W H Wilson Tang

Lerner Research Institute, Cleveland, Ohio, United States

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Publications (503)3337.89 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Race has seldomly been reported in the major clinical trials of cardiac resynchronization therapy (CRT). When described, African Americans (AAs) were substantially under-represented. This study sought to compare reverse ventricular remodeling and long-term outcomes in AAs versus European Americans (EAs) with advanced heart failure who underwent CRT. We extracted demographic (including race), clinical, and echocardiographic data on patients with advanced heart failure who underwent CRT with a left ventricular ejection fraction (LVEF) ≤35% and a QRS duration ≥120 ms. Long-term outcomes were compared between AAs and EAs. In patients in whom follow-up echocardiograms were available, improvement in LVEF (defined as an absolute improvement ≥5%) was compared between races. From a cohort of 662 patients, there were 88 AAs and 574 EAs. At a mean follow-up of 5.0 ± 2.5 years, survival rate free of left ventricular assist device (LVAD) and heart transplant was 54.5% for AAs and 53.8% for EAs (log-rank p = 0.997). In multivariate analysis, there was no difference in survival free of heart transplant or LVAD based on race (hazard ratio 1.1 [0.74 to 1.56], p = 0.72, EAs race as referent); 424 patients had a follow-up echocardiogram (55.4% EAs and 64.7% AAs). In multivariate analysis, there was no difference in the incidence of response based on race (1.1 [0.6 to 2.1, p = 0.80], EAs as referent). AAs derive similar benefits with CRT compared with EAs in terms of improvement in LVEF and long-term survival free of LVAD and heart transplant.
    The American journal of cardiology 09/2015; 116(7):1101-5. DOI:10.1016/j.amjcard.2015.07.016 · 3.28 Impact Factor
  • Daniel Li · Jennifer Kirsop · W H Wilson Tang
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    ABSTRACT: What we understand about diabetes from decades of genetics research is now being supplemented with exciting new evidence based on a better understanding of how one of the biggest "environmental" factors the body is exposed to is influencing the pathogenesis of disease. The recent discovery that certain dietary nutrients possessing a trimethylamine (TMA) moiety (namely choline/phosphatidylcholine and L-carnitine) participate in the development of atherosclerotic heart disease has renewed attention towards the contributions of gut microbiota in the development of cardiovascular diseases. Collectively, animal and human studies reveal that conversion of these nutrient precursors to trimethylamine N-oxide (TMAO) depends on both microbial composition and host factors, and can be induced by dietary exposures. In addition, circulating TMAO levels are strongly linked to cardiovascular disease risks and various adverse cardio-renal consequences. Our group and others have further demonstrated that circulating TMAO levels are elevated in patients with type 2 diabetes mellitus compared to healthy controls and gut microbiota-dependent phosphatidylcholine metabolism has been implicated in metabolic dysregulation and insulin resistance in animal models. Therefore, preventive strategies to minimize adverse consequences associated with TMAO generation in the diabetic population are warranted.
    Current Diabetes Reports 09/2015; 15(9):634. DOI:10.1007/s11892-015-0634-1 · 3.08 Impact Factor
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    ABSTRACT: Background: Worsening renal function in heart failure may be related to increased venous congestion, decreased cardiac output, or both. Diuretics are universally used in acute decompensated heart failure, but they may be ineffective and may lead to azotemia. We aimed to compare the decongestive properties of a urine output-guided diuretic adjustment and standard therapy for the management of cardiorenal syndrome in acute decompensated heart failure. Methods and results: Data were pooled from subjects randomized to the stepwise pharmacologic care algorithm (SPCA) in the CARRESS-HF trial and those who developed cardiorenal syndrome (rise in creatinine >0.3 mg/dL) in the DOSE-AHF and ROSE-AHF trials. Patients treated with SPCA (n = 94) were compared with patients treated with standard decongestive therapy (SDT) that included intravenous loop diuretic use (DOSE-AHF and ROSE-AHF; n = 107) at the time of cardiorenal syndrome and followed for net fluid balance, weight loss, and changing renal function. The SPCA group had higher degrees of jugular venous pressure (P < .0001) at the time of cardiorenal syndrome. The group that received SPCA had more weight change (-3.4 ± 5.2 lb) and more net fluid loss (1.705 ± 1.417 L) after 24 hours than the SDT group (-0.8 ± 3.4 lb and 0.892 ± 1.395 L, respectively; P < .001 for both) with a slight improvement in renal function (creatinine change -0.1 ± 0.3 vs 0.0 ± 0.3 mg/dL, respectively; P = .03). Conclusions: Compared with SDT, patients who received an intensification of medication therapy for treating persisting congestion had greater net fluid and weight loss without being associated with renal compromise.
