Amir Lerman

Mayo Foundation for Medical Education and Research, Rochester, Michigan, United States

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Publications (527)3363.29 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Spontaneous coronary artery dissection (SCAD) is an increasingly recognized nonatherosclerotic cause of acute coronary syndrome. The angiographic characteristics of SCAD are largely undetermined. The goal of this study was to determine the prevalence of coronary tortuosity in SCAD and whether it may be implicated in the disease.
    Circulation Cardiovascular Interventions 08/2014; · 6.54 Impact Factor
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    ABSTRACT: Endothelial progenitor cells (EPCs) participate in renal repair, but their number and function may be impaired by exposure to cardiovascular risk factors. The number of circulating EPCs is decreased in essential and renovascular hypertensive patients, but the effects of hypertension on EPC function are incompletely understood. We hypothesized that EPC function was preserved under well-controlled conditions in treated hypertensive patients. Patients with atherosclerotic renal artery stenosis (ARAS; n=22) or essential hypertension (n=24) were studied during controlled sodium intake and antihypertensive regimen. Late-outgrowth EPCs were isolated from the inferior vena cava (IVC) and renal vein blood of ARAS and essential hypertension patients and a peripheral vein of matched normotensive controls (n=18). The angiogenic function of EPCs was assessed in vitro, and multidetector computed tomography was used to measure single-kidney hemodynamics and function in ARAS and essential hypertension patients. Inflammatory biomarkers and EPC homing signal levels and renal release were calculated. Inferior vena cava and renal vein-obtained EPC function were similar in ARAS and essential hypertension patients and comparable to that in normal controls (tube length, 171.86±16.846, 191.09±14.222, 174.925±19.774 μm, respectively). Function of renal vein-obtained EPCs directly correlated with stenotic kidney glomerular filtration rate, EPC homing factors, and anti-inflammatory mediator levels in ARAS patients. Therefore, EPC function was relatively preserved in ARAS patients, although it directly correlated with renal function. Adequate EPC function supports the feasibility of using autologous EPCs as a therapeutic option in essential and renovascular hypertensive patients. Homing signals and inflammatory mediators may potentially regulate EPC angiogenic function.
    Hypertension 07/2014; · 6.87 Impact Factor
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    ABSTRACT: The aim of this study was to determine if renin inhibition is able to improve the survival of transplanted stem cells in a mouse model of myocardial infarction. Myocardial infarction was induced in FVB/NJ inbred mice (n = 23). Bone marrow-derived mouse mesenchymal stromal cells (mMSCs, 3 × 10(5)) expressing the reporter gene firefly luciferase were delivered intramyocardially (n = 12) and monitored non-invasively by bioluminescence imaging. A group of these mice (n = 6) received aliskiren (15 mg/kg/day) via an osmotic pump implanted subcutaneously. The survival of mMSCs was significantly increased in those animals that received aliskiren leading to a significant improvement in systolic function after myocardial infarction. Histological analysis revealed a significant reduction in inflammation and collagen deposition in those mice that received aliskiren compared to controls. Renin inhibition of the ischemic myocardium is able to modulate the microenvironment improving the survival and efficacy of transplanted mMSCs in a mouse model of myocardial infarction.
    Journal of Cardiovascular Translational Research 07/2014; · 3.06 Impact Factor
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    ABSTRACT: Erectile dysfunction (ED) is associated with an increased risk for cardiovascular disease, stroke, and all-cause mortality, independent of conventional cardiovascular risk factors. Coronary endothelial dysfunction is independently associated with ED in men with early coronary atherosclerosis. We aimed to investigate whether coronary microvascular dysfunction predicts development of ED in patients presenting with coronary atherosclerosis without critical stenoses.
    Coronary artery disease. 07/2014;
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    ABSTRACT: This study aims to investigate trends of cardiovascular disease (CVD) risk factor profiles over 17 years in percutaneous coronary intervention (PCI) patients at the Mayo Clinic.
    07/2014; 47(4):216-29.
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    ABSTRACT: The mechanisms responsible for renal injury in atherosclerotic renovascular disease (ARVD) are incompletely understood, and few therapeutic options are available to reverse it. We hypothesized that chronic renal damage involves mitochondrial injury, and that mitochondrial protection would reduce renal fibrosis and dysfunction in ARVD pigs.
