Peter Ganz

University of California, San Francisco, San Francisco, California, United States

Are you Peter Ganz?

Claim your profile

Publications (206)2147.95 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Background and aims: Endothelial cell-selective adhesion molecule (ESAM) is selectively expressed on vascular endothelium and is postulated to play a role in atherogenesis. We investigated the association of serum soluble ESAM (sESAM) levels with subsequent cardiovascular outcomes in patients with stable ischemic heart disease. Methods: We measured sESAM levels in 981 patients with stable coronary disease enrolled between September 2000 and December 2002 in a prospective cohort study. Poisson regression models were used to define the relationship between baseline sESAM levels and cardiovascular outcomes, including myocardial infarction, heart failure hospitalization, and mortality. Results: There were 293 occurrences of the composite endpoint over a median follow-up of 8.9 years. After adjusting for demographic and clinical risk factors, participants in the highest sESAM quartile (compared to the lower three sESAM quartiles) had a higher rate of the composite endpoint (incident rate ratio (IRR) 1.52 (95% CI 1.16-1.99) as well as of its individual components: myocardial infarction (IRR 1.64 (1.06-2.55)), heart failure hospitalizations (IRR 1.96 (1.32-2.81)), and death (IRR 1.5 (1.2-1.89)). These associations were no longer significant after adjustment for estimated glomerular filtration rate. Conclusions: sESAM levels associate with myocardial infarction, heart failure, and death after adjustment for demographic and clinical risk factors, but not after adjustment for kidney function. sESAM may be involved in the pathogenesis of concurrent kidney and cardiovascular disease.
    Atherosclerosis 10/2015; 243(2). DOI:10.1016/j.atherosclerosis.2015.10.092 · 3.99 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Growth differentiation factor 11 and/or its homologue growth differentiation factor 8 (GDF11/8) reverses age-related cardiac hypertrophy and vascular ageing in mice. We investigated whether GDF11/8 associates with cardiovascular outcomes, left ventricular hypertrophy (LVH), or age in humans. We measured plasma GDF11/8 levels in 928 participants with stable ischaemic heart disease in the Heart and Soul study. We adjudicated heart failure hospitalization, stroke, myocardial infarction, death, and their composite endpoint. Left ventricular hypertrophy was evaluated by echocardiography. We used multivariable Cox proportional hazards models to compare rates of cardiovascular events and death across GDF11/8 quartiles and logistic regression models to evaluate the association between GDF11/8 and LVH. Four hundred and fifty participants (48.5%) experienced a cardiovascular event or death during 8.9 years of follow-up. The adjusted risk of the composite endpoint was lower in the highest compared with the lowest GDF11/8 quartile [hazard ratio (HR), 0.45; 95% confidence interval (CI), 0.33-0.60; P < 0.001]. We replicated this relationship of GDF11/8 to adverse events in 971 participants in the HUNT3 cohort (adjusted HR, 0.34; 95% CI, 0.23-0.51; P < 0.001). Left ventricular hypertrophy was present in 368 participants (39.7%) at baseline. Participants in the highest quartile of GDF11/8 were less likely to have LVH than those in the lowest quartile (adjusted OR, 0.55; 95% CI, 0.35-0.86; P = 0.009). GDF11/8 levels were lower in older individuals (P < 0.001). In patients with stable ischaemic heart disease, higher GDF11/8 levels are associated with lower risk of cardiovascular events and death. Our findings suggest that GDF11/8 has similar cardioprotective properties in humans to those demonstrated in mice. Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2015. For permissions please email:
