Steven E Nissen

South Australian Health and Medical Research Institute, Adelaide Hills, South Australia, Australia

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Publications (467)5730.54 Total impact

  • 12/2015; 10(4):191-192. DOI:10.1007/s12467-012-0144-6
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    ABSTRACT: Background: Bromodomain and extra-terminal (BET) proteins regulate transcription of lipoprotein and inflammatory factors implicated in atherosclerosis. The impact of BET inhibition on atherosclerosis progression is unknown. Methods: ASSURE was a double-blind, randomized, multicenter trial in which 323 patients with angiographic coronary disease and low high-density lipoprotein cholesterol (HDL-C) levels were randomized in a 3:1 fashion to treatment with the BET protein inhibitor RVX-208 200 mg or placebo for 26 weeks. Plaque progression was measured with serial intravascular ultrasound imaging. Lipid levels, safety, and tolerability were also assessed. Results: During treatment, apolipoprotein (apo)A-I increased by 10.6 % with placebo (P < 0.001 compared with baseline) and 12.8 % with RVX-208 (P < 0.001 compared with baseline), between groups P = 0.18. HDL-C increased by 9.1 % with placebo (P < 0.001 compared with baseline) and 11.1 % with RVX-208 (P < 0.001 compared with baseline), between groups P = 0.24. Low-density lipoprotein cholesterol (LDL-C) decreased by 17.9 % with placebo (P < 0.001 compared with baseline) and 15.8 % with RVX-208 (P < 0.001 compared with baseline), between groups P = 0.55. The primary endpoint, the change in percent atheroma volume, decreased 0.30 % in placebo-treated patients (P = 0.23 compared with baseline) and 0.40 % in the RVX-208 group (P = 0.08 compared with baseline), between groups P = 0.81. Total atheroma volume decreased 3.8 mm(3) in the placebo group (P = 0.01 compared with baseline) and 4.2 mm(3) in the RVX-208 group (P < 0.001 compared with baseline), P = 0.86 between groups. A greater incidence of elevated liver enzymes was observed in RVX-208-treated patients (7.1 vs. 0 %, P = 0.009). Conclusion: Administration of the BET protein inhibitor RVX-208 showed no greater increase in apoA-I or HDL-C or incremental regression of atherosclerosis than administration of placebo. Trial registration: identifier-NCT01067820.
    American Journal of Cardiovascular Drugs 09/2015; DOI:10.1007/s40256-015-0146-z · 2.42 Impact Factor
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    ABSTRACT: Background: Obesity is associated with adverse atherosclerotic cardiovascular events. While various metabolic abnormalities associated with obesity promote plaque formation, the morphological phenotype of atherosclerotic plaque has not been well characterized in the setting of obesity. Frequency-domain optical coherence tomography (FD-OCT) enables in vivo visualization of plaque microstructures associated with vulnerability. We characterized plaque microstructures in obese patients. Methods: FD-OCT imaging was performed in 308 patients with coronary artery disease undergoing percutaneous coronary intervention. Patients were stratified according to the presence or absence of obesity (body mass index > 30 kg/m(2)). Plaques in obese (n = 129) and non-obese (n = 179) patients were compared with regard to clinical characteristics and FD-OCT-derived features of plaque vulnerability. Results: Obese patients were more likely to be younger (p = 0.01), female (p = 0.01) and have a history of hypertension (p = 0.01). Higher levels of triglyceride (p < 0.0001) and glucose (p = 0.02), whereas a lower level of high-density lipoprotein cholesterol (HDL-C) (p = 0.02) was observed in obese patients. FD-OCT imaging demonstrated thinner fibrous caps (85.3 ± 31.1 vs 110.1 ± 32.4 µm, p = 0.01) and a higher prevalence of thin-cap fibroatheroma (28.8 vs 14.3%, p = 0.01) in obese patients, which remained significant after controlling for differences in clinical characteristics. Achieving a low-density lipoprotein cholesterol (LDL-C) level < 1.8 mmol/l was associated with thicker fibrous caps in obese patients, but only to the level observed in non-obese patients with suboptimal lipid control. Conclusions: Obese patients harbor more vulnerable plaques in association with atherogenic risk factors. The limited benefit of lipid control suggests the need to adopt novel anti-atherosclerotic strategies in higher-risk patients.
