Mihai Gheorghiade

Northwestern University, Evanston, Illinois, United States

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Publications (762)5440.9 Total impact

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    ABSTRACT: The relationship between resting heart rate (RHR) and incident heart failure (HF) has been questioned. RHR was assessed at baseline in 7073 participants in 3 prospective cohorts (Cardiovascular Health Study, Health ABC study and Kuopio Ischemic Heart Disease Study) that recorded 1189 incident HF outcomes during 92 702 person-years of follow-up. Mean age of participants was 67 (9.9) years and mean RHR was 64.6 (11.1) bpm. Baseline RHR correlated (P<0.001) positively with body mass index (r=0.10), fasting glucose (r=0.18), and C-reactive protein (r=0.20); and inversely with serum creatinine (r=-0.05) and albumin (r=-0.05). Baseline RHR was non-linearly associated with HF risk. The age and sex-adjusted hazard ratio for HF comparing the top (>72 bpm) versus the bottom (<57 bpm) quartile of baseline RHR was 1.48 (95% confidence interval [CI] 1.26 to 1.74) and was modestly attenuated (1.30, 95% CI 1.10 to 1.53) with further adjustment for body mass index, history of diabetes, hypertension, smoking status, serum creatinine, and left ventricular hypertrophy. These findings remained consistent in analyses accounting for incident coronary heart disease, excluding individuals with prior cardiovascular events, or those taking beta-blockers; and in subgroups defined by several individual participant characteristics. In a pooled random effects meta-analysis of 7 population-based studies (43 051 participants and 3476 HF events), the overall hazard ratio comparing top versus bottom fourth of RHR was 1.40 (95% CI: 1.19 to 1.64). There is a non-linear association between RHR and incident HF. Further research is needed to understand the physiologic foundations of this association. © 2015 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.
    Journal of the American Heart Association 12/2015; 4(1). DOI:10.1161/JAHA.114.001364 · 4.31 Impact Factor
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    ABSTRACT: Aims: In the EVEREST trial, tolvaptan improved symptoms and body weight during hospitalization for heart failure (HF), but did not improve post-discharge cardiovascular outcomes. We hypothesized that this disconnect between the short- and long-term effects may be related to changes in serum osmolality. We describe the longitudinal profile of osmolality and its response to tolvaptan during and after hospitalization for HF. Methods and results: EVEREST enrolled 4133 patients hospitalized for HF and reduced EF. Serum osmolality data were available in 3744 (91%). We assessed the effects of tolvaptan on serum osmolality and related these effects to in-hospital changes in body weight and physician-assessed symptoms. Calculated values of osmolality, determined from serum sodium, blood urea nitrogen, and glucose, were 3-4 mOsm/kg higher than concurrently measured serum osmolality at enrolment and discharge in both treatment arms. During hospitalization in the placebo group, serum osmolality slightly increased throughout hospitalization, whereas serum sodium decreased and blood urea nitrogen increased until discharge. Tolvaptan increased osmolality by hospital day 1, but this effect diminished by post-discharge week 4-8 and disappeared by post-discharge week 56. In-hospital changes in osmolality were poorly correlated with in-hospital changes in body weight and physician-assessed dyspnoea. Conclusion: Tolvaptan increased serum osmolality during hospitalization for HF, a time frame when the drug also improved signs and symptoms of HF. However, this effect on osmolality declined in the early post-discharge period, when tolvaptan failed to influence clinical outcomes. Serum osmolality, which can be estimated based on readily available laboratory parameters, may be a marker or a target of response to tolvaptan.
