Gregg W Stone

Erasmus Universiteit Rotterdam, Rotterdam, South Holland, Netherlands

Are you Gregg W Stone?

Claim your profile

Publications (930)9924.15 Total impact

  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Background The incidence, predictors, and prognostic impact of post-discharge bleeding (PDB) after percutaneous coronary intervention (PCI) with drug-eluting stent (DES) implantation are unclear. Objectives This study sought to characterize the determinants and consequences of PDB after PCI. Methods The prospective ADAPT-DES (Assessment of Dual Antiplatelet Therapy With Drug-Eluting Stents) study was used to determine the incidence and predictors of clinically relevant bleeding events occurring within 2 years after hospital discharge. The effect of PDB on subsequent 2-year all-cause mortality was estimated by time-adjusted Cox proportional hazards regression. Results Among 8,582 “all-comers” who underwent successful PCI with DES in the ADAPT-DES study, PDB occurred in 535 of 8,577 hospital survivors (6.2%) at a median time of 300 days (interquartile range: 130 to 509 days) post-discharge. Gastrointestinal bleeding (61.7%) was the most frequent source of PDB. Predictors of PDB included older age, lower baseline hemoglobin, lower platelet reactivity on clopidogrel, and use of chronic oral anticoagulation therapy. PDB was associated with higher crude rates of all-cause mortality (13.0% vs. 3.2%; p < 0.0001). Following multivariable adjustment, PDB was strongly associated with 2-year mortality (hazard ratio [HR]: 5.03; p < 0.0001), with an effect size greater than that of post-discharge myocardial infarction (PDMI) (HR: 1.92; p = 0.009). Conclusions After successful PCI with DES in an unrestricted patient population, PDB is not uncommon and has a strong relationship with subsequent all-cause mortality, greater that that associated with PDMI. Efforts to reduce PDB may further improve prognosis after successful DES implantation. (Assessment of Dual Antiplatelet Therapy With Drug-Eluting Stents [ADAPT-DES]; NCT00638794)
    Journal of the American College of Cardiology 09/2015; 66(9). DOI:10.1016/j.jacc.2015.06.1323 · 15.34 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The long-term risk associated with different coronary artery disease (CAD) presentations in women undergoing percutaneous coronary intervention (PCI) with drug-eluting stents (DES) is poorly characterized. We pooled patient-level data for women enrolled in 26 randomized clinical trials. Of 11,577 women included in the pooled database, 10,133 with known clinical presentation received a DES. Of them, 5,760 (57%) had stable angina pectoris (SAP), 3,594 (35%) had unstable angina pectoris (UAP) or non-ST-segment-elevation myocardial infarction (NSTEMI), and 779 (8%) had ST-segment-elevation myocardial infarction (STEMI) as clinical presentation. A stepwise increase in 3-year crude cumulative mortality was observed in the transition from SAP to STEMI (4.9% vs 6.1% vs 9.4%; p <0.01). Conversely, no differences in crude mortality rates were observed between 1 and 3 years across clinical presentations. After multivariable adjustment, STEMI was independently associated with greater risk of 3-year mortality (hazard ratio [HR] 3.45; 95% confidence interval [CI] 1.99 to 5.98; p <0.01), whereas no differences were observed between UAP or NSTEMI and SAP (HR 0.99; 95% CI 0.73 to 1.34; p = 0.94). In women with ACS, use of new-generation DES was associated with reduced risk of major adverse cardiac events (HR 0.58; 95% CI 0.34 to 0.98). The magnitude and direction of the effect with new-generation DES was uniform between women with or without ACS (pinteraction = 0.66). In conclusion, in women across the clinical spectrum of CAD, STEMI was associated with a greater risk of long-term mortality. Conversely, the adjusted risk of mortality between UAP or NSTEMI and SAP was similar. New-generation DESs provide improved long-term clinical outcomes irrespective of the clinical presentation in women. Copyright © 2015 Elsevier Inc. All rights reserved.
