In selected patients with multivessel coronary disease, PTCA and CABG as initial treatments resulted in equivalent improvement in angina after one year. However, in order to achieve similar clinical outcomes, the patients treated with PTCA were more likely to require further interventions and antianginal drugs, whereas the patients treated with CABG were more likely to sustain an acute myocardial infarction at the time of the procedure.

Thrombi located in the left atrial appendage are frequently not detected with conventional two-dimensional echocardiography. The transesophageal echocardiographic approach readily visualizes left atrial morphology and may be used as an alternative. In 6 of 21 patients with mitral valve stenosis, a left atrial appendage thrombus was diagnosed by transesophageal two-dimensional echocardiography when transthoracic echocardiography had failed. The transesophageal echocardiographic findings were confirmed at surgery for mitral valve replacement in all cases.

BACKGROUND Aortic dissection requires prompt and reliable diagnosis to reduce the high mortality. The purpose of this study was to assess the reliability of both ECG-triggered magnetic resonance imaging (MRI) and transesophageal two-dimensional echocardiography combined with color-coded Doppler flow imaging (TEE) for the diagnosis of thoracic aortic dissection and associated epiphenomena. METHODS AND RESULTS Fifty-three consecutive patients with clinically suspected aortic dissection were subjected to a dual noninvasive imaging protocol in random order; imaging results were compared and validated against the independent morphological "gold standard" of intraoperative findings (n = 27), necropsy (n = 7), and/or contrast angiography (n = 53). No serious side effects were encountered with either imaging method. In contrast to a precursory screening transthoracic echogram, the sensitivities of both MRI and TEE were 100% for detecting a dissection of the thoracic aorta irrespective of its location. The specificity of TEE, however, was lower than the specificity of MRI for a dissection (TEE, 68.2% versus MRI, 100%; p less than 0.005), which resulted mainly from false-positive TEE findings confined to the ascending segment of the aorta (TEE, 78.8% versus MRI, 100%; p less than 0.01). In addition, MRI proved to be more sensitive than TEE in detecting the formation of thrombus in the false lumen of both the aortic arch (p less than 0.01) and the descending segment of the aorta (p less than 0.05). There were no discrepancies between the two imaging techniques in detecting the site of entry to a dissection, aortic regurgitation, or pericardial effusion. CONCLUSIONS Both MRI and TEE are atraumatic, safe, and highly sensitive methods to identify and classify acute and subacute dissections of the entire thoracic aorta. TEE, however, is associated with lower specificity for lesions in the ascending aorta. These results may still favor TEE as a semi-invasive diagnostic procedure after a precursory screening transthoracic echogram in suspected aortic dissection, but they establish MRI as an excellent method to avoid false-positive findings. Anatomic mapping by MRI may emerge as the most comprehensive approach and morphological standard to guide surgical interventions.

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Thromboxane released from activated platelets and prostacyclin of the vessel wall may act as potent antagonistic modulators of platelet aggregability and coronary vascular tone. Therefore, urinary excretion of their major metabolites, 2,3-dinor-thromboxane B2 and 2,3-dinor-6-ketoprostaglandin F1 alpha, was studied in 16 patients presenting with prolonged angina at rest. The 10 patients whose condition did not improve under vigorous antianginal treatment within 48 hours exhibited higher thromboxane metabolite excretion than did the 6 patients who responded to therapy (2,208 +/- 1,542 versus 609 +/- 312 ng/g creatinine; p less than 0.001). Elevated values were also found in four of eight patients with sustained postinfarction angina. Enhanced thromboxane metabolite excretion was frequently associated with angiographic evidence of thrombus formation. When nine patients were restudied in a stable phase after 11 +/- 5 months, thromboxane metabolite excretion was consistently normal or high normal. Excretion of prostacyclin metabolites was not depressed in any patient but correlated weakly with thromboxane (r = 0.41). Thus, enhanced thromboxane production as an index of platelet activation may identify patients with active thrombus formation who could benefit most from platelet inhibitory treatment.