Elevated Admission Serum Creatinine Predicts Poor Myocardial Blood Flow (Full title below)
- Volume 21 - Issue 10 - October, 2009
- Posted on: 10/7/09
- 0 Comments
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Statistical analysis. Analyses were performed using SPSS software, version 13.0 (SPSS, Inc., Chicago, Illinois). Continuous data are expressed as mean values ± standard deviation. The student’s t-test was used to analyze continuous variables. Categorical variables were analyzed by the chi-square or Fisher’s exact test. Relative risks (RRs) were calculated to investigate the effects on poor myocardial perfusion and 1-year mortality. Logistic regression models were used to identify the clinical and angiographic variables correlated with poor myocardial perfusion and deaths at 1-year follow up. Univariate correlations with p-values of < 0.1 were entered into multivariate models to determine the independent correlations to poor myocardial perfusion and deaths at 1-year follow up. A p-value < 0.05 was considered statistically significant.
Results
Baseline clinical characteristics. Baseline clinical characteristics of the patients grouped by admission serum creatinine level are provided in Table 1. Patients with elevated serum creatinine were older, more often male, more likely to have hypertension, previous myocardial infarction (MI), in-hospital worsened creatinine defined as a 25% elevation in serum creatinine or an absolute increase of 0.5 mg/dl during hospitalization compared to the admission level, higher admission and discharge creatinine levels, and were more prone to show symptoms of congestive heart failure on presentation. Differences in concomitant therapy and device use including thrombus aspirator and drug-eluting stents (DES) during PCI between the two groups had no statistical significance. None of the patients underwent thrombolysis prior to their PCI, which may have affected TIMI flow evaluation.
Angiographic and ECG characteristics. Patients in the elevated group were more likely to have multivessel disease. There were no significant differences between the two groups in terms of frequency of TFGs 3 in the IRA after PCI, however CTFCs were higher in the elevated group. There were more frequent TMPGs 0–1 in the elevated group. In addition, significant ΣSTe recovery occurred less frequently in the elevated group (Table 2).
Clinical and echocardiographic outcomes. In-hospital and 1-year deaths were significantly higher in patients with elevated serum creatinine (4.7% vs. 1.2%, p < 0.05; 7.0% vs. 2.4%, p < 0.05). There were no differences between the two groups in terms of major adverse cardiac events (MACE) at discharge (5.6% vs. 7.0%, p > 0.05), however there were statistical differences in MACE at 1-year follow up (14.0% vs. 7.3%, p < 0.05). LVEF was lower in the elevated group compared to the normal group before discharge and at 1-year follow up (Table 3).
Admission serum creatinine ≥ 1.3 mg/dl (relative risk [RR] = 1.41, 95% confidence interval [CI]: 1.24–2.69), TMPGs 0–2 (RR = 1.54, 95% CI: 1.27–2.09), age ≥ 70 years (RR = 1.09, 95% CI: 1.04–1.19), previous MI (RR = 1.24, 95% CI: 1.05–1.84), in-hospital worsened creatinine (RR = 1.40, 95% CI: 0.96–1.74), Killip Class II–IV (RR = 1.96, 95% CI: 1.56–2.38), number of narrowed coronary arteries (RR = 1.32, 95% CI: 1.05–1.79), TFGs 0–2 (RR = 1.17, 95% CI: 1.01–1.54), and significant ΣSTe recovery (RR = 2.35, 95% CI: 1.24–4.23) were independent predictors of a higher rate of 1-year mortality in STEMI patients undergoing primary PCI (Table 4).












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