Anterior Myocardial Infarction

Etiology

Plaque Rupture (also known as plaque fissure) 

Most AWMIs occur due to the disruption of atherosclerotic plaque, leading to exposure to thrombogenic contents. A thrombus forms when blood flow encounters the necrotic core within the coronary artery. Atherosclerotic plaque rupture, also known as plaque fissure, is characterized by a necrotic core with an eroded thin cap, followed by thrombus formation, and is the most common cause of anterior MI.[4] 

Anterior myocardial infarction (MI) occurs due to sustained ischemia caused by the occlusion of the left anterior descending (LAD) artery—this acute reduction of blood supply to the myocardium results in necrosis of the heart muscle.

The thrombus formed at the site of plaque rupture in anterior myocardial infarction (MI) typically exhibits a white appearance (platelet-rich) at the site of rupture while appearing red at the margins (composed of red blood cells and fibrin). Thrombus formation involves a complex interplay of different cellular and non-cellular components within the blood. The breakdown of the extracellular matrix is a key factor in the exact cause of plaque rupture, with matrix metalloproteinases (MMPs) playing a significant role.

MMPs contribute to the degradation of the extracellular matrix, leading to positive remodeling and core expansion, which contribute to plaque progression. The initial disruption of fibrillar collagen occurs through the action of MMPs, creating a vulnerability within the plaque. Additionally, apoptosis of smooth muscle cells and macrophages, as well as elastolysis, may also contribute to plaque rupture. These processes collectively contribute to the pathophysiology of plaque rupture and subsequent thrombus formation in conditions such as anterior myocardial infarction.[5]

Plaque Erosion

Plaque erosion is the second most common cause of acute coronary syndrome, differing from plaque rupture by the absence of fibrous cap disintegration or fissure. In plaque erosion, there is a lack of communication between the necrotic core and the luminal thrombus.

The thrombus appears white and contains abundant neutrophils, while smooth muscle cells are interspersed. The necrotic core is small, and there is a lack of endothelial lining due to apoptosis. This allows the blood components to encounter the collagen, leading to thrombus formation.

The site of plaque erosion is rich in proteoglycan and hyaluronan, in contrast to the site of plaque rupture, which has little. Optical coherence tomography can help differentiate between plaque erosion and rupture.[6]

Microvascular and Coronary Spasm

Spasm is a significant cause of acute coronary syndrome without thrombus formation. In these cases, the constriction of the microvessels or coronary arteries leads to inadequate blood supply to the myocardium, resulting in ischemia and subsequent symptoms of acute coronary syndrome.

This phenomenon, often called vasospastic angina or variant angina, can occur spontaneously or be triggered by various factors, such as stress, cold temperatures, or certain medications.

AWMI Risk Factors

• Hypertension
• Diabetes mellitus
• Smoking
• Dyslipidemia
• Family history of premature coronary artery disease
• Overweight or obesity
• Age and gender
• Inflammation
• Diet - high glycemic index and low fiber, red meat, trans-fatty acid. 
• Lack of exercise

Epidemiology

The incidence of acute myocardial infarction demonstrates an age-dependent increase and exhibits variation with gender. Findings from the Framingham study revealed that over 10 years, the incidence of MI was 12.9 per 1,000 males (aged 30 to 34) and 5.2 per 1,000 females (aged 35 to 44). This increased by 8 to 9 times in people aged 55 to 64.[7] However, AMI's epidemiology has changed with advancements in diagnosis and management. A 2000 to 2014 study analyzed the annual change in percentages for AMI hospitalizations, including ST-elevation and non-ST elevation MI. The findings indicate a significant decline in AMI hospitalizations per 100,000 person-years across all ethnicities after adjusting for age and gender.[8]  

Across the United States, a notable disparity exists in outcomes for AMI, with certain states experiencing poorer results. Lagging states exhibit higher incidence and prevalence rates of AMI, increased mortality associated with AMI, and lower life expectancy overall.[9] Compared with the developed world, South-Asian countries face a relatively higher burden of AMI and coronary artery disease (CAD).[10] 

CAD remains a significant public health concern. According to 2013 data, cardiovascular disease, including CAD, accounts for approximately 1 in every 3 deaths in the United States.[11] For every hospitalized patient with MI, an estimated 30 patients have stable angina. Furthermore, the prevalence of CAD increases with age for both men and women.[12] While the prevalence of CAD has not decreased, the mortality rate from MI has declined. This encouraging trend can be attributed to advancements in treatment strategies and improved management of MI.

