mitral regurgitation (MR)
Posterior leaflet tethering – A degree of ischemic MR is seen in ~30% of acute MI. Inferior MI with localized inferior/posterior akinesis pulls the posterior papillary muscle posterolaterally, with subsequent tethering of the posterior mitral leaflet (predominantly). This tether- ing may lead to severe MR, a dynamic form of MR that may be mild at rest and severe with increased ventricular loading. Tethering may also occur with anterior MI and is usually a posterior tethering as well. In anterior MI, posterior tethering is secondary to global LV dilatation.
Papillary muscle rupture – Severe MR may result from rupture of a papillary muscle head, usually the posterior papillary muscle in the context of an inferior or posterior MI (two-thirds of severe MR cases in the SHOCK registry).121 The posterior papillary muscle is supplied by one artery, the PDA (from a dominant RCA or LCx), whereas the anterolateral muscle has a dual blood supply from the LAD (usuallyfirst diagonal) and the LCx. Papillary muscle rupture occurs in ~1% of MIs, and, unlike ventricular septal rupture, the infarct is relatively small in 50% of the cases. Each papillary muscle extends chordae to both leaflets, and therefore flailing of either or both leaflets may occur with rupture of either papillary muscle.Echo distinguishes papillary muscle rupture (treated surgically) from leaflet tethering (initially treated with revascularization and supportive measures). In the former, the leaflet(s) are flail, prolapsed, with flailing of chordae and flailing of an echogenic piece of papillary muscle; in the latter, the posterior leaflet is restricted and the jet is usually posterior.
B.Ventricular septal rupture (VSR) occurs in ~1% of MIs (only 0.2% of reperfused MIs). Anterior MI (LAD) and inferior MI (mainly RCA) were equally common causes of VSR in the SHOCK registry, while other registries suggest that anterior MI is slightly more common.122 Patients with a wrap-around LAD have less septal collaterals and are at a higher risk of septal rupture with anterior MI. The location is apical septal in anterior MI and basal inferior in inferior MI. VSR leads to a severe left-to-right shunting with severe hypotension and LV volume overload.
C.Free wall rupture occurs in ~2% of MIs and is the most common and most underdiagnosed mechanical complication (≤1.5% of patients treated with PCI, 3% of patients treated with thrombolysis, 6% of patients not reperfused).123,124 The most common location is anterior MI (LAD culprit); the second most common location is lateral MI (LCx culprit).125
Free wall rupture often leads to tamponade and a bradycardic pulseless electrical activity. It commonly has one of the following pro- dromes: chest pain, re-elevation of ST segments, bradycardia, or syncope from a vagal shock.124 In ~30% of the cases, it is preceded by a concealed rupture and a moderate pericardial effusion, where the pericardium temporarily seals the rupture.124
Risk factors for VSR and free wall rupture: female sex, older age, first MI, absence of collaterals, history of HTN, anterior MI. Also, the use of NSAIDs or steroids increases the risk of rupture. Anticoagulants do not clearly increase the risk of rupture.
Reperfusion with thrombolysis or PCI reduces the incidence of all mechanical complications. While early thrombolysis reduces the risk of free wall rupture, late thrombolysis >12 hours, particularly in elderly patients, may increase the risk of free wall rupture according to a meta-analysis of thrombolytic trials.126,127
The majority of patients with VSR have multivessel disease, while patients with papillary muscle or free wall rupture usually have a single-vessel disease with good LV function.
D. Clinical manifestations
Patients with either MR or VSR present with cardiogenic shock and pulmonary edema.
Pulmonary edema is less marked with VSR than with MR. Patients with VSR can typically lie supine, which is not the case with MR.
The murmur may be faint or absent with 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