Predictors of left atrium appendage clot detection despite on-target warfarin prevention for atrial fibrillation.

BACKGROUND AND PURPOSE: The antithrombotic management of atrial fibrillation (AF) is currently based on clinical scores (CHADS(2) or CHA(2)DS(2)VASc). The prevalence of left atrium (LA) thrombi in effectively anticoagulated AF patients has been reported as being up to 7.7 %. We tried to correlate LA/LA appendage (LAA) thrombus detection with possible clinical predictors in warfarin-treated patients. METHODS: We performed trans-esophageal echocardiography on 430 patients (mean age, 60.3 ± 9.8 years) receiving oral anticoagulant (OAC) therapy and undergoing pulmonary vein isolation. In 10/430 (2.3 %), an LA thrombus was found despite therapeutic OAC (mean INR 2.6 ± 0.6; range, 2.0-3.8) over the previous 4 weeks. RESULTS: Two study groups were identified: 1. T-positive group = with LAA thrombus (10 patients) 2. T-negative group = without LAA thrombus (420 patients) The T-positive patients had a higher CHADS(2) score (1.5 ± 0.7 versus 0.7 ± 0.8; p = 0.004), a lower LVEF (54.7 ± 9.5 % versus 60.2 ± 7.4; p = 0.02), and a larger LA size (LA diameter, 56 ± 12.2 mm versus 46 ± 6.5 mm; p < 0.001and normalized LA volume: 140.2 ± 66 ml/m² vs. 67 ± 39 ml/m²; p < 0.05). On multivariate analysis, a larger LA diameter and normalized LA volume (OR, 1.14; 95 % C.I., 1.04-1.26; p = 0.006 and OR, 1.02; 95 % C.I., 1.01-1.03; p = 0.001, respectively) and a higher CHA(2)DS(2)VASc score (OR, 2.4; 95 % C.I., 1.4-4.2; p = 0.001) predicted left atrium appendage (LAA) thrombus. In another 42/430 (9.8 %) patients, an LA spontaneous echo-contrast (SEC) was detected. Thus, cumulatively, 52/430 (12.1 %) patients had either LAA thrombi (10 patients) or SEC (42 patients). LA diameter continued to predict the presence of either thrombi or SEC (OR, 1.14; 95 % C.I., 1.07-1.2; p < 0.05). CONCLUSIONS: We found a 2.3 % prevalence of LA thrombus (12.1 % when SEC was also considered). The thrombus was present despite on-target warfarin prevention. In addition to a higher CHA(2)DS(2)VASc score, a larger LA size was a strong predictor of clot detection.

Tricuspid valve endocarditis: repair with the use of artificial chordae.

We report on a patient who developed tricuspid valve endocarditis on a permanent endocardial pacemaker lead. At operation the endocardial lead was removed and accurate debridement of the tricuspid tissue was performed. Tricuspid valve reconstruction included commissural plication and the construction of artificial polytetrafluoroethylene chordae from the anterior leaflet to the anterior papillary muscle to obtain valve competence.

Silent ischemia and loss of reversible myocardial dysfunction following myocardial infarction.

Sixty-seven asymptomatic patients were enrolled after a first uncomplicated myocardial infarction (MI) so as to study the relevance of reversible myocardial dysfunction in determining left ventricular function soon after the acute episodes and 12 months later. Moreover, the potential role of silent ischemia in conditioning the evolutive aspects of contractile dysfunction has been investigated. Postextrasystolic potentiation during two-dimensional echocardiographic (2-D echo) monitoring has been used to detect the presence of viable myocardium in asynergic myocardial segments. Results of electrocardiographic (ECG) ambulatory monitoring at predischarge determined patient groups: Group A included 49 patients without ST changes during monitoring, while Group B included 18 patients with silent ischemia. Incidence of reversible myocardial dysfunction was similar in the two study groups (82 vs. 86%, p = NS). Group B patients were older (59.6 +/- 6.7 vs. 50.6 +/- 10.6 years, p < 0.015) and had lower ejection fractions (EFs, 43.4 +/- 6.4% vs. 51.2 +/- 8.3%, p = 0.026) and higher at-rest wall-motion scores (WMSs, 11.4 +/- 5.9 vs. 7.2 +/- 3.8, p = 0.019). Left ventricular end-diastolic volume (LVEDV) and potentiated WMS did not differ. At 1-year examination, Group B patients exhibited a greater LVEDV index (96 +/- 6.5 vs. 70.7 +/- 14 ml/m2, p < 0.002) with a worsening both in rest and in potentiated wall-motion score index (12.8 +/- 4.6 vs. 5.3 +/- 1.8, p < 0.001; 9.2 +/- 3.6 vs. 4.8 +/- 2.2, p < 0.001, respectively). Left ventricular EF remained significantly depressed in Group B patients (42 +/- 8.7% vs. 55.5 +/- 8.1%, p < 0.002).(ABSTRACT TRUNCATED AT 250 WORDS)

Reversible and irreversible left ventricular dysfunction after acute myocardial infarction.

Left ventricular function after acute myocardial infarction depends on several mechanisms leading to left ventricular remodeling: (a) infarct size and healing and (b) adaptive changes involving both the dysfunctioning but viable myocardium (hibernating and stunned myocardium) and the nonischemic myocardium. The prognosis after acute myocardial infarction is strongly related to regional and global left ventricular function and the loss of dysfunctioning viable myocardium is a main factor in the worsening in left ventricular function in survivors of the acute phase. Thus, medical strategies should exert their beneficial effect on the "mechanical instability" of ventricular myocardium by saving the viable myocardium. beta-Blocker therapy has been shown to be effective in improving the prognosis via anti-ischemic and antiarrhythmic actions. The combination of metoprolol and nisoldipine seems to be able to preserve the contractile function of viable myocardium in the first 6 months after acute myocardial infarction.