Marvin A Konstam

Tufts Medical Center, Boston, Massachusetts, United States

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Publications (390)3293.84 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Congestion is a primary reason for hospitalization in patients with acute heart failure (AHF). Despite inpatient diuretics and vasodilators targeting decongestion, persistent congestion is present in many AHF patients at discharge and more severe congestion is associated with increased morbidity and mortality. Moreover, hospitalized AHF patients may have renal insufficiency, hyponatremia, or an inadequate response to traditional diuretic therapy despite dose escalation. Current alternative treatment strategies to relieve congestion, such as ultrafiltration, may also result in renal dysfunction to a greater extent than medical therapy in certain AHF populations. Truly novel approaches to volume management would be advantageous to improve dyspnea and clinical outcomes while minimizing the risks of worsening renal function and electrolyte abnormalities. One effective new strategy may be utilization of aquaretic vasopressin antagonists. A member of this class, the oral vasopressin-2 receptor antagonist tolvaptan, provides benefits related to decongestion and symptom relief in AHF patients. Tolvaptan may allow for less intensification of loop diuretic therapy and a lower incidence of worsening renal function during decongestion. In this article, we summarize evidence for decongestion benefits with tolvaptan in AHF and describe the design of the Targeting Acute Congestion With Tolvaptan in Congestive Heart Failure Study (TACTICS) and Study to Evaluate Challenging Responses to Therapy in Congestive Heart Failure (SECRET of CHF) trials.
    Circulation Heart Failure 09/2015; 8(5):997-1005. DOI:10.1161/CIRCHEARTFAILURE.115.002259 · 5.89 Impact Factor
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    ABSTRACT: Background: In the current era, where advanced heart failure (AHF) has become an American Board of Internal Medicine (ABIM) certified subspecialty, new data are needed to benchmark and value levels of clinical effort performed by AHF specialists (AHFMDs). Methods and results: A 36-question survey was sent to 728 AHFMDs members of the Heart Failure Society of America, and 224 (31% responded). Overall, 56% worked in academic medical centers (AMCs) and were younger (48 ± 9 years vs. 52 ± 10 years, p < 0.01) and had a higher proportion of women (34% vs. 21%, p < 0.01) compared to non-AMCs. The percentage of time in clinical care was lower in AMC (64 ± 19% vs. 78 ± 18 %, p = 0.002), with similar concentration on E&M services (79 ± 18 % in AMC vs. 72 ± 18 % in non-AMC, p = NS). The majority of non-clinical time was spent in program administration (10% in both AMCs and non-AMCs) and education/ research (15% in AMC vs. 5% in non-AMCs). Although 69% of respondents were compensated by work relative value units (wRVUs), only a small percentage knew their target or the amount of RVU generated. The mean annual wRVUs generated were lower in AMC compared to non-AMC (5452 ±1961 vs. 9071 ± 3484), p < 0.001). The annual compensation in AMC was lower than non-AMC (45% vs. 10% below $250,000 and 17% vs. 61% over $350,000, p < 0.001) and the satisfaction with compensation was higher in non-AMCs. Conclusions: AHFMDs compensation is largely dependent by practice type (AMC vs. non-AMC) and clinical productivity, as measured by wRVUs. These data provide an opportunity for benchmarking work effort and compensation for AHFMDs, allowing distinction from segments of cardiologists with greater opportunity to accrue procedural wRVUs. They also show several differences between AMC and non-AMC that should be considered when formulating work assignment and compensation for AHFMDs.