    Cardiovascular research. 06/2014;
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    ABSTRACT: Endothelial dysfunction is highly prevalent and associated with adverse outcomes among patients without obstructive coronary artery disease (CAD). Angiotensin II inhibition may improve endothelial function, but with continued treatment, "aldosterone escape" may occur. Thus, it is unknown if adding aldosterone blockade further improves endothelial function.
    American heart journal. 06/2014; 167(6):826-32.
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    ABSTRACT: Renovascular hypertension alters cardiac structure and function. Autophagy is activated during left ventricular hypertrophy and linked to adverse cardiac function. The angiotensin II receptor blocker, valsartan, lowers blood pressure and is cardioprotective, but whether it modulates autophagy in the myocardium is unclear. We hypothesized that valsartan would alleviate autophagy and improve left ventricular myocardial mitochondrial turnover in swine renovascular hypertension. Domestic pigs were randomized to control, unilateral renovascular hypertension, and renovascular hypertension treated with valsartan (320 mg/d) or conventional triple therapy (reserpine+hydralazine+hydrochlorothiazide) for 4 weeks after 6 weeks of renovascular hypertension (n=7 each group). Left ventricular remodeling, function, and myocardial oxygenation and microcirculation were assessed by multidetector computer tomography, blood oxygen level-dependent MRI, and microcomputer tomography. Myocardial autophagy, markers for mitochondrial degradation and biogenesis, and mitochondrial respiratory-chain proteins were examined ex vivo. Renovascular hypertension induced left ventricular hypertrophy and myocardial hypoxia, enhanced cellular autophagy and mitochondrial degradation, and suppressed mitochondrial biogenesis. Valsartan and triple therapy similarly decreased blood pressure, but valsartan solely alleviated left ventricular hypertrophy, ameliorated myocardial autophagy and mitophagy, and increased mitochondrial biogenesis. In contrast, triple therapy only slightly attenuated autophagy and preserved mitochondrial proteins, but elicited no improvement in mitophagy. These data suggest a novel potential role of valsartan in modulating myocardial autophagy and mitochondrial turnover in renovascular hypertension-induced hypertensive heart disease, which may possibly bolster cardiac repair via a blood pressure-independent manner.
    Hypertension 04/2014; · 6.87 Impact Factor
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    ABSTRACT: Single nucleotide polymorphisms (SNPs) are the most common source of genetic variation. Although microvascular pathology is associated with cardiovascular events, genetic phenotypes causing microvascular disease remain largely unknown. This study identifies sex-specific SNPs associated with coronary microvascular dysfunction. Six hundred and forty-three patients without significant obstructive coronary heart disease were enrolled, referred for cardiac catheterization, and underwent invasive coronary microcirculatory assessment. Patient data were collected from 1529 autosomal SNPs and seven X chromosome SNPs, which were selected to represent the variability from 76 candidate genes with published associations with coronary vasoreactivity, angiogenesis, inflammation, vascular calcification, atherosclerosis risk factors, female hormones, blood coagulation, or coronary heart disease. Coronary flow reserve (CFR) was assessed by an intracoronary injection of adenosine. Patients were categorized according to a CFR above or below 2.5 and were stratified by sex.After adjusting for age, sex, and BMI, this study shows that SNPs within VEGFA and CDKN2B-AS1 are associated with abnormal CFR (P<0.005). SNPs within MYH15, VEGFA, and NT5E are associated with abnormal CFR in men. No SNPs were associated with abnormal CFR in women. Genetic variations within defined regions of VEGFA and CDKN2B-AS1 genes are associated with coronary microvascular dysfunction. Furthermore, sex-specific allelic variants within MYH15, VEGFA, and NT5E are associated with an increased risk of coronary microvascular dysfunction in men.
