Circulation: Arrhythmia and Electrophysiology
Previous studies of costs related to device infections have been limited to those during the hospitalization. This study, which included costs incurred during subsequent care found very high 1- year costs associated with device infections. These substantial costs support dedication of resources to reduce infection rates.
Incidence, Treatment Intensity, and Incremental Annual Expenditures for Patients Experiencing a Cardiac Implantable Electronic Device Infection
Evidence From a Large US Payer Database 1-Year Post Implantation
M. Rizwan Sohail, MD Elizabeth L. Eby, MPH Michael P. Ryan, MS Candace Gunnarsson, EdD Laura A. Wright, PhD Arnold J. Greenspon, MD
Correspondence to: Elizabeth L. Eby, MPH, Medtronic, Plc, 8200 Coral Sea St NE, Mounds View, MN 55112. E-mail
Background: Because of the increasing use of cardiac implantable electronic devices (CIEDs), it is important to estimate the incidence and annual healthcare expenditures associated with CIED infections.
Methods and Results: Patients with a record of an initial or replacement (full implant or generator only) CIED implant during the calendar years 2009 to 2012 in MarketScan Commercial Claims and Medicare Supplemental database were identified. CIED infections were classified into 4 categories: (1) infection not managed by inpatient admission nor implant removal, (2) infection managed by inpatient admission but no implant removal, (3) infection managed by an implant removal either in an inpatient or in an outpatient setting, and (4) infection with severe sepsis and managed in an inpatient setting with implant removal. Using separate models for initial and replacement cohorts, annualized incidence of infection and incremental annual expenditures by treatment intensity were estimated. Cumulative incidence of infection at 1 year post implant was 1.18% for initial CIED implants and 2.37% for replacement. Median time to infection was 35 days for initial and 23 days for replacement. Incremental healthcare expenditures by treatment intensity categories for initial implant patients at 1 year were $16 651, $104 077, $45 291, and $279 744. For replacement patients, incremental expenditures at 1 year by treatment intensity categories were $26 857, $43 541, $48 759, and $362 606.
Conclusions: The management of CIED infections results in a substantial healthcare burden with a significant increase in annual expenditures the year after implant when device infection occurs.
Circ Arrhythm Electrophysiol. 2016;9:e003929, doi:10.1161/CIRCEP.116.003929.
Circulation: Cardiovascular Genetics
In this study, two novel genetic loci were identified via genome-wide association study with systolic blood pressure in specific age epochs. This suggests that genetic determinants of blood pressure begin in childhood and vary across the lifespan.
International Genome-Wide Association Study Consortium Identifies Novel Loci Associated With Blood Pressure in Children and Adolescents
Priyakumari Ganesh Parmar, PhD H. Rob Taal, MD, PhD Nicholas J. Timpson, PhD Elisabeth Thiering, PhD Terho Lehtimäki, MD, PhD Marcella Marinelli, PhD Penelope A. Lind, PhD Laura D. Howe, PhD Germaine Verwoert, PhD Ville Aalto, MSc Andre G. Uitterlinden, PhD Laurent Briollais, PhD Dave M. Evans, PhD Margie J. Wright, PhD John P. Newnham, MD John B. Whitfield, PhD Leo-Pekka Lyytikäinen, MD Fernando Rivadeneira, MD, PhD Dorrett I. Boomsma, PhD Jorma Viikari, MD, PhD Matthew W. Gillman, MD SM, Beate St Pourcain, PhD Jouke-Jan Hottenga, PhD Grant W. Montgomery, PhD Albert Hofman, MD, PhD Mika Kähönen, MD, PhD Nicholas G. Martin, PhD Martin D. Tobin, PhD Ollie Raitakari, MD, PhD Jesus Vioque, MD, PhD Vincent W.V. Jaddoe, MD, PhD Marjo-Riita Jarvelin, MD, PhD Lawrence J. Beilin, MD Joachim Heinrich, PhD Cornelia M. van Duijn, PhD Craig E. Pennell, MD, PhD Debbie A. Lawlor, MD, PhD Lyle J. Palmer, PhD Early Genetics and Lifecourse Epidemiology Consortium
Correspondence to: Priyakumari Ganesh Parmar, PhD, Auckland University of Technology, 90 Akoranga Dr, Northcote, Auckland, 0627, New Zealand. E-mailor Debbie A. Lawlor, MD, PhD, MRC IEU, Oakfield House, Oakfield Grove, Bristol, BS8 2BN, United Kingdom. E-mail
Background: Our aim was to identify genetic variants associated with blood pressure (BP) in childhood and adolescence.