    Journal of cardiac failure 09/2015; DOI:10.1016/j.cardfail.2015.08.340 · 3.05 Impact Factor
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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: 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: Previous reports have provided conflicting data regarding the relationship between length of stay (LOS) and subsequent readmission risk among patients hospitalized for heart failure (HF). We performed a post-hoc analysis of the Efficacy of Vasopressin Antagonism in Heart Failure Outcome Study with Tolvaptan (EVEREST) trial to evaluate the differences in LOS overall and between geographic regions (North America, South America, Western Europe, and Eastern Europe) in association with all-cause and cause-specific [HF, cardiovascular (CV) non-HF, and non-CV] readmissions within 30 days of discharge after HF hospitalization. The present analysis included 4020 patients enrolled from 20 countries who were alive at discharge. Median [interquartile range (IQR)] LOS was 8 (4-11) days. The 30-day readmission rates were 15.7% [95% confidence interval (CI) 14.6-16.8] for all-cause; 5.6% (95% CI 4.9-6.3) for HF; 4.4% (95% CI 3.8-5.1) for CV non-HF; and 5.8% (95% CI 5.1-6.6) for non-CV readmissions. There was a positive correlation between LOS and all-cause readmissions (r = 0.09, 95% CI 0.06-0.12). The adjusted odds ratio for the top (≥14 days) vs. the bottom (≤3 days) quintile for LOS was 1.39 (95% CI 0. 92-2.11) for all-cause readmissions, 0.43 (95% CI 0.24-0.79) for HF, 2.99 (95% CI 1.49-6.02) for CV non-HF, and 1.72 (95% CI 1.05-2.81) for non-CV readmissions. With the exception of Western Europe, these findings remained largely consistent across geographic regions. In this large multinational cohort of hospitalized HF patients, longer LOS was associated with a higher risk for all-cause, CV non-HF, and non-CV readmissions, but a lower risk of HF readmissions within 30 days of discharge. These results may inform strategies to reduce readmissions. © 2015 The Authors European Journal of Heart Failure © 2015 European Society of Cardiology.
    European Journal of Heart Failure 05/2015; DOI:10.1002/ejhf.282 · 6.53 Impact Factor
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    P Rossignol · N Girerd · D Gregory · J Massaro · M.A. Konstam · F Zannad
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    ABSTRACT: Recent data have highlighted shortcomings of the usual blood pressure (BP) hypothesis in several populations, and emphasized the importance of visit-to-visit variability of BP in predicting cardiovascular events. Herein, we aimed at assessing the association between visit-to-visit BP variability and outcomes in chronic heart failure (CHF) patients enrolled in the Heart failure Endpoint evaluation of Angiotensin II Antagonist Losartan (HEAAL). The HEAAL study randomized 3834 patients with HF and reduced ejection fraction administered 150mg or 50mg losartan daily in a double blind, randomized, controlled trial. The patients were followed up for up to 6.8years after randomization, and BP was measured at 3 time points in the first year and at semi-annual visits in the years thereafter. Three measures of visit-to-visit BP variability were computed for each subject: the standard deviation, the coefficient of variation and the average absolute visit-to-visit variation. Cox proportional hazard models were used to investigate the relationship between variations in systolic blood pressure, baseline covariates and the time to death or heart failure hospitalization (i.e. primary outcome). In multivariate analyses stratified on baseline BP, the patients with higher visit-to visit BP variability exhibited poorer outcomes (average absolute difference in SBP in mmHg:hazard ratio: 1.023 [95% CI (1.013, 1.034), P<0.0001]), independent from high dose losartan (still beneficial). For the first time, visit-to-visit BP variability was found elevated in CHF patients with reduced ejection fraction, and associated with poorer cardiovascular outcomes. Such assessments should be prioritized for testing prevention strategies in CHF. This study is registered with the, number NCT00090259. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.
    International journal of cardiology 03/2015; 187(1):183-189. DOI:10.1016/j.ijcard.2015.03.169 · 4.04 Impact Factor
  • Journal of the American College of Cardiology 03/2015; 65(17). DOI:10.1016/j.jacc.2015.03.031 · 16.50 Impact Factor
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    ABSTRACT: Objectives: This study investigated the dose-related effect of losartan on changes in renal function using datafromthe HEAAL (Heart failure Endpoint evaluation of Angiotensin II Antagonist Losartan) trial. Background: Angiotensin receptor blockers adversely affect renal function in patients with heart failure (HF). Thetime course and dose dependency of this time course, as well as the clinical implications of these changes in renalfunction, are not well described. Methods: Subjects in the HEAAL dataset (n= 3,843) were studied. Changes in estimated glomerular filtration rate (eGFR) over time were compared between dose groups. The association between the timing of incident increases in serum creatinine (SCr) >0.3 mg/dl and clinical outcomes was explored. Results: Compared with 50 mg, 150 mg losartan led to a greater reduction in eGFR across time (mean difference: -3.79 ml/min/1.73 m2; p< 0.0001). This difference was driven by early changes, and differences in eGFR after 4 months were not significant (mean difference: 0.40 ml/min/1.73 m2; p= 0.16). Although an increase in SCr >0.3 mg/dl from baseline was associated with increased risk of death or hospitalization for HF (hazard ratio [HR]: 1.36; p<0.0001), the relationship was not significant if the change occurred before 4 months (HR: 1.09; p= 0.20). Despite increased risk of worsening renal function, 150 mg losartan was associated with reduced risk of death or hospitalization for HF compared with 50 mg (HR: 0.85; p< 0.0001). Conclusions: Compared with 50 mg, 150 mg losartan is associated with an increased risk of acute rise in SCr, as well as with greater long-term reductions in eGFR. Despite these effects, high-dose losartan retains its net clinical benefit andis associated with reduced risk of death or hospitalization for HF. (Study to Evaluate Potential Decrease in Hospitalization Events, Time Between Events, and Increasing Longevity in Patients With Symptomatic Heart Failure; NCT00090259).
