Percutaneous coronary intervention and beyond for ST-elevation acute myocardial infarction
Department of Cardiology, I.R.C.C.S. Ospedale Maggiore Policlinico, Milan, Italy
* Corresponding author. Tel: +39 02 55033532; fax: +39 02 55033530. E-mail address: gbdanzi{at}tin.it
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Abstract |
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 Top Abstract IntroductionPercutaneous coronary...Adjunctive pharmacological...Prevention of embolizationImplementation of myocardial...Unsolved issues in cardiogenic...References |
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The short- and long-term prognosis of acute myocardial infarction (MI) has markedly improved over the past 20 years, from 19% in 1986 to the current 5–6%. One of the reasons for this decrease is the introduction of more effective myocardial reperfusion techniques, as it has been clearly demonstrated that the rapidity, extent, and durability of reperfusion are an important prognostic determinant. Primary percutaneous coronary intervention has been shown to be superior to fibrinolytic treatment because it leads to a higher reperfusion rate. Myocardial salvage after the timely revascularization of an infarct-related artery critically depends on coronary blood flow to the area at risk, and therefore the adequacy of arterial reperfusion in acute MI depends not only on the persistent arterial patency, but also on the integrity of the distal circulation. At the microcirculatory level, distal embolization from the lesion site, the release of vasoconstrictive platelet mediators, and vascular reperfusion injury due to cardiac inflammatory responses may all compromise recovery, and therefore efficacious treatment of acute MI requires the restoration of patent epicardial flow and the preservation of microvascular integrity. The various techniques currently being evaluated for their ability to reduce final infarct size will be discussed.
Key Words: Myocardial infarction • PTCA • Angioplasty
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Introduction |
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TopAbstractIntroductionPercutaneous coronary...Adjunctive pharmacological...Prevention of embolizationImplementation of myocardial...Unsolved issues in cardiogenic...References |
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It has been demonstrated that myocardial reperfusion relieves or reduces ischaemia and necrosis, but is followed by morphological and functional changes that ultimately lead to tissue damage. The salvaging of a jeopardized myocardium seems to be primarily determined by: (i) time to the reperfusion and patency of the infarct-related artery, (ii) microcirculatory perfusion, and (iii) myocyte preservation after the ischaemia–reperfusion sequence. The relevance of vascular damage in the natural history of myocardial infarction (MI) is consistent with the benefits achieved by treatment strategies directly aimed at protecting the coronary circulation from reperfusion damage.1
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Percutaneous coronary intervention |
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TopAbstractIntroductionPercutaneous coronary...Adjunctive pharmacological...Prevention of embolizationImplementation of myocardial...Unsolved issues in cardiogenic...References |
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Primary percutaneous coronary intervention (PCI) is strongly recommended as the reperfusion strategy of choice for patients with ST-elevation acute MI (STEMI) at centres experienced in interventional management and swift door-to-balloon times (<2 h from hospital admission).2,3 The main evidence favouring mechanical reperfusion over fibrinolysis comes from a meta-analysis published in 2003, which included 23 randomized trials comparing primary PCI with thrombolysis in a total of 7739 patients:4 primary PCI was better than thrombolytic therapy at reducing overall mortality (7 vs. 9%, P=0.0002), non-fatal re-MI (3 vs. 7%, P<0.0001), stroke (1 vs. 2%, P=0.0004), and the composite of these events (8 vs. 14%, P<0.0001). The reduction in these outcomes was significant after both short- and long-term follow-up.