    European Journal of Heart Failure 10/2015; DOI:10.1002/ejhf.415 · 6.53 Impact Factor
  • Erik B Schelbert · Timothy C Wong · Mihai Gheorghiade
    Journal of the American Heart Association 09/2015; 4(9). DOI:10.1161/JAHA.115.002491 · 4.31 Impact Factor
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    ABSTRACT: Myocardial recovery in heart failure (HF) is possible, but its determinants are not fully defined. At least partial functional improvement is possible with current evidence-based therapies. However, once significant HF symptoms develop, patients have varied trajectories, including: 1) structural and functional recovery; 2) stabilization (remission); and 3) acceleration to end-stage HF/death. All 3 trajectories may be interrupted by sudden death. These trajectories may represent the interplay of heterogeneous causality, genetic predeterminants, and disease phenotypes. Enhanced phenotypic description with cardiac magnetic resonance imaging, molecular imaging, or circulating biomarkers of the heterogeneous HF population may provide insights regarding specific biological targets amenable to existing and novel therapeutic strategies. The identification of patients in "remission," before progression to the end stage of predominantly nonviable tissue (e.g., fibrosis), has implications for clinical practice and future trials because such patients may be more likely to experience myocardial recovery (cardiac reserve). The identification of dysfunctional but viable myocardium and its diverse pathophysiological causes may provide opportunities to investigate existing and novel therapeutics aimed at enhancing myocardial recovery.
    09/2015; 3(9):661-9. DOI:10.1016/j.jchf.2015.04.011
  • Stephen J Greene · Mihai Gheorghiade
    European Journal of Heart Failure 08/2015; 17(9). DOI:10.1002/ejhf.335 · 6.53 Impact Factor
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    ABSTRACT: Acute worsening heart failure (WHF) is seen in a sizable portion of patients hospitalized for heart failure, and is increasingly being recognized as an entity that is associated with an adverse in-hospital course. WHF is generally defined as worsening heart failure symptoms and signs requiring an intensification of therapy, and is reported to be seen in anywhere from 5% to 42% of heart failure admissions. It is difficult to ascertain the exact epidemiology of WHF due to varying definitions used in the literature. Studies indicate that WHF cannot be precisely predicted on the basis of baseline variables assessed at the time of admission. Recent data suggest that some experimental therapies may reduce the risk of development of WHF among hospitalized heart failure patients, and this is associated with a reduction in risk of subsequent post-discharge cardiovascular mortality. In this respect, WHF holds promise as a endpoint for acute heart failure clinical trials to better elucidate the benefit of targeted novel therapies. Better understanding of the pathophysiology and a consensus on the definition of WHF will further improve our epidemiological and clinical understanding of this entity. © 2015 The Authors European Journal of Heart Failure © 2015 European Society of Cardiology.
    European Journal of Heart Failure 08/2015; DOI:10.1002/ejhf.333 · 6.53 Impact Factor
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    ABSTRACT: Acute heart failure (AHF) is a complex syndrome with presentations ranging from hypotensive cardiogenic shock to hypertensive emergency with pulmonary edema. Most patients with AHF present with worsening of chronic HF signs and symptoms over days to weeks, and significant heterogeneity exists. It can, therefore, be challenging to characterize the overall population. The complexity of defining the AHF phenotype has been cited as a contributing cause for neutral results in most pharmacologic trials in patients with AHF. Dyspnea has been a routine inclusion criterion for AHF for over a decade, but the utility of current instruments for dyspnea assessment has been called into question. Furthermore, the threshold of clinical severity that prompts patient admission of an HF clinic visit may vary substantially across regions in global trials. Therefore, the inclusion of cardiac-specific biomarkers has been incorporated into AHF trials as 1 strategy to support inclusion of the target patient population and potentially enrich the population with patients at risk for clinical outcomes. In conclusion, we discuss strategies to support appropriate patient selection in AHF trials with an emphasis on using biomarker criteria that may improve the likelihood of success with future AHF clinical trials. Copyright © 2015 Elsevier Inc. All rights reserved.
