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Gender differences in J point height exist. Previous studies suggest male sex hormones mediate effects on cardiovascular disease through myocardial repolarization. Our objective was to assess whether male and female sex hormones are associated with J point amplitude in healthy subjects. We conducted a cross-sectional study of 475 healthy, mixed racial population of men, and premenopausal women (age 33 ± 9 years, 56% male). Baseline J point amplitude (JPA) was obtained from continuous surface electrocardiograms. Plasma testosterone (T), dihydrotestosterone, estrone, 17-estradiol (E2), and sex hormone–binding globulin were measured. A free testosterone index (FTI) was calculated. Multivariate regression analysis stratified by gender and electrocardiographic lead location was used to determine independent predictors of maximum JPA. Regression analysis demonstrated FTI levels were positively associated with JPA in lateral leads (β = +0.01, p <0.05) in men but not in women. Total testosterone was positively associated with anterior electrocardiographic lead JPA in women (β = +0.5, p <0.02), but not in men. E2 was positively associated with inferior lead JPA (β = +1.2, p <0.03) in men but not in women. Total testosterone levels were positively associated with JPA in anterior leads (β = +0.054, p <0.05) in women. Male volunteers in the highest tertile of FTI demonstrated greater lateral JPA compared with the lowest tertile (p <0.05). Women in the highest tertile of FTI demonstrated greater anterior lead JPA compared with the lowest tertile (p <0.05). In conclusion, in a young, healthy population, the female sex hormone E2 and an FTI are independent determinants of JPA in men, whereas T is associated with JPA in women.

Patients with left ventricular dysfunction due to nonischemic dilated cardiomyopathy are at substantial risk for sudden death from ventricular arrhythmias. This study found that prophylactic implantation of a cardioverter–defibrillator did not improve overall survival but significantly reduced the risk of death from cardiac arrhythmias. Prophylactic implantation of a cardioverter–defibrillator did not improve overall survival. Patients with nonischemic dilated cardiomyopathy often die suddenly. 1 Although therapy with angiotensin-converting–enzyme (ACE) inhibitors and beta-blockers has increased survival in clinical trials of patients with left ventricular dysfunction due to nonischemic and ischemic cardiomyopathies, such patients still have a substantial risk of sudden death from cardiac causes despite receiving adequate doses of both pharmacologic agents. 2 , 3 The implantable cardioverter–defibrillator (ICD) prevents sudden death in patients who have had an episode of ventricular tachycardia or cardiac arrest, 4 as well as in selected patients who have coronary disease and left ventricular dysfunction. 5 – 7 However, no large-scale studies have examined the role of . . .

Background Eleven criteria correlating electrocardiogram (ECG) findings with reduced left ventricular ejection fraction (LVEF) have been previously published. These have not been compared head‐to‐head in a single study. We studied their value as a screening test to identify patients with reduced LVEF estimated by cardiac magnetic resonance (CMR) imaging. Methods ECGs and CMR from 548 patients (age 61 + 11 years, 79% male) with previous myocardial infarction (MI), from the DETERMINE and PRE‐DETERMINE studies, were analyzed. Sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) of each criterion for identifying patients with LVEF ≤ 30% and ≤ 40% were studied. A useful screening test should have high sensitivity and NPV. Results Mean LVEF was 40% (SD = 11%); 264 patients (48.2%) had LVEF ≤ 40%, and 96 patients (17.5%) had LVEF ≤ 30%. Six of 11 criteria were associated with a significant lower LVEF, but had poor sensitivity to identify LVEF ≤ 30% (range 2.1%–55.2%) or LVEF ≤ 40% (1.1%–51.1%); NPVs were good for LVEF ≤ 30% (range 82.8%–85.9%) but not for LVEF ≤ 40% (range 52.1%–60.6%). Goldberger's third criterion (RV4/SV4 < 1) and combinations of maximal QRS duration > 124 ms + either Goldberger's third criterion or Goldberger's first criterion (SV1 or SV2 + RV5 or RV6 ≥ 3.5 mV) had high specificity (95.4%–100%) for LVEF ≤ 40%, although seen in only 48 (8.8%) patients; predictive values were similar on subgroup analysis. Conclusions None of the ECG criteria qualified as a good screening test. Three criteria had high specificity for LVEF ≤ 40%, although seen in < 9% of patients. Whether other ECG criteria can better identify LV dysfunction remains to be determined.

The DEFibrillators In Non-Ischemic Cardiomyopathy Treatment Evaluation (DEFINITE) was a multi-center, randomized, investigator-initiated trial. Patients enrolled in the trial had non-ischemic cardiomyopathy (LVEF 10 PVCs/hr or non-sustained ventricular tachycardia defined as 3 to 15 beats at a rate of >120 bpm) on Holter monitor or telemetry within the past 6 months. All patients received standard oral medical therapy for heart failure including angiotensin converting enzyme inhibitors and beta-blockers. Patients were randomized to implantable cardioverter defibrillator (ICD) versus no ICD. Patients were followed for 2 to 3 years. The primary endpoint was total mortality. Quality of life and pharmacoeconomics analysis was also performed. A registry tracked patients who met basic inclusion criteria but were not randomized. We estimated an annual total mortality of 15% at 2 years in the treatment arm that did not receive an ICD. The ICD was expected to reduce mortality by 50%. Approximately 229 patients were required in each treatment group. Forty-five centers were included in this trial that was designed to last an estimated 4 years. Enrollment was projected to occur over 2 1/2 years with a post enrollment follow-up of 1 1/2 years.