Acute Myocardial Infarction

Etiology

Acute myocardial infarction occurs due to decreased coronary blood flow, leading to insufficient oxygen supply to the heart and cardiac ischemia. Decreased coronary blood flow is multifactorial. Atherosclerotic plaques classically rupture and lead to thrombosis, contributing to acutely decreased blood flow in the coronary. Other etiologies of myocardial ischemia include coronary artery embolism, which accounts for 2.9% of patients, cocaine-induced ischemia, coronary dissection, and coronary vasospasm.[4][5]

Nonmodifiable Risk Factors

• Sex
• Age
• Family history
• Male pattern baldness

Modifiable Risk Factors

• Smoking
• Dyslipidemia
• Diabetes mellitus
• Hypertension
• Obesity
• Sedentary lifestyle
• Poor oral hygiene
• Presence of peripheral vascular disease
• Elevated levels of homocysteine

Other Causes of MI

• Trauma
• Vasculitis
• Drug use (cocaine)
• Coronary artery anomalies
• Coronary artery emboli
• Aortic dissection
• Excess demand on the heart (hyperthyroidism, anemia)

Epidemiology

Approximately 70% of fatal AMI cases are attributed to occlusion caused by atherosclerotic plaques. As atherosclerosis is the predominant cause of AMI, risk-factors for atherosclerotic disease are often mitigated in disease prevention. Modifiable risk factors account for 90% of AMI cases in men and 94% in women. These modifiable risk factors include cigarette smoking, physical inactivity, hypertension, obesity, elevated cholesterol levels (particularly LDL), and high triglyceride levels. In contrast, age, sex, and family history are nonmodifiable risk factors for atherosclerosis and AMI.[6][7]

Pathophysiology

The rupture of an atherosclerotic plaque initiates an inflammatory response of monocytes and macrophages, leading to thrombus formation and platelet aggregation. This process decreases oxygen delivery through the coronary artery, resulting in inadequate oxygenation of the myocardium (see Image. Specimen Showing MI). The subsequent inability to produce ATP in the mitochondria triggers an ischemic cascade, ultimately leading to apoptosis (cell death) of the endocardium or myocardial infarction.

With some exceptions due to genetic variation, coronary arteries exhibit unique and diagnostic territorial distributions. For example, the left anterior descending coronary artery supplies blood flow to the interventricular septum, anterolateral wall, and ventricular apex. The left circumflex artery supplies blood to the inferolateral wall. The right coronary artery supplies the right ventricle. The inferior wall is supplied either by the left circumflex or right coronary artery.[8]

Histopathology

The histological changes observed in MI evolve throughout the disease course. At time 0, no microscopic histologic changes are observed. Within 0.5 to 4 hours, light microscopy reveals waviness of fibers at the tissue periphery along with glycogen depletion. At 4 to 12 hours, the myocardium undergoes coagulation necrosis and edema. At 12 to 24 hours, the gross specimen appears dark and mottled, with contraction band necrosis and neutrophil predominance observed on histopathology. 

Subsequently, nuclei reduction occurs between 1 to 3 days, and then, within the next 3 to 7 days, macrophages emerge to clear apoptotic cells. Granulation tissue appears at 7 to 10 days, and collagen type I deposition occurs after 10 days. Ultimately, after 2 months, the myocardium undergoes scarring.

History and Physical

The history and physical examination alone may not always diagnose AMI definitively. The history should focus on the onset, quality, and associated symptoms. Recent studies suggest that diaphoresis and bilateral arm radiating pain are more commonly associated with MI in men. Other associated symptoms may include the following:

• Lightheadedness
• Anxiety
• Cough
• Choking sensation
• Diaphoresis
• Wheezing
• Irregular heart rate

The physical examination should include the patient’s vital signs and appearance, including diaphoresis, pulmonary evaluation, and cardiac auscultation. Specific vital aspects of the examination are as follows:

• Heart rate: Tachycardia, atrial fibrillation, or ventricular arrhythmia may be present, indicating cardiac electrical disturbances.

• Pulses: Unequal pulses may be observed if the patient has an aortic dissection, indicating a potential arterial problem.

• Blood pressure: Blood pressure is typically high in AMI but may become hypotensive if the patient is in shock due to compromised cardiac function.

• Respiratory findings: Tachypnea and fever may be present, indicating an inflammatory response.

• Neck veins: Distended neck veins may be observed, suggesting right ventricular failure and increased central venous pressure.

• Cardiac findings: The heart may exhibit lateral displacement of the apical impulse, a soft S1 sound, a palpable S4 sound, and a new mitral regurgitation murmur. A loud holosystolic murmur radiating to the sternum may indicate ventricular septal rupture.

