Amir Lerman

St. Mary's Hospital (WI, USA), Madison, Wisconsin, United States

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Publications (694)

  • [Show abstract] [Hide abstract] ABSTRACT: The objective of this study was to determine the incidence of arrhythmias and device (internal cardiac defibrillator/cardiac resynchronization therapy defibrillator) therapies in patients with a diagnosis of cardiomyopathy and anthracycline exposure.
    Article · Sep 2016 · JACC Clinical Electrophysiology
  • Yasushi Matsuzawa · Mahmoud Suleiman · Raviteja R Guddeti · [...] · Amir Lerman
    [Show abstract] [Hide abstract] ABSTRACT: Background: The mechanisms of atrial fibrillation (AF) are highly divergent. The prevalence of AF increases significantly with age, and underling mechanisms might vary with age. Endothelial dysfunction may be associated with AF and atrial arrhythmia recurrence after catheter ablation. We tested the hypothesis that the impact of endothelial dysfunction on arrhythmia recurrence following catheter ablation is age dependent. Methods and results: This study enrolled 92 participants with AF undergoing catheter ablation. Endothelial function was assessed by peripheral arterial tonometry before ablation, and the natural logarithmic transformation of reactive hyperemia index was calculated. Endothelial dysfunction was defined as a natural logarithmic transformation of reactive hyperemia index <0.618 (median). Participants were followed for atrial tachycardia, flutter, and fibrillation recurrence for a median of 14 months. The mean age was 57±10 years. There was significant interaction between age and endothelial dysfunction in association with recurrence of AF (P=0.029) and any atrial arrhythmia (P=0.015), and the risk associated with endothelial dysfunction for arrhythmia recurrence was higher in younger versus older participants. Participants were divided into 2 age groups at a threshold of 60 years. Among participants aged ≤60 years, multivariate Cox proportional hazards analysis revealed the independent association between endothelial dysfunction and increased risk of arrhythmia recurrence (hazard ratio for AF 4.18 [95% CI 1.33-15.82], P=0.014, and for any atrial arrhythmia 3.62 [95% CI 1.29-11.81], P=0.014). Kaplan-Meier analysis showed that participants with endothelial dysfunction had significantly higher rates of recurrence of AF (P=0.01) and any atrial arrhythmia (P=0.002). Conclusions: The risk associated with endothelial dysfunction for arrhythmia recurrence following catheter ablation was age dependent and was higher in younger participants.
    Article · Sep 2016 · Journal of the American Heart Association
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    Full-text available · Article · Sep 2016 · Journal of the American Heart Association
  • Raviteja R Guddeti · Abhiram Prasad · Yasushi Matsuzawa · [...] · Amir Lerman
    [Show abstract] [Hide abstract] ABSTRACT: Objectives Percutaneous coronary intervention (PCI) for acute coronary syndromes frequently fails to restore myocardial perfusion despite establishing epicardial vessel patency. Endothelin-1 (ET-1) is a potent vasoconstrictor, and its expression is increased in atherosclerosis and after PCI. In this study, we aim to define the role of endothelin in regulating coronary microvascular blood flow and myocardial perfusion following PCI in patients with non-ST elevation acute coronary syndromes (NSTACS), by assessing whether adjunctive therapy with a selective endothelin A (ETA) receptor antagonist acutely improves postprocedural coronary microvascular blood flow. Methods In a randomised, double-blinded, placebo-controlled trial, 23 NSTACS patients were enrolled to receive an intracoronary infusion of placebo (n=11) or BQ-123 (n=12) immediately before PCI. Post-PCI coronary microvascular blood flow and myocardial perfusion were assessed by measuring Doppler-derived average peak velocity (APV), and cardiac biomarker levels were quantified. Results Compared with the placebo group, APV was significantly higher in the drug group immediately after PCI (30 (20, 37) vs 19 (9, 26) cm/s; p=0.03). Hyperaemic APV, measured post-adenosine administration, was higher in the BQ-123 group, but the difference did not achieve statistical significance (56 (48, 72) vs 46 (34, 64) cm/s; p=0.090). Maximum coronary flow reserve postprocedure was not different between the two groups (2.1 (1.6, 2.3) vs 2.5 (1.8, 3.0)). Per cent change in creatine kinase isoenzyme MB from the time of PCI to 8 and 16 hours post-PCI was significantly lower in the drug group compared with the placebo group (−17 (−26, −10) vs 26 (−15, 134); p=0.02 and −17 (−38, 14) vs 107 (2, 446); p=0.007, respectively). Conclusions Endothelin is a mediator of microvascular dysfunction during PCI in NSTACS, and adjunctive selective ETA antagonist may augment myocardial perfusion during PCI. Trial registration number NCT00586820; Results.
