acute MR, because of the near-equalization of LV and LA pressures. The murmur is usually loud in VSR and is associated with a thrill at the left lower sternal border.
E. Diagnosis
1 Transthoracic echo (TTE) is the initial test. TTE shows a left-to-right shunt in VSR. It may miss severe acute MR because of the narrowing of the pressure difference between the LV and the LA, leading to attenuation of the regurgitant color flow. TTE may show a pericardial effusion with layered echodensities, corresponding to blood, in free wall rupture; however, it may miss a sealed rupture (an effusion is not seen in 25% of sealed ruptures).125
2 If the severity/mechanism of MR is unclear on TTE in a patient with shock, perform transesophageal echocardiography.
3 MRI is needed when a sealed free wall rupture is suspected but not well delineated by echo.
4 Right heart catheterization may also be useful to diagnose VSR and MR:In VSR, there is O2 saturation step-up ≥7% between RA and RV.In MR, PCWP tracing has a giant V wave; however, a large V wave is also seen with VSR or severe LV failure. In both MR and VSR,PCWP is higher than LVEDP.
5 Left ventriculography may be performed during PCI in a patient with cardiogenic shock. It allows the diagnosis of severe MR, VSR, or free wall rupture.
F. Treatment
All mechanical complications are treated by emergent surgical repair and coronary revascularization. Surgery reduces mortality from 90–100% to ~20–50%.
1 MR – Papillary muscle rupture dictates emergent valvular surgery + CABG. Place IABP preoperatively and administer IV vasodilators (nitroprusside) as in all cases of acute severe MR. Mitral valve replacement is most often performed as it is more expeditious than repair, and it is difficult to sew necrotic tissue. The operative mortality is 20–40%.121When severe acute MR is secondary to acute mitral leaflet tethering, the patient may be treated with percutaneous revascularization, vasodilators and temporary IABP support. It is expected that leaflet tethering improves once the function of the reperfused territory improves.128-130 This is not the case in chronic leaflet tethering seen with chronic infarction. Surgery should be considered a second-line therapy for those patients who do not improve with medical therapy.
2 VSR – The operative mortality is high, ~50%, as it is difficult to sew the necrotic friable septum. Mortality is higher in basal-inferior VSR, because the latter is more serpiginous and often associated with RV infarct. Prepare the patient with IABP/nitroprusside/inotropes. Even a small VSR requires surgical repair, as the tear may rapidly and unpredictably progress to hemodynamic collapse.
The long-term survival of patients who survive any of the three mechanical complications is good.
Figure 2.6 Dynamic left ventricular outflow tract obstruction in apical infarction.
G. Another mechanical complication: dynamic left ventricular outflow tract obstruction
This complication occurs in 1–2% of MIs and up to 12% of anterior MIs in women. It is due to anteroapical akinesis associated with a compensatory hyperkinesis of the LV base. This narrows the LVOT and leads to drawing of the mitral valve to the septum and systolic ante- rior motion (SAM) of the mitral valve, similar to HOCM (Figure 2.6).131
Hypotension and pulmonary edema may subsequently occur. Clinically, a new, dynamic systolic murmur, similar to HOCM murmur, is heard. MR murmur (SAM) may also be heard.
As opposed to the treatment of cardiogenic shock, inotropes, diuretics, and IABP should be avoided, as they worsen the basal hyper- kinesis and LVOT narrowing. β-Blockers are used to reduce the LVOT hyperkinesis. α-Agonists may be used in case of hypotension.
III. Recurrent infarction and ischemia
Within 30 days, recurrent infarction or ischemia occurs in ~10–15% of patients treated with fibrinolytic therapy, vs. <4% of patients treated with PCI (less so with stenting, ~2%).26,44,45 Recurrent infarction is usually due to reocclusion and is also called “infarct extension,” which is different from “infarct expansion” (LV remodeling).
It is diagnosed based on clinical grounds, ECG, and a reincrease of a downtrending troponin by >20%.
Treatment – Escalate β-blockers, NTG, and readminister anticoagulants. Emergent PCI is indicated in STEMI or hemodynamic instability. Otherwise, a non-urgent coronary angiogram is usually performed. For recurrent ST elevation, the fibrin-specific fibrinolytics may be (re-)administered if PCI cannot be performed in a timely fashion.
IV. Tachyarrhythmias
A. Ventricular tachyarrhythmias: VF and sudden death
Improvements in reperfusion therapy have reduced the 30-day mortality of a STEMI patient presenting to the hospital from 15% to 5–6%. Yet, out-of-hospital mortality remains very high, and is responsible for most MI fatalities, mainly in the first hour after MI onset. In fact, the risk of out-of-hospital cardiac arrest in STEMI is ~30%,132,133 mainly in the first hour after STEMI onset, when over half of all VF episodes occur;134 and between hours 1 and 4, where most of the remaining VF events occur.
Conversely, for patients who make it to the hospital without cardiac arrest, the risk of primary VF within 48 hours is ~4%, mostly in the first 4 hours after symptom onset, and the risk of VT and/or VF is ~10%.135
B. Ventricular tachyarrhythmias: VF
In the reperfusion era, sustained VF occurs in 4% of patients hospitalized with acute STEMI. There are three types of VF, mostly character- ized in fibrinolytic trials:
Primary VF is defined as VF occurring in the first 48 hours after MI without an associated shock or severe HF. It occurs because of rapid potassium fluxes with increased automaticity and dispersion of repolarization, or increased sympathetic or vagal tone. It mostly occurs in the first 4 hours. Primary VF, whether in the first 4 hours or at 4–48 hours, is associated with a 2–4 times increased in-hospital mortality, from the VF episode itself, VF recurrence, or the larger ischemic burden. However, VF does not affect long-term mortality in survivors, even on unadjusted analyses.135–137 In fact, primary VF correlates with the extent of initial ischemia and is much more commonly seen in STEMI than NSTEMI, but does not correlate with the eventual infarct size and is at least as frequently seen in inferior as in anterior MI (GISSI-2, Apex-AMI analyses). Sinus bradycardia or pauses may precipitate VF in patients with inferior MI.Even after primary PCI, a small but significant proportion of patients have VT/VF at 24–48 hours (~1.5% of patients).138,139 This post-PCI VT/VF carries an increase in short-term,139 but not long-term, mortality.
Post-PCI VF may reflect stent thrombosis and warrants thorough clinical and ECG investigation.
Secondary VF is defined as VF occurring in association with HF or shock (<48 h or >48 h) and portends
