IV: cardiogenic shock (mortality = 50–60%)
Note that Killip classification is only applied at presentation. It also has a prognostic value in NSTE-ACS.
B. TIMI risk score for STEMI
Depending on the STEMI TIMI risk score (Table 2.3), the 30-day mortality of fibrinolytic-treated STEMI patients ranges from 1% to 35%.97 The benefit of reperfusion is highest in the higher risk groups.
C.Troponin I peaks at a level of 50–300 ng/ml (at ~24 h), CK typically peaks at 2500–5000 units/l (at 18–24 h). Reperfusion therapy makes these biomarkers peak earlier and often at higher levels; however, the total volume of CK or troponin released is smaller, i.e., the distribution curves over time are narrower and the decline is faster (3–4 days for troponin I). The CK or troponin mass, rather than the CK or troponin peak, correlates with the infarct size and the prognosis. Aborted STEMI, whether aborted spontaneously or with very early reperfusion, is characterized by a biomarker rise that is usually mild (CK-MB <2× normal).
XII. LV remodeling and infarct expansion after MI (see Figure 2.5)
XIII. Discharge, EF improvement, ICD
A. Discharge medications
See Chapter 1, Section VI.
B.EF improves 1–3 months after discharge and justifies follow-up echocardiography for risk assessment. There are two explanations for EF improvement:
LV dysfunction that occurs immediately after MI is partly due to post-ischemic stunning rather than necrosis. When an artery occludes transiently, necrosis occurs in part of the myocardium, while dysfunction without necrosis, called stunning, occurs in other parts. The stunned myocardium recovers over the course of days to weeks after arterial recanalization.
ACE-Is, β-blockers, and aldosterone antagonists reduce LV remodeling and LV size, allowing an increase in EF for the same amount of necrotic myocardium (Figure 2.5). Each one of these drugs allows an EF improvement of up to 5%.
C. ICD
The risk of sudden death is highest in the first 30 days after MI (1.2%) and increases with HF and severe LV dysfunction (~3%).98 However, placing an ICD in the first 40 days after MI has not been shown to reduce the overall mortality; it reduces sudden-death mortality by 50%, but the patients prone to early sudden death are typically high-risk patients also prone to dying from pump failure or recurrent MI.99,100 Early ICD placement only changes the mode of death of these patients, from sudden death to pump-failure death (conversion hypothesis). Also, early LV dysfunction/stunning may improve and some patients may turn out to be at a lower long-term risk than expected, and thus would not require an ICD. Therefore, ICD is indicated for primary prevention of VT/VF if EF is ≤35% at 40 days post-MI.
On the other hand, ICD is indicated early on, before hospital discharge, for the patient who develops sustained VT or VF anytime beyond the first 2 days after MI.
Table 2.3 STEMI TIMI risk score.
| Variable | Score |
|---|---|
| Age ≥65 yr / ≥75 yr | 2 for ≥65; 3 for ≥75 |
| SBP <100 mmHg | 3 |
| Sinus tachycardia >100 bpm | 2 |
| Killip class ≥ II | 2 |
| Anterior location of MI or LBBB | 1 |
| Prior history of diabetes, HTN, or angina | 1 |
| Time to treatment >4 h after symptom onset | 1 |
| Weight <67 kg (higher bleeding with fibrinolytics) | 1 |
30-day mortality according to the score: score ≤2 → <2.2%; score 3–4 → 4–7%; score ≥5→ >12%.
Figure 2.5, Stages of negative LV remodeling post-MI, also called infarct expansion.
For the same amount of necrosis, the dashed infarcted area thins and stretches out (from 1 to 2). Then, this stretched infarcted area increases tension at its edges (arrows), which eventually leads to progressive dilatation of the normal, non-necrotic myocardium (from 2 to 3). The dilatation occurs as a compensatory attempt to increase stroke volume, albeit counterproductive and maladaptive. The LV loses its normal elliptical shape and becomes a sphere, which further increases wall stress and reduces the efficiency of the non-infarcted myocardium.
Thus, for the same amount of tissue necrosis the infarcted area and the EF vary largely, depending on:
1 Loading conditions.
2 Opening of the occluded artery, even at a time when necrosis has already occurred (e.g., 3–24 h). Reperfusion accelerates myocardial scar formation and turgor and reduces the thinning of the necrotic area, even if it does not salvage myocardium beyond 3–6 hours.
3 Medical therapy: ACE-Is reduce afterload and exert a direct myocardial effect that reduces LV dilatation and reduces fibrosis in peri-infarct areas. Aldosterone antagonists also exert a direct myocardial effect that reduces LV dilatation and fibrosis. β-Blockers reduce the high wall stress induced by the sympathetic tone. Diuretics reduce preload and afterload.
2. STEMI COMPLICATIONS
I. Cardiogenic shock
A. Differential diagnosis (see Table 2.4)
Clinically, RV-related shock leads to a high JVP and clear lungs, whereas LV-related shock leads to a high JVP with pulmonary edema. PCWP is frequently increased in RV shock, with a mean PCWP of 23 mmHg, because of concomitant LV failure and RV/ LV interdependence.101
When a patient with inferior MI develops cardiogenic shock, consider the following:
RV shock
Mechanical
