Intravenous N-acetylcysteine for preventing contrast-induced nephropathy: a randomised trial.

BACKGROUND: Studies evaluating the role of N-acetylcysteine in patients undergoing coronary angiography have yielded inconsistent data. Less is known about patients with normal renal function at baseline. METHODS: Prospective, double-blind, placebo-controlled trial to determine the benefits of intravenous N-acetylcysteine as an adjunct to hydration in this kind of population. Patients were randomly assigned to receive either N-acetylcysteine (600 mg twice daily) or placebo, in addition to 0.45% intravenous saline. The primary end point was development of contrast-induced nephropathy, defined as an acute increase in the serum creatinine concentration > or = 0.5 mg/dl and/or > 25% increase above baseline level at 48 h after contrast dosing. RESULTS: A total of 216 patients were studied: N-acetylcysteine = 107 and placebo = 109. Treatment groups were similar with respect to baseline clinical characteristics. Overall incidence of contrast-induced nephropathy was 10.2%, 10.3% in the N-acetylcysteine group and 10.1% in the placebo group. Furthermore, no significant differences were observed when considering the non-diabetic population, although there was a trend towards a protective effect of N-acetylcysteine in the subgroup of 47 patients with both hypertension and diabetes. There were no significant changes in serum urea nitrogen concentrations. The incidence of in-hospital adverse clinical events was low: no patient with contrast-induced nephropathy required dialysis, the median Coronary Unit stay was 4.5 vs. 4 days, and the mortality rate was 2.8% vs. 4.6% in the N-acetylcysteine and placebo groups, respectively (p=NS). CONCLUSIONS: The prophylactic administration of intravenous N-acetylcysteine provides no additional benefit to saline hydration in high-risk coronary patients with normal renal function.

Early results of direct coronary stenting in consecutive patients when multivessel, complex, long lesions, and small vessels are included.

BACKGROUND: Direct coronary stenting is the dominant technique for coronary stent implantation, but previous randomized studies have strongly selected lesions to treat. To evaluate whether the results can be generalized to routine clinical practice, all consecutive patients with direct stenting in 15 hospitals were entered into a prospective registry. Single vessels and simple lesions, but also multivessel, complex and long lesions, and small vessels size (< or =2.5 mm) were included. Immediately results as well as clinical events within 30 days after the procedure were evaluated. METHODS: Between April and November 2002, direct coronary stenting was performed in 452 consecutive patients (559 lesions) at 15 sites. Stents edge-protected by "sleeves" (SOX technology, NIR Stent, Boston Scientific) or with short transitional edge protection (STEP technology, Multilink Stents, Guidant) were selected to minimize vessel injury outside the stent edges during balloon inflation/deployment. RESULTS: Stents were successfully implanted in 96% of lesions. Lesions were multivessel in 27%, type B2-C in 40%, very angulated in 28%, calcified in 18%, and longer than 20 mm in 10% of patients. Vessels were smaller than < or =2.5 mm in 27% of patients. Direct coronary stenting was unsuccessful in 25 lesions (24 patients) characterized by more unstable angina (p=0.07), more treated lesions (p<0.01), and more distal locations (p=0.001). Dissection occurred in 6% of patients, and one stent embolised. The 30-day follow-up period included 1 death (due to subacute occlusion), 11 (2.4%) acute myocardial infarctions (8 non-Q wave), and one stroke (following carotid surgery). CONCLUSIONS: Direct coronary stenting yielded excellent results at 30 days although some expanded indications will be included.

[Relationship of C-reactive protein levels with angiographic findings and markers of necrosis in non-ST-segment elevation acute coronary syndrome]. / Relación de los valores de proteína C reactiva con los hallazgos angiográficos y los marcadores de necrosis en el síndrome coronario agudo sin elevación del segmento ST.

INTRODUCTION AND OBJECTIVES: The mechanism responsible for elevated C-reactive protein levels (inflammation of the ruptured atherosclerotic plaque or myocardial necrosis) in acute coronary syndromes is controversial. The aim of this study was to investigate the relationship between C-reactive protein levels and angiographic complexity of the culprit lesion and troponin elevation in patients with non-ST elevation acute coronary syndromes. PATIENTS AND METHOD: The study group consisted of 125 patients with single-vessel disease. Troponin-I and C-reactive protein were measured, and the complexity of the culprit lesion was analyzed (TIMI flow and thrombus). Information on age, sex, smoking habit, hypertension, hypercholesterolemia and diabetes was obtained from the medical record. RESULTS: The quartile distribution of C-reactive protein showed more patients with TIMI flow < 3 (31%, 28%, 18%, and 55%; P=.02), thrombus (3%, 6%, 7%, and 28%; P=.007) and troponin-I elevation (19%, 44%, 50%, and 66%; P=.003) in the fourth quartile. Multivariate analysis showed both thrombus (OR = 4.1; 95% CI, 1.2-14.3; P=.03) and troponin elevation (OR = 2.6; 95% CI, 1.1-6.3; P=.03) to be associated with C-reactive protein > 18 mg/L (fourth quartile cut-off). When treated as a continuous variable, higher levels of C-reactive protein were also associated with thrombus (P=.02) and troponin elevation (P=.003). No other clinical variables were related with C-reactive protein levels. CONCLUSIONS: Both angiographic complexity of the culprit lesion and elevated troponin level are related with increased C-reactive protein levels in non-ST elevation acute coronary syndromes.

[Prognostic factors in unstable angina with dynamic electrocardiographic changes. Value of fibrinogen]. / Factores pronósticos en la angina inestable con cambios dinámicos del electrocardiograma. Valor del fibrinógeno.

INTRODUCTION AND OBJECTIVES: The prognosis of unstable angina varies between series depending on the inclusion criteria and management protocol used. The aim of this study was to analyze in-hospital events and their predictors in a homogeneous single-center series of patients with unstable angina. MATERIAL AND METHODS: A total of 246 patients with the following inclusion criteria were studied: 1) resting anginal pain, 2) transient electrocardiographic changes during anginal pain, 3) normal CK-MB levels and 4) exclusion of postinfarction angina. All patients were treated with aspirin and enoxaparin (1 mg/kg/12 h). Coronary angiography was performed in the case of recurrent angina or ischemia in Bruce I-II stage during the predischarge effort stress test. The variables recorded were risk factors, history of ischemic heart disease, history of coronary surgery, ECG upon admission, and fibrinogen. RESULTS: During the hospital stay the following events were recorded: 36% recurrent angina, 58% cardiac catheterization, and 5,7% major events (infarction or death). Multivariate analysis found recurrent angina to be more frequent in patients with a history of coronary bypass surgery (p = 0.004. OR = 22; CI 95%, 3-182), ST-segment changes (p = 0.01. OR = 4.7, CI 95%; 1.4-15.9) and higher fibrinogen (p = 0.002. OR = 1,4, CI 95%; 1.1-1.7). Fibrinogen was the only variable related to cardiac catheterization (p = 0,009. OR = 1.3. CI 95%, 1.1-1.6) and major events (p = 0.001. OR = 2.0. CI 95%, 1.4-3.1). CONCLUSIONS: 1) Unstable angina with electrocardiographic changes was associated to a high rate of in-hospital events. 2) Fibrinogen was related to any event, and previous by-pass surgery and ST changes were related to recurrent angina.