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Mr Yonathan Hasin
Prof. D Ghanim
The main mechanical complications (MC) of acute myocardial infarction are ventricular septal rupture(VSR), free wall rupture(FWR), and ischemic mitral regurgitation (IMR). In the chronic phase, negative remodeling and aneurysm formation may occur. The pathophysiological mechanism of MC post AMI is complete lack of perfusion leading to myocardial necrosis, neutrophil infiltration, activation of matrix metalloproteinases (MMPS) and degradation of collagen struts by serine protease leading to slippage of myocytes, wall thinning, increased wall stress and ventricular dilatation, and finally wall disruption and rupture.
The incidence of ventricular septal rupture(VSR), infarct expansion, free wall rupture(FWR), and ischemic mitral regurgitation (IMR) is quite low, but the contribution of these complications to total mortality from AMI is high. The incidence of any degree of infarct expansion is about 30-50 percent of anterior wall MI and in more then 75 percent of patients dying from AMI. Infarct expansion is associated with high mortality and complications such as heart failure and LV aneurysm formation (2).
In general there is no way to predict the occurance of these complications, but CRP level measurements early after MI can predict infarct expansion, cardiac rupture, LV aneurysm formation and one year cardiac death (1). The main risk determinants of infarct expansion are large transmural infarct, LAD occlusion, lack of LV hypertrophy, and high intramural tension.
There are no effective therapeutic interventions to treat MI expansion, but any intervention that normalises wall stress by reducing intraventricular pressures and radius and increasing wall thickness can attenuate early and late remodeling. Early revascularisation with fibrinolysis or primary PCI can limit infarct size, transmurality and can at times attenuate infarct expansion(3). ACE-inhibitors and B-Blockers attenuate late remodeling but there is no data related to early remodeling.
MMPS inhibition is promising and has been shown to attenuate early LV remodeling in animals but experience in humans is still missing(4). MMPs’ activity depends on their transcription, activation, and inhibition. MMP transcription is stimulated by IL-1, PDGF, and TNF- , and inhibited by TGF-ß, retinoids, heparin, and corticosteroids. Activation of latent pro-MMPs to active MMPs is stimulated largely by (uPA)/plasmin system, and inhibited by TIMPs. Inhibition of activated MMPs by TIMPs and drugs, such as tetracyclines, anthracyclines, synthetic TIMP inhibitors, regulate the proteolysis of ECCM(5).
The incidence of VSR in the pre-thrombolytic era was between 1-3 percent, and has declined with the use of fibrinolytic agents to 0.2 percent(5). The time of occurrence has changed from 3-5 days from the onset of the AMI in the pre-thrombolytic era to less than 24 hours with thrombolysis(6). The known risk determinants for this complication are, advanced age, female sex, no previous smoking, anterior MI, worse killip class and, increased heart rate on admission(6). On angiography, there is a higher occurance of total occlusion of the IRA (57%), usually the LAD, less collaterals with low TIMI flow and low ejection fraction(7). The Shunt degree depends on the size of the VSD, the ratio of pulmonic vascular resistance to systemic resistance and the the contractility of both ventricules.
Mortality at 30 days is higher in patients with VSR than in those without this complication (73.8% versus 6.8%, P<0.001). Patients with VSDs selected for surgical repair have better outcomes than patients treated medically (30-day mortality, 47% versus 94%) (7). When the clinical presentation is cardiogenic shock with RV dysfunction in the setting of inferior wall MI, the prognosis is grave.
FWR develops with large transmural anterior wall MI, that involves more than 20 percent of the LV. It is usually preceded by infarct expansion, it appears in the junction of the infarct and the normal muscle and it rarely occurs in the thickened ventricule with good collaterals. It can present as an acute tear with immediate death or subacute allowing opportunity for intervention. Rupture can occur as early as the first day after infarction, although it most often occurs later in the first week in the setting of myocardial necrosis and neutrophilic infiltration(9).
It is a fatal compliction that contributes to 10 percent of AMI mortality and it is the second cause of death after pump failure(5). The incidence of FWR can probably be reduced by reducing infarct size with immediate reperfusion, avoiding agents that interfere with the healing process like steroids and NSAID, and attenuating wall stress. Survival depends on immediate diagnosis, hemodynamic stabilisation and prompt surgical repair(5). Delayed thrombolysis increases the risk and primary PCI reduces it(9).
In the acute stage of AMI, the etiology of mitral regurgitation is either papillary muscle dysfunction/ rupture or rupture of chordae. In the chronic stage, mitral annulus dilation, tethering of mitral leaflets and localised wall motion abnormalities are the mechanisms underlying MR. In the acute setting the volume of regurgitation, LV function and LA compliance determine the clinical presentation and the prognosis.
Patients with chronic ischemic MR have a higher cardiovascular mortality rate compaired to no MR (29 % vs 12%, p<0.001, 3.5 y follow up ), higher rate of persistently occluded IRA (27.3% vs 15.2%, p=0, 001), larger LV volume and they develop more often severe heart failure(12). A MR increase significantly the 5 year cardiac and total mortality of patients with reduced LV function with a relative risk of 1.83 and 1.88 respectively(13).
Mitral valve replacement is the procedure of choice for acute MR, yet mitral valve repair may be feasible(11). In the Shock trial, patients with cardiogenic shock and severe MR had inferior wall MI in 55 percent of the cases and posterior MI in 32 percent. Mean LVEF was 37 percent and in-hospital mortality was 55 percent. The majority did not undergo mitral valve surgery, but among those who were operated mean LVEF was higher and in-hospital mortality was lower, at 39 percent(10).
Prevention of all these severe complications can be achieved by/with : 1-Early and efficient reperfusion and surgical repair 2-Preventing reperfusion injury 3-Preventing breakdown of extracellular collagen, necrosis and apoptosis. 4-Preserving the microcirculation 5-Modulation of tissue repair like hypertrophy and fibrosis
The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.
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