According to a study, it was found that the incidence of anterior ST-elevation MI (STEMI) accounts for approximately 33% of all STEMIs.[13] Additionally, the incidence of cardiogenic shock in AMI ranges from 5% to 15%.[14]

Pathophysiology

Erosion or rupture of the atherosclerotic plaque in LAD leads to thrombus formation. Erosion of the plaque exposes thrombogenic lipid core or subendothelial tissue, leading to enhanced vascular inflammatory activity and thrombus formation.[15] The disruption of endothelial continuity facilitates the accumulation of thrombogenic blood components, forming a thrombus. The integrity of the fibrous cap is maintained through a delicate equilibrium between collagen synthesis and degradation.

Various cytokines, such as interferon-gamma, tumor necrosis factor, macrophage chemoattractant proteins, and macrophage colony-stimulating factors, participate in the inflammatory response. The central region of the thrombus is predominantly composed of platelets, giving it a 'white' appearance. In contrast, the proximal and distal ends of the thrombus appear 'red' due to the accumulation of fibrin and red blood cells. A thrombus and vasospasm can reduce blood supply to the myocardium, leading to ischemia and subsequent myocardial infarction.

The consequences of acute myocardial infarction arise as a result of the following series of pathophysiological events: 

Systolic dysfunction and cardiogenic shock: Disruption in the blood supply along the LAD leads to compromised myocardium contractility. Consequently, several manifestations may occur, including dyssynchrony (uncoordinated contraction of different myocardial segments), hypokinesia (reduced endocardial thickening), akinesia (absent endocardial thickening), or dyskinesia (paradoxical endocardial motion and bulging of the endocardial layer).

The non-infarcted segments of the myocardium may exhibit compensatory hyperkinesia, which usually resolves in 2 weeks following the ischemic insult. Ischemia in remote areas of the heart can arise from the loss of collateral circulation originating from the occluded artery or a previous occlusion.

This systolic dysfunction causes a decrease in cardiac output, stroke volume, and blood pressure. The rate of pressure change (dP/dt) also drops, leading to an increase in end-systolic ventricular volume. Conversely, a drop in end-systolic volume is one of the most significant predictors of outcomes in acute myocardial infarction.

Ventricular dyskinesia creates a mechanical disadvantage, contributing to decreased stroke volume. The elongation and dilation of ischemic segments further promote the expansion of the infarct.[16] A noticeable decline in ejection fraction is observed when more than 15% of the myocardium is compromised. Clinical indications of heart failure and cardiogenic shock typically become evident after losing 40% of the myocardium.

As ejection fraction decreases, left ventricular end-diastolic pressures increase, and dP/dt decreases. The rate of change in ventricular pressure during isovolumetric contraction, known as dP/dt, represents ventricular contractile function. A value below 1,000 mmHg/sec is considered abnormal. 

Diastolic dysfunction: Characterized by elevated left ventricular filling pressures and altered dP/dt. In ischemia, ventricular relaxation is slowed, increasing filling pressures within the left ventricle.[17]

Circulatory regulation: Reduced stroke volume and cardiac output result in reduced coronary perfusion pressure, worsening ischemia. This cycle may lead to cardiogenic shock.

Myocardial infarction also initiates a systemic inflammatory response in the body. The release of inflammatory cytokines contributes to hypotension by causing vasodilation and reduced systemic vascular resistance. In addition, the depressed left ventricular function increases left ventricular volume, leading to elevated wall tension and increased afterload. This further decreases stroke volume, exacerbating ischemia.

Hyperkinesia of non-infarcted segments serves as a compensatory mechanism to mitigate the reduction in stroke volume. The increased left ventricular end-diastolic pressure (LVEDP) causes pulmonary congestion and hypoxemia, contributing to ischemia. 

Histopathology

The gross pathological, histochemical, light microscopic, and ultrastructural findings vary with coronary occlusion and ischemia onset.