    Article · Aug 2016
  • Kyoung-Ha Park · Tao Sun · Felipe Diez-Delhoyo · [...] · Amir Lerman
    [Show abstract] [Hide abstract] ABSTRACT: Background and aims: The vasa vasorum (VV) plays a role in the initial phase of atherosclerosis, and abnormalities in microvascular function may be sensitive measures of the early development of atherosclerosis. The current study was designed to access the association between coronary microvascular function and VV density in patients undergoing cardiac catheterization. Methods: Twenty-four patients with early coronary artery disease underwent endothelium-dependent (coronary blood flow, CBF) and endothelium-independent (coronary flow velocity reserve, CFVR) coronary microvascular function testing, and optical coherence tomography (OCT) imaging of the left anterior descending coronary artery (LAD). Using an intracoronary Doppler guidewire, CBF was examined by evaluating changes in blood flow in response to acetylcholine and CFVR in response to adenosine. VV density (VV volume/vessel volume × 100, %VV) of the proximal 10 mm of the LAD was quantified by OCT. Results: The median values (Q1, Q3) of CFVR, % changes in CBF in response to acetylcholine, and the %VV were 2.70 (2.30, 2.90), -16.82 (-42.34, 54.52), and 2.62 (2.35, 3.35), respectively. %VV correlated inversely with CBF (r = -0.614, p = 0.001) and directly with CFVR (r = 0.423, p = 0.040). Multivariate analysis showed that only %VV was significantly correlated with CBF and the association was independent of other clinical variables, Framingham risk score, body mass index, and a family history of coronary heart disease. Conclusions: This study demonstrates that VV density has negative correlation with endothelium-dependent microvascular function in patients with early coronary atherosclerosis. These observations link adventitial VV structure and function to microvascular dysfunction in early coronary atherosclerosis.
    Article · Aug 2016 · Atherosclerosis
  • Soumen Jana · Amir Lerman
    [Show abstract] [Hide abstract] ABSTRACT: A two-dimensional (2D) nanofibrous membrane cannot keep its morphology and shape intact without an underlying support such as glass coverslip (GC). As cellular processes and the behavior of cells depend on the mechanical properties of a substrate, an underlying support that generally has higher stiffness than a nanofibrous membrane could have unwanted influence on culturing cells. In this study, we investigated the influence of a GC on the cells by preparing a 2D standalone concentric nanofibrous (CN) substrate and a CN membrane with an underlying glass coverslip (CN-GC) substrate. We then cultured stiffness-sensitive valvular interstitial cells (VICs) onto them. Sole GC substrate was used as a negative control. While VICs were stretched and spindle-shaped on the CN substrates, they were flat and rectangular-shaped on the CN-GC substrates. On the GC substrates, all the VICs formed an almost continuous flat sheet of cells spreading in all directions without any alignment. VICs showed fibroblast phenotype on the CN substrates whereas same VICs showed myofibroblast phenotype on the CN-GC and GC substrates. Further, GC substrates bent due to contraction of cultured cells. Collagen fibril deposit rates were lowest on the CN substrates and highest on the GC substrates. These findings indicate that cellular processes and behavior can be influenced by the underlying supporting substrate in a nanofibrous membrane system, which is very significant for tissue engineering and regenerative medicine where cell is a vital ingredient. We have proposed several easy means to fabricate standalone 2D nanofibrous substrates without any underlying support for in vitro and in vivo research and applications.
