Inferior Myocardial Infarction

Etiology

Atherosclerosis is characterized by the accumulation of fatty deposits (plaque) within the arterial intima. Atherosclerosis can begin in childhood with the development of fatty streaks that progress with age into fibrous cholesterol plaques. When this process involves the coronary arteries, it is called coronary artery disease. The portion of the plaque adjacent to the vessel's lumen is the fibrous cap, and thinner, inflamed caps have a higher risk of rupture. When coronary artery plaques rupture, highly thrombogenic substances inside the plaque are released into the blood, leading to rapid thrombus formation, sudden occlusion of the coronary artery, ischemia, and possible infarction (death of myocardial tissue). Acute coronary syndrome results from the loss of integrity of the protective covering over an atherosclerotic plaque. Rupture of a plaque within a coronary artery that perfuses the inferior wall of the heart results in an inferior MI.[5]

Epidemiology

Myocardial infarction is a leading cause of global morbidity and mortality. Due to advances in medical care, patient education, and risk factor management, the incidence of MI has declined in the United States. Modifiable risk factors include hypertension, hyperlipidemia, tobacco use, diabetes mellitus, obesity, physical inactivity, and psychosocial stress. The nonmodifiable risk factors are age and family history. The risk of MI increases with age, and men have a higher risk than women. Black individuals have higher mortality rates from MI than White individuals, reflecting disparities in patient care. Inferior wall MIs account for 40% to 50% of all MIs and have a better prognosis than other anatomic territories, with a mortality rate of 2% to 9%. However, up to 40% of inferior wall MIs involve the right ventricle, which is associated with worse outcomes.[1][6][7]

Pathophysiology

The pathophysiology of MI involves rupture of a coronary artery plaque, platelet aggregation and thrombus formation, and distal occlusion of the vessel lumen resulting in diminished flow. This narrowing or occlusion of a vessel can progress to myocardial ischemia and necrosis. The RCA runs in the AV groove and continues to the posterior interventricular groove, where it gives rise to the PDA and supplies the inferior wall in right-dominant circulation. In left-dominant circulation, the PDA arises from the LCx. A lesion in the RCA usually causes inferior wall infarction. 

The RCA perfuses the SA and AV node, so bradycardia, AV nodal block, and arrhythmias are associated with inferior wall MIs.[8] Sinus bradycardia is common in early inferior ST-segment elevation myocardial infarction. For example, results from a study demonstrated that sinus bradycardia was 3 times more common in inferior MIs than in anterior MIs. Furthermore, proximal RCA occlusion caused sinus bradycardia more often than mid- or distal RCA occlusion, and LCx occlusion was not associated with sinus bradycardia.[9] 

AV nodal block is common in inferior wall MIs because the posterolateral RCA supplies part of the AV node in right-dominant circulation. RCA occlusion causes the inferior myocardial wall to release acetylcholine, contributing to bradycardia and AV nodal block.[8][9] Transient, second-degree, Mobitz type I AV nodal block is more common in inferior MI caused by RCA occlusion. Second-degree, Mobitz type II AV nodal block carries a worse prognosis when present.[9] The Bezold-Jarisch reflex is a triad of hypotension, bradycardia, and peripheral vasodilation, often caused by an inferior wall MI. This reflex is caused by stimulation of cardiopulmonary mechanoreceptors associated with unmyelinated, vagal nerve afferent C fibers.[9]

Histopathology

Atherosclerosis involving the coronary arteries is known as coronary artery disease (CAD). The histopathologic features of CAD evolve and can be divided into several stages. The initial lesions of atherosclerosis often begin in childhood as fatty streaks. These lesions do not disrupt the arterial architecture and commonly occur in adolescents and young adults. Over time, these fatty streaks can develop into atherosclerotic plaques. Characteristics of atheromatous plaques include a fibrous cap and a necrotic lipid core. Eventually, these fibrous caps can rupture, releasing the contents of the necrotic lipid core into the blood, which can result in thrombus formation. Depending on the size and magnitude of the thrombus, occlusion of the coronary artery can occur, leading to ischemia and potential infarction.[10]

History and Physical

The history should elicit the onset and character of symptoms, including chest pain or shortness of breath. A past medical history of diabetes mellitus, CAD, prior MI, and hypertension is pertinent. Family history of CAD and social history of tobacco use are also important factors. Medication history, including the recent use of phosphodiesterase type 5 inhibitors, can uncover contraindications to the use of nitroglycerin. Physical examination should include vital signs (heart rate, blood pressure, oxygen saturation) and evaluation for jugular venous distension (suggestive of right ventricular infarction), assessment of heart rhythm, and auscultation for murmurs and gallops. Evidence of volume overload, such as peripheral edema or pulmonary crackles (rales) on lung examination, should also be noted.