• Gross alterations become evident after 6 to 12 hours. Gross pathology reveals evidence of transmural infarction or myocardial necrosis in most cases of occlusion myocardial infarction (OMI). However, within hours of infarction, histo-chemically, the necrotic area appears pale with triphenyl tetrazolium chloride, indicating a lack of staining, whereas the uninfarcted area appears brick red.[18]  
• The primary sequence of events in myocardial infarction involves hemorrhagic myocardial necrosis, followed by contraction band necrosis, and eventually, delayed inflammation and repair. 
• Temporally, a sequential series of changes can be observed in myocardial infarction, beginning with the waviness of myocardial fibers, coagulation necrosis, myocardial edema, focal hemorrhage, and neutrophilic infiltration. This is followed by ongoing coagulation necrosis and pallor due to shrunken cells and contraction band necrosis. Subsequently, there is loss of striation (around 8 hours) and further necrosis with continued neutrophilic infiltration. This cascade of events leads to the disintegration of myocardial fibers and subsequent phagocytosis, resulting in a soft yellow-brown core surrounded by a hyperemic border. After complete phagocytosis, granulation tissue formation occurs along with neo-vascularization and a fibrous reaction (around 14 days), ultimately forming an organized fibrous scar (approximately 3 months). 
• Electron microscopy reveals early signs of myocardial damage, such as depletion of glycogen granules and swelling of mitochondrial and sarcolemma, which can be observed as early as 20 minutes after the onset of ischemia. This is followed by further mitochondrial disruption, formation of amorphous aggregates, and relaxation of myofibrils, typically occurring around 60 minutes. Finally, irreversible structural damage to myocardial cells begins manifesting within 20 minutes to 2 hours of the ischemic insult. 

History and Physical

History

Patients commonly present with classic angina symptoms, which can occur either at rest or at a lower activity level than what they typically experience. The intensity of the pain experienced by patients varies. Still, it is often most severe in individuals who seek medical attention due to their inability to tolerate the discomfort or extreme exhaustion following the episode of pain. The pain classically lasts longer than 30 minutes and can persist for hours if revascularization is not performed. Patients typically describe the pain as constricting, squeezing, or a heavy sensation in the chest. The discomfort is commonly felt retrosternally and may radiate to the bilateral shoulder, jaw/neck, or left arm. The pain may also cause numbness or tingling sensation in the ulnar aspect of the arm.

Women may present with atypical symptoms, necessitating more suspicion and careful evaluation. Some patients may show atypical symptoms such as heart failure, extreme nervousness, apprehension, or even psychosis. Additionally, symptoms of systemic embolization can also be observed in some cases. 

Associated symptoms include dyspnea, palpitations, anxiety, nausea, vomiting, and diaphoresis. History should include characteristics and duration of symptoms, aggravating and relieving factors, and the patient's functional capacity. In addition, patients should undergo a quick evaluation for risk factors like diabetes, smoking, hyperlipidemia, hypertension, obesity, previous history of CAD, family history, illicit drug use, and medication history and compliance. 

Physical Examination

Patients with anterior wall myocardial infarction may exhibit the following signs:

• Anxious, restless, anguished face
• Clutching chest or holding a clenched fist against the sternum (Levine sign)
• Signs of heart failure, such as cold and pale skin, perspiration, propped-up position in bed, gasping for breath, or frothy pink sputum
• Cardiogenic shock signs include cool, clammy skin, severe nail beds and lips cyanosis, and hemodynamic instability.
• Tachycardia
• Uncomplicated cases may be normotensive, while previously hypertensive patients may exhibit an adrenergic response with elevated blood pressure. In cardiogenic shock, the systolic blood pressure is typically <90 mmHg.
• Fever may present in extensive ST-elevation myocardial infarction (STEMI).
• Tachypnea can occur due to anxiety, stress, or heart failure. Cheyne-Stokes respiration (periodic breathing) may be observed in cardiogenic shock, heart failure, or prior cerebrovascular disease cases.
• Jugular venous pressure (JVP) is usually normal in anterior STEMI.
• Carotid pulse may be weak if stroke volume is reduced, and it may be brief and sharp in cases of mitral regurgitation or ventricular septal rupture with a left-to-right shunt. In addition, pulsus alternans (alternating strong and weak pulses) may be present in severe left ventricular dysfunction.
• Pulmonary rales may be auscultated in the chest if heart failure is present.
• Precordial palpation may reveal normal findings or palpable S4 (forceful atrial contraction to fill a non-compliant left ventricle due to ischemia). Outward movement of a dyskinetic left ventricle may coincide with an S3 sound.
• Precordial auscultation may reveal a soft or muffled S1, paradoxical splitting of S2 (in the presence of left bundle branch block), an S3 sound (indicative of severe left ventricular dysfunction or increased flow due to mitral regurgitation or ventricular septal rupture), and an S4 sound (almost universally present). In addition, a pansystolic murmur of mitral regurgitation or a pansystolic murmur with a thrill of ventricular septal rupture may be heard. Finally, frictional rubs may occur, typically appearing on the 2nd to 3rd day (but can range from 1 day to 2 weeks).

