Peter Ganz

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

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Publications (135)1049.41 Total impact

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    ABSTRACT: IntroductionErectile 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.AimThe 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 MeasuresFramingham CVD risk and change in Framingham CVD risk were the main outcome measures.ResultsTransient 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. Fang SC, Rosen RC, Vita JA, Ganz P, and Kupelian V. Changes in erectile dysfunction over time in relation to Framingham cardiovascular risk in the Boston Area Community Health (BACH) Survey. J Sex Med **;**:**–**.
    Journal of Sexual Medicine 11/2014; · 3.51 Impact Factor
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    ABSTRACT: 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.
    Journal of the American Heart Association. 10/2014; 3(5):e001267.
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    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. · 4.65 Impact Factor
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    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; · 4.91 Impact Factor
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    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. 01/2014;
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    ABSTRACT: An association between erectile dysfunction and cardiovascular disease has long been recognized, and studies suggest that erectile dysfunction is an independent marker of cardiovascular disease risk. Therefore, assessment and management of erectile dysfunction may help identify and reduce the risk of future cardiovascular events, particularly in younger men. The initial erectile dysfunction evaluation should distinguish between predominantly vasculogenic erectile dysfunction and erectile dysfunction of other etiologies. For men believed to have predominantly vasculogenic erectile dysfunction, we recommend that initial cardiovascular risk stratification be based on the Framingham Risk Score. Management of men with erectile dysfunction who are at low risk for cardiovascular disease should focus on risk-factor control; men at high risk, including those with cardiovascular symptoms, should be referred to a cardiologist. Intermediate-risk men should undergo noninvasive evaluation for subclinical atherosclerosis. A growing body of evidence supports the use of emerging prognostic markers to further understand cardiovascular risk in men with erectile dysfunction, but few markers have been prospectively evaluated in this population. In conclusion, we support cardiovascular risk stratification and risk-factor management in all men with vasculogenic erectile dysfunction.
    The American journal of medicine 11/2013; · 5.30 Impact Factor
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    ABSTRACT: Endothelial dysfunction is a possible mechanism to explain the association between atherosclerosis and kidney disease. This study evaluated circulating soluble endothelial cell-selective adhesion molecule (sESAM), a marker of endothelial dysfunction, as a risk factor for kidney function decline and albuminuria. In the Heart and Soul Study, we measured sESAM from baseline serum samples and defined elevated levels of sESAM by the highest quartile (quartile 4 [Q4]: >65.4 ng/mL). We evaluated the associations of high sESAM with baseline estimated glomerular filtration rate (eGFR) and ratio of urine albumin to creatinine (ACR), and with longitudinal changes in eGFR and ACR. Among 990 participants with sESAM measurements, median sESAM was 54.5 ng/mL (interquartile range, 45.3-65.8). After multivariable adjustment, elevated levels of sESAM were strongly and independently associated with baseline reduced eGFR <60 mL/min per 1.73 m(2) (odds ratio [OR], 11.44; P<0.0001) and ACR ≥30 mg/g (OR, 5.23; P<0.0001). Associations of sESAM (Q4 versus quartile 1 [Q1]) with change in ACR (β=54.47; P<0.0001) were also significant after full adjustment. The association with change in eGFR (1.56%; P=0.0049) was not statistically significant after application of the Bonferroni correction for multiple markers. In unadjusted models, sESAM was associated with rapid kidney function loss, defined as 3% annual eGFR decline (OR, 2.28; P=0.0003), although this was attenuated by adjustment (OR, 2.11; P=0.0095). sESAM is associated with albuminuria and reduced kidney function in both cross-sectional and longitudinal analyses. These findings implicate endothelial dysfunction as a potential contributor to the elevated kidney disease risk in persons with cardiovascular disease.
