Acute Kidney Injury After Primary Angioplasty: Is Contrast-Induced Nephropathy the Culprit?

BACKGROUND: Acute kidney injury (AKI) following primary percutaneous coronary intervention (pPCI) is frequently interpreted as contrast-induced AKI but may result from other insults. We aimed to determine the causal association of contrast material exposure and the incidence of AKI following pPCI using a control group of propensity score-matched patients with ST-segment-elevation myocardial infarction who were not exposed to contrast material. METHODS AND RESULTS: We studied 2025 patients with ST-segment-elevation myocardial infarction who underwent pPCI and 1025 patients receiving fibrinolysis or no reperfusion who were not exposed to contrast material during the first 72 hours of hospital stay (control group). AKI was defined as creatinine of ≥0.5 mg/dL or >25% rise within 72 hours. AKI rates were similar in the pPCI and control groups (10.3% versus 12.1%, respectively; P=0.38). Propensity score matching resulted in 931 matched pairs with PCI and no PCI, with balanced baseline covariates (standardized difference <0.1). Among propensity score-matched patients, AKI rates were not significantly different with and without PCI (8.6% versus 10.9%, P=0.12). In the pPCI cohort, independent predictors of AKI included age ≥70 years, insulin-treated diabetes mellitus, diuretic therapy, anterior infarction, baseline estimated glomerular filtration rate, and variables related to the presence of pump failure (higher Killip class, intra-aortic balloon pump use) and reduced left ventricular ejection fraction but not contrast material dose. A risk score based on the PCI cohort had similar discriminatory capacity for AKI in the control group (C statistic 0.81±0.02 and 0.78±0.02, respectively; P=0.26). CONCLUSIONS: The development of AKI in patients with ST-segment-elevation myocardial infarction undergoing pPCI is mainly related to older age, baseline estimated glomerular filtration rate, heart failure, and hemodynamic instability. Risk for AKI is similar among ST-segment-elevation myocardial infarction patients with and without contrast material exposure.

Fasting glucose is an important independent risk factor for 30-day mortality in patients with acute myocardial infarction: a prospective study.

BACKGROUND: Stress hyperglycemia in patients with acute myocardial infarction has been associated with increased mortality. Most studies looked at the relationship between admission glucose (AG) and outcome; limited information is available about the clinical significance of fasting glucose (FG). METHODS AND RESULTS: We prospectively studied the relationship between FG and 30-day mortality in 735 nondiabetic patients with acute myocardial infarction. FG (> or =8-hour fast within 24 hours of admission) and AG were measured in each patient. At 30 days, 9 deaths (2%) occurred in patients with normal FG, and 11 (10%), 14 (13%), and 31 (29%) deaths occurred in the first, second, and third tertiles of elevated FG, respectively. Compared with normal FG (<110 mg/dL), the adjusted OR for 30-day mortality progressively increased with higher tertiles of elevated FG (first tertile, 4.6; 95% CI, 1.7 to 12.7; P=0.003; second tertile, 6.4; 95% CI, 2.5 to 16.6; P<0.0001; third tertile, 11.5; 95% CI, 4.7 to 20.0; P<0.0001). Compared with patients categorized as having normal AG (<140 mg/d), the adjusted ORs for tertiles of elevated AG were as follows: first tertile, 1.4 (95% CI, 0.5 to 3.8; P=0.54); second tertile, 3.0 (95% CI, 1.3 to 7.0; P=0.01); and third tertile, 4.4 (95% CI, 2.0 to 9.7; P<0.0001). Compared with patients with normal FG and AG, the adjusted ORs for 30-day mortality were 0.71 (95% CI, 0.15 to 3.4; P=0.67) in patients with elevated AG and normal FG, 3.4 (95% CI, 1.1 to 10.4; P=0.03) for patients with normal AG glucose and elevated FG, and 9.6 (95% CI, 3.5 to 26.0; P<0.0001) for patients with both elevated FG and AG. Comparing nested models showed that including AG failed to improve the prediction of the model based on FG (chi2=5.4, 3 df, P=0.15). In contrast, the addition of FG classes to the model based on AG improved model prediction (chi2=22.4, 3 df, P<0.0001). CONCLUSIONS: There is a graded relation between elevated FG and AG and 30-day mortality in patients with acute myocardial infarction. FG is superior to AG in the assessment of short-term risk.

Haptoglobin polymorphism predicts 30-day mortality and heart failure in patients with diabetes and acute myocardial infarction.

Patients with diabetes presenting with acute myocardial infarction (AMI) have an increased rate of death and heart failure. Patients with diabetes homozygous for the haptoglobin (Hp) 1 allele (Hp 1-1) develop fewer vascular complications. We tested the hypothesis that Hp type is related to the outcome of patients with diabetes presenting with AMI. We prospectively assessed the relationship between Hp type and 30-day mortality and heart failure in 1,437 patients with AMI (506 with diabetes). Multivariate logistic regression identified a significant interaction between Hp type and diabetes status on these outcome measures. Hp type was not related to outcome among patients without diabetes. In contrast, Hp 1-1 was associated with a strong protective effect with regard to the primary end point of death (OR 0.14, P = 0.015) and for death and heart failure (OR 0.35; 95% CI 0.15-0.86, P = 0.018) among patients with diabetes. Finally, among patients with diabetes, Hp 1-1 was associated with smaller infarct size. This study demonstrates that in patients with diabetes and AMI, the Hp type is an important determinant of clinical outcome and infarct size.