The results of DANAMI 2 (Danish Trial in Acute Myocardial Infarction-2) suggested that transferring patients for primary PCI is associated with better outcomes than local thrombolysis if the transfer time is <3 h,5 whereas the PRAGUE-2 (Primary Angioplasty in Patients Transferred from General Community Hospital to PCI Units Versus Emergency Thrombolysis) trial found better outcomes with primary PCI only in patients treated >3 h after symptom onset.6 The American College of Cardiology/American Heart Association (ACC/AHA) guidelines warn that the benefit of primary PCI is lost if treatment is delayed by >60 min.2
Although thrombolysis has been shown to produce no benefit after 12 h from symptom onset, the BRAVE-2 (Bavarian Reperfusion Alternative Evaluation 2) study [results presented by A. Kastrati at the American College of Cardiology (ACC) Annual Scientific Session, Orlando, FL, USA, March 2005] showed for the first time that late restoration of TIMI (thrombolysis in MI) 3 grade flow offers some advantages. The study randomized 365 asymptomatic MI patients presenting >12 h after symptom onset to angiography (and PCI if necessary) or conventional medical therapy. The effect of reperfusion was evaluated on the basis of infarct size, and it was found that the patients undergoing PCI had smaller infarcts than those treated non-invasively. The current guidelines still do not recommend reperfusion for MI patients presenting >12 h after symptom onset.
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Adjunctive pharmacological therapy |
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TopAbstractIntroductionPercutaneous coronary...Adjunctive pharmacological...Prevention of embolizationImplementation of myocardial...Unsolved issues in cardiogenic...References |
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Abciximab is still the only glycoprotein IIb/IIIa inhibitor that has been proved to be clinically effective in combination with PCI for AMI,7 and five trials have found that it leads to significant reductions in 30-day ischaemic events.8–12 The results of the CADILLAC (Controlled Abciximab and Device Investigation to Lower Late Angioplasty Complications) trial (2082 patients),8 RAPPORT (ReoPro and Primary PTCA Organization and Randomized Trial) (483 patients),9 and the ISAR-2 (Intracoronary Stenting and Antithrombotic Regimen-2) trial (401 patients)10 agreed, showing a significant enhancement in 30-day event-free survival, and also indicated the absence of any substantial long-term effect. In contrast, the results of the ADMIRAL (Abciximab Before Direct Angioplasty and Stenting in Myocardial Infarction Regarding Acute and Long-term Follow-up) study11 suggested more sustained efficacy so far as abciximab treatment was associated with a higher incidence of post-procedural epicardial TIMI-3 grade flow and less than half the rate of 30-day major adverse cardiac events (MACE), a benefit that was maintained after 6 months. It can be hypothesized that the lack of effect of abciximab in the stenting arm of the CADILLAC trial was due to the very early administration of thienopyridines or to the low-risk profile of the enrolled patients as demonstrated by the low incidence of adverse events.
The ACE (Abciximab and Carbostent Evaluation) trial demonstrated the highly beneficial effects of abciximab after 6 and 12 months of follow-up: 1-year survival rate in the abciximab group was 95±2% compared with 88±2% in the stent-alone group (P=0.017).12 It also revealed a potent protective effect of abciximab against stent thrombosis, which occurred in only 0.5% of the patients randomized to receive a stent plus abciximab but in 5% of those randomized to receive a stent alone (P=0.01).13
It can be concluded that the immediate administration of abciximab is beneficial in acute MI patients scheduled for primary PCI, as recommended by current clinical European and ACC/AHA guidelines.2–3 However, it should be noted that several recent reports have emphasized the value of tirofiban, when administered as a single high-dose bolus (SHDB) of 25 µg/kg followed by a standard infusion, as an affordable and safer alternative to abciximab.14–16 In TARGET (Tirofiban and ReoPro Give Similar Efficacy Outcomes Trial),17 in patients undergoing PCI, abciximab was superior to tirofiban with respect to the pre-specified combined endpoint. The superiority of abciximab was driven by a higher rate of peri-procedural MI in the tirofiban arm, suggesting inadequate early platelet inhibition with the bolus regimen (10 µg/kg) used. Subsequent dose-ranging studies showed that increasing the tirofiban bolus dose from 10 to 25 µg/kg was necessary to obtain an optimal level of platelet inhibition,14,15 and initial clinical trials with the high bolus appear highly promising.