    The American Journal of Cardiology 09/2015; DOI:10.1016/j.amjcard.2015.06.010 · 3.43 Impact Factor
  • Yaling Han · Yi Li · Gregg W Stone
    JAMA The Journal of the American Medical Association 08/2015; 314(6):625. DOI:10.1001/jama.2015.7384 · 30.39 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Contrast-induced acute kidney injury (CI-AKI), defined as a serum creatinine increase ≥0.5 mg/dL or ≥25% within 72 hours after contrast exposure, is a common complication of procedures requiring contrast media and is associated with increased short- and long-term morbidity and mortality. Few studies describe the effects of CI-AKI in a large-scale acute coronary syndrome population, and the relationship between CI-AKI and bleeding events has not been extensively explored. We sought to evaluate the impact of CI-AKI after percutaneous coronary intervention in patients presenting with acute coronary syndrome. We pooled patient-level data for 9512 patients from the percutaneous coronary intervention cohorts of the Harmonizing Outcomes With Revascularization and Stents in Acute Myocardial Infarction (HORIZONS-AMI) and Acute Catheterization and Urgent Intervention Triage Strategy (ACUITY) multicenter randomized trials. Patients were classified according to CI-AKI development, and cardiovascular outcomes at 30 days and 1 year were compared between groups. A total of 1212 patients (12.7%) developed CI-AKI. Patients with CI-AKI were older, with a more extensive comorbidity profile than without CI-AKI. Multivariable analysis confirmed several previously identified predictors of CI-AKI, including diabetes mellitus, contrast volume, age, and baseline hemoglobin. Mortality rates were significantly higher in the CI-AKI group at 30 days (4.9% versus 0.7%; P<0.0001) and 1 year (9.8% versus 2.9%; P<0.0001), as were rates of 1-year myocardial infarction, definite/probable stent thrombosis, target lesion revascularization, and major adverse cardiac events. Major bleeding (13.8% versus 5.4%; hazard ratio, 2.64; 95% confidence interval, 2.21-3.15; P<0.0001) was also higher in patients with CI-AKI. After multivariable adjustment, results were unchanged. CI-AKI after percutaneous coronary intervention in patients presenting with acute coronary syndrome is independently associated with increased risk of short- and long-term ischemic and hemorrhagic events. URL: http://www.clinicaltrials.gov. Unique identifiers: NCT00433966 (HORIZONS-AMI) and ACUITY (NCT00093158). © 2015 American Heart Association, Inc.
    Circulation Cardiovascular Interventions 08/2015; 8(8):e002475. DOI:10.1161/CIRCINTERVENTIONS.114.002475 · 6.98 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Dual antiplatelet therapy reduces the risk of myocardial infarction, stent thrombosis, and cardiovascular mortality after percutaneous coronary intervention, but the optimal duration of therapy remains unclear. Stent thrombosis, one of the most feared complications of coronary intervention, is associated with high mortality and morbidity and is related in part to technical and patient-specific factors. Advances in device technology and better understanding of the pathophysiology of stent thrombosis have reduced the frequency of this devastating complication. Bioresorbable vascular scaffolds possess a number of advantageous features and are currently undergoing active investigation. Bioresorbable vascular scaffolds have been demonstrated to restore physiologic vasomotion, allow for late lumen enlargement, and upon full resorption remove the nidus for very late polymer reactions and resolve concerns of stent malapposition and side branch jailing. Based on the results from recent large-scale randomized trials, the optimal duration of dual antiplatelet therapy may depend on the choice of device type, as well as the individual patient risk of ischemic versus hemorrhagic complications. © 2015 Wiley Periodicals, Inc. © 2015 Wiley Periodicals, Inc.
