Myocardial Injury After Apparently Successful Coronary Stenting With or Without Balloon Dilation: Direct Versus Conventional Ste


Timur Timurkaynak, MD, Murat Ozdemir, MD, Atiye Cengel, MD, Haci Ciftci, MD, Mustafa Cemri, MD, Guliz Erdem, Ridvan Yalcin, MD, Bulent Boyaci, MD, Ovsev Dortlemez, MD, Halis Dortlemez, MD

Direct stenting (DS) without balloon predilation is a novel approach in the percutaneous treatment of coronary artery lesions. This approach, besides reducing aggression to the vessel wall, may also significantly lower the rate of procedural ischemic complications because the dissections created by balloon inflation are immediately sealed by the endoprosthesis. Stenting without balloon dilation may decrease trauma, incidence of dissection and distal embolization, leading to a better outcome.1–4

Cardiac enzymes troponin T, troponin I, creatine kinase (CK) and its isoform CKMB are particularly useful not only for the diagnosis of myocardial infarction, but also for the diagnosis of myocardial necrosis.5,6 However, troponins were shown to be more sensitive than CKMB7,8 for the detection of this minor damage missed by conventional markers which are prognostically important.9–11 The reported incidence of troponin T or I release after percutaneous coronary intervention (PCI) ranges between 13–44%, with the incidence higher after stenting.7,12,13
We hypothesized that DS would decrease the myocardial injury because it causes less trauma. However, data regarding the potential benefits of direct stenting in this field are scarce. The purpose of this study was to measure cardiac troponin T (cTnT), CK and CKMB fraction after apparently successful elective stent implantation with conventional stenting (CS) or stenting without balloon predilation (DS) and to compare the procedural myocardial injury between these two approaches.


We reviewed our institutional interventional database and identified all patients who underwent percutaneous coronary intervention from May 1999 to February 2001. Cases with infarcted myocardium at the intervened artery site, recent myocardial infarction (MI), pre-procedural enzyme elevation, bundle branch block morphology in electrocardiogram, and sidebranch arising from the lesion location were excluded. We identified 60 patients who fulfilled our criteria. These patients were then divided into two groups: 1) conventional stenting (CS) patients (n = 23); and 2) direct stenting (DS) patients (n = 37).
PCI was performed after obtaining multiple views of the coronary lesion. After crossing the lesion with a 0.014´´ guidewire, interventionist preference determined the procedure to be performed. Initial balloon dilation in the CS group was carried out with percutaneous transluminal coronary angioplasty balloons inflated at nominal pressures (6–8 atmospheres). Multiple balloon inflations were performed if needed. Stenting in both groups was accomplished with the use of second-generation, pre-loaded tubular stents (Jostent and ACS MultiLink) which were implanted at high pressure (> 12 atmospheres). Stent-artery ratio was 1.1:1. DS was accomplished with the delivery balloon and a high-pressure single inflation. Post-dilation was not performed in any patients in either group. During the procedure, an intravenous bolus dose of 10,000 units of standard heparin was given to maintain an activated clotting time > 300 seconds and continued for 6 hours in addition to ticlopidine (250 mg twice daily for 30 days) or clopidogrel (300 mg loading dose, then 75 mg/day for 30 days) and aspirin (300 mg, indefinitely). Glycoprotein IIb/IIIa receptor blockers were not used in any patients. Quantitative coronary angiography (QCA) was performed with the use of an automatic edge detection system (General Electric DLX Angiographic Systems, GE Medical Systems Europe, Sedex, France).
Troponin T, CK and CKMB measurements were done just before and 16 hours after the intervention. A second-generation commercial ELISA cTnT assay (Boehringer Mannheim Corporation) was used to measure cTnT with a cut-off of 0.1 ng/dl. Total CK (normal < 195 IU/L) and CKMB (normal < 24 IU/L) activities were measured with a Hitachi 917 (Boehringer, Mannheim, Germany) analyzer with the automatic enzyme immunoassay method. Routine 12-lead electrocardiograms were done before, immediately after and the day after the procedure.

Statistical analysis. Data were expressed as means ± standard deviation for continuous variables and as frequencies for categorical variables. Continuous variables were compared by Mann-Whitney U-test and categorical variables by Chi-square test. Comparisons were made between DS and CS groups and between normal and abnormal biochemical markers. CTnT was labeled negative if the level was < 0.1 ng/dl, and positive if the level was > 0.1 ng/dl; the difference between the groups was analyzed with the Chi-square test. Mean cTnT values were compared with the Mann-Whitney U-test. A p-value < 0.05 was considered statistically significant.