• Pulmonary findings: Wheezing and rales may be heard if the patient has developed pulmonary edema, indicating fluid accumulation in the lungs.

• Extremities: Edema or cyanosis may be present in the extremities, with a sensation of coldness due to compromised circulation.

Evaluation

Early and prompt ECG testing should be employed in all patients presenting with chest pain. Women may experience atypical symptoms such as abdominal pain or dizziness and may present without chest pain (see Image. Myocardial Infarction Warning Signs in Women). Older patients often present with shortness of breath rather than chest pain in cases of MI. All of the aforementioned presentations should prompt ECG testing.[9][10][11]

The ECG is a highly specific diagnostic tool for MI, with a specificity of 95% to 97%. However, its sensitivity is relatively low, at approximately 30%. Right-sided, posterior lead placement and repeat ECG testing can increase ECG sensitivity. For example, peaked T-waves on ECG, known as "hyperacute T waves," often indicate early ischemia and will progress to ST elevation. When present, ST-elevation findings greater than 2 mm in 2 contiguous leads on ECG (inferior: leads II, III, aVF; septal: equal V1, V2; anterior: V3, V4; lateral: I, aVL, V5, V6) are indicative of a STEMI (see Image. ECG With Pardee Waves Indicating AMI). Often, ST depressions are visualized in opposite anatomical regions of the myocardium.

Diagnosing STEMI using the ECG can be challenging, particularly in patients with a left bundle branch block and pacemakers. However, specific criteria have been identified to aid in the diagnosis. Sgarbossa criteria suggest isolated ST elevations in lead aVR can indicate left main coronary artery occlusion in the appropriate clinical setting. Wellens criteria noted deeply biphasic T waves in leads V2 and V3, often predictive of an impending proximal left anterior descending artery occlusion, potentially leading to devastating anterior wall myocardial infarction.

Patients presenting with symptoms of MI may not exhibit diagnostic ST-elevation ECG abnormalities. In cases in which patients have typical chest pain but no obvious ST elevation, further investigation for NSTEMI is warranted. Subtle abnormalities on ECG, such as ST depressions and T-wave changes, may be present. Serial ECGs can be helpful in looking for dynamic changes. ECG findings without acute changes or any abnormalities are common in NSTEMI.

Diagnostic guidelines can aid practitioners in determining whether additional testing helps identify patients with NSTEMI. Considering the limited sensitivity of ECG in STEMI detection, troponin levels have become an almost universally employed diagnostic tool for patients with a clinical history suggestive of MI. The HEART score has been validated and popularized. The HEART score incorporates the clinician's suspicion, patient risk factors, ECG findings, and troponin levels to assess the patient's risk level.

Laboratory Studies

A cardiac troponin test should be the only cardiac marker test ordered. CDC, lipid profile, renal function, and metabolic panel are relevant labs. 

Cardiac biomarkers are helpful in the diagnosis of AMI, particularly NSTEMI. Troponin, creatine kinase-MB (CK-MB), and LDH are cardiac markers observed.

A troponin test is the most specific lab test for early detection of AMI; levels of the troponin isoforms I and T are measured. Troponin levels peak at 12 hours and remain elevated for 7 days. High-sensitivity troponin has been approved for use in the United States after being heavily studied and utilized in Europe. Although it is more sensitive than conventional troponin, it is also less specific. Thus, potential challenges include numerous false-positive interpretations.[3]

The level of CK-MB, an isoenzyme of creatine kinase usually found in the myocardium, reaches its peak at 10 hours and normalizes within 2 to 3 days. CK-MB is also not clinically utilized due to its low specificity, rapid rise, and normalization. 

LDH levels reach their peak after 72 hours and return to normal within 10 to 14 days. In clinical practice, LDH is not used to diagnose acute MI. 

B-type natriuretic peptide (BNP) should not be ordered as a marker for MI; instead, it is more valuable for risk stratification, particularly in patients with MI who subsequently develop heart failure.

Cardiac Imaging

Cardiac angiography is used to perform the percutaneous coronary intervention (PCI) procedure or determine obstructions in the coronary vessels.

An ECG is used to assess wall motion, degree of valve abnormality, ischemic mitral regurgitation, and presence of cardiac tamponade.

