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Unlabelled: Predictive factors of a favourable response to beta-blocker therapy are still unknown and the role of heart rate remains controversial., Aim: To investigate the relation between heart rate and the response to chronic metoprolol treatment in patients with dilated cardiomyopathy (DCM)., Methods: Ninety-eight consecutive patients with DCM, left ventricular ejection fraction (LVEF) < or = 0.40 and blood pressure < or = 140/90 mmHg were treated with metoprolol, associated with digitalis, diuretics and ACE-inhibitors. After 24 +/- 6 months, 48 patients (49%) were classified as "improved" on the basis of a clinical/instrumental score., Results: Rest, mean 24-hour and maximal exercise heart rate were all significantly and directly related to the probability of improvement, but heart rate at rest, supine and in upright position, showed the highest predictive power. The relationship between heart rate and improvement with metoprolol appeared to be non-linear, with an increasing probability in patients with higher heart rate, but with a fall of the slope in cases with extreme tachycardia. By dividing our study population on the basis of the most important clinical variables, this complex relation was evident only in patients at a more advanced stage of the disease., Conclusion: Our analysis confirms the strict relationship between heart rate and improvement with chronic metoprolol therapy in patients with DCM. This relation seems to be non-linear and is influenced by the severity of the disease.

A spontaneous episode of bundle branch reentry ventricular tachycardia was recorded in a 50 year old man few weeks after operation for a severe aortic valve regurgitation. After surgery, the patient developed recurrent syncope and showed a bradycardia-dependent left bundle branch block and a HV interval of 70 ms. A bundle branch reentry ventricular tachycardia with left bundle branch block morphology, easily induced during premature ventricular stimulation, occurred spontaneously after the longest sinus cycle of a sequence conducted to the ventricles with a left bundle branch block morphology of the QRS complexes. During left bundle branch block an incomplete and concealed anterograde conduction along the left bundle branch was supposed to be present and its disappearance was considered the trigger mechanism of the spontaneous ventricular tachycardia. The negative results obtained with the signal-averaged ECG in our case support the concept that intramyocardial delay is not essential for this type of ventricular tachycardia.

Background: Patients with non rheumatic atrial fibrillation (NRAF) have an increased risk for thromboembolic complications. Recent evidence suggests that left atrial appendage function (contraction, filling dynamics) may provide clues to the thrombogenic potential of this structure. The aim of this study was to identify left atrial spontaneous echocontrast and thrombus between patients with NRAF and their relationship with left atrial appendage function., Methods: Transthoracic (TTE) and biplane or multiplane transesophageal echocardiography (TEE) were performed in 143 patients with chronic NRAF enrolled in the Trieste Area Study on non rheumatic Atrial Fibrillation (TASAF), an ongoing prospective community study with a follow-up period of 2 years. The maximal and minimal areas of the left atrial appendage were measured during three cardiac cycles and the peak emptying and filling velocities profile were obtained by pulsed wave Doppler at the orifice of the left atrial appendage. The left atrium and appendage were inspected for thrombus and spontaneous echocontrast., Results: Left atrial appendage thrombus was present in 37 patients (26%) and spontaneous echocontrast in 60 patients (42%), 45% of patients with spontaneous echocontrast had thrombus. Univariate analysis identified positive correlation of thrombus with duration of atrial fibrillation (p = 0.05), hypertension (p = 0.01), left atrial area (p = 0.005), mitral annular calcification (p = 0.01), left ventricular dysfunction (p = 0.03) and a non significant correlation with the mitral valve prolapse (p = 0.08) in the TTE. The presence of mitral regurgitation did not demonstrate a protective effect (p = 0.73) against thrombosis. The variables of left atrial appendage function identifying a subgroup of patients with increased risk of thrombus formation were: shortening fraction of the area in the horizontal and vertical sections (p = 0.0001 and p = 0.002 respectively), the peak filling and emptying velocity in horizontal (p = 0.0001 equal for both) and vertical sections (p = 0.0001 equal for both). In summary these patients have a larger left atrial maximal area (p = 0.004) and a lower flow velocity profile (p < 0.00001) and more intense spontaneous echocontrast (p < 0.00001) than the others. Spontaneous echocontrast was correlated with left ventricular dysfunction (p = 0.008), left atrial area (p = 0.02) and there was a non-significant correlation with mitral annular calcification (p = 0.09) and lower left ventricular shortening fraction (p = 0.06). Transesophageal echocardiography variables have identified the subgroup of patients with an increased risk of echocontrast formation. This was positively associated with a low flow velocity profile (p = 0.0001), a left atrial appendage low shortening fraction in horizontal section (p = 0.001) and in vertical section (p = 0.05) and a low peak filling velocity in horizontal section (p = 0.003) and in vertical section (p = 0.004) and a low peak emptying velocity in horizontal section (p = 0.003) and in vertical section (p = 0.001). Prophylactic therapy with anticoagulant or antiplatelet agents has little benefits in our experience., Conclusions: Spontaneous echocontrast and low flow profile velocity (low peak emptying and filling velocity) and increased area of left atrial appendage were strongly associated with left atrial and/or appendage thrombus in patients with NRAF. The assessment of left atrial appendage function by TEE is an important component of the comprehensive evaluation of potentially increased risk of thrombus formation.