    Journal of cardiac failure 08/2015; DOI:10.1016/j.cardfail.2015.07.007 · 3.05 Impact Factor
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    ABSTRACT: Acute decompensated heart failure (ADHF) can be complicated by electrolyte abnormalities, but the major focus has been concentrated on the clinical significance of serum sodium levels. This study sought to determine the prognostic significance of serum chloride levels in relation to serum sodium levels in patients with ADHF. We reviewed 1,318 consecutive patients with chronic heart failure admitted for ADHF to the Cleveland Clinic between July 2008 and December 2013. We also validated our findings in an independent ADHF cohort from the University of Pennsylvania (n = 876). Admission serum chloride levels during hospitalization for ADHF were independently and inversely associated with long-term mortality (hazard ratio [HR] per unit change: 0.94; 95% confidence interval [CI]: 0.92 to 0.95; p < 0.001). After multivariable risk adjustment, admission chloride levels remained independently associated with mortality (HR per unit change: 0.93; 95% CI: 0.90 to 0.97; p < 0.001) in contrast to admission sodium levels, which were no longer significant (p > 0.05). Results were similar in the validation cohort in unadjusted (HR per unit change for mortality risk within 1 year: 0.93; 95% CI: 0.91 to 0.95; p < 0.001) and multivariable risk-adjusted analysis (HR per unit change for mortality risk within 1 year: 0.95; 95% CI: 0.92 to 0.99; p = 0.01). These observations in a contemporary advanced ADHF cohort suggest that serum chloride levels at admission are independently and inversely associated with mortality. The prognostic value of serum sodium in ADHF was diminished compared with chloride. Copyright © 2015 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
    Journal of the American College of Cardiology 08/2015; 66(6):659-66. DOI:10.1016/j.jacc.2015.06.007 · 16.50 Impact Factor
  • W H Wilson Tang
    Journal of the American Society of Nephrology 07/2015; DOI:10.1681/ASN.2015050576 · 9.34 Impact Factor
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    ABSTRACT: The aim of this study was to assess the haemodynamic response and tolerance to aggressive oral hydralazine/isosorbide dinitrate (HYD/ISDN) up-titration after intravenous vasodilator therapy in advanced decompensated heart failure (ADHF). Medical records of 147 consecutive ADHF patients who underwent placement of a pulmonary artery catheter and received intravenous vasodilator therapy were reviewed. Intravenous sodium nitroprusside and sodium nitroglycerin as first-line agent for those with preserved blood pressures were utilized in 143 and 32 patients, respectively. Sixty-one percent of patients were converted to oral HYD/ISDN combination therapy through a standardized conversion protocol. These patients had a significantly higher admission mean pulmonary arterial wedge pressure compared with patients not converted (28 ± 7 vs. 25 ± 8 mmHg, respectively; P-value 0.024). Beneficial haemodynamic response to decongestive therapy, defined as low cardiac filling pressures and cardiac index ≥2.20 L/min/m(2) without emergent hypotension, was achieved in 32% and 29% of patients who did or did not receive oral HYD/ISDN, respectively (P-value 0.762). HYD/ISDN dosing was progressively and consistently decreased up to the moment of hospital discharge and during outpatient follow-up, primarily due to incident hypotension. The use of a standardized haemodynamically guided up-titration protocol for conversion from intravenous to oral vasodilators may warrant subsequent dose reductions upon stabilization. © 2015 The Authors European Journal of Heart Failure © 2015 European Society of Cardiology.
