Practical Cardiovascular Medicine. Elias B. Hanna

      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 complication

       Relative sinus bradycardia or AV block

       Prior MI or LV dysfunction

       Superdominant RCA with apical, posterior, or lateral involvement

      In the SHOCK trial and registry, ~60% of patients with LV shock had anterior MI, while 34% had inferior MI without any acute anterior involvement.^73,102 Concerning the latter 34% of patients, 14% had prior MI and 11% had concomitant apical, posterior or lateral involvement, while only 9% had isolated, new inferior MI.¹⁰²

      B. Pathophysiology of LV-related cardiogenic shock and failure in acute MI

      In the SHOCK trial, LVEF was ~30 ± 12%, implying that at least half the patients only had a moderate LV insult and a moderate reduction of LV systolic function.⁷³ Also, ~40% of patients had non-anterior MI, mainly inferior MI.^73,102 Thus, an EF that is well tolerated in chronic HF may be associated with cardiogenic shock in acute MI. In a way, this is similar to tolerating chronic MR or AI vs. developing shock with acute MR or AI. Beside systolic dysfunction, several mechanisms explain cardiogenic shock in acute MI:

       While the progressive LV dilatation that occurs chronically raises afterload and is maladaptive, some early degree of LV dilatation is adaptive and increases stroke volume at a given LV contractility. Also, some degree of LA dilatation is adaptive and lessens the rise in backward pressure. This is similar to the chronic LV adaptation to MR or AI. In fact, half of patients with cardiogenic shock have a small or normal-size LV, which represents failure of the mechanism of acute LV dilatation.103,104

Table 2.4 Differential diagnosis of shock in MI.

LV-related cardiogenic shock: anterior MI, MI with a prior history of MI or LV dysfunction, or MI in a patient with multivessel CAD. Cardiogenic shock occurs in 4–7% of STEMI (vs. 2.5% of NSTEMI). It is occasionally present on admission, and more typically develops soon after admission, at a median of 5.5 hours after MI onset (vs. a later shock development, at ~3 days, in NSTEMI with three-vessel disease).RV infarct: RV-related shock should be considered whenever hypotension occurs in inferior MI. RV infarct occurs in 30% of inferior MIs, mainly with proximal RCA occlusion. Only one-half of RV infarcts produce clinical RV failure.Mechanical complications (mitral regurgitation, ventricular septal rupture, free wall rupture) or tamponade.Arrhythmias (inappropriate bradycardia, advanced AV block, VT).Vagal stimulation and vagal shock in inferior MI. It manifests as bradycardia with clear lungs and low JVP. It is treated with atropine and fluid administration.Hypovolemic hypotension: hypotension with clear lungs, low JVP, and no bradycardia. May attempt small fluid challenge in this situation.

      During or after PCI, shock may develop from the use of sedative and vasodilatory drugs in a patient with limited cardiac output reserve, or from