    European Heart Journal 08/2015; DOI:10.1093/eurheartj/ehv385 · 15.20 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: To describe the efficacy and tolerability of continuous nitroglycerin for treatment of hot flashes. Perimenopausal and postmenopausal women reporting at least seven hot flashes per day were recruited into a single-arm, dose-escalation trial of continuous transdermal nitroglycerin. Participants were started on a generic 0.1 mg/hour nitroglycerin patch applied daily without patch-free periods. During 4 weeks, participants escalated dosage weekly to 0.2, 0.4, or 0.6 mg/hour as tolerated, then discontinued nitroglycerin during the final week. Changes in hot flash frequency and severity were assessed using symptom diaries. Paired t tests examined change in outcomes between baseline and maximal-dose therapy and after discontinuation of nitroglycerin. Of the 19 participants, mean age was 51.4 (±4.3) years. Women reported an average 10.6 (±3.0) hot flashes and 7.1 (±3.8) moderate-to-severe hot flashes per day at baseline. Eleven women escalated to 0.6 mg/hour, three to 0.4 mg/hour, two to 0.2 mg/hour, and one remained on 0.1 mg/hour nitroglycerin. Two discontinued nitroglycerin before the first outcomes assessment. Among the remaining 17 women, the average daily frequency of hot flashes decreased by 54% and the average frequency of moderate-to-severe hot flashes decreased by 69% from baseline to maximum-dose therapy (P < 0.001 for both). After discontinuing nitroglycerin, participants reported an average 23% increase in frequency of any hot flashes (P = 0.041) and 96% increase in moderate-to-severe hot flashes (P < 0.001). Continuous nitroglycerin may substantially and reversibly decrease hot flash frequency and severity. If confirmed in a randomized blinded trial, it may offer a novel nonhormonal hot flash treatment.
    Menopause (New York, N.Y.) 08/2015; DOI:10.1097/GME.0000000000000520 · 3.36 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Patients with stable coronary heart disease (CHD) have widely varying prognoses and treatment options. Validated models for risk stratification of patients with CHD are needed. We sought to evaluate traditional and novel risk factors as predictors of secondary cardiovascular (CV) events, and to develop a prediction model that could be used to risk stratify patients with stable CHD. We used independent derivation (912 participants in the Heart and Soul Study) and validation (2876 participants in the PEACE trial) cohorts of patients with stable CHD to develop a risk prediction model using Cox proportional hazards models. The outcome was CV events, defined as myocardial infarction, stroke, or CV death. The annual rate of CV events was 3.4% in the derivation cohort and 2.2% in the validation cohort. With the exception of smoking, traditional risk factors (including age, sex, body mass index, hypertension, dyslipidemia, and diabetes) did not emerge as the top predictors of secondary CV events. The top 4 predictors of secondary events were the following: N-terminal pro-type brain natriuretic peptide, high-sensitivity cardiac troponin T, urinary albumin:creatinine ratio, and current smoking. The 5-year C-index for this 4-predictor model was 0.73 in the derivation cohort and 0.65 in the validation cohort. As compared with variables in the Framingham secondary events model, the Heart and Soul risk model resulted in net reclassification improvement of 0.47 (95% CI 0.25 to 0.73) in the derivation cohort and 0.18 (95% CI 0.01 to 0.40) in the validation cohort. Novel risk factors are superior to traditional risk factors for predicting 5-year risk of secondary events in patients with stable CHD. © 2015 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.
