Background: Chronic left bundle branch block (LBBB) can lead to LBBB-mediated cardiomyopathy from left ventricular dysynchrony. His-bundle pacing (HBP) results in direct electrical synchrony using the native His-Purkinje system, providing a novel treatment for this cardiomyopathy. Objective: To assess the feasibility of HBP for cardiac resynchronization therapy (CRT) in LBBB-mediated cardiomyopathy patients. Methods: Retrospective database review was conducted on patients who underwent CRT by the HBP capable provider at Indiana University Health and Eskenazi Hospital from August 2015 to August 2017. A subset of patients who met the predefined syndrome criteria of LBBB-mediated cardiomyopathy who underwent HBP were identified. Clinical, echocardiographic, and electrocardiographic variables were extracted at baseline and follow-up. Results: Nine patients had cardiomyopathy and LBBB. Among those two were lost to follow-up. Seven patients were included in the analysis. The average time from device implantation to the last follow-up was 14.5 months. Left ventricular ejection fraction improved on average from 25% to 50% (p = .0001). The left ventricular endsystolic dimension decreased from 47 to 37 mm (p = .003) and the left ventricular end-diastolic dimension decreased from 55 to 48 mm (p = .03). QRS duration with HBP-CRT decreased from 152 to 115 ms. New York Heart Association classification improved from an average of 2.7-2. Conclusion: HBP is a viable technique for pursuing CRT in patients with LBBBmediated cardiomyopathy.
The impact of heart failure (HF) on long-term survival in patients with critical limb ischemia (CLI) has not been well described. Outcomes stratified by left ventricular ejection fraction (EF) are also unknown. A single center retrospective chart review was performed for patients who underwent treatment for CLI from 2006 to 2013. Baseline demographics, procedural data and outcomes were analyzed. HF diagnosis was based on appropriate signs and symptoms as well as results of non-invasive testing. Among 381 CLI patients, 120 (31%) had a history of HF and 261 (69%) had no history of heart failure (no-HF). Within the HF group, 74 (62%) had HF with preserved ejection fraction (HFpEF) and 46 (38%) had HF with reduced ejection fraction (HFrEF). The average EF for those with no-HF, HFpEF and HFrEF were 59±13% vs 56±9% vs 30±9%, respectively. The likelihood of having concomitant coronary artery disease (CAD) was lowest in the no-HF group (43%), higher in the HFpEF group (70%) and highest in the HFrEF group (83%) ( p=0.001). Five-year survival was on average twofold higher in the no-HF group (43%) compared to both the HFpEF (19%, p=0.001) and HFrEF groups (24%, p=0.001). Long-term survival rates did not differ between the two HF groups ( p=0.50). There was no difference in 5-year freedom from major amputation or freedom from major adverse limb events between the no-HF, HFpEF and HFrEF groups, respectively. Overall, the combination of CLI and HF is associated with poor 5-year survival, independent of the degree of left ventricular systolic dysfunction.
Detailed histories were extracted, including age of diagnosis, treatment modality, IGF-1 levels, cardiovascular medications, and clinical outcomes. Where available, we compared pretreatment imaging to most recent findings to quantify changes in cardiac function. Results: The study cohort consisted of 21 patients (42%) with dilated cardiomyopathy, 25 patients (50%) with hypertrophic phenotype and 4 patients (8%) with ischemic cardiomyopathy. Hypertension (61%), diabetes mellitus (36%) and obstructive sleep apnea (48%) were the most common comorbidities. Successful treatment of acromegaly resulted in a clinically-relevant improvement in mean LV ejection fraction in the DCM cohort from 38% to 49% (p = 0.05) and mean LV diastolic diameter from 66 to 60 mm (p = 0.20). Additionally, an improvement in LV mass index was seen in the hypertrophic phenotype from 117 to 104 g/m 2 (p = 0.05). Heart rate, QRS and QTC intervals were statistically unchanged. Conclusions: Contrary to prior research, treatment of human growth hormone excess resulted in an improvement in dilated as well as hypertrophic phenotypes, though not necessarily independent of guideline-directed medical therapy. This highlights the importance of effective treatment of GH excess states in reducing the prevalent cardiovascular morbidity and mortality in patients with acromegaly.
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