Angiotensin receptor type 1 single nucleotide polymorphism 1166A/C is associated with malignant arrhythmias and altered circulating miR-155 levels in patients with chronic heart failure.

Background: Sudden cardiac death (SCD) from ventricular tachyarrhythmias accounts for approximately 450,000 annual deaths in the United States; many of these cases involve patients with chronic heart failure (HF). Prediction of which HF patients are most susceptible to SCD is difficult, and it is uncertain whether gene polymorphisms associated with HF outcomes are also linked to arrhythmic risk.

Methods: We evaluated 485 patients with chronic HF to see whether the angiotensin receptor type 1 (AT1R) 1166A/C or angiotensin-converting enzyme insertion/deletion (ACE I/D) polymorphisms were associated with a higher rate of ventricular arrhythmias requiring implantable cardioverter defibrillator (ICD) therapies over a 5-year period.

Mitochondrial reactive oxygen species and calcium uptake regulate activation of phagocytic NADPH oxidase.

Production of superoxide (O(2)(·-)) by NADPH oxidases contributes to the development of hypertension and atherosclerosis. Factors responsible for activation of NADPH oxidases are not well understood; interestingly, cardiovascular disease is associated with both altered NADPH oxidase activity and age-associated mitochondrial dysfunction. We hypothesized that mitochondrial dysfunction may contribute to activation of NADPH oxidase.

Prediction of atrial fibrillation following cardiac surgery using rough set derived rules.

Atrial fibrillation (AF) and flutter are common following cardiac surgery, increasing costs and morbidity. Cardiologists need a method to discern those patients who are at high risk for this arrhythmia in order to attempt to treat them by either pharmacologic or non-pharmacologic means. We performed a retrospective analysis of 377 CABG patients, of which 94 developed AF post-operatively.