    Journal of the American Heart Association 07/2015; 4(7). DOI:10.1161/JAHA.114.001646 · 4.31 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Myocardial perfusion scintigraphy (MPS) is used widely to assess cardiovascular risk in patients with chest pain. The utility of carotid intima-media thickness (CIMT) and endothelial function as assessed by reactive hyperemia-peripheral arterial tonometry index (RHI) in risk stratifying patients with angina-like symptoms needs to be defined. We investigated whether the addition of CIMT and RHI to Framingham Cardiovascular Risk Score (FCVRS) and MPS improves comprehensive cardiovascular risk prediction in patients presenting with angina-like symptoms. We enrolled 343 consecutive patients with angina-like symptoms suspected of having stable angina. MPS, CIMT, and RHI were performed and patients were followed for cardiovascular events for a median of 5.3years (range 4.4-6.2). Patients were stratified by FCVRS and MPS. During the follow-up, 57 patients (16.6%) had cardiovascular events. Among patients without perfusion defect, low RHI was significantly associated with cardiovascular events in the intermediate and high FCVRS groups (hazard ratio (HR) [95% confidence interval (CI)] of RHI≤2.11 was 6.99 [1.34-128] in the intermediate FCVRS group and 6.08 [1.08-114] in the high FCVRS group). Furthermore, although MPS did not predict, only RHI predicted hard cardiovascular events (cardiovascular death, myocardial infarction, and stroke) independent from FCVRS, and adding RHI to FCVRS improved net reclassification index (20.9%, 95% CI 0.8-41.1, p=0.04). Especially, RHI was significantly associated with hard cardiovascular events in the high FCVRS group (HR [95% CI] of RHI≤1.93 was 5.66 [1.54-36.4], p=0.007). Peripheral endothelial function may improve discrimination in identifying at-risk patients for future cardiovascular events when added to FCVRS-MPS-based risk stratification. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.
    International journal of cardiology 07/2015; 190(1). DOI:10.1016/j.ijcard.2015.04.124 · 4.04 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: This study sought to determine whether biomarkers ST2, growth differentiation factor (GDF)-15, N-terminal pro-B-type natriuretic peptide (NT-proBNP), and high-sensitivity troponin I are elevated in patients infected with human immunodeficiency virus (HIV) and are associated with cardiovascular dysfunction and all-cause mortality. HIV-infected patients have high rates of cardiovascular disease. Markers of myocardial stress may identify at-risk patients and provide additional prognostic information. Biomarkers and echocardiograms were assessed in 332 HIV-infected patients and 50 age- and sex-matched control subjects. Left ventricular systolic dysfunction was defined as ejection fraction <50%, diastolic dysfunction (DD) as stage 1 or higher, and pulmonary hypertension as pulmonary artery systolic pressure ≥35 mm Hg. Mortality data were obtained from the National Death Index. Patients with HIV had a median age of 49 years, and 80% were male. Compared with control subjects, HIV-infected patients had higher adjusted percent estimates of all biomarkers except ST2 and interleukin-6. Among HIV-infected patients, 45% had DD; only ST2 was associated with DD (relative risk [RR]: 1.36; p = 0.047). Left ventricular systolic dysfunction was rare in this cohort (5%). Pulmonary hypertension was present in 27% of HIV-infected patients and was associated with GDF-15 (RR: 1.18; p = 0.04), NT-proBNP (RR: 1.18; p = 0.007), and cystatin C (RR: 1.54; p = 0.03). Thirty-eight deaths occurred among HIV-infected patients over a median of 6.1 years. In adjusted analysis, all-cause mortality was independently predicted by ST2 (hazard ratio [HR]: 2.04; p = 0.010), GDF-15 (HR: 1.42; p = 0.0054), high-sensitivity C-reactive protein (HR: 1.25; p = 0.023), and D-dimer (HR: 1.49; p = 0.029). Relationships were unchanged when analyses were restricted to virally suppressed HIV-infected patients receiving antiretroviral therapy. Among HIV-infected patients, ST2 and GDF-15 were associated with both cardiovascular dysfunction and all-cause mortality, and these variables may be useful at identifying those at risk for developing cardiovascular events and death. Copyright © 2015 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
    06/2015; 3(8). DOI:10.1016/j.jchf.2015.03.007