Methods and Results: Genome-wide association study data from participating European ancestry cohorts of the Early Genetics and Lifecourse Epidemiology (EAGLE) Consortium was meta-analyzed across 3 epochs; prepuberty (4–7 years), puberty (8–12 years), and postpuberty (13–20 years). Two novel loci were identified as having genome-wide associations with systolic BP across specific age epochs: rs1563894 (ITGA11, located in active H3K27Ac mark and transcription factor chromatin immunoprecipitation and 5′-C-phosphate-G-3′ methylation site) during prepuberty (P=2.86×10–8) and rs872256 during puberty (P=8.67×10–9). Several single-nucleotide polymorphism clusters were also associated with childhood BP at P<5×10–3. Using a P value threshold of <5×10–3, we found some overlap in variants across the different age epochs within our study and between several single-nucleotide polymorphisms in any of the 3 epochs and adult BP-related single-nucleotide polymorphisms.
Conclusions: Our results suggest that genetic determinants of BP act from childhood, develop over the lifecourse, and show some evidence of age-specific effects.
Circ Cardiovasc Genet. 2016;9:266-278. doi:10.1161/CIRCGENETICS.115.001190.
Circulation: Cardiovascular Imaging
Echocardiographic predictors of sudden cardiac death in the general population included reduced left ventricular ejection fraction, mitral annular calcification, mitral E/A >1.5 or <0.7, increased left ventricular mass, and increased left atrial diameter. These predictors provided incremental value compared with clinical risk factors in predicting sudden cardiac death, which may allow clinicians to use this information to better understand who may be at risk.
Echocardiographic Predictors of Sudden Cardiac Death
The Atherosclerosis Risk in Communities Study and Cardiovascular Health Study
Suma H. Konety, MD, MS Ryan J. Koene, MD Faye L. Norby, MS, MPH Tony Wilsdon, MS Alvaro Alonso, MD, PhD David Siscovick, MD, MPH Nona Sotoodehnia, MD, MPH John Gottdiener, MD Ervin R. Fox, MD Lin Y. Chen, MD, MS Selcuk Adabag, MD, MS Aaron R. Folsom, MD, MPH
Correspondence to: Suma H. Konety, MD, MS, Cardiovascular Division, Department of Medicine, University of Minnesota, 420 Delaware St SE, MMC 508, Minneapolis, MN 55455. E-mail
Background: This study assessed the echocardiographic predictors of sudden cardiac death (SCD) within 2 population-based cohorts.
Methods and Results: Echocardiograms were obtained on 2383 participants (1993–1995) from the ARIC study (Atherosclerosis Risk in Communities; 100% black) and 5366 participants (1987–1989 and 1994–1995) from the CHS (Cardiovascular Health Study). The main outcome was physician-adjudicated SCD. We used Cox proportional-hazards models with incident coronary heart disease and heart failure as time-dependent covariates to assess the association between echocardiographic variables and SCD, adjusting for Framingham risk score variables, coronary heart disease, and renal function. Cohort-specific results were meta-analyzed. During a median follow-up of 7.3 and 13.1 years, 44 ARIC study participants and 275 CHS participants had SCD, respectively. In the meta-analyzed results, the adjusted hazard ratios (95% confidence intervals) for predictors of SCD were 3.07 (2.29–4.11) for reduced left ventricular ejection fraction; 1.85 (1.36–2.52) for mitral annular calcification; 1.64 (1.07–2.51) for mitral E/A >1.5, and 1.52 (1.14–2.02) for mitral E/A <0.7 (versus mitral E/A 0.7–1.5); 1.30 (1.15–1.48) per 1 SD increase in left ventricular mass; and 1.15 (1.02–1.30) per 1 SD increase in left atrial diameter. A receiver-operating characteristic model for prediction of SCD using Framingham risk score variables had a C statistic of 0.61 for ARIC study and 0.67 for CHS; the full multivariable model including all echocardiographic variables had a C statistic of 0.76 for ARIC study and 0.74 for CHS.
Conclusions: In addition to reduced left ventricular ejection fraction, we identified other echocardiographic-derived variables predictive for SCD that provided incremental value compared with clinical risk factors.
Circ Cardiovasc Imaging. 2016;9:e004431. doi:10.1161/CIRCIMAGING.115.004431.
Circulation: Cardiovascular Interventions
Few studies have evaluated the impact of routine use of fractional flow reserve (FFR) on clinical decision-making in “real world” cohorts. This analyses from a large registry showed that FFR influenced clinical care in almost 50% of cases, and may reduce downstream need for noninvasive stress testing and new procedures.
