Mortality and cause of death in patients with chronic non-rheumatic atrial fibrillation after a two-year follow-up.

BACKGROUND: Non-rheumatic atrial fibrillation (NRAF) is a very common arrhythmia but its role in the prognosis and cardiovascular mortality is controversial. In particular, cause and predictors of death are not completely known. METHODS: We analyzed the cause of death and the possible predictors of cardiovascular mortality in 664 outpatients (mean age 72 +/- 9 years old) enrolled in the "Trieste Area Study on Non-Rheumatic Atrial Fibrillation" (TASAF), a prospective community study, after a follow-up of 27 +/- 9 months. The mean duration of the arrhythmia at enrollment was 59 months (range 1-360 months). Only 42 patients (6.3%) were on anticoagulants by general practitioners and 205 (30.8%) were on antiplatelet drugs. RESULTS: Of these patients, 110 (16.5%) died: 28 (25.5%) due to a cerebral or peripheral thromboembolism, 10 (8.2%) of sudden death, 46 (42.7%) of expected cardiac death and 25 (22.7%) of non-cardiac causes. In one patient, the cause of death was uncertain. Sixty-nine patients underwent postmortem examination. In univariate analysis, left ventricular dysfunction (p = 0.03) and an enlarged left atrium (p = 0.03) proved to be directly related to increased cardiovascular mortality. Both in univariate and Cox proportional hazards model analysis, aging (odds ratio 1.09, IC 95% 1.05-1.12, p = 0.00001), history of heart failure (odds ratio 1.27, IC 95% 1.01-1.60, p = 0.036), cardiomegaly (odds ratio 1.35, IC 95% 1.01-1.81, p = 0.040), diabetes mellitus (odds ratio 1.35, IC 95% 0.99-1.84, p = 0.058) and previous myocardial infarction (odds ratio 1.56, IC 95% 1.20-2.03, p = 0.0007) were all independent risk factors for cardiovascular mortality. A history of cerebral or systemic embolism (23 versus 12%, p = 0.09) and, above all, one or more recurrences before enrollment (11 versus 2.3%, p = 0.04), were associated with embolic mortality. CONCLUSIONS: Patients with NRAF have an increased risk of cardiovascular death. Aging, the presence of diabetes, cardiomegaly on chest x-ray, heart failure and a previous myocardial infarction were independent risk factors for cardiovascular mortality. A history of embolism at enrollment significantly conditioned the embolic mortality rate but above all, embolic events during follow-up determined a very high percentage of total deaths (25.5% of all causes). A proper anticoagulant therapy should strongly be advised to all patients with no contraindications.

Electrocardiography of myocarditis revisited: clinical and prognostic significance of electrocardiographic changes.

To clarify the clinical and prognostic value of the ECG, an ECG review was undertaken in 45 consecutive patients with a histologic diagnosis of active myocarditis (29 men and boys and 16 women and girls; age, 36.8 +/- 15 years; idiopathic myocarditis, 39 cases). In patients (21) with symptoms of recent onset (less than or equal to 1 month) AV block and repolarization abnormalities were the prevailing ECG features at the time of admission, and a pseudoinfarction pattern (Q waves plus ST-segment elevation) frequently heralded a rapidly fatal course ("fulminant myocarditis"). Left atrial enlargement and atrial fibrillation, left ventricular hypertrophy and LBBB, which prevailed in patients who had symptoms for longer periods, corresponded to the most severe degree of left ventricular dysfunction during the initial hemodynamic and echocardiographic evaluation. The overall mortality rate after 58 +/- 24 months from the time of diagnosis was 29%. Abnormal QRS complexes and LBBB were markers of poor survival, independently of initial indexes of left and right ventricular function, both of which indicate an increased propensity for sudden cardiac death.

The use of associated propafenone in patients with amiodarone-resistant ventricular tachycardia.

To clarify the risk-benefit ratio involved in association of antiarrhythmic drugs, a combined therapy of amiodarone and propafenone was tested by means of continuous electrocardiographic monitoring, analysis of levels of the drug in the plasma and programmed electrical stimulation in a selected group of 10 patients who had left ventricular dysfunction and spontaneous relapses of sustained ventricular tachycardia despite treatment with amiodarone. Induction of sustained ventricular tachycardia, possible in each case during treatment with amiodarone, was suppressed after addition of propafenone in 2 patients (responders), who had the best ejection fractions of the entire group (greater than 45%). Worsening of spontaneous tachycardias developed in 4 cases during the combined therapy. These ventricular arrhythmias, although generally at a low rate, sometimes had the potential to degenerate into ventricular fibrillation and disappeared after both discontinuation of propafenone or increase of its dosage (1 patient). Of the six cases undergoing chronic combined treatment, only the responders to premature electrical stimulation were completely protected from recurrences of arrhythmia. Three cases, on the other hand, needed permanent endocardial pacing for symptomatic bradyarrhythmias. The combination of treatment with amiodarone and propafenone, although potentially useful in limiting dosages of and toxicity from amiodarone, is frequently associated with undesirable, and occasionally has severe, side-effects. The best candidates for this pharmacological association seem to be patients without severely depressed left ventricular function who have a greater probability of not presenting the inducibility of ventricular tachycardia after the addition of propafenone to the regimen for treatment.

Chest thump and ventricular tachycardia.

Chest thump is a simple method of treatment of some paraxysmal arrhythmias. Its therapeutic efficacy, electrophysiological bases and clinical utility have been studied in 17 patients during 45 episodes of ventricular tachycardia (VT). Thumping the precordium interrupted the VT in 22 episodes. Three types of interruption of VT have been observed: (1) In 15 episodes, single ventricular premature beats induced by the blow, occurring randomly in the cycle, stopped the arrhythmia; (2) In 5 episodes, a run of premature beats, induced by a rapid succession of blows, interrupted the tachycardia; (3) In 2 episodes, chest thump caused a short period of asystole followed by sinus rhythm. Chest thump is an antiarrhythmic treatment of definite clinical utility. The complications are rare, although there is a possibility of ventricular fibrillation. Therefore, it should be performed only under careful supervision.