Acute Myocardial Infarction: Complications

Acute Myocardial Infarction: Complications

Retesh Bajaj

Anantharaman Ramasamy

Vincenzo Tufaro

Arjun K. Ghosh


The advent of coronary reperfusion therapy has substantially reduced the incidence of complications following acute myocardial infarction (MI). However, their occurrence is still associated with significant morbidity and mortality. Cardiac complications can be broadly divided into mechanical, arrhythmic, and pericardial. A high index of suspicion and vigilance must be maintained to ensure these rare, but important, complications are diagnosed in a timely manner and appropriately managed.


Ischemic injury frequently results in structural and mechanical changes in the myocardium, the magnitude of which is directly related to the amount of muscle affected and, therefore, impacted by extent of infarction. Structural complications and their severity are more common in patients who have sustained a transmural infarction in comparison to a nontransmural infarction. Patients who have not been treated with coronary reperfusion therapy have a significantly higher risk of mechanical cardiac complications. The incidence of mechanical complications has diminished to approximately 1% in the era of reperfusion therapy,1 but the mortality rate remains high.

These complications can present acutely as life-threatening deteriorations in the immediate aftermath of a MI or more chronically, related to scar formation and remodeling of the heart as its architecture modifies to maintain cardiac output after the injury.

Acute Mechanical Complications

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

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

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

Cardiac Free Wall Rupture

Cardiac rupture is commonest within four days of ST-elevation MI (STEMI) and more likely to affect the LV anteroapical wall (although RV involvement has been reported). Rates of cardiac rupture in acute MI patients who did not receive reperfusion therapy are as high as 6%. The incidence has halved in the last 30 years because of the use of reperfusion therapy,10 but the mortality rate (>70%) is the highest among all acute mechanical complications and may account for up to 20% of acute mortality associated with MI.11 Risk factors associated with cardiac free wall rupture include older age, female gender, and first MI.

The presentation is typically dramatic with sudden cardiac tamponade, although individuals with a slow leak of blood into the pericardium may note nonspecific symptoms including chest pain and signs ranging from minimal hemodynamic changes to frank hemodynamic collapse. Electromechanical dissociation on the ECG without preceding cardiac failure in the context of MI has been reported as a very specific sign of cardiac rupture.12

Early recognition and treatment are essential. In the unstable patient with cardiac tamponade, emergency pericardiocentesis can be lifesaving, but emergent surgical repair (ie, resecting the infarcted area and applying a patch to the ruptured zone) is the definitive treatment option. Perioperative mortality remains high because surgery on the friable and necrotic myocardium is technically challenging.

Ventricular Septal Rupture

Ventricular septal rupture classically develops 3 to 5 days post MI. It complicates 2 to 3 of every 1000 MIs13 with a higher incidence among older females. The mortality rate approaches 100% without closure.14 The anatomic location of the ventricular septal rupture is relevant as it impacts mortality: apicoanterior septal ruptures are associated with an LAD infarction and carry a better prognosis than posterior septal ruptures that are associated with occlusion of the posterior descending artery.15 The latter are associated with RV dysfunction and are anatomically more challenging to treat (Figure 7.1). The dissection plane of the rupture can take a serpiginous route (ie, the LV entry and RV exit sites occur in different locations)16 and is best assessed using transthoracic echocardiography with color flow imaging.

The acute left-to-right shunt results in hemodynamic compromise and biventricular failure. The presentation can be acute with pulmonary edema, and a new, harsh pansystolic murmur with a thrill may be found at the left sternal border.