    Catheterization and Cardiovascular Interventions 08/2015; DOI:10.1002/ccd.26099 · 2.40 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: In the Providing Regional Observations to Study Predictors of Events in the Coronary Tree (PROSPECT) study, plaque burden, plaque composition, and minimal luminal area were associated with an increased risk of adverse cardiovascular events arising from untreated atherosclerotic lesions (vulnerable plaques) in patients with acute coronary syndromes (ACS). We sought to evaluate the utility of biomarker profiling and clinical risk factors to predict 3-year all-cause and nonculprit lesion-related major adverse cardiac events (MACEs). Of 697 patients who underwent successful percutaneous coronary intervention (PCI) for ACS, an array of 28 baseline biomarkers was analyzed. Median follow-up was 3.4 years. Beta2-microglobulin displayed the strongest predictive power of all variables assessed for all-cause and nonculprit lesion-related MACE. In a classification and regression tree analysis, patients with beta2-microglobulin >1.92 mg/L had an estimated 28.7% 3-year incidence of all-cause MACE; C-peptide <1.32 ng/ml was associated with a further increase in MACE to 51.2%. In a classification and regression tree analysis for untreated nonculprit lesion-related MACE, beta2-microglobulin >1.92 mg/L identified a cohort with a 3-year rate of 18.5%, and C-peptide <2.22 ng/ml was associated with a further increase to 25.5%. By multivariable analysis, beta2-microglobulin was the strongest predictor of all-cause and nonculprit MACE during follow-up. High-density lipoprotein (HDL), transferrin, and history of angina pectoris were also independent predictors of all-cause MACE, and HDL was an independent predictor of nonculprit MACE. In conclusion, in the PROSPECT study, beta2-microglobulin strongly predicted all-cause and nonculprit lesion-related MACE within 3 years after PCI in ACS. C-peptide and HDL provided further risk stratification to identify angiographically mild nonculprit lesions prone to future MACE. Copyright © 2015 Elsevier Inc. All rights reserved.
    The American journal of cardiology 07/2015; DOI:10.1016/j.amjcard.2015.07.017 · 3.43 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Prior aspirin treatment is considered a risk factor for adverse outcomes in acute coronary syndrome (ACS) patients. The relationships between aspirin pretreatment and findings on quantitative coronary angiography (QCA) and intravascular ultrasound (IVUS), as well as clinical outcomes, are not well understood. In the PROSPECT trial, QCA and triple-vessel IVUS imaging were performed after successful percutaneous coronary intervention (PCI) of the culprit lesion(s) in ACS patients. We compared patients receiving aspirin within 7 days of enrollment to those naive to aspirin. Propensity score matching was performed to adjust for differences in baseline characteristics. Aspirin-pretreated patients (n = 236; 35%) were older and more likely to have known coronary disease than those without pretreatment (P≤.01 for all). Pretreated patients had more untreated non-culprit lesions with angiographic and IVUS characteristics predictive of future events (53.1% vs 38.6%; P<.001). There were no significant differences in overall major adverse cardiac event (MACE) rates at 3 years between the aspirin and no-aspirin groups (23.6% vs 18.8%, respectively; P=.17) in unadjusted or propensity-adjusted analyses. Prior aspirin use was not an independent predictor of MACE at 3 years (hazard ratio, 1.21; 95% confidence interval, 0.73-2.01; P=.45). In the PROSPECT trial, aspirin pretreatment identifies an older population with more advanced coronary disease. Aspirin pretreatment was not an independent predictor of MACE in ACS patients treated with an early invasive strategy. The extent to which aspirin pretreatment is a risk factor for adverse events after PCI in ACS should be revisited.
