Continuing Education Activity

Anterior myocardial infarction (AMI) is a common heart disease associated with significant mortality and morbidity. Advancements in diagnosis and treatment options have led to a favorable outcome. This activity reviews the evaluation and management of anterior myocardial infarction and highlights the role of the interprofessional team in the care of patients with this condition.

Objectives:

• Describe the pathophysiology of anterior myocardial infarction.
• Review the appropriate evaluation process for anterior myocardial infarction.
• Outline the management options for anterior myocardial infarction.
• Summarize the importance of communication and care coordination amongst the interprofessional team to enhance the care of patients with anterior myocardial infarction.

Introduction

Myocardial infarction (MI) remains the leading cause of death worldwide. [1] Coronary artery disease is a major but preventable cause of morbidity and mortality. Myocardial infarction is defined as the irreversible necrosis of heart muscle resulting from a decrease in blood supply to the heart due to coronary artery occlusion. Clinically MI is diagnosed when rising cardiac biomarkers detect the acute myocardial injury, and there is evidence of acute myocardial ischemia (supported by either patient symptoms, EKG changes, or imaging evidence). [2] Anterior myocardial infarction is a type of myocardial infarction occurring due to a decrease in blood supply to the anterior wall of the heart.

Classification of anterior myocardial infarction is based on EKG findings as follows:[3]

1. Anteroseptal – ST-segment elevation in leads V1 to V4
2. Anteroapical (or mid-anterior) – ST-segment elevation in leads V3-V4
3. Anterolateral – ST-segment elevation in leads V3 to V6
4. Extensive anterior – ST-segment elevation in leads V1 to V6

Etiology

The anterior myocardium receives vascular supply via the left anterior descending (LAD) coronary artery. Sustained ischemia due to LAD artery occlusion leads to anterior MI. Atherosclerotic plaque rupture, followed by thrombus formation is the most common cause of anterior MI. [4] This acute reduction of blood supply to the myocardium results in necrosis of the heart muscle. Certain factors are associated with a higher likelihood of CAD and MI. Five main risk factors for CAD are hypertension, hyperlipidemia, diabetes, obesity, and smoking. The presence of one or more risk factors increases the risk of cardiovascular events. [5]

Epidemiology

Coronary artery disease (CAD) remains a significant public health issue. As per 2013 data, one in every three deaths in the United States is attributable to cardiovascular disease. [6] For every hospitalized patient with MI, there are about 30 patients with stable angina. The prevalence of CAD increases with age for both men and women. [7] The prevalence of CAD has not decreased, but the mortality from MI has been decreasing. This fact is likely due to advanced treatment strategies and better management. One study determined that the incidence of anterior ST-elevation MI (STEMI) is approximately 33% of all STEMIs. [8]

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. [9] The breach in the endothelial continuity invites thrombogenic blood components to aggregate and result in thrombus formation. Fibrous cap integrity is a consequence of a balance between collagen synthesis and degradation. Various cytokines participate in the inflammatory response such as interferon-gamma, tumor necrosis factor, macrophage chemoattractant proteins, and macrophage colony-stimulating factors. The core of the thrombus is platelet rich and 'white' whereas the proximal and distal ends appear 'red' due to fibrin and red blood cell accumulation. Thrombus and/or vasospasm lead to a decrease in blood supply to the myocardium causing ischemia and then infarction. 

History and Physical

A careful history and physical exam are cornerstones for the diagnosis of anterior MI. Patients typically present with chest pain. Associated symptoms can be dyspnea, palpitations, anxiety, nausea, vomiting, and diaphoresis. History should include characteristics and duration of symptoms, aggravating and relieving factors, and functional capacity of the patient. Patients should undergo evaluation for risk factors like diabetes, smoking, hyperlipidemia, hypertension, obesity, previous history of CAD, family history, illicit drug use, and medication history and compliance. 

The physical exam may elicit clues to cardiovascular disease like hypotension/ hypertension, tachypnea, tachycardia/ arrhythmia, jugular venous distension, heart murmurs, lung crackles, and peripheral edema. A good history and physical exam are critical prior to diagnostic testing to estimate the pretest likelihood of ischemia.

Evaluation

Any patient suspected of myocardial ischemia or infarction should undergo an evaluation with EKG and measurement of cardiac biomarkers.