    JACC: Heart Failure 03/2015; 3(3):214-23. DOI:10.1016/j.jchf.2014.11.004
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    ABSTRACT: We investigated the clinical profiles associated with serum uric acid (sUA) levels in a large cohort of patients hospitalized for worsening chronic heart failure with ejection fraction (EF) ≤40%, with specific focus on gender, race, and renal function based interactions. In 3,955 of 4,133 patients (96%) with baseline sUA data, clinical characteristics and outcomes were compared across sUA quartiles. The primary end points were all-cause mortality and a composite of cardiovascular mortality or heart failure hospitalization. Interaction analyses were performed for gender, race, and baseline renal function. Median follow-up was 9.9 months. Mean sUA was 9.1 ± 2.8 mg/dl and was higher in men than in women (9.3 ± 2.7 vs 8.7 ± 3.0 mg/dl, p <0.001) and in blacks than in whites (10.0 ± 2.7 vs 9.0 ± 2.8 mg/dl, p <0.001). Higher sUA was associated with lower systolic blood pressure and EF, higher natriuretic peptides, and more impaired renal function. After accounting for 24 baseline covariates, in patients with enrollment estimated glomerular filtration rate ≥30 ml/min/1.73 m(2), sUA was strongly associated with increased all-cause mortality (hazard ratio 1.44, 95% confidence interval 1.22 to 1.69, p <0.001) and the composite end point (hazard ratio 1.44, 95% confidence interval 1.26 to 1.64, p <0.001). However, in patients with estimated glomerular filtration rate <30 ml/min/1.73 m(2), sUA was not related with either end point (both p >0.4). Adjusted interaction analyses for gender, race, and admission allopurinol use were not significant. In conclusion, sUA is commonly elevated in patients hospitalized for worsening chronic heart failure and reduced EF, especially in men and blacks. The prognostic use of sUA differs by baseline renal function, suggesting different biologic and pathophysiologic significance of sUA among those with and without significant renal dysfunction.
    The American Journal of Cardiology 09/2014; 114(11). DOI:10.1016/j.amjcard.2014.09.008 · 3.28 Impact Factor
  • Alanna A Morris · Javed Butler · Marvin A Konstam
    Journal of cardiac failure 08/2014; 20(10). DOI:10.1016/j.cardfail.2014.08.007 · 3.05 Impact Factor
  • Journal of Cardiac Failure 08/2014; 20(8S):S103-S104. DOI:10.1016/j.cardfail.2014.06.291 · 3.05 Impact Factor
  • Journal of Cardiac Failure 08/2014; 20(8S):S102. DOI:10.1016/j.cardfail.2014.06.287 · 3.05 Impact Factor
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    ABSTRACT: Despite the well-established benefits of mineralocorticoid receptor agonists (MRAs) in heart failure with reduced ejection fraction, safety concerns remain in patients with concomitant diabetes mellitus (DM) because of common renal and electrolyte abnormalities in this population. We analyzed all-cause mortality and composite cardiovascular mortality and HF hospitalization over a median 9.9 months among 1,998 patients in the placebo arm of the Efficacy of Vasopressin Antagonism in Heart Failure Outcome Study With Tolvaptan (EVEREST) trial by DM status and discharge MRA use. Of the 750 patients with DM, 59.2% were receiving MRAs compared with 62.5% in the non-DM patients. DM patients not receiving MRAs were older, more likely to be men, with an ischemic heart failure etiology and slightly worse renal function compared with those receiving MRAs. After adjustment for baseline risk factors, among DM patients, MRA use was not associated with either mortality (hazard ratio [HR] 0.93; 95% confidence interval [CI] 0.75 to 1.15) or the composite end point (HR 0.94; 95% CI 0.80 to 1.10). Similar findings were seen in non-DM patients (mortality [HR 1.01; 95% CI 0.84 to 1.22] or the composite end point [HR 0.98; 95% CI 0.85 to 1.13] [p >0.43 for DM interaction]). In conclusion, in-hospital initiation of MRA therapy was low (15% to 20%), and overall discharge MRA use was only 60% (with regional variation), regardless of DM status. There does not appear to be clear, clinically significant in-hospital hemodynamic or even renal differences between those on and off MRA. Discharge MRA use was not associated with postdischarge end points in patients hospitalized for worsening heart failure with reduced ejection fraction and co-morbid DM. DM does not appear to influence the effectiveness of MRA therapy.
