Bicuspid aortic valves have a larger annulus size, sinus of Valsalva and ascending aorta dimensions. In addition, the BAV aortic annuli appear circular and most will fit currently available commercial valved stents.
Background. Atrial fibrillation (AF) is a common arrhythmia in adults with congenital heart disease (CHD). Long-term antiarrhythmic therapy (AAT) in these patients has significant shortcomings. The safety and efficacy of pulmonary vein antrum isolation (PVAI) for the treatment of AF in CHD is presently unknown. Hypothesis. We hypothesized that PVAI for AF in patients with CHD is effective and safe. Methods. We reviewed a prospective cohort of 4315 patients (age Ն 18) undergoing PVAI for drug refractory AF at a single institution and identified 36 consecutive patients with CHD (single ventricle physiology, tetralogy of Fallot, coarctation of the aorta, ventricular septal defects, atrial septal defects (ASD) and cardiomyopathy resulting from anomalous origin of the left main coronary from the pulmonary artery). A second cohort of 355 consecutive patients with noncongenital structural heart disease (NSHD) (coronary artery disease, valvular heart disease, ejection fraction <50%, or prior noncongenital cardiac surgery) undergoing PVAI during the same time period was used as a control. Success was defined as freedom from AF starting two months after PVAI in the absence AAT until the end of follow-up. Partial success was defined as freedom from AF in the presence of AAT until the end of follow-up. Combined success was defined as the sum of success and partial success. We compared the outcomes with the use of propensity-score matching in the overall cohort. Results. Patients with NSHD were older and had higher prevalence of hypertension (P < .01), diabetes (P < .01) and hyperlipidemia (P < .01). The most common CHD lesion was ASD (61%) and the most common NSHD lesion was valvular heart disease (57%). After one PVAI, success was achieved in 42% and 53% at 300 days in the CHD and NSHD groups respectively. Four-year success was achieved in 27% and 36% in the CHD and NSHD groups, respectively. There were no significant differences in the success rates between patients groups (P = .46), nor were there any differences in left atrial size or changes in ejection fraction after one or two PVAI in the respective groups. Complication rates between the CHD and NSHD groups were similar (15% vs. 11%, P = .42) except for a higher risk of vascular site complications in patients with CHD (8% vs. 1%, P < .05). Conclusion. PVAI is an attractive treatment modality in drug refractory AF in CHD, with combined success rates in excess of 60%. The maintenance of sinus rhythm after PVAI in CHD appears similar to that of NSHD and warrants prospective validation.
The normal heart responds to changes in its metabolic milieu by changing relative oxidation rates of energy providing substrates. We hypothesized that this flexibility is lost when genetically obese rats are fed a high caloric, high fat ‘Western’ diet (WD).
Male Zucker obese (ZO) and Zucker lean (ZL) rats were fed either control or WD composed of 10 kcal% and 45 kcal% fat respectively for 7 or 28 days. Cardiac triglycerides and mRNA transcript levels were measured in situ. Substrate oxidation rates and cardiac power were measured ex vivo. Hearts from ZO rats fed WD for 7 days showed decreased cardiac power and increased cardiac triglyceride content, but no change in oleate oxidation rates or mRNA transcript levels of pyruvate dehydrogenase kinase-4 (PDK-4), uncoupling protein-3 (UCP-3), mitochondrial (MTE-1) and cytosolic thioesterase 1(CTE-1). When fed WD for 28 days, ZO rats showed no further decrease in cardiac power and no further increase in intramyocardial triglyceride levels compared to ZO rats fed the same diet for 7 days only, but did show significantly increased oleate oxidation rates and transcript levels of CTE-1, MTE-1, PDK-4 and UCP-3. In contrast, hearts from ZL rats fed WD showed increased rates of oleate oxidation and increased transcript levels of the fatty acid responsive genes investigated, and no further deterioration of contractile function.
We conclude that exposing a genetic model of obesity to the nutrient stress of WD results in an early reversible loss of metabolic flexibility of the heart which is accompanied by contractile dysfunction.
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