EKG changes - Anterior wall ischemia/infarction presents as ST elevation in some or all of leads V1 through V6. In anterior MI, the EKG is useful to predict the LAD occlusion site relative to its major side branches.[10] ST-segment elevation in leads I, aVL, and V1 through V4 and 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, suggests anterior wall ischemia/infarction, most likely due to occlusion of the distal portion of the LAD.[11][12] EKG also provides prognostic information in anterior MI. More leads with ST-elevation indicate a larger area of infarction and an increased risk of mortality.[13]

More on ECKGGGG mechanism etc. 

Lab studies should include troponins, a complete metabolic panel, a complete blood count, B-type natriuretic peptide, and a coagulation profile.

A chest X-ray (CXR) should be obtained, and bedside echocardiography should be a consideration if available. CXR helps in the diagnosis of pulmonary edema. The presence of pulmonary edema confers a poor prognosis. Transthoracic echocardiography (TTE) can help diagnose acute MI by wall motion abnormalities and rule out alternate causes of chest pain like pericardial effusion, aortic valve stenosis, and aortic dissection. It can also estimate left ventricle ejection fraction, which also helps to estimate prognosis. This testing not only helps in diagnosis but also provides prognostic information.[13]

ECHO:

Treatment / Management

The management of myocardial infarction should focus on hemodynamic stability, pain relief, increasing oxygen supply to the heart, and decreasing myocardium oxygen demand.

1. Oxygen: Supplemental oxygen should be administered to patients with arterial oxygen saturation of less than 90%.

2. Nitrates: Patients with ongoing chest pain should receive sublingual nitroglycerin 0.4 mg every 5 minutes for a total of 3 doses, and after that, an assessment should take place regarding the need for IV nitroglycerin. Intravenous nitroglycerin is indicated for the relief of ongoing ischemic discomfort, control of BP, or maintenance with nitroglycerin. Avoid nitrates in patients with systolic BP less than 90 mm Hg, severe bradycardia, suspected RV infarction and those who have received a phosphodiesterase inhibitor with in the last 24 hours

3. Analgesia: Administer morphine sulfate for pain relief. 

4. Aspirin: Give an initial dose of 162 mg to 325 mg.

5. Beta-blockers: Administer oral beta-blockers in patients without contraindications and in the presence of tachyarrhythmia or hypertension.

6. Reperfusion: Reperfusion is the mainstay of treatment in acute MI. Patients with acute anterior STEMI should undergo percutaneous coronary intervention (PCI) within 90 minutes of first medical contact. If the patient is at a non- PCI capable hospital, the door-in door-out time should be less than 30 minutes with the transfer of the patient to a PCI capable hospital. The expectation is that the first medical contact to intervention time will be as soon as possible, ideally less than 120 minutes. 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 or restenosis will require urgent transfer to a PCI capable hospital. Patients with STEMI having ischemic symptoms for less than 12 hours, patients with absolute contraindication to fibrinolytic therapy irrespective of time delay from first medical contact, cardiogenic shock, or acute severe heart failure irrespective of time delay from the first medical contact should undergo emergent PCI. Early reperfusion leads to decreased complications and better prognosis. PCI has demonstrated superiority to thrombolytic therapy in reducing the short term and long term adverse cardiac events in patients with anterior acute MI.[14][15]  

7. Anticoagulation: Anticoagulation with heparin or low molecular weight heparin after thrombolysis and during PCI is required to prevent thrombosis.

8. Adjunctive therapy should include P2Y12 inhibitors, a statin, an angiotensin-converting enzyme inhibitor/ angiotensin receptor blocker (ACEi/ ARB), and spironolactone within 24 hours in a stable patient.

9. Patients undergoing PCI should receive the following:

• Aspirin: 162 to 325 mg loading and 81 mg daily maintenance indefinitely
• Clopidogrel: 600 mg as early as possible or at the time of PCI and 75 mg daily maintenance dose OR
• Prasugrel: 60 mg at the time of PCI and 10 mg daily maintenance dose OR
• Ticagrelor: 180 mg as early as possible or at the time of PCI and 90 mg twice daily maintenance dose.

