that forms a myocardial pocket. Dyskinesis without an aneurysm implies that the myocardium protrudes only during systole, whereas an aneu- rysm protrudes in both systole and diastole, forming a separate chamber, and always has thin walls. LV aneurysm usually reflects the presence of extensive transmural necrosis; contrarily, dyskinesis may be seen with acute reversible ischemia, post-ischemic stunning, or takotsubo cardiomyopahty without any necrosis, in which case the myocardial wall is not thin (it may appear thin in systole from the lack of thickening, but it is not thin in diastole). Dyskinesis without an aneurysm is much more common than a true aneurysm.
LV aneurysm is a form of adverse LV remodeling and dilatation of the necrotic area. ~50% develop acutely in the first 48 hours, from early dilatation of the necrotic, expansile myocardium, and the remainder usually appear within 2 weeks.157 The mature, thick scar appears several weeks later, followed by calcifications. The early use of ACE-I, β-blocker, and aggressive blood pressure control prevents LV aneurysm from appearing or expanding.
An aneurysm leads to increased preload and afterload, and a double mortality for the same EF.158 LV aneurysm occurs in 5% of STEMI cases, mainly anteroapical STEMI (80% of LV aneurysms are anteroapical; the rest are inferoposterior). LV aneurysm may initiate or worsen: (i) HF, (ii) angina (from the adverse loading conditions), (iii) VT, and (iv) mural thrombosis.
The diagnosis is made by echo. ST elevation that persists >3 weeks suggests LV aneurysm, but may also be seen with a dyskinetic, often non-viable wall.
Treatment consists of standard HF therapy which aims to reverse LV remodeling. Aneurysmectomy is indicated for refractory HF or refractory VT, mainly in conjunction with CABG. Operative mortality is <10%.
B. LV pseudoaneurysm
Pseudoaneurysm is a myocardial rupture that has been sealed by pericardium, organized thrombus and fibrosis. Unlike a true LV aneurysm, the LV pseudoaneurysmal wall does not contain any myocardium. Note that thrombus is layered inside both the LV aneurysm and LV pseudoaneurysm. A pseudoaneurysm may also be seen after trauma or cardiac surgery (especially mitral surgery, at the posterobasal level) (Figure 2.7).
A pseudoaneurysm has a 40–50% risk of progressing to a full rupture, and thus warrants urgent surgical suturing. Rupture often occurs in the first week,159 but rupture of chronic pseudoaneurysms, even small pseudoaneurysms, has been described.160 Conversely, a true aneurysm does not rupture (it may, rarely, rupture in the first 2 weeks of MI, but does not rupture later on, once it is fully fibrosed).
The distinction between a true LV aneurysm and a pseudoaneurysm is made by echo: a pseudoaneurysm has a narrow neck with a neck-to-internal diameter ratio <0.5,161 although occasionally in large cases, it can be 0.5–1.159 Doppler may also support the diagnosis of
pseudoaneurysm by showing a to-and-fro turbulent flow through the narrow neck, which corresponds to a murmur on exam. However, echo-Doppler does not always allow this distinction. MRI may be used in equivocal cases and shows loss of epicardial fat across the pseudoaneurysm.
Figure 2.7 LV aneurysm and LV pseudoaneurysm.
In comparison with the normal LV, note the bulging pocket seen in LV aneurysm and LV pseudoaneurysm. The aneurysmal wall consists of thin scarred myocardium ± clot, whereas the pseudoaneurysmal wall consists of adherent pericardium and clot (stars). The neck of the LV pseudoaneurysm is narrow; the neck/internal diameter ratio is <0.5 in pseudoaneurysm vs. >0.5, usually 0.8–1, in aneurysm (ratio of double arrows). The dyskinetic motion of the aneurysm is indicated by the horizontal arrows.
Left ventriculography is also highly accurate in distinguishing an aneurysm from a pseudoaneurysm.159 In case of a pseudoaneurysm, it shows a pocket with a contrast stain that persists over multiple beats. Moreover, in contrast with a true aneurysm, the coronary arteries do not extend over the pseudoaneurysmal wall.
VII. Pericardial complications
A. Acute post-infarction pericarditis
In the reperfusion era, inflammatory pericarditis occurs in ~5% of STEMIs, usually large or anterior STEMIs (it was more common in the pre-reperfusion era, ~10–20%). Less commonly, it may occur in large NSTEMIs. The incidence is higher if only pericarditic chest pain is used to define post-infarction pericarditis, without mandating a rub.162 On the other hand, asymptomatic rubs are also common in the first 48 hours of MI. Pericarditis, including asymptomatic rub, correlates with a larger MI size, and thus carries a worse prognosis despite being innocuous per se.
A minimal or small pericardial effusion is seen in up to a third of patients with MI.163 Pericarditis and pericardial effusion do not neces- sarily coincide. Over half of pericarditis cases are not associated with any effusion; similarly, half of pericardial effusions are not inflammatory (no rub), and rather result from pump failure and transudation.163
1 Diagnosis – Pericarditis develops in the first few days of MI, most commonly the first or second day, and usually lasts a few days only. The pain is typically pleuritic, and radiation to the trapezius is characteristic. A fleeting rub may be heard. On ECG, a pattern of diffuse pericarditis with diffuse ST elevation is rare (<20%);162 rather, pericarditis is localized to the infarcted area with ECG findings of localized ST elevation. The latter may simulate reinfarction or may be overshadowed by the pre-existing ST elevation. The persistence of upright T waves or the reversal from inverted T waves to upright T waves very early after MI is 100% sensitive for the diagnosis of pericarditis, but may also be seen with ischemia (normally, inverted T waves are seen a few hours after MI onset, and persist several days at least).164
2 Treatment – NSAIDs should not be used post-MI because of the risk of adverse LV remodeling and free wall rupture. High-dose aspirin (325–650 mg Q 6–8 h) may be used; alternatively, acetaminophen or colchicine may be used for this transient process.The risk of hemorrhagic transformation of acute post-MI pericarditis is theoretical and very rarely reported. Thus, pericarditis should not alter the antiplatelet regimen and anticoagulation may be continued in patients who need it, with close monitoring. However, in the presence of a moderate or large effusion, anticoagulants are preferably discontinued (antiplatelet agents are usually continued).
B. Pericardial effusion
Small pericardial effusions (5–9 mm) are seen in 5% of STEMIs, usually appearing during the first 5 days and slowly resolving over several weeks.165,166 A small pericardial effusion may be secondary to pericarditis or to pump failure and may be associated with an increase in long-term mortality. It is not usually associated with a free wall rupture unless it progresses to a moderate effusion, which happens in a minority of patients.166 Echo surveillance is warranted even for a small effusion.
Moderate or large pericardial effusions (≥10 mm) were seen in 5% of STEMIs before the reperfusion era, and are probably less common in the PCI era. A moderate pericardial effusion, even if asymptomatic, is associated with an 8% risk of death from free wall rupture, which tends to occur over a week late. While it may result from pump failure or pericarditis in some patients, a moderate pericardial effusion represents a sealed, subacute myocardial rupture with self-limited bleeding in a substantial proportion of patients. A large effusion with tamponade or pulseless electrical activity is usually due to free wall rupture and warrants emergent surgical repair. A moderate effusion, if diagnosed on a pre-discharge echo or in a symptomatic patient, warrants at least more prolonged monitoring, close echo surveillance, and potentially a cardiac MRI to diagnose impending rupture. Anticoagulation should be discontinued.
C. Dressler syndrome