Treatment / Management

All patients with STEMI and NSTEMI require immediate administration of nonenteric-coated, chewable aspirin with a loading dose of 162 mg to 325 mg.[12] Additionally, patients should have intravenous access established, and oxygen supplementation should be administered if their oxygen saturation falls below 91%. Opioids may be used for pain control in addition to sublingual nitroglycerin if the patient's blood pressure is within an acceptable range.[13][14][15](B2)

The primary treatment approach for STEMI involves immediate reperfusion. The preferred method is emergent PCI. Before PCI, patients should receive dual antiplatelet therapy, which includes intravenous heparin infusion and an adenosine diphosphate inhibitor receptor (P2Y12 inhibitor), most commonly ticagrelor. A glycoprotein IIb/IIIa inhibitor or direct thrombin inhibitor may also be administered during the PCI procedure. If PCI is unavailable within 90 minutes of diagnosing STEMI, reperfusion using an intravenous thrombolytic agent should be attempted.

In stable asymptomatic patients with NSTEMI, the initial management approach is typically medical, focusing on using antiplatelet agents and other appropriate medications. However, PCI can be performed within 48 hours of admission if necessary. This delayed PCI strategy has been shown to potentially improve in-hospital mortality and decrease the length of hospital stay for NSTEMI patients.

In NSTEMI patients who experience refractory ischemia or ischemia with hemodynamic or electrical instability, PCI should be performed emergently.

Before discharge for acute MI, patients may routinely be prescribed aspirin, a high-dose statin, a beta-blocker, and possibly an ACE inhibitor.

If PCI is considered the treatment option for an acute MI, it is recommended to perform the procedure within 12 hours of symptom onset. If fibrinolytic therapy is considered the primary reperfusion strategy, it should be initiated within 120 minutes. In addition to reperfusion strategies, parenteral anticoagulation is recommended for all patients with acute MI, regardless of whether they undergo PCI or receive fibrinolytic therapy.

Differential Diagnosis

Differential diagnoses for AMI include the following: 

• Aortic dissection: This is a life-threatening condition with a tear in the inner layer of the aorta, leading to the separation of the layers and potential obstruction of blood flow.

• Pericarditis: Inflammation of the pericardium can cause chest pain that may resemble an AMI.

• Acute gastritis: Inflammation of the stomach lining can cause upper abdominal pain that may be mistaken for cardiac-related chest pain.

• Acute cholecystitis: Inflammation of the gallbladder can cause right upper-quadrant abdominal pain that can radiate to the chest and mimic cardiac symptoms.

• Asthma: Acute asthma exacerbation can lead to shortness of breath, wheezing, and chest tightness, which may be mistaken for cardiac symptoms.

• Esophagitis: Inflammation of the esophagus can cause chest pain, mainly if it is related to gastroesophageal reflux disease (GERD) or other esophageal disorders.

• Myocarditis: Heart muscle inflammation can present with chest pain and other symptoms similar to AMI.

• Pneumothorax: A collapsed lung can cause sudden chest pain and difficulty breathing, mimicking cardiac-related symptoms.

• Pulmonary embolism: Blockage of a pulmonary artery by a blood clot can lead to chest pain, shortness of breath, and other symptoms that may resemble an AMI.

Prognosis

AMI carries a significant risk of mortality outside of the hospital environment. Data indicate that at least one-third of patients succumb to the condition before reaching the hospital, and an additional 40% to 50% do not survive upon arrival. Furthermore, another 5% to 10% of patients will experience mortality within the first 12 months after an MI.

The prognosis of AMI depends on the extent of muscle damage. Better outcomes are seen in patients who undergo early perfusion, including thrombolytic therapy within 30 minutes of arrival or PCI within 90 minutes. Patients with preserved ejection fraction have better outcomes than those with reduced ejection fraction. 

Medical management following an AMI is crucial for improving long-term outcomes. Initiating medications, such as aspirin, beta-blockers, and ACE inhibitors, is standard practice to help prevent recurrent cardiovascular events.

Factors that negatively affect prognosis include the following:

• Diabetes
• Advanced age
• Prior MI, peripheral vascular disease, or stroke
• Delayed reperfusion
• Diminished ejection fraction (the strongest predictor)
• Presence of congestive heart failure
• Elevated C-reactive protein and BNP levels
• Depression

A high readmission rate affects about 50% of patients within the first 12 months after the initial MI. The overall prognosis depends on factors such as the ejection fraction, age, and comorbidities. Patients who do not undergo revascularization procedures have poorer outcomes than those who undergo revascularization. The most favorable prognosis is observed in patients with early and successful reperfusion and preserved left ventricular function.[16][17][18]

Complications

Primary complications of AMI include the following:

• New-onset mitral regurgitation
• Ventricular septal rupture
• Left ventricular aneurysm
• Arrhythmias
• Emboli