Citations

Background— Current risk models for predicting long-term mortality after percutaneous coronary intervention are restricted to all-cause mortality. We sought to develop novel risk models for the prediction of cardiac and noncardiac mortality after percutaneous coronary intervention. Methods and Results— We retrospectively evaluated patients who underwent index percutaneous coronary intervention at Mayo Clinic from 2003 to 2008. Long-term deaths were ascertained through scheduled prospective surveillance. Cause of death was determined via telephone interviews, medical records, and autopsy reports. Fine and Gray extension of Cox proportional hazards models was used to model cause-specific cumulative incidence. Candidate variables and interactions were chosen a priori, without variable selection methods. Resulting models were mapped to an integer-based risk score. The study comprised 6636 patients followed up over a median of 62 months (25th, 75th percentiles: 45, 77 months). There were 1488 deaths, 518 (35%) cardiac, 938 (63%) noncardiac, and 32 (2%) unknown. The 5-year predicted cardiac mortality ranged from 0.6% to 97%, with a corrected c -statistic of 0.82. Risk factors for cardiac death included age, body mass index, ejection fraction, and history of congestive heart failure. The integer score for noncardiac death included age, medicine index, body mass index, current smoker, noncardiac Charlson index and cardiac Charlson index, and accommodated significant age-based interactions for smoking and the 2 Charlson indices. Predicted noncardiac mortality at 5 years ranged from 0.2% to 81%, with a corrected c -statistic of 0.77. Conclusions— We report novel risk models to predict cardiac and noncardiac long-term mortality after percutaneous coronary intervention.

Background— Post-percutaneous coronary intervention (PCI) bleeding complications are an important quality metric. We sought to characterize site-level variation in post-PCI bleeding and explore the influence of patient and procedural factors on hospital bleeding performance. Methods and Results— Hospital-level bleeding performance was compared pre- and postadjustment using the newly revised CathPCI Registry ® bleeding risk model (c-index, 0.77) among 1292 National Cardiovascular Data Registry ® hospitals performing >50 PCIs from 7/2009 to 9/2012 (n=1 984 998 procedures). Using random effects models, outlier sites were identified based on 95% confidence intervals around the hospital’s random intercept. Bleeding 72 hours post-PCI was defined as: arterial access site, retroperitoneal, gastrointestinal, or genitourinary bleeding; intracranial hemorrhage; cardiac tamponade; nonbypass surgery–related blood transfusion with preprocedure hemoglobin ≥8 g/dL; or absolute decrease in hemoglobin value ≥3 g/dL with preprocedure hemoglobin ≤16 g/dL. Overall, the median unadjusted post-PCI bleeding rate was 5.2% and varied among hospitals from 2.6% to 10.4% (5th, 95th percentiles). Center-level bleeding variation persisted after case-mix adjustment (2.8%–9.5%; 5th, 95th percentiles). Although hospitals’ observed and risk-adjusted bleeding ranks were correlated (Spearman ρ: 0.88), individual rankings shifted after risk-adjustment (median Δ rank order: ±91.5; interquartile range: 37.0, 185.5). Outlier classification changed postadjustment for 29.3%, 16.1%, and 26.5% of low-, non-, and high-outlier sites, respectively. Hospital use of bleeding avoidance strategies (bivalirudin, radial access, or vascular closure device) was associated with risk-adjusted bleeding rates. Conclusions— Despite adjustment for patient case-mix, there is wide variation in rates of hospital PCI-related bleeding in the United States. Opportunities may exist for best performers to share practices with other sites.

Background— Spontaneous coronary artery dissection (SCAD) is an increasingly recognized nonatherosclerotic cause of acute coronary syndrome. The angiographic characteristics of SCAD are largely undetermined. The goal of this study was to determine the prevalence of coronary tortuosity in SCAD and whether it may be implicated in the disease. Methods and Results— Patients with confirmed SCAD (n=246; 45.3±8.9 years; 96% women) and 313 control patients without SCAD or coronary artery disease who underwent coronary angiography were included in this case–control study. Angiograms were reviewed for coronary tortuosity and assigned a tortuosity score. Tortuosity was common in patients presenting with their first SCAD event (78% versus 17% in controls; P <0.0001; tortuosity score, 4.41±1.73 versus 2.33±1.49 in controls; P <0.0001) despite a low prevalence of hypertension (34%). Recurrent SCAD (n=40) occurred within segments of tortuosity in 80% of cases. Severe tortuosity (≥2 consecutive curvatures ≥180°) was associated with a higher risk of recurrent SCAD (hazard ratio, 3.29; 95% confidence interval, 0.99–8.29; P =0.05). Tortuosity score >5 was associated with a trend toward higher risk of recurrent SCAD ( P =0.16). Prespecified angiographic markers of tortuosity including corkscrew appearance and multivessel symmetrical tortuosity were associated with extracoronary vasculopathy including fibromuscular dysplasia ( P <0.05 for both). Conclusions— Coronary artery tortuosity is highly prevalent in the SCAD population and is associated with recurrent SCAD. Recurrent SCAD most often occurs within segments of tortuosity. Angiographic features of SCAD are associated with extracoronary vasculopathy, including fibromuscular dysplasia. These findings suggest that coronary tortuosity may serve as a marker or potential mechanism for SCAD.