    The Journal of invasive cardiology 07/2015; · 0.82 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Mitral regurgitation (MR) is one of the most prevalent valve disorders and has numerous etiologies, including primary (organic) MR, due to underlying degenerative/structural mitral valve (MV) pathology, and secondary (functional) MR, which is principally caused by global or regional left ventricular remodeling and/or severe left atrial dilation. Diagnosis and optimal management of MR requires integration of valve disease and heart failure specialists, MV cardiac surgeons, interventional cardiologists with expertise in structural heart disease, and imaging experts. The introduction of transcatheter MV therapies has highlighted the need for a consensus approach to pragmatic clinical trial design and uniform endpoint definitions to evaluate outcomes in patients with MR. The Mitral Valve Academic Research Consortium is a collaboration between leading academic research organizations and physician-scientists specializing in MV disease from the United States and Europe. Three in-person meetings were held in Virginia and New York during which 44 heart failure, valve, and imaging experts, MV surgeons and interventional cardiologists, clinical trial specialists and statisticians, and representatives from the U.S. Food and Drug Administration considered all aspects of MV pathophysiology, prognosis, and therapies, culminating in a 2-part document describing consensus recommendations for clinical trial design (Part 1) and endpoint definitions (Part 2) to guide evaluation of transcatheter and surgical therapies for MR. The adoption of these recommendations will afford robustness and consistency in the comparative effectiveness evaluation of new devices and approaches to treat MR. These principles may be useful for regulatory assessment of new transcatheter MV devices, as well as for monitoring local and regional outcomes to guide quality improvement initiatives. Copyright © 2015 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
    European Heart Journal 07/2015; 66(3). DOI:10.1093/eurheartj/ehv333 · 14.72 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Mitral regurgitation (MR) is one of the most prevalent valve disorders and has numerous etiologies, including primary (organic) MR, due to underlying degenerative/structural mitral valve (MV) pathology, and secondary (functional) MR, which is principally caused by global or regional left ventricular remodeling and/or severe left atrial dilation. Diagnosis and optimal management of MR requires integration of valve disease and heart failure specialists, MV cardiac surgeons, interventional cardiologists with expertise in structural heart disease, and imaging experts. The introduction of transcatheter MV therapies has highlighted the need for a consensus approach to pragmatic clinical trial design and uniform endpoint definitions to evaluate outcomes in patients with MR. The Mitral Valve Academic Research Consortium is a collaboration between leading academic research organizations and physician-scientists specializing in MV disease from the United States and Europe. Three in-person meetings were held in Virginia and New York during which 44 heart failure, valve, and imaging experts, MV surgeons and interventional cardiologists, clinical trial specialists and statisticians, and representatives from the U.S. Food and Drug Administration considered all aspects of MV pathophysiology, prognosis, and therapies, culminating in a 2-part document describing consensus recommendations for clinical trial design (Part 1) and endpoint definitions (Part 2) to guide evaluation of transcatheter and surgical therapies for MR. The adoption of these recommendations will afford robustness and consistency in the comparative effectiveness evaluation of new devices and approaches to treat MR. These principles may be useful for regulatory assessment of new transcatheter MV devices, as well as for monitoring local and regional outcomes to guide quality improvement initiatives. Copyright © 2015 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
    European Heart Journal 07/2015; 66(3). DOI:10.1093/eurheartj/ehv281 · 14.72 Impact Factor
  • JACC. Cardiovascular imaging 07/2015; DOI:10.1016/j.jcmg.2015.02.019 · 6.99 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Despite the large number of novel therapies under basic scientific investigation, the translation of cardioprotective strategies targeting reperfusion injury to improve patient outcomes following percutaneous coronary intervention (PCI) for myocardial infarction (MI) has been disappointing. The varying susceptibility of an individual to reperfusion injury, as well as the narrow window of opportunity in which to intervene, adds significant complexity. Here, we discuss the unmet need and challenges of translating cardioprotective strategies into clinical practice, review the pathophysiology of microvascular dysfunction and lethal reperfusion as they relate to promising novel therapeutics, and evaluate recent and ongoing clinical trials in the field. Copyright © 2015 Elsevier Ltd. All rights reserved.
