the pharmacologic-therapy group and those in the ultrafiltration group (a loss of 5.5±5.1 kg [12.1±11.3 lb] and 5.7±3.9 kg [12.6±8.5 lb], respectively; P=0.58). A higher percentage of patients in the ultrafiltration group than in the pharmacologic-therapy group had a serious adverse event (72% vs. 57%, P=0.03).
Conclusions
In a randomized trial involving patients hospitalized for acute decompensated heart failure, worsened renal function, and persistent congestion, the use of a stepped pharmacologic-therapy algorithm was superior to a strategy of ultrafiltration for the preservation of renal function at 96 hours, with a similar amount of weight loss with the two approaches. Ultrafiltration was associated with a higher rate of adverse events. (Funded by the National Heart, Lung, and Blood Institute; ClinicalTrials.gov number, NCT00608491.)
Tuesday, November 6, 2012
Obesity: Role of Government & Policy
Circulation 2012;126:2345
Obesity : Role of Policy and Government in the Obesity Epidemic
Nicole L. Novak, MSc; Kelly D. Brownell, PhD
From the Rudd Center for Food Policy and Obesity, Department of Psychology, Department of Epidemiology and Public Health, Yale University, New Haven, CT.
Correspondence to Nicole L. Novak, Rudd Center for Food Policy and Obesity, 309 Edwards St, New Haven, CT 06511. E-mail nicole.l.novak@gmail.com.
In 2001, the Surgeon General's “Call to Action to Prevent and Decrease Overweight and Obesity”1 identified obesity as a key public health priority for the United States. Obesity rates were higher than ever, with 61% of adults nationwide overweight or obese. In the intervening years, several administrations have declared a commitment to deal with the problem, and the food industry has issued numerous pledges for change, yet the prevalence of overweight and obesity has risen further, to 68%.2 Children have been particularly affected; >19% of school-aged children were obese in 2007 to 2008 compared with just 6% in the late 1970s.3 Disease rates join high healthcare costs, so everyone is affected personally, economically, or both.4,5
A wide range of government policies and programs have been implemented, including the development of national clinical guidelines, nutrition labeling on packaged foods, education and social marketing efforts, and more recently, calorie labeling on restaurant menus and federal efforts to increase access and financing for fresh fruits and vegetables. However, most of these efforts focus on clinical and educational factors or on community interventions and, until recently, have rarely addressed environmental drivers of obesity. There is growing theoretical and scientific support for policies that intervene on environmental determinants of overeating. The implementation of some policies is facing resistance from the food and beverage industries.
Obesity : Role of Policy and Government in the Obesity Epidemic
Nicole L. Novak, MSc; Kelly D. Brownell, PhD
From the Rudd Center for Food Policy and Obesity, Department of Psychology, Department of Epidemiology and Public Health, Yale University, New Haven, CT.
(Click on image to enlarge)
Correspondence to Nicole L. Novak, Rudd Center for Food Policy and Obesity, 309 Edwards St, New Haven, CT 06511. E-mail nicole.l.novak@gmail.com.
In 2001, the Surgeon General's “Call to Action to Prevent and Decrease Overweight and Obesity”1 identified obesity as a key public health priority for the United States. Obesity rates were higher than ever, with 61% of adults nationwide overweight or obese. In the intervening years, several administrations have declared a commitment to deal with the problem, and the food industry has issued numerous pledges for change, yet the prevalence of overweight and obesity has risen further, to 68%.2 Children have been particularly affected; >19% of school-aged children were obese in 2007 to 2008 compared with just 6% in the late 1970s.3 Disease rates join high healthcare costs, so everyone is affected personally, economically, or both.4,5
A wide range of government policies and programs have been implemented, including the development of national clinical guidelines, nutrition labeling on packaged foods, education and social marketing efforts, and more recently, calorie labeling on restaurant menus and federal efforts to increase access and financing for fresh fruits and vegetables. However, most of these efforts focus on clinical and educational factors or on community interventions and, until recently, have rarely addressed environmental drivers of obesity. There is growing theoretical and scientific support for policies that intervene on environmental determinants of overeating. The implementation of some policies is facing resistance from the food and beverage industries.
Saturday, October 20, 2012
SVT prophylaxis in infants: Digoxin vs. Propranolol
Circ Arrhythm Electrophysiol. 2012 Oct 1;5(5):984-91. doi: 10.1161/CIRCEP.112.972620. Epub 2012 Sep 8.