    Arteriosclerosis Thrombosis and Vascular Biology 10/2013; · 6.34 Impact Factor
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    ABSTRACT: Current guidelines advocate primary percutaneous coronary intervention as the therapy of choice for ST-segment elevation myocardial infarction (STEMI) when available. Little is known about the outcomes of patients without a culprit lesion after referral for primary percutaneous coronary intervention for a presumed STEMI. Subjects were identified within a registry containing consecutive patients who underwent emergent angiography for a potential STEMI from October 2008 to July 2012. Vital status was obtained from the medical record and Social Security Death Index. Cox proportional hazards models were created to evaluate the relation between the angiographic findings and cardiovascular outcomes, including major adverse cardiovascular events (MACE) and mortality. Among 539 patients who underwent emergent angiography, 65 (12%) had no coronary artery disease (CAD), 110 (20%) had CAD without a culprit lesion, and 364 (68%) had a culprit lesion. Kaplan-Meier analysis of MACE demonstrated that patients with CAD who lack a culprit lesion had a similar rate of MACE to those with a culprit lesion (p = 0.64), and both groups had significantly increased risk compared with those with no CAD (hazard ratio [HR] 1.9, 95% confidence interval [CI] 1.01 to 3.41 and HR 2.0, 95% CI 1.15 to 3.54, respectively). Kaplan-Meier analysis of mortality illustrated a nonsignificant trend toward increased mortality in patients having a culprit lesion (HR 1.7, 95% CI 0.59 to 4.80) and those having CAD without a culprit lesion (HR 1.2, 95% CI 0.39 to 3.81) compared with those with no CAD. In conclusion, patients found to have CAD without a culprit lesion in emergent angiography after a presumptive STEMI diagnosis have similar long-term rates of MACE compared with those requiring emergent revascularization.
    The American journal of cardiology 09/2013; · 3.58 Impact Factor
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    ABSTRACT: An isolated posterior myocardial infarction (PMI) is associated with significant morbidity and mortality. Because physicians often fail to recognize this diagnosis, there may be delays in the timely revascularization of these patients. The present study sought to identify the clinical characteristics and reperfusion times among patients presenting with isolated PMI. We identified subjects with isolated PMI within a registry of all catheterization laboratory activations for ST-elevation myocardial infarction (STEMI) from 2008 to 2012. Association between PMI and revascularization within 90 minutes was evaluated by logistic regression. Among 318 patients who underwent revascularization for STEMI, a total of 20 (6%) had electrocardiographic evidence of an isolated PMI. Compared to non-PMI STEMI, subjects with PMI were more often female (45% vs 22%; P=.02) and less likely to have chest pain (40% vs 75%; P<.01). The median door-to-activation (25.5 min vs 12 min; P<.01), activation-to-laboratory (36.5 min vs 29 min; P<.01) and door-to-balloon times (107 min vs 72 min; P<.01) were longer among subjects with PMI, with fewer patients achieving reperfusion within 90 minutes (30% vs 71%; P<.01). After multivariable adjustment, individuals with PMI had 82% lower odds (adjusted odds ratio, 0.18; 95% confidence interval, 0.06-0.50) of achieving coronary reperfusion within 90 minutes. Door-to-activation time accounted for 96% of variation in the total revascularization time (R²=0.96; P<.0001). Door-to-activation time was prolonged for those with PMI, resulting in longer door-to-balloon times and fewer patients revascularized within the recommended time. An isolated PMI should be considered among individuals presenting with symptoms consistent with myocardial infarction.