    Article · Jul 2016
  • Taek-Geun Kwon · Rajiv Gulati · Yasushi Matsuzawa · [...] · Amir Lerman
    Article · Jul 2016
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    [Show abstract] [Hide abstract] ABSTRACT: Mitochondrial injury contributes to renal dysfunction in several models of renal disease, but its involvement in human hypertension remains unknown. Fragments of the mitochondrial genome released from dying cells are considered surrogate markers of mitochondrial injury. We hypothesized that hypertension would be associated with increased urine mitochondrial DNA (mtDNA) copy numbers. We prospectively measured systemic and urinary copy number of the mtDNA genes cytochrome-c oxidase-3 and NADH dehydrogenase subunit-1 by quantitative polymerase chain reaction in essential (n=25) and renovascular (RVH, n=34) hypertensive patients and compared them with healthy volunteers (n=22). Urinary kidney injury molecule-1 and neutrophil gelatinase-associated lipocalin served as indices of renal injury. Renal blood flow and oxygenation were assessed by multidetector computed tomography and blood oxygen level-dependent magnetic resonance imaging. Blood pressure, urinary neutrophil gelatinase-associated lipocalin, and kidney injury molecule-1 were similarly elevated in essential hypertension and RVH, and estimated glomerular filtration rate was lower in RVH versus healthy volunteers and essential hypertension. Renal blood flow was lower in RVH compared with essential hypertension. Urinary mtDNA copy number was higher in hypertension compared with healthy volunteers, directly correlated with urinary neutrophil gelatinase-associated lipocalin and kidney injury molecule-1 and inversely with estimated glomerular filtration rate. In RVH, urinary mtDNA copy number correlated directly with intrarenal hypoxia. Furthermore, in an additional validation cohort, urinary mtDNA copy number was higher in RVH compared with healthy volunteers (n=10 each). The change in serum creatinine levels and estimated glomerular filtration rate 3 months after medical therapy without or with revascularization correlated with the change in urinary mtDNA. Therefore, elevated urinary mtDNA copy numbers in hypertensive patients correlated with markers of renal injury and dysfunction, implicating mitochondrial injury in kidney damage in human hypertension.
    Full-text available · Article · Jun 2016 · Hypertension
  • Alfonso Eirin · Amir Lerman · Lilach O. Lerman
    [Show abstract] [Hide abstract] ABSTRACT: Renal disease affects millions of people worldwide, imposing an enormous financial burden for health-care systems. Recent evidence suggests that mitochondria play an important role in the pathogenesis of different forms of renal disease, including genetic defects, acute kidney injury, chronic kidney disease, aging, renal tumors, and transplant nephropathy. Renal mitochondrial abnormalities and dysfunction affect several cellular pathways, leading to increased oxidative stress, apoptosis, microvascular loss, and fibrosis, all of which compromise renal function. Over recent years, compounds that specifically target mitochondria have emerged as promising therapeutic options for patients with renal disease. Although the most compelling evidence is based on preclinical studies, several compounds are currently being tested in clinical trials. This chapter provides an overview of the involvement of mitochondrial dysfunction in renal disease and summarizes the current knowledge on mitochondria-targeted strategies to attenuate renal disease.
    Chapter · Jun 2016
  • [Show abstract] [Hide abstract] ABSTRACT: Microvascular rarefaction distal to renal artery stenosis is linked to renal dysfunction and poor outcomes. Low-energy shockwave therapy stimulates angiogenesis, but the effect on the kidney microvasculature is unknown. We hypothesized that low-energy shockwave therapy would restore the microcirculation and alleviate renal dysfunction in renovascular disease. Normal pigs and pigs subjected to 3 weeks of renal artery stenosis were treated with six sessions of low-energy shockwave (biweekly for 3 consecutive weeks) or left untreated. We assessed BP, urinary protein, stenotic renal blood flow, GFR, microvascular structure, and oxygenation in vivo 4 weeks after completion of treatment, and then, we assessed expression of angiogenic factors and mechanotransducers (focal adhesion kinase and β1-integrin) ex vivo A 3-week low-energy shockwave regimen attenuated renovascular hypertension, normalized stenotic kidney microvascular density and oxygenation, stabilized function, and alleviated fibrosis in pigs subjected to renal artery stenosis. These effects associated with elevated renal expression of angiogenic factors and mechanotransducers, particularly in proximal tubular cells. In additional pigs with prolonged (6 weeks) renal artery stenosis, shockwave therapy also decreased BP and improved GFR, microvascular density, and oxygenation in the stenotic kidney. This shockwave regimen did not cause detectable kidney injury in normal pigs. In conclusion, low-energy shockwave therapy improves stenotic kidney function, likely in part by mechanotransduction-mediated expression of angiogenic factors in proximal tubular cells, and it may ameliorate renovascular hypertension. Low-energy shockwave therapy may serve as a novel noninvasive intervention in the management of renovascular disease.