Evaluation

Electrocardiogram (ECG): Anterior wall ischemia or infarction is typically characterized by ST elevation in some or all of leads V1 through V6 on an ECG. The ECG findings can help predict the occlusion site in the left anterior LAD relative to its major side branches.[19] 

In AWMI, specific patterns of ST-segment elevation and depression can provide diagnostic information. The ECG findings in anterior MI also have prognostic implications. A greater number of leads with ST-segment elevation indicates a larger area of infarction and is associated with an increased risk of mortality.[20]

• ST-segment elevation in leads I, aVL, and V1 through V4, along with ST-segment depression in leads II, III, and aVF, suggests an anterior wall or antero-basal ischemia/infarction most likely due to occlusion of the proximal portion of the LAD.
• ST-segment elevation in leads V3 through V6 and no ST-segment depression in leads II, III, and aVF, ischemia, most likely due to occlusion of the distal portion of the LAD.[21][22]  
• Anterior myocardial infarction is characterized by ST elevations in precordial leads. The specific leads corresponding to different regions are as follows: V1-V2 are septal leads, V3-V4 are anterior leads, and V5-V6 are lateral leads. Therefore, analyzing territorial changes in these leads can help determine the area of the myocardium at risk.
  • A septal infarct is denoted by ST elevation in leads V1-V2
  • An anterior infarction is indicated by ST elevation in leads V2-V5
  • An anteroseptal infarction is identified by ST elevation in leads V1-V4
  • An anterolateral is denoted by ST elevation in leads V3-V6, I, and aVL
  • Extensive anterior/anterolateral wall MI is marked by ST elevation in leads V1-V6, I, and aVL[23]

Cardiac enzymes: Troponin-I is the preferred test for diagnosing patients with anterior wall infarction. However, awaiting the results should not delay reperfusion in patients with clinical evidence of ischemia and anterior ST elevation on EKG. When using a high-sensitivity assay, evidence of ischemia can be obtained within 2 to 3 hours of presentation. Serial testing is recommended for patients with suspected acute coronary syndrome (ACS) with negative initial troponin results.  

Serologic testing: Renal function test, liver function test, and lipid panel are essential components of a comprehensive assessment of anterior myocardial infarction.

Chest X-ray (CXR): In patients without heart failure, CXR is typically unremarkable. However, in the setting of pulmonary edema, it may show interstitial prominence, alveolar infiltrates, and hilar cephalization of pulmonary vessels. The presence of pulmonary edema is associated with a poor prognosis.

Transthoracic echocardiogram (TTE): Urgent revascularization should not be delayed in patients with anterior ST-elevation myocardial infarction (STEMI). However, TTE can be helpful if symptoms or ECG changes are equivocal. TTE helps defines wall motion abnormalities in a territorial distribution of the LAD artery. Wall motion abnormalities are seen in the apical, anterior septal, and anterior segments.

Additionally, TTE is valuable in identifying mechanical complications, such as ventricular septal rupture, mitral regurgitation, aneurysm, and pseudoaneurysm in myocardial infarction and cardiogenic shock. Ejection fraction, initially determined by echocardiogram, strongly predicts survival and cardiovascular outcomes in patients with anterior myocardial infarction.

Cardiovascular Magnetic Resonance (CMR): In patients presenting with late anterior wall infarction, CMR is instrumental in assessing myocardial viability. Measurement of end-diastolic wall thickness helps assess transmurality of the infarction. A wall thickness of less than 6 mm is less likely to show functional recovery following revascularization.