In the first randomized head-to-head comparison between tirofiban, administered as SHDB, and abciximab during primary PCI,16 our group found no differences in terms of MACE or recovery of left ventricular function (primary endpoint of the study) between the two drugs. Similar results were reported for the STRATEGY (High-Dose Bolus Tirofiban and Sirolimus Eluting Stent Versus Abciximab and Bare Metal Stent in Acute Myocardial Infarction) trial (presented at the American College of Cardiology Annual Scientific Session, Orlando, FL, USA, March 2005), which also found that tirofiban was associated with a trend towards a reduction in bleeding and a significant reduction in thrombocytopenia.
The on-going TENACITY (The Tirofiban Evaluation of Novel Dosing vs. Abciximab with Clopidrogel and Inhibition of Thrombin Study) trial will specifically address the issue of whether, in a broad PCI population that includes patients with STEMI, tirofiban administered as SHDB will perform similarly in terms of 30 days MACE with respect to a standard regimen of abciximab.
Various mechanisms contribute to ischaemia–reperfusion injury, including the production of oxygen free radicals, neutrophil activation, endothelial and myocyte oedema, the loss of antioxidant enzymes, and cardiomyocyte apoptosis, and a number of pharmacological approaches are being evaluated as a means of reducing this process.
Adenosine, an endogenous purine nucleoside, antagonizes many of the biochemical and physiological mechanisms involved in ischaemia–reperfusion injury, and experimental animal models have shown that adenosine pre-treatment reduces ischaemia–reperfusion damage, limits infarct size, and improves ventricular function.18 Hori et al.,19 who investigated the pathophysiology of acute embolization in small coronary vessels and the role of adenosine in 39 dogs, showed maintained or even enhanced epicardial flow due to adenosine-related hyperaemia of the myocardium surrounding the embolized microregions, with blood shunting around the areas of obstruction. In humans, the intracoronary administration of adenosine as an adjunct to primary angioplasty has led to controversial results: in a small randomized study, Marzilli et al.20 found that patients receiving adenosine showed a lower incidence of no-reflow and a significant improvement in the final TIMI grade flow than those treated with saline infusion, but the ADMIRE (AmP579 Delivery for Myocardial Infarction Reduction) study of 311 patients undergoing primary percutaneous transluminal coronary angioplasty (PTCA) found that adenosine had no significant effect on infarct size.21 The use of intracoronary adenosine in current interventional practice is limited to the treatment of no-reflow.
Another possible pharmacological strategy is complement activation, an important mediator of inflammatory damage that is associated with larger infarctions and poor clinical outcomes. The COMMA (Complement Inhibitor in Myocardial Infarction Treated With Angioplasty) trial randomized 960 patients undergoing primary PCI to placebo or pexelizumab, an antibody fragment C5 complement inhibitor, and showed that, although pexelizumab did not reach its primary 72-h endpoint of reducing infarct size, its administration was associated with a dose-dependent and statistically significant 70% reduction in 90-day mortality.22 Patel et al.23 showed that baseline and serial measurements of white blood cells and body temperature during the first few days after the onset of acute MI treated with thrombolytics or PCI in patients enrolled in two phase II trials [COMPLY (Complement Inhibitor in Myocardial Infarction Treated with Thrombolytics) and COMMA] could limit infarct size as well as mortality and heart failure after 90 days.