    09/2015; 22(10):1331-9. DOI:10.1177/2047487315598711
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    ABSTRACT: Objectives: Pathological studies demonstrate the dual significance of plaque burden (PB) and lipid composition for mediating coronary plaque vulnerability. We evaluated relationships between intravascular ultrasound (IVUS)-derived PB and arterial remodeling with near-infrared spectroscopy (NIRS)-derived lipid content in ex vivo and in vivo human coronary arteries. Approach and results: Ex vivo coronary NIRS and IVUS imaging was performed through blood in 116 coronary arteries of 51 autopsied hearts, followed by 2-mm block sectioning (n=2070) and histological grading according to modified American Heart Association criteria. Lesions were defined as the most heavily diseased 2-mm block per imaged artery on IVUS. IVUS-derived PB and NIRS-derived lipid core burden index (LCBI) of each block and lesion were analyzed. Block-level analysis demonstrated significant trends of increasing PB and LCBI across more complex atheroma (Ptrend <0.001 for both LCBI and PB). Lesion-based analyses demonstrated the highest LCBI and remodeling index within coronary fibroatheroma (Ptrend <0.001 and 0.02 versus all plaque groups, respectively). Prediction models demonstrated similar abilities of PB, LCBI, and remodeling index for discriminating fibroatheroma (c indices: 0.675, 0.712, and 0.672, respectively). A combined PB+LCBI analysis significantly improved fibroatheroma detection accuracy (c index 0.77, P=0.028 versus PB; net-reclassification index 43%, P=0.003), whereas further adding remodeling index did not (c index 0.80, P=0.27 versus PB+LCBI). In vivo comparisons of 43 age- and sex-matched patients (to the autopsy cohort) undergoing combined NIRS-IVUS coronary imaging yielded similar associations to those demonstrated ex vivo. Conclusions: Adding NIRS to conventional IVUS-derived PB imaging significantly improves the ability to detect more active, potentially vulnerable coronary atheroma.
    Arteriosclerosis Thrombosis and Vascular Biology 09/2015; DOI:10.1161/ATVBAHA.115.306118 · 6.00 Impact Factor
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    ABSTRACT: Objective: Lowering low-density lipoprotein cholesterol (LDL-C) with statins reduces cardiovascular events and slows plaque progression. While this therapeutic approach has been reported to favorably modify plaque composition, this is not well characterized in humans. Also, the benefit of achieving LDL-C levels below current recommended targets remains unknown. Frequency-domain optical coherence tomography (FD-OCT) enables visualization of plaque microstructures associated with plaque instability. We investigated plaque morphologies in patients with low LDL-C levels by using FD-OCT. Methods: 293 and 122 non-obstructive lipid and fibrous plaques in 280 stable statin-treated CAD patients were evaluated by FD-OCT imaging in vessels requiring percutaneous coronary intervention. Study subjects were stratified according to achieved LDL-C levels (<50, 50-70, 70-100, <100 mg/dL). FD-OCT derived plaque microstructures were compared. Results: LDL-C levels <50 mg/dL and <70 mg/dL were observed in 13.9% (39/280) and 29.2% (82/280) of patients, respectively. Patients with LDL-C <50 mg/dL were more likely to be older (p < 0.001) and receive a high-dose statin (p = 0.01). On FD-OCT imaging, patients with LDL-C <50 mg/dL were more likely to have fibrous plaque (51.7, 43.2, 22.2 and 12.3%, p = 0.01) and less likely to have lipid plaques (48.2, 56.7, 77.7 and 87.6%, p = 0.01). In addition, LDL-C level was significantly associated with lipid arc (173 ± 76, 175 ± 88, 196 ± 102 and 234 ± 85°, p = 0.01) and fibrous cap thickness (139.9 ± 93.9, 103.1 ± 66.4, 92.5 ± 48.5 and 92.1 ± 47.8 um, p = 0.001). In particular, the smallest lipid arc and thickest fibrous cap were observed in patients who achieved LDL-C <50 mg/dL. Multivariable analysis revealed LDL-C levels (beta coefficient -0.254, p = 0.009) and high-dose statin use (beta coefficient 1.814, p = 0.003) to independently associate with fibrous cap thickness. Conclusions: More stable plaque features were observed within non-obstructive atheromas in patients with very low LDL-C levels. These findings underscore LDL-C level to stabilize plaques in patients with CAD and high residual atherosclerotic risk.
