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Hyperuricemia occurs frequently in patients with myeloproliferative and lymphoproliferative disorders and in patients with congenital heart disease associated with polycythemia. Whether hyperuricemia is common in patients with severe pulmonary hypertension is not known.In the Pulmonary Hypertension Center at the University of Colorado Health Sciences Center between September 1991 and August 1997, 442 consecutive patients were evaluated with right heart catheterization; 191 patients also had a measurement of the serum uric acid (UA) in close temporal proximity to the hemodynamic evaluation.Of the 191 patients with a complete data set, 99 patients had primary pulmonary hypertension (PPH) and 92 had secondary pulmonary hypertension. For the entire cohort with severe pulmonary hypertension (n = 191), there was a positive correlation between the natural logarithm of the serum UA (lnUA) and the mean right atrial pressure (RAP; r = 0.47; p0.001). When analyzed separately, the correlation between lnUA and RAP was stronger in the patients with PPH (r = 0.642; p0.001). This correlation cannot be explained by diuretic use or impaired hepatocellular function. Neither mean pulmonary artery pressure nor cardiac output was as well correlated with the RAP when compared with the lnUA. Some patients with PPH had serum UA measurements repeated during treatment with chronic IV prostacyclin infusion. Eleven of these 18 patients (61%) demonstrated a decrease in serum UA during prostacyclin treatment.There is a positive correlation between the RAP elevation and the serum UA levels in patients with PPH. Serum UA levels drop in some, but not all PPH patients during chronic prostacyclin infusion therapy.

We report two cases of the inadvertent insertion of a saphenous vein bypass graft into the anterior cardiac vein creating an aortocoronary vein fistula. The clinical recognition, evaluation, and management are discussed. Suggestions on surgical technique to help minimize or eliminate this potential complication daring saphenous vein bypass surgery are proposed.

Based upon our experience with a cohort of 46 patients referred to the UCHSC from April, 1980 to April, 1987 for evaluation and treatment of PPH, we currently assess acute pulmonary vasoreactivity as defined by the patient's response to intravenous PGI 2 during the initial diagnostic catheterization. A 3 to 5 day trial of high dose oral diltiazem treatment (720 mg/day maximum) is given while monitoring the patient in the clinical research center to detect significant side effects including arrhythmias, orthostatic systemic hypotension, arterial desaturation, and worsened right ventricular dysfunction. We believe it is necessary to recatheterize each patient to establish the efficacy of calcium antagonist treatment prior to discharge. Those patients who are responsive to diltiazem are discharged and followed in our pulmonary hypertension clinic. Since an occasional patient will deteriorate after several weeks of therapy, repeat right heart catheterization after 8 weeks of treatment is used to determine which patients should be continued on diltiazem for chronic therapy. Approximately 30 percent of our patients with PPH have been improved on diltiazem treatment. Most patients who have a good response to treatment after eight weeks continue to benefit from longterm treatment. It appears that the response to an acute infusion of PGI 2 is useful in safely identifying those PPH patients who are likely to benefit from vasodilator therapy. Debilitated patients who are unresponsive to PGI 2 and vasodilator therapy are considered potential candidates for cardiopulmonary transplantation.

Regional myocardial blood flow before and after intravenous dipyridamole (0.56 mg/kg) was measured during cardiac catheterization in 11 patients using the 133Xe washout technique. Significant increases in heart rate (75 +/- 4 vs 87 +/- 6, p less than 0.004) and decreases in systolic blood pressure (144 +/- 8 vs 131 +/- 7, p less than 0.02) were observed with dipyridamole infusion. However, double product and cardiac output did not differ before or after drug infusion. Regional myocardial blood flow increased from 67 +/- 3 (SEM) to 117 +/- 3 ml/100 mg/min in myocardial segments supplied by nonobstructed coronary arteries. In stenotic coronary arteries, flow increased from 57 +/- 5 to 79 +/- 9 ml/100 mg/min with dipyridamole. We conclude that dipyridamole infusion results in flow differences which discriminate stenotic from nonstenotic coronary arteries.