Risk of Sudden Cardiac Death in Patients Undergoing Cancer Treatment.

The risk of sudden cardiac death (SCD) in patients with cancer receiving cancer therapies is not well defined. In this study we aimed to (1) evaluate the risk of SCD during the first 6 months of cancer treatment and (2) identify risk factors (RFs) for SCD in patients who underwent active cancer treatment. The study population comprised 8,356 patients who received any cancer treatment at the University of Rochester Medical Center from 2011 to 2020. The primary end point was the occurrence of SCD within 6 months of cancer treatment. SCD was defined by using the modified Hinkle-Thaler classification. The mean age at the time of cancer treatment was 64 ± 14 years and 49% were women. All-cause mortality occurred in 834 patients (10%), of whom 51 (6%) were identified as SCD. The cumulative probability of SCD at 6 months was 0.6%. Age <74 years (0.042), history of congestive heart failure (0.058) and lung cancer (0.004) were identified as independent RFs for SCD in the multivariate Cox regression models. The cumulative probability of SCD at 6 months from cancer treatment initiation was significantly higher in patients with ≥2 RFs (1.6%) than in patients with 0 or 1 RF (0.5%) (log-rank p <0.001). In conclusion, our findings suggest that active cancer treatment is associated with SCD risk that is more pronounced in younger patients (< 74 years), patients with cancer and a history of heart failure, and those who underwent treatment for lung cancer. Future studies should address appropriate modalities for prevention and protection in this high-risk population.

Relation of brain natriuretic peptide level to extent of left ventricular scarring in patients with chronic heart failure secondary to ischemic cardiomyopathy.

Multiple factors influence brain natriuretic peptide (BNP) release in patients with heart failure. We hypothesized that extensive myocardial scarring could result in an attenuated BNP response. A total of 115 patients with New York Heart Association class III chronic heart failure and ischemic cardiomyopathy were evaluated for ischemia, hibernation, and myocardial scarring by dipyridamole-rubidium-positron emission tomographic scanning with fluorine-18, 2-fluoro-2-deoxyyglucose. Plasma BNP levels were determined within 2 weeks of the study. Left ventricular dimension and function were evaluated by echocardiography. Patients were categorized as having <33% myocardial scar (n=67) or>or=33% myocardial scar (n=48). BNP measurements were correlated with amount of myocardial scarring. Compared with patients with less scar, those with >or=33% scar had lower BNP levels (mean 317+/-364 vs 635+/-852 pg/ml, median 212 vs 357, p=0.016). Using multiple regression analysis, presence of scarring was associated with decreased BNP response (p=0.022). Further, patients with <33% scar in whom a higher BNP level was noted had more ischemia (51% vs 27%, p=0.01) and greater myocardial hibernation (22+/-14% vs 12+/-7%, p=0.02) compared with patients with >or=33% scar. In conclusion, in patients with chronic heart failure, a decreased BNP response indicated extensive myocardial scarring.

Effect of biventricular pacing during a ventricular sensed event.

Loss of biventricular (BiV) pacing occurs during ventricular sensed events such as frequent ventricular ectopy, nonsustained ventricular tachycardia, and intrinsic atrioventricular nodal conduction, such as in atrial fibrillation. Ventricular sense response (VSR) pacing, a novel cardiac resynchronization therapy pacing strategy, maintains BiV pacing during these sensed ventricular events. Patients who underwent echocardiographic optimization after BiV pacemaker implantation were enrolled, and aortic velocity-time integrals (VTIs) were recorded and compared during intrinsic conduction without pacing, optimized BiV pacing, and intrinsic conduction with VSR pacing alone. Thirty-two patients were enrolled (mean age 68 +/- 11 years, 78% men), with a mean baseline QRS duration of 164 +/- 24 ms and a mean left ventricular ejection fraction of 23 +/- 10%. The mean aortic VTI during intrinsic conduction with VSR pacing was 16.5 +/- 3.6 cm, compared with 15.3 +/- 3.4 cm during intrinsic conduction without pacing (p <0.001). The mean aortic VTI with optimized BiV pacing was 17.3 +/- 3.6 cm, significantly better (p <0.001) compared with intrinsic conduction without pacing. Improvements in aortic VTI were higher with optimized BiV pacing compared with VSR pacing alone (p = 0.02). In the subgroup of patients with left bundle branch block-type activation, the hemodynamic improvements realized with VSR pacing were similar to optimized BiV pacing. Mean aortic VTI improvements with VSR were similar in patients with ischemic and nonischemic cardiomyopathy. In conclusion, a cardiac resynchronization therapy algorithm that maintains BiV pacing during a ventricular sensed event appears to have an aortic VTI response that is significantly better compared with intrinsic conduction without pacing.