Clinical outcomes of PTCA in chronic renal failure: a case-control study for comorbid features and evaluation of dialysis dependence.

We compared clinical outcomes following percutaneous transluminal coronary angioplasty (PTCA) for 77 chronic renal failure (CRF) (dialysis and nondialysis) patients and a control group matched for history of myocardial revascularization, specific revascularization procedure, gender, age, diabetes, number of native vessels diseased, number of vessels dilated, and the specific vessel(s) dilated. CRF patients had a higher incidence of peripheral vascular disease, hypertension, and more complex PTCA target lesion types than controls: 5% vs. 16% Type A, 12% vs. 28% Type B1, 44% vs. 41% Type B2, 39% vs. 15% Type C (p < 0.001). The primary success rate for PTCA in CRF patients and controls was 89% and 97% (p < 0.05). Survival analysis 24 months following PTCA showed a lower composite cardiac event-free survival (angiographic restenosis, myocardial infarction, coronary artery bypass surgery, and cardiac death) for those with CRF than controls, 54% vs. 69% (p = 0.002). Over the study period, 26 CRF patients died (11 from cardiac causes) compared to only 3 control patients (one from a cardiac cause); p < 0.001 for all cause and p < 0.003 for cardiac mortality. We also compared PTCA results between two categories of CRF patients. The first consisted of 49 end-stage renal disease (ESRD) patients on dialysis and the second included 28 patients not on dialysis (13 with creatinine > 2. 0 mg/dL and 15 with ESRD post-renal transplant). Both subgroups had similar coronary anatomy, including PTCA, target lesion type, and acute and long-term outcomes. In conclusion, we observed acceptable primary success and complication rates for PTCA in CRF patients compared with controls matched for comorbid features despite more complex target lesion morphology. Poorer long-term outcomes, however, were apparent for those with CRF regardless of dialysis dependence and likely relate to more extensive atherosclerosis and complex target coronary lesions at index PTCA as well as other features related to CRF.

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

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 microg/l were categorized into group 1 (n=23). The remaining 60 patients (pre-procedural cTnI=0.8 microg/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 microg/l) in groups 2, 3 and 4 was associated with higher risk of complications 30 days post-procedure.

Improved detection of minor ischemic myocardial injury with measurement of serum cardiac troponin I.

This study compared the diagnostic accuracy of the measurement of serum cardiac troponin I (cTnI) with creatine kinase (CK) MB mass in patients with minor myocardial injury whose measured total CK activity did not exceed twice the upper reference limit (300 U/L for men; 200 U/L for women). Forty-eight consecutive patients presenting with chest pain and with in-hospital documentation of myocardial injury were enrolled. Electrocardiogram, echocardiogram, and serial serum CK-MB mass, cTnI, and total CK were measured over 36 h after admission. Peak total CK activity was within normal limits in 28 patients (58%). The mean (+/- SD) peak CK-MB mass and cTnI concentrations were: 16.4 (11.8) micrograms/L and 132 (13.0) micrograms/L; respectively. The peak biochemical marker index (defined as CK-MB or cTnI divided by its respective upper reference limit) was significantly (P < 0.05) higher for cTnI than for CK-MB from 7 to 36 h. The clinical sensitivity for detection of myocardial injury for cTnI was 100% [95% confidence interval (CI): 87.2% to 100%], compared with 81.8% (CI: 67.3% to 91.8%) for CK-MB. Thus, cTnI was more sensitive than CK-MB mass for detection of myocardial injury in patients with small increases of total CK.