Conventional Versus Direct Stenting in Acute Myocardial Infarction: Effect on Immediate
Coronary Blood Flow

Timur Timurkaynak, MD, Murat Ozdemir, MD, Atiye Cengel, MD, Mustafa Cemri, MD, Haci Ciftci, MD, Ridvan Yalcin, MD, Bulent Boyaci, MD, Ovsev Dortlemez, MD, Halis Dortlemez, MD
Timur Timurkaynak, MD, Murat Ozdemir, MD, Atiye Cengel, MD, Mustafa Cemri, MD, Haci Ciftci, MD, Ridvan Yalcin, MD, Bulent Boyaci, MD, Ovsev Dortlemez, MD, Halis Dortlemez, MD
Although thrombus-containing lesions were previously considered as a contraindication for stenting, accumulating data regarding stenting in acute myocardial infarction (AMI) and in the presence of angiographically apparent thrombus reveal promising results with a very low acute and subacute thrombosis rates.1–8 Obtaining TIMI 3 flow with percutaneous coronary intervention (PCI) was associated with a better prognosis in AMI.9 Brisk TIMI 3 flow immediately after intervention minimizes the ischemic insult on myocardium. GUSTO trial demonstrated a poorer clinical outcome in cases where TIMI 3 flow cannot be obtained.10 Primary angioplasty and thrombolytic therapy are the major treatment modalities for rapid and complete reperfusion in patients with acute ST-segment elevation MI. If initial thrombolytic therapy fails, rescue percutaneous coronary intervention (PCI) or coronary bypass graft (CABG) surgery is attempted. However, PTCA-related major complications occurred in patients with unstable angina, likely because of the plaque fissuring and thrombus that is frequently present. Abrupt closure (no re-flow) at the angioplasty site occurs in 11–50% of patients who undergo balloon angioplasty in the setting of AMI.11–13 Primary thrombus propagation may be more important when dilation is performed in the setting of pre-existing thrombus (unstable angina and myocardial infarction).14 No re-flow, still a dreadful complication after percutaneous interventions, may limit the procedural success. Infarct-related artery (IRA) occlusion and dissections are the major complications after PTCA in AMI leading to impaired clinical sequel.15,16 However, stenting by overcoming these potential complications may improve the blood flow in this thrombogenic milieu. Direct stenting (stenting without balloon predilation), is a novel approach in percutaneous treatment of coronary artery lesions. Stenting without balloon dilation may decrease the trauma, incidence of dissection and distal embolization leading to a better outcome.17–20 However, there is no data regarding these potential benefits of direct stenting in the setting of AMI. The aim of this study was to evaluate the impact of a novel percutaneous coronary intervention technique, direct stenting on the angiographic results and compare it to conventional stenting performed in the setting of AMI. Methods Study population. We reviewed the institutional interventional database from February 1998 through February 2001 at our center and identified all the patients who underwent primary and rescue angioplasty. The inclusion criteria were chest pain longer than 30 minutes in duration, presentation within 12 hours after the onset of symptoms, and ST-segment elevation > 0.1 mV in two contiguous electrocardiographic leads for primary angioplasty. Criteria for rescue angioplasty were recurrence of previously subsided chest pain or ST-segment re-elevation after successful thrombolytic therapy or ongoing chest pain without any ST-segment resolution, despite thrombolytic therapy. We identified 54 patients meeting the above-mentioned criteria. We excluded 6 patients because of the presence of cardiogenic shock and 2 patients because of AMI due to subacute stent thrombosis, in whom only PTCA was performed. Two patients in whom PTCA was performed without stenting as a bridge to CABG were also excluded. The remaining 44 (29 primary and 15 rescue PTCA) patients were then divided into two groups: group A consisted of patients who had undergone conventional stenting (23 patients), and group B were those who had undergone direct stenting (21 patients). Angioplasty procedure. PCI was performed after obtaining two orthogonal views of the IRA. After crossing the lesion with a 0.014´´ guidewire, the state of TIMI flow (TIMI flow > 0) determined the procedure to be performed (direct stenting or not) in the majority of the patients in addition to operator preference. Initial balloon dilation in the conventional stenting group was carried out with undersized PTCA balloons inflated at nominal pressures (6–8 atm). Multiple balloon inflations were used if needed. Stenting in both groups was accomplished with the use of second generation preloaded tubular stents (Jostent and ACS Multilink) and implanted with high pressure (> 12 atm). Stent-to-artery ratio was 1.1/1. Direct stenting was accomplished with the delivery balloon with a high pressure single inflation. Postdilation