Percutaneous coronary intervention is an alternative to CABG for patients with medically refractory myocardial ischemia and a high risk of adverse outcomes with CABG.

We studied the ability of a single oral dose of aspirin to inhibit prostacyclin synthesis by human arterial and venous tissue and to inhibit thromboxane A2 synthesis by platelets in 70 patients who were undergoing aortocoronary bypass. A dose of 40, 80, or 325 mg of aspirin was administered 12 to 16 hours before surgery. The generation of thromboxane in serum--which provides an estimate of platelet thromboxane production--was reduced from the control value by 77, 95, and 99 per cent after single doses of 40, 80, and 325 mg of aspirin, respectively. By contrast, prostacyclin production in aortic tissue that was removed at operation was reduced by only 35, 38, and 75 per cent, respectively, in response to these doses. Production of prostacyclin in saphenous-vein tissue (not tested after 40 mg of aspirin) fell only slightly and not significantly after 80 mg but was reduced by 85 per cent after 325 mg. These findings indicate that a low dose of aspirin (40 to 80 mg) can largely inhibit platelet aggregation and thromboxane synthesis but has much less effect on prostacyclin production in arterial and venous endothelium.

Air pollution is positively associated with increased daily incidence of myocardial infarction and cardiovascular mortality. We hypothesize that air pollutants, primarily vapor phase organic compounds, cause an enhancement of coronary vascular constriction. Such events may predispose susceptible individuals to anginal symptoms and/or exacerbation of infarction. To develop this hypothesis, we studied the effects of nonparticulate diesel exhaust constituents on (1) electrocardiographic traces from ApoE-/- mice exposed whole-body and (2) isolated, pressurized septal coronary arteries from ApoE-/- mice. ApoE-/- mice were implanted with radiotelemetry devices to assess electrocardiogram (ECG) waveforms continuously throughout exposures (6 h/day x 3 days) to diesel exhaust (0.5 and 3.6 mg/m3) in whole-body inhalation chambers with or without particulates filtered. Significant bradycardia and T-wave depression were observed, regardless of the presence of particulates. Pulmonary inflammation was present only in the whole exhaust-exposed animals at the highest concentration. Fresh diesel exhaust or air was bubbled through the physiologic saline tissue bath prior to experiments to enable the isolated tissue exposure; exposed saline contained elevated levels of several volatile carbonyls and alkanes, but low to absent levels of polycyclic aromatic hydrocarbons. Vessels were then assayed for constrictive and dilatory function. Diesel components enhanced the vasoconstrictive effects of endothelin-1 and reduced the dilatory response to sodium nitroprusside. These data demonstrate that nonparticulate compounds in whole diesel exhaust elicit ECG changes consistent with myocardial ischemia. Furthermore, the volatile organic compounds in the vapor phase caused enhanced constriction and reduced dilatation in isolated coronary arteries caused by nonparticulate components of diesel exhaust.

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