    The American Journal of Cardiology 06/2014; 114(5). DOI:10.1016/j.amjcard.2014.05.064 · 3.28 Impact Factor
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    ABSTRACT: Angiotensin receptor antagonists (ARBs) improve outcomes in patients with heart failure (HF) with reduced left ventricular ejection fraction, but may induce hyperkalemia (HK) and/or a worsening of renal function (WRF). The incidence and risk factors of HK and its inter-relationship with WRF, as well as associations with clinical outcome (death or admission for HF i.e. the primary outcome) in 3846 HF patients enrolled in the double blind HEAAL trial (losartan 150mg/d vs. 50mg/d) were assessed. Worsening of renal function was defined as a decrease in eGFR >20% from baseline and HK as serum K >5.5 or >5mmol/L. Higher dose of losartan increased serum potassium. Episodes of HK >5mmol/L or WRF occurred at least once in about half of the patients. WRF was associated with higher occurrence of HK (HR 1.19 (1.06-1.34)) and vice versa (HR 1.35 (1.19-1.53)), but preceded HK in only about half of the events. High dose losartan improved outcome despite more frequent WRF and HK, both being independently associated with adverse outcomes in multivariate analyses. HK and WRF are common in HF patients. Both can be predicted from baseline risk factors and are therefore potentially preventable. Although associated with worse outcome, occurrence of any does not hinder the efficacy of high dose losartan. HK was associated with WRF and worse outcomes. Whether therapy targeting specifically HK may maximize the survival benefit derived from renin angiotensin aldosterone inhibitor use should be appropriately tested in future trials.
    International journal of cardiology 02/2014; 173(3). DOI:10.1016/j.ijcard.2014.02.034 · 4.04 Impact Factor
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    ABSTRACT: Objectives The purpose of this study was to characterize the relationship between heart rate and post-discharge outcomes in patients with hospitalization for heart failure (HHF) with reduced ejection fraction (EF) in sinus rhythm. Background A reduction in heart rate improves clinical outcomes in patients with chronic heart failure and in sinus rhythm, but the association between heart rate and post-discharge outcomes in patients with HHF is presently unclear. Methods This post-hoc analysis of the EVEREST (Efficacy of Vasopressin Antagonism in Heart Failure: Outcome Study With Tolvaptan) trial examined 1,947 patients with HHF and EF ≤40% not in atrial fibrillation/flutter or pacemaker dependent. Results The median follow-up period was 9.9 months. At baseline, patients with a higher heart rate tended to be younger with lower EF and were more likely to have worse New York Heart Association functional class and higher natriuretic peptide levels. After adjustment for clinical risk factors, baseline heart rate was not predictive of all-cause mortality (p ≥ 0.066). However, at ≥70 beats/min, every 5-beat increase in 1-week post-discharge heart rate was independently associated with increased all-cause mortality (hazard ratio: 1.13 [95% confidence interval: 1.05 to 1.22]; p = 0.002). Similarly, every 5-beat increase ≥70 beats/min in 4-week post-discharge heart rate was predictive of all-cause mortality (hazard ratio: 1.12 [95% confidence interval: 1.05 to 1.19]; p = 0.001). Conclusions In this large cohort of patients with HHF with reduced EF and in sinus rhythm, baseline heart rate did not correlate with all-cause mortality. In contrast, at ≥70 beats/min, higher heart rate in the early post-discharge period was independently predictive of death during subsequent follow-up. Further study of post-discharge heart rate as a potential therapeutic target in this high-risk population is encouraged.