    European Journal of Heart Failure 07/2015; DOI:10.1002/ejhf.324 · 6.53 Impact Factor
  • W H Wilson Tang · Stanley L Hazen
    Journal of the American College of Cardiology 07/2015; 66(1):96-7. DOI:10.1016/j.jacc.2014.12.080 · 16.50 Impact Factor
  • Stuart M Zeltzer · David O Taylor · W H Wilson Tang
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    ABSTRACT: Diet and nutrition are moving to the forefront of modern primary and preventive care to help address the rising burden of chronic diseases among the general population. Such a movement has yet to occur formally across the field of transplantation. We therefore looked to establish the current base of knowledge regarding diet, nutrition and solid-organ transplantation. A limited number of focused studies looking into the dietary habits of solid-organ transplant patients have been performed and many of the available studies have detailed the nutritional status in the peri-operative period. Frequently described, however, is the heavy incidence of metabolic abnormalities, such as obesity, dyslipidemia and diabetes, occurring after solid-organ transplantation. Optimistically, several studies have noted improvement in several metabolic abnormalities with the use of dietary interventions in the post-transplant period. Despite these positive results, few consensus guidelines for post-transplant diet have been established and nutritional support among transplant programs remains limited. Although there are many hurdles to implementation of detailed dietary recommendations and nutritional support for transplant patients, creating such programs and guidelines could dramatically impact long-term outcomes and burden of chronic metabolic disease for transplant recipients. Copyright © 2015 International Society for Heart and Lung Transplantation. Published by Elsevier Inc. All rights reserved.
    The Journal of heart and lung transplantation: the official publication of the International Society for Heart Transplantation 07/2015; DOI:10.1016/j.healun.2015.06.014 · 6.65 Impact Factor
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    ABSTRACT: RNA sequencing (RNA-Seq) allows an unbiased survey of the entire transcriptome in a high-throughput manner. A major application of RNA-Seq is to detect differential isoform expression across experimental conditions, which is of great biological interest due to its direct relevance to protein function and disease pathogenesis. Detection of differential isoform expression is challenging because of uncertainty in isoform expression estimation owing to ambiguous reads and variability in precision of the estimates across samples. It is desirable to have a method that can account for these issues and is flexible enough to allow adjustment for covariates. In this paper, we present MetaDiff, a random-effects meta-regression model that naturally fits for the above purposes. Through extensive simulations and analysis of an RNA-Seq dataset on human heart failure, we show that the random-effects meta-regression approach is computationally fast, reliable, and can improve the power of differential expression analysis while controlling for false positives due to the effect of covariates or confounding variables. In contrast, several existing methods either fail to control false discovery rate or have reduced power in the presence of covariates or confounding variables. The source code, compiled JAR package and documentation of MetaDiff are freely available at https://github.com/jiach/MetaDiff. Our results indicate that random-effects meta-regression offers a flexible framework for differential expression analysis of isoforms, particularly when gene expression is influenced by other variables.
    BMC Bioinformatics 07/2015; 16(1):208. DOI:10.1186/s12859-015-0623-z · 2.58 Impact Factor
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    Frederik H Verbrugge · W H Wilson Tang · Stanley L Hazen
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    ABSTRACT: Carbamylation constitutes a posttranslational modification of proteins or amino acids and results from different pathways in vivo. First is the non-enzymatic reaction between isocyanic acid, a decomposition product of urea, and either the N-terminus or the ɛ-amino group of lysine residues. Isocyanic acid levels, while low in vivo, are in equilibrium with urea and are thus increased in chronic and end-stage renal diseases. An alternative pathway involves the leukocyte heme protein myeloperoxidase, which catalyzes the oxidation of thiocyanate in the presence of hydrogen peroxide, producing isocyanate at inflammation sites. Notably, plasma thiocyanate levels are increased in smokers, and leukocyte-driven protein carbamylation occurs both within human and animal atherosclerotic plaques, as well as on plasma proteins. Protein carbamylation is considered a hallmark of molecular aging and is implicated in many pathological conditions. Recently, it has been shown that carbamylated low-density lipoprotein (LDL) induces endothelial dysfunction via lectin-like-oxidized LDL receptor-1 activation and increased reactive oxygen species production, leading to endothelial nitric oxide synthase uncoupling. Moreover, carbamylated LDL harbors atherogenic activities, including both binding to macrophage scavenger receptors inducing cholesterol accumulation and foam-cell formation, as well as promoting vascular smooth muscle proliferation. In contrast, high-density lipoprotein loses its anti-apoptotic activity after carbamylation, contributing to endothelial cell death. In addition to involvement in atherogenesis, protein carbamylation levels have emerged as a particularly strong predictor of both prevalent and incident cardiovascular disease risk. Recent studies also suggest that protein carbamylation may serve as a potential therapeutic target for the prevention of atherosclerotic heart disease.Kidney International advance online publication, 10 June 2015; doi:10.1038/ki.2015.166.