  • Journal of the American College of Cardiology 03/2015; 65(10):A2132. DOI:10.1016/S0735-1097(15)62132-5 · 16.50 Impact Factor

  • Journal of the American College of Cardiology 03/2015; 65(10):A999. DOI:10.1016/S0735-1097(15)60999-8 · 16.50 Impact Factor

  • Journal of the American College of Cardiology 03/2015; 65(10):A2156. DOI:10.1016/S0735-1097(15)62156-8 · 16.50 Impact Factor

  • Journal of the American College of Cardiology 03/2015; 65(10):A1478. DOI:10.1016/S0735-1097(15)61478-4 · 16.50 Impact Factor

  • Journal of the American College of Cardiology 03/2015; 65(10):A1543. DOI:10.1016/S0735-1097(15)61543-1 · 16.50 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The endothelium is a key mediator of vascular homeostasis and cardiovascular health. Molecular research on the human endothelium may provide insight into the mechanisms underlying cardiovascular disease. Prior methodology used to isolate human endothelial cells has suffered from poor yields and contamination with other cell types. We thus sought to develop a minimally invasive technique to obtain endothelial cells derived from human subjects with higher yields and purity. Nine healthy volunteers underwent endothelial cell harvesting from antecubital veins using guidewires. Fluorescence-activated cell sorting (FACS) was subsequently used to purify endothelial cells from contaminating cells using endothelial surface markers (CD34 / CD105 / CD146) with the concomitant absence of leukocyte and platelet specific markers (CD11b / CD45). Endothelial lineage in the purified cell population was confirmed by expression of endothelial specific genes and microRNA using quantitative polymerase chain reaction (PCR). A median of 4,212 (IQR: 2161 - 6583) endothelial cells were isolated from each subject. Quantitative PCR demonstrated higher expression of von Willebrand Factor (vWF, P<0.001), nitric oxide synthase 3 (NOS3, P<0.001) and vascular cell adhesion molecule 1 (VCAM-1, P<0.003) in the endothelial population compared to similarly isolated leukocytes. Similarly, the level of endothelial specific microRNA-126 was higher in the purified endothelial cells (P<0.001). This state-of-the-art technique isolates human endothelial cells for molecular analysis in higher purity and greater numbers than previously possible. This approach will expedite research on the molecular mechanisms of human cardiovascular disease, elucidating its pathophysiology and potential therapeutic targets.
    PLoS ONE 02/2015; 10(2-2):e0118081. DOI:10.1371/journal.pone.0118081 · 3.23 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Introduction: Erectile dysfunction (ED) is associated with cardiovascular disease (CVD); however, the association between change in ED status over time and future underlying CVD risk is unclear. Aim: The aim of this study was to investigate the association between change in ED status and Framingham CVD risk, as well change in Framingham risk. Methods: We studied 965 men free of CVD in the Boston Area Community Health (BACH) Survey, a longitudinal cohort study with three assessments. ED was assessed with the five-item International Index of Erectile Function at BACH I (2002-2005) and BACH II (2007-2010) and classified as no ED/transient ED/persistent ED. CVD risk was assessed with 10-year Framingham CVD risk algorithm at BACH I and BACH III (2010-2012). Linear regression models controlled for baseline age, socio-demographic and lifestyle factors, as well as baseline Framingham risk. Models were also stratified by age (≥/< 50 years). Main Outcome Measures: Framingham CVD risk and change in Framingham CVD risk were the main outcome measures. Results: Transient and persistent ED was significantly associated with increased Framingham risk and change in risk over time in univariate and age-adjusted models. In younger men, persistent ED was associated with a Framingham risk that was 1.58 percentage points higher (95% confidence interval [CI]: 0.11, 3.06) and in older men, a Framingham risk that was 2.54 percentage points higher (95% CI: -1.5, 6.59), compared with those without ED. Change in Framingham risk over time was also associated with transient and persistent ED in men <50 years, but not in older men. Conclusions: Data suggest that even after taking into account other CVD risk factors, transient and persistent ED is associated with Framingham CVD risk and a greater increase in Framingham risk over time, particularly in younger men. Findings further support clinical assessment of CVD risk in men presenting with ED, especially those under 50 years.
