Acute mechanical complications of MI include sequelae from left or right ventricular systolic impairment or a loss of structural integrity that results in cardiac wall rupture, papillary muscle rupture, or ventricular septal rupture. Broadly, the latter share the same pathogenesis: myocyte necrosis, interstitial edema, inflammation, and matrix metalloproteinase secretion and activations that lead to degradation of the extracellular matrix impairing structural integrity.²,³,⁴ Complete coronary occlusion and transmural infarction are the biggest risk factors for acute mechanical complication, with the timing of clinical presentation occurring in a bimodal distribution; most manifest within the first 24 hours of MI and the remainder in the following week.⁵ The clinical presentations include an acute deterioration in symptoms that may be nonspecific, new or worse chest pain, cardiogenic shock, and sudden cardiac death. In patients with these presentations, urgent transthoracic echocardiography is critical in establishing the diagnosis. Mechanical complications can also be diagnosed on contrast ventriculography at the time of angiography or by alternative imaging modalities such as computerized tomographic (CT) scanning (if performed to rule out dissection or pulmonary embolus for symptoms) or cardiac magnetic resonance imaging (MRI).

Optimal management of acute mechanical complications involves a multidisciplinary team including cardiologists, cardiothoracic surgeons, intensivists, and advanced imaging specialists, and should ideally occur in specialized cardiac centers equipped to care for these high-risk patients.

Cardiogenic shock is defined by persistent hypotension (systolic blood pressure ≤90 mm Hg) despite adequate volume replacement accompanied by signs of hypoperfusion (oliguria, cool peripheries, altered mental status, or end-organ hypoperfusion).⁶ Although cardiogenic shock can result from structural complications (ie, septal rupture, papillary muscle rupture, ventricular septal defect, etc), the commonest cause remains depressed left ventricular (LV) function and less commonly right ventricular (RV) infarction. The incidence of cardiogenic shock following acute MI is variably described in registries as between 3% and 13%. Despite a reduction in incidence as a result of coronary reperfusion, it remains a leading cause of death with in-hospital mortality rates of 50% or more. Patients are most likely to develop cardiogenic shock within the first 24 hours of admission after MI. Elevation of serum lactate and creatinine levels is associated with a higher mortality, as is RV dysfunction complicating LV failure. Accordingly, echocardiography is helpful in assessing LV and RV function. The treatment of cardiogenic shock complicating MI is multipronged⁷: early revascularization of the infarct-related artery with percutaneous coronary intervention (PCI) is recommended (or failing that, coronary artery bypass graft surgery [CABG]), followed by hemodynamic monitoring and support in an intensive care environment. Most patients with cardiogenic shock have multivessel coronary disease, and the management strategy of nonculprit vessels has been a subject of recent study. The CULPRITSHOCK⁸ trial found a reduction in death and renal failure at 30 days in patients undergoing PCI to the culprit-vessel only
as compared to complete revascularization. This has been reflected in a recommendation to defer non-infarct-related artery PCI.⁷ Mechanical support measures may be considered in individualized cases, but at present there is a lack of evidence for these to be used routinely.

Right ventricular infarction complicates up to 50% of inferior MIs and can be diagnosed by detecting ST elevation in electrocardiographic leads aVR and V1 or the right precordial leads (V3R and V4R). The presence of RV infarction increases the risk of cardiogenic shock, arrhythmia, and death with reported mortality at one year being 18% in those with isolated right coronary artery lesions and 27% in the presence of left and right coronary artery disease. Most RV MIs involve a dominant right coronary artery occluded proximal to the RV branches, but it may be associated with a left-dominant circumflex occlusion, or rarely the left anterior descending (LAD) if it provides collaterals to the RV free wall. As a result of the coronary anatomy involved, RV MI may be complicated by bradyarrhythmia and atrioventricular (AV) nodal block. The classic triad of hypotension, clear lung fields, and elevated jugular venous pressure (JVP) is also associated with RV MI. Between 25% and 50% of affected patients may suffer hemodynamic compromise owing to acute RV dilatation and the effects of ventricular interdependence resulting in decreased LV filling and contributing to systemic hypoperfusion.