    Kidney International 06/2015; 88(3). DOI:10.1038/ki.2015.166 · 8.56 Impact Factor
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    ABSTRACT: The objective of this study was to investigate determinants of the natriuretic response to diuretics in decompensated heart failure (HF) and the relationship with decongestion, neurohumoral activation and clinical outcome in the contemporary era of HF management. In this prospective, single-centre cohort study, consecutive patients with decompensated HF (n = 54) and left ventricular ejection fraction 45% received protocol-driven diuretic therapy until complete disappearance of congestion signs. Urine was collected during three consecutive 24-h intervals. Natriuretic response was defined as absolute natriuresis (mmol) per mg of intravenous bumetanide administered. Natriuresis was 146 mmol (76-206 mmol), 74 mmol (37-167 mmol) and 74 mmol (53-134 mmol) per mg intravenous bumetanide administered during the first, second and third 24-h interval, respectively. Diastolic blood pressure (beta = 23.048 +/- 10.788; P-value = 0.036), plasma aldosterone (beta = -25.722?11.560; P-value=0.029), and combination therapy with acetazolamide (beta = 103.241 +/- 40.962; P-value = 0.014) were independent predictors of the natriuretic response. Patients with a stronger natriuretic response demonstrated more pronounced decreases in plasma NT-proBNP levels (P-value = 0.025), while a weaker response was associated with higher peak plasma aldosterone levels (P-value = 0.013) and plasma renin activity (P-value = 0.033). Natriuresis per loop diuretic dose predicted freedom from all-cause mortality or HF readmissions, independently of baseline renal function (HR 0.40, 95% CI 0.16-0.98; P-value = 0.045). More effective natriuresis in decompensated HF patients with reduced ejection fraction and volume overload is associated with better decongestion, less neurohumoral activation and predicts favourable clinical outcome independently from renal function per se. Acetazolamide warrants further evaluation in large prospective trials to increase the natriuretic response to loop diuretics.
    Acta cardiologica 06/2015; 70(3):265-73. DOI:10.2143/AC.70.3.3080630 · 0.65 Impact Factor
  • W.H. Wilson Tang · Justin L. Grodin
    JACC: Heart Failure 05/2015; 3(5). DOI:10.1016/j.jchf.2015.02.003
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    ABSTRACT: Oxidative stress may contribute to heart failure (HF) progression. Inhibiting xanthine oxidase in hyperuricemic HF patients may improve outcomes. We randomly assigned 253 patients with symptomatic HF, left ventricular ejection fraction ≤40%, and serum uric acid levels ≥9.5 mg/dL to receive allopurinol (target dose, 600 mg daily) or placebo in a double-blind, multicenter trial. The primary composite end point at 24 weeks was based on survival, worsening HF, and patient global assessment. Secondary end points included change in quality of life, submaximal exercise capacity, and left ventricular ejection fraction. Uric acid levels were significantly reduced with allopurinol in comparison with placebo (treatment difference, -4.2 [-4.9, -3.5] mg/dL and -3.5 [-4.2, -2.7] mg/dL at 12 and 24 weeks, respectively, both P<0.0001). At 24 weeks, there was no significant difference in clinical status between the allopurinol- and placebo-treated patients (worsened 45% versus 46%, unchanged 42% versus 34%, improved 13% versus 19%, respectively; P=0.68). At 12 and 24 weeks, there was no significant difference in change in Kansas City Cardiomyopathy Questionnaire scores or 6-minute walk distances between the 2 groups. At 24 weeks, left ventricular ejection fraction did not change in either group or between groups. Rash occurred more frequently with allopurinol (10% versus 2%, P=0.01), but there was no difference in serious adverse event rates between the groups (20% versus 15%, P=0.36). In high-risk HF patients with reduced ejection fraction and elevated uric acid levels, xanthine oxidase inhibition with allopurinol failed to improve clinical status, exercise capacity, quality of life, or left ventricular ejection fraction at 24 weeks. URL: http://www.clinicaltrials.gov. Unique identifier: NCT00987415. © 2015 American Heart Association, Inc.
