Outcomes of Blacks Versus Whites with Cardiomyopathy.

Racial disparities in health outcomes have been widely documented in medicine, including in cardiovascular care. While some progress has been made, these disparities have continued to plague our healthcare system. Patients with cardiomyopathy are at an increased risk of death and cardiovascular hospitalizations. In the present analysis, we examined the baseline characteristics and outcomes of black and white men and women with cardiomyopathy. All patients with cardiomyopathy (left ventricular ejection fraction (LVEF) < 50%) cared for at University of Pittsburgh Medical Center (UPMC) between 2011 and 2017 were included in this analysis. Patients were stratified by race, and outcomes were compared between Black and White patients using Cox proportional hazard models. Of a total of 18,003 cardiomyopathy patients, 15,804 were white (88%), 1,824 were black (10%) and 375 identified as other (2%). Over a median follow-up time of 3.4 years, 7,899 patients died. Black patients were on average a decade younger (p <0.001) and demonstrated lower unadjusted all-cause mortality (hazard ratio [HR]: 0.83%; 95% CI 0.77 to 0.90; p < 0.001). However, after adjusting for age and other comorbidities, black patients had higher all-cause mortality compared to white patients (HR: 1.15, 95% CI 1.07 to 1.25; p < 0.001). These differences were seen in both men (HR:1.19, 95% CI 1.08 to 1.33; p < 0.001) and women (HR:1.12, 95% CI 0.99 to 1.25; p = 0.065). In conclusion, our data demonstrate higher all-cause mortality in black compared to white men and women with cardiomyopathy. These findings are likely explained, at least in part, by significantly higher rates of comorbidities in black patients. Earlier interventions targeting these comorbidities may mitigate the risk of progression to heart failure and improve outcomes.

Advances in mechanisms of atrial fibrillation: structural remodeling, high-frequency fractionated electrograms, and reentrant AF drivers.

The mechanisms to explain atrial fibrillation (AF) have been widely debated. Although contemporary experimental techniques have provided more insight, hypotheses regarding AF propagation conceived in the early half of the century remain minimally altered and relevant today. Modern mapping technologies have implicated multiwavelet reentry as the electrophysiologic basis to explain AF propagation within the atrial myocardium; however, reentry has also been observed within pulmonary veins and may behave as a focal trigger. The ability to terminate AF by catheter ablation has provided additional clues to explain AF induction and sustenance. The presence of complex fractionated electrograms (CFAE) and subsequent successful CFAE-directed ablation suggest that diseased atrial myocardium is a necessary substrate for AF maintenance. Atrial remodeling creates differential areas of refractory periods and conduction velocity, which, in turn, creates a suitable environment for AF. This review addresses the complex relationship between remodeled atrial myocardium and reentry and explores the role of CFAEs in AF maintenance.

Commotio cordis.

Sudden arrhythmic death as a result of a blunt chest wall blow has been termed Commotio Cordis (CC). CC is being reported with increasing frequency with more than 180 cases now described in the United States Commotio Cordis Registry. The clinical spectrum is diverse; however young athletes tend to be most at risk, with victims commonly being struck by projectiles regarded as standard implements of the sport. Sudden death is instantaneous and victims are most often found in ventricular fibrillation (VF). Chest blows are not of sufficient magnitude to cause any significant damage to overlying thoracic structures and autopsy is notable for the absence of any structural cardiac injury. Development of an experimental model has allowed for substantial insights into the underlying mechanisms of sudden death. In anesthetized juvenile swine, induction of VF is instantaneous following chest impacts that occur during a vulnerable window before the T wave peak. Other critical variables, including the impact velocity and location, and the hardness of the impact object have also been identified. Rapid left ventricular pressure rise following chest impact likely results in activation of ion channels via mechano-electric coupling. The generation of inward current through mechano-sensitive ion channels results in augmentation of repolarization and non-uniform myocardial activation, and is the cause of premature ventricular depolarizations that are triggers of VF in CC. Currently available chest protectors commonly used in sport are not adequately designed to prevent CC. The development of more effective chest protectors and the widespread availability of automated external defibrillators at youth sporting events could improve the safety of young athletes.

Testing of a new T-wave subtraction algorithm as an aid to localizing ectopic atrial beats.

BACKGROUND: Identifying the timing and morphology of an ectopic P wave from the surface electrogram can aid in the diagnosis and localization of atrial arrhythmias. Given the relatively short coupling interval of atrial ectopic beats, the P wave is often obscured by the larger amplitude QRS-T wave complex. A method to uncover such "buried" P waves using a standard 12-lead surface ECG would be clinically useful and could potentially be a noninvasive guide to catheter ablation of focal atrial tachycardia. METHODS: We developed an automated computerized program (BARD DUO LAB SYSTEM trade mark ) designed to subtract the QRS-T wave complex from the surface electrogram and uncover a previously obscured P wave. The purpose of the present study was to validate this program. The surface ECG from 21 patients undergoing atrial pacing during electrophysiologic study (group I) and 10 patients with atrial tachycardia (group II) were analyzed and the derived P-wave morphology assessed using correlation waveform analysis (CWA) and visual grading by three reviewers. RESULTS: The algorithm successfully uncovered the P wave in each surface ECG. For the 21 patients in group I, average CWA comparing the derived P wave with the previous paced P wave was 83%. Average CWA for group II was 82%. Visual grading of the match between derived P waves and paced P waves revealed a 21/21 match in group I patients and a 12/12 match in 9/10 of group II patients. CONCLUSIONS: An ectopic atrial P wave obscured by a coincident QRS-T wave complex can be accurately uncovered using this new algorithm. Addition of this technique to existing methods may improve the diagnosis of atrial arrhythmias and aid in the localization and ablation of ectopic atrial foci.