Evaluation

Evaluation should include an electrocardiogram (ECG) for detecting ST-segment changes, including ST-segment elevation in the inferior leads (II, III, aVF) with reciprocal change in other leads. Serial troponin levels, a complete blood count, a basic metabolic panel, and coagulation studies should be performed in all patients in anticipation of percutaneous coronary intervention or thrombolytic therapy. Patients presenting with typical chest pain symptoms and an ECG revealing ST-segment elevation should proceed directly to the cardiac catheterization lab for primary percutaneous coronary intervention if available.[11] 

The ECG remains the initial test of choice. Traditionally, reciprocal ST-segment depression is observed in leads electrically opposite to the infarct location; however, ST-segment depression can occur in any lead, with the infarct area acting as the negative pole.[11] Inferior MI is associated with ST-segment elevations in the inferior leads (II, III, and aVF). (See Image. Electrocardiogram With Pardee Waves).

The relative magnitude of ST elevation in lead II versus lead III can sometimes help distinguish whether the RCA or the LCx is involved. If ST-segment elevation in lead III is higher than in lead II, the RCA is likely involved. When the ST-segment elevation magnitude is greater in lead II compared with lead III, the LCx is more likely to be involved. Reciprocal ST-segment depression is most common in the lateral leads I and aVL. RCA involvement may also produce ST-segment elevation in the right-sided leads.[12][13] The most common ECG finding associated with an inferior wall myocardial infarction is ST-segment elevation in leads II, III, and aVF, accompanied by reciprocal ST-segment depression in leads I and aVL. Results from a large meta-analysis found that the most sensitive and specific findings for inferior MI were ST-segment elevation in lead III, along with concurrent ST-segment depression in lead I.[7]

Treatment / Management

If ST-segment elevation is present on the ECG, the patient should receive emergent coronary angiography with primary percutaneous coronary intervention; the goal door-to-balloon time is less than 90 minutes. If the facility does not have a cardiac catheterization lab or transport times are outside this time window, thrombolysis should be considered. If right ventricular infarction is suspected, nitrates should be avoided due to the risk of hypotension, and intravenous crystalloids should be provided to optimize preload. The right ventricle contains less myocardium than the left ventricle and depends on adequate preload to maintain cardiac output. If there is damage to the right ventricle, preload reduction from nitrates could result in significant hypotension. Treatment with intravenous crystalloids and, if necessary, vasopressors is required in the setting of hypotension. Other treatments include an oral aspirin dose of 162 mg to 325 mg, intravenous unfractionated heparin, and additional antiplatelet agents such as clopidogrel or prasugrel.[14][15][16](A1)

High-grade conduction abnormalities are associated with higher mortality. Temporary transvenous pacing is recommended in cases of complete AV nodal block that does not improve with reperfusion. When pacing is not available, intravenous isoproterenol, dopamine, or epinephrine has been used temporarily.[1] (B3)

Differential Diagnosis

The differential diagnosis of acute chest pain can be extensive. Symptoms that indicate an increased likelihood of cardiac disease include exertional chest pain, diaphoresis, nausea and vomiting, and radiation of pain to the arm or jaw. Other life-threatening illnesses to consider include pulmonary embolism, acute aortic dissection, pneumothorax, esophageal rupture, and cardiac tamponade. Atypical symptoms may occur, especially in women, older adults, and individuals with diabetes mellitus. Because myocardial ischemia symptoms include nausea, vomiting, epigastric pain, and fatigue, it is imperative to consider the cardiac causes of these symptoms and not dismiss them as gastrointestinal tract illnesses.

Pertinent Studies and Ongoing Trials

The recently reported Fractional Flow Reserve Versus Optical Coherence Tomography to Guide Revascularization of Intermediate Coronary Stenoses (FORZA) trial and the OCT-Features Of moRphology, coMposItion anD instABility of culprit and not culprit coronary pLaquE in ACS patient (OCT-FORMIDABLE) have evaluated the use of fractional flow reserve and optical coherence tomography to help risk-stratify patients for interventional cardiac procedures.[17]

Prognosis

The mortality rate of inferior wall MI is approximately 2% to 9%.[7] While inferior wall MIs usually have a favorable prognosis, a few factors may increase mortality. Approximately 40% of inferior wall infarctions also involve the right ventricle. Right ventricular infarctions are very preload-dependent, and nitrates may precipitate hypotension. Obtaining an ECG using right-sided leads and noting ST-segment elevations in V₄R may suggest the diagnosis. If timely treatment does not occur, myocyte death increases, and there is a risk of cardiogenic shock. Additionally, AV nodal block and bradycardia may occur because the RCA supplies blood to the SA and AV nodes. A high-grade AV nodal block (defined as a second-degree, Mobitz type II or third-degree AV nodal block) occurs in 19% of patients with acute inferior wall myocardial infarction. The amount of collateral circulation to the AV node impacts the incidence of heart block. If there are concomitant perfusion abnormalities in other coronary arteries, collateral circulation to the AV node is reduced, and the likelihood of AV nodal block increases. 

Complications

The complications of inferior myocardial infarctions include:

• Cardiogenic shock
• AV nodal block
• Bradyarrhythmias
• Ventricular fibrillation