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The relation of bundle branch block (BBB) with adverse outcome is controversial. We hypothesized that increased QRS duration is an independent predictor of cardiovascular (CV) mortality in a cross-sectional US population. This is a retrospective cohort study on prospectively collected data to assess the relationship between QRS duration on routine ECG and CV mortality. Participants included 8,527 patients with ECG data available from the National Health and Nutrition Examination Survey data set, representing 74,062,796 individuals in the United States. Mean age was 60.5 ± 13.6 years. Most subjects were white (87%) and women (53%). During the follow-up period of 106,244.6 person-years, 1,433 CV deaths occurred. Multivariate analysis revealed that the highest quartile of QRS duration was associated with higher CV mortality than lowest quartile (hazard ratio [HR] 1.3, 95% confidence interval [CI] 1.01 to 1.7, p = 0.04) after adjustment for established risk factors. Both left BBB (HR 2.4, 95% CI 1.3 to 4.7, p = 0.009) and right BBB (HR 1.90, 95% CI 1.2 to 3.0, p = 0.008) were significantly associated with increased CV mortality. The addition of the QRS duration in 10-millisecond increments to the Framingham Risk Score model resulted in 4.4% overall net reclassification improvement (95% CI 0.02 to 0.04; p = 0.00006). In conclusion, increased QRS duration was found to be an independent predictor of CV mortality in this cross-sectional US population. A model including QRS duration in addition to traditional risk factors was associated with improved CV risk prediction.

Many medications used to treat atrial fibrillation (AF) also reduce blood pressure (BP). The relation between BP and mortality is unclear in patients with AF. We performed a post hoc analysis of 3,947 participants from the Atrial Fibrillation Follow-Up Investigation of Rhythm Management trial. Systolic blood pressure (SBP) and diastolic blood pressure (DBP) at baseline and follow-up were categorized by 10-mm Hg increments. The end points were all-cause mortality (ACM) and secondary outcome (combination of ACM, ventricular tachycardia and/or fibrillation, pulseless electrical activity, significant bradycardia, stroke, major bleeding, myocardial infarction, and pulmonary embolism). SBP and DBP followed a “U-shaped” curve with respect to primary and secondary outcomes after multivariate analysis. A nonlinear Cox proportional hazards model showed that the incidence of ACM was lowest at 140/78 mm Hg. Subgroup analyses revealed similar U-shaped curves. There was an increased ACM observed with BP <110/60 mm Hg (hazard ratio 2.4, p <0.01, respectively, for SBP and DBP). In conclusion, in patients with AF, U-shaped relation existed between BP and ACM. These data suggest that the optimal BP target in patients with AF may be greater than the general population and that pharmacologic therapy to treat AF may be associated with ACM or adverse events if BP is reduced to <110/60 mm Hg.

Electrocardiographic lead aVR is often ignored in clinical practice. The aim of this study was to investigate whether ST-T wave amplitude in lead aVR predicts cardiovascular (CV) mortality and if this variable adds value to a traditional risk prediction model. A total of 7,928 participants enrolled in the National Health and Nutrition Examination Survey (NHANES) III with electrocardiographic data available were included. Each participant had 13.5 ± 3.8 years of follow-up. The study sample was stratified according to ST-segment amplitude and T-wave amplitude in lead aVR. ST-segment elevation (>8 μV) in lead aVR was predictive of CV mortality in the multivariate analysis when not accounting for T-wave amplitude. The finding lost significance after including T-wave amplitude in the model. A positive T wave in lead aVR (>0 mV) was the strongest multivariate predictor of CV mortality (hazard ratio 3.37, p <0.01). The addition of T-wave amplitude in lead aVR to the Framingham risk score led to a net reclassification improvement of 2.7% of subjects with CV events and 2.3% of subjects with no events (p <0.01). Furthermore, in the intermediate-risk category, 20.0% of the subjects in the CV event group and 9.1% of subjects in the no-event group were appropriately reclassified. The absolute integrated discrimination improvement was 0.012 (p <0.01), and the relative integrated discrimination improvement was 11%. In conclusion, T-wave amplitude in lead aVR independently predicts CV mortality in a cross-sectional United States population. Adding T-wave abnormalities in lead aVR to the Framingham risk score improves model discrimination and calibration with better reclassification of intermediate-risk subjects.

