Monitoring plasma cardiac troponin I for the detection of myocardial injury after percutaneous transluminal coronary angioplasty

Vincent Ricchiuti, Wendy S. Shear, Timothy D Henry, Pamela R. Paulsen, Elizabeth A. Miller, Fred S. Apple

Research output: Contribution to journalArticlepeer-review

12 Scopus citations

Abstract

The objective of this study was to detect myocardial injury defined by an increase of plasma cardiac troponin I (cTnI) following percutaneous transluminal coronary angioplasty (PTCA) and compare plasma cTnI with the risk of cardiac complications at 30 days. Plasma cTnI, creatine kinase (CK) MB, and total CK were determined in 83 patients before (baseline) and 6, 12 and 24 h after PTCA. Thirty-eight patients underwent conventional PTCA, 39 PTCA-stent and six rotational atherectomy. Patients with acute myocardial infarction (AMI) and increased pre-procedural cTnI >0.8 μg/l were categorized into group 1 (n = 23). The remaining 60 patients (pre-procedural cTnI = 0.8 μg/l) were categorized as follows: Group 2 (n = 15) AMI; group 3 (n = 20) unstable angina (UA); group 4 (n = 25) coronary artery disease (CAD). Twelve hours post-procedure, all three cardiac markers were more frequently increased over baseline in group 2 patients (40-60%) compared to patients in group 3 (5-29%, P < 0.03) or group 4 (0.5-5%, P < 0.01). This was also true for patients undergoing PTCA-stent compared to conventional PTCA or rotational atherectomy (27-40 vs. 4-14%, P < 0.02). cTnI was more sensitive (60%) to detect release of myocardial protein after PTCA compared to total CK (47%) or CKMB (43%). A moderate increase of cTnI (0.8-1.5 μg/l) in groups 2, 3 and 4 was associated with higher risk of complications 30 days post-procedure.

Original languageEnglish (US)
Pages (from-to)161-170
Number of pages10
JournalClinica Chimica Acta
Volume302
Issue number1-2
DOIs
StatePublished - 2000

Bibliographical note

Funding Information:
This work was supported in part by a grant from Dade Behring Inc. We thank Claude Gronifer PhD for his statistical support.

Keywords

  • Angioplasty
  • Cardiac troponin
  • Myocardial damage

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