    Coronary artery disease 04/2014; · 1.56 Impact Factor
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    ABSTRACT: Atherosclerotic renovascular disease (ARVD) is associated with high rates of coronary events and predicts mortality among patients with coronary artery disease (CAD). However, the impact of coronary atherosclerosis on renal outcomes after revascularization of ARVD is unclear. We hypothesized that CAD negatively impacts renal functional outcomes among patients with ARVD undergoing renal artery revascularization. Patients with ARVD who underwent echocardiography at Mayo Clinic, Rochester, Minnesota, USA between 2004 and 2012 were identified retrospectively and included if they had ejection fraction more than 50%. Renal and overall outcomes were compared among atherosclerotic renovascular disease patients with coronary artery disease (ARVD-C, n = 75) and without coronary artery disease (ARVD, n = 56) , within 1 year from initial revascularization and included blood pressure control, renal function, and incident cardiovascular/cerebrovascular events. Degree of renal artery stenosis was similar in both groups. ARVD-C had higher prevalence of diabetes, peripheral artery disease (PAD), and cerebrovascular disease, and lower baseline renal function. Risk of developing end-stage renal disease was higher in ARVD-C (11 vs. 2%, P = 0.05). Despite better control of blood pressure and cholesterol levels, renal function postrevascularization worsened in 15% of ARVD-C compared with 2% of ARVD (P = 0.01). Differences in clinical outcomes remained statistically significant after adjustment for covariables, including sex, baseline blood pressure, renal function, underlying diabetes, cholesterol levels, and medications. Similar differences in clinical outcomes were also associated with PAD and cerebrovascular disease. CAD in patients with ARVD is a predictor of worse outcomes after renal revascularization, likely reflecting diffuse atherosclerotic disease. Further studies are needed to develop strategies to manage patients with vascular comorbidities and improve their outcomes.
    Journal of Hypertension 03/2014; · 4.22 Impact Factor
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    ABSTRACT: Background There is a paucity of data on the temporal trends of cardiovascular risk factors in patients undergoing percutaneous coronary intervention (PCI). We investigated the secular trends of risk profiles of patients undergoing PCI without prior history of cardiovascular disease (CVD).HypothesisCVD risk factors are changed over time.Methods This time-trend analysis from 1994 to 2010 was performed within the Mayo Clinic PCI Registry. Outcome measures were prevalence of CVD risk factors, including the Framingham risk score (FRS), at the time of admission for PCI.ResultsDuring this period, 12,055 patients without a history of CVD (mean age, 65.0 ± 12.4 years, 67% male) underwent PCI at the Mayo Clinic. Age distribution slightly shifted toward older age (P for trend <0.05), but sex did not change over time. Despite a higher prevalence of hypertension, hypercholesterolemia, and diabetes mellitus over time, actual blood pressure and lipid profiles improved (P for trend <0.001). Over time, FRS and 10-year CVD risk improved significantly (7.3 ± 3.2 to 6.5 ± 3.3, P for trend <0.001; and 11.0 to 9.0, P for trend <0.001, respectively). Body mass index, not included in the FRS, increased significantly (29.0 ± 5.2 to 30.1 ± 6.2 kg/m2, P for trend <0.001), whereas smoking prevalence did not change.Conclusions The current study demonstrates that although traditional FRS and its associated predicted 10-year cardiovascular risk declined over time, the prevalence of risk factors increased in patients undergoing PCI. The study suggests the need for a new risk-factor assessment in this patient population.
    Clinical Cardiology 03/2014; · 1.83 Impact Factor
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    ABSTRACT: Obesity associated with metabolic derangements (ObM) worsens the prognosis of patients with coronary artery stenosis (CAS), but the underlying cardiac pathophysiologic mechanisms remain elusive. We tested the hypothesis that ObM exacerbates cardiomyocyte loss distal to moderate CAS. Obesity-prone pigs were randomized to 4 groups (n=6 each): lean-sham, ObM-sham, lean-CAS, and ObM-CAS. Lean and ObM pigs were maintained on a 12-week standard or atherogenic diet, respectively, and left circumflex CAS then induced by placing local-irritant coils. Cardiac structure, function, and myocardial oxygenation were assessed 4 weeks later by computed-tomography and Blood-Oxygenation-Level-Dependent (BOLD)-magnetic resonance imaging (MRI), the microcirculation with micro-computed-tomography, and injury mechanisms by immunoblotting and histology. ObM pigs showed obesity, dyslipidemia, and insulin resistance. The degree of CAS (range 50-70%) was similar in lean and ObM pigs, and resting myocardial perfusion and global cardiac function remained unchanged. Increased angiogenesis distal to the moderate CAS observed in lean was attenuated in ObM pigs, which also showed microvascular dysfunction and increased inflammation (M1-macrophages, TNF-α expression), oxidative stress (gp91), hypoxia (BOLD-MRI), and fibrosis (Sirius-red and trichrome). Furthermore, lean-CAS showed increased myocardial autophagy, which was blunted in ObM pigs (downregulated expression of ULK1 and Atg-12, p<0.05 vs. lean CAS) and associated with marked apoptosis. The interaction diet xstenosis synergistically inhibited angiogenic, autophagic, and fibrogenic activities. ObM exacerbates structural and functional myocardial injury distal to moderate CAS with preserved myocardial perfusion, possibly due to impaired cardiomyocyte turnover.