Most clinicians regard isolated, minor, or nonspecific ST-segment and T-wave (NS-STT) abnormalities to be incidental, often transient, and benign findings in asymptomatic patients. We sought to evaluate whether isolated NS-STT abnormalities on routine electrocardiograms (ECGs) are associated with increased risk of cardiovascular mortality (CM) and all-cause mortality (AM) in a cross-sectional United States population without known coronary artery disease. We included all adults 40 to 90 years of age without known coronary artery disease or risk equivalent based on history and laboratory values, enrolled in the NHANES III from 1988 to 1994, with electrocardiographic data available, and a total follow-up period of 59,781.75 patient-years. NS-STT abnormalities were defined by Minnesota Coding. Subjects were excluded if their mortality data were missing or if they had major electrocardiographic abnormalities, heart rate >120 beats/min, nonsinus rhythm, cardiac infarction/injury score ≥20 on ECG, left ventricular hypertrophy by Minnesota Codes 3.1 and 3.3, or patient-reported history coronary artery disease, congestive heart failure, stroke, diabetes, or peripheral arterial disease. The remaining 4,426 subjects were stratified by presence or absence of NS-STT abnormalities. Mortality was judged based on International Classification of Diseases, Tenth Revision coding linked to the National Death Index. Cox proportional hazard ratio was used for multivariate analysis, showing that CM (hazards ratio 1.71, 95% confidence interval 1.04 to 2.83, p = 0.04) and AM (hazards ratio 1.37, 95% confidence interval 1.03 to 1.81, p = 0.02) were significantly higher in the isolated NS-STT abnormalities group. In conclusion, isolated NS-STT abnormalities on ECG were associated with a higher incidence of CM and AM in this large nationally representative cross-sectional cohort without known coronary artery disease or coronary artery disease risk equivalents.

Although left ventricular (LV) hypertrophy has been proposed as a factor predisposing to atrial fibrillation (AF), its relevance to prognosis and selection of therapeutic strategies is unclear. We identified 2,105 patients with echocardiographic data on LV mass enrolled in the Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) trial. LV hypertrophy was defined as increased LV mass, stratified by American Society of Echocardiography criteria. The primary end point was all-cause mortality, secondary end point was as per AFFIRM trial definition, and tertiary end point was cardiovascular hospitalizations. We compared “strict” versus “lenient” rate control in patients with increased LV mass, and studied association of heart failure (HF) with preserved and decreased systolic function in patients with increased LV mass. Over 6 years, 332 deaths (15.7%) were reported. Adjusted hazard ratio (HR) of severely increased LV mass for all-cause mortality was 1.34 (95% confidence interval [CI] 1.01 to 1.79, p = 0.045) for the overall population and 1.61 (95% CI 1.09 to 2.37, p = 0.016) for the rhythm-control arm. Increased LV mass was a predictor of cardiovascular hospitalizations in the lenient rate-control group (HR 1.72, 95% CI 1.05 to 2.82, p = 0.03) but not in the strict rate-control group. Severely increased LV mass was predictive of cardiovascular hospitalizations in patients with HF with preserved (HR 1.8, 95% CI 1.0 to 3.2, p = 0.03) and decreased LV systolic function (HR 2.4, 95% CI 1.1 to 5.2, p = 0.02). Thus, LV hypertrophy is a significant independent predictor of mortality in patients with AF, especially those managed with rhythm control. In patients with LV hypertrophy, strict rate control may be associated with better outcomes than lenient rate control. LV hypertrophy portends higher cardiovascular morbidity in patients with AF and HF.