    The American journal of cardiology 07/2015; DOI:10.1016/j.amjcard.2015.07.049 · 3.28 Impact Factor
  • Source
    Michele Senni · Antonello Gavazzi · Mihai Gheorghiade · Javed Butler
    European Journal of Heart Failure 07/2015; 17(8). DOI:10.1002/ejhf.315 · 6.53 Impact Factor
  • Muthiah Vaduganathan · Javed Butler · Bertram Pitt · Mihai Gheorghiade
    Circulation Heart Failure 07/2015; 8(4):826-31. DOI:10.1161/CIRCHEARTFAILURE.115.002271 · 5.89 Impact Factor
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    ABSTRACT: Congestion is the most common reason for admissions and readmissions for heart failure (HF). The vast majority of hospitalized HF patients appear to respond readily to loop diuretics, but available data suggest that a significant proportion are being discharged with persistent evidence of congestion. Although novel therapies targeting congestion should continue to be developed, currently available agents may be utilized more optimally to facilitate complete decongestion. The combination of loop diuretics, natriuretic doses of mineralocorticoid receptor antagonists and vasopressin antagonists represents a regimen of currently available therapies that affects early and persistent decongestion, while limiting the associated risks of electrolyte disturbances, hemodynamic fluctuations, renal dysfunction and mortality.
    Expert Review of Cardiovascular Therapy 07/2015; 13(7):799-809. DOI:10.1586/14779072.2015.1053872
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    ABSTRACT: A systematic assessment of the temporal trends in heart failure (HF) clinical trials is lacking. 154 phase II-IV HF trials including 162,725 patients published between 2001 and 2012 in 8 high impact factor journals were reviewed. Median number of participants and sites per trial were 367 (IQR 133-1450) and 38 (5-101), respectively. Median enrollment duration was 2.2 (1.5-3.3) years. The majority of studies investigated treatment for chronic HF (82.5%) and investigated HFrEF 109 (71.4%), while 27 trials (17.5%) enrolled patients with mixed EF and 9 enrolled HFpEF (5.8%) patients alone. Enrollment rates did not significantly change over time (median 0.49; IQR 0.34-0.98 patients/site/month; p=0.53). Trials meeting their primary endpoint decreased over time from 73.5% in 2001-2003 to 52.5% in 2010-2012 (p=0.08) and were more often smaller and utilized non-mortality endpoints. Industry trials were larger with shorter enrollment duration, were more concentrated in North America, and more likely to be positive. Trials conducted exclusively outside North America and Western Europe had the highest enrollment rates (median 1.95; IQR 1.34-4.11). Contemporary HF clinical trials display slow enrollment rates and decreased rates of positive outcomes over time. Positive trials tended to be smaller size with higher proportion of surrogate endpoints. Copyright © 2015 Elsevier Inc. All rights reserved.
    Journal of cardiac failure 06/2015; DOI:10.1016/j.cardfail.2015.06.014 · 3.05 Impact Factor
  • Sadiya S Khan · Javed Butler · Haris Subacius · Mihai Gheorghiade
    The American journal of cardiology 06/2015; 116(5). DOI:10.1016/j.amjcard.2015.06.001 · 3.28 Impact Factor
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    ABSTRACT: Agents with vasodilator properties (AVDs) are frequently used in the treatment of acute heart failure (AHF). AVDs rapidly reduce preload and afterload, improve left ventricle to aorta and right ventricle to pulmonary artery coupling, and may improve symptoms. Early biomarker changes after AVD administration have suggested potentially beneficial effects on cardiac stretch, vascular tone, and renal function. AVDs that reduce haemodynamic congestion without causing hypoperfusion might be effective in preventing worsening organ dysfunction. Existing AVDs have been associated with different results on outcomes in randomized clinical trials, and observational studies have suggested that AVDs may be associated with a clinical outcome benefit. Lessons have been learned from past AVD trials in AHF regarding preventing hypotension, selecting the optimal endpoint, refining dyspnoea measurements, and achieving early randomization and treatment initiation. These lessons have been applied to the design of ongoing pivotal clinical trials, which aim to ascertain if AVDs improve clinical outcomes. The developing body of evidence suggests that AVDs may be a clinically effective therapy to reduce symptoms, but more importantly to prevent end-organ damage and improve clinical outcomes for specific patients with AHF. The results of ongoing trials will provide more clarity on the role of AVDs in the treatment of AHF. © 2015 The Authors European Journal of Heart Failure © 2015 European Society of Cardiology.
