Update on ST elevation Myocardial infarction

Update on ST Elevation Myocardial infarction: acute myocardial infarction in women; immediate multivessel versus culprit vessel PCI in cardiogenic shock and is post-procedural anticoagulation needed after primary PCI? During the last two decades the management of ST elevation myocardial infarction (STEMI) has evolved considerably throughout Europe through the organisation of regional STEMI networks and the increasing use of primary percutaneous coronary intervention (PCI) as preferred reperfusion strategy. Inclusion of out of hospital emergency physicians and other prehospital healthcare professionals is of uttermost importance in order to keep the delay between first medical contact and the first balloon dilatation as short as possible. Involvement of prehospital emergency teams resulted in the French RESCUe registry over a period of 5 years in a progressive reduction of the delay between first medical contact and the first balloon dilatation and also in progressive increase of primary PCI.1 The delay between onset of symptoms and calling the emergency medical system (patient delay) affects significantly the treatment delay before initiation of reperfusion therapy. The implementation of a national primary PCI strategy in Denmark apparently resulted in an increased public awareness on the symptoms of a heart attack as a mild reduction of the patient delay was observed over a 7-year period.2 Patient delay remains however substantial and is most problematic in the elderly, diabetics, female patients and when symptoms arise during the night. A significant number of patients with ST-elevation myocardial infarction (STEMI) present with multivessel coronary artery disease (MVD). The indication and timing of coronary intervention on non-culprit lesions is still a matter of debate. A post-hoc analysis of the AIDA STEMI trial shows that PCI of the culprit lesion alone had no negative effect on reperfusion success and myocardial salvage in patients with MVD as compared to STEMI patients with single vessel disease.3 However, the presence of MVD is an independent risk factor associated with a threefold increase of major adverse cardiac events during long term follow-up. This study indicates that immediate multivessel PCI is not necessary in order to improve myocardial reperfusion but that a staged revascularisation of non-culprit lesions may be good strategy to improve the long-term outcome of STEMI patients with MVD. At present, there is no consensus on the optimal revascularisation of MVD in STEMI patients presenting with cardiogenic shock. In a post-hoc analysis of the randomized IABP-SHOCK II trial that investigated the effect of intra-aortic balloon pump on the outcome of acute myocardial infarction (AMI) complicated by cardiogenic shock, MVD was present in 75% of the patients4. In contrast with ESC STEMI guidelines that recommend to consider immediate PCI of all significant non-infarct related lesions5, two thirds of the MVD patients were treated with primary PCI of the culprit artery only and staged PCI procedures or coronary bypass surgery were only rarely performed. Immediate multivessel PCI that was performed in only 37% of the patients, was not associated with any benefit on long-term mortality, immediate TIMI 3 patency or on any of the secondary clinical endpoints. It appears therefore that primary PCI of the culprit artery alone is sufficient as immediate revascularisation procedure in patients with AMI complicated by cardiogenic shock. The final verdict on the optimal revascularisation strategy in cardiogenic shock will come when the results of the ongoing prospective multicentre CULPRIT-SHOCK trial will be communicated. Analysis of the multicentre VIRGO study shows that compared to men young and middle-aged women with AMI represent a fundamentally distinct, higher-risk population with a poorer prognosis over the long term.6 A higher burden of classical cardiovascular risk factors and a higher prevalence of comorbidities may explain only in part the worse outcome of these patients. Additional factors are a poorer psychosocial status, a longer delay between symptom onset and presentation, more atypical symptoms and a lower frequency of timely performed reperfusion. In only 50% of the patients with diffuse ectatic coronary arteries a TIMI grade 3 flow is achieved immediately after primary PCI for STEMI.7 Many of these patients however show a normalisation of the epicardial coronary flow during the chronic phase and the mortality is much lower than expected on the basis of the high prevalence of a TIMI grade 2 or less flow. It is speculated that the intracoronary thrombus in these patients may have a different composition since it is formed due to flow sluggishness in ectacic coronary arteries. Platelets play an important role in intracoronary thrombus formation in acute coronary syndromes. Anterior STEMI patients with high platelet counts (>400k) on admission showed a lower prevalence of a TIMI grade 3 flow before primary PCI and a lower left ventricular systolic function both on admission and before discharge whereas patients with lower platelet counts showed higher coronary flow grades and a better left ventricular systolic function.8 These observations are in line with earlier studies with intravenous thrombolysis. Myocardial inflammation is supposed to play an important role in the acute phase of AMI and in the post-infarction remodelling. State of the art cardiac magnetic resonance imaging in STEMI patients showed that peak levels of routine inflammatory markers (C-reactive protein) were significantly correlated to the extent of myocardial injury and the degree of left ventricular (LV) dysfunction in the acute setting after primary PCI as well as 4 months thereafter.9 The addition of these biomarkers to cardiac troponins did not add to the prediction of LV dysfunction at follow-up. The rise of inflammatory markers appears therefore to be only reactive to myocardial necrosis without any further direct negative effect on the adverse post-infarction remodelling. Following primary PCI STEMI patients remain at high risk for recurrent ischemia or other adverse thrombotic events such as deep venous thrombosis or pulmonary thromboembolism. Routine anticoagulation is frequently used for several days after the intervention in order to prevent early thrombotic complications. The evidence for this therapy is unclear and any preventive effect may be offset by an increased bleeding complication rate. A post-hoc analysis of the HORIZONS-AMI trial showed no beneficial effect of routine post-procedural anticoagulation on short term clinical outcome.10 In the analysis of the combined EUROMAX and HORIZONS-AMI trials data set post-procedural anticoagulation was associated with higher bleeding rates without any reduction in ischaemic events.11 Therefore, routine post-procedural anticoagulation after primary PCI seems to have an unfavourable effect and should be avoided unless a well-established indication is present. Spontaneous coronary artery rupture is a rare potentially fatal disease. An illustrative case and a review of the literature12 is presented at the end of this issue.