    Journal of Sexual Medicine 11/2014; 12(1). DOI:10.1111/jsm.12715 · 3.15 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Background Individuals with rheumatoid arthritis (RA) are at increased risk for cardiovascular disease, partly due to systemic inflammation and endothelial dysfunction. B‐cells play an important pathogenic role in the inflammatory process that drives RA disease activity. Rituximab, a chimeric murine/human monoclonal antibody that depletes B‐cells, is an effective therapy for RA. The purpose of this study was to determine whether B‐cell depletion with rituximab reduces systemic inflammation and improves macrovascular (brachial artery flow‐mediated dilation, FMD) and microvascular (reactive hyperemia) endothelial function in RA patients. Methods and Results RA patients received a single course of rituximab (1000 mg IV infusion at baseline and on day 15). FMD, reactive hyperemia, inflammatory markers, and clinical assessments were performed at baseline, week 12, and week 24. Twenty patients (95% female, median age 54 years) completed the study. Following treatment, FMD improved from a baseline of 4.5±0.4% to 6.4±0.6% at 12 weeks (mean±SE; P<0.0001), followed by a decline at week 24; a similar pattern was observed for hyperemic velocity. Significant decreases in RA disease scores, high‐sensitivity C‐reactive protein, erythrocyte sedimentation rate, and circulating CD19+ B‐cells were sustained through week 24. Cholesterol and triglycerides became significantly although modestly elevated during the study. Conclusions Depletion of B‐cells with rituximab improved macrovascular and microvascular endothelial function and reduced systemic inflammation, despite modest elevation in lipids. Given these results, rituximab should be evaluated in the future for its possible role in reducing excess cardiovascular risk in RA. Clinical Trial Registration URL Unique identifier: NCT00844714.
    Journal of the American Heart Association 10/2014; 3(5):e001267. DOI:10.1161/JAHA.114.001267 · 4.31 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Purpose Increasing evidence of a link between erectile dysfunction (ED) and cardiovascular disease (CVD) suggests a shared vascular etiology with endothelial dysfunction as a plausible underlying biological mechanism. Whether this association is different for large arterial compared to microvascular endothelium has yet to be established. The objective of this study was to investigate the association of ED with macrovascular and microvascular endothelial function. Materials and Methods A sample of 390 men (mean age 55.5 years) was recruited from the Boston Area Community Health (BACH) Survey, a population-based survey of urologic symptoms. ED was assessed using the 5-item International Index of Erectile Function (IIEF-5). Brachial artery flow-mediated dilation (FMD) (%), a measure of macrovascular function, and hyperemic flow velocity (cm/s), a measure of microvascular function, were assessed by ultrasound. Linear regression was used to assess the association of ED and endothelial function and adjust for potential confounders. Results Reactive hyperemia was lower in men with ED (mean (SE) of 97.1(2.5) cm/s) compared to those without ED (106.0(1.6) cm/s, p=0.003). However, the difference in FMD between men with and without ED was statistically non-sginficant (6.6(0.33) vs. 7.2(0.24), p=0.147).The ED and reactive hyperemia association was attenuated but remained statistically significant for men with moderate to severe ED (IIEF-5<12) after adjusting for traditional cardiovascular risk factors (p=0.038). Conclusions These results provide evidence of microvascular more than macrovascular endothelial dysfunction as a potential contributor to the development of ED and as an underlying mechanism linking ED and cariovascular disease.
    The Journal of Urology 09/2014; 193(2). DOI:10.1016/j.juro.2014.08.108 · 4.47 Impact Factor
  • Source

