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Aims/hypothesis Using modern echocardiography, we quantified the extent of global myocardial function and

Summary Oral administration of 1 g of acetazolamide to 8 normal subjects studied at sea level and in normoxia caused an acute increase in cerebral blood flow (CBF). During the subsequent prolonged oral treatment with 1 g of acetazolamide daily, CBF returned to normal within 2 days. The alveolar CO2 tension decreased gradually to 70% of the control value, indicating hyperventilation. At sea level hyperventilation will not increase brain oxygenation significantly in normal man, as the arterial oxygen content only increases minimally, while CBF is unchanged. At high altitude the beneficial effects of acetazolamide on the symptoms of acute mountain sickness may well be due to an improved oxygen supply to the brain, as hyperventilation will, at the low ambient PO2, cause a significant increase of the arterial oxygen content, while CBF presumably is unaffected by the drug. During hypoxia at high altitude the overall effect of prolonged acetazolamide treatment may thus be equivalent to a descent by several hundred metres.

Background: Data are sparse regarding the association between C-reactive protein (CRP) and percutaneous coronary intervention (PCI) in long-term prognosis. Previous studies have shown that PCI evokes an inflammatory response. We tested the hypothesis that the CRP response to PCI has a prognostic value. Methods: We investigated 891 consecutive patients presenting with stable or unstable angina pectoris, with serum concentrations of cardiac troponin T <0.03 g/L, who were undergoing a variety of PCIs. Serum concentrations of CRP and cardiac troponin T were determined before and the day after PCI. The mean follow-up time after PCI was 2.6 years, and the endpoint was death or nonfatal myocardial infarction. Results: Seventy-six patients reached the endpoint (4.6% death, 3.9% nonfatal myocardial infarction), whereas 21% developed myocardial infarction during the procedure. CRP increased more than 2-fold after the procedure. Patients in the third tertile of the CRP response to PCI had an increased risk for death or nonfatal myocardial infarction in multivariate analysis. Conclusions: Increased serum CRP in response to PCI is an independent predictor of death or nonfatal myocardial infarction independent of myocardial injury during the procedure. CRP determinations might be of value in risk stratification after PCI.

Endothelin (ET)-1 receptor blockade improves endothelial function in the forearm of patients with atherosclerosis. The aim was to investigate whether intracoronary ET receptor blockade improves coronary endothelial function and increases blood flow in patients with coronary artery disease. Ten patients received a 60-minute infusion of either the selective ETA receptor antagonist BQ123 (40 nmol/min, n = 6) or BQ123 + the ETB receptor antagonist BQ788 (40 nmol/min, n = 4). In all patients, substance P, an endothelium-dependent vasodilator, did not increase baseline coronary flow reserve with thermodilution (CFRThermo) (0.71 +/- 0.14 s during NaCl versus 0.59 +/- 0.14 s during substance P) or baseline quantitative coronary angiography (QCA) (2.74 +/- 0.16 mm versus 2.83 +/- 0.20 mm). After ET receptor blockade, however, the response to substance P was significantly improved as determined both by CFRThermo (0.62 +/- 0.14 s during NaCl versus 0.48 +/- 0.10 s during substance P, p < 0.05) and by QCA (2.70 +/- 0.18 mm versus 2.85 +/- 0.19 mm, p < 0.05). In addition, ET blockade increased blood flow in all patients by 16% +/- 10% (n = 10, p < 0.05) and in the BQ123 group by 22% +/- 16% (n = 6, p < 0.05). Furthermore, ETA blockade increased blood flow significantly more than did dual ETA/ETB blockade (p < 0.05). These findings indicate that ET receptor blockade may be a new therapeutic strategy to improve coronary vascular function in patients with coronary artery disease.

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