ABSTRACT
This prospective study (September 1989 to November 1990) was undertaken to evaluate the utility of transesophageal echocardiography in acute peripheral ischaemic syndromes. After embolectomy or thrombolysis, 87 patients with an average age of 69.7 years underwent not only the usual investigations (conventional echocardiography, abdominal ultrasonography and Holter monitoring) but also transesophageal echocardiography within 2 days of the ischaemic events (lower limb 84%, multiple embolism 11%, recurrent embolism 13%). Atrial fibrillation was documented in 44 patients (50.5%), 19 patients had chronic arterial disease (22%), 8 patients had valvular heart disease (9%) and 2 patients had a blood disorder (2%). Transthoracic echocardiography only demonstrated one left ventricular apical thrombus whereas transesophageal echocardiography showed residual thrombus in 22 patients (25%) mainly in the left auricle but also in the descending thoracic aorta (8 patients) as a mobile, pediculated thrombus or lining an aortic aneurysm, thereby opening up new therapeutic possibilities. In addition, double aortic dissection was diagnosed in a patient who was not echogenic, isolated spontaneous contrast in 20 patients (23%) and other abnormalities in 7 patients (8%). Statistical analysis showed a significant relationship between the presence of thrombus and/or spontaneous contrast in the left atrium and/or left auricle and the size of the left atrium (Fisher test - p = 0.0073), and the presence of a supraventricular arrhythmia (chi 2 test).
Subject(s)
Echocardiography/methods , Embolism/diagnostic imaging , Peripheral Vascular Diseases/diagnostic imaging , Adult , Aged , Aged, 80 and over , Atrial Fibrillation/complications , Embolism/complications , Esophagus , Female , Heart Atria , Heart Diseases/diagnostic imaging , Heart Diseases/etiology , Heart Valve Diseases/complications , Humans , Male , Middle Aged , Peripheral Vascular Diseases/etiology , Prospective Studies , Thrombosis/diagnostic imaging , Thrombosis/etiologyABSTRACT
It has been shown previously that an increase in cytoplasmic Ca2+ concentration depresses the GABA-A response. However, little attention has been paid to the Ca2+ source involved. In the present study, we show that the Ca2+ increase triggered by caffeine-induced Ca2+ release from the intracellular pool inhibits the GABA-A response, whereas Ca2+ influx through voltage-activated Ca2+ channels has no effect on this response.