Treatment involves surgical closure, which may be complicated by the technical challenges of operating on necrosed myocardial tissue. More recently, percutaneous closure devices have been introduced and may be an option in experienced centers.17,18 Initial observational studies reported that postoperative survival was better for surgery deferred for a week; however, this was likely owing to survival bias, because early surgery is usually performed on individuals with marked hemodynamic instability and circulatory compromise. Consequently, it is now recommended that surgery or percutaneous treatment not be delayed. Afterload reduction with nitrates (in patients with a blood pressure that allows this) and intra-aortic balloon pump placement may stabilize patients with hemodynamic compromise until definitive surgery can be performed or a closure device is inserted.17

Papillary Muscle Rupture

Acute papillary muscle rupture is most commonly associated with inferior MIs and typically occurs 2 and 7 days after infarction. The posteromedial papillary muscle is 10 times more likely to be involved than the anterolateral papillary muscle, because it has a single blood supply from either the right or left circumflex coronary; the anterolateral papillary muscle is typically supplied by both the LAD and the left circumflex arteries. Papillary muscle rupture may be partial or complete and can result in a new pansystolic murmur; however, the murmur may be soft or inaudible in the presence of cardiac failure. The acute mitral regurgitation that results is typically poorly tolerated,
resulting in pulmonary edema and a high mortality without treatment in the first 24 hours.

Surgical options include mitral valve repair or replacement depending on anatomy and extent of the rupture. In patients who are deemed to be inoperable, successful treatment with the percutaneous MitraClip (Abbott, Lake Bluff, Illinois, USA) has been reported.19,20


Acute mechanical complications after MI represent a collection of life-threatening scenarios that may be difficult to diagnose and effectively treat. Accordingly, early involvement of cardiology and cardiothoracic teams is essential. Mechanical circulatory support devices such as intra-aortic balloon pumps21 may aid stabilization, improve hemodynamics, and delay deterioration until definitive treatment (ie, surgery or percutaneous) can be provided. More recently, extracorporeal membrane oxygenation in experienced centers has been used as an adjunct22 to allow time for more definitive surgical management.


Ventricular remodeling after MI is common with secondary progression to heart failure. Up to 20% of patients older than 65 years who have survived an MI will develop heart failure.23 The process of healing that follows an MI leads to thinning of the myocardium and elongation of the infarcted region in response to myocardial wall stress, resulting in topographic changes to the ventricle—a process termed “infarct expansion.” Depending on the size and extension of the infarction, this can result in a spectrum of effects—from no impairment of ventricular function to significant remodeling and ventricular aneurysm formation to depression of systolic function owing to loss of myocytes. These architectural changes can result in significant morbidity as well as risk of secondary complications.

Left Ventricular Aneurysms

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.

Left Ventricular Thrombus

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

Ventricular Failure

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.


Cardiac arrhythmias are a known complication of acute MI. Myocardial ischemia and infarction often lead to intracellular metabolic derangement and autonomic dysfunction that can lead to cardiac arrhythmias. Clinical characteristics such as infarct size, hemodynamic instability, pre-existing conduction
disease, and use of ionotropic support agents may exacerbate myocardial ischemia and provoke cardiac arrhythmias. Although the majority of patients with cardiac arrhythmias post MI may be asymptomatic, patients can present with a variety of symptoms such as palpitations, chest pain, breathlessness, syncope, or cardiac arrest. Timely recognition and management are essential because these arrhythmias—both tachycardic or bradycardic episodes—can provoke hemodynamic instability and lead to life-threatening rhythm disturbances and cardiac death.


Atrial Arrhythmias

Sinus Tachycardia. A marked rise in sinus node discharge is common during the acute phase of MI. This is usually associated with the chest pain and anxiety surrounding the presentation, which often resolve following administration of pain relief and revascularization. However, a physiologic tachycardia as a compensatory mechanism for reduced stroke volume may indicate pump failure, which is associated with poor prognosis. Studies have shown that sinus tachycardia in patients with acute MI is associated with larger proportion of anterior infarcts, multiple infarct sites, and higher mean peak biomarker release.34 These patients are also more likely to suffer from post-MI complications such as peri-infarct pericarditis and an increased risk of in-hospital mortality. Early and cautious administration of beta blockers to lower the sympathetic tone should be considered in these patients.