    AJP Heart and Circulatory Physiology 02/2014; · 3.63 Impact Factor
  • Jing Li, Amir Lerman
    Circulation Journal 01/2014; · 3.58 Impact Factor
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    ABSTRACT: Background: Myocardial bridging (MB) results in compression of the coronary artery lumen in systole, extending into diastole with resultant hemodynamic alternation as reflected by fractional flow reserve (FFR). MB has also been associated with coronary endothelial dysfunction. The objective of this study was to investigate relationship between FFR with dobutamine challenge and coronary microvascular endothelial dysfunction in symptomatic MB. Methods and Results: Seventeen consecutive patients who had cardiac catheterization assessment of MB were enrolled. The patients were divided into 2 groups according to normal (% increase in coronary blood flow [%CBF] ≥50%, n=7) or impaired (%CBF <50%, n=10) coronary microvascular endothelial function assessed on vasoreactivity in the coronary artery with intracoronary infusion of acetylcholine (Ach). Myocardial ischemia was then assessed using FFR at rest and during i.v. dobutamine infusion challenge across the MB with intracoronary pressure wires. FFR was significantly decreased at peak dobutamine infusion compared to at rest in the impaired group (0.85±0.06 vs. 0.91±0.05, P=0.001), but not in the normal group (0.93±0.05 vs. 0.91±0.07, P=0.618). Both FFR at rest and at peak dobutamine infusion had a positive correlation with %CBF by Ach in the impaired group (r(2)=0.46, P=0.030; r(2)=0.52, P=0.018, respectively). Conclusions: Microvascular endothelial dysfunction was associated with decreased FFR at peak dobutamine stress in patients with symptomatic MB.
    Circulation Journal 01/2014; · 3.58 Impact Factor
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    ABSTRACT: Cardiovascular disease (CVD) is the leading cause of morbidity, mortality, and cost in Western society. Employer-sponsored work health programs (WHPs) and Web-based portals for monitoring and providing guidance based on participants' health risk assessments are emerging, yet online technologies to improve CVD health in the workplace are relatively unproven. We hypothesized that an online WHP, comprehensively addressing multiple facets of CVD, can be successfully implemented and improve the health of participants. A cohort of employees in Tennessee (n = 1,602) was subjected to a health risk assessment at baseline. Those who did not meet all 5 healthy benchmarks (n = 836)-body mass index, blood pressure, glucose, total cholesterol, and smoking status-were prospectively assigned to a Web-based personal health assistant and had repeat measurements taken at 90 days. Of those who both completed the personal health assistant program and underwent baseline plus 90-day assessments (508/836, 61%), 75% were female, mean age was 46.5 ± 11.1 years, and the mean number of risk factors at baseline was 1.1 ± 0.9 with a mean 10-year Framingham Risk Score of 2.9%. This cohort demonstrated a significant reduction in total cholesterol (P < .0001), low-density lipoprotein cholesterol (P < .0001), triglycerides (P < .0001), systolic blood pressure (P = .009), glucose (P = .004), weight (P = .001), and body mass index (P = .001). Most of the participants improved at least 1 risk factor. Framingham Risk 10-year cardiovascular risk percentages were significantly reduced (P = .003). This study in a prospective cohort of community-dwelling employees suggests that an online WHP can provide a viable means to improve surrogates of CVD risk factors.
