Effect of Direct Stent Implantation on Minor Myocardial Injury

Comparison of abnormal cardiac troponin T values at 12 hours and 24 hours after coronary interventions in both groups. Group I, stenting without predilatation; Group II, stenting with predilatation.
Author(s): 

Yusuf Atmaca, MD, Fatih Ertas, MD, Sadi Gülec, MD, Irem Dincer, MD, Dervis Oral, MD

Coronary stenting is established as a common technique to improve outcomes of percutaneous transluminal coronary angioplasty (PTCA) and to reduce incidence of emergency coronary artery bypass grafting after PTCA.1 The standard coronary stent implantation technique requires routine predilatation of the target lesion with a balloon catheter. This technique, although universally used, usually requires the use of a balloon and has the potential for dissections and/or other complications such as abrupt vessel closure, elastic recoil, suboptimal result, sidebranch occlusion and distal embolization.2 Although abrupt vessel closure, coronary dissection, elastic recoil and suboptimal result can be prevented with the use of stent implantation, minor myocardial injury (MMI), probably resulting from the longer ischemia duration, sidebranch occlusion and distal embolization, remains a problem using conventional implantation techniques.
Cardiac troponin T (cTnT) is a regulatory contractile protein, which is not normally found in blood. Its appearance in the circulation is a clear signal of cardiac myocyte damage.3,4 The use of serum troponin T level as a means of assessing MMI, which affects the prognosis, has not been fully clarified in patients with direct stenting (stenting without predilatation).
This is the first prospective, nonrandomized study to investigate the incidence of MMI following direct stent implantation. In the present study, we compared direct stenting in patients with stable angina and simple lesion morphology with the conventional implantation technique with respect to MMI and 6 month prognosis by using cTnT.

METHODS

Patient population. From November 1999 to April 2001, a total of 910 patients with Canadian Cardiac Society Class II stable angina pectoris underwent percutaneous coronary interventions in our institution. Only patients with type A de novo lesions in large native coronary arteries were enrolled prospectively in this nonrandomized study. Patients with renal dysfunction, pericardial disease, cardiomyopathy, unstable angina, acute myocardial infarction within 2 weeks, 12-lead resting electrocardiogram with right or left bundle branch block, paced rhythm or complete atrioventricular block, aortocoronary bypass operation within 2 weeks and recent myocarditis were excluded. Furthermore, patients with a lesion located in a vessel that had excessive proximal tortuosity and patients in whom the target lesion was highly calcified were excluded.
The primary endpoint of the study was MMI in-hospital and the secondary endpoint was the major clinical events (death, acute myocardial infarction and repeat revascularization) in-hospital and at 6 months. The study protocol was approved by the local ethics committee and a written informed consent was requested of all patients before undergoing coronary interventions.

Invasive procedure. Coronary angiography was made with the Judkins technique from the right femoral artery. Coronary lesions were assessed by multiple orthogonal views with coronary angiography and visually evaluated for morphologic features similar to those reported by the ACC/AHA.5
Stent implantation was performed by 3 different invasive cardiologists according to standard clinical practice. A 6 French guiding catheter was used in all patients for whom coronary intervention was decided during the coronary angiography. A standard 0.014´´ guidewire was passed through the target lesion. The decision whether to perform predilatation for other lesions that were suitable for both procedures (stenting with or without predilatation) was made by the operators.
If a decision was made to proceed without predilatation, the stent was usually deployed at the nominal pressure of the stent balloon and a high-pressure balloon was subsequently used for dilatation within the stent at 14–16 atmospheres (atm). If the stent failed to cross the lesion, standard predilatation with a balloon was performed, followed by a further attempt to cross with the stent. If a decision was made to proceed with predilatation, balloon dilatation with 8 atm was performed and stent(s) were subsequently deployed. Balloon inflation time (BIT) and the number of balloon inflations were recorded during the interventions. Total BIT in seconds was obtained by adding the times of each inflation.
Results before and after coronary interventions were evaluated quantitatively by coronary angiography (Philips DC). Angiographic success was defined as < 30% residual diameter stenosis after stent implantation for both groups. After stenting, all patients received aspirin 300 mg/day and ticlopidine 500 mg/day. Ticlopidine was discontinued after 1 month.

Electrocardiographic (ECG) monitoring. All patients were monitored continuously during the interventions and then transferred in an intensive care unit after the procedure. A 12-lead ECG was taken just before and immediately after coronary stenting for exclusion of acute ischemia. A significant ST-segment depression was defined as horizontal or down-sloping depression of ST segment > 0.1 mV and 0.08 seconds after the J point that persisted for more than 1 minute.

