Comparison of sirolimus eluting stent with bioresorbable polymer to everolimus eluting stent with permanent polymer in bifurcation lesions: Results from CENTURY II trial.

OBJECTIVE: To demonstrate the safety and efficacy of a new sirolimus eluting stent with bioresorbable polymer, Ultimaster, (BP-SES) compared with everolimus-eluting, permanent polymer, Xience stent (PP-EES) in bifurcation lesions with respect to the freedom from Target Lesion Failure at 1-year. METHODS: Within 1,119 patients enrolled in the CENTURY II randomized controlled multicenter trial, 194 patients were treated for bifurcation lesions and randomized to either BP-SES (n = 95) or PP-EES (n = 99). The primary endpoint was freedom from target lesion failure (TLF) composite endpoint [cardiac death, MI not clearly attributable to a non-target vessel, and clinically driven target lesion revascularization (TLR)] at 1-year. RESULTS: Baseline patient demographic, angiographic, and stenting characteristics were similar in both study arms. A single stent technique with provisional or "cross over" stenting were the most widely used in both arms (93.2% BP-SES vs. 92.4% PP-EES). Freedom from TLF at 1-year was 94.7% for BP-SES and 91.9% for PP-EES (P for noninferiority 0.031). The rate of clinically driven target lesion revascularization (TLR) at 1-year was 3.2% for BP-SES and 3.0% for PP-EES (P = 0.95). There were no significant differences detected in any of the individual clinical endpoints or other secondary clinical endpoints between the study arms at 1-year follow up. CONCLUSIONS: The new bioresorbable polymer sirolimus-eluting stent showed safety and efficacy profiles similar to durable polymer everolimus-eluting in the treatment of patients with bifurcation lesions at 1-year follow up. © 2015 Wiley Periodicals, Inc.

Increased susceptibility of low-density lipoprotein (LDL) to oxidation by gamma-radiolysis with age.

The susceptibility to oxidation of freshly isolated LDL from healthy normolipidemic individuals in three age groups was estimated by exposure of LDL to ionizing radiation followed by analyses of vitamin E, TBARS, conjugated dienes, and fluorescent products. The results clearly showed that LDL from elderly subjects was the most susceptible to oxidative damage in vitro. In particular, the greater susceptibility of LDL from elderly subjects in comparison to that from young subjects may be attributed to the much lower (4-fold) concentration of LDL vitamin E in the elderly subjects. The present study reinforces the notion that the susceptibility of LDL to oxidation increases with age.

Multicenter patency trial of intravenous anistreplase compared with streptokinase in acute myocardial infarction. The TEAM-2 Study Investigators.

Thrombolytic therapy has been shown to improve clinical outcome when administered early after the onset of symptoms of acute myocardial infarction; the mechanism of benefit is believed to be reestablishment and maintenance of coronary artery patency. Anistreplase is a second generation thrombolytic agent that is easily administered and has a long duration of action. To compare anistreplase (30 units/2-5 min) and therapy with the Food and Drug Administration-approved regimen of intravenous streptokinase (1.5 million units/60 min), a randomized, double-blind, multicenter patency trial was undertaken in 370 patients less than 76 years of age with electrocardiographic ST segment elevation who could be treated within 4 hours of symptom onset. Coronary patency was determined by reading, in a blinded fashion, angiograms obtained early (90-240 minutes; mean, 140 minutes) and later (18-48 hours; mean, 28 hours) after beginning therapy. Early total patency (defined as Thrombolysis in Myocardial Infarction grade 2 or 3 perfusion) was high after both anistreplase (132/183 = 72%) and streptokinase (129/176 = 73%) therapy, and overall patency patterns were similar, although patent arteries showed "complete" (grade 3) perfusion more often after anistreplase (83%) than streptokinase (72%) (p = 0.03). Similarly, residual coronary stenosis, determined quantitatively by a validated computer-assisted method, was slightly less in patent arteries early after anistreplase (mean stenosis diameter, 74.0%) than streptokinase (77.2%, p = 0.02). In patients with patent arteries without other early interventions, reocclusion risk within 1-2 days was defined angiographically and found to be very low (anistreplase = 1/96, streptokinase = 2/94). Average coronary perfusion grade was greater, and percent residual stenosis was less, at follow-up than on initial evaluation and did not differ between treatment groups. Enzymatic and electrocardiographic evolution was not significantly different in the two groups. Despite rapid injection, anistreplase was associated with only a small (4-5 mm Hg), transient (at 5-10 minutes) mean differential fall in blood pressure. In-hospital mortality rates were comparable for anistreplase and streptokinase (5.9%, 7.1%). Stroke occurred in one (0.5%) and three (1.6%) patients, respectively; one stroke was hemorrhagic. Other serious bleeding events and adverse experiences occurred uncommonly and with similar frequency in the two groups. Thus, for the end points of our study (patency, safety), anistreplase and streptokinase showed overall favorable and relatively comparable outcomes, with a few differences.(ABSTRACT TRUNCATED AT 400 WORDS)

Failure of diltiazem to prevent restenosis after percutaneous transluminal coronary angioplasty.

This prospective randomized trial was carried out in 92 patients who underwent a successful percutaneous transluminal coronary angioplasty (PTCA) and had no evidence of coronary spasm before PTCA. All patients were premedicated with calcium antagonists and platelet inhibitors and received platelet inhibitors (aspirin and dipyridamole) for 6 months after PTCA. The diltiazem group (46 patients with 50 stenoses successfully dilated) received diltiazem, 90 mg three times a day by mouth for 3 months after PTCA; in the control group (46 patients, 53 stenoses), calcium antagonists were discontinued immediately after PTCA. All patients underwent a control angiogram 5 to 10 months after PTCA unless recurrence of angina dictated its need earlier. Baseline characteristics were similar in both groups, except for the number of diseased vessels greater than or equal to 70%, which was higher in the control group (1.2 +/- 0.55 vs 0.9 +/- 0.39 for the diltiazem group, p less than 0.05). In the diltiazem group, the degree of stenosis increased from 38 +/- 15% immediately after PTCA to 42 +/- 23% at repeat angiography 8.24 +/- 4.79 months after PTCA and there were seven restenoses. In the control group, the degree of stenosis increased from 37 +/- 12% to 44 +/- 23% at repeat angiography 8.26 +/- 4.91 months after PTCA and there were 10 restenoses (NS vs the diltiazem group). In conclusion, in patients without variant angina before PTCA, adjunction of diltiazem to platelet inhibitors does not decrease the incidence of restenosis. These data suggest that coronary spasm is not the major mechanism of restenosis.

Symptomatic coronary artery spasm following radiotherapy for Hodgkin's disease.

Four years after mediastinal radiation for Hodgkin's lymphoma, a 32-year-old man developed angina at rest and with varying levels of physical activity. At coronary arteriography, 40 percent to 50 percent stenoses were seen in the left coronary artery; ergonovine induced severe coronary spasm. Treatment with diltiazem eliminated all anginal attacks.