Mihai Gheorghiade

Northwestern University, Evanston, Illinois, United States

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Publications (770)5514.7 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
  • Hussein Abu Daya · Mihai Gheorghiade · Erik B. Schelbert ·

    Circulation 11/2015; 132(21):e248-e248. DOI:10.1161/CIRCULATIONAHA.115.017796 · 14.43 Impact Factor
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    ABSTRACT: Heart failure is a clinical syndrome that manifests from various cardiac and noncardiac abnormalities. Accordingly, rapid and readily accessible methods for diagnosis and risk stratification are invaluable for providing clinical care, deciding allocation of scare resources, and designing selection criteria for clinical trials. Natriuretic peptides represent one of the most important diagnostic and prognostic tools available for the care of heart failure patients. Natriuretic peptide testing has the distinct advantage of objectivity, reproducibility, and widespread availability.The concept of tailoring heart failure management to achieve a target value of natriuretic peptides has been tested in various clinical trials and may be considered as an effective method for longitudinal biomonitoring and guiding escalation of heart failure therapies with overall favorable results.Although heart failure trials support efficacy and safety of natriuretic peptide-guided therapy as compared with usual care, the relationship between natriuretic peptide trajectory and clinical benefit has not been uniform across the trials, and certain subgroups have not shown robust benefit. Furthermore, the precise natriuretic peptide value ranges and time intervals of testing are still under investigation. If natriuretic peptides fail to decrease following intensification of therapy, further work is needed to clarify the optimal pharmacologic approach. Despite decreasing natriuretic peptide levels, some patients may present with other high-risk features (e.g. elevated troponin). A multimarker panel investigating multiple pathological processes will likely be an optimal alternative, but this will require prospective validation.Future research will be needed to clarify the type and magnitude of the target natriuretic peptide therapeutic response, as well as the duration of natriuretic peptide-guided therapy in heart failure patients.
    Journal of Cardiovascular Medicine 11/2015; DOI:10.2459/JCM.0000000000000392 · 1.51 Impact Factor
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    ABSTRACT: Background: The association between natriuretic peptides and clinical outcome in asymptomatic hypertensive and diabetic patients with no clinical evidence of heart failure (HF) is still unclear. We assessed the prognostic value of NT-pro BNP, and its interactions with age and gender, in a cohort of asymptomatic, stage A/B HF hypertensive and diabetic patients enrolled in primary care. Methods: NT-proBNP was measured in 1012 asymptomatic subjects with systemic hypertension and/or type-2 diabetes (age 66.6 ± 7.8 years, 48 % males) with no clinical evidence of HF. Patients were prospectively followed over 49.8 ± 6.7 months for the development of cardiac death, HF hospitalization, and nonfatal myocardial infarction. Results: Patients with NT-proBNP above the 80th age- and gender-specific percentile showed a threefold risk of events as compared to those with NT-proBNP under this cut-off [hazard ratio 3.2 (2.6-8.3), p < 0.0001]. In multivariable analysis, NT-proBNP added independent and incremental prognostic information to a predictive model including established risk factors (p < 0.0001). After stratification by age, increased NT-proBNP predicted outcome among patients in the second and third age tertiles, but not among those in the first tertile. Increased NT-proBNP was associated with a 3.6-fold risk in women and a 2.9-fold risk in men. Addition of the gender-NT-proBNP interaction to prognostic models further improved prediction of events (p = 0.014). Conclusions: NT-proBNP measurement adds independent and incremental information for the prediction of clinical outcome in asymptomatic, stage A-B HF hypertensive and diabetic patients taken from primary care. This prognostic value might be further evident in the elderly and among women.
    Clinical Research in Cardiology 11/2015; DOI:10.1007/s00392-015-0937-x · 4.56 Impact Factor
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    ABSTRACT: Importance: Worsening chronic heart failure (HF) is a major public health problem. Objective: To determine the optimal dose and tolerability of vericiguat, a soluble guanylate cyclase stimulator, in patients with worsening chronic HF and reduced left ventricular ejection fraction (LVEF). Design, setting, and participants: Dose-finding phase 2 study that randomized 456 patients across Europe, North America, and Asia between November 2013 and January 2015, with follow-up ending June 2015. Patients were clinically stable with LVEF less than 45% within 4 weeks of a worsening chronic HF event, defined as worsening signs and symptoms of congestion and elevated natriuretic peptide level requiring hospitalization or outpatient intravenous diuretic. Interventions: Placebo (n = 92) or 1 of 4 daily target doses of oral vericiguat (1.25 mg [n = 91], 2.5 mg [n = 91], 5 mg [n = 91], 10 mg [n = 91]) for 12 weeks. Main outcomes and measures: The primary end point was change from baseline to week 12 in log-transformed level of N-terminal pro-B-type natriuretic peptide (NT-proBNP). The primary analysis specified pooled comparison of the 3 highest-dose vericiguat groups with placebo, and secondary analysis evaluated a dose-response relationship with vericiguat and the primary end point. Results: Overall, 351 patients (77.0%) completed treatment with the study drug with valid 12-week NT-proBNP levels and no major protocol deviation and were eligible for primary end point evaluation. In primary analysis, change in log-transformed NT-proBNP levels from baseline to week 12 was not significantly different between the pooled vericiguat group (log-transformed: baseline, 