10. Patients undergoing fibrinolytic therapy:

• Adjunctive antithrombotic therapy
• Aspirin: 162 to 325 mg loading dose, 81 to 325 mg maintenance dose
• Clopidogrel: Age < 75 years 300 mg loading dose, 75 mg maintenance. Age >75 years, no loading dose and 75 mg daily for 14 days and up to 1 year

11. Secondary prevention for STEMI

• Complete smoking cessation
• Blood pressure control
• Lipid management
• Weight management goal BMI: 18.5 to 24.9 kg/m^2.
• Diabetes management: Goal HBA1c <7%
• Renin-angiotensin-aldosterone system blockers - In anterior MI patients start an ACEi or start ARB if intolerant to ACEi
• Aldosterone antagonists: For patients with STEMI who are receiving an ACE inhibitor and a beta-blocker, and who have a left ventricular ejection fraction less than or equal to 40 percent and either heart failure or diabetes
• Beta-blockers: Start in all patients unless contraindicated

12. Cardiac rehabilitation - This includes exercise training and counseling, education on heart-healthy living, and counseling to reduce stress.

Differential Diagnosis

• Aortic dissection
• Cardiac tamponade
• Pulmonary embolism
• Tension pneumothorax
• Esophageal perforation
• Esophageal spasm
• Gastroesophageal reflux disease (GERD) or peptic acid disease
• Musculoskeletal pain
• Pericarditis
• Myocarditis

Prognosis

Studies have demonstrated that the prognosis of patients with anterior MI is worse when compared to those with inferior or posterior MI.[16][17] Patients with anterior MI usually have a complicated hospital course as compared to inferior/posterior MI.[16][18] Anterior MI is associated with an increased incidence of acute heart failure, ventricular fibrillation, and death.[19][20] Following discharge, patients with anterior MI correlated with poor long-term prognosis.[16] Anterior MI associated with right bundle branch block (RBBB) predicts poor prognosis.[21]

Complications

• Cardiogenic shock: Cardiogenic shock complicating anterior MI is associated with higher hospital mortality when compared to inferior MI.[22]
• Left ventricular dysfunction
• Left ventricular mural thrombus. Left ventricular mural thrombus is a frequent complication with systolic dysfunction due to anterior MI.[23][24] TTE can be used with high accuracy for diagnosis when suspicious of a thrombus.[25] This condition can lead to stroke or peripheral ischemia.
• Ventricular septal rupture
• Free wall rupture
• Pericardial effusion from free wall rupture
• Acute mitral regurgitation (MR) from papillary muscle rupture
• Pericarditis
• Sudden cardiac death secondary to ventricular tachycardia/ventricular fibrillation (VT/VF): VT/VF that occurs after 48 hours requires an implantable cardioverter-defibrillator (ICD) placement. An ICD is indicated in patients 40 days post-MI with a left ventricular ejection fraction (LVEF) of 35% with a New York Heart Association (NYHA) class II or III, patients 40 days post-MI LVEF of 30% with NYHA class I, and patients with nonsustained ventricular tachycardia (NSVT), an LVEF of <40% and inducible VT on an electrophysiology study (EPS).
• Conduction abnormalities including Mobitz type II block at the level of His bundle or below His bundle and RBBB with either left anterior fascicular block or left posterior fascicular block
• Left ventricular aneurysm

Deterrence and Patient Education

Combining strategies based on the individual level, the health care level, and the population level will help improve compliance and prevention of further cardiovascular events. The individual-level approach includes patient education regarding lifestyle changes and adherence to medical treatments. Weight loss, smoking cessation, regular exercise, and dietary changes all help to improve patient outcomes. Participation in cardiac rehabilitation programs should also be encouraged. Health care level strategies include facilitating, encouraging, and rewarding patients and clinicians to improve health by optimizing modifiable risk factors. Population-based strategies target a healthy lifestyle in the community.[6]

A large burden provides a useful window for healthcare physicians to improve the outcomes of this disease entity. 

Enhancing Healthcare Team Outcomes

Coronary artery disease prevalence has not decreased for decades. Modifying the risk factors is the mainstay for reducing the risk of CAD. Primary clinicians should educate patients about the likelihood of CAD associated with these risk factors. A team approach involving primary clinicians, nurses, pharmacists, dietitians, behavioral therapists, and social workers can help the patient in the optimization of risk factors. Anterior MI, like any other MI, benefits from early intervention and optimal medical therapy after reperfusion. Hospital teams involving emergency clinicians, hospitalists, cardiologists, and emergency and intensive care unit (ICU) nurses can work together to provide early intervention and reduce the time from medical contact to PCI. Post- reperfusion care in the ICU and patient education immediately after the event helps in improved patient compliance. Referral to cardiac rehabilitation and timely communication with the primary clinician at the time of discharge helps to close the loop and ensures the patient gets appropriate care after a significant cardiovascular event.