    Article · Jun 2016 · Journal of the American Society of Nephrology
  • Kyoung-Ha Park · Tao Sun · Zhi Liu · [...] · Amir Lerman
    [Show abstract] [Hide abstract] ABSTRACT: Background: Cardiac allograft vasculopathy (CAV) is an accelerated form of coronary artery disease, and optical coherence tomography (OCT) provides detailed microstructural information. The current study was designed to test the hypothesis that markers of plaque vulnerability derived from OCT could predict CAV progression after heart transplantation (HTx). Methods: In 34 consecutive patients (median 3.1 years from HTx), intravascular ultrasound (IVUS) and OCT were performed in the left anterior descending artery (LAD) during routine annual coronary angiography. The presence of vulnerability markers, such as lipid pools, thin-cap fibroatheroma, macrophages and microchannels, was assessed in 100 consecutive frames of OCT in 20-mm segments of proximal LAD. The total number of appearances of vulnerable markers was defined as the vulnerability score (VS). Plaque volume (PV) was measured in the same study segment using IVUS at baseline and at 1-year follow-up, and the association between the baseline VS and the subsequent change in percent PV (PV / vessel volume × 100 [%PV]) was evaluated. Results: Follow-up IVUS study was conducted after 12.5 ± 1.3 months. The mean VS was 59.9 ± 44.6. Compared with the initial %PV, the follow-up %PV increased in the study segment (25.6 ± 13.7% to 31.8 ± 17.5%, p < 0.001). The correlations between baseline VS and Δ%PV were significant in the study segment (r = 0.757, p < 0.001). On multivariable analysis, only the VS correlated significantly with Δ%PV. Conclusions: Our results demonstrate that the markers of plaque vulnerability in OCT can predict the progression of CAV. Therefore, in patients with HTx, OCT may aid in determining prognosis and guiding therapy related to CAV.
    Article · Jun 2016 · The Journal of heart and lung transplantation: the official publication of the International Society for Heart Transplantation
  • Jae Yoon Park · Amir Lerman · Joerg Herrmann
    [Show abstract] [Hide abstract] ABSTRACT: Despite advances in therapy, coronary artery disease (CAD) remains the leading cause of morbidity and mortality worldwide. Over the past years, the utilization of revascularization procedures has been refined, and in the best interest of the patient and to reduce the healthcare burden of CAD, it is paramount that patients are appropriately selected for therapies aiming at improving their symptoms and prognosis. Fractional flow reserve (FFR) is the current invasive standard test to identify hemodynamically significant coronary artery stenoses with resultant implications for revascularization and clinical outcomes. In this review, we discuss the current evidence behind the use of FFR as well as new trends in the application of this technique to help guide clinicians in making the best management decisions for patients with CAD.