The study population consisted of 60 patients with a mean age of 57.1 ± 10.4 years who presented with stable angina pectoris. Of these 60 patients, a total of 37 underwent DS and 23 underwent CS. The reason for stenting in the CS group was suboptimal procedure in 7, nonocclusive dissection in 4 and primary procedure in 12 patients. All stents were > 2.5 mm. Stenting was successful in all patients. There was no stent loss or imprecise stent placement in the DS group.
There were no abnormalities in any of the 3 enzymes in either group before the procedure. At 16 hours, cTnT was elevated in 5 out of 23 patients (21.7%) in the CS group and 4 out of 37 patients (10.8%) in the DS group. Although both the incidence and mean numerical values of cTnT were observed to be higher in the CS group than in the DS group at 16 hours post-procedure, these values did not reach statistical significance (p > 0.05) (Table 1).
CK and CKMB levels were not elevated (above 2 times normal) in any of the patients. Only 2 patients had CK elevation > 200 IU 16 hours post-procedure. Patient and angiographic variables of the troponin positive and negative groups are listed in Tables 2 and 3. The increase in cTnT was not clearly predictable by any factor. There was no association between lesion type, stenosis severity, balloon length or inflation duration with the release of cTnT (Table 3).


The extensive use of stents in the treatment of coronary artery disease led cardiologists to simplify the procedure by introducing the concept of stenting without predilation, i.e., direct stenting. Several studies confirmed the safety and feasibility of the procedure with success rates greater than 90%.1,2,4 In addition to reductions in procedure time, fluoroscopy time and procedural costs, balloon-induced dissections were also reported to be lower.1,2
Animal studies revealed that endothelial denudation was lower in the DS group compared to the CS group, which may mean less vascular wall trauma and thrombosis risk.3,14 Also, Webb et al. reported less atheromatous embolic debris during intervention in saphenous vein grafts with DS compared to CS, which may lead to a lesser degree of myocardial damage.4 The authors reported that stents reduced thrombus dislodgement and embolization by entrapping friable material. Repeated balloon inflations to obtain a greater luminal diameter are also eliminated.15 We also hypothesized that limitation of vessel trauma to the stented segment might decrease the myocardial injury in the DS group. Avoiding vessel trauma outside the stented segment by avoiding predilation with long balloons (a lesion that could usually be stented with a 9 mm stent is predilated with a 20 mm balloon) may decrease procedure-related complications. However, although the incidence of cTnT release is higher in the CS group than in the DS group (21.8% versus 10.8%, respectively), these values did not reach statistical significance (p > 0.05). This could have been due to the small number of patients involved. There was no difference in balloon length between the groups. However, the potential pitfalls of DS should always be kept in mind. Although stenosis severity was not reported to be an indicator of successful direct stenting,1 passing a stent through a severe undilated stenosis might be more traumatic, leading to increased distal embolization.
Most studies reported that elevation of enzymes after PCI has been linked to the occurrence of in-lab complications. Post-procedural CKMB elevation was previously reported to be due to prolonged ischemia, sidebranch occlusion, peri-procedural transient vessel occlusion and distal embolization.16–21 Since we excluded patients with a sidebranch arising from the lesion, there was no sidebranch occlusion in our cohort. This might explain the lack of detectable CKMB elevation in this cohort. Transient ischemia without cell necrosis was also reported to lead minor amounts of cTnI elevation.22,23 Although we found no difference between the transient occlusion time of the groups with elevated and normal cTnT levels in our cohort, elimination of the balloon predilation prior to stenting might decrease the duration of ischemia and related necrosis.
The reported incidence of troponin T or I release was higher after stenting compared to balloon angioplasty.7,12,13 Shyu et al. recently reported that incidence of cTnT release was 29% with stenting compared to 13% with PTCA (p < 0.05).7 The authors speculated that deeper injury to the vessel wall caused by the stent might have led to this increase in cTnT level. We also found a high incidence of cTnT elevation in the CS group similar to Shyu et al.; however, the incidence was quite low in the DS group. Besides, cTnI release was also reported to be high, ranging from 27–29.6% in the literature.24,25 In both studies,24,25 if we exclude the cases with sidebranch occlusion, the incidence of troponin elevation decreases to 17.4% and 18.4%, respectively, which is similar to our CS group (21.8%). However, the incidence observed in the DS group is the lowest value reported in the literature after stenting.
Glycoprotein receptor blockers are now well-established adjuncts for elective PCI and have been shown to significantly reduce the incidence of post-procedural myocardial necrosis.26,27 These agents led to reductions in death, recurrent MI, or urgent revascularization and improved microvascular perfusion.28–30 We did not use GP receptor blockers in any of our patients.
We found no pre-procedure clinical or angiographic variables that predicted cTnT elevation in the 2 groups. Lesion type, stenosis severity, balloon length and inflation duration were not predictors of marker elevation. The inflation duration was short compared to the literature;25 besides, there was no sidebranch arising from the lesion, and there were no in-lab complications. We could not find any explanation for the elevation of cTnT in this patient cohort with apparently successful interventions. As Garbarz et al. reported, cardiac troponins might be an oversensitive marker in the setting of uncomplicated PCI.24

Study limitations. This is a single-center, retrospective and non-randomized study with a small, selected number of patients. This may have limited our statistical power to detect a significant difference in enzyme elevation between different stenting modalities. In addition, the small number of patients might also have accounted for a possible bias in the selection of treatment and our inability to identify the predictors of troponin elevation. However, these data provide the framework upon which to base larger prospective evaluations in patients undergoing stent implantation. Randomized studies with larger patient populations should be conducted to compare the two different approaches.


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