    Atherosclerosis 08/2015; 242(2):490-495. DOI:10.1016/j.atherosclerosis.2015.08.005 · 3.99 Impact Factor
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    ABSTRACT: To determine the 2-year outcomes of Roux-en-Y gastric bypass (RYGB) and sleeve gastrectomy (SG) vs. intensive medical therapy (IMT) on lean body mass, total bone mass, and bone mineral density (BMD) measures from the STAMPEDE trial. 54 subjects (BMI: 36 ± 1 kg/m(2) , age: 48 ± 4 years) with type 2 diabetes (T2DM) (HbA1c : 9.7 ± 2%) were randomized to IMT, RYGB, or SG and underwent DXA at baseline and at 1 and 2 years. At 2 years, the reduction in BMI was similar after RYGB and SG and was greater than IMT (P < 0.001). Lean mass was reduced by ∼10%, total bone mineral content reduced by ∼8%, and hip BMD reduced by ∼9% in both surgical groups and was significantly greater than IMT despite increases in vitamin D intake in all groups. The change in hip BMD correlated with weight loss (r = 0.84, P < 0.0001) and changes in lean mass (r = 0.74, P < 0.0001) and leptin (r = 0.53, P < 0.0001). Peripheral fractures were self-reported in RYGB (4/18 patients), SG (2/19 patients), and IMT (4/16 patients). Surgically induced weight loss is associated with modest reductions in lean mass, bone mineral content, and BMD, despite calcium and vitamin D supplementation in patients with T2DM. Awareness for bone loss is indicated for patients undergoing bariatric procedures. © 2015 The Obesity Society.
    Obesity 07/2015; DOI:10.1002/oby.21150 · 3.73 Impact Factor
  • Journal of the American College of Cardiology 07/2015; 66(3):328-9. DOI:10.1016/j.jacc.2015.05.023 · 16.50 Impact Factor
  • Rishi Puri · Steven E Nissen · Stephen J Nicholls
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    ABSTRACT: Whether statins are equi-efficacious in women and men continues to be debated. The potential antiatherosclerotic effects of high-intensity statin therapy on coronary atheroma in women compared with men have only very recently been characterized. This review aims to summarize the evidence underlying these recent observations. Coronary intravascular ultrasound (IVUS) is a highly sensitive plaque imaging tool, and serial changes of plaque burden on IVUS are known to associate with incident cardiovascular events. Study of coronary atheroma by intravascular ultrasound: effect of rosuvastatin versus atorvastatin was a randomized controlled trial employing serial IVUS to evaluate the antiatherosclerotic efficacy of high-dose rosuvastatin and atorvastatin during a 24-month study period. Study of coronary atheroma by intravascular ultrasound: effect of rosuvastatin versus atorvastatin revealed significantly greater coronary atheroma regression in women compared with men, particularly in the setting of lower achieved LDL cholesterol. Results of this analysis also identified a significant interaction between sex and type of statin used. These findings support the broad use of statins, especially high-intensity statins, in women with coronary artery disease, who may in fact derive greater benefit than men. These findings also suggest the need for dedicated clinical trials involving women, supporting the notion of more personalized therapeutic strategies for tackling atherosclerotic disease.