    Article · Jun 2016 · Trends in cardiovascular medicine
  • [Show abstract] [Hide abstract] ABSTRACT: Background Renovascular hypertension (RVH) impairs cardiac structure and left ventricular (LV) function, but whether mitochondrial injury is implicated in RVH‐induced myocardial damage and dysfunction has not been defined. We hypothesized that cardiac remodeling in swine RVH is partly attributable to cardiac mitochondrial injury. Methods and Results After 12 weeks of hypercholesterolemic (HC)‐RVH or control (n=14 each), pigs were treated for another 4 weeks with vehicle or with the mitochondrial‐targeted peptide (MTP), Bendavia (0.1 mg/kg subcutaneously, 5 days/week), which stabilizes mitochondrial inner‐membrane cardiolipin (n=7 each). Cardiac function was subsequently assessed by multidetector‐computed tomography and oxygenation by blood‐oxygen‐level–dependent magnetic resonance imaging. Cardiolipin content, mitochondrial biogenesis, as well as sarcoplasmic‐reticulum calcium cycling, myocardial tissue injury, and coronary endothelial function were assessed ex vivo. Additionally, mitochondrial cardiolipin content, oxidative stress, and bioenergetics were assessed in rat cardiomyocytes incubated with tert‐butyl hydroperoxide (tBHP) untreated or treated with MTP. Chronic mitoprotection in vivo restored cardiolipin content and mitochondrial biogenesis. Thapsigargin‐sensitive sarcoplasmic reticulum Ca²⁺‐ATPase activity that declined in HC‐RVH normalized in MTP‐treated pigs. Mitoprotection also improved LV relaxation (E/A ratio) and ameliorated cardiac hypertrophy, without affecting blood pressure or systolic function. Myocardial remodeling and coronary endothelial function improved only in MTP‐treated pigs. In tBHP‐treated cardiomyocytes, mitochondrial targeting attenuated a fall in cardiolipin content and bioenergetics. Conclusions Chronic mitoprotection blunted myocardial hypertrophy, improved LV relaxation, and attenuated myocardial cellular and microvascular remodeling, despite sustained HC‐RVH, suggesting that mitochondrial injury partly contributes to hypertensive cardiomyopathy.
    Article · Jun 2016 · Journal of the American Heart Association
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    [Show abstract] [Hide abstract] ABSTRACT: Significance: Adipose-derived stromal cell (ASC) function might decline in a disease milieu, but it remains unclear whether ASC function varies during the development of obesity. This study tested the hypothesis that microenvironmental inflammatory changes during development of metabolic disorders in obesity affect ASC function. It was found that ASCs show increased propensity for differentiation into adipocytes, which is partly mediated by upregulated tumor necrosis factor-α (TNF-α), likely in their adipose tissue microenvironment. Furthermore, TNF-α magnified obese ASC senescence, although it did not regulate their anti-inflammatory properties. Thus, adipose tissue inflammation might be a novel therapeutic target to avert ASC maldifferentiation and senescence.
    Full-text available · Article · May 2016 · STEM CELLS TRANSLATIONAL MEDICINE
  • Zhi Liu · Yasushi Matsuzawa · Joerg Herrmann · [...] · Amir Lerman
    [Show abstract] [Hide abstract] ABSTRACT: Background: FFR of deferred PCI lesions can predict future cardiovascular events. However, the prognostic utility of FFR remains unclear in diabetic patients in view of the potential impact of the diffuse nature of vascular disease process. We aimed to study the relation between fractional flow reserve (FFR) values and long-term outcomes of diabetic and non-diabetic patients with deferred percutaneous coronary intervention (PCI). Methods: Patients with FFR assessment and deferred PCI (n=630) were enrolled and stratified according to diabetes mellitus (DM) status and FFR values. Patients were followed over a median of 39months. Cox proportional hazard regression models were used to analyze the association between clinical endpoints and clinical factors such as DM and FFR. Results: In non-diabetics (n=450), higher FFR values were associated with less cardiovascular events (hazard ratio (HR) for death and myocardial infarction (MI) [95% confidence interval (CI)], 0.61[0.44 to 0.86] per 0.1 increase in FFR, p=0.007; HR for revascularization [95%CI], 0.66[0.49 to 0.9] per 0.1 increase in FFR, p=0.006). In diabetics (n=180), there was no difference in death and MI across the range of FFR values. Among those patients with an FFR >0.85, diabetics had a more than two-fold higher risk of death and MI than non-diabetics (HR [95% CI], 2.20 [1.19 to 4.01], p=0.015). Conclusion: Among non-diabetic patients with deferred PCI, a higher FFR was associated with lower rates of death, MI and revascularization. On the contrary in diabetic patients with deferred revascularization, FFR was not able to differentiate the risk of cardiovascular events.