    European Journal of Heart Failure 06/2015; 17(7). DOI:10.1002/ejhf.294 · 6.53 Impact Factor
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    ABSTRACT: Efficient conduct of clinical trials is essential for the timely generation of critical medical knowledge. We systematically assessed size, duration, enrollment rates, and geographic distribution of randomized cardiovascular trials published between 2001 and 2012 in the 8 highest-impact journals in general medicine and cardiology. Of the 1,224 trials, 27.0% were conducted in North America, 36.5% in Western Europe, and 7.7% in other countries, and 28.8% were multiregional. Trials enrolled a median of 452 patients (interquartile range 167-1,530) in 20 sites (2-76). Median duration was 2.1 (1.3-3.3) years, with an estimated enrollment rate of 1.1 (0.5-3.5) patients/site per month. Between 2001-2003 and 2009-2012, the proportion of North American trials decreased from 34.5% to 25.7% (P = .006), whereas that of multiregional trials (from 26.0% to 30.3%; P = .046) and trials conducted in other countries (from 4.6% to 10.3%; P = .012) increased. Over time, trials involved more patients (from 400 to 500 [median]; P = .032) and sites (from 20 to 22; P = .049), multiregional trials involved more countries (from 12 to 18; P = .031), and enrollment rate declined from 1.2 to 0.9 patients/site per month (P = .017). The proportion of trials meeting their primary end point ("positive") decreased from 69% to 57% (P < .001). Trials with higher enrollment rates were more likely to be positive (odds ratio 1.20 per doubling, 95% CI 1.12-1.29), as were industry-sponsored compared with government-sponsored trials (odds ratio 2.62, 95% CI 1.67-4.12). From 2001 to 2012, cardiovascular clinical trials have become larger, more global, and less likely to meet their primary end point. Enrollment rates have declined, requiring more sites and regions. Copyright © 2015 Elsevier Inc. All rights reserved.
    American Heart Journal 05/2015; 170(2). DOI:10.1016/j.ahj.2015.05.006 · 4.46 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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    ABSTRACT: This study sought to investigate regional variation in clinical characteristics, therapy utilization, and post-discharge outcomes among patients hospitalized for heart failure (HHF) enrolled in the multinational ASTRONAUT (Aliskiren Trial on Acute Heart Failure Outcomes) trial. The ASTRONAUT trial randomized 1615 HHF patients with ejection fraction ≤40% to aliskiren or placebo. Enrolled patients were from Eastern Europe (n = 495, 30.7%), Asia/Pacific (n = 439, 27.2%), Western Europe (n = 395, 24.5%), Latin America (n = 163, 10.1%), and North America (n = 123, 7.6%). Marked differences were seen across geographic regions in terms of baseline demographics, vital signs, laboratory tests, co-morbidity burden, and use of guideline-recommended therapies. All-cause death at 12 months ranged from 7.3% in North America to 26.7% in Asia/Pacific, with differences largely driven by sudden cardiac death. Rates of repeat HHF at 12 months ranged from 22.7% in Latin America to 43.9% in North America. After adjustment for patient characteristics, region was an independent predictor of death at 12 months, with highest risk in Asia/Pacific (hazard ratio 3.04, 95% confidence interval 1.47-6.29, compared with North America) and lowest risk in North America and Western Europe. There was no association between region and the composite of cardiovascular mortality or HHF. For patients enrolled in this HHF trial, baseline characteristics and risk of death differed markedly by geographic region. Rates of death and repeat HHF demonstrated a general inverse relationship. Global differences in patient characteristics and outcomes should be accounted for when designing future HHF clinical trials. © 2015 The Authors European Journal of Heart Failure © 2015 European Society of Cardiology.