    Current opinion in lipidology 06/2015; 26(4). DOI:10.1097/MOL.0000000000000195 · 5.66 Impact Factor
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    ABSTRACT: -Although dofetilide is widely used in the United States for rhythm control of atrial fibrillation (AF), there is limited post-approval safety data in the AF population despite its known risk of Torsade de pointes (TdP). -We conducted a retrospective chart review of a cohort of 1,404 patients initially loaded on dofetilide for AF suppression at the Cleveland Clinic from 2008-2012 to evaluate the incidence and risk factors for in-hospital adverse events as well as the long-term safety of continued use. Of the 17 patients with TdP during loading (1.2%), 10 had a cardiac arrest requiring resuscitation (one death), 5 had syncope/pre-syncope and 2 were asymptomatic. Dofetilide loading was stopped for 105 patients (7.5%) due to QTc prolongation or TdP. Variables correlated with TdP were 1) female gender, 2) 500 mcg dose, 3) reduced ejection fraction, and 4) increase in QTc from baseline. One-year all-cause mortality was higher in patients who continued dofetilide compared to those who discontinued use (HR 2.48, 95%CI 1.08 to 5.71, p=0.03). Those patients who had a TdP event had higher one-year all-cause mortality than those who did not (17.6% vs. 3% at one year, p<0.001). -Dofetilide loading has a low but finite risk of TdP and other adverse events that warrant the current FDA-mandated practice of inpatient monitoring during drug loading. In this cohort, all-cause mortality was higher at one year in those patients continued on dofetilide as well as in those patients who experienced TdP while loading.
    Circulation Arrhythmia and Electrophysiology 06/2015; 8(4). DOI:10.1161/CIRCEP.114.002339 · 4.51 Impact Factor
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    Steven E Nissen
    JAMA The Journal of the American Medical Association 05/2015; 313(18):1813-1814. DOI:10.1001/jama.2015.4138 · 35.29 Impact Factor
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    ABSTRACT: Aortic atherosclerosis has been linked with worse peri- and post-procedural outcomes following a range of aortic procedures. Yet, there are currently no standardized methods for non-invasive volumetric pan-aortic plaque assessment. We propose a novel means of more accurately assessing plaque volume across whole aortic segments using computed tomography angiography (CTA) imaging. Sixty patients who underwent CTA prior to trans-catheter aortic valve implantation were included in this analysis. Specialized software analysis (3mensio Vascular™, Pie Medical, Maastricht, Netherlands) was used to reconstruct images using a centerline approach, thus creating true cross-sectional aortic images, akin to those images produced with intravascular ultrasonography. Following aortic segmentation (from the aortic valve to the renal artery origin), atheroma areas were measured across multiple contiguous evenly spaced (10 mm) cross-sections. Percent atheroma volume (PAV), total atheroma volume (TAV) and calcium score were calculated. In our populations (age 79.9 ± 8.5 years, male 52 %, diabetes 27 %, CAD 84 %, PVD 20 %), mean ± SD number of cross sections measured for each patient was 35.1 ± 3.5 sections. Mean aortic PAV and TAV were 33.2 ± 2.51 % and 83,509 ± 17,078 mm3, respectively. Median (IQR) calcium score was 1.5 (0.7–2.5). Mean (SD) inter-observer coefficient of variation and agreement for plaque area among 4 different analysts was 14.1 (5.4), and the mean (95 % CI) Lin’s concordance correlation coefficient was 0.79 (0.62–0.89), effectively simulating a Core Laboratory scenario. We provide an initial validation of cross-sectional volumetric aortic atheroma assessment using CTA. This proposed methodology highlights the potential for utilizing non-invasive aortic plaque imaging for risk prediction across a range of clinical scenarios.
