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Background The outcome of patients with diabetes after myocardial infarction (MI) has traditionally been worse than in their nondiabetic counterparts before and during the thrombolytic therapy era. Whether the fate of patients with diabetes might improve with mechanical intervention, particularly with primary stenting, has not previously been studied. Methods We compared the angiographic and clinical outcome of 76 nondiabetic patients (aged 61 +/- 14 years; 66% male) and 28 patients with diabetes (aged 65 +/- 12 years; 64% male) consecutively treated with primary stenting for acute MI. Coronary Thrombolysis In Myocardial Infarction grade 3 flow was restored in 96% of diabetic and 97% of nondiabetic patients. Results Angiographic results after stent deployment were similar in the 2 groups. At 1-month follow-up, all patients in both groups were alive. Patients with diabetes had a much higher incidence of stent thrombosis (18% vs 1%; P = .003), which accounted for the majority of the major cardiac events at 1 month (21% vs 4%; P = .009). At a mean follow-up of 315 +/- 13 days, 99% of nondiabetic and 89% of patients with diabetes were alive (P = .04). Overall freedom from a major cardiac event (death, MI, target vessel revascularization) at 315 +/- 13 day follow-up was 88% for nondiabetics and 54% for patients with diabetes (P = .0003). By multivariate analysis, diabetes mellitus was the most important predictor for development of 1-month (RR 9.89; 95% confidence interval, 1.6-30) and late major cardiovascular events (RR 8.39; 95% confidence interval, 2.93-24). Conclusions Primary stenting in acute MI is highly effective in restoring immediate TIMI 3 coronary flow in nondiabetic patients and patients with diabetes. This procedure may improve benefit in terms of mortality rate to both groups, particularly in patients with diabetes, compared with previous reports with thrombolytic therapy. Nevertheless, stent thrombosis and major cardiovascular events at 1 month and late follow-up are more frequent in patients with diabetes. (Am Heart J 1999;138:446-55.)

Using polystyrene replicas of microfabricated silicon wafers bearing multiple 1.5 μm spaced, 2.0 μm wide ridges (=2.0 μm spaced, 1.5 μm wide grooves) of different heights (0.116–2.4 μm), appressoria were induced in six cereal rusts (Puccinia graminisf. sp.tritici, P. graminisf. sp.avenae, P. graminisf. sp.secalis, P. reconditaf. sp.tritici, P. coronataf. sp.avenaeandP. hordei). The pattern of response to different ridge heights was not correlated with either host or rust species. OnlyP. graminisf. sp.secalisformed significantly large numbers of appressoria (<65.0% differentiation) on singles ridges spaced 50 μm apart. Formation of appressoria on host leaves was found to be very efficient, with 92–95% of germlings encountering stomata differentiating appressoria over them. On polystyrene replicas of host leaves, however, the efficiency was much less and varied significantly between rusts (4–63% differentiation). Again, the variation was not correlated with host or rust species. Our results indicate that whilst topographical signals are sufficient to induce appressoriain vitro,host topography alone is not sufficient to explain the high efficiency of appressorium induction observedin vivo.

Two outbreaks of babesiasis are described. In one, cattle were introduced to tick-infested ground in an endemic area; 68 animals developed redwater and eight died. Indirect immunofluorescent tests on blood samples taken five months after the first case had been diagnosed showed that 58% of the calves and 92% of the cows had babesial antibody. Whereas 88% of the inexperienced, seropositive animals required treatment for redwater, only 13% of the experienced, seropositive animals had manifest disease. On the second farm, tick infested cattle, introduced from an endemic area, were grazed for several months in fields subsequently occupied by dairy cattle. Seven of the dairy cows developed characteristic symptoms of babesiasis. Whereas 55% of the cows were found to have babesial antibody, only 13% of these seropositive animals had shown signs of the infection.

Limited histopathologic studies of failed cardiac allografts have demonstrated that cardiac allograft vasculopathy extends into the donor aorta; however, no study has examined the development of allograft aortic intimal proliferation in vivo in conjunction with coronary intimal hyperplasia. By using simultaneous intracoronary and intraaortic ultrasound, we studied 20 consecutive heart transplant recipients at 2.5 +/- 2.1 years after transplantation. The degree of coronary intimal thickening was strongly correlated with the development of intraaortic intimal hyperplasia ( r = 0.90; p < 0.0001). Multivariate predictors of aortic intimal thickening included years after transplant ( r = 0.47; p = 0.03), serum cholesterol level ( r = 0.65, p = 0.003), and serum triglyceride level ( r = 0.51; p = 0.03). Allograft aortopathy occurs in a similar manner to allograft coronary disease, thus providing support for the notion that an immunologic stimulus operating across the allograft vascular bed may be responsible for the development of cardiac allograft vasculopathy. Furthermore, this investigation provides insight into the putative role of hyperlipidemia in allograft vascular disease. (Am Heart J 1997;133:698-702.)