    Circulation 05/2015; 131(20). DOI:10.1161/CIRCULATIONAHA.114.014536 · 14.43 Impact Factor
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    ABSTRACT: Diuretic unresponsiveness often occurs during hospital admission for acute heart failure (AHF) and is associated with adverse outcome. This study aims to investigate determinants, clinical outcome, and the effects of nesiritide on diuretic response early after admission for AHF. Diuretic response, defined as weight loss per 40 mg of furosemide or equivalent, was examined from hospital admission to 48 hours in 4,379 patients from the ASCEND-HF trial. As an additional analysis, a urinary diuretic response metric was investigated in 5,268 patients using urine volume from hospital admission to 24 hours per 40 mg of furosemide or equivalent. Mean diuretic response was -0.42 kg/40 mg of furosemide (interquartile range -1.0, -0.05). Poor responders had lower blood pressure, more frequent diabetes, long-term use of loop diuretics, poorer baseline renal function, and lower urine output (all P < .01). Randomized nesiritide treatment was not associated with diuretic response (P = .987). Good diuretic response was independently associated with a significantly decreased risk of 30-day all-cause mortality or heart failure rehospitalization (odds ratio 0.44, 95% CI 0.29-0.65, highest vs lowest quintile, P < .001). Diuretic response based on urine output per 40 mg of furosemide showed similar results in terms of clinical predictors, association with outcome, and the absence of an effect of nesiritide. Poor diuretic response early after hospital admission for AHF is associated with low blood pressure, renal impairment, low urine output, and an increased risk of death or rehospitalization early after discharge. Nesiritide had a neutral effect on diuretic response. Copyright © 2015 Elsevier Inc. All rights reserved.
    Journal of the American College of Cardiology 05/2015; 65(10). DOI:10.1016/j.ahj.2015.05.003 · 16.50 Impact Factor
  • Antonio L Perez · W H Wilson Tang
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    ABSTRACT: Opinion statement: The pathogenesis of idiopathic cardiomyopathies is likely highly complex and remains elusive. Environmental toxins have been hypothesized to possibly cause a subset of cardiomyopathies. Epidemiological, preclinical, and small clinical studies have investigated the role of numerous elements and compounds in the pathogenesis of these myocardial disorders. In this review, we present the evidence implicating elements and environmental compounds in myocardial toxicity, including antimony, cobalt, mercury, aluminum, copper, and acrolein. We discuss their sources, toxic effects, and epidemiology, as well as identify groups at risk for toxic exposure. Through our discussion, we highlight areas where further investigation into the clinical effects of these possible toxins is warranted.
    Current Treatment Options in Cardiovascular Medicine 05/2015; 17(5):381. DOI:10.1007/s11936-015-0381-2
  • Dhssraj Singh · Akanksha Thakur · W H Wilson Tang
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    ABSTRACT: The success achieved in advances in cancer therapy has been marred by development of cardiotoxicity, which causes significant morbidity and mortality. This has led to the development of surveillance protocols for cardiotoxicity utilizing multimodality imaging techniques and investigation of various drugs to treat and prevent cardiotoxicity in this subset of patients. Cardiac biomarkers hold important diagnostic and prognostic value in various cardiac diseases. In this review, we discuss the use of biomarkers in patients receiving chemotherapy, highlighting data behind the use of troponin, B-type natriuretic peptide, and myeloperoxidase. We also discuss the use of dexrazoxane, angiotensin-converting enzyme inhibitors, and beta blockers in the treatment and prevention of chemotherapy-induced cardiotoxicity. Cardiac biomarkers may serve an important role in selecting patients that are at high risk of cardiotoxicity and can potentially be used to guide the administration of drugs to treat and prevent cardiotoxicity.