Impact of Routine Fractional Flow Reserve Evaluation During Coronary Angiography on Management Strategy and Clinical Outcome
One-Year Results of the POST-IT Multicenter Registry
Sergio Bravo Baptista, MD Luís Raposo, MD Lino Santos, MD Ruben Ramos, MD Rita Calé, MD Elisabete Jorge, MD, PhD Carina Machado, MD Marco Costa, MD Eduardo Infante de Oliveira, MD João Costa, MD João Pipa, MD Nuno Fonseca, MD Jorge Guardado, MD Bruno Silva, MD Maria-João Sousa, MD João Carlos Silva, MD Alberto Rodrigues, MD Luís Seca, MD Renato Fernandes, MD
Correspondence to: Sergio Bravo Baptista, MD, Cardiology Department, Hospital Prof. Doutor Fernando da Fonseca, IC 19, 2720-276 Amadora, Portugal. E-mailor Luís Raposo, MD, Cardiology Department, UNICARV, Hospital de Santa Cruz, CHLO, Av. Professor Reinaldo dos Santos, 2790-134 Carnaxide, Portugal. E-mail
Background: Penetration of fractional flow reserve (FFR) in clinical practice varies extensively, and the applicability of results from randomized trials is understudied. We describe the extent to which the information gained from routine FFR affects patient management strategy and clinical outcome.
Methods and Results: Nonselected patients undergoing coronary angiography, in which at least 1 lesion was interrogated by FFR, were prospectively enrolled in a multicenter registry. FFR-driven change in management strategy (medical therapy, revascularization, or additional stress imaging) was assessed per-lesion and per-patient, and the agreement between final and initial strategies was recorded. Cardiovascular death, myocardial infarction, or unplanned revascularization (MACE) at 1 year was recorded. A total of 1293 lesions were evaluated in 918 patients (mean FFR, 0.81±0.1). Management plan changed in 406 patients (44.2%) and 584 lesions (45.2%). One-year MACE was 6.9%; patients in whom all lesions were deferred had a lower MACE rate (5.3%) than those with at least 1 lesion revascularized (7.3%) or left untreated despite FFR≤0.80 (13.6%; log-rankP=0.014). At the lesion level, deferral of those with an FFR≤0.80 was associated with a 3.1-fold increase in the hazard of cardiovascular death/myocardial infarction/target lesion revascularization (P=0.012). Independent predictors of target lesion revascularization in the deferred lesions were proximal location of the lesion, B2/C type and FFR.
Conclusions: Routine FFR assessment of coronary lesions safely changes management strategy in almost half of the cases. Also, it accurately identifies patients and lesions with a low likelihood of events, in which revascularization can be safely deferred, as opposed to those at high risk when ischemic lesions are left untreated, thus confirming results from randomized trials.
Circ Cardiovasc Interv. 2016;9:e003288. doi:10.1161/CIRCINTERVENTIONS.115.003288.
Circulation: Cardiovascular Quality and Outcomes
This study evaluated the impact of the addition of niacin with laropiprant to statin-based therapy on health-related quality of life and costs. Niacin/laropiprant was associated with worse quality of life–adjusted survival and increased hospital costs.
Effects of Vascular and Nonvascular Adverse Events and of Extended-Release Niacin With Laropiprant on Health and Healthcare Costs
Seamus Kent, MSc Richard Haynes, DM, FRCP Jemma C. Hopewell, PhD Sarah Parish, DPhil Alastair Gray, PhD Martin J. Landray, PhD, FRCP Rory Collins, FMedSci, FRS Jane Armitage, FRCP, FFPH Borislava Mihaylova, DPhil On behalf of the HPS2-THRIVE Collaborative Group
Correspondence to: Borislava Mihaylova, Health Economics Research Centre, Nuffield Department of Population Health, University of Oxford, Old Rd Campus, Oxford, OX3 7LF, United Kingdom. E-mail
Background: Extended-release niacin with laropiprant did not significantly reduce the risk of major vascular events and increased the risk of serious adverse events in Heart Protection Study 2-Treatment of HDL to Reduce the Incidence of Vascular Events (HPS2-THRIVE), but its net effects on health and healthcare costs are unknown.