Late gadolinium enhancement involves the administration of gadolinium-based contrast agents, which highlight areas of scar tissue. Transmural hyperenhancement, indicating the presence of contrast uptake throughout the full thickness of the myocardium, suggests transmural infarction and lack of viability. Additionally, dobutamine stress CMR can be employed to assess viability by evaluating the contractile reserve of the myocardium. 

A transesophageal echocardiogram (TEE) is a valuable imaging modality utilized in cases with uncertainty or limited visualization of cardiac structures and mechanical complications with a TTE.

Treatment / Management

Managing myocardial infarction should focus on hemodynamic stability, pain relief, avoiding hypoxia, decreasing myocardial oxygen demand, and providing the earliest possible revascularization. 

Nitrates: In patients with ongoing chest pain suggestive of myocardial infarction, administering sublingual nitroglycerin can help alleviate symptoms and improve coronary blood flow. The recommended dose is 0.4 mg of sublingual nitroglycerin, which can be repeated every 5 minutes for 3 doses if the pain persists. 

If the chest pain persists or there is inadequate relief, the need for intravenous (IV) nitroglycerin should be considered. IV nitroglycerin can provide more sustained and controlled vasodilation and may be necessary in severe or refractory chest pain cases. Nitrites should be avoided in patients with systolic BP less than 90 mm Hg, severe bradycardia, suspected RV infarction, and those receiving a phosphodiesterase inhibitor within the last 24 hours.

Oxygen: Maintaining adequate oxygenation is crucial to meet the myocardial oxygen demand. Supplemental oxygen should be considered when the arterial oxygen saturation (SpO2) falls below 90%. For patients without COPD, supplemental oxygen can be administered at a flow rate of 2 to 4 liters per minute via nasal cannula. This standard starting range can be adjusted based on the patient's response and subsequent oxygen saturation levels.

Analgesia: Administration of morphine can be beneficial in providing pain relief, alleviating anxiety, and assisting in managing pulmonary edema.

Aspirin: An initial dose of 162 mg to 325 mg of aspirin is recommended for all patients with AMI before undergoing percutaneous coronary intervention (PCI). It should be continued indefinitely as part of long-term management.

Adjunct antithrombotic therapy for patients presenting to PCI facility: Antiplatelet therapy with P2Y12 receptor inhibitors is essential to managing myocardial infarction. The choice of specific P2Y12 inhibitor and dosing regimen may vary depending on several factors, including the patient's characteristics and the clinical scenario. The commonly used P2Y12 inhibitors and their recommended dosing regimens are as follows:

1. Clopidogrel:
   • Loading Dose: A loading dose of 600 mg of clopidogrel should be administered as early as possible or at the time of percutaneous coronary intervention (PCI).
   • Maintenance Dose: Following the loading dose, a daily maintenance dose of 75 mg of clopidogrel should be continued for the prescribed duration, typically up to 12 months or as determined by the treating physician.
2. Prasugrel:
   • Loading Dose: A loading dose of 60 mg of prasugrel should be given at the time of PCI.
   • Maintenance Dose: A daily maintenance dose of 10 mg of prasugrel is recommended after the loading dose.
3. Ticagrelor:
   • Loading Dose: An loading dose of 180 mg of ticagrelor should be administered as early as possible or at the time of PCI.
   • Maintenance Dose: Following the loading dose, a twice-daily maintenance dose of 90 mg of ticagrelor should be continued.

Reperfusion: Reperfusion is the mainstay of treatment in acute MI. In patients with anterior STEMI, timely PCI is recommended.

• PCI within 90 minutes of First Medical Contact (FMC): In patients with anterior STEMI, the goal is to perform PCI within 90 minutes of initial medical contact. This includes the time from the patient's arrival at the hospital or when medical personnel first assess the patient.

• Door-in-Door-out (DIDO) time for non-PCI-capable hospitals: If the patient initially presents to a hospital without PCI capabilities, the DIDO time should be less than 30 minutes. This refers to the time it takes for the patient to be transferred from a non-PCI-capable hospital to a PCI-capable hospital.

• The recommended goal is to achieve a first medical contact to intervention time of fewer than 120 minutes, aiming for prompt reperfusion to restore blood flow to the affected coronary artery. 