    Current Heart Failure Reports 04/2015; 12(3). DOI:10.1007/s11897-015-0258-4
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    ABSTRACT: Patients hospitalized for acute decompensated heart failure (ADHF) are at high risk for early mortality and rehospitalization. Risk stratification of ADHF using clinically available data on admission is increasingly important to integrate with clinical pathways. Our goal was to create a simple method of screening patients upon admission to identify those with increased risk of future adverse events. Using ASCEND-HF, a pragmatic clinical trial conducted in 398 sites globally, we developed and validated logistic regression risk models for (a) 30-day mortality/HF rehospitalization, (b) 30-day mortality/all-cause rehospitalization, (c) 30-day all-cause mortality, and (d) 180-day all-cause mortality. Fifty-one candidate variables were evaluated based on prior publications and clinical review. Final models were selected based on stepwise selection with entry and a staying criterion of P < .01. The 30-day mortality model was externally validated, and coefficients were converted to an additive risk score. Among 7,141 patients, the median age was 67 years, 34% were female, and 80% had a left ventricular ejection fraction <40%. The models had between 5 and 12 risk factors with c-indices ranging from 0.68 to 0.75. A simplified score, including age, systolic blood pressure, sodium, blood urea nitrogen, and dyspnea at rest, discriminated 30-day mortality risk from 0.5% (score 0) to 53% (score 10). Commonly available clinical variables provide simple risk stratification for clinical outcomes among patients with ADHF, and these models may be considered for integration into routine clinical care. Copyright © 2015. Published by Elsevier Inc.
    American Heart Journal 04/2015; 170(2). DOI:10.1016/j.ahj.2015.04.006 · 4.46 Impact Factor
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    ABSTRACT: The benefits of biventricular pacing in patients with cardiac resynchronization therapy (CRT) remain poorly understood in those with right bundle branch block (RBBB). The aim of this study was to examine the differences in several speckle tracking-derived parameters, including left ventricular torsion and longitudinal strain with CRT on and off for patients with underlying left bundle branch block (LBBB) and RBBB. Twelve patients with CRT and RBBB were compared with a similar group of patients with underlying LBBB who were sent for evaluation and atrioventricular optimization. Echocardiographic images were acquired with biventricular pacing on and off. The 2 groups had similar baseline characteristics, including age, the ejection fraction, and QRS duration. During intrinsic conduction (CRT off), patients with LBBB had lower torsion angles than those with RBBB (2.3 ± 1.0° in those with LBBB vs 6.3 ± 1.0° in those with RBBB, p = 0.03) but trended toward improvements in torsional parameters, including torsional angle and peak untwisting velocity with CRT on, whereas these parameters worsened in patients with RBBB. Compared with CRT off, analyses of septal and lateral strain curves showed significant improvements in septal strain during 100% and 200% of systole with CRT on in patients with LBBB, whereas biventricular pacing resulted in a trend toward worsening of septal strain in patients with RBBB. Negligible changes were noted in lateral strain values. In conclusion, CRT favorably improves regional mechanics in patients with LBBB primarily involving the ventricular septum, with a negligible positive impact on cardiac function in patients with underlying RBBB. Copyright © 2015 Elsevier Inc. All rights reserved.
    The American Journal of Cardiology 04/2015; 115(7). DOI:10.1016/j.amjcard.2015.01.018 · 3.28 Impact Factor
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    ABSTRACT: Background Cardiac pump function is often quantified by left ventricular ejection fraction by various imaging modalities. As the heart is commonly conceptualized as a hydraulic pump, cardiac power describes the hydraulic function of the heart. We aim to describe the prognostic value of resting cardiac power index (CPI) in ambulatory patients with advanced heart failure.Methods and resultsWe calculated CPI in 495 sequential ambulatory patients with advanced heart failure who underwent invasive haemodynamic assessment with longitudinal follow-up of adverse outcomes (all-cause mortality, cardiac transplantation, or ventricular assist device placement). The median CPI was 0.44 W/m2 (interquartile range 0.37, 0.52). Over a median of 3.3 years, there were 117 deaths, 104 transplants, and 20 ventricular assist device placements in our cohort. Diminished CPI (<0.44 W/m2) was associated with increased adverse outcomes [hazard ratio (HR) 2.4, 95% confidence interval (CI) 1.8–3.1, P < 0.0001). The prognostic value of CPI remained significant after adjustment for age, gender, pulmonary capillary wedge pressure, cardiac index, pulmonary vascular resistance, left ventricular ejection fraction, and creatinine [HR 1.5, 95% CI 1.03–2.3, P = 0.04). Furthermore, CPI can risk stratify independently of peak oxygen consumption (HR 2.2, 95% CI 1.4–3.4, P = 0.0003).Conclusion Resting cardiac power index provides independent and incremental prediction in adverse outcomes beyond traditional haemodynamic and cardio-renal risk factors.