    The International Journal of Cardiovascular Imaging 05/2015; DOI:10.1007/s10554-015-0674-2 · 1.81 Impact Factor
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    ABSTRACT: Background: Statins can regress coronary atheroma and lower clinical events. Although pre-clinical studies suggest procalcific effects of statins in vitro, it remains unclear if statins can modulate coronary atheroma calcification in vivo. Objectives: This study compared changes in coronary atheroma volume and calcium indices (CaI) in patients receiving high-intensity statin therapy (HIST), low-intensity statin therapy (LIST), and no-statin therapy. Methods: In a post-hoc patient-level analysis of 8 prospective randomized trials using serial coronary intravascular ultrasound, serial changes in coronary percent atheroma volume (PAV) and CaI were measured across matched coronary segments in patients with coronary artery disease. Results: Following propensity-weighted adjustment for differences in baseline and changes in clinical, laboratory, and ultrasonic characteristics, HIST (n = 1,545) associated with PAV regression from baseline (-0.6 ± 0.1%; p < 0.001), whereas both LIST (n = 1,726) and no-statin therapy (n = 224) associated with PAV progression (+0.8 ± 0.1% and +1.0 ± 0.1%; p < 0.001, respectively; p < 0.001 for both HIST vs. LIST and HIST vs. no-statin; p = 0.35 for LIST vs. no-statin). Significant increases in CaI from baseline were noted across all groups (median [interquartile range] HIST, +0.044 [0.0-0.12]; LIST, +0.038 [0.0-0.11]; no-statin, +0.020 [0.0-0.10]; p < 0.001 for all), which could relate to statin intensity (p = 0.03 for LIST vs. no-statin; p = 0.007 for HIST vs. no-statin; p = 0.18 for HIST vs. LIST). No correlations were found between changes in CaI and on-treatment levels of atherogenic and antiatherogenic lipoproteins, and C-reactive protein, in either of the HIST groups or the no-statin group. Conclusions: Independent of their plaque-regressive effects, statins promote coronary atheroma calcification. These findings provide insight as to how statins may stabilize plaque beyond their effects on plaque regression.
    Journal of the American College of Cardiology 04/2015; 65(13). DOI:10.1016/j.jacc.2015.01.036 · 16.50 Impact Factor
  • Diabetes Care 03/2015; 38(3):e32-3. DOI:10.2337/dc14-2035 · 8.42 Impact Factor
  • Journal of the American College of Cardiology 03/2015; 65(10):A1591. DOI:10.1016/S0735-1097(15)61591-1 · 16.50 Impact Factor
  • Journal of the American College of Cardiology 03/2015; 65(10):A1411. DOI:10.1016/S0735-1097(15)61411-5 · 16.50 Impact Factor
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    ABSTRACT: Lowering low-density lipoprotein cholesterol (LDL-C) with statins has been demonstrated to slow plaque progression. This antiatherosclerotic effect in patients with minimal LDL-C lowering has not been investigated. Six hundred forty-seven patients with angiographic coronary artery disease who were commenced on statin therapy underwent serial imaging with intravascular ultrasound. Responders were defined as a percentage reduction in LDL-C of <15%. Disease progression was compared in responders (n=517) and hyporesponders (n=130) to statin therapy. Twenty percentage of patients demonstrated minimal changes in LDL-C, despite commencement of statin therapy. Statin hyporesponders were younger (55 versus 57 years; P=0.01), more likely to be male (79% versus 66%; P=0.005), and obese (body mass index, 31.5±6.1 versus 30.3±5.9 kg/m(2); P=0.04) and less likely to have a history of dyslipidemia (50% versus 66%; P<0.001). Baseline levels of systolic blood pressure (127±15 versus 132±17 mm Hg; P=0.01) and LDL-C (2.5±0.6 versus 3.4±0.8 mmol/L; P<0.001) were lower in statin hyporesponders. Baseline percent atheroma volume was similar between statin hyporesponders and responders (36.9±9.8% versus 38.3±9.2%; P=0.13). On serial evaluation, greater progression of percent atheroma volume (1.19±0.48% versus 0.09±0.43%; P=0.003) was observed in statin hyporesponders. After adjusting for baseline clinical characteristics and measures of plaque burden, statin hyporesponders still exhibited greater atheroma progression (+0.83±0.58% versus -0.21±0.52%; P=0.006). A substantial proportion of patients with coronary artery disease fail to achieve effective reductions in LDL-C, despite prescription of statin therapy. Greater progression of atherosclerosis is observed in these patients. Our current study underscores monitoring LDL-C level after the commencement of statin to ensure adequate response to statin therapy. © 2015 American Heart Association, Inc.