    Trends in Pharmacological Sciences 07/2015; DOI:10.1016/j.tips.2015.06.004 · 9.99 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: There is a common misperception in the cardiology community that most acute coronary events arise from ruptures of mildly stenotic plaques. This notion has emanated from multiple studies that had measured the degree of angiographic luminal narrowing in culprit plaques months to years before myocardial infarction. However, angiographic studies within 3 months before myocardial infarction, immediately after myocardial infarction with thrombus aspiration or fibrinolytic therapy, and postmortem pathological observations have all shown that culprit plaques in acute myocardial infarction are severely stenotic. Serial angiographic studies also have demonstrated a sudden rapid lesion progression before most cases of acute coronary syndromes. The possible mechanisms for such rapid plaque progression and consequent luminal obstruction include recurrent plaque rupture and healing and intraplaque neovascularization and hemorrhage with deposition of erythrocyte-derived free cholesterol. Moreover, recent intravascular and noninvasive imaging studies have demonstrated that plaques which result in coronary events have larger plaque volume and necrotic core size with greater positive vessel remodeling compared with plaques, which remain asymptomatic during several years follow-up, although these large atheromatous vulnerable plaques may angiographically seem mild. As such, it is these vulnerable plaques which are more prone to rapid plaque progression or are those in which plaque progression is more likely to become clinically evident. Therefore, in addition to characterizing plaque morphology, inflammatory activity, and severity, detection of the rate of plaque progression might identify vulnerable plaques with an increased potential for adverse outcomes. © 2015 American Heart Association, Inc.
    Circulation Research 06/2015; 117(1):99-104. DOI:10.1161/CIRCRESAHA.117.305637 · 11.09 Impact Factor
  • Gerald S. Werner · Harvey Hecht · Gregg W. Stone
    JACC. Cardiovascular imaging 06/2015; DOI:10.1016/j.jcmg.2015.04.009 · 6.99 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: For many years, coronary artery bypass graft surgery has been the gold standard for revascularization of patients with left main disease; however, increasing evidence suggests that percutaneous coronary intervention with drug-eluting stents may be an acceptable alternative or even preferred in select cases. This review will present clinical evidence examining the outcomes of drug-eluting stents compared to coronary artery bypass graft surgery for unprotected left main coronary artery disease and discuss the anatomic factors, patient variables, and clinical strategies that may dictate choice of revascularization modality for patients with left main disease. If percutaneous coronary intervention is selected to treat unprotected left main disease, meticulous technique is essential to optimize outcomes, including use of procedural physiology and imaging guidance, optimal stent and adjunct pharmacology use, and expert management of the distal bifurcation. Finally, issues of equipoise and uncertainty are identified, representing areas for future investigation. © 2015, Wiley Periodicals, Inc.
    Journal of Interventional Cardiology 06/2015; DOI:10.1111/joic.12211 · 1.32 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: The optimal revascularization strategy in patients with acute coronary syndrome (ACS) and proximal left anterior descending (pLAD) coronary artery lesions is not well defined. The aim of this study was to compare the outcomes of ACS patients with pLAD culprit lesions receiving percutaneous coronary intervention (PCI) vs coronary artery bypass graft (CABG). The ACUITY trial was a multicenter, prospective trial of patients with ACS treated with an early invasive strategy. Major adverse cardiac event (MACE; defined as death, myocardial infarction [MI], and repeat revascularization) and stroke were compared at 30 days and 1 year between PCI and CABG in patients with significant stenosis of the pLAD undergoing revascularization. Postprocedural major bleeding was evaluated at 30 days. Among patients with a significant pLAD stenosis (n = 842), a total of 562 (66.7%) underwent PCI and 280 (33.3%) underwent CABG. Baseline characteristics, including age, sex, diabetes, and TIMI risk score, were well matched between groups; however, patients undergoing PCI were more likely to have had previous CABG (21.9% vs 6.4%; P<.001). Death, MI, MACE, and stroke rates did not differ between groups at 1 year. PCI patients had lower bleeding rates (8.1% vs 52.4%; P<.001) and blood product transfusion at 30 days (4.5% vs 41.3%; P<.001), but higher rates of unplanned revascularization at 1 year (12.7% vs 5.2%; P<.01). These results were consistent in patients with single vs multivessel disease and in diabetics vs non-diabetics. Among ACS patients with pLAD culprit lesions, an initial revascularization strategy of PCI compared with CABG yields similar 1-year death, MI, and MACE rates, although unplanned revascularization is more common after PCI.
