Background: The previous 50 years have seen major changes in the epidemiology of infective endocarditis (IE). Aim: To evaluate local risk factors, clinical manifestations, microbiology, echocardiographic features, morbidity and mortality in patients with definite IE. Design: Prospective observational study. Method : Over a ten year period, patients referred with probable IE were evaluated. All had received a standardized diagnostic evaluation as per department protocol. Epidemiological data were documented; underlying risk factors for IE were noted. Initial evaluation and follow-up included documentation of vascular or immunological phenomena, morbidity and mortality. Results: Of 90 patients referred with probable IE, 50 had definite IE. The mean age was 36 yrs with a male predominance (1.2:1). Rheumatic heart disease was present in 20 (40%). Eight had mitral valve prolapse and congenital heart disease respectively, and three had prosthetic valves. All had denied the use of intravenous recreational drugs and 11 had normal valve endocarditis. Cardiac murmur (98%) and fever (96%) were commonly observed. Six patients had renal involvement and ten patients had embolic episodes. Vegetations were seen in 80% of patients. 70% were managed medically, 10% surgically, and mortality was 20%. An etiological diagnosis was made in 29 patients with viridans streptococci the most common isolate. Conclusions: Infective endocarditis in Oman is a disease of younger adults, with a male predominance. Rheumatic heart disease is the major predisposing factor. Degenerative heart disease and intravenous drug abuse are not important risk factors. Local mortality rates are similar to published rates but the proportion of "culture-negative" IE was higher. Large vegetations were important prognostically.

Genetic alterations of various ion channels produce heritable cardiac arrhythmias that predispose affected individuals to sudden death. The investigation of such 'channelopathies' continues to yield remarkable insights into the molecular basis of cardiac excitability. The concept of channelopathies is not restricted to genetic disorders; notably, changes in the expression or post-translational modification of ion channels underlie the fatal arrhythmias associated with heart failure. Recognizing the fundamental defects in channelopathies provides the basis for new strategies of treatment, including tailored pharmacotherapy and gene therapy.