## Overview of ST Elevation Myocardial Infarction Involving Right Coronary Artery (I21.11) ### Pathophysiology and Anatomical Significance ST-elevation myocardial infarction (STEMI) involving the right coronary artery (RCA) represents a critical cardiovascular emergency. The RCA typically originates from the right aortic sinus and supplies the right atrium, right ventricle, the inferior portion of the left ventricle, and the posterior third of the interventricular septum. In approximately 80% of individuals with right-dominant circulation, the RCA also gives rise to the posterior descending artery (PDA). Crucially, the RCA supplies the sinoatrial (SA) node in 60% of people and the atrioventricular (AV) node in 90%. Therefore, an acute occlusion of the RCA, usually due to atherosclerotic plaque rupture and subsequent thrombus formation, not only results in inferior wall ischemia but frequently leads to conduction disturbances and right ventricular dysfunction. The localized ischemia leads to the loss of myocardial contractility and can result in significant hemodynamic instability depending on the extent of the vessel involved and the presence of collateral circulation. ### Clinical Presentation and Right Ventricular Involvement Patients typically present with acute substernal chest pressure, often described as crushing or heavy, which may radiate to the jaw, neck, or left arm. However, RCA occlusions often present with significant autonomic symptoms, including nausea, vomiting, and diaphoresis, which are attributed to increased vagal tone (Bezold-Jarisch reflex) common in inferior wall infarctions. A subset of patients diagnosed with I21.11 will experience right ventricular infarction (RVI). These patients may present with a specific clinical triad of hypotension, clear lung fields on auscultation, and elevated jugular venous pressure. Recognizing RVI is paramount because these patients are highly preload-dependent; the standard administration of nitrates or diuretics can cause a profound and dangerous drop in blood pressure. ### Diagnostic Evaluation and ECG Criteria The diagnosis is primarily established via a 12-lead electrocardiogram (ECG) showing ST-segment elevation in the inferior leads (II, III, and aVF). In the specific context of an RCA occlusion, ST elevation in lead III is often greater than in lead II, and ST depression is frequently observed in leads I and aVL as a reciprocal change. To evaluate for associated right ventricular involvement, clinicians should obtain right-sided leads (V3R to V6R); ST elevation of 1 mm or more in lead V4R is highly specific for RV infarction. Laboratory findings include the rising and falling pattern of cardiac biomarkers, specifically high-sensitivity troponin T or I, which indicates myocardial necrosis. ### Standard of Care and Management The gold standard of treatment for I21.11 is immediate reperfusion therapy. Primary Percutaneous Coronary Intervention (PCI) is the preferred modality if it can be performed within 90 minutes of first medical contact. If PCI is unavailable within a reasonable timeframe, fibrinolytic therapy should be administered within 30 minutes of hospital arrival, provided there are no contraindications. Adjuvant pharmacological therapy includes aspirin, P2Y12 inhibitors (such as ticagrelor or clopidogrel), and anticoagulation (typically unfractionated heparin or bivalirudin). For patients experiencing RCA-associated bradycardia or high-degree AV block, atropine or temporary transvenous pacing may be required. Fluid resuscitation is the first line for hypotension in the setting of RV infarction, avoiding preload-reducing agents. Long-term management focuses on secondary prevention through the use of beta-blockers, ACE inhibitors, high-intensity statins, and lifestyle modifications including smoking cessation and cardiac rehabilitation.