• If the door-in-door-out time is greater than 30 minutes, and the first medical contact to intervention time is greater than 120 minutes, a fibrinolytic agent should be administered within 30 minutes of arrival. Evidence of failed reperfusion will require urgent transfer to a PCI-capable hospital.

• Patients with STEMI who meet the criteria should undergo emergent PCI as the preferred reperfusion strategy. Indications for emergent PCI are as follows: ischemic symptoms for less than 12 hours, absolute contraindication to fibrinolytic therapy regardless of time delay from the first medical contact, cardiogenic shock, or acute severe heart failure. 
  • Early reperfusion leads to decreased complications and a better prognosis. PCI has demonstrated superiority to thrombolytic therapy in reducing short-term and long-term adverse cardiac events in patients with anterior acute MI.[24][25] 
  • Routine thrombectomy before PCI is not recommended. PCI of the non-infarct related artery may be considered in stable patients during primary PCI or as a staged procedure.[26]
(A1)

Treatment at a non-PCI capable facility with a delay of more than 120 minutes from FMC to primary PCI: Thrombolytic therapy should be given if the onset of symptoms is less than 12 hours (class I) or the onset of symptoms is 12 to 24 hours, but there is clinical evidence of ongoing ischemia with potential for large myocardium damage or hemodynamic instability. If a patient develops cardiogenic shock or has refractory heart failure after receiving thrombolytic therapy, they should be transferred for immediate angiography and possible PCI. A patient may also require transfer for immediate angiography and possible PCI if there is evidence of failed reperfusion or re-occlusion of the infarct-related artery after thrombolytic therapy. For stable patients who have received successful thrombolysis, elective PCI can be considered between 3 and 24 hours after thrombolysis to assess further and treat the coronary artery. 

Adjunctive antithrombotic therapy for patients undergoing fibrinolytic therapy: 

1. Aspirin:
   • Loading dose: 162 to 325 mg
   • Maintenance dose: 81 to 325 mg maintenance dose
2. Clopidogrel:
   • Loading dose for age <75: 300 mg loading dose
   • Maintenance dose for age <75: 75 mg maintenance.
   • Loading dose for age >75: no loading dose
   • Maintenance dose for age>75: 75 mg daily for 14 days and up to 1 year
3. Unfractionated Heparin (UFH):
   • Maintain aPTT 1.5 to 2 times of control
   • Based on the age and renal function, enoxaparin may be considered. 

Anticoagulation: Anticoagulation with unfractionated heparin (UFH) or low molecular weight heparin (LMWH) after thrombolysis and during PCI is necessary to prevent thrombosis. In patients undergoing PCI, UFH boluses should be administered to maintain activated partial thromboplastin time (aPTT), taking into consideration whether Glycoprotein IIb/IIIa inhibitor is being used. Alternatively, bivalirudin can be used as an anticoagulant during PCI. However, fondaparinux should not be used as a sole anticoagulant in STEMI.

Beta-blocker: Administer oral beta-blockers in patients without contraindications, especially in tachyarrhythmia or hypertension. Beta-blockers are commonly used to manage acute MI for several beneficial effects, such as reduction of myocardial oxygen demand, prevention of reinfarction, antiarrhythmic effects, and improvement of left ventricular function.

High-intensity statin therapy: To manage AMI, patients without contraindications should be prescribed high-intensity statin therapy, such as atorvastatin 80 mg.

Adjunctive therapy: Adjunctive therapy plays a crucial role in managing AMI. These include:

• P2Y12 inhibitors: medications such as clopidogrel, prasugrel, and ticagrelor, are antiplatelet agents that help prevent further clot formation and reduce the risk of recurrent cardiovascular events. These are typically initiated with aspirin and continued for a specific time, depending on the patient's clinical presentation and chosen agent.
• Angiotensin-converting enzyme inhibitor/angiotensin receptor blocker (ACEi/ ARB): these medications help reduce afterload, promote vasodilation, and inhibit the adverse remodeling of the heart following MI. ACE inhibitors are indicated in patients with left ventricular dysfunction, heart failure, to other high-risk features
• Spironolactone: a potassium-sparing diuretic and aldosterone antagonist, has reduced mortality and morbidity in patients with heart failure and reduced ejection fraction.  