    The Journal of invasive cardiology 06/2015; · 0.82 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: The preferred revascularization strategy for diabetic patients with acute coronary syndromes and multivessel coronary artery disease is uncertain. We evaluated the outcomes of diabetic patients with moderate and high-risk acute coronary syndrome and multivessel disease managed with percutaneous coronary intervention (PCI) versus coronary artery bypass grafting (CABG). Among 13 819 moderate and high-risk acute coronary syndrome patients enrolled in the Acute Catheterization and Early Intervention Triage Strategy (ACUITY) trial, 1772 diabetic patients had multivessel disease with left anterior descending artery involvement and were managed by PCI (n=1349) or CABG (n=423). Propensity scoring was applied to adjust for differences in baseline clinical and angiographic characteristics, yielding a total of 326 matched patients (163 managed by PCI and 163 managed by CABG). At 30 days, treatment with PCI compared with CABG was associated with lower rates of major bleeding (15.3% versus 55.6%; P<0.0001), blood transfusions (9.2% versus 43.2%; P<0.0001), and acute kidney injury (13.4% versus 33.6%; P<0.0001), but more unplanned revascularization procedures (6.9% versus 1.9%; P=0.03). At 1 year PCI was associated with higher rates of repeat revascularization procedures (19.5% versus 5.2%; P=0.0001), with nonsignificantly different rates of myocardial infarction, stroke, and death at either 30 days or 1 year. In the large-scale ACUITY trial, diabetic patients with acute coronary syndrome and multivessel disease treated with PCI rather than CABG had less bleeding and acute kidney injury, greater need for repeat revascularization procedures, and comparable rates of myocardial infarction, stroke, and death through 1-year follow-up. URL: http://www.clinicaltrials.gov. Unique identifier: NCT00093158. © 2015 American Heart Association, Inc.
    Circulation Cardiovascular Interventions 06/2015; 8(6). DOI:10.1161/CIRCINTERVENTIONS.114.002032 · 6.98 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Chronic kidney disease (CKD) is associated with increased rates of adverse events after percutaneous coronary intervention. We sought to determine the impact of CKD on platelet reactivity in clopidogrel-treated patients and whether high platelet reactivity (HPR) confers a similar or differential risk for adverse events among patients with CKD and non-CKD. We performed a post hoc analysis of the Assessment of Dual Antiplatelet Therapy With Drug-Eluting Stents (ADAPT-DES) registry, which included 8582 patients undergoing percutaneous coronary intervention with drug-eluting stents and platelet function testing using the VerifyNow assay. We compared HPR and its impact on ischemic and bleeding events >2 years among patients with CKD and non-CKD. Patients with CKD (n=1367) were older, more often female, diabetic, and had lower ejection fraction compared with their non-CKD counterparts (n=7043). Although HPR prevalence increased with worsening renal function in unadjusted analyses, these associations were no longer present after adjustment. Major adverse cardiac event rates at 2 years among those without CKD or HPR, HPR alone, CKD alone, and both CKD and HPR were 9.0%, 11.2%, 13.3%, and 17.5%, respectively (P<0.001). Associations between HPR and adverse events were uniform across CKD strata without evidence of interaction. HPR is more common among those with versus without CKD, an association that is attributable to confounding risk factors that are more prevalent in CKD. The impact of HPR on ischemic and bleeding events is similar irrespective of CKD status. URL: http://www.clinicaltrials.gov. Unique identifier: NCT00638794. © 2015 American Heart Association, Inc.
