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Background: Several weeks of prophylactic anticoagulation are routinely prescribed before and after electrical cardioversion of atrial fibrillation. Recent studies have supported the use of transesophageal echocardiography to guide early cardioversion: patients in whom no thrombus is observed are treated with heparin followed by one month of warfarin therapy after the procedure. This kind of treatment requires hospital admission during heparin infusion, because of the need for monitoring partial thromboplastin time., Aim of the Study: To evaluate if a short at-home treatment (three days) with warfarin is sufficient to reach a good level of anticoagulation, in order to permit safe electrical cardioversion in day-hospital for patients who show no thrombi on transesophageal echocardiography., Methods: One hundred twenty-four patients with atrial fibrillation, who were candidates for cardioversion, were treated with warfarin: 10 mg the first and second day, 5 mg the third day in group A patients (n = 79); 15 mg the first day, 10 mg the second and third day in group B patients (n = 45). On the fourth day, INR value was measured and if it was < 2, warfarin therapy was prolonged until patients reached a good level of anticoagulation. Transesophageal echocardiography was performed when the INR was > or = 2, and patients were cardioverted with DC shock if there were no thrombi. The patients were discharged on the same day of the procedure, and warfarin therapy was continued for 4 weeks there-after. If a thrombus was detected, patients repeated transesophageal echocardiography after 6 weeks of warfarin therapy, and were cardioverted if the thrombus disappeared. Otherwise, cardioversion was deferred and they received prolonged warfarin treatment. If there was poor visualization of the left atrial appendage, patients received conventional warfarin therapy for 3 weeks before and 4 weeks after electrical cardioversion., Results: Mean INR value after three days of warfarin treatment was 2.41 in group A patients and 3.02 in group B patients. Twenty-one patients from group A and 3 patients from group B required anticoagulant therapy for a mean of 3.3 and 5.1 days, respectively, before reaching a good level of anticoagulation (INR value > or = 2). Eight patients reverted spontaneously to sinus rhythm before transesophageal echocardiography. Eighteen thrombi (15.5%) were identified on the transesophageal echocardiography, all of which were in the left atrial appendage. In 11 cases, thrombus disappeared after 6 weeks of warfarin therapy. In 7 patients (6%), the atrial appendage was not sufficiently visualized. Electrical cardioversion was performed on 109 patients and was successful in 88 (80.7%). None of them experienced a clinical thromboembolic event., Conclusions: In the majority of patients in atrial fibrillation, a short at-home warfarin treatment is sufficient to reach a good level of anticoagulation in order to permit safe electrical cardioversion in a day-hospital situation. Larger initial doses can achieve even better results. This treatment algorithm minimizes the anticoagulation period, hospital stay, overall duration of atrial fibrillation and the time required for the mechanical function of the left atrium to return.

Background: Thromboembolic complications after electrical cardioversion (CV) of atrial fibrillation (AF) have been attributed to the dislodgment of preexistent left atrial thrombus during the resumption of atrial contraction. Transesophageal echocardiography (TEE) has been used to identify patients without thrombus, who potentially could undergo CV without anticoagulation. However, embolic events after CV in patients without evidence of thrombus on TEE have recently been reported., Aim of the Study: To evaluate if absence of thrombi or prethrombotic conditions such as spontaneous echo contrast or left atrial appendage disfunction can justify electrical CV without anticoagulant therapy., Methods: Seventy-four patients with AF and candidates for CV underwent monoplane TEE. Patients were cardioverted without anticoagulation in case of: 1) absence of thrombus and/or spontaneous echocardiographic contrast and 2) good visualization of left atrial appendage, with a well defined peak blood flow velocity greater than 20 cm/sec. In all other cases, patients underwent anticoagulant therapy which started 3 weeks before CV and continued for 4 weeks afterwards., Results: Forty-six patients, without thrombus or "prethrombotic" conditions, did not receive anticoagulation, while 28 followed traditional therapy with warfarin. Four patients with a thrombus in the left atrial appendage were identified: 1 died of cerebral embolism 3 days after the beginning of anticoagulation, in another one CV was definitely deferred because of the persistence of thrombus after 1 month of warfarin therapy. One patient, with left atrial appendage disfunction, died suddenly after 5 days of anticoagulation. Two patients reverted spontaneously in sinus rhythm. Two patients refused electrical CV. The remaining 67 patients underwent electrical CV which was successful in 56 of them. Cerebral embolism occurred 24 hours after CV in one patient who did not receive anticoagulation. Repeat TEE soon after embolism showed absence of thrombus or spontaneous echo contrast, but the presence of low flow velocity in the left atrial appendage., Conclusions: In patients in AF candidates for CV, exclusion of thrombi or prethrombotic conditions by TEE does not exclude the risk of thromboembolic events and the need for anticoagulant therapy. Left atrial appendage function can be stunned or impaired immediately after CV, favouring a thrombogenic milieu and subsequent embolic events. Therapeutic anticoagulation at the time of as well as after cardioversion is actually recommended.