7.969; 12 weeks, 7.567; difference, -0.402; geometric means: baseline, 2890 pg/mL; 12 weeks, 1932 pg/mL) and placebo (log-transformed: baseline, 8.283; 12 weeks, 8.002; difference, -0.280; geometric means: baseline, 3955 pg/mL; 12 weeks, 2988 pg/mL) (difference of means, -0.122; 90% CI, -0.32 to 0.07; ratio of geometric means, 0.885, 90% CI, 0.73-1.08; P = .15). The exploratory secondary analysis suggested a dose-response relationship whereby higher vericiguat doses were associated with greater reductions in NT-proBNP level (P < .02). Rates of any adverse event were 77.2% and 71.4% among the placebo and 10-mg vericiguat groups, respectively. Conclusions and relevance: Among patients with worsening chronic HF and reduced LVEF, compared with placebo, vericiguat did not have a statistically significant effect on change in NT-proBNP level at 12 weeks but was well-tolerated. Further clinical trials of vericiguat based on the dose-response relationship in this study are needed to determine the potential role of this drug for patients with worsening chronic HF. Trial registration: clinicaltrials.gov Identifier: NCT01951625.
    JAMA The Journal of the American Medical Association 11/2015; DOI:10.1001/jama.2015.15734 · 35.29 Impact Factor
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    ABSTRACT: Over the past 1.5 decades, numerous stem cell trials have been performed in patients with cardiovascular disease. Although encouraging outcome signals have been reported, these have been small, leading to uncertainty as to whether they will translate into significantly improved outcomes. A reassessment of the rationale for the use of stem cells in cardiovascular disease is therefore timely. Such a rationale should include analyses of why previous trials have not produced significant benefit and address whether mechanisms contributing to disease progression might benefit from known activities of stem cells. The present paper provides such a reassessment, focusing on patients with left ventricular systolic dysfunction, either nonischemic or ischemic. We conclude that many mechanisms contributing to progressive left ventricular dysfunction are matched by stem cell activities that could attenuate the myocardial effect of such mechanisms. This suggests that stem cell strategies may improve patient outcomes and justifies further testing.
    Journal of the American College of Cardiology 11/2015; 66(18):2038-2047. DOI:10.1016/j.jacc.2015.09.010 · 16.50 Impact Factor
  • Waqas Qureshi · javed butler · Sean P. Collins · Alec Moorman · Mihai Gheorghiade ·
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    ABSTRACT: Hospitalization for heart failure is common condition and refers to the various acute heart failure syndromes that require urgent treatment. The chapter provides an overview of the classification, pathophysiology, management principles and current treatment modalities for hospitalization for heart failure. It also emphasizes the various diagnostic as well as prognostic evaluations of heart failure patients. However, the understanding and treatment still remains deficient in the wake of development of newer drugs, devices and novel approaches to decrease this immense health care problem that can improve morbidity, mortality and quality of life of our patients.
    Management of Heart Failure: Volume 1, 2nd edited by Baliga RR, Haas GJ, 10/2015: chapter 6: pages 113-149; Springer., ISBN: 978-1-4471-6656-6
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    ABSTRACT: Aims: This article describes an ongoing study investigating the safety and efficacy of ischemia-tolerant mesenchymal stem cell (MSC) therapy in patients with nonischemic heart failure and dysfunctional viable myocardium without scarring. This study will follow principles of the previously described mechanistic translational-phase concept whereby the effect of the study agent on laboratory and imaging markers of cardiac structure and function will be tested in a small homogenous cohort with the goal to enhance the understanding of the effect of interventions on cardiac remodeling and performance. Study design: This single-blind, placebo-controlled, crossover, multicenter, randomized study will assess the safety, tolerability, and preliminary efficacy of a single intravenous (i.v.) dose of allogeneic ischemia-tolerant MSCs in individuals with heart failure of nonischemic cause, ejection fraction 40% or less, and dysfunctional viable myocardium who have been receiving guideline-directed medical therapy. Eligible patients will have no evidence of baseline replacement scarring on delayed-enhancement cardiac magnetic resonance (CMR). Approximately 20 patients will be randomized in a 1 : 1 ratio to receive an i.v. infusion of ischemia-tolerant MSCs or placebo. At 90 days, the two groups will undergo crossover and received the alternative treatment. The primary endpoint is safety, as evaluated through at least 1-year post-MSC infusion. Additional efficacy endpoints will include measures of cardiac structure and function, as evaluated by serial cine-CMR and transthoracic echocardiography at 90 and 180 days post-initial infusion. Conclusion: This pilot study will explore the safety and effects on cardiac structure and function of i.v. injection of ischemia-tolerant MSCs in a small homogenous cohort of nonischemic heart failure patients with reduced ejection fraction and absent replacement scarring on CMR. This study also represents a prospective mechanistic translational-phase study using baseline and serial CMR imaging in heart failure patients and serves as a potential model for design of future heart failure trials (ClinicalTrials.gov identifier: NCT02467387).
    Journal of Cardiovascular Medicine 10/2015; DOI:10.2459/JCM.0000000000000303 · 1.51 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
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    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; 116(8). DOI:10.1016/j.amjcard.2015.07.049 · 3.28 Impact Factor
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    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

