cut through the true apex. Delayed-enhancement MRI allows an accurate diagnosis and allows the distinction between thrombus and the underlying myocardial scar.172
Treatment – Warfarin anticoagulation almost abolishes the embolization risk.168,170,172 In addition, warfarin allows intrinsic lysis of the thrombus or, at least, organization and endothelialization. In fact, ~60-70% of LV thrombi resolve within 6–12 months of anticoagulation, while the rest organize and become laminated. It is believed that an organized thrombus actually has beneficial effects, as it adheres to the dyskinetic apex preventing further infarct expansion and reducing the paradoxical myocardial motion by a plugging effect.
Thus, ACC guidelines recommend the use of warfarin for at least 3 months in patients with LV thrombus (class IIa), as most emboli occur within 3 months of MI.171 Warfarin may be beneficial beyond 3 months in patients who continue to have a low bleeding risk and a high embolic risk, such as: (i) history of embolization; (ii) severe HF or LV dilatation with EF<35%, ischemic or not. One study of patients with LV thrombus, most of whom had ischemic cardiomyopathy with apical akinesis, suggested a benefit of prolonged anticoagulant therapy >3 months, particularly if EF<35%.173 It is unclear whether dual antiplatelet therapy has any effect on LV thrombus, and thus, anticoagulation seems warranted on top of antiplatelet therapy, particularly for the first 3 months. NOACs have been used and found to be comparable to warfarin in one retrospective study,173 but significantly inferior in a larger study.174
IX. Early and late mortality after STEMI
Over half of the STEMI fatalities occur suddenly outside the hospital (VF). For patients who present to the hospital, the short-term mortality (30 days) is, on average, 4–5% for patients treated with primary PCI, 6–7% for patients treated with fibrinolytics, and ~11–12% for patients not treated with reperfusion therapy. This varies according to the risk criteria listed in Section 1.XI (Killip class and TIMI risk score), the ST-segment response to reperfusion therapy, and the coronary microvascular perfusion achieved with reperfusion therapy.
Afterward, the yearly mortality is 2–6% depending on the degree of LV dysfunction, the presence of HF, and the presence and extent of residual severe CAD.
The risk of sudden death is highest in the first 30 days after MI (1.2%), followed by a 1.2% sudden death risk per year.98 The risk is higher in patients with HF or severe LV dysfunction (2.5–3%).
Note that NSTEMI has the same short- and long-term mortality as STEMI (but lower in-hospital mortality).175
Appendix 1. Out-of-hospital cardiac arrest: role of early coronary angiography and therapeutic hypothermia
Of 100 patients suffering out-of-hospital cardiac arrest (OHCA), ~30–40 are successfully resuscitated in the field with return of spontaneous circulation and reach the hospital. Of those 30–40, ~5–10 survive to hospital discharge (5–10% overall survival).176 A better survival is seen in patients whose initial rhythm is VF/VT (22% survival to discharge). In patients with VF, the survival decreases by 7–10% for each minute of delay to defibrillation. The prognosis is very poor in patients with non-shockable rhythm: survival to hospital discharge 10% for PEA and 2% for asystole. Some patients with non-shockable rhythm develop VT/VF during the course of resuscitation, but they should still be considered as non-shockable rhythm for the purposes of prognosis and therapy.177
A. Decision to perform immediate coronary angiography and role of post-resuscitation ECG
The large COACT trial randomized comatose patients with resuscitated OHCA, whose initial rhythm was VT/VF, and whose post-arrest ECG did not show STEMI (~70% of OHCA), to immediate coronary angiography vs. coronary angiography delayed until neurological recovery. The 90-day survival was similar in both groups (~65%).178 There was no benefit of immediate coronary angiography, even though the trial selected patients with favorable features for neurological recovery (mostly witnessed arrest, with only 2 min from arrest to basic life support, and 15 min to return of spontaneous circulation, pH 7.2). Importantly, while most patients had CAD (~65%, including prior PCI or CABG in ~35%), most of this CAD was chronic stable CAD (CTO 37%) and VT/VF was related to ischemic cardiomyopathy and old scars/infarcts rather than active ischemia; only ~5% of patients had acute thrombotic occlusion and ~15% had unstable coronary lesions. Another large trial, TOMAHAWK, confirmed this lack of benefit from immediate coronary angiography, which was conversely associated with a trend toward more death and severe neurological deficit; a culprit coronary lesion was identified in 39% of patients.179–181
The initial neurological status, upon return of spontaneous circulation, is a strong determinant of survival. In patients who regain consciousness early on or who display response to pain or stimuli, the survival to hospital discharge with good neurological status is >90%.181,182 Conversely, the prognosis is particularly poor in patients who are totally unresponsive, who are missing multiple brainstem reflexes, or who display early myoclonic jerks.
In addition, older age (>75-80), initial non-shockable rhythm, unwitnessed arrest or delayed initiation of cardiac compressions (>10 min), prolonged resuscitation before return of spontaneous circulation (>20 min, >3 doses of epinephrine required), and low pH<7.2 indicate a poor likelihood of neurological recovery and argue against immediate coronary angiography, particularly in the absence of ST elevation (ESC).2,183 Proper cardiac compressions only provide ~20% of the normal cardiac output.
Overall, immediate coronary angiography is indicated in the following cases (ESC, SCAI 2020):2,177
Post-resuscitation ECG consistent with STEMI and favorable neurological predictors are present. If multiple unfavorable predictors are present in a comatose patient, treatment is individualized, and coronary angiography may be deferred (SCAI).
In the absence of ST elevation, quickly evaluate for non-cardiac causes (intracranial hemorrhage, respiratory failure, PE, sepsis), take into consideration Q waves (old scar?) and pronounced ST depression (active ischemia?), and consider urgent echocardiography. Coronary angiography does not need to be performed immediately, unless: (a) myocardial ischemia appears likely, with (b) persistent shock and (c) no poor neurological predictors.
Note that, when indicated, immediate coronary angiography is performed in patients who are successfully resuscitated and whose systemic pressure is maintained on reasonable and stable doses of vasopressors. The performance of PCI in patients actively receiving chest compressions, using an external compression device, did not improve the grim mortality in one study and was not recommended in an expert viewpoint.176,184
Note: 5–15% of patients with ST elevation and OHCA do not have acute coronary occlusion.179-181 In those cases, ST elevation is related to a myocardial injury from the cardiac arrest itself, hyperkalemia, PE, or intracranial hemorrhage. One Korean study has shown that up to 19% of OHCA patients with ST elevation or, more so, ST depression have intracranial hemorrhage as a cause of the OHCA.
B. Role of post-resuscitation echocardiography
Echo often shows LV dysfunction that is non-specific, as it may be secondary to acute ischemia but also post-cardiac arrest myocardial stunning or chronic cardiomyopathy. Echo may be more specific in some settings, particularly when segmental dysfunction is present: (i) segmental akinesis of a thin myocardium with Q waves and no ST elevation suggests an old infarct and a scar-related VF, rather than acute ischemia VF; (ii) segmental akinesis without Q waves suggests acute ischemia; (iii) preserved LV function with akinetic or dilated RV suggests massive PE.