Results of our prospective, randomised pilot trial to evaluate the clinical effects and the angiographic correlates of early thrombolysis in patients with unstable angina are reported. Sixty-seven patients had coronary angiography 10 +/- 8 (median 7) hours after an episode of transient chest pain at rest with reversible ischaemic changes on the electrocardiogram. Patients with left main disease (4), or diffuse coronary disease and unidentified ischemia-producing lesions (13) were excluded, as were those without severe (greater than or equal to 70%) stenosis (10). Intracoronary thrombus was identified at angiography in 7 patients (17%) and complex coronary lesions in 5 (12%) of the remaining 40 patients who were randomised to either intracoronary streptokinase 250,000 IU followed by intravenous heparin along with conventional treatment (20 patients), or to conventional treatment alone (20 patients). All patients received Aspirin. No differences between the streptokinase and the conventional treatment groups were observed with respect to demographic and clinical characteristics at admission to the study. During observation in the intensive care unit for 3 +/- 1 days, 8 patients (40%) with streptokinase and 10 (50%) with conventional treatment were free from angina and infarction (p = 0.75; 95% confidence interval for the difference in response rates = -20 to 40%). There were no bleeding complications and no patient died. Patients enrolled in our study had fewer coronary thrombi at angiography than currently reported. Our data did not show that adjunct treatment with streptokinase and heparin is superior to conventional treatment alone in these patients.

Cardiac involvement is commonly seen in the carcinoid syndrome (C.S.). However echocardiographic observations in this condition are still very scanty. In two patients with the C.S. and clinical signs of tricuspid insufficiency (plus mild pulmonic stenosis in one case) two-dimensional echocardiography showed: 1) right ventricular overload with normal left heart valves and chambers; 2) a peculiar aspect of the tricuspid valve, whose three leaflets were markedly thickened and retracted. The anterior leaflet was almost fixed in a semi-open position while the septal and posterior leaflets appeared as rigid structures fixed in an open position, extending from the annulus into the right ventricular cavity. In both cases only the posterior cusp of the pulmonary valve could be visualized. The afore-mentioned changes exactly reproduce the pathological features of the tricuspid valve in the carcinoid heart disease and so far, have not been observed in other conditions.

On the basis of a personal observation and from a complete review of the existing literature, clinical and instrumental findings of right atrial myxoma are described. The clinical presentation appears to be rather characteristic. The presence of systemic symptoms, peripheral venous hypertension and/or right heart failure without apparent cause are a clue to the diagnosis especially in an adult woman. The presence of abnormal sounds and/or murmurs in the tricuspid area and intermittence of the signs of obstruction are further support to the diagnosis. The diagnosis can always be made non-invasively by echocardiography, though some pitfalls seem to be inherent to the M-mode technique. The accuracy of two-dimensional echocardiography in the diagnosis of the right atrial myxoma is such that no further investigations are necessary before surgery.

Severe and reversible electrocardiographic abnormalities (first degree atrioventricular block, left bundle branch block, ventricular fibrillation), were induced by the administration of Arfonad in a patient with type III acute aortic dissection previously chronically treated with alpha-methyl-dopa. Any other possible cause of the electrocardiographic changes was excluded on the basis of clinical findings and laboratory studies. The explanation of the electrocardiographic abnormalities induced by Arfonad are not readily apparent, also on careful review of the literature. We suggest a strict electrocardiographic monitoring during Arfonad administration especially in patients with cardiac conduction defects and previous administration of cardiac cathecholamines depleting drugs.