Sindrom Koroner Akut

01Pathophysiology

Acute coronary syndrome (ACS) is a continuum of myocardial ischemia caused by an abrupt reduction in coronary blood flow. The central event is rupture or erosion of a vulnerable atherosclerotic plaque in a coronary artery. Vulnerable plaques have a thin fibrous cap overlying a large lipid-rich necrotic core. When the cap breaks, the thrombogenic lipid core is exposed to circulating blood, triggering platelet adhesion, activation, and aggregation, followed by activation of the coagulation cascade. This results in an intraluminal thrombus that partially or completely occludes the vessel.
The degree and duration of occlusion determine the clinical syndrome. A completely occlusive thrombus that persists causes transmural ischemia and necrosis, which is STEMI. A partially occlusive or transiently occlusive thrombus causes subendocardial ischemia: if myocyte death occurs (troponin rises), it is NSTEMI; if ischemia is reversible without necrosis, it is unstable angina.
The subendocardium is the region most vulnerable to ischemia because it is farthest from the epicardial blood supply and experiences the highest wall tension during systole. This explains why partial occlusion injures the subendocardium first, producing ST-depression rather than ST-elevation.
Oxygen supply-demand mismatch (type 2 MI) is a separate mechanism where the coronary arteries are not acutely thrombosed, but myocardial oxygen demand exceeds supply due to conditions such as severe anemia, sustained tachyarrhythmia, hypotension, or sepsis. This distinction matters because the management is directed at the underlying trigger rather than at reperfusion therapy.

02Classification and Clinical Manifestation

Clinical presentation varies by the territory of the occluded artery:

Atypical presentations are a common exam trap. Women, elderly patients (>75), and diabetic patients may present without classic chest pain. Instead, they may report isolated dyspnea, nausea, vomiting, fatigue, or syncope. Diabetic patients develop autonomic neuropathy that blunts the perception of ischemic pain, which is why their infarctions are described as "silent."

03Diagnostic Workup

The ECG is the single most important initial test and dictates the management pathway. In a patient with chest pain, the ECG separates STEMI (requiring emergent reperfusion) from NSTEMI/UA (managed medically first, with possible invasive strategy). You must obtain it within 10 minutes of presentation.
Troponin is the most sensitive and preferred biomarker. High-sensitivity troponin assays allow earlier detection but are also elevated in non-ACS conditions such as heart failure, myocarditis, pulmonary embolism, renal failure, and sepsis. The key distinguishing feature of acute MI is a rise-and-fall pattern rather than a chronically stable elevation.
CK-MB has a narrower detection window. Its primary remaining utility is detecting reinfarction: if a patient who had an MI five days ago develops new chest pain, troponin may still be elevated from the first event, but CK-MB would have already normalized and a new rise confirms a second infarction.
Coronary angiography is both diagnostic and therapeutic. For STEMI, it is performed emergently as part of primary PCI. For NSTEMI, the timing of angiography depends on risk stratification (within 24 hours for high-risk features such as recurrent ischemia, hemodynamic instability, or elevated TIMI/GRACE score).

04Management and Treatment

Acute stabilization follows the mnemonic framework of initial therapies: aspirin, anticoagulation, P2Y12 inhibitor, beta-blocker, statin, and nitroglycerin. All patients with suspected ACS receive aspirin immediately. Dual antiplatelet therapy (DAPT) with aspirin plus a P2Y12 inhibitor is the cornerstone of antithrombotic management for at least 12 months after the event.
For STEMