Читать книгу Practical Cardiovascular Medicine - Elias B. Hanna - Страница 120

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.