    European Journal of Heart Failure 04/2015; 17(6). DOI:10.1002/ejhf.280 · 6.53 Impact Factor
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    ABSTRACT: Thrombin is a critical element of crosstalk between pathways contributing to worsening of established heart failure (HF). The aim of this study is to explore the efficacy and safety of rivaroxaban 2.5 mg bid compared with placebo (with standard care) after an exacerbation of HF in patients with reduced ejection fraction (HF-rEF) and documented coronary artery disease. This is an international prospective, multicentre, randomized, double-blind, placebo-controlled, event-driven study of approximately 5000 patients for a targeted 984 events. Patients must have a recent symptomatic exacerbation of HF, increased plasma concentrations of natriuretic peptides (B-type natriuretic peptide ≥200 pg/mL or N-terminal pro-B-type natriuretic peptide ≥800 pg/mL), with left ventricular ejection fraction ≤40% and coronary artery disease. Patients requiring anticoagulation for atrial fibrillation or other conditions will be excluded. After an index event (overnight hospitalization, emergency department or observation unit admission, or unscheduled outpatient parenteral treatment for worsening HF), patients will be randomized 1:1 to rivaroxaban or placebo (with standard of care). The primary efficacy outcome event is a composite of all-cause mortality, myocardial infarction or stroke. The principal safety outcome events are the composite of fatal bleeding or bleeding into a critical space with potential permanent disability, bleeding events requiring hospitalization and major bleeding events according to International Society on Thrombosis and Haemostasis bleeding criteria. COMMANDER HF is the first prospective study of a target-specific oral antithrombotic agent in HF. It will provide important information regarding rivaroxaban use following an HF event in an HF-rEF patient population with coronary artery disease. © 2015 The Authors. European Journal of Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology.
    European Journal of Heart Failure 04/2015; 17(7). DOI:10.1002/ejhf.266 · 6.53 Impact Factor
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    ABSTRACT: With one possible exception, the last decade of clinical trials in hospitalized heart failure (HHF) patients has failed to demonstrate improvement in long-term clinical outcomes. This trend necessitates a need to evaluate optimal drug development strategies and standards of trial conduct. It has become increasingly important to recognize the heterogeneity among HHF patients and the differential characterization of novel drug candidates. Targeting these agents to specific subpopulations may afford optimal net response related to the particular mode of action of the drug. Analyses of previous trials demonstrate profound differences in the baseline characteristics of patients enrolled across global regions and participating sites. Such differences may influence risks for events and interpretation of results. Therefore, the actual execution of trials and the epidemiology of HHF populations at the investigative sites must be taken into consideration. Collaboration among participating sites including the provision of registry data tailored to the planned development program will optimize trial conduct. Observational data prior to study initiation may enable sites to feedback and engage in protocol development to allow for feasible and valid clinical trial conduct. This site-centered, epidemiology-based network environment may facilitate studies in specific patient populations and promote optimal data collection and clear interpretation of drug safety and efficacy. This review summarizes the roundtable discussion held by a multidisciplinary team of representatives from academia, National Institutes of Health, industry, regulatory agencies, payers, and contract and academic research organizations to answer the question: Who should be targeted for novel therapies in HHF?
    Heart Failure Reviews 04/2015; 20(4). DOI:10.1007/s10741-015-9485-8 · 3.79 Impact Factor
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    ABSTRACT: Device uptake and development have progressed over the last decade, but few quantitative data exist examining the overall operating characteristics and temporal trends of these clinical trials. We performed a systematic analysis of all cardiovascular device clinical trials from 2001 to 2012 published in medical and cardiovascular journals with the 8 highest impact factors. Of the 1,224 identified cardiovascular clinical trials, 299 (24.4%) focused specifically on devices. Each trial included a median of 335 patients (162 to 745) recruited from a median of 14 sites (3 to 38) over a median enrollment duration of 1.9 years (1.2 to 3.3). Median enrollment rate was 1.1 patients/site/month (0.5 to 4.2). Most device trials targeted coronary artery disease (55.2%), followed by arrhythmias (17.4%). Most were industry sponsored (53.6%) and included mortality as a primary end point (69.6%). The median number of patients (225 to 499, p <0.001 for trend) and enrolling sites (11 to 19, p = 0.07 for trend) increased from 2001 to 2012. During the study period, multinational enrollment grew and approached 50% (p = 0.03), whereas trials enrolling in North America exclusively decreased from 30% to 17% (p = 0.10 for trend). Approximately 70% of device trials met their primary end points; this rate did not significantly change over time. In conclusion, this descriptive study of the contemporary cardiovascular device clinical trials highlights recent trends toward larger, more international trial programs. These aggregate data may help inform future cardiovascular device development. Copyright © 2015 Elsevier Inc. All rights reserved.
