BackgroundExcessive daytime sleepiness (EDS), a common symptom among patients with sleep‐disordered breathing, is closely associated with the development of cardiovascular diseases, but its long‐term prognostic value is not completely understood. The aim of this study was to investigate whether EDS would be an independent prognostic factor after myocardial infarction.Methods and ResultsWe prospectively recruited 112 post–myocardial infarction patients. The Epworth Sleepiness Scale was completed before polysomnography, and EDS was defined as a score ≥11. After exclusion of 8 patients who accepted treatment with continuous positive airway pressure, 104 patients were followed up for 48 months. The primary composite end point was major adverse cardiac events. Patients with EDS had higher rates of major adverse cardiac events (48.4% versus 27.4%, χ2=5.27, P=0.022) and reinfarction (29.0% versus 5.5%, χ2=13.51, P=0.0002) compared with those without EDS. In the Cox proportional hazards model, patients with EDS had 2.15 times (95% confidence interval, 1.08–4.18; P=0.030) higher crude risk of major adverse cardiac events, with prognostic significance persisting after adjusting for age, diabetes mellitus, depression, left ventricular ejection fraction, apnea–hypopnea index, and nocturnal nadir oxygen saturation (hazard ratio: 2.13, 95% confidence interval, 1.04–4.26, P=0.039). Furthermore, among participants with moderate to severe sleep‐disordered breathing, the presence of EDS was associated with higher risk of major adverse cardiac events than those without EDS, after adjusting for age and nadir oxygen saturation (hazard ratio: 3.17, 95% confidence interval, 1.22–7.76, P=0.019).Conclusions EDS may be an independent prognostic factor of adverse outcome in post–myocardial infarction patients with moderate to severe sleep‐disordered breathing. Evaluation of EDS may shed new light on risk stratification and identify treatment responders for this patient population.

Although great strides have been made in the areas of ventricular pacing, it is still appreciated that dyssynchrony can be malignant, and that appropriately placed pacing leads may ameliorate mechanical dyssynchrony. However, the unknowns at present include:1. The mechanisms by which ventricular pacing itself can induce dyssynchrony;2. Whether or not various pacing locations can decrease the deleterious effects caused by ventricular pacing;3. The impact of novel methods of pacing, such as atrioventricular septal, lead-less, and far-field surface stimulation;4. The utility of ECG and echocardiography in predicting response to therapy and/or development of dyssynchrony in the setting of cardiac resynchronization therapy (CRT) lead placement;5. The impact of ventricular pacing-induced dyssynchrony on valvular function, and how lead position correlates to potential improvement.This review examines the existing literature to put these issues into context, to provide a basis for understanding how electrical, mechanical, and functional aspects of the heart can be distorted with ventricular pacing. We highlight the central role of the mitral valve and its function as it relates to pacing strategies, especially in the setting of CRT. We also provide future directions for improved pacing modalities via alternative pacing sites and speculate over mechanisms on how lead position may affect the critical function of the mitral valve and thus overall efficacy of CRT.

Rapid advances in genetic technologies have led to expanding use of diagnostic, research, and direct-to-consumer exome and genome sequencing. Incidentally identified variants from this sequencing represent a significant and growing challenge to interpret and translate into clinical care and include variants in genes associated with heritable cardiovascular disease such as cardiac ion channelopathies, cardiomyopathies, thoracic aortic disease, dyslipidemias, and congenital/structural heart disease. These variants need to be properly reported, the risk of associated disease accurately assessed, and clinical management implemented to prevent or lessen the disease so that cardiovascular genomic medicine can become both predictive and preventive. The goal of this American Heart Association consensus statement is to provide guidance to clinicians who are called on to evaluate patients with incidentally identified genetic variants in monogenic cardiovascular disease genes and to assist them in the interpretation and clinical application of variants. This scientific statement outlines a framework through which clinicians can assess the pathogenicity of an incidental variant, which includes a clinical evaluation of the patient and the patient’s family and re-evaluation of the genetic variant in question. Furthermore, this guidance underscores the importance of a multidisciplinary team to address these challenging clinical evaluations and highlights how clinicians can effectively interface with specialty centers.

Study Objectives: A strong association between sleep-disordered breathing (SDB) and atrial fibrillation and/or atrial flutter (AF) has consistently been observed in epidemiologic and interventional studies. The effect of positive airway pressure (PAP) on AF recurrence is inconclusive. This study sought to evaluate the effectiveness of PAP therapy for SDB on AF recurrence. Methods: This was a single-center, retrospective study conducted at a tertiary referral center. All adult patients who had SDB on polysomnography and underwent AF intervention (ablation or cardioversion) following polysomnography from January 1992-December 2014 were analyzed. Primary outcome was time to first-documented recurrence of AF after AF intervention by Kaplan-Meier estimates. Results: Among 30,188 patients with obstructive and central SDB, 429 had this diagnosis before AF intervention; 269 were "PAP-adherent users," the remaining 160 were "PAP-nonusers." Patients in both groups had similar age, sex, body mass index (BMI), ejection fraction, left atrial volume index (LAVI), antiarrhythmic medications, diabetes mellitus, systemic hypertension, and heart failure diagnoses. Time to recurrence of AF postintervention was no different in PAP-adherent users and nonusers (4.8 and 4.1 months respectively, P =.7). Cardioversion (compared to catheter ablation) was the strongest independent predictor of recurrent AF (hazard ratio [HR] 2.02, 95% confidence interval [CI] 1.39-2.94, P < .001). BMI and LAVI were also significant predictors of recurrence in adjusted analyses (HR 1.01, 95% CI 1.003-1.023, P = .10 and HR 1.01, 95% CI 1.001-1.019, P = .024 respectively). Conclusions: Our study found no effect of PAP treatment of SDB on time to recurrence of AF post-AF intervention. Increased risk of recurrent AF was associated with high BMI and LAVI. These findings may affect the clinical management of AF.

We report an unusual case of an isolated right ventricular infarction with haemodynamic compromise caused by spontaneous isolated proximal occlusion of the right ventricular branch of the right coronary artery (RCA), successfully treated by balloon angioplasty. A 58-year-old gentleman presented with epigastric pain radiating into both arms. Electrocardiograph with right ventricular leads confirmed ST elevation in V4R and a diagnosis of isolated right ventricular infarction was made. Urgent primary percutaneous intervention was performed which revealed occlusion of the right ventricular branch of the RCA. During the procedure, the patient's blood pressure dropped to 80/40 mmHg, and echocardiography showed impaired right ventricular systolic function. Despite aggressive fluid resuscitation, the patient remained hypotensive, continued to have chest pain and persistent electrocardiograph changes, and hence balloon angioplasty was performed on the proximal right ventricular branch which restored flow to the vessel and revealed a severe ostial stenosis. This was treated with further balloon angioplasty which restored TIMI 3 flow with resolution of patient's symptoms. Repeat echocardiography showed complete resolution of the ST-elevation in leads V4R and V5R and partial resolution in V1. Subsequent dobutamine-stress echocardiography at 4 wk showed good left and right ventricular contractions. The patient was discharged after a 3-d in-patient stay without any complications.