Prognostic value of cardiac troponin I elevation after percutaneous coronary intervention in patients with chronic renal insufficiency: A 12-month outcome analysis
✍ Scribed by Luis Gruberg; Shmuel Fuchs; Ron Waksman; Augusto D. Pichard; Kenneth M. Kent; John R. Laird; Hongsheng Wu; Sayed Elsayyad; Craig M. Allen; Lowell F. Satler
- Publisher
- John Wiley and Sons
- Year
- 2002
- Tongue
- English
- Weight
- 68 KB
- Volume
- 55
- Category
- Article
- ISSN
- 1522-1946
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✦ Synopsis
Abstract
Serum cardiac troponin I (cTnI) is a highly specific marker for myocardial damage in patients with chronic renal insufficiency (CRI), unlike creatine kinase myocardial band fraction (CK‐MB), which may be elevated in the absence of myocardial injury in patients with CRI. We studied 116 consecutive CRI patients (serum creatinine ≥ 1.8 mg/dL, not on dialysis) with normal baseline cTnI levels who underwent successful percutaneous coronary intervention (PCI). Patients were divided into two groups: group 1, elevated postprocedural cTnI (n = 50), and group 2, normal cTnI (n = 66). Patients with elevated cTnI were older and had a higher incidence of postinfarction angina and lower creatinine clearance compared to patients who did not have cTnI elevation. Atheroablative devices (rotational and directional atherectomy and excimer laser coronary angioplasty) were more frequently used in group 1 patients (27.1% vs. 18.5%; P = 0.04). In‐hospital mortality, cardiac mortality, and Q‐wave myocardial infarction rates did not differ between the two groups. At 12‐month follow‐up, total mortality rates were significantly higher in group 1 (28.0% vs. 9.9%; P = 0.002). Multivariate analysis showed that cTnI was an independent predictor of late mortality (OR = 2.26; CI = 1.07–4.77; P = 0.03). Thus, in patients with CRI, elevated cTnI levels after successful PCI is an important predictor of poor long‐term outcome. Our data suggest that patients with cTnI elevation > 3 times above normal values are particularly at higher risk. Cathet Cardiovasc Intervent 2002;55:174–179. © 2002 Wiley‐Liss, Inc.