The incidence and risk factors for new onset atrial fibrillation in the PROSPER study

Aims Atrial fibrillation/flutter (AF) is the most common arrhythmia in older people. It associates with reduced exercise capacity, increased risk of stroke, and mortality. We aimed to determine retrospectively whether pravastatin reduces the incidence of AF and whether any electrocardiographic measures or clinical conditions might be risk factors for its development. Methods and results The PROspective Study of Pravastatin in the Elderly at Risk (PROSPER) was a randomized, double-blind controlled trial that recruited 5804 individuals aged 70-82 years with a history of, or risk factors for, vascular disease. A total of 2891 were allocated to pravastatin and 2913 to placebo; mean follow-up was 3.2 years. Electrocardiograms (ECGs), which were recorded at baseline, annually thereafter, and at run-out, were processed by computer and reviewed manually. In all, 264 of 2912 (9.1%) of the placebo group and 283 of 2888 (9.8%) of the pravastatin-treated group developed AF [hazard ratio 1.08 (0.92,1.28), P = 0.35)]. Multivariate analysis showed that PR and QTc intervals, age, left ventricular hypertrophy, and ST-T abnormalities were related to development of AF after adjustment for many variables including alcohol consumption, which itself was univariately predictive of developing AF. Previous myocardial infarction on the ECG was not a risk factor. A history of vascular disease was strongly linked with developing AF but not diabetes and hypertension. Conclusion Pravastatin does not reduce the incidence of AF in older people at risk of vascular disease, at least in the short-medium term. Risk factors for AF include older age, prolongation of PR or QTc intervals, left ventricular hypertrophy, and ST-T abnormalities on the EC

Cardiovascular magnetic resonance in systemic hypertension

Systemic hypertension is a highly prevalent potentially modifiable cardiovascular risk factor. Imaging plays an important role in the diagnosis of underlying causes for hypertension, in assessing cardiovascular complications of hypertension, and in understanding the pathophysiology of the disease process. Cardiovascular magnetic resonance (CMR) provides accurate and reproducible measures of ventricular volumes, mass, function and haemodynamics as well as uniquely allowing tissue characterization of diffuse and focal fibrosis. In addition, CMR is well suited for exclusion of common secondary causes for hypertension. We review the current and emerging clinical and research applications of CMR in hypertension

Events in the cardiac arrhythmia suppression trial (CAST): Mortality in the entire population enrolled

To test the hypothesis that suppression of ventricular arrhythmias by antiarrhythmic drugs after myocardial infarction improves survival, the Cardiac Arrhythmia Suppression Trial (CAST) was initiated. Suppression was evaluated before randomization during an open label titration period. Patients whose arrhythmias were suppressed were randomized in the main study and those whose arrhythmias were partially suppressed were randomized in a substudy. Overall survival and survival free of arrhythmic death or cardiac arrest were higher in patients treated with encainide or flecainide than in patients treated with placebo. However, the death rate in patients randomized to placebo therapy was lower than expected. This report describes the survival experience of all patients enrolled in CAST and compares it with mortality in other studies of patients with ventricular arrhythmias after myocardial infarction.As of April 18, 1989, 2,371 patients had enrolled in CAST and entered prerandomization, open label titration: 1,913 (81%) were randomized to double-blind, placebo-controlled therapy (1,775 patients whose arrhythmias were suppressed and 138 patients whose arrhythmias were partially suppressed during open label titration); and 458 patients (19%) were not randomized because they were still in titration, had died during titration or had withdrawn. Including all patients who enrolled in CAST, the actuarial (Kaplan-Meier) estimate of 1-year mortality was 10.3%.To estimate the “natural” mortality rate of patients enrolled in CAST, an analysis was done that adjusted for deaths that might be attributable to encainide or flecainide treatment either during prerandomization, open label drug titration or after randomization. Because the censoring procedure excluded patients treated with encainide or flecainide after randomization, the mortality estimate will be less than the unadjusted mortality estimate of 10.3%. A minimal 1-year “natural” mortality rate of 6.3% was estimated by assuming that all deaths during open label titration with encainide or flecainide were due to drug treatment and that after randomization all excess mortality in the group randomized to active treatment was also due to drug effect. A maximal 1-year “natural” mortality rate of 8.4% was estimated by assuming that no deaths during open label titration with encainide or flecainide were due to drug treatment and that after randomization all excess mortality in the group randomized to active treatment was due to drug effect. Thus, the “natural” overall mortality rate in CAST, falling somewhere between 6.3% and 8.4%, is similar to rates observed in other postinfarction natural history studies, suggesting that the low mortality rate in the group randomized to placebo is largely due to the process of selecting only those enrolled patients for the randomized phase of CAST whose ventricular arrhythmias were suppressed in the prerandomization open label titration phase

Idiopathic dilated cardiomyopathy in the young: Clinical profile and natural history

The clinical profile and course of documented cases of idiopathic dilated cardiomyopathy in children have been poorly characterized. Twenty-four patients (median age 2 years, range < 1 month to 18 years) with idiopathic dilated cardiomyopathy were identified from Mayo Clinic records from 1973 to 1982. The most common presentation was congestive heart failure (92% of patients). Echocardiography (22 patients) generally revealed a dilated left ventricle with reduced fractional shortening (mean 14%) and ejection fraction (mean 26%): Two-dimensional echocardiographic evidence of left ventricular thrombus was present in 3 (23%) of 13 patients. Median cardiac index and left ventricular end-diastolic pressure (19 patients) were 2.5 liters/min per m2and 22 mm Hg, respectively. Myocardial biopsy in eight patients showed nonspecific findings without active inflammation or evidence of endocardial fibroelastosis.On follow-up (mean duration 33 months, range 0 to 149), systemic arterial embolism had occurred in 2 (8%) of 24 patients. Fifteen of 24 patients had died (63% survival at 1 year and 34% survival at 5 years of followup). The cause of death was congestive heart failure in 11, complications after cardiac transplantation in 3 and sudden cardiac death in 1. Nine patients are alive at a mean follow-up time of 65 months (range 26 to 149); five are asymptomatic. Serial determination of left ventricular systolic function, available in all survivors, showed improvement in six patients and no significant change in three. Severe mitral insufficiency was present only in patients who ultimately died. A recent viral syndrome was noted more frequently in patients who survived. There were no clinical or laboratory variables that were sensitive and specific predictors of outcome. Although the prognosis of idiopathic dilated cardiomyopathy in children is usually grave, a minority show unpredictable clinical improvement