Heart failure in patients with diabetes undergoing primary percutaneous coronary intervention.

INTRODUCTION: Diabetes mellitus is associated with increased risk after acute coronary syndromes. Primary percutaneous coronary intervention is the most effective method of reperfusion for acute ST-elevation myocardial infarction and can limit the ischaemic damage to the left ventricle. However, there are few data on the impact of diabetes mellitus on the risk of heart failure following primary percutaneous coronary intervention. METHODS: We studied 958 ST-elevation myocardial infarction patients treated with primary percutaneous coronary intervention, of whom 263 (27.5%) had diabetes mellitus, with 67 (7.0%) treated with insulin. The primary end points of the study were re-admission for heart failure. Secondary end points were all-cause mortality and recurrent infarctions. The follow-up period was 5 years after hospital discharge. RESULTS: The cumulative incidence of re-admission for heart failure was 8.4%, 15.2% and 26.7% in patients without diabetes mellitus, non-insulin-treated and insulin-treated diabetes mellitus, respectively. Compared with patients without diabetes mellitus, the adjusted hazard ratio for heart failure was 1.95 (95% confidence intervals 1.30-2.93) and 3.09 (95% confidence intervals 1.71-5.60) in non-insulin-treated and insulin-treated diabetes mellitus, respectively. The corresponding hazard ratios for mortality were 1.03 (95% confidence intervals 0.68-1.55) and 2.04 (95% confidence intervals 1.22-3.42), respectively. There was a J-shaped association between fasting glucose levels in the acute phase and risk of mortality (P=0.0001) and a direct association with heart failure (P=0.03). CONCLUSION: Despite modern treatment of ST-elevation myocardial infarction and high levels of guideline-based medical care, diabetes mellitus had an independent adverse effect on the risk of re-admissions for heart failure, which was particularly high among insulin-treated patients.

Admission C-reactive protein levels and 30-day mortality in patients with acute myocardial infarction.

BACKGROUND: Elevated C-reactive protein levels are associated with an increased risk of subsequent cardiovascular events in patients with unstable angina. However, limited information is available concerning the value of C-reactive protein levels in patients with acute myocardial infarction. METHODS: We prospectively studied 448 consecutive patients (mean [+/- SD] age, 60 +/- 12 years) with acute myocardial infarction. Serum C-reactive protein levels were measured within 12 to 24 hours of symptom onset, and divided into tertiles. Infarct size was determined by echocardiographic examination that was performed on day 2 or 3. Patients were followed for 30 days for mortality and subsequent cardiac events. RESULTS: At 30 days, 4 deaths (3%) occurred in patients in the lowest C-reactive protein tertile, 15 (10%) in patients in the middle tertile (P = 0.02 vs. the lowest tertile), and 33 (22%) in patients in the highest tertile (P <0.001 vs. the lowest tertile). In a multivariate analysis, C-reactive protein in the upper tertile was associated with 30-day mortality (relative risk = 3.0; 95% confidence interval [CI]: 1.3 to 7.2; P = 0.01) and the development of heart failure (odds ratio = 2.6; 95% CI: 1.5 to 4.6; P = 0.0006). C-reactive protein levels were not associated with the development of postinfarction angina, recurrent myocardial infarction, or the need for revascularization. CONCLUSION: Plasma C-reactive protein level obtained within 12 to 24 hours of symptom onset is an independent marker of 30-day mortality and the development of heart failure in patients with acute myocardial infarction. These findings suggest that C-reactive protein levels may be related to inflammatory processes associated with infarct expansion and postinfarction ventricular remodeling.

Fasting glucose in acute myocardial infarction: incremental value for long-term mortality and relationship with left ventricular systolic function.

OBJECTIVE: Elevation of blood glucose is a common metabolic disorder among patients with acute myocardial infarction (AMI) and is associated with adverse prognosis. However, few data are available concerning the long-term prognostic value of elevated fasting glucose during the acute phase of infarction. RESEARCH DESIGN AND METHODS: We prospectively studied the relationship between fasting glucose and long-term mortality in patients with AMI. Fasting glucose was determined after an >/=8 h fast within 24 h of admission. The median duration of follow-up was 24 months (range 6-48). All multivariable Cox models were adjusted for the Global Registry of Acute Coronary Events (GRACE) risk score. RESULTS: In nondiabetic patients (n = 1,101), compared with patients with normal fasting glucose (<100 mg/dl), the adjusted hazard ratio for mortality progressively increased with higher tertiles of elevated fasting glucose (first tertile 1.5 [95% CI 0.8-2.9], P = 0.19; second tertile 3.2 [1.9-5.5], P < 0.0001; third tertile 5.7 [3.5-9.3], P < 0.0001). The c statistic of the model containing the GRACE risk score increased when fasting glucose data were added (0.8 +/- 0.02-0.85 +/- 0.02, P = 0.004). Fasting glucose remained an independent predictor of mortality after further adjustment for ejection fraction. Elevated fasting glucose did not predict mortality in patients with diabetes (n = 462). CONCLUSIONS: Fasting glucose is a simple robust tool for predicting long-term mortality in nondiabetic patients with AMI. Fasting glucose provides incremental prognostic information when added to the GRACE risk score and left ventricular ejection fraction. Fasting glucose is not a useful prognostic marker in patients with diabetes.