    12/2013; 1(6):488–496. DOI:10.1016/j.jchf.2013.08.005
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    ABSTRACT: Importance Small studies suggest that low-dose dopamine or low-dose nesiritide may enhance decongestion and preserve renal function in patients with acute heart failure and renal dysfunction; however, neither strategy has been rigorously tested.Objective To test the 2 independent hypotheses that, compared with placebo, addition of low-dose dopamine (2 μg/kg/min) or low-dose nesiritide (0.005 μg/kg/min without bolus) to diuretic therapy will enhance decongestion and preserve renal function in patients with acute heart failure and renal dysfunction.Design, Setting, and Participants Multicenter, double-blind, placebo-controlled clinical trial (Renal Optimization Strategies Evaluation [ROSE]) of 360 hospitalized patients with acute heart failure and renal dysfunction (estimated glomerular filtration rate of 15-60 mL/min/1.73 m2), randomized within 24 hours of admission. Enrollment occurred from September 2010 to March 2013 across 26 sites in North America.Interventions Participants were randomized in an open, 1:1 allocation ratio to the dopamine or nesiritide strategy. Within each strategy, participants were randomized in a double-blind, 2:1 ratio to active treatment or placebo. The dopamine (n = 122) and nesiritide (n = 119) groups were independently compared with the pooled placebo group (n = 119).Main Outcomes and Measures Coprimary end points included 72-hour cumulative urine volume (decongestion end point) and the change in serum cystatin C from enrollment to 72 hours (renal function end point).Results Compared with placebo, low-dose dopamine had no significant effect on 72-hour cumulative urine volume (dopamine, 8524 mL; 95% CI, 7917-9131 vs placebo, 8296 mL; 95% CI, 7762-8830 ; difference, 229 mL; 95% CI, −714 to 1171 mL; P = .59) or on the change in cystatin C level (dopamine, 0.12 mg/L; 95% CI, 0.06-0.18 vs placebo, 0.11 mg/L; 95% CI, 0.06-0.16; difference, 0.01; 95% CI, −0.08 to 0.10; P = .72). Similarly, low-dose nesiritide had no significant effect on 72-hour cumulative urine volume (nesiritide, 8574 mL; 95% CI, 8014-9134 vs placebo, 8296mL; 95% CI, 7762-8830; difference, 279 mL; 95% CI, −618 to 1176 mL; P = .49) or on the change in cystatin C level (nesiritide, 0.07 mg/L; 95% CI, 0.01-0.13 vs placebo, 0.11 mg/L; 95% CI, 0.06-0.16; difference, −0.04; 95% CI, −0.13 to 0.05; P = .36). Compared with placebo, there was no effect of low-dose dopamine or nesiritide on secondary end points reflective of decongestion, renal function, or clinical outcomes.Conclusion and Relevance In participants with acute heart failure and renal dysfunction, neither low-dose dopamine nor low-dose nesiritide enhanced decongestion or improved renal function when added to diuretic therapy.Trial Registration Identifier: NCT01132846
    JAMA The Journal of the American Medical Association 11/2013; 310(23). DOI:10.1001/jama.2013.282190 · 35.29 Impact Factor
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    John Gordon Harold · Patrick O'Gara · Joseph A Hill · Marvin A Konstam
    Journal of the American College of Cardiology 11/2013; 62(19):1811-2. DOI:10.1016/j.jacc.2013.10.001 · 16.50 Impact Factor
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    Journal of the American College of Cardiology 10/2013; 62(15):1394-1395. DOI:10.1016/j.jacc.2013.09.003 · 16.50 Impact Factor
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    ABSTRACT: Serum magnesium levels may be impacted by neurohormonal activation, renal function, and diuretics. The clinical profile and prognostic significance of serum magnesium level concentration in patients hospitalized for heart failure (HF) with reduced ejection fraction is unclear. In this retrospective analysis of the placebo group of the Efficacy of Vasopressin Antagonism in Heart Failure Outcome Study with Tolvaptan trial, we evaluated 1,982 patients hospitalized for worsening HF with ejection fractions ≤40%. Baseline magnesium levels were measured within 48 hours of admission and analyzed as a continuous