Severe Tricuspid Regurgitation in a Patient with a Transvenous Dual-chamber Pacemaker: Considerations for Diagnosis and Management.

Cardiac implantable electronic device leads can contribute to tricuspid regurgitation and also complicate surgical and transcatheter interventions to manage tricuspid regurgitation. Here we present a case of a patient with sinus node dysfunction and complete heart block who underwent extraction of a right ventricular pacing lead before tricuspid valve surgery. We review the data regarding the contribution of leads to tricuspid regurgitation and the benefits of lead extraction, risks of jailing leads during tricuspid interventions, and pacing considerations around tricuspid valve procedures.

Atrial flutter after surgical maze: incidence, diagnosis, and management.

PURPOSE OF REVIEW: The prevalence of atrial fibrillation is increasing and surgical ablation is becoming more common, both as a stand-alone procedure and when performed concomitantly with other cardiac surgery. Although surgical ablation is effective, with it unique challenges arise, including iatrogenic macroreentrant tachycardias that are often highly symptomatic and difficult to manage conservatively. RECENT FINDINGS: Postsurgical ablation, localization of the arrhythmic circuit is difficult to determine using surface ECG alone because of alterations in the atrial myocardium, and multiple different pathways are often present. Most, however, localize to the left atrium, and percutaneous catheter ablation is emerging as an effective treatment modality. SUMMARY: Patients with complex postoperative arrhythmias should be referred to a dedicated atrial fibrillation center when possible and symptomatic arrhythmias mapped and ablated. Knowledge of the previously performed surgical lesion set is of vital importance in understanding the mechanism of the arrhythmia and increasing procedural success rates. VIDEO ABSTRACT: http://links.lww.com/HCO/A31.

Image integration using intracardiac ultrasound and 3D reconstruction for scar mapping and ablation of ventricular tachycardia.

BACKGROUND: Ablation of ventricular tachycardia (VT) reduces implantable cardioverter defibrillator shocks. Intracardiac ultrasound (ICE) can visualize and quantify the function of all left ventricular wall segments. We thus hypothesized that ICE could identify scar tissue and provide a guide to facilitate substrate-guided VT ablation. METHODS: Eighteen patients underwent VT ablation with real time ICE mapping from the right atrium and ventricle with online 3D-image reconstruction of scar segments. The left ventricle was also scar mapped by traditional electroanatomic mapping (CARTO) for comparison. Images from these 2 scar mapping techniques were compared to each other as well as to a preprocedure transthoracic echocardiogram. RESULTS: The average age was 65 +/- 12 years and 12 (67%) were male (15 [83%] had ischemic cardiomyopathy). Two patients (12%) had recurrence of their clinical VT (1 remained on an antiarrhythmic medication, the other had a repeat ablation) over a follow-up of 127 +/- 33 days. No periprocedural or long-term adverse events occurred. A total of 248 wall segments were analyzed. All 3 modalities were concordant in scar identification in 193 (78%) segments. The ICE segments correlated with the electroanatomic map in 213 (86%) segments versus 198 (80%), which correlated with transthoracic echocardiography and electroanatomic mapping (P = 0.046). Specifically, the ICE wall motion scores were closer to the electroanatomic mapping in the basal segments and showed a higher accuracy in ischemic heart disease. CONCLUSION: These data demonstrate that real time ICE images provide accurate chamber geometries and scar boundaries of the left ventricle. These scar borders were more accurate than transthoracic echocardiography and illustrate the feasibility of ICE for substrate-based ablation for VT.

Lamin A/C deficiency as a cause of familial dilated cardiomyopathy.

PURPOSE OF REVIEW: Familial dilated cardiomyopathy is an underrecognized form of dilated cardiomyopathy. Lamin A/C deficiency is probably the most common cause of familial dilated cardiomyopathy. This review will focus on the emerging knowledge of epidemiology, diagnosis, and treatment of patients with lamin A/C deficiency, as well as possible disease mechanisms. RECENT FINDINGS: Screening of patients with dilated cardiomyopathy continues to indicate that lamin A/C deficiency is a significant cause. Multiple novel mutations have been found, suggesting that many mutations are limited to individuals or families. It is unknown how mutations cause the syndrome, although an animal model has shown that lamin A/C insufficiency causes apoptosis, particularly in the conduction system. Inheritance is predominantly autosomal dominant, but penetrance is variable. For symptomatic patients, the course is malignant, with conduction system disease, atrial fibrillation, heart failure, and sudden cardiac death. The data are contradictory, and currently, there is no clear marker for when a lamin A/C-deficient patient is at risk for sudden death. SUMMARY: Lamin A/C deficiency is an important cause of dilated cardiomyopathy, and diagnosis requires that clinicians have a high index of suspicion. Our knowledge of the mechanisms, diagnosis, and treatment of lamin A/C deficiency is incomplete. It is clear that patients with this condition have a malignant course and need to be followed aggressively.

Common issues in sports cardiology.

Many cardiac conditions found in athletes are amenable to athletic participation if well-managed. As always, a respect for the causes of sudden cardiac death in athletes is paramount. Although rare, sudden cardiac death in athletes is frequently preventable by careful pre-participation screening. The authors hope that more athletes will undergo screening, and that basic investigations, including but not limited to electrocardiography, will become more widespread. A high degree of surveillance for cardiac pathology in athletes is the duty of any sports medicine practitioner.