A new protocol using sodium bicarbonate for the prevention of contrast-induced nephropathy in patients undergoing coronary angiography.

Contrast-induced nephropathy (CIN) is associated with increased morbidity and mortality rates. Although a previous study reported that pretreatment with sodium bicarbonate is more effective than sodium chloride for prophylaxis of CIN, this has not been a universal finding. We performed a prospective randomized trial to investigate whether CIN can be avoided using sodium bicarbonate. In total 155 patients with a glomerular filtration rate (GFR) <60 ml/min/1.73 m(2) who were undergoing coronary angiography were enrolled. We assigned patients to sodium chloride plus sodium bicarbonate (bicarbonate group, n = 78) or sodium chloride alone (chloride group, n = 77). Infusion of sodium bicarbonate at 1 ml/kg/hour continued from 3 hours before to 6 hours after coronary angiography. CIN was defined as a 25% increase in serum creatinine from baseline value or an absolute increase of ≥0.5 mg/dl, which appeared within 2 days of contrast. Baseline GFR was not significantly different between the 2 groups. Patients in the bicarbonate group had a higher GFR than those in the chloride group on day 2 (45.8 ± 13.4 vs 40.9 ± 14.6 ml/min/1.73 m(2), p = 0.031) and at 1 month (49.5 ± 14.7 vs 43.7 ± 15.5 ml/min/1.73 m(2), p = 0.019). CIN occurred in 10 patients (13%) in the chloride group but in only 2 patients (2.6%) in the bicarbonate group (p = 0.012). Sodium chloride plus sodium bicarbonate is more effective than sodium chloride alone for prophylaxis of CIN and can lead to retention of better long-term renal function.

Contrast-induced nephropathy in patients undergoing emergency percutaneous coronary intervention for acute coronary syndrome.

Contrast-induced nephropathy (CIN) is associated with significantly increased morbidity and mortality after coronary angiography and percutaneous coronary intervention (PCI). The aim of the present study was to assess the clinical features and in-hospital outcomes of CIN after emergency PCI. The serum creatinine (SCr) concentration was measured from days 0 to 30 in 338 consecutive patients with acute coronary syndrome undergoing emergency PCI. CIN was defined as an increase in SCr of >25% or >0.5 mg/dl within 2 days after PCI. Overall, 94 patients (28%) developed CIN. The mean SCr on admission was not significantly different between patients with CIN and those without CIN. The CIN group had significantly greater SCr at days 1, 2, and 30 than did the no CIN group. Multivariate analysis showed female gender (odds ratio [OR] 2.38, 95% confidence interval [CI] 1.12 to 5.07, p = 0.025), a culprit lesion in the left anterior descending artery (OR 2.37, 95% CI 1.31 to 4.27, p = 0.0042), contrast agent volume >200 ml (OR 3.60, 95% CI 1.96 to 6.62, p <0.001) and end-diastolic pulmonary arterial pressure >15 mm Hg (OR 2.03, 95% CI 1.02 to 4.04, p <0.01) to all correlate independently with CIN. The in-hospital mortality rate was greater in the CIN group than in the no CIN group (9.6% vs 3.3%, respectively; p = 0.025). In conclusion, CIN is a frequent complication of emergency PCI for acute coronary syndrome and is associated with a greater mortality rate and persistent renal dysfunction.

High risk factors for valvular heart disease from dopamine agonists in patients with Parkinson's disease.

An association between ergot-derived dopamine agonists and asymptomatic valvular heart disease in Parkinson's disease has been established. For safe use of these agonists, it is important to specify those at high risk for valvular heart disease among patients with Parkinson's disease. We performed a nested case-control study of 223 patients with Parkinson's disease. In results of multivariable logistic analyses, use of pergolide, use of cabergoline, age, male sex, and hypertension were independent significant risk factors for left-sided valvular regurgitation. In patients receiving cabergoline or pergolide, elderly (>or=70 years) hypertensive patients had a markedly high risk for valvular regurgitation (odds ratio 94.5) as compared to non-elderly (<70 years) patients without hypertension. The risk of valvular regurgitation caused by pergolide or cabergoline was found to be highly enhanced by comorbid hypertension or aging, suggesting that special attention should be paid when prescribing cabergoline or pergolide for those patients.

Nicorandil suppressed myocardial injury after percutaneous coronary intervention.

BACKGROUND: Nicorandil exerts beneficial effects as an adjunctive therapy for patients with ischemic heart disease. This study was designed to assess the effects of nicorandil on the myocardial protective benefits of elective percutaneous coronary intervention (PCI). METHODS: We randomly divided 49 patients scheduled to undergo elective PCI into two groups, nicorandil and control. Before PCI, the former received an intravenous bolus injection of nicorandil (4 mg), followed by continuous infusion at 6 mg/h for 24 h after intervention. Oral administration of nicorandil was continued until follow-up coronary angiography (CAG). Serial venous blood samples, for measurement of creatine kinase (CK), creatine kinase MB isoform (CK-MB), troponin I (TnI) and myoglobin, were obtained before PCI, and at 0 h, 4 h, 24 h and 48 h after PCI. Left ventricular function and left ventricular wall motion were evaluated by means of contrast ventriculography before PCI and follow-up CAG. RESULTS: At 24 h after PCI, elevations of cardiac enzymes were significantly suppressed in the nicorandil as compared to the control group; CK (78.1+/-34.9 versus 117.4+/-137.9 U/l, P=0.0141), CK-MB (1.57+/-1.90 versus 2.67+/-4.50 U/l, P=0.0485) and TnI (0.37+/-0.55 versus 0.86+/-1.65 ng/ml, P=0.0101). Regional left ventricular wall motion was significantly improved at follow-up in the nicorandil as compared to the control group. CONCLUSIONS: Nicorandil suppressed elevations of cardiac enzymes after elective PCI and left ventricular wall motion was also significantly improved at follow-up, suggesting that nicorandil enhances the myocardial protective effect of PCI against angioplasty-related myocardial injury.