    American heart journal 01/2014; 167(1):93-100. · 4.65 Impact Factor
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    ABSTRACT: Background Endothelial dysfunction is highly prevalent and associated with adverse outcomes among patients without obstructive coronary artery disease (CAD). Angiotensin II inhibition may improve endothelial function, but with continued treatment “aldosterone escape” may occur. Thus it is unknown if adding aldosterone blockade further improves endothelial function. Methods In a double-blind, parallel-group, repeated measures study, women with symptoms and signs of ischemia, no significant CAD, and coronary endothelial dysfunction receiving an angiotensin converting enzyme-inhibitor (ACE-I) or receptor blocker were randomized to aldosterone blockade or placebo. The primary outcome at 16 weeks was percent change in coronary diameter to ACh and secondary outcomes coronary flow reserve to adenosine, both adjusted for baseline reactivity. Results Forty-one women completed the treatment period with repeat coronary reactivity testing. Their mean age was 54 ± 10 years, body mass index 30 ± 7.4 kg/m2, 12% had diabetes, and 15% had metabolic syndrome. There were no significant differences between treatment groups. At baseline, the percent change in reference vessel coronary diameter to ACh was −5.0% in the aldosterone blockade group and −3.4% in the placebo group, and at 16 weeks, −7.2% in the aldosterone blockade group versus −14.3% in the placebo group (p = 0.15). At 16 weeks, the change in coronary flow reserve to intracoronary adenosine was −0.13 in the aldosterone blockade group versus −0.25 in the placebo group (p = 0.66). Conclusion Adding aldosterone receptor blockade to angiotensin II inhibition did not improve coronary endothelial or microvascular function among women with signs and symptoms of ischemia in the setting of non-obstructive CAD.
    American Heart Journal. 01/2014;
  • Joerg Herrmann, Amir Lerman
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    ABSTRACT: Over the past decades there have been great advancements in the survival outcome of patients with cancer. As a consequence, treatment regimens are being extended to patient populations, which would not have qualified in the past based on co-morbidities and age. Furthermore, the anti-cancer regimens, which have been and are being used, can cause considerable morbidity and even mortality. In fact, new drugs such as tyrosine kinase inhibitors have yielded unanticipated side effects in frequency and severity. The cardiovascular disease spectrum is an important element in all of these. In order to optimize the outcome of cancer patients with cardiovascular diseases existing prior to cancer treatment or developing as a consequence of it, a new discipline called “cardio-oncology” has evolved over the past few years. Herein we review the latest developments in this field including cardiotoxicities, vascular toxicities, and arrhythmias. This field is taking on more shape as cardiologists, oncologists, and hematologists are forming alliances, programs, and clinics, supported by the development of expert consensus statements on best management approaches and care of the cancer patient with cardiovascular diseases.
    Trends in Cardiovascular Medicine. 01/2014;
  • JACC. Cardiovascular imaging 01/2014; 7(1):103-4. · 14.29 Impact Factor
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    ABSTRACT: Objective To assess the safety and efficacy of extracorporeal shockwave myocardial revascularization (ESMR) therapy in treating patients with refractory angina pectoris. Patients and Methods A single-arm multicenter prospective trial to assess safety and efficacy of the ESMR therapy in patients with refractory angina (class III/IV angina) was performed. Screening exercise treadmill tests and pharmacological single-photon emission computed tomography (SPECT) were performed for all patients to assess exercise capacity and ischemic burden. Patients were treated with 9 sessions of ESMR to ischemic areas over 9 weeks. Efficacy end points were exercise capacity by using treadmill test as well as ischemic burden on pharmacological SPECT at 4 months after the last ESMR treatment. Safety measures included electrocardiography, echocardiography, troponin, creatine kinase, and brain natriuretic peptide testing, and pain questionnaires. Results Fifteen patients with medically refractory angina and no revascularization options were enrolled. There was a statistically significant mean increase of 122.3±156.9 seconds (38% increase compared with baseline; P=.01) in exercise treadmill time from baseline (319.8±157.2 seconds) to last follow-up after the ESMR treatment (422.1±183.3 seconds). There was no improvement in the summed stress perfusion scores after pharmacologically induced stress SPECT at 4 months after the last ESMR treatment in comparison to that at screening; however, SPECT summed stress score revealed that untreated areas had greater progression in ischemic burden vs treated areas (3.69±6.2 vs 0.31±4.5; P=.03). There was no significant change in the mean summed echo score from baseline to posttreatment (0.4±5.1; P=.70). The ESMR therapy was performed safely without any adverse events in electrocardiography, echocardiography, troponins, creatine kinase, or brain natriuretic peptide. Pain during the ESMR treatment was minimal (a score of 0.5±1.2 to 1.1±1.2 out of 10). Conclusion In this multicenter feasibility study, ESMR seems to be a safe and efficacious treatment for patients with refractory angina pectoris. However, larger sham-controlled trials will be required to confirm these findings.