Blood sampling. Blood samples were drawn from an antecubital vein just before the procedure and 12 and 24 hours after the procedure. Serum troponin T concentration was then measured by “Cardiac T Quantitative” equipment (Boehringer, Mannheim, Germany). The results were evaluated within 20 minutes by the “Cardiac Reader”. While the values remaining under 0.05 ngr/ml were shown as negative by the Cardiac Reader, the upper values were assessed quantitatively.

Clinical follow-up. All patients were followed up during the hospital stay and then with telephone contact up to 6 months with respect to major clinical events (death, acute myocardial infarction, repeat revascularization). Deaths were classified as cardiac in origin if associated with congestive heart failure, acute myocardial infarction or sudden cardiac death (< 1 hour after symptom onset). Revascularization of the target lesion was defined as either bypass surgery or balloon angioplasty involving the intervention segments. Coronary angiography was not performed except for those who had symptoms or signs of ischemia.

Statistical analysis. Continuous variables were expressed as means ± SD and were compared by student’s t-test. Categorical variables were compared by the Chi-square test. Comparisons were made between the direct stenting group and the stenting with predilatation group. A p-value < 0.05 was considered statistically significant.

RESULTS

One-hundred and fifty-four patients (17%) were considered eligible for direct stenting without predilatation by 3 operators who independently reviewed the coronary angiograms. The patients were then divided into 2 arms based on the stenting technique used: direct stenting without predilatation, Group I (n = 78); and stenting with predilatation, Group II (n = 76). All patients underwent only single-vessel procedures. There was no significant difference between Groups I and II with respect to baseline clinical characteristics (Table 1).

Troponin T measurement. Basal cTnT measurements were negative in all patients. cTnT level was found to be increased in 4 out of 78 patients (5.1%) in Group I and 16 out of 76 patients (21%) in Group II at both 12 hours and 24 hours postintervention as shown in Figure 1 (p < 0.007). The amount of cTnT release was significantly higher in Group II than in Group I (0.28 ± 0.04 ngr/ml for Group I at 12 hours vs. 0.51 ± 0.12 ngr/ml for Group II at 12 hours, p < 0.001; 0.28 ± 0.06 ngr/ml for Group I at 24 hours vs. 0.51 ± 0.10 ngr/ml for Group II at 24 hours, p < 0.0004) (Table 2).

Angiographic data. A total of 176 lesions were treated with 168 stents (51 Multi-Link Duet or Tetra stents, 57 NIR stents, 33 Jostents, and 27 AVE GFX stents). There were no major complications or sidebranch occlusions during or immediately postprocedure. Furthermore, no GP IIb/IIIa agents were used during or postprocedure.
Angiographic features of the 2 groups were similar except for the following procedural factors: total BIT (30.3 ± 4.6 seconds in Group I vs. 122.7 ± 4.3 seconds in Group II); number of balloon inflations (1.4 ± 0.4 inflations in Group I vs. 3.1 ± 1.1 inflations in Group II); and percent diameter stenosis (80.4 ± 2.9% in Group I vs. 84.6 ± 3.4% in Group II) (Table 3).
We compared the total BIT and the number of balloon inflations in patients with or without elevation of cTnT level within the 2 groups. The total BIT was found to be significantly higher in patients with abnormal cTnT levels than in those with normal cTnT levels in Group II (120.3 ± 4.7 seconds vs. 118.2 ± 1.3 seconds, respectively; p < 0.002), but there was not a significant difference in Group I (32.4 ± 2.1 seconds vs. 30.6 ± 2.4 seconds, respectively; p > 0.05). Furthermore, there was no statistically significant difference with respect to the number of balloon inflations in patients with normal and abnormal cTnT levels in either group (1.2 ± 0.2 inflations vs. 1.3 ± 0.4 inflations in Group I, p > 0.05; 3.2 ± 0.9 inflations vs. 3.0 ± 1.4 inflations in Group II, p > 0.05)

Clinical follow-up. There were no complications during or after the procedure in any patient. In Group II, two patients with abnormal cTnT levels died suddenly by the end of the sixth month. No major clinical events were seen during the in-hospital period. Six month clinical outcomes were obtained in 96.6% of patients with a mean duration of 6.1 ± 1.1 months. During this period, ten patients (9 with normal and 1 with abnormal cTnT level, p > 0.05) in Group I and 12 patients (8 with normal and 4 with abnormal cTnT level, p > 0.05) in Group II underwent repeat revascularization because of refractory chest pain. None of the patients had acute myocardial infarction. Therefore, the major clinical event rate was 12.8% in Group I and 18.4% in Group II (p > 0.05).

DISCUSSION


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