Manage episode 215385127 series 1452724
Paul Wang: Welcome to the monthly podcast, On the Beat for Circulation: Arrhythmia and Electrophysiology. I'm Dr Paul Wang, editor-in-chief, with some of the key highlights from this month's issue. In our first paper from the Finland Group Registry, Nordenswan and her colleagues have further defined the risk of sudden cardiac death in ventricular arrhythmias in patients with cardiac sarcoidosis. While it has been observed that there's a high risk of lethal arrhythmias in cardiac sarcoidosis patients with high grade AV block, the incidents in these patients with lone AV block, in the absence of known VT or left ventricular dysfunction, has not been described. From the patients with myocardial inflammatory diseases in their registry, the authors identified 143 cardiac sarcoidosis patients with high grade AV block. Of these patients, 90 had lone AV block. For these patients, the five-year composite incidence of sudden cardiac death or VT was 24%, in comparison with 54% in AV block with ventricular tachycardia or severe left ventricular dysfunction, and 24% with AV block in non-severe left ventricular dysfunction.
These findings support implementation of an implantable cardioverter defibrillator for cardiac sarcoidosis patients with lone AV block. A recent study by Gold and Colleagues suggests atrial ventricular optimization improves reverse remodeling in patients with significant intraventricular electrical delay. In this sub-study of the Smart AV Trial, 275 subjects were randomized to either electrogram-based AV optimization, smart delay, or nominal AV delay, 120 milliseconds. In this mostly male cohort, with a mean age of 65 years, and a left ventricular ejection fraction of 28% at follow up, at six months the benefit of AV optimization increased as intraventricular electrical delay prolonged, defined as the time between the peaks of the right and left ventricular electrograms. The longest cohort trial of intraventricular conduction delay had 4.26 times greater odds of remodeling response with AV optimization compared with nominal AV delay. This suggests that the left ventricular lead position in AV optimization might have a synergistic effect in reverse remodeling in cardiac resynchronization patients.
Concerns have long been raised that anorexia nervosa causes QT interval prolongation predisposing these individuals to life-threatening ventricular arrhythmias and sudden cardiac death. Fredrickson and Associates made progress in challenging this conclusion, demonstrating that despite a slightly increased incidence in borderline mean QTC, greater than 440 milliseconds, in 430 female anorexia nervosa patients, compared to 123 healthy controls from the Danish Civil Register, there was no difference in the risk of prolonged corrected QT interval greater than 460 milliseconds between the two groups.
However, during a 10-year follow up, anorexia nervosa patients had a slightly increased risk of ventricular tachycardiac, aborted cardiac arrest, and cardiac arrest compared to healthy controls. Incidence of 0.5% in the anorexia nervosa patients versus 0.07% in healthy controls. In addition, anorexia nervosa patients had a significantly increased risk of all-cause mortality with a hazard ratio of 11.2 over 10 years compared to population-based cohort, suggesting that anorexia nervosa increases the risk of medical complications, including cardiac complications, but these are not directly related to anorexia nervosa's effects on corrected QT interval.
In our next paper, Ahmed Karim Talib and Associates reported on the outcomes of endocardial ablation of drug-resistant ventricular fibrillation in Brugada syndrome. Endocardial mapping ablation was performed in 21 patients with one or more episodes of ventricular fibrillation. Endocardial mapping revealed low voltage fractionated endocardial electrograms in 19% of patients. All patients underwent ablation of ventricular fibrillation triggers, followed by endocardial substrate modification. Noninducibility of ventricular fibrillation and normalization of Brugada ECG was documented in 14, in three patients, respectively. During a mean follow up of 54 months, seven patients, or 33%, experienced ventricular fibrillation recurrences, presence of cruris notching in D1 was associated with the presence of low-voltage fractionated endocardial electrograms in ablation failure.
In our next paper, Jae Yeong Cho and Associates tried to elucidate the mechanism of sudden cardiac death in patients with heart failure with preserved ejection fraction using an ambulatory recording in a rat model. They showed that rats who had a clinical phenotype of heart failure with preserved ejection fraction had prolonged QT and QTC intervals and reduced heart rate variability compared to the controls. Importantly, the rats with heart failure and preserved ejection fraction had significantly higher rates of spontaneous ventricular arrhythmias, and about a third died suddenly with ventricular arrhythmia being the terminal rhythm.
In our next paper, Elad Anter and Colleagues used a novel mapping algorithm which integrated atrial activation mapping, vector analysis, and the physiologic constraints of atrial excitation to determine an atrial arrhythmias mechanism in circuitry. Ander's group initially applied this technique to historical controls and found that atrial tachycardias were diagnosed and their termination site predicted with 92.5% accuracy. When this algorithm was then applied prospectively to mapping of unknown atrial arrhythmias in 20 patients, this technique was able to identify macroreentrant, localized reentrant in focal tachycardias, even when standard mapping techniques had failed. This enhanced mapping capability allowed for significantly shorter ablation time when compared to historical controls, 3.2 +/- 1.7 minutes versus 17.3 +/- 6.6 minutes.
In our next paper Richard Walton and Colleagues explored the anatomical and electrical characteristics of the moderator band which provides a substrate for macroreentrant ventricular tachycardia. Ventricular wedge preparations with intact moderator bands were studied from humans in two cases and sheep in 15 cases. The moderator band structure was remarkably organized as two excitable yet uncoupled compartments of myocardium in [inaudible 00:07:45]. In humans, actual potential duration was significantly shorter in the moderator band than the right ventricular myocardium. S1, S2 moderator band pacing induced unidirectional propagation via the moderator band myocardium, permitting sustained macroreentrant ventricular tachycardia.
In sheep, the instance of ventricular tachycardia for right ventricular moderator band, or S1 right ventricular, and S2 moderator band pacing was 1.3%, 5.1%, and 10.3%, respectively. Severing the moderator band led to ventricular tachycardiac termination, confirming a primary arrhythmic role. Inducible preparations had shorter actual potential durations in the moderator band than right ventricle, whereas noninducible preparations showed no difference.
In our final paper, Witt and Associates studied the outcomes of 1421 patients who underwent ICD generator placement at Mayo Clinic, Minnesota and Beth Israel Deaconess Medical Center. During a mean follow up of 2.7 years appropriate ICD therapy occurred in 30.6% of the patients, predicted by low left ventricular ejection fraction and history of appropriate ICD therapy prior to generator replacement. On the other hand, 23.7% died prior to appropriate ICD therapy, predicted by old age, low left ventricular ejection fraction, diabetes mellitus, chronic lung disease, peripheral vascular disease, low hemoglobin level, and low glomerular filtration rate. The progressive increase in mortality after ICD generator change was observed in those who had aggregation of non-cardiac co-morbidities.
That's it for this month. We hope that you'll find the Journal to be the go-to place for everyone interested in the field. See you next time.
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