    Circulation Cardiovascular Interventions 06/2015; 8(6):e001683. DOI:10.1161/CIRCINTERVENTIONS.115.001683 · 6.98 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Overdosing of parenteral antithrombotic therapies can increase the risk of bleeding. Cangrelor is a potent intravenous platelet P2Y12 receptor antagonist with rapid onset and offset of action. In patients undergoing percutaneous coronary interventions (PCI), compared with control, cangrelor (30 µg/kg bolus, followed immediately by a 4 µg/kg per minute infusion for 2-4 h or until the conclusion of the index PCI, whichever was longer) reduces periprocedural thrombotic complications without an increase in major bleeding complications, although minor bleeding is increased. The impact of cangrelor overdosing on bleeding is unknown and represented the aim of this analysis. Patients with cangrelor overdosing were identified among safety population patients enrolled in the CHAMPION program (n = 25,107). Overdose was defined as administration of an excess >20 % of the bolus dose (30 μg/kg) and/or infusion rate (4 μg/kg per min). Bleeding complications were assessed. Among the safety analysis population in the CHAMPION program, 12,565 patients received cangrelor. A total of 36 overdosed cangrelor patients (0.29 %) were identified in this pooled analysis (20 with both bolus and infusion, 5 with bolus only, and 11 with infusion only). In the majority of patients, the dose did not exceed 2.5 times the recommended dose. Bleeding events were balanced between treatment arms and were consistent with those in the overall CHAMPION program. Only one overdosed patient experienced a serious bleed. There was no correlation between bleeding and magnitude of cangrelor overdose. In a large clinical trial program of patients undergoing PCI, cangrelor overdosing was rare and not associated with an increase in bleeding complications, an observation that may be attributed to its very short-half life and rapid offset of action.
    Journal of Thrombosis and Thrombolysis 05/2015; 65(10). DOI:10.1007/s11239-015-1233-3 · 2.17 Impact Factor
  • Joseph F. Sabik · Gregg W. Stone
    Journal of the American College of Cardiology 05/2015; 65(20). DOI:10.1016/j.jacc.2015.04.006 · 15.34 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Although smoking is a risk factor for coronary atherosclerosis, the age-related impact on lesion characteristics and plaque instability remains unclear. In ADAPT-DES, 780 patients with 916 culprit lesions were evaluated by preprocedural grayscale and virtual histology-intravascular ultrasound. Current smokers (smoking within 1 month) more often presented with acute coronary syndrome (67 vs. 51 vs. 51%, P<0.05) compared with former smokers (no smoking for >1 month) or nonsmokers. In patients 65 or more years of age, current smokers (vs. nonsmokers) showed larger normalized volumes of plaque and media [8.6 (7.8-9.4) vs. 7.2 (6.8-7.7) mm/mm, P=0.016] and external elastic membrane [14.4 (13.2-15.5) vs. 12.8 (12.2-13.4) mm/mm, P=0.05]. At the minimal lumen area site, despite a greater plaque burden, the larger external elastic membrane area [14.4 (13.1-15.7) vs. 12.0 (11.3-12.7) mm, P=0.003] contributed toward preserving the minimal lumen area [2.6 (2.4-2.7) vs. 2.6 (2.5-2.7) mm, P=0.91] in current smokers (vs. nonsmokers) 65 or more years of age. Moreover, current smokers (vs. nonsmokers) 65 or more years of age showed a greater normalized necrotic core volume [1.19 (0.96-1.46) vs. 0.75 (0.66-0.85) mm/mm, P=0.0007], more thin-cap fibroatheromas (61 vs. 48%, P=0.04), and plaque ruptures (38 vs. 26%, P=0.051). Conversely, in patients younger than 65 years of age, there was no significant difference in culprit lesion morphology among current, former, and nonsmokers. In patients 65 or more years (not in patients<65 years), smoking increased culprit lesion plaque instability (greater plaque with more necrotic core, thin-cap fibroatheromas, positive remodeling, and plaque ruptures).