    Journal of the American College of Cardiology 04/2014; 63(12):A780. DOI:10.1016/S0735-1097(14)60780-4 · 16.50 Impact Factor
  • Source

    Journal of the American College of Cardiology 04/2014; 63(12):A28. DOI:10.1016/S0735-1097(14)60028-0 · 16.50 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: A posterior myocardial infarction (PMI) is associated with significant morbidity and delays in recognition may prevent the timely revascularization of these patients. The present study sought to evaluate the reperfusion times and in-hospital outcomes among patients with an isolated PMI. Clinical characteristics and reperfusion times were compared between those with an isolated PMI and those with all other ST-elevation myocardial infarctions (STEMI) in the NCDR ACTION-GWTG Registry from 2007 to 2012. Logistic generalized estimating equations were used to examine risk-adjusted mortality. Among 117,739 subjects with a STEMI, 824 (0.7%) had evidence of an isolated PMI. The median time between patient arrival and initial electrocardiogram was similar between those with an isolated PMI and those with a non-PMI STEMI (6 vs. 6 minutes, P = .48). However, the median time from initial electrocardiogram to percutaneous coronary intervention was significantly longer among subjects with a PMI (69 vs 61 minutes, P < .01) and fewer patients achieved a door-to-balloon time less than 90 minutes (83% vs 89%, P < .01). After multivariable adjustment, in-hospital mortality was similar for PMI patients compared to those with a non-PMI STEMI (AOR: 1.11, 95% CI: 0.83-1.50). The door-to-balloon times are significantly longer for those with an isolated PMI resulting in fewer patients receiving reperfusion within the guideline recommended time period. Ongoing educational initiatives to increase recognition of a PMI are needed to improve the reperfusion times and outcomes associated with this condition.
    American heart journal 03/2014; 167(3):350-4. DOI:10.1016/j.ahj.2013.11.011 · 4.46 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: To examine the relationship between asymmetric dimethylarginine (ADMA) and HIV-associated pulmonary arterial hypertension (PAH). HIV infection is an independent risk factor for PAH, but the underlying pathogenesis remains unclear. Chronic inflammation resulting in nitric oxide-mediated endothelial dysfunction is a key mechanism underlying other types of PAH. ADMA is an endogenous inhibitor of endothelial nitric oxide synthase. Among uninfected individuals, ADMA is associated with PAH and predicts disease-related mortality. We measured ADMA, high sensitivity C-reactive protein, interleukin-6 (IL-6), D-dimer, and pulmonary artery systolic pressure (PASP) using echocardiography in HIV-infected individuals. Right heart catheterization (RHC) was performed in individuals with a PASP at least 30 mmHg. We performed multivariable analysis to identify factors associated with high PASP by echocardiogram and PAH by RHC. Among 214 HIV-infected individuals, the median age was 50 years, 82% were men, 71% were on antiretroviral therapy, and 4.2% carried a prior diagnosis of PAH. ADMA and IL-6 were associated with increased values of PASP following multivariable adjustment (7.2% per 0.1 μmol/l, P = 0.0049 and 3.9% per doubling, P = 0.027, respectively). In adjusted analysis among the 85 participants who underwent RHC, ADMA and IL-6 were associated with higher values of mean PAP (14.2% per 0.1 μmol/l, P = 0.0014 and 5.8% per doubling, P = 0.038, respectively). However, only ADMA was associated with PAH (prevalence ratio = 1.74, P = 0.029). Elevated levels of ADMA are independently associated with PAH among HIV-infected individuals. Our findings suggest that chronic HIV-associated inflammation leading to an accumulation of ADMA and subsequent nitric oxide-mediated endothelial dysfunction may represent a novel mechanism for HIV-associated PAH.
    AIDS (London, England) 01/2014; 28(4). DOI:10.1097/QAD.0000000000000124 · 5.55 Impact Factor
  • Source

Publication Stats

16k Citations
2,147.95 Total Impact Points


  • 2008-2015
    • University of California, San Francisco
      • • Division of Cardiology
      • • Department of Medicine
      San Francisco, California, United States
  • 2009-2013
    • San Francisco VA Medical Center
      San Francisco, California, United States
  • 2012
    • University of California, Davis
      Davis, California, United States
  • 1982-2011
    • Harvard University
      Cambridge, Massachusetts, United States
  • 1985-2010
    • Harvard Medical School
      • Department of Medicine
      Boston, Massachusetts, United States
  • 1984-2007
    • Brigham and Women's Hospital
      • • Department of Medicine
      • • Division of Cardiovascular Medicine
      Boston, Massachusetts, United States
  • 1985-1996
    • University of Massachusetts Boston
      Boston, Massachusetts, United States