Glucose–insulin–potassium (GIK) infusion as adjunctive therapy in patients with ST-elevation MI improves ventricular function and decreases ventricular arrhythmias. The original GIPS (Glucose–Insulin–Potassium Study) showed that 30-day mortality was reduced in MI patients without heart failure who received GIK in addition to PTCA.24 However, after randomizing 889 patients with acute MI to reperfusion therapy plus GIK infusion or reperfusion therapy alone within 6 h of symptom onset, the results of GIPS-II (presented by Felix Zijlstra at the ACC Annual Scientific Session, Orlando, FL, USA, March 2005) showed that GIK therapy failed to reduce the primary endpoint of 30-day mortality. Similar results were obtained in CREATE-ECLA (Clinical Trial of Reviparin and Metabolic Modulation in Acute Myocardial Infraction Treatment Evaluation-Estudios Cardiologicos Latinoamerica).25
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Prevention of embolization |
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TopAbstractIntroductionPercutaneous coronary...Adjunctive pharmacological...Prevention of embolizationImplementation of myocardial...Unsolved issues in cardiogenic...References |
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The net effect of reperfusion is usually beneficial, but microvessel disruption and the macro- and microembolization of atherothrombotic debris during PCI for acute MI are frequent and may obstruct the coronary microvessel network, thus decreasing the efficacy of mechanical reperfusion and myocardial salvage.26 The no-reflow phenomenon is due to a lack of reperfusion at the microcirculatory level with a post-procedural TIMI grade flow of <3 or the dissociation of epicardial and myocardial flow. Three different approaches are currently used to prevent distal embolization in clinical practice: direct stenting without pre-dilation, thrombectomy, and the use of anti-embolic protection devices.
Direct stenting without pre-dilation
Direct stenting without pre-dilation may decrease embolization and the incidence of no-reflow.27
Thrombectomy
Thrombectomy is a more specific approach to the problem of intra-PCI embolization, and one randomized trial has found that rheolytic thrombectomy is effective in decreasing embolization in patients undergoing PCI on venous grafts or native coronary vessels with massive thromboses.28 In a further small study, Antoniucci et al.29 randomized 100 patients to direct infarct artery stenting with or without previous rheolytic thrombectomy using a second-generation 4FR catheter (Angiojet®, Possis Inc., MN, USA), and demonstrated that rheolytic thrombectomy before routine direct infarct artery stenting is highly feasible and provides more effective myocardial reperfusion, as shown by more frequent early ST-segment resolution, lower TIMI frame count values, and smaller infarcts, than stenting alone.
Beran et al.30 showed that, in comparison with conventional PCI alone, pre-treatment with the X-sizer catheter system (EndiCOR Inc., San Clemente, CA, USA) improves epicardial flow and coronary microcirculatory function, and leads to more rapid ST-segment resolution: ST-resolution of >50% was observed immediately after the intervention in 82.6% of the patients treated with the X-sizer compared with 52.2% of those in the control group (P<0.03). Multivariate analysis identified X-sizer application as the only independent predictor of an ST-resolution of >50% (odds ratio, 4.35; P<0.04). Similar conclusions were reached by Napodano et al.31 in a study of 92 acute MI patients with angiographic evidence of a thrombus: thrombectomy performed using the X-sizer catheter led to better myocardial reperfusion (as assessed by myocardial blush and ST-segment resolution) than conventional stenting.
However, a preliminary report from the large AiMI (Angiojet in Myocardial Infarction) study of 480 patients randomized to primary PCI or rheolytic thrombectomy (presented at the TCT Meeting, Washington DC, USA, September 2004) indicated no evidence of a reduction in infarct size (evaluated by means of resting Tc-99 m sestamibi scans) and, although the study was not powered for clinical endpoints, there was a significant between-group difference in mortality, with a remarkably low death rate in the control arm (0.8 vs. 4.6%, P=0.02).
Anti-embolic protection devices
A plethora of anti-embolic protection devices are available, but the results concerning their effect in patients with acute MI are still inconclusive. The Guardwire® (Medtronic, MN, USA) is the prototype occlusive protection system and was found to be effective against embolization in patients with diseased saphenous vein grafts.32 Stone et al.33 conducted the first randomized trial of the usefulness of Guardwire distal protection devices during primary PCI in 501 patients who underwent primary or rescue PCI within 6 h of symptom onset and were randomized to undergo PCI with balloon occlusion and the use of an aspiration protection system or angioplasty without distal protection. Although the aspiration system effectively retrieved embolic debris in most patients (73%), it did not lead to improved microvascular flow, a greater success rate, reduced infarct size, or enhanced event-free survival (10.0 vs. 11%, P=0.66) in comparison with the control group.