Differential Diagnosis

The differential diagnosis of anterior wall myocardial infarction (MI) includes the following conditions:

• Aortic dissection
• Unstable angina
• Stable angina
• Vasospastic angina
• Takotsubo cardiomyopathy
• Myocardial trauma
• Massive pulmonary embolism
• Tension pneumothorax
• Esophageal perforation
• Esophageal spasm
• Gastroesophageal reflux disease or peptic acid disease
• Musculoskeletal pain
• Acute pericarditis
• Myocarditis
• Pulmonary embolism

Staging

Killip classification is a widely used system for assessing the 30-day prognosis in patients with STEMI. It helps categorize the severity of heart failure and determines the risk of adverse outcomes. The Killip classification is as follows:

• Killip class I: This class indicates no evidence of heart failure.
• Killip class II: This class represents mild signs of heart failure, such as bibasal rales, a third heart sound (S3), and raised JVP. However, despite these findings, the patient's clinical condition is stable.
• Killip class III: This class denotes the presence of acute pulmonary edema. Patients in this category experience significant respiratory distress due to fluid accumulation in the lungs.
• Killip class IV: This class represents cardiogenic shock, the most severe form of heart failure. Patients in this category exhibit profound hemodynamic instability, characterized by severe hypotension, reduced cardiac output, and end-organ hypoperfusion. In addition, they may have cold and clammy skin, altered mental status, and signs of peripheral vasoconstriction.

Prognosis

The in-hospital mortality rates associated with each classification are as follows:[27]

• Killip class I: 6% 
• Killip class II: 17%
• Killip class III: 38%
• Killip class IV: 81%

The anatomical location of occlusion of the LAD artery also predicts the 30-day and 1-year mortality in anterior myocardial infarction. 

Studies have demonstrated that the prognosis of patients with anterior MI is worse than those with inferior or posterior MI.[28][29] Patients with anterior MI usually have a complicated hospital course compared to inferior/posterior MI.[3][28] Anterior MI is associated with an increased incidence of acute heart failure, ventricular fibrillation, and death.[30][31] Following discharge, patients with an anterior MI are associated with poorer long-term prognoses than those with other types of MI.[28] Additionally, anterior MI associated with right bundle branch block (RBBB) predicts poor prognosis.[32]

Complications

Anterior wall myocardial infarction can be associated with various complications, including:

• Cardiogenic shock: In severe cases of AWMI, extensive damage to the left ventricle can cause a significant decrease in cardiac output, leading to cardiogenic shock. Cardiogenic shock complicating anterior MI is associated with higher hospital mortality when compared with inferior MI.[33]
• Left ventricular dysfunction: AWMI involves a significant portion of the left ventricle, which can lead to impaired left ventricular function. This can result in decreased EF, compromised cardiac output, and an increased risk of heart failure.
• Left ventricular mural thrombus is a frequent complication with systolic dysfunction due to anterior MI.[34][35] TTE can be used with high accuracy for diagnosis when suspicious of a thrombus.[36] This condition can lead to stroke or peripheral ischemia.
• Ventricular septal rupture in the ventricular spetum results in communication between the left and right ventricles. This condition requires urgent surgical intervention.
• Free wall rupture is rare but can lead to cardiac tamponade and hemodynamic instability. Emergency surgical repair is required.
• Pericardial effusion: Due to free wall rupture, causing an accumulation of fluid in the pericardial sac. This requires pericardiocentesis or surgical drainage.
• Acute pericarditis: AWMI can cause inflammation of the pericardium. 
• Dressler syndrome: Delayed autoimmune response following MI, characterized by pericarditis, pleuritis, and fever. It typically occurs weeks to months after the initial event.
• Sudden cardiac death: AWMI increases the risk of life-threatening arrhythmias, such as ventricular tachycardia/ventricular fibrillation (VT/VF), which can result in sudden cardiac death.
• Conduction abnormalities: AWMI can lead to conduction abnormalities, including blocks at the level of the His bundle or below and bundle branch blocks.
• Left ventricular aneurysm: In some cases, AWMI can form a left ventricular aneurysm, which is a localized abnormal bulging of the ventricular wall. Aneurysms can lead to heart failure, arrhythmias, and thromboembolic events.