was not performed in any patients in both groups. In cases of multivessel disease, only the culprit vessel was treated. During the procedure, an intraveneous bolus dose of 10,000 units of standard heparin was given to maintain an activated clotting time > 300 seconds; this was continued for 6–24 hours. Standard heparin was then replaced with enoxaparin (1 mg/12 hours) in addition to ticlopidine (250 mg bid for 30 days) and aspirin (300 mg, indefinitely). Glycoprotein (GP) IIb/IIIa receptor antagonists were not used in any patients. Angiographic evaluation. Angiograms were reviewed and graded by two independent film readers unaware of the study purpose to assess TIMI flow grades.21 Contrast flow through the epicardial artery was graded using the standard TIMI trial flow scale of 0 to 3. “No re-flow” was defined as an acute impairment of blood flow to TIMI 0-1 after successful dilation. TIMI 2 flow was defined as “Slow Flow”. Angiographic success was defined as TIMI flow grade >= 2. Slow flow or no re-flow phenomena were treated with intracoronary nitroglycerin (200 µg) followed by intracoronary Verapamil (150–250 µg). We used an angiographic thrombus scoring system based on the size of the thrombus (0 = no thrombus; 1 = intraluminal haziness; 2 = definite thrombus 2 vessel diameters) before stenting (after balloon predilation in group A and after guidewire crossing in group B) between the two groups.22,23 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). Multivessel disease was defined as at least one major non-IRA with more than 50% stenosis. Statistical analysis. Data were expressed as the mean ± SD for continuous variables and as frequencies for the categorical variables. Continuous variables were compared by the Mann-Whitney U test and categorical variables by the X2 test. A p value of = 2) after stenting were similar in both groups (p > 0.05). Although there was no difference in thrombus score between groups A and B (2.3 ± 1.4 vs. 2.1 ± 1.2; p > 0.05), final TIMI 3 flow was significantly better in group B after stenting (65% vs. 95%; p 0.05), final TIMI 3 flow was significantly lower in group A (65% vs. 95%; p 0.05). Total occlusion of the IRA was observed in 3 patients (14%) when the stent was delivered to the lesion for implantation in group B with successful recanalization after deployment. However, there was no stent loss or geographic miss in this group. The majority of the stents deployed were Jostent (65%) (JOSTENT Flex Supreme System, Jomed International AB, Helsingborg, Sweden) and ACS Multilink (34%) (Duet, Tristar and Tetra, Guidant/ACS, Sunnyvale, California). All stents were successfully implanted without any crossing failure. Discussion Angiographically apparent intracoronary thrombus has been documented to be a strong correlate of acute coronary occlusion during PTCA.24,25 Besides local activation of platelets and coagulation factors, liberation of clot-bound-thrombin due to mechanical disruption of thrombus after balloon dilation were reported to be the responsible mechanisms.26–28 Ballon dilation of diffusely diseased sapheneous vein grafts carries a major risk of abrupt closure or distal coronary embolization, likely due in part to the frequent presence of thrombus within these degenerated vessels.29 Extensive use of stents in the treatment of coronary artery disease led the cardiologists to simplify the procedure by introducing the concept of stenting without predilation, named direct stenting.17,30 Several studies confirmed the safety and feasibility of the procedure with success rates greater than 90%.17,18,20 Besides reductions in procedure time, fluoroscopy time and costs, balloon-induced dissections were reported to be lower.17,18 Obtaining TIMI 3 flow is the ultimate goal after PCI. In a meta-analysis, TIMI 3 flow was found to be associated with significantly less mortality compared to all the other TIMI flow grades including the TIMI 2.31 Recently, CADILLAC study also demonstrated that stenting with or without GP IIb/IIIa receptor blockers is superior to PTCA in the setting of AMI — the authors concluded that it should be the default therapy in this setting in experienced centers.32 In the present study, TIMI flow grades before stenting (after balloon predilation in group A and after guidewire crossing in group B) were similar. However, the final TIMI flow grades were significantly better in group B after stenting, despite the absence of any difference in thrombus burden between the groups. The reason for this difference could be the lesser trauma in group B leading to lesser flow impairment by trapping the thrombus. The trauma caused by balloon predilation might have caused distal embolization of the thrombi and debris. Animal studies revealed that endothelial denudation is less in the direct stenting group compared to conventional stenting, which may mean less