The effect of rate versus rhythm control in patients with atrial fibrillation who have undergone previous pacemaker (PM) implantation is unknown. We evaluated the mortality in patients with atrial fibrillation and a PM randomized to rate or rhythm control treatment strategies. The Atrial Fibrillation Follow-up Investigation of Rhythm Management data set was stratified by the presence (n = 250) or absence (n = 3,810) of a PM at randomization into the rate or rhythm control arm. Kaplan-Meier curves were used for univariate analysis, and proportional hazards were used for multivariate analysis. The subjects with a PM (n = 250) were older (73 vs 69 years, p <0.01) and had a greater prevalence of coronary artery disease (53% vs 37%, p <0.01) and congestive heart failure (33% vs 23%, p <0.01). All-cause mortality was significantly greater in the PM patients who were randomized to the rhythm control arm (n = 128) than in the patients enrolled in the rate control arm with or without a PM (n = 2,027, p <0.01) and those in the rhythm control arm without a PM (n = 1,905, p <0.01). Multivariate analysis revealed that predictors of all-cause mortality included PM patients randomized to the rhythm control arm (hazard ratio 2.59, 95% confidence interval 1.46 to 4.58, p <0.01) and the presence of congestive heart failure (hazard ratio 2.42, 95% confidence interval 1.40 to 4.16, p <0.01). In conclusion, all-cause mortality was greater among patients with atrial fibrillation with a PM, who were randomized to the rhythm control arm of the Atrial Fibrillation Follow-up Investigation of Rhythm Management study compared with all other patients enrolled in the Atrial Fibrillation Follow-up Investigation of Rhythm Management study. The rhythm control strategy in patients with a PM was an independent predictor of mortality.

Abstract Background Cardiac sarcoidosis (CS) is associated with poor prognosis, yet the clinical diagnosis is often challenging. Advanced cardiac imaging including cardiac magnetic resonance (CMR) and positron emission tomographic (PET) have emerged as useful modalities to diagnose CS. Case summary A 66-year-old woman presented with palpitations. A 24-h Holter monitor detected a high premature ventricular contraction burden of 25.6%. She underwent two transthoracic echocardiograms; both showed normal results. Stress perfusion CMR did not show any evidence of ischaemic aetiology; however, myocardial lesions detected by late gadolinium enhancement (LGE) imaging raised suspicion for CS. While there was no myocardial uptake of fluorodeoxyglucose (FDG) in subsequent cardiac PET, high FDG uptake was seen in hilar lymph nodes. Lymph node biopsy confirmed the diagnosis of sarcoidosis. Discussion Cardiac magnetic resonance and PET imaging are designed to evaluate different aspects CS pathophysiology. The characteristic LGE in the absence of increased FDG uptake suggested inactive CS with residual myocardial scarring.

Lipomatous metaplasia in chronic postmyocardial infarction scars is a common and underappreciated finding seen in histopathology and cardiac MRI. Evidence suggests that lipomatous metaplasia is capable of altering the electroconductivity of the myocardium leading to re-entry pathways that are implicated in the pathogenesis of postmyocardial infarction arrhythmogenesis. We report a case of a patient who presented with non-sustained ventricular tachycardia and was found to have lipomatous metaplasia of a prior myocardial infarct-related scar.

We describe a case of 49-year-old man who presented with chest pain and was diagnosed with non-ST elevation myocardial infarction. Transthoracic echocardiogram (TTE) showed severe global hypokinesis of left ventricle with ejection fraction of 25%–30%. Left heart catheterisation showed severe right coronary stenosis and focal 60%–70% distal left anterior descending artery stenosis. Cardiac MRI (CMR) was done for evaluation of viability which showed a large pseudoaneurysm which was missed on TTE and left ventriculogram. Our case demonstrates the increasing importance of cardiac MRI in the diagnosis of left ventricular pseudoaneurysm. In our case left ventricular pseudoaneurysm was missed on TTE and left ventriculogram. It was diagnosed on CMR which was ordered for evaluation of myocardium viability.