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This study has examined the prognostic significance of troponin-I (Tn-I) levels after catheter-based coronary interventions in coronary arteries and saphenous vein grafts lesions. Tn-I and creatine kinase-MB (CK-MB) fraction levels were measured at 6 and 18 to 24 hours after catheter-based coronary intervention in 1,129 consecutive patients with normal preintervention plasma levels of Tn-I, and CK-MB levels below the cutoff for myocardial infarction. Patients were stratified according to maximal postangioplasty Tn-I levels. Group I (n = 784) had no elevated Tn-I (<0.15 ng/ml), group II (n = 170) had Tn-I at 0.15 to 0.45 ng/ml, and group III (n = 175) had Tn-I elevation >0.45 ng/ml. Major in-hospital complications (death, 0-wave infarction, and emergent coronary bypass grafting) and out-of-hospital intermediate-term (8 months) outcomes were compared between the 3 groups. Tn-I elevation >0.45 ng/ml was associated with increased risk of mortality (group III, 1.6%; group II, 0.6%; and group I, 0.1%; p = 0.019) and major in-hospital complications (3.2%, 1.7%, and 0.5%; p = 0.004). There was no difference in death (1.8%, 3.2%, and 2.4%; p = 0.74), Q-wave infarction (0.6%, 0%, and 0.3%; p = 0.66), or target lesion revascularization (10.1%, 9.0%, and 9.3%; p = 0.86) between the 3 groups at follow-up. Cardiac event-free survival was similar between groups (p = 0.3). By multivariate analysis, Tn-I >0.45 ng/ml was an independent predictor for major in-hospital complications (odds ratio 2.1, 95% confidence interval 1.2 to 3.9, p = 0.01). The degree of risk was also associated with the conjoint elevation of Tn-I and CK-MB levels (odds ratio 1.1, 95% confidence interval 1.02 to 1.2, p = 0.01). We conclude that Tn-I levels >3 times the normal limit and conjoint elevation of Tn-I and CK-MB levels after coronary angioplasty are associated with increased risk of major in-hospital complications, but have no incremental risk of adverse intermediate-term (8 months) clinical outcomes.

In phase 1 of this study, 60 patients undergoing coronary angioplasty were randomized to receive saline, dopamine, or aminophylline; the overall incidence of contrast-induced renal failure was 38%, without difference among the 3 groups. In phase 2 of this study, 72 patients with established contrast-induced renal failure were randomized to receive saline or dopamine; dopamine had a deleterious effect on the severity of renal failure, prolonging the course.

Left ventricular outflow obstruction in patients with idiopathic hypertrophic subaortic stenosis or obstructive asymmetric septal hypertrophy is due to abnormal forward motion during systole of the anterior mitral leaflet. To determine why some patients with this disease hav left ventricular outflow obstruction whereas others do not, we studied a large number of patiens with assymetric septal hypertrophy using both one- and two-dimensional echocardiography. In 100 patients with asymmetric septal hypertrophy and 22 normal subjects, mitral valve position at the onset of systole was quantitated by measuring the distance from the ventricular septum to the mitral valve and the distance from the mitral valve to the posterior left ventricular wall. None of the normal subjects and only 3 (6 percent) of 51 patients with nonobstructive asymmetric septal hypertrophy had a septal-mitral valve distance of less than 20 mm compared with 23 (66 percent) of 35 patients with obstructive asymmetric septal hypertrophy. Moreover, the mitral valve at the onset of systole was actually positioned forward in the left ventricular activity. Two-dimensional studies in 11 patients with obstructive asymmetric septal hypertrophy revealed that contraction of the malaligned papillary muscles did not cause the abnormal forward mitral valve motion. We propose that the left ventricular outflow obstruction in patients with obstructive asymmetric septal hypertrophy occurs as a result of two factors: (1) narrowing of the left ventricular outflow tract at the onset of systole, and (2) hydrodynamic forces generated by contraction on the left ventricle.

Postoperative echocardiogram often demonstrate persistent right ventricular dilatation and paradoxic ventricular septal motion after repair of an atrial septal defect. To determine the prevalence, causes and significance of these echocardiographic abnormalities, 31 patients were studied with catheterization and echocardiography before and after repair of an atrial septal defect. Before operation, every patient manifested right ventricular dilatation, and all but one had abnormal septal motion. After operation, right ventricular dilatation was noted in 24 (77%) and abnormal septal motion in 21 (68%) patients despite the absence of residual left to right shunting in 30 (97%). These echocardiographic abnormalities could be correlated with age at operation and length of postoperative follow-up study but did not correlate with the degree of preoperative right ventricular enlargement or with shunt size or right ventricular pressure before or after operation. There was no associated functional deficit as demonstrated by the normal maximal oxygen consumption in all 13 patients who underwent treadmill exercise testing 5 to 38 months after operation; these patients included 9 with persistent right ventricular enlargement and abnormal septal motion.