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Objective-To compare the value of current transthoracic echocardiographic systems and transoesophageal echocardiography for assessing left atrial appendage function and imaging thrombi. Design-Single blind prospective study. Patients were first investigated by transthoracic echocardiography and thereafter by a second investigator using transoesophageal echocardiography. The feasibility of imaging the left atrial appendage, recording its velocities, and identifying thrombi within the appendage were determined by both methods. Patients-117 consecutive patients with a stroke or transient neurological deficit. Setting-Tertiary cardiac and neurological care centre. Results-Imaging of the complete appendage was feasible in 75% of the patients by transthoracic echocardiography and in 95% by transoesophageal echocardiography. Both methods were concordant for the detection of thrombi in 10 cases. Transoesophageal echocardiography revealed two additional thrombi. In one of these patients, transthoracic echocardiography was not feasible and in the other the thrombus had been missed by transthoracic examination. In patients with adequate transthoracic echogenicity, the specificity and sensitivity of detecting left atrial appendage thrombi were 100% and 91%, respectively. Recording of left atrial appendage velocities by transthoracic echocardiography was feasible in 69% of cases. None of the patients with a velocity > 0.3 m/s had left atrial appendage thrombi. In the one patient in whom transthoracic echocardiographic evaluation missed a left atrial appendage thrombus, the peak emptying velocity of the left atrial appendage was 0.25 m/s. Conclusions-A new generation echocardiographic system allows for the transthoracic detection of left atrial appendage thrombi and accurate determination of left atrial appendage function in most patients with a neurological deficit. (Heart 1999;81:192-198)

Internal atrial defibrillation causes depressed left atrial chamber and appendage function and may result in the subacute accumulation of spontaneous echo contrast and development of new thrombi after cardioversion. These findings have important clinical implications for anticoagulation therapy before and after low energy internal atrial defibrillation in patients with atrial fibrillation.

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Objective-To analyse profiles of coronary artery flow velocity at rest in patients with aortic stenosis and to determine whether changes of the coronary artery flow velocities are related to symptoms in patients with aortic stenosis. Design-A prospective study investigating the significance of aortic valve area, pressure gradient across the aortic valve, systolic left ventricular wall stress index, ejection fraction, and left ventricular mass index in the coronary flow velocity profile of aortic stenosis; and comparing flow velocity profiles between symptomatic and asymptomatic patients with aortic stenosis using transoesophageal Doppler echocardiography to obtain coronary artery flow velocities of the left anterior descending coronary artery. Setting-Tertiary referral cardiac centre. Patients-Fifty eight patients with aortic stenosis and 15 controls with normal coronary arteries. Results-Adequate recordings of the profile of coronary artery flow velocities were obtained in 46 patients (79%). Left ventricular wall stress was the only significant haemodynamic variable for determining peak systolic velocity (r = -0-83, F = 88 5, P < 0.001). The pressure gradient across the aortic valve was the only contributor for explaining peak diastolic velocity (r = 0 56, F = 20-9, P < 0.001).Controls and asymptomatic patients with aortic stenosis (n = 12) did not differ for peak systolic velocity [32.8 (SEM 9.7) v 27-0 (8.7) cmls, NS] and peak diastolic velocity [58-3 (18.7) v 61'9 (13.5) cmls, NS]. In contrast, patients with angina (n = 12) or syncope (n = 8) had lower peak systolic velocities and higher peak diastolic velocities than asymptomatic patients (P < 0.01). Peak systolic and diastolic velocities were -7 7 (22 5) cm/s and 81'7 (17.6) cmls for patients with angina, and -19-5 (22.3) cmls and 94*0 (20.9) cmls for patients with syncope.Asymptomatic patients and patients with dyspnoea (n = 14) did not differ. Conclusions-Increased pressure gradient across the aortic valve and enhanced systolic wall stress result in characteristic changes of the profile of coronary flow velocities in patients with aortic stenosis. Decreased or reversed systolic flow velocities are compensated by enhanced diastolic flow velocities, particularly in patients with angina and syncope. This characteristic pattern of the profile of coronary artery flow velocities in patients with angina or syncope may be useful for differentiating those patients from asymptomatic patients.