    Arteriosclerosis Thrombosis and Vascular Biology 02/2015; 35(4). DOI:10.1161/ATVBAHA.114.304477 · 6.00 Impact Factor
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    ABSTRACT: Controversy exists regarding benefits of raising HDL-C in statin-treated coronary artery disease (CAD) patients. We assessed the anti-atherosclerotic efficacy of raising HDL-C in statin-treated individuals with CAD across a range of achieved LDL-C, including lower (<70 mg/dL) versus higher (≥70 mg/dL) levels. In seven prospective randomized trials utilizing serial coronary intravascular ultrasound, 3469 statin-treated CAD patients were stratified according to achieved LDL-C (< vs ≥70 mg/dL) and changes in HDL-C (≥ vs < median), as well as across a broader spectrum of changes in HDL-C and achieved LDL-C levels. Changes in coronary percent atheroma volume and MACE (cardiovascular death, non-fatal MI, stroke, coronary revascularization, hospitalization for unstable angina) were evaluated across these groups. Overall, median change in HDL-C was +6.03%, and mean achieved LDL-C in the lower and higher LDL-C groups were 55.1 ± 11 and 97.4 ± 22 mg/dL, respectively. Following multivariable adjustment, in patients with achieved LDL-C < 70 mg/dL, greater HDL-C-raising did not associate with disease progression/regression. In those with achieved LDL-C ≥ 70 mg/dL, greater HDL-C-raising associated with less disease progression (OR 0.80 (95% CI 0.67, 0.97)) and MACE (HR 0.78 (95% CI 0.64, 0.96)). Greater increases in HDL-C (up to 25% from baseline) across the continuous range of on-treatment LDL-C levels associated with less disease progression )OR 0.90 (95% CI 0.83, 0.98)) and lower MACE (HR 0.87 (95% CI 0.77, 0.998)). Increasing HDL-C via a broad spectrum of mechanisms appears beneficial in statin-treated CAD patients, but is likely of greater benefit in patients with achieved LDL-C levels ≥70 mg/dL. © The European Society of Cardiology 2015 Reprints and permissions:
    European Journal of Preventive Cardiology 02/2015; DOI:10.1177/2047487315572920 · 3.32 Impact Factor
  • Journal of the American College of Cardiology 02/2015; 65(6):630-632. DOI:10.1016/j.jacc.2014.11.039 · 16.50 Impact Factor
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    ABSTRACT: Objective This study investigated the effect of type 2 diabetes duration on glucose regulation 24 months post-bariatric surgery.Methods Twenty-seven adults with short- (<5 years) and long-duration (≥10 years) type 2 diabetes received a mixed-meal tolerance test at baseline and 24 months postsurgery. Body weight, insulin sensitivity, first- and second-phase meal-stimulated insulin secretion, disposition index (i.e., DI or pancreatic β-cell function), and incretin responses were examined.ResultsAdults with short-duration type 2 diabetes had better HbA1c, greater insulin secretory capacity, and greater DI compared with adults with long-duration type 2 diabetes, despite similar weight loss and incretin responses. Diabetes duration correlated with smaller improvements in HbA1c and DI but not weight loss.Conclusions Enhanced β-cell function characterizes the effect of bariatric surgery in adults with diabetes for <5 years, independent of weight loss or incretins. Additional therapy postsurgery may be required to improve glycemia for people with long-standing type 2 diabetes.