The Study of Antiarrhythmic Medications in Infancy (SAMIS): A Multicenter, Randomized Controlled Trial Comparing the Efficacy and Safety of Digoxin Versus Propranolol for Prophylaxis of Supraventricular Tachycardia in Infants.
Sanatani S, Potts JE, Reed JH, Saul JP, Stephenson EA, Gibbs KA, Anderson CC, Mackie AS, Ro PS, Tisma-Dupanovic S, Kanter RJ, Batra AS, Fournier A, Blaufox AD, Singh HR, Ross BA, Wong KK, Bar-Cohen Y, McCrindle BW, Etheridge SP.
Background- Supraventricular tachycardia (SVT) is one of the most common conditions requiring emergent cardiac care in children, yet its management has never been subjected to a randomized controlled clinical trial. The purpose of this study was to compare the efficacy and safety of the 2 most commonly used medications for antiarrhythmic prophylaxis of SVT in infants: digoxin and propranolol.
Methods and Results- A randomized, double-blind, multicenter study of infants <4 atrioventricular="atrioventricular" comparing="comparing" digoxin="digoxin" excluding="excluding" months="months" nodal="nodal" or="or" propranolol.="propranolol." reciprocating="reciprocating" reentrant="reentrant" svt="svt" tachycardia="tachycardia" with="with" wolff-parkinson-white="wolff-parkinson-white">The primary end point was recurrence of SVT requiring medical intervention.
Time to recurrence and adverse events were secondary outcomes.
Sixty-one patients completed the study, 27 randomized to digoxin and 34 to propranolol.
SVT recurred in 19% of patients on digoxin and 31% of patients on propranolol (P=0.25).
No first recurrence occurred after 110 days of treatment.
The 6-month recurrence-free status was 79% for patients on digoxin and 67% for patients on propranolol (P=0.34), and there were no first recurrences in either group between 6 and 12 months. There were no deaths and no serious adverse events related to study medication.
Conclusions- There was no difference in SVT recurrence in infants treated with digoxin versus propranolol. The current standard practice may be treating infants longer than required and indicates the need for a placebo-controlled trial.
Clinical Trial Registration Information- http://clinicaltrials.gov; NCT-00390546.
The Study of Antiarrhythmic Medications in Infancy (SAMIS): A Multicenter, Randomized Controlled Trial Comparing the Efficacy and Safety of Digoxin Versus Propranolol for Prophylaxis of Supraventricular Tachycardia in Infants.
Sanatani S, Potts JE, Reed JH, Saul JP, Stephenson EA, Gibbs KA, Anderson CC, Mackie AS, Ro PS, Tisma-Dupanovic S, Kanter RJ, Batra AS, Fournier A, Blaufox AD, Singh HR, Ross BA, Wong KK, Bar-Cohen Y, McCrindle BW, Etheridge SP.
Background- Supraventricular tachycardia (SVT) is one of the most common conditions requiring emergent cardiac care in children, yet its management has never been subjected to a randomized controlled clinical trial. The purpose of this study was to compare the efficacy and safety of the 2 most commonly used medications for antiarrhythmic prophylaxis of SVT in infants: digoxin and propranolol.
Methods and Results- A randomized, double-blind, multicenter study of infants <4 atrioventricular="atrioventricular" comparing="comparing" digoxin="digoxin" excluding="excluding" months="months" nodal="nodal" or="or" propranolol.="propranolol." reciprocating="reciprocating" reentrant="reentrant" svt="svt" tachycardia="tachycardia" with="with" wolff-parkinson-white="wolff-parkinson-white">The primary end point was recurrence of SVT requiring medical intervention.
Time to recurrence and adverse events were secondary outcomes.
Sixty-one patients completed the study, 27 randomized to digoxin and 34 to propranolol.
SVT recurred in 19% of patients on digoxin and 31% of patients on propranolol (P=0.25).
No first recurrence occurred after 110 days of treatment.
The 6-month recurrence-free status was 79% for patients on digoxin and 67% for patients on propranolol (P=0.34), and there were no first recurrences in either group between 6 and 12 months. There were no deaths and no serious adverse events related to study medication.
Conclusions- There was no difference in SVT recurrence in infants treated with digoxin versus propranolol. The current standard practice may be treating infants longer than required and indicates the need for a placebo-controlled trial.
Clinical Trial Registration Information- http://clinicaltrials.gov; NCT-00390546.
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