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Implementation of myocardial reperfusion with other techniques |
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TopAbstractIntroductionPercutaneous coronary...Adjunctive pharmacological...Prevention of embolizationImplementation of myocardial...Unsolved issues in cardiogenic...References |
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It has been suggested that hypothermia may have a positive effect on microcirculatory perfusion and myocyte preservation, because cooling the myocardium before reperfusion protects against ischaemic and reperfusion injury by reducing metabolic demand and limiting infarct size. A randomized feasibility study of 42 acute MI patients within 6 h of symptom onset showed that it was possible to achieve endovascular cooling of 3–4°C in all of the 18 patients randomized to cooling without any major negative effects.34 The median infarct size (as assessed by means of 1-month Tc-99 m 2-methoxy-2-methylpropylisonitrile scintigraphy) was very small in both groups.
Another strategy that could prevent the negative effects of PCI and optimize myocardial salvage and functional recovery is the hyperoxaemic coronary infusion of aqueous oxygen, a liquid-phase combination of water and medical-grade oxygen mixed with arterial blood. Regional organ or tissue perfusion is achieved using a blood loop (TherOx Inc., Irvine, CA, USA) that allows precise control of pO2 (oxygen tension) when aqueous oxygen is mixed with arterial blood.35 Experimental36 and clinical studies37 have shown that correcting hypoxaemia or inducing hyperoxaemia attenuates microvascular dysfunction and reperfusion of ischaemia. A non-randomized study of 29 patients with acute MI demonstrated the feasibility of 90-min hyperoxaemic reperfusion after stenting of the infarct-related vessel.37 O'Neil et al., in the preliminary report of the AMIHOT (Acute Myocardial Infarction with Hyperoxemic Therapy) trial (presented at the TCT Meeting, Washington DC, USA, September 2004), assessed the effectiveness of this integrated reperfusion technique in 134 patients and 135 controls. ST-segment resolution was significantly better in the anterior MI group and showed a favourable trend in the cohort as a whole; there was also a favourable whole-cohort trend in terms of infarct size (determined by means of sestamibi scans), with a significant reduction in the patients treated within 6 h of symptom onset. The 30-day MACE rate was not significantly different in the two groups.
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Unsolved issues in cardiogenic shock |
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TopAbstractIntroductionPercutaneous coronary...Adjunctive pharmacological...Prevention of embolizationImplementation of myocardial...Unsolved issues in cardiogenic...References |
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Although only partial and limited information is available from small groups of patients undergoing coronary angiography, the 7–8% incidence of post-acute MI cardiogenic shock has apparently not declined with modern treatment. The SHOCK (Should We Emergently Revascularize Occluded Coronary for Cardiogenic Shock) trial found significantly better 1-year survival in patients undergoing emergency revascularization (47%) than in those who were initially medically stabilized (34%),38 but the rate of early mortality due to cardiogenic shock remains high. It has been suggested that vasorelaxant and myocardial depressant nitric oxide-derived species may play a critical role in the pathophysiology of shock on the basis of the favourable results of a small, single-centre, prospective trial involving 30 patients randomized to supportive care plus the L-NAME nitric oxide synthase inhibitor or supportive care alone, which found a 40% difference in absolute mortality between the two groups.39 The multicentre SHOCK-2 trial, designed to investigate the outcomes of cardiogenic shock patients after treatment with nitric oxide synthase inhibitor, has not yet been completed.
Ongoing trials will assess the effectiveness of adjunctive reperfusion techniques, and it likely seems that at least some of them will be incorporated in the future treatment of patients with acute MI.
Conflict of interest: none declared.
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References |
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