    The Journal of invasive cardiology 08/2013; 25(8):371-5. · 1.57 Impact Factor
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    International journal of cardiology 07/2013; · 6.18 Impact Factor
  • Peter Ganz, Priscilla Y Hsue
    European Heart Journal 06/2013; · 14.72 Impact Factor
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    ABSTRACT: OBJECTIVES: To compare asymmetric dimethylarginine (ADMA) among HIV-infected and uninfected individuals and to evaluate predictors of ADMA in HIV infection. BACKGROUND: HIV-infected individuals have high rates of atherosclerosis. Endothelial dysfunction is central to atherogenesis and is one possible mechanism underlying this increased cardiovascular risk. ADMA is an endogenous inhibitor of endothelial nitric oxide synthase. Among uninfected individuals, higher ADMA levels predict cardiovascular events and mortality. The association between HIV infection, HIV-related factors, and ADMA has not been well described. METHODS: We compared ADMA in 248 HIV-infected individuals and 50 uninfected controls. We performed multivariable analysis using traditional cardiovascular and HIV-specific factors as covariates to identify factors associated with ADMA. RESULTS: HIV-infected men were older, less often Caucasian, more hypertensive, and had lower HDL than uninfected men. The median duration of HIV infection was 13 years, median CD4+ count was 592 cells/μL, 76% had an undetectable viral load, and 76% were on antiretroviral therapy. ADMA levels were modestly higher in HIV-infected individuals than controls [median (IQR): 0.46 μM (0.41-0.52) vs. 0.44 μM (0.38-0.46), p = 0.019], but the association lost statistical significance after controlling for cardiovascular risk factors (+0.028 μM, p = 0.054). Lower CD4+ count and both detectable and higher viral load were independently associated with increased ADMA. CONCLUSIONS: ADMA levels were modestly elevated in the setting of HIV infection. Notably, a greater HIV-associated inflammatory burden, as evidenced by lower CD4+ counts and higher viral loads, was associated with increased ADMA levels. Our findings suggest that HIV infection impairs endothelial function and predisposes to atherosclerosis through chronic inflammation and subsequent accumulation of ADMA.
    Atherosclerosis 04/2013; · 3.71 Impact Factor
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    ABSTRACT: Prompt percutaneous coronary intervention is associated with improved survival in patients presenting with cardiac arrest. Few studies, however, have focused on patients with cardiac arrest not selected for coronary angiography. The aim of the present study was to evaluate the clinical characteristics and outcomes of patients with cardiac arrest denied emergent angiography. Patients with cardiac arrest were identified within a registry that included all catheterization laboratory activations from 2008 to 2012. Logistic regression and proportional-hazards models were created to assess the clinical characteristics and mortality associated with denying emergent angiography. Among 664 patients referred for catheterization, 110 (17%) had cardiac arrest, and 26 of these patients did not undergo emergent angiography. Most subjects (69%) were turned down for angiography for clinical reasons and a minority for perceived futility (27%). After multivariate adjustment, pulseless electrical activity as the initial arrest rhythm (adjusted odds ratio [AOR] 13.27, 95% confidence interval [CI] 1.76 to 100.12), <1.0 mm of ST-segment elevation (AOR 10.26, 95% CI 1.68 to 62.73), female gender (AOR 4.45, 95% CI 1.04 to 19.08), and advancing age (AOR 1.10 per year, 95% CI 1.04 to 1.16) were associated with increased odds of withholding angiography. The mortality rate was markedly higher for patients who were denied emergent angiography (hazard ratio 3.64, 95% CI 2.05 to 6.49), even after adjustment for medical acuity (hazard ratio 2.29, 95% CI 1.19 to 4.41). In conclusion, older subjects, women, and patients without ST-segment elevation were more commonly denied emergent angiography after cardiac arrest. Patients denied emergent angiography had increased mortality that persisted after adjustment for illness severity.
    The American journal of cardiology 02/2013; · 3.58 Impact Factor
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    ABSTRACT: The association of prediabetic states with endothelial dysfunction measured by flow-mediated dilation (FMD) or endothelial biomarker levels remains controversial. We examined data from 5 ethnic groups to determine the association between glucose categories and FMD or endothelial biomarkers. We determined whether these associations vary by ethnic group or body mass index. We used data from 3516 participants from 5 race/ethnic groups with brachial FMD, endothelial biomarkers, and glucose category (normal, impaired fasting glucose [IFG], and diabetes) measures. There were significant ethnic differences in FMD, biomarker levels, and the prevalence of IFG and diabetes. However, all 5 ethnic groups showed similar patterns of higher FMD for the IFG group compared with the normal glucose and diabetes groups, which was most significant among whites and Asian Indians. Associations between glucose categories and endothelial biomarkers were more uniform, with the IFG and diabetes groups having higher biomarker levels than the normal glucose group. These associations did not change with further adjustment for fasting insulin levels. Whites with normal BMI had higher FMD values with higher glucose levels, but those with BMI in the overweight or obese categories had the inverse association (P for interaction=0.01). The discordance of IFG being associated with higher FMD but more abnormal endothelial biomarker levels is a novel finding. This higher FMD for the IFG group was most notable in whites of normal BMI. The higher FMD among those with impaired fasting glucose may reflect differences in insulin signaling pathways between the endothelium and skeletal muscle.