Treatment includes restoration of flow in the RV branches and hemodynamic support—specifically intravascular volume infusion and avoiding medications, such as nitrates, that reduce preload. Volume supplementation should be attempted with careful assessment of the patient’s fluid status and, if possible, with hemodynamic monitoring. Although RV infarction is a preload-dependent condition, excessive RV dilatation as a result of volume replacement may lead to further hemodynamic compromise as a result of impaired left heart filling caused by ventricular interdependence.⁹

LV aneurysms are fibrous, noncontractile outpouchings of the myocardial wall and most commonly occur in the anteroapical region. The anteroapical region has a relatively thinner wall anatomically as well as the greatest geometric curvature, predisposing it to aneurysm formation³,²⁴ in the context of transmural anterior infarction. Posterior and inferior wall aneurysms have been described but are much less common (Figure 7.2), and pseudoaneurysms that occur owing to chronic myocardial rupture are rarer still. Pseudoaneurysms are formed when the cardiac rupture is contained by the pericardium, organizing thrombus, and hematoma (ie, no myocardial tissue) and are considered a surgical emergency. Specific risk factors for aneurysm formation include hypertension, the use of steroids, and nonsteroidal anti-inflammatory drugs (NSAIDs).²⁵

LV aneurysms may be entirely asymptomatic or the patient may complain of symptoms of heart failure owing to the impaired LV systolic function that would typically accompany significant anterior wall dyskinesia. Clinical signs depend on the size of the aneurysm; however, a diffuse, pansystolic apical thrust with a double impulse because of late systolic expansion of the aneurysmal sac has been detected on palpation of the left chest wall. A third heart sound may be present on auscultation because the aneurysmal sac may contribute to rapid ventricular filling.

A classic finding is the persistence of ST segment elevation in the ECG leads corresponding to the infarct region: ST elevation in V1-V6 in the presence of loss of R wave progression and well-established Q waves signifies a transmural infarction in the anterior region.²⁶,²⁷ The mechanism for this is unclear but may be caused by traction and mechanical stress affecting the normal myocardium surrounding the aneurysm.

Aneurysms can be diagnosed on transthoracic echocardiography and most may be apparent early, often within days of the infarction. A previous study²⁸ found that it is rare for new aneurysms to develop beyond 3 months postinfarction.

The aneurysmal LV has a risk of rupture, is a locus of ventricular arrhythmias, and increases the risk of development of intraventricular thrombus that may embolize. Treatment with surgery is an option and is considered for aneurysms to mitigate these risks.

LV pseudoaneurysms have a predilection for the lateral or diaphragmatic wall and are at a higher risk of rupture.²⁹ They result from quick hematoma formation or pericardial adhesions that limit bleeds from a cardiac rupture. Given the anatomic location, imaging with CT angiography or cardiac MRI is often helpful³⁰ in delineating the topography.

LV thrombus formation is an important complication after acute MI that is associated with worse outcomes owing to the risk of systematic embolization. The pathogenesis is related to both blood stasis as a result of regionally depressed myocardial function, hypercoagulability in the aftermath of an MI, and activation of the clotting cascade by necrosed myocardial tissue.³¹ Although the risk of thrombus formation has reduced in the PCI era, it can complicate up to 25% of anterior MIs and 15% of all MIs that are not treated with reperfusion therapy.³¹ Other causes of myocardial injury that result in regional LV dysfunction—such as Takotsubo cardiomyopathy—may also result in LV thrombus formation. The diagnosis can be made on transthoracic echocardiography, but this imaging modality has a relatively low sensitivity; in suspected cases, a contrast echocardiogram or cardiac MRI is helpful in confirming the diagnosis, The treatment is with oral anticoagulation, most commonly with warfarin in addition to dual antiplatelet therapy for up to 6 months.³²

Ultimately, loss of myocardial tissue owing to ischemic necrosis can result in depression of systolic function and mechanical change or remodeling as a consequence of a complex interplay of neurohormonal factors and homeostatic mechanisms attempting to maintain cardiac output in the presence of weakened musculature. Chronic heart failure in the long term should be managed broadly as heart failure from other causes and should be treated by a specialist with serial interval imaging to assess ventricular function.

Early revascularization is the only therapy that has been shown to reduce in-hospital mortality in acute MI complicated by heart failure and may be guided by viability imaging studies. Beta blockers should be avoided in the first 24 hours after an MI with heart failure, and patients should be reviewed for reconsideration daily. There is evidence for administration of angiotensin converting enzyme (ACE) inhibitors within the first 24 hours to reduce mortality after hospital discharge (unless contraindicated by hypotension, acute kidney injury, renal failure, or drug allergy), and for administration of aldosterone antagonists in the first 7 days after an MI.³³ Angiotensin receptor blockers may be substituted for ACE inhibitors if contraindicated by drug allergy.