    European Journal of Heart Failure 04/2015; 17(7). DOI:10.1002/ejhf.268 · 6.53 Impact Factor
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    ABSTRACT: Discordance between left- and right-sided filling pressures occurs in a subset of patients presenting with acute decompensated heart failure (ADHF). We hypothesized that a disproportionately increased right atrial pressure (RAP) relative to the pulmonary capillary wedge pressure (PCWP) would be associated with both renal dysfunction and mortality in ADHF. A total of 367 patients admitted with ADHF with elevated intracardiac filling pressures were treated with intensive medical therapy guided by invasive hemodynamic monitoring. Baseline characteristics, hemodynamics, and renal function at admission were stratified by RAP/PCWP quartiles. The association of RAP/PCWP quartile with all-cause mortality after a median follow-up of 2.4 years was assessed in univariable and multivariable models, which included adjustment for the RAP. The median RAP/PCWP was 0.58 (interquartile range 0.43-0.75). Increasing RAP/PCWP was inversely associated with estimated glomerular filtration rate at baseline and with treatment (P < .0001) independently of RAP. High RAP/PCWP was associated with increased mortality (quartile 4 vs 1: hazard ratio [95% CI] 2.1 [1.3-3.5], P = .002). The association of RAP/PCWP with mortality persisted after adjustment for age, gender, mean arterial pressure, RAP, cardiac index, pulmonary vascular resistance, and estimated glomerular filtration rate (hazard ratio 2.4 [1.4-3.9], P = .007). A disproportionate increase in right to left ventricular filling pressures is associated with renal dysfunction and mortality, independently of the right atrial pressure. Copyright © 2015 Elsevier Inc. All rights reserved.
    American Heart Journal 02/2015; 169(6). DOI:10.1016/j.ahj.2015.02.017 · 4.46 Impact Factor

Publication Stats

9k Citations
3,337.89 Total Impact Points


  • 2008–2015
    • Lerner Research Institute
      • Department of Cellular and Molecular Medicine
      Cleveland, Ohio, United States
    • Rede Sarah de Hospitais de Reabilitação
      Brasília, Federal, Brazil
  • 2003–2015
    • Cleveland Clinic
      • • Department of Cell Biology
      • • Department of Cardiovascular Medicine
      • • Department of Cardiology
      Cleveland, Ohio, United States
  • 2014
    • Henry Ford Hospital
      Detroit, Michigan, United States
  • 2013
    • London School of Hygiene and Tropical Medicine
      Londinium, England, United Kingdom
    • MetroHealth Medical Center
      Cleveland, Ohio, United States
  • 2012–2013
    • Universiteit Hasselt
      • Faculty of Medicine and Life Sciences
      Hasselt, Flanders, Belgium
    • NCI-Frederick
      Фредерик, Maryland, United States
    • Cleveland Clinic Laboratories
      Cleveland, Ohio, United States
    • Baylor College of Medicine
      Houston, Texas, United States
  • 2005–2013
    • Case Western Reserve University
      • Division of Cardiovascular Medicine
      Cleveland, Ohio, United States
    • University of Alabama at Birmingham
      • Department of Medicine
      Birmingham, Alabama, United States
  • 2008–2012
    • Metropolitan Heart and Vascular Institute
      Minneapolis, Minnesota, United States
  • 2011
    • Allegheny General Hospital
      Pittsburgh, Pennsylvania, United States
  • 1999–2011
    • Stanford Medicine
      • Division of Cardiovascular Medicine
      Stanford, California, United States
  • 2009
    • University of Western Sydney
      • School of Nursing and Midwifery
      Penrith, New South Wales, Australia
  • 2007
    • VA San Diego Healthcare System
      San Diego, California, United States
    • IST Austria
      Klosterneuberg, Lower Austria, Austria
  • 2006
    • University of Maryland, Baltimore
      Baltimore, Maryland, United States
  • 2004
    • University of Texas Southwestern Medical Center
      • Department of Internal Medicine
      Dallas, Texas, United States
    • University of North Carolina at Chapel Hill
      North Carolina, United States
  • 2001–2004
    • Stanford University
      • Division of Cardiovascular Medicine
      Palo Alto, California, United States