    Journal of the American Heart Association. 01/2013; 2(1):e004283.
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    ABSTRACT: With adoption of telemedicine, physicians are increasingly asked to diagnose ST-segment elevation myocardial infarctions (STEMIs) based on electrocardiograms (ECGs) with minimal associated clinical information. We sought to determine physicians' diagnostic agreement and accuracy when interpreting potential STEMI ECGs. A cross-sectional survey was performed consisting of 36 deidentified ECGs that had previously resulted in putative STEMI diagnoses. Emergency physicians, cardiologists, and interventional cardiologists participated in the survey. For each ECG, physicians were asked, "based on the ECG above, is there a blocked coronary artery present causing a STEMI?" The reference standard for ascertaining the STEMI diagnosis was subsequent emergent coronary arteriography. Responses were analyzed with generalized estimating equations to account for nested and repeated measures. One hundred twenty-four physicians interpreted a total of 4392 ECGs. Among all physicians, interreader agreement (kappa) for ECG interpretation was 0.33, reflecting poor agreement. The sensitivity to identify "true" STEMIs was 65% (95% CI: 63 to 67) and the specificity was 79% (95% CI: 77 to 81). There was a 6% increase in the odds of accurate ECG interpretation for every 5 years of experience since medical school graduation (OR 1.06, 95% CI: 1.02 to 1.10, P=0.01). After adjusting for experience, there was no significant difference in the odds of accurate interpretation by specialty-Emergency Medicine (reference), General Cardiology (AOR 0.97, 95% CI: 0.79 to 1.2, P=0.80), or Interventional Cardiology physicians (AOR 1.24, 95% CI: 0.93 to 1.7, P=0.15). There is significant physician disagreement in interpreting ECGs with features concerning for STEMI. Such ECGs lack the necessary sensitivity and specificity to act as a suitable "stand-alone" diagnostic test.
    Journal of the American Heart Association. 01/2013; 2(5):e000268.
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    ABSTRACT: In acute coronary syndromes, C-reactive protein (CRP) strongly relates to subsequent death, but surprisingly not to recurrent myocardial infarction. Other biomarkers may reflect different processes related to these outcomes. We assessed 8 inflammatory and vascular biomarkers and the risk of death and recurrent nonfatal cardiovascular events in the 16 weeks after an acute coronary syndrome. We measured blood concentrations of CRP, serum amyloid A (SAA), interleukin-6 (IL-6), soluble intercellular adhesion molecule (ICAM), soluble vascular cell adhesion molecule (VCAM), E-selectin, P-selectin, and tissue plasminogen activator antigen (tPA) 24 to 96 hours after presentation with acute coronary syndrome in 2925 subjects participating in a multicenter study. Biomarkers were related to the risk of death, and recurrent nonfatal acute coronary syndromes (myocardial infarction or unstable angina) over 16 weeks using Cox proportional hazard models. On univariate analyses, baseline CRP (P=0.006), SAA (P=0.012), and IL-6 (P<0.001) were related to death, but not to recurrent nonfatal acute coronary syndromes. VCAM and tPA related to the risk of death (P<0.001, P=0.021, respectively) and to nonfatal acute coronary syndromes (P=0.021, P=0.049, respectively). Adjusting for significant covariates reduced the strength of the associations; however, CRP and SAA continued to relate to death. In acute coronary syndromes, the CRP inflammatory axis relates to the risk of death and may reflect myocardial injury. VCAM and tPA may have greater specificity for processes reflecting inflammation and thrombosis in the epicardial arteries, which determine recurrent coronary events.