Background Assessing hospital quality in the performance of carotid endarterectomy ( CEA ) requires appropriate risk adjustment across hospitals with varying case mixes. The aim of this study was to develop and validate a prediction model to assess the risk of in‐hospital stroke or death after CEA that could aid in the assessment of hospital quality. Methods and Results Patients from National Cardiovascular Data Registry (NCDR)'s Carotid Artery Revascularization and Endarterectomy (CARE) Registry undergoing CEA without acute evolving stroke from 2005 to 2013 were included. In‐hospital stroke or death was modeled using hierarchical logistic regression with 20 candidate variables and accounting for hospital‐level clustering. Internal validation was achieved with bootstrapping; model discrimination and calibration were assessed. A total of 213 (1.7%) primary end point events occurred during 12 889 procedures. Independent predictors of stroke or death included age, prior peripheral artery disease, diabetes mellitus, prior coronary artery disease, having a symptomatic carotid lesion, having a contralateral carotid occlusion, or having New York Heart Association Class III or IV heart failure. The model was well calibrated and demonstrated moderate discriminative ability (c‐statistic 0.65). The NCDR CEA score was then developed to support simple, prospective risk quantification in the clinical setting. Conclusions The NCDR CEA score, comprising 7 clinical variables, predicts in‐hospital stroke or death after CEA . This model can be used to estimate hospital risk‐adjusted outcomes for CEA and to assist with the assessment of hospital quality.

ABSTRACTBackgroundThere is a paucity of data on the temporal trends of cardiovascular risk factors in patients undergoing percutaneous coronary intervention (PCI). We investigated the secular trends of risk profiles of patients undergoing PCI without prior history of cardiovascular disease (CVD).HypothesisCVD risk factors are changed over time.MethodsThis time‐trend analysis from 1994 to 2010 was performed within the Mayo Clinic PCI Registry. Outcome measures were prevalence of CVD risk factors, including the Framingham risk score (FRS), at the time of admission for PCI.ResultsDuring this period, 12,055 patients without a history of CVD (mean age, 65.0 ± 12.4 years, 67% male) underwent PCI at the Mayo Clinic. Age distribution slightly shifted toward older age (P for trend <0.05), but sex did not change over time. Despite a higher prevalence of hypertension, hypercholesterolemia, and diabetes mellitus over time, actual blood pressure and lipid profiles improved (P for trend <0.001). Over time, FRS and 10‐year CVD risk improved significantly (7.3 ± 3.2 to 6.5 ± 3.3, P for trend <0.001; and 11.0 to 9.0, P for trend <0.001, respectively). Body mass index, not included in the FRS, increased significantly (29.0 ± 5.2 to 30.1 ± 6.2 kg/m2, P for trend <0.001), whereas smoking prevalence did not change.ConclusionsThe current study demonstrates that although traditional FRS and its associated predicted 10‐year cardiovascular risk declined over time, the prevalence of risk factors increased in patients undergoing PCI. The study suggests the need for a new risk‐factor assessment in this patient population.

Background— The impact of changing demographics on causes of long-term death after percutaneous coronary intervention (PCI) remains incompletely defined. Methods and Results— We evaluated trends in cause-specific long-term mortality after index PCI performed at a single center from 1991 to 2008. Deaths were ascertained by scheduled prospective surveillance. Cause was determined via telephone interviews, medical records, autopsy reports, and death certificates. Competing-risks analysis of cause-specific mortality was performed using 3 time periods of PCI (1991–1996, 1997–2002, and 2003–2008). Final follow-up was December 31, 2012. A total of 19 077 patients survived index PCI hospitalization, of whom 6988 subsequently died (37%, 4.48 per 100 person-years). Cause was determined in 6857 (98.1%). Across 3 time periods, there was a 33% decline in cardiac deaths at 5 years after PCI (incidence: 9.8%, 7.4%, and 6.6%) but a 57% increase in noncardiac deaths (7.1%, 8.5%, and 11.2%). Only 36.8% of deaths in the recent era were cardiac. Similar trends were observed regardless of age, extent of coronary disease, or PCI indication. After adjustment for baseline variables, there was a 50% temporal decline in cardiac mortality but no change in noncardiac mortality. The decline in cardiac mortality was driven by fewer deaths from myocardial infarction/sudden death ( P <0.001) but not heart failure ( P =0.85). The increase in noncardiac mortality was primarily attributable to cancer and chronic diseases ( P <0.001). Conclusions— This study found a marked temporal switch from predominantly cardiac to predominantly noncardiac causes of death after PCI over 2 decades. The decline in cardiac mortality was independent of changes in baseline clinical characteristics. These findings have implications for patient care and clinical trial design.

Objectives: To determine the prevalence and relationship of frailty and health-related quality of life (HRQOL) among residents of long-term care [nursing homes (NH) and assisted living (AL)] facilities. Methods: Residents of NH and AL facilities in La Crosse County, Wisconsin, were recruited 1/2009-6/2010 and assessed for frailty (gait speed, unintended weight loss, grip strength), comorbidity (Charlson index), and HRQOL [Short Form (SF)-36]. Results: Among 137 participants, 85% were frail. Frail residents were older, had more comorbidities (2.0 vs. 0, p < .001) and lower mean SF-36 Physical Component Score (PCS, 32 vs. 48, p < .001). Following adjustments for age, sex, and comorbidities, compared to nonfrail residents, frail residents had lower SF-36 PCS (mean difference −14.7, 95% CI. −19.3,−10.1, p < .001). Frailty, comorbidity, and HRQOL did not differ between NH and AL facilities. Discussion: Frail residents had lower HRQOL, suggesting that preventing frailty may lead to better HRQOL among residents of long-term care facilities.