    Article · May 2016 · International journal of cardiology
  • [Show abstract] [Hide abstract] ABSTRACT: Rationale: Coronary endothelial dysfunction (ED)-an early marker of atherosclerosis-increases the risk of cardiovascular events. Objective: We tested the hypothesis that cholesterol efflux capacity and HDL particle concentration predict coronary ED better than HDL-cholesterol (HDL-C). Methods and results: We studied 80 subjects with non-obstructive (<30% stenosis) coronary artery disease. ED was defined as <50% change in coronary blood flow in response to intra-coronary infusions of acetylcholine during diagnostic coronary angiography. Cholesterol efflux capacity and HDL particle concentration (HDL-PIMA) were assessed with validated assays. Cholesterol efflux capacity and HDL-PIMA were both strong, inverse predictors of ED (P<0.001 and 0.005, respectively). In contrast, HDL-C and other traditional lipid risk factors did not differ significantly between control and ED subjects. Large HDL particles were markedly decreased in ED subjects (33%; P=0.005). After correction for HDL-C, both efflux capacity and HDL-PIMA remained significant predictors of ED status. HDL-PIMA explained cholesterol efflux capacity more effectively than HDL-C (r=0.54 and 0.36, respectively). The efflux capacities of isolated HDL and serum HDL correlated strongly (r=0.49). Conclusions: Cholesterol efflux capacity and HDL-PIMA are reduced in subjects with coronary ED, independently of HDL-C. Alterations in HDL-PIMA and HDL itself account for a much larger fraction of the variation in cholesterol efflux capacity than does HDL-C. A selective decrease in large HDL particles may contribute to impaired cholesterol efflux capacity in ED subjects. These observations support a role for HDL size, concentration and function as markers-and perhaps mediators-of coronary atherosclerosis in humans.
    Article · Apr 2016 · Circulation Research
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    R Jay Widmer · Thomas G Allison · Brendie Keane · [...] · Amir Lerman
    [Show abstract] [Hide abstract] ABSTRACT: Cardiovascular disease (CVD) is the leading cause of morbidity and mortality in the US. Emerging employer-sponsored work health programs (WHP) and Digital Health Intervention (DHI) provide monitoring and guidance based on participants' health risk assessments, but with uncertain success. DHI-mobile technology including online and smartphone interventions-has previously been found to be beneficial in reducing CVD outcomes and risk factors, however its use and efficacy in a large, multisite, primary prevention cohort has not been described to date. We analyzed usage of DHI and change in intermediate markers of CVD over the course of one year in 30,974 participants of a WHP across 81 organizations in 42 states between 2011 and 2014, stratified by participation log-ins categorized as no (n = 14,173), very low (
    Full-text available · Article · Apr 2016 · PLoS ONE
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    [Show abstract] [Hide abstract] ABSTRACT: BACKGROUND:The diagnosis and management of cardiovascular complications have become a clinical concern for oncologists, cardiologists, surgeons, interventional radiologists, radiation therapy physicians, internists, nurses, pharmacists, administrators, and all the stakeholders involved in the care of cancer patients. Anticancer therapies have extended the lives of patients with cancer, but for some this benefit is attenuated by adverse cardiovascular effects.METHODS:This review article aims to provide an overview of the rationale of setting up a cardio-oncology unit and reflect on our own experience establishing this service, and conclude with some fundamental aspects of consideration for evaluation and management of patients with cancer and cardiovascular diseases.RESULTS:Cardiotoxicity can lead to congestive heart failure and cardiac death. In fact, chemotherapy-related cardiac dysfunction may carry one of the worst prognoses of all types of cardiomyopathies, and has a profound impact on morbidity and mortality in oncology patients. Other complex clinical situations involve cancer patients who might benefit from a highly curative drug in terms of cancer survival but face limitations of its administration because of concomitant cardiovascular diseases. Indeed, the balance between the benefits and risks of the cancer therapy regimen in the context of the cardiovascular status of the individual patient can sometimes be extraordinarily challenging. A subspecialty with a multidisciplinary integrative approach between oncologists, hematologists, cardiologists, among others has thus emerged to address these issues, termed cardio-oncology. Cardio-oncology addresses the spectrum of prevention, detection, monitoring and treatment of cancer patients with cardiovascular diseases, or at risk for cardiotoxicity, in a multidisciplinary manner. In this field, cardiologists assist oncologists and hematologists with cardiovascular recommendations. This can be mediated through e-consultations or face-to-face evaluations.CONCLUSION:Cardio-oncology is a subspecialty that assists in the overall care of cancer patients with and without cardiovascular disease in an interdisciplinary fashion. We believe that this partnership of sharing responsibilities and experiences among health-care team members can potentially decrease cancer therapeutics-related cardiovascular complications and improve clinical outcomes.