variable and in quartiles. The primary end points of all-cause mortality (ACM) and cardiovascular mortality or HF rehospitalization were analyzed using Cox regression models. Mean baseline magnesium level was 2.1 ± 0.3 mg/dl. Compared with the lowest quartile, patients in the highest magnesium level quartile were more likely to be older, men, have lower heart rates and blood pressures, have ischemic HF origin, and have higher creatinine and natriuretic peptide levels (all p <0.003). During a median follow-up of 9.9 months, every 1-mg/dl increase in magnesium level was associated with higher ACM (hazard ratio [HR] 1.77; 95% confidence interval [CI] 1.35 to 2.32; p <0.001) and the composite end point (HR 1.44; 95% CI 1.15 to 1.81; p = 0.002). However, after adjustment for known baseline covariates, serum magnesium level was no longer an independent predictor of either ACM (HR 0.94, 95% CI 0.69 to 1.28; p = 0.7) or the composite end point (HR 1.01, 95% CI 0.79 to 1.30; p = 0.9). In conclusion, despite theoretical concerns, baseline magnesium level was not independently associated with worse outcomes in this cohort. Further research is needed to understand the importance of serum magnesium levels in specific HF patient populations.
    The American journal of cardiology 10/2013; 112(11). DOI:10.1016/j.amjcard.2013.07.020 · 3.28 Impact Factor
  • Journal of Cardiac Failure 08/2013; 19(8):S73. DOI:10.1016/j.cardfail.2013.06.237 · 3.05 Impact Factor

Publication Stats

20k Citations
3,293.84 Total Impact Points


  • 1983–2015
    • Tufts Medical Center
      • • Division of Cardiology
      • • Department of Medicine
      Boston, Massachusetts, United States
  • 2013
    • American University Washington D.C.
      Washington, Washington, D.C., United States
    • American College of Cardiology
      Washington, Washington, D.C., United States
  • 1984–2013
    • Tufts University
      • • Division of Cardiology
      • • Tufts Center for Conservation Medicine
      • • Department of Medicine
      Georgia, United States
    • Boston University
      • Department of Chemistry
      Boston, Massachusetts, United States
  • 2012
    • San Francisco VA Medical Center
      San Francisco, California, United States
  • 1985–2012
    • University of Massachusetts Boston
      • Department of Counseling and School Psychology
      Boston, Massachusetts, United States
  • 2010
    • University of Wisconsin - Milwaukee
      Milwaukee, Wisconsin, United States
  • 1983–2010
    • Boston Medical Center
      Boston, Massachusetts, United States
  • 2009
    • Rutgers New Jersey Medical School
      Newark, New Jersey, United States
  • 2007
    • Northwestern University
      • Division of Gastroenterology and Hepatology
      Evanston, Illinois, United States
    • Treatment Research Institute, Philadelphia PA
      Filadelfia, Pennsylvania, United States
  • 1998–2006
    • New England Baptist Hospital
      Boston, Massachusetts, United States
  • 2005
    • Blue Water Task Force
      Big Sky, Montana, United States
  • 2004
    • University of California, Los Angeles
      Los Angeles, California, United States
    • Medical University of South Carolina
      Charleston, South Carolina, United States
  • 2003
    • University of Pittsburgh
      Pittsburgh, Pennsylvania, United States
  • 1981–2003
    • Harvard Medical School
      • Department of Medicine
      Boston, Massachusetts, United States
  • 1991–2002
    • Beverly Hospital, Boston MA
      BVY, Massachusetts, United States
  • 1996
    • University of Ottawa
      Ottawa, Ontario, Canada
  • 1984–1996
    • Harvard University
      Cambridge, Massachusetts, United States
  • 1995
    • U.S. Department of Health and Human Services
      Washington, Washington, D.C., United States
    • University of North Carolina at Chapel Hill
      • Department of Biostatistics
      North Carolina, United States
  • 1992
    • University of Texas Health Science Center at Houston
      • Medical School
      Houston, Texas, United States
  • 1990
    • Good Samaritan Hospital
      Cincinnati, Ohio, United States