Methods and Results: 25 673 participants aged 50 to 80 years with previous cardiovascular disease were randomized to 2 g of extended-release niacin with 40 mg of laropiprant daily versus matching placebo, in addition to effective statin-based low-density lipoprotein cholesterol–lowering treatment. The net effects of niacin–laropiprant on quality–adjusted life years and hospital care costs (2012 UK £; converted into US $ using purchasing power parity index) during 4 years in HPS2-THRIVE were evaluated using estimates of the impact of serious adverse events on health-related quality of life and hospital care costs. During the study, participants assigned niacin–laropiprant experienced marginally but not statistically significantly lower survival (0.012 fewer years [standard error (SE) 0.007]), fewer quality-adjusted life years (0.023 [SE 0.007] fewer using UK EQ-5D scores; 0.020 [SE 0.006] fewer using US EQ-5D scores) and accrued greater hospital costs (UK £101 [SE £37]; US $145 [SE $53]). Stroke, heart failure, musculoskeletal events, gastrointestinal events, and infections were associated with significant decreases in health-related quality of life in both the year of the event and in subsequent years. All serious vascular and nonvascular events were associated with substantial increases in hospital care costs.
Conclusions: In HPS2-THRIVE, the addition of extended-release niacin–laropiprant to statin-based therapy reduced quality of life–adjusted survival and increased hospital costs.
Circ Cardiovasc Qual Outcomes. 2016;9:348-354. doi:10.1161/CIRCOUTCOMES.115.002592.
Circulation: Heart Failure
While the concept of complete recovery of left ventricular function and complete reverse remodeling after implantation of Left Ventricular Assist Devices (LVAD) is highly compelling, the rates of recovery reported over the years have varied widely. This large dataset suggests that recovery sufficient to enable LVAD explant is uncommon (≈ 1% per year), though partial recovery is more common (≈ 10%). Understanding the factors enabling recovery, developing treatments to speed the process and identifying patients to be targeted as most likely to recover are important areas for future research.
Myocardial Recovery in Patients Receiving Contemporary Left Ventricular Assist Devices
Results From the Interagency Registry for Mechanically Assisted Circulatory Support (INTERMACS)
Veli K. Topkara, MD, MSc A. Reshad Garan, MD Barry Fine, MD, PhD Amandine F. Godier-Furnémont, PhD Alexander Breskin, BS, MPH Barbara Cagliostro, RN, MSN Melana Yuzefpolskaya, MD Koji Takeda, MD, PhD Hiroo Takayama, MD, PhD Donna M. Mancini, MD Yoshifumi Naka, MD, PhD Paolo C. Colombo, MD
Correspondence to: Veli K. Topkara, MD, MSc, Columbia University Medical Center, Division of Cardiology, Heart Failure, Columbia University Medical Center–New York Presbyterian, 622 West 168th St, PH9-977, New York, NY. E-mail
Background: Time course and predictors of myocardial recovery on contemporary left ventricular assist device support are poorly defined because of limited number of recovery patients at any implanting center. This study sought to investigate myocardial recovery using multicenter data from the Interagency Registry for Mechanically Assisted Circulatory Support (INTERMACS).
Methods and Results: Thirteen thousand four hundred fifty-four adult patients were studied. Device explant rates for myocardial recovery were 0.9% at 1-year, 1.9% at 2-year, and 3.1% at 3-year follow-up. Independent predictors of device explantation for recovery were age <50 years (odds ratio [OR] 2.5), nonischemic etiology (OR 5.4), time since initial diagnosis <2 years (OR 3.4), suboptimal heart failure therapy before implant (OR 2.2), left ventricular end-diastolic diameter <6.5 cm (OR 1.7), pulmonary systolic artery pressure <50 mm Hg (OR 2.0), blood urea nitrogen <30 mg/dL (OR 3.3), and axial-flow device (OR 7.6). Patients with myocarditis (7.7%), postpartum cardiomyopathy (4.4%), and adriamycin-induced cardiomyopathy (4.1%) had highest rates of device explantation for recovery. Use of neurohormonal blockers on left ventricular assist device support was significantly higher in patients who were explanted for recovery. Importantly, 9% of all left ventricular assist device patients who were not explanted for recovery have demonstrated substantial improvement in left ventricular ejection fraction (partial recovery) and had remarkable overlap in clinical characteristic profile compared with patients who were explanted for recovery (complete recovery). Complete and partial recovery rates have declined in parallel with recent changes observed in device indications and technology.
Conclusions: Myocardial recovery is a spectrum of improvement rather than a binary clinical end point. One in every 10 left ventricular assist device patients demonstrates partial or complete myocardial recovery and should be targeted for functional assessment and optimization.
Circ Heart Fail. 2016;9:e003157. doi:10.1161/CIRCHEARTFAILURE.116.003157.
- © 2016 American Heart Association, Inc.