    Mayo Clinic Proceedings 01/2014; 89(3):346–354. · 5.79 Impact Factor
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    ABSTRACT: Background p38 MAPK inhibition has potential myocardial protective effects. We assessed losmapimod, a potent oral p38 MAPK inhibitor, in patients with non-ST-segment elevation myocardial infarction (NSTEMI) in a double-blind, randomised, placebo-controlled trial. Methods From October, 2009, to November, 2011, NSTEMI patients were assigned oral losmapimod (7·5 mg or 15·0 mg loading dose followed by 7·5 mg twice daily) or matching placebo in a 3:3:2 ratio. Safety outcomes were serious adverse events and alanine aminotransferase (ALT) concentrations over 12 weeks, and cardiac events (death, myocardial infarction, recurrent ischaemia, stroke, and heart failure) at 90 days. Efficacy outcomes were high-sensitivity C-reactive protein (hsCRP) and B-type natriuretic peptide (BNP) concentrations at 72 h and 12 weeks, and troponin I area under the curve (AUC) over 72 h. The losmapimod groups were pooled for analysis. This trial is registered with ClinicalTrials.gov, number NCT00910962. Findings Of 535 patients enrolled, 526 (98%) received at least one dose of study treatment (losmapimod n=388 and placebo n=138). Safety outcomes did not differ between groups. HsCRP concentrations at 72 h were lower in the losmapimod group than in the placebo group (geometric mean 64·1 nmol/L, 95% CI 53·0–77·6 vs 110·8 nmol/L, 83·1–147·7; p=0·0009) but were similar at 12 weeks. Early geometric mean BNP concentrations were similar at 72 h but significantly lower in the losmapimod group at 12 weeks (37·2 ng/L, 95% CI 32·3–42·9 vs 49·4 ng/L, 38·7–63·0; p=0·04). Mean troponin I AUC values did not differ. Interpretation p38 MAPK inhibition with oral losmapimod was well tolerated in NSTEMI patients and might improve outcomes after acute coronary syndromes. Funding GlaxoSmithKline.
    Lancet. 01/2014;

Publication Stats

16k Citations
3,363.29 Total Impact Points

Institutions

  • 1991–2014
    • Mayo Foundation for Medical Education and Research
      • • Division of Cardiovascular Diseases
      • • Division of Nephrology and Hypertension
      • • Department of Internal Medicine
      • • Cardiorenal Research Laboratory
      • • Mayo Medical School
      Rochester, Michigan, United States
  • 1990–2014
    • Mayo Clinic - Rochester
      • • Department of Cardiovascular Diseases
      • • Department of Hospital Internal Medicine
      • • Department of Cardiovascular Surgery
      Rochester, Minnesota, United States
  • 2013
    • Columbia University
      New York City, New York, United States
    • University of Pittsburgh
      Pittsburgh, Pennsylvania, United States
  • 2012–2013
    • Konyang University
      Ronsan, South Chungcheong, South Korea
    • Capital Medical University
      • Department of Cardiology
      Beijing, Beijing Shi, China
    • Yale-New Haven Hospital
      New Haven, Connecticut, United States
    • University of California, Los Angeles
      Los Angeles, California, United States
    • Erasmus Universiteit Rotterdam
      Rotterdam, South Holland, Netherlands
  • 2011
    • University of Texas Health Science Center at Houston
      Houston, Texas, United States
  • 2010
    • Gachon University
      Sŏngnam, Gyeonggi Province, South Korea
  • 2002–2009
    • University of Minnesota Rochester
      Rochester, Minnesota, United States
  • 2008
    • Duke University Medical Center
      Durham, North Carolina, United States
    • Vanderbilt University
      Nashville, Michigan, United States
  • 2006–2008
    • Konyang University Hospital
      Gaigeturi, Jeju, South Korea
    • Cedars-Sinai Medical Center
      • Division of Cardiology
      Los Angeles, CA, United States
  • 2006–2007
    • University of Naples Federico II
      Napoli, Campania, Italy
  • 2005
    • University of Birmingham
      Birmingham, England, United Kingdom
  • 2003
    • Technion - Israel Institute of Technology
      H̱efa, Haifa District, Israel
    • Aarhus University
      Aarhus, Central Jutland, Denmark
  • 2001
    • Second University of Naples
      Caserta, Campania, Italy
  • 1999
    • Rabin Medical Center
      • Department of Cardiology
      Tel Aviv, Tel Aviv, Israel
    • Yonsei University
      • Department of Internal Medicine
      Seoul, Seoul, South Korea
  • 1995
    • Tel Aviv University
      Tell Afif, Tel Aviv, Israel