Drug-eluting versus bare metal stenting in acute myocardial infarction. A clinical review.

Coronary heart disease is a leading cause of death around the world. The treatment of acute myocardial infarction has evolved with the advent of novel thrombolytic agents, anticoagulants, antiplatelets, and innovative percutaneous techniques. The development of drug-eluting stents has dramatically lowered the risk of in-stent restenosis compared to bare metal stents. Clinicians in the United States and Europe have begun utilizing DES in the setting of AMI despite the fact that no practice guidelines exist to support their use. Lingering concerns exist about the reported increased risk of early and late stent thrombosis after DES implantation. In this review, we will highlight the >7,500 patients studied in randomized controlled trials and >30,000 registry patients comparing drug-eluting and bare metal stent implantation during acute myocardial infarction. In the selected patient populations of the 13 randomized controlled trials comparing drug-eluting and bare metal stent implantation, death/re-infarction/stent thrombosis were not different between groups while target vessel revascularization was significantly lower in the drug-eluting stent patients. In the "real world" registry studies, mortality/target vessel revascularization/stent thrombosis were less frequent in the first year after drug-eluting stent implantation while re-infarction was not different between the groups. While multiple questions remain regarding long-term follow up and especially late stent thrombosis, it appears that drug-eluting stents are effective at decreasing target vessel revascularization while not being associated with an elevated risk of death/re-infarction/stent thrombosis in the first year post myocardial infarction.

Cardiac conduction abnormalities in endocarditis defined by the Duke criteria.

BACKGROUND: Cardiac conduction abnormalities occur in endocarditis and have been associated with infection extension and increased mortality. There have been no prospective studies of electrocardiographic (ECG) conduction changes in endocarditis. We examined the incidence of ECG changes in a large prospective cohort with suspected endocarditis and correlated changes with echocardiographic evidence of invasive infection and mortality. METHODS: One hundred thirty-seven of 1396 (10%) suspected cases of endocarditis were classified as "definite" or "possible" by the Duke criteria and had an interpretable ECG. ECG conduction changes were classified as old (pre-existing hospitalization), new (evident on admission or developed during hospitalization), or indeterminate. New or indeterminate abnormalities were considered "ECG conduction changes." Echocardiogram results were reviewed to identify infected valves and invasive infection. RESULTS: ECG conduction changes were present in 36 of 137 (26%) patients. Patients with ECG conduction changes were more often male (69% vs 46%, P =.005) and had prosthetic valves (47% vs 23%, P <.001). There were no significant differences in microbiology results or treatment with cardiac surgery. In 76 (55%) patients, at least one infected valve was identified by echocardiography; 15 of 76 (20%) patients were determined to have evidence of invasive infection. Eight of 15 (53%) invasive infections exhibited ECG conduction changes compared with 16 of 61 (26%) isolated valve infections (P =.046). Eleven of 36 (31%) patients with ECG conduction changes died during hospitalization compared with 15 of 101 (15%) patients without changes (P =.039). CONCLUSIONS: ECG conduction changes commonly occur in endocarditis despite more sensitive diagnostic criteria and are associated with increased mortality and invasive infection.

Coronary artery restenosis after atherectomy is primarily due to negative remodeling.

The primary cause of restenosis following directional coronary atherectomy (DCA) remains obscure. "Negative remodeling," a decrease in vessel area, is believed to be more causative than is increase in plaque area. The DCA technique used in these patients, designed to facilitate the removal of plaque, should allow a more precise evaluation of the relative roles of these two mechanisms. Twenty-five patients underwent DCA. In 17, complete angiographic and intravascular ultrasound (IVUS) images were obtained before and after DCA and at follow-up (6 to 9 months). Internal elastic lamina (IEL), lumen, and plaque areas were calculated at preatherectomy, postatherectomy, and follow-up. Postatherectomy, the mean IEL area increased by 32% and the mean plaque area decreased by 51%, resulting in a significant mean increase in lumen area, 500%. At follow-up when compared to postatherectomy, the change in IEL area was variable; however, the mean did not change significantly (p = 0.58). Plaque area change, when standardized for initial vessel size, was small (mean increase 2.8 +/- 3.5%). The mean lumen area did not decrease significantly at follow-up (p = 0.43). A highly significant correlation (r = 0.96) was noted between IEL area change and lumen area at follow-up. In contrast, the correlation between plaque area change and lumen area change over the same period was much less significant (r = 0.64). These data indicate that decrease in IEL area primarily is responsible for restenosis.