    Journal of the American Heart Association. 01/2013; 2(1):e003103.
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    ABSTRACT: Background- Little is known about the components of door-to-balloon time among patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention. We assessed the role of time from hospital arrival to ST-segment elevation myocardial infarction diagnosis (door-to-activation time) on door-to-balloon time in contemporary practice and evaluated factors that influence door-to-activation times. Methods and Results- Registry data on 347 consecutive patients diagnosed with a ST-segment elevation myocardial infarction in the emergency department over 30 months at 2 urban primary percutaneous coronary intervention centers were analyzed. The primary study end point was the time from hospital arrival to catheterization laboratory activation by the emergency department physician, and we assessed factors associated with this period. Door-to-balloon time and its other components were secondary study end points. The median door-to-activation time was 19 minutes (interquartile range, 9-54). Variation in door-to-activation times explained 93% of the variation in door-to-balloon times and demonstrated the strongest correlation with door-to-balloon times (r=0.97). Achieving a door-to-activation time of ≤20 minutes resulted in an 89% chance of achieving a door-to-balloon time of ≤90 minutes compared with only 28% for patients with a door-to-activation time >20 minutes. Factors significantly associated with door-to-activation time include the following: prehospital ECG use (61% shorter, 95% confidence interval, -50 to -72%; P<0.001) and computed tomography scan use in the emergency department (245% longer, 95% confidence interval, +50 to +399%; P=0.001). Conclusions- The interval from hospital arrival to ST-segment elevation myocardial infarction diagnosis and catheterization laboratory activation (door-to-activation time) is a strong driver of overall door-to-balloon times. Achieving a door-to-activation time ≤20 minutes was key to achieving a door-to-balloon time ≤90 minutes. Delays in door-to-activation time are not associated with delays in other aspects of the primary percutaneous coronary intervention process.
    Circulation Cardiovascular Quality and Outcomes 09/2012; 5(5):672-9. · 5.66 Impact Factor
  • Circulation 08/2012; 126(6):753-67. · 15.20 Impact Factor

Publication Stats

9k Citations
1,049.41 Total Impact Points

Institutions

  • 2009–2014
    • University of California, San Francisco
      • Division of Cardiology
      San Francisco, California, United States
  • 2013
    • University of Washington Seattle
      • Division of Cardiology
      Seattle, WA, United States
  • 2009–2013
    • San Francisco VA Medical Center
      San Francisco, California, United States
  • 2012
    • University of California, Davis
      • Division of Cardiovascular Medicine
      Davis, CA, United States
  • 2011–2012
    • Massachusetts General Hospital
      • Division of Cardiology
      Boston, MA, United States
    • Northwestern University
      • Division of Cardiology (Dept. of Medicine)
      Evanston, IL, United States
  • 1984–2012
    • Brigham and Women's Hospital
      • • Center for Brain Mind Medicine
      • • Department of Medicine
      Boston, MA, United States
  • 2009–2010
    • New England Research Institutes
      Watertown, Massachusetts, United States
  • 2000–2010
    • Boston Children's Hospital
      • Division of Nephrology
      Boston, MA, United States
  • 1991–2010
    • Harvard Medical School
      • Department of Medicine
      Boston, Massachusetts, United States
  • 2006–2008
    • Partners HealthCare
      Boston, Massachusetts, United States
  • 2007
    • University of Cambridge
      • Department of Public Health and Primary Care
      Cambridge, ENG, United Kingdom
  • 2004
    • Institut de recherches cliniques de Montréal
      Montréal, Quebec, Canada
    • Boston University
      • Whitaker Cardiovascular Institute
      Boston, MA, United States
  • 1996
    • University of South Florida
      Tampa, Florida, United States
  • 1995
    • University of Massachusetts Boston
      Boston, Massachusetts, United States