vascular wall trauma and thrombosis risk.19,33 Besides, Webb et al. reported lesser atheromatous embolic debris during intervention in saphenous vein grafts with direct stenting approach compared to conventional stenting, which may lead to “no re-flow” phenomenon.20 Although small numbers limit the conclusion, in our study, there were three “no re-flow” cases (13%) all in the conventional stenting group. The final TIMI flow grades were significantly better in group B after stenting, despite the absence of any difference in thrombus burden between the groups. In the presence of thrombi, stents may act as a jail for the thrombus and prevent distal propagation. However, the potential pitfalls of direct stenting should always be kept in mind. Although stenosis severity was not reported to be an indicator of successful direct stenting,17,31,34 passing a stent through a severe undilated stenosis might be more traumatic.35 However, direct stenting may not be an appropriate approach in all lesion subsets and requires distal opacification of the vessel for an accurate assessment of lesion characteristics and stent choice. In the present study, five patients with TIMI 0 flow achieved a distal opacification immediately after guidewire crossing the lesion, which enabled us to apply direct stenting in these patients. We observed total occlusion of the vessel during stent implantation, making the correct positioning difficult in 3 patients (14%), of which, there was no geographic miss. As a majority of acute coronary syndromes develop on lesions with a diameter stenosis less than 50% and are associated with a soft thrombotic occlusion, direct stenting in these lesion subsets seems to be a safe approach.36,37 We didn’t observe any “no re-flow” in our direct stenting group. Hamon et al. performed direct stenting in acute coronary syndromes and reported a very low rate of reversible “no re-flow” in this high-risk patient population.37 Recently, Capozzolo et al. reported a statistically better postprocedural angiographic flow in patients undergoing primary PTCA treated with direct stenting compared to patients treated with conventional stenting (p
1. Kaul U, Aggarwal R, Jain P, Wasir HS. Safety and efficacy of intracoronary stenting for thrombus containing lesions. Am J Cardiol 1996;77:425–427. 2. Alfonso F, Rodriguez P, Phillips PD, et al. Clinical and angiographic implications of coronary stenting in thrombus containing lesion. J Am Coll Cardiol 1997;29:725–733. 3. Kaul U, Singh B, Sudan D, et al. Primary stenting in acute myocardial infarction. A 30 day follow up study. Cathet Cardiovasc Intervent 1999;46:4–10. 4. Suryapranata H, Hoorntje JCA, de Boer MJ, Zijlstra F. Randomized comparison of primary stenting with primary balloon angioplasty in acute myocardial infarction. Circulation 1997;96:I–327. 5. Antoniucci D, Santoro GM, Bolognese L, et al. A clinical trial comparing primary stenting of the infarct-related artery with optimal primary angioplasty for acute myocardial infarction: Results from the Florence Randomized Elective Stenting in Acute Coronary Occlusions (FRESCO) trial. J Am Coll Cardiol 1998;31:1234–1239. 6. Saito S, Hosokawa G. Primary Palmaz-Schatz stent implantation for acute myocardial infarction: The final results of Japanese PASTA (Primary Angioplasty Versus Stent Implantation in AMI in Japan) trial. Circulation 1997;96:I–595. 7. Schömig A, Neuman FJ, Walter H, et al. Coronary stent placement in patients with acute myocardial infarction: Comparison of clinical and angiographic outcome after randomization to antiplatelet or anticoagulant therapy. J Am Coll Cardiol 1997;29:28–34. 8. Monassier JP, Hamon M, Elias J, et al. Early versus late coronary stenting following acute myocardial infarction. Results of the SENTIM I Study. Cathet Cardiovasc Diagn 1997;42:243–248. 9. van’t Hof A, Liem A, Suryapranata H, et al. Angiographic assessment of myocardial reperfusion in patients treated with primary angioplasty for acute myocardial infarction. Circulation 1998;97:2302–2306. 10. Morton JK, Joseph AM, Frank VA, et al. Determination of angiographic (TIMIGRADE) blood flow by intracoronary doppler flow velocity during acute myocardial infarction. Circulation 1996;94:1545–1552. 11. Piana RN, Paik GY, Mosucci M, et al. Incidence and treatment of no reflow after percutaneous coronary intervention. Circulation 1994;89:2514–2518. 12. Marzilli M, Gliozheni E, Marraccini P, Fedele S. Primary coronary angioplasty in acute myocardial infarction: Clinical correlates of the “no reflow” phenomenon. Int J Cardiol 1998;65(Suppl 1):S23–S28. 13. Morishima I, Sone T, Mokuno S, et al. Clinical significance of no-reflow phenomenon observed on angiography after successful treatment of acute myocardial infarction with percutaneous transluminal coronary angioplasty. Am Heart J 1995;130:239–243. 14. Waller BF, Fry E, Peters TF, et al. Abrupt (