18 research outputs found

    998-61 Population Prevalence of Wolff-Parkinson-White Syndrome

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    Little is known about the epidemiology of Wolff-Parkinson-White (WPW) syndrome in the general population. Virtually all previous studies have been either case series from tertiary care centers or limited to young adult males screened for military training. To date, there are no detailed studies of the prevalence of WPW in the general population. To determine the prevalence of WPW in the general population, we used the Marshfield Epidemiologic Study Area (MESA), a population laboratory of 50,000 people residing in 12 contiguous zip codes in central Wisconsin. Prevalence was determined as of 7/1/91 among MESA residents who had a diagnosis of WPW between 1/1/79 and 6/30/91. Cases were identified by reviewing the medical records and electrocardiograms of: a) all 32 MESA residents with the WPW diagnosis identified by International Classification of Diseases, 9th Revision (ICD-9) Code 426.7 as a hospital discharge or outpatient clinic diagnosis, b) 600 patients with suspected supraventricular arrhythmias identified by three ICD 9 codes, and c) all patients who had an invasive electrophysiology study for overt WPW syndrome in our institution over the last 10 years.ResultsWe identified 25 prevalent cases of WPW resulting in an overall population prevalence of 5.1/10,000 (95% C.I., 3.1–7.1).Age specific-prevalence rates per 10,000 were: 0–19 years –2.0; 20–39 years –5.5; 40–59 years –9.6; > 60 years –4.8. There was no significant difference in males versus females. Al1 25 verified cases were identified from the 32 potential cases with ICD-9 Code 426.7, indicating that this code is 100% sensitive and has a 78% positive predictive value for WPW syndrome.Conclusions1) The prevalence of WPW in the general population is lower than that reported in selected populations and appears to be highest in those of late middle-age. 2) Based on the findings of our study, we estimate that there are approximately 130,000 individuals in the United States with electrocardiographic documentation of WPW

    Comparison of Inappropriate Shocks and Other Health Outcomes Between Single- and Dual-Chamber Implantable Cardioverter-Defibrillators for Primary Prevention of Sudden Cardiac Death: Results From the Cardiovascular Research Network Longitudinal Study of Implantable Cardioverter-Defibrillators

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    BACKGROUND: In US clinical practice, many patients who undergo placement of an implantable cardioverter-defibrillator (ICD) for primary prevention of sudden cardiac death receive dual-chamber devices. The superiority of dual-chamber over single-chamber devices in reducing the risk of inappropriate ICD shocks in clinical practice has not been established. The objective of this study was to compare risk of adverse outcomes, including inappropriate shocks, between single- and dual-chamber ICDs for primary prevention. METHODS AND RESULTS: We identified patients receiving a single- or dual-chamber ICD for primary prevention who did not have an indication for pacing from 15 hospitals within 7 integrated health delivery systems in the Longitudinal Study of Implantable Cardioverter-Defibrillators from 2006 to 2009. The primary outcome was time to first inappropriate shock. ICD shocks were adjudicated for appropriateness. Other outcomes included all-cause hospitalization, heart failure hospitalization, and death. Patient, clinician, and hospital-level factors were accounted for using propensity score weighting methods. Among 1042 patients without pacing indications, 54.0% (n=563) received a single-chamber device and 46.0% (n=479) received a dual-chamber device. In a propensity-weighted analysis, device type was not significantly associated with inappropriate shock (hazard ratio, 0.91; 95% confidence interval, 0.59-1.38 [P=0.65]), all-cause hospitalization (hazard ratio, 1.03; 95% confidence interval, 0.87-1.21 [P=0.76]), heart failure hospitalization (hazard ratio, 0.93; 95% confidence interval, 0.72-1.21 [P=0.59]), or death (hazard ratio, 1.19; 95% confidence interval, 0.93-1.53 [P=0.17]). CONCLUSIONS: Among patients who received an ICD for primary prevention without indications for pacing, dual-chamber devices were not associated with lower risk of inappropriate shock or differences in hospitalization or death compared with single-chamber devices. This study does not justify the use of dual-chamber devices to minimize inappropriate shocks

    Evaluation of Genetic Factors for Warfarin Dose Prediction

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    Objectives: Warfarin is a commonly prescribed anticoagulant drug used to prevent thromboses that may arise as a consequence of orthopedic and vascular surgery or underlying cardiovascular disease. Warfarin is associated with a notoriously narrow therapeutic window where small variations in dosing may result in hemorrhagic or thrombotic complications. To ultimately improve dosing of warfarin, we evaluated models for stable maintenance dose that incorporated both clinical and genetic factors. Method: A model was constructed by evaluating the contribution to dosing variability of the following clinical factors: age, gender, body surface area, and presence or absence of prosthetic heart valves or diabetes. The model was then sequentially expanded by incorporating polymorphisms of cytochrome P450 (CYP) 2C9; vitamin K 2,3 epoxide reductase complex, subunit 1 (VKORC1); gamma carboxylase; factor VII; and apolipoprotein (Apo) E genes. Results: Of genetic factors evaluated in the model, CYP2C9 and VKORC1 each contributed substantially to dose variability, and together with clinical factors explained 56% of the individual variability in stable warfarin dose. In contrast, gamma carboxylase, factor VII and Apo E polymorphisms contributed little to dose variability. Conclusion: The importance of CYP2C9 and VKORC1 to patient-specific dose of warfarin has been confirmed, while polymorphisms of gamma carboxylase, factor VII and Apo E genes did not substantially contribute to predictive models for stable warfarin dose

    Missense mutations in the rod domain of the lamin A/C gene as causes of dilated cardiomyopathy and conduction-system disease

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    Inherited mutations cause approximately 35 percent of cases of dilated cardiomyopathy; however, few genes associated with this disease have been identified. Previously, we located a gene defect that was responsible for autosomal dominant dilated cardiomyopathy and conduction-system disease on chromosome 1p1-q21, where nuclear-envelope proteins lamin A and lamin C are encoded by the LMNA (lamin A/C) gene. Mutations in the head or tail domain of this gene cause Emery-Dreifuss muscular dystrophy, a childhood-onset disease characterized by joint contractures and in some cases by abnormalities of cardiac conduction during adulthood
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