    Full-text available · Article · Apr 2016
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    Satoshi Yoshino · Rebecca Cilluffo · Megha Prasad · [...] · Amir Lerman
    [Show abstract] [Hide abstract] ABSTRACT: Table S1. Patient Characteristics Table S2. SNPs Associated With Macrovascular/Epicardial Endothelial Dysfunction Significant Only Among Females Table S3. SNPs Associated With Macrovascular/Epicardial Endothelial Dysfunction Significant Only Among Males
    File available · Dataset · Apr 2016
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    Chaim Locker · Hartzell V. Schaff · Richard C. Daly · [...] · Amir Lerman
    [Show abstract] [Hide abstract] ABSTRACT: Objective: To compare long-term survival with multiple arterial coronary artery bypass grafting (CABG) (MultArt) versus percutaneous coronary intervention (PCI) in patients with multivessel disease (MVD). Methods: We reviewed 12,615 patients with MVD with isolated primary CABG or PCI from 1993 to 2009. Patients with CABG (n = 6667) were grouped according to the number of arterial grafts into left internal thoracic artery (LITA)/saphenous vein (SV) (n = 5712) or MultArt (n = 955); patients with PCI (n = 5948) were grouped into balloon angioplasty (BA) (n = 1020), drug-eluting stent (DES) (n = 1686), and bare metal stent (BMS) (n = 3242). Results: Unadjusted long-term survival was lower for CABG than PCI (15-year survival, 34% vs 46%; P < .001); however, in patients with MultArt, survival was greater than LITA/SV, BA, BMS (15-year survival, 65% vs 31%, 47%, 45%, respectively; P < .001), and DES (8-year survival, 87% vs 70%; P < .001). In matched analyses, 15-year survival of MultArt was higher than BA (66% vs 57%; P = .002), LITA/SV (64% vs 56%; P = .02), and BMS (5-year survival 94% vs 90%; P = .01), and similar to DES at 8 years. In multivariate analysis, compared with MultArt, LITA/SV had worse survival (hazard ratio [HR], 1.29; 95% confidence interval [CI], 1.09-1.52; P = .003). BMS (HR, 0.87; 95% CI, 0.80-0.94; P < .001) and DES (HR, 0.76; 95% CI, 0.66-0.88; P < .001) had improved survival versus LITA/SV but not versus MultArt (HR, 1.12; 95% CI, 0.94-1.34; P = .21, and HR, 0.98; 95% CI, 0.79-1.21; P = .83, respectively). Secondary analyses for treatment crossover indicated lower survival for LITA/SV versus MultArt and PCI. Conclusions: In patients with MVD undergoing primary revascularization, MultArt increased survival benefit versus LITA/SV compared with PCI. Use of MultArt must increase.
    Full-text available · Article · Apr 2016 · The Journal of thoracic and cardiovascular surgery

Publication Stats

30k Citations


  • 2015
    • St. Mary's Hospital (WI, USA)
      Madison, Wisconsin, United States
    • Sun Yat-Sen University
      • Department of Vascular Surgery
      Shengcheng, Guangdong, China
  • 2000-2015
    • Mayo Foundation for Medical Education and Research
      • Division of Cardiovascular Diseases
      Рочестер, Michigan, United States
  • 1999-2012
    • Mayo Clinic - Rochester
      • • Department of Cardiovascular Diseases
      • • Department of Internal Medicine
      Rochester, Minnesota, United States
  • 2011
    • University of Florida
      Gainesville, Florida, United States
  • 2003
    • Aarhus University
      Aarhus, Central Jutland, Denmark
    • Second University of Naples
      Caserta, Campania, Italy
  • 2002
    • Deutsches Herzzentrum München
      München, Bavaria, Germany
    • Saint Louis University
      Сент-Луис, Michigan, United States
  • 1998
    • University of Rome Tor Vergata
      Roma, Latium, Italy
    • University of Zurich
      Zürich, Zurich, Switzerland