Publication Stats

29k Citations
5,514.70 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
  • 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
    • University of Wisconsin - Milwaukee
      Milwaukee, Wisconsin, United States
    • Medtronic
      Minneapolis, Minnesota, 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
    • University of California, Los Angeles
      • Department of Medicine
      Los Ángeles, California, United States
    • Attikon University Hospital
      • Department of Cardiology
      Athínai, Attica, Greece
  • 2007
    • University of Alabama at Birmingham
      • Department of Medicine
      Birmingham, Alabama, United States
    • Tufts Medical Center
      • Division of Cardiology
      Boston, Massachusetts, 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
    • The institute for clinical research and development
      San José, California, United States
  • 2004-2006
    • Sapienza University of Rome
      • Department of Cardiovascular, Respiratory, Nephrologic and Geriatric Sciences
      Roma, Latium, Italy
  • 2002-2006
    • University of North Carolina at Chapel Hill
      • Department of Medicine
      North Carolina, United States
  • 1998
    • San Francisco VA Medical Center
      San Francisco, California, 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
  • 1984
    • Brown University
      Providence, Rhode Island, United States
  • 1983
    • National Heart, Lung, and Blood Institute
      베서스다, Maryland, United States
  • 1980
    • Providence Hospital
      Mobile, Alabama, United States