    Coronary artery disease 05/2015; DOI:10.1097/MCA.0000000000000268 · 1.30 Impact Factor

Publication Stats

29k Citations
9,924.15 Total Impact Points

Institutions

  • 2015
    • Erasmus Universiteit Rotterdam
      • Department of Cardiology
      Rotterdam, South Holland, Netherlands
  • 2009–2015
    • New York Presbyterian Hospital
      • Department of Cardiology
      New York, New York, United States
    • Harvard University
      Cambridge, Massachusetts, United States
    • Centre Hospitalier Universitaire de Caen
      Caen, Lower Normandy, France
    • Duke University Medical Center
      • Duke Clinical Research Institute
      Durham, NC, United States
  • 2005–2015
    • CUNY Graduate Center
      New York, New York, United States
    • Isala Klinieken
      Zwolle, Overijssel, Netherlands
    • Chiba University
      Tiba, Chiba, Japan
    • Boston Scientific
      Boston, Massachusetts, United States
  • 2004–2015
    • Columbia University
      • Division of Cardiology
      New York, New York, United States
    • Brigham and Women's Hospital
      Boston, Massachusetts, United States
    • Allegheny General Hospital
      Pittsburgh, Pennsylvania, United States
  • 2000–2014
    • Cardiovascular Research Foundation
      New York, New York, United States
    • Cornell University
      Итак, New York, United States
  • 2013
    • The Christ Hospital
      Cincinnati, Ohio, United States
    • Florida Hospital
      Florida, United States
  • 2010–2013
    • Yale-New Haven Hospital
      New Haven, Connecticut, United States
    • Lehigh Valley Health Network
      Allentown, Pennsylvania, United States
    • Kaiser Permanente
      • Department of Cardiology
      Oakland, CA, United States
    • Mayo Clinic - Rochester
      • Department of Cardiovascular Diseases
      Рочестер, Minnesota, United States
    • Fortis Escorts Heart Institute
      New Dilli, NCT, India
    • University of Catania
      • Department of Surgery (CHIR)
      Catania, Sicily, Italy
  • 2012
    • Icahn School of Medicine at Mount Sinai
      • Division of Cardiology
      Manhattan, New York, United States
    • Mount Sinai Medical Center
      New York City, New York, United States
  • 2011
    • University of California, Los Angeles
      Los Ángeles, California, United States
    • Methodist Hospitals
      Gary, Indiana, United States
    • Gracie Square Hospital, New York, NY
      New York, New York, United States
    • Saint Luke's Health System (KS, USA)
      Kansas City, Kansas, United States
    • Auckland City Hospital
      Окленд, Auckland, New Zealand
  • 2001–2008
    • Lenox Hill Hospital
      New York, New York, United States
  • 2007
    • University of Hamburg
      Hamburg, Hamburg, Germany
    • Rambam Medical Center
      • Department of Cardiology
      H̱efa, Haifa District, Israel
  • 2006
    • University of Southampton
      Southampton, England, United Kingdom
    • Mid-Columbia Medical Center
      DLS, Oregon, United States
  • 2002–2005
    • Hospital General Universitario Gregorio Marañón
      Madrid, Madrid, Spain
  • 1999–2004
    • Washington Hospital Center
      Washington, Washington, D.C., United States
  • 2003
    • Duke University
      Durham, North Carolina, United States
    • Stanford University
      • Division of Cardiovascular Medicine
      Palo Alto, California, United States
  • 1995–2002
    • William Beaumont Army Medical Center
      El Paso, Texas, United States
    • Beaumont Hospital
      Dublin, Leinster, Ireland
  • 1995–1999
    • El Camino Hospital
      Mountain View, California, United States
  • 1989–1996
    • St. Luke's Hospital
      Cedar Rapids, Iowa, United States
  • 1990
    • University of Missouri - Kansas City
      Kansas City, Missouri, United States