    Obesity 02/2015; 23(3). DOI:10.1002/oby.21021 · 3.73 Impact Factor
  • Heart, Lung and Circulation 01/2015; 24:S331. DOI:10.1016/j.hlc.2015.06.512 · 1.44 Impact Factor

Publication Stats

29k Citations
5,730.54 Total Impact Points


  • 2015
    • South Australian Health and Medical Research Institute
      Adelaide Hills, South Australia, Australia
  • 2013–2015
    • University of Adelaide
      • South Australian Research and Development Institute (SARDI)
      Tarndarnya, South Australia, Australia
  • 2001–2015
    • Cleveland Clinic
      • • Department of Cardiology
      • • Department of Cardiovascular Medicine
      Cleveland, Ohio, United States
    • Stanford University
      Stanford, California, United States
  • 2010–2014
    • Metropolitan Heart and Vascular Institute
      Minneapolis, Minnesota, United States
  • 1991–2012
    • Case Western Reserve University
      • • Division of General Internal Medicine and Geriatrics
      • • Department of Biomedical Engineering
      • • Department of Epidemiology and Biostatistics
      Cleveland, Ohio, United States
    • Lexington VA Medical Center
      Washington, Washington, D.C., United States
  • 2011
    • University of Florida
      Gainesville, Florida, United States
    • Queen's University Belfast
      • Centre for Public Health
      Béal Feirste, Northern Ireland, United Kingdom
  • 2008
    • Sungkyunkwan University
      Sŏul, Seoul, South Korea
  • 2007
    • Northwestern University
      Evanston, Illinois, United States
    • Washington Hospital Center
      Washington, Washington, D.C., United States
  • 2005–2007
    • Montreal Heart Institute
      Montréal, Quebec, Canada
    • The Ohio State University
      Columbus, Ohio, United States
  • 1994–2007
    • American College of Cardiology
      Washington, Washington, D.C., United States
  • 2006
    • University of Colorado
      Denver, Colorado, United States
    • Baylor College of Medicine
      Houston, Texas, United States
    • Brigham and Women's Hospital
      Boston, Massachusetts, United States
  • 2004
    • University of California, San Diego
      • Department of Medicine
      San Diego, California, United States
  • 2003
    • University of Washington Seattle
      Seattle, Washington, United States
    • Toho University
      Edo, Tōkyō, Japan
    • Hospital of the University of Pennsylvania
      • Division of Cardiovascular Medicine
      Filadelfia, Pennsylvania, United States
    • Lerner Research Institute
      Cleveland, Ohio, United States
  • 2001–2003
    • Yale University
      • Section of Cardiovascular Medicine
      New Haven, Connecticut, United States
  • 2000
    • University of Pennsylvania
      Filadelfia, Pennsylvania, United States
  • 1998
    • Cleveland Clinic Laboratories
      Cleveland, Ohio, United States
  • 1994–1995
    • National Cerebral and Cardiovascular Center
      • Department of Cardiovascular Medicine
      Ōsaka, Ōsaka, Japan
  • 1990–1992
    • Lexington Medical Center
      West Columbia, South Carolina, United States
  • 1987–1991
    • University of Kentucky
      • • Department of Medicine
      • • College of Medicine
      Lexington, Kentucky, United States
  • 1989
    • Università di Pisa
      • Department of Clinical and Experimental Medicine
      Pisa, Tuscany, Italy
  • 1986
    • United States Department of Veterans Affairs
      Бедфорд, Massachusetts, United States