Premature Atrial Ectopics. Premature atrial ectopics (PACs) are the most of common type of atrial arrhythmias in patients with acute MI. They are characterized by abnormal morphology of the P waves. These may be because of increased sympathetic tone, atrial distensions from either left or right ventricular infarction, or atrial ischemia/infarction. PACs rarely cause symptoms; therefore, suppressive treatment is not required in these patients.35

Supraventricular Tachycardias. Paroxysmal or persistent supraventricular tachycardia (SVT) including atrial tachycardia (AT) and atrioventricular nodal ventricular tachycardia (AVNT) are relatively rare in patients with acute MI. Most of these arrhythmias are transient and cause no symptoms.36 However, when present with rapid ventricular response, patients can be highly symptomatic with associated hemodynamic collapse. Management is directed toward controlling the rapid ventricular rate. This can be attempted by carotid sinus massage or Valsalva maneuver, both of which increase the vagal tone and alter the AV nodal properties. Intravenous adenosine can be useful to terminate these arrhythmias, but resuscitation facilities with an external defibrillator should be available because a small number of patients develop ventricular fibrillation from adenosine. Intravenous beta blockers and calcium channel blockers may also be used to slow the rapid ventricular rate, but this should be done cautiously to avoid hypotension in patients with acute MI. Hemodynamically unstable patients should be treated with urgent, synchronized direct current cardioversion to terminate these arrhythmias.

Atrial Fibrillation. The incidence of atrial fibrillation (AF) in the setting of acute MI has been reported to be 7% to 21%.37 Rapid and irregular ventricular rates may impair coronary perfusion and LV function, which can lead to symptoms such as chest pain, palpitations, and breathlessness. Coronary ischemia, irregular RR intervals, and enhanced sympathetic nervous system in the presence of atrial fibrillation can lead to life-threatening ventricular arrhythmias. Advanced heart failure (Killip class IV) is the most significant predictor of development of AF in acute MI.38 In addition, advanced age, male gender, and admission heart rate greater than 100 beats per minute are associated with the development of AF.

AF in the setting of acute MI is associated with increased morbidity and mortality39 independent of age, diabetes mellitus, hypertension, history of previous MI, cardiac failure, or coronary revascularization status. However, it is unclear if AF is purely a complication of MI or a severity marker of the acute infarction. The TRACE study concluded that the excess mortality in these patients is likely related to sudden and non-sudden cardiac deaths.40

Traditional antiplatelet therapy have not reduced the risk of thromboembolism in patients with AF. The addition of oral anticoagulant to antiplatelets increases the absolute risk of major hemorrhage. Accordingly, patients with AF undergoing primary PCI should be treated with newer third-generation drug-eluting stents with shorter duration of antiplatelet therapy, because they will require long-term oral anticoagulation.41

The management of AF in acute MI should focus on adequate rate control that can be achieved with administration of beta blockers or calcium channels blockers. However, this should be done cautiously in patients who have suffered large infarcts with LV dysfunction because the negative chronotropic effect of these medications can further compromise their hemodynamic status. Class 1C antiarrhythmic agents such as flecainide and propafenone are contraindicated in patients with coronary artery disease and should be avoided. Prompt treatment with synchronized DC cardioversion should be considered when patients with AF present with hemodynamic instability.

Ventricular Arrhythmias

Premature Ventricular Contractions. Premature ventricular contractions (PVCs) occur frequently in patients with acute MI (Figure 7.3). They rarely cause hemodynamic compromise and do not require specific treatments. Frequent PVCs may be related to electrolyte imbalance, so plasma levels of potassium and magnesium should be checked and corrected accordingly.42 Frequent PVCs persisting longer than 48 hours are associated with increased long-term arrhythmic risk, especially in patients with impaired LV function.43

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May 8, 2022 | Posted by in CARDIOLOGY | Comments Off on Acute Myocardial Infarction: Complications
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