    The American Journal of Cardiology 04/2015; 116(2). DOI:10.1016/j.amjcard.2015.03.062 · 3.28 Impact Factor
  • Stephen J Greene · Mihai Gheorghiade
    Journal of the American College of Cardiology 03/2015; 65(10):1061-1062. DOI:10.1016/j.jacc.2014.11.064 · 16.50 Impact Factor

Publication Stats

27k Citations
5,440.90 Total Impact Points


  • 1999–2015
    • Northwestern University
      • • Center for Cardiovascular Innovation
      • • Feinberg School of Medicine
      • • Division of Gastroenterology and Hepatology
      Evanston, Illinois, United States
  • 1994–2015
    • University of Illinois at Chicago
      • Section of Cardiology
      Chicago, Illinois, United States
  • 2013
    • Vanderbilt University
      • Department of Emergency Medicine
      Nashville, Michigan, United States
    • Durham University
      Durham, England, United Kingdom
    • Harvard Medical School
      • Department of Medicine
      Boston, MA, United States
  • 2012
    • Stanford Medicine
      • Department of Medicine
      Stanford, California, United States
  • 2002–2012
    • Duke University Medical Center
      • Department of Medicine
      Durham, North Carolina, United States
  • 2011
    • University of Pittsburgh
      Pittsburgh, Pennsylvania, United States
  • 2004–2011
    • Duke University
      Durham, North Carolina, United States
  • 1995–2011
    • University of Chicago
      • Department of Medicine
      Chicago, Illinois, United States
    • Henry Ford Health System
      Detroit, Michigan, United States
    • Oakland University
      • Department of Physics
      Рочестер, Michigan, United States
  • 2010
    • Medtronic
      Minneapolis, Minnesota, United States
    • University of Wisconsin - Milwaukee
      Milwaukee, Wisconsin, United States
    • Università degli Studi di Brescia
      • Department of Clinical and Experimental Sciences
      Brescia, Lombardy, Italy
    • Wayne State University
      • Department of Emergency Medicine
      Detroit, MI, United States
  • 1999–2010
    • Northwestern Memorial Hospital
      Chicago, Illinois, United States
  • 2009
    • Cleveland Clinic
      Cleveland, Ohio, United States
  • 2008
    • Attikon University Hospital
      • Department of Cardiology
      Athínai, Attica, Greece
  • 1998–2008
    • University of California, Los Angeles
      • • Department of Medicine
      • • Division of Cardiology
      Los Ángeles, California, United States
  • 2007
    • Tufts Medical Center
      • Division of Cardiology
      Boston, Massachusetts, United States
    • University of Alabama at Birmingham
      • Department of Medicine
      Birmingham, Alabama, United States
  • 2002–2007
    • The University of Chicago Medical Center
      • Department of Cardiology
      Chicago, Illinois, United States
  • 1987–2007
    • Henry Ford Hospital
      • Department of Internal Medicine
      Detroit, Michigan, United States
  • 2006
    • European Hospital
      Roma, Latium, Italy
    • The institute for clinical research and development
      San José, California, United States
  • 2002–2006
    • University of North Carolina at Chapel Hill
      • Department of Medicine
      North Carolina, United States
  • 1998–2006
    • Sapienza University of Rome
      • Department of Cardiovascular, Respiratory, Nephrologic and Geriatric Sciences
      Roma, Latium, Italy
  • 2005
    • University of Michigan
      Ann Arbor, Michigan, United States
  • 1997
    • Northeastern Illinois University
      Chicago, Illinois, United States
  • 1989
    • Virginia Hospital Center
      Arlington, Virginia, United States
  • 1986
    • Baylor College of Medicine
      • Section of Cardiology
      Houston, Texas, United States
  • 1985–1986
    • University of Virginia
      Charlottesville, Virginia, United States
  • 1980–1984
    • Providence Hospital
      Mobile, Alabama, United States
  • 1983
    • National Heart, Lung, and Blood Institute
      베서스다, Maryland, United States