The diagnostic yield of transesophageal and transthoracic echocardiography for identifying a cardiac source of embolism was compared in 79 patients presenting with unexplained stroke or transient ischemic attack. There were 35 men and 44 women with a mean age of 59 years (range 17 to 84); 52% had clinical cardiac disease. Both transthoracic and transesophageal echocardiograms were performed using Doppler color flow and contrast imaging. Transesophageal echocardiography identified a potential cardiac source of embolism in 57% of the overall study group compared with only 15% by transthoracic echocardiography (p less than 0.0005). Compared with transthoracic echocardiography, transesophageal echocardiography more frequently identified atrial septal aneurysm associated with a patent foramen ovale (9 versus 1 of 79 patients, p less than 0.005), left atrial thrombus or tumor (6 versus 0 of 79 patients, p less than 0.05) and left atrial spontaneous contrast (13 versus 0 of 79 patients, p less than 0.0005). All cases of left atrial thrombus or spontaneous contrast were identified in patients with clinically identified cardiac disease. In the 38 patients with no cardiac disease, transesophageal echocardiography identified isolated atrial septal aneurysm and atrial septal aneurysm with a patent foramen ovale more frequently than transthoracic echocardiography (8 versus 2 of 38 patients, p less than 0.05). The two techniques had a similar rate of identifying apical thrombus and mitral valve prolapse. Overall, transesophageal echocardiography identified abnormalities in 39% of patients with no cardiac disease versus 19% for transthoracic echocardiography (p less than 0.005). Thus, transesophageal echocardiography identifies potential cardiac sources of embolism in the majority of patients presenting with unexplained stroke.(ABSTRACT TRUNCATED AT 250 WORDS)
To assess the use of adenosine as an alternative agent for determination of coronary vasodilator reserve, hemodynamics and coronary blood flow velocity were measured at rest and during peak hyperemic responses to continuous intravenous adenosine infusion (50, 100 and 150 micrograms/kg per min for 3 min) and intracoronary papaverine (10 mg) in 34 patients (17 without [group 1] and 17 with [group 2] significant left coronary artery disease), and in 17 patients (11 without and 6 with left coronary artery disease) after low dose (2.5 mg) intravenous bolus injection of adenosine. The maximal adenosine dose did not change mean arterial pressure (-10 +/- 14% and -6 +/- 12% for groups 1 and 2, respectively) but increased the heart rate (15 +/- 18% and 13 +/- 16, respectively). For continuous adenosine infusions, mean coronary flow velocity increased 64 +/- 104%, 122 +/- 94% and 198 +/- 59% and 15 +/- 51%, 110 +/- 95% and 109 +/- 86% in groups 1 and 2, respectively for each of the three doses. Mean coronary flow velocity increased significantly after 100 and 150 micrograms/kg of adenosine and 10 mg of intracoronary papaverine (48 +/- 25, 52 +/- 19 and 54 +/- 21 cm/s, respectively; all p less than 0.05 vs. baseline) and was significantly higher than in group 2 (37 +/- 24, 32 +/- 16, 41 +/- 23 cm/s; all p less than 0.05 vs. group 1). The coronary vasodilator reserve ratio (calculated as the ratio of hyperemic to basal mean flow velocity) for adenosine and papaverine was 2.94 +/- 1.50 and 2.94 +/- 1.00, respectively, in group 1 and was significantly and similarly reduced in group 2 (2.16 +/- 0.81 and 2.38 +/- 0.78, respectively; both p less than 0.05 vs. group 1). Low dose bolus injection of adenosine increased mean velocity equivalently to that after continuous infusion of 100 micrograms/kg, but less than after papaverine. There was a strong correlation between adenosine infusion and papaverine for both mean coronary flow velocity and coronary vasodilator reserve ratio (r2 = 0.871 and 0.325; SEE = 0.068 and 0.189, respectively; both p less than 0.0005). No patient had significant arrhythmias or prolongation of the corrected QT (QTc) interval with adenosine, but papaverine increased the QT (QTc) interval from 445 +/- 44 to 501 +/- 43 ms (p less than 0.001 vs. both maximal adenosine and baseline) and produced nonsustained ventricular tachycardia in one patient.(ABSTRACT TRUNCATED AT 400 WORDS)
The contour of the epicardial coronary vessels may change considerably during coronary angioplasty. We report the extreme and unique "accordion-like" wrinkling of the mid right coronary artery as a result of distal guidewire entrapment during coronary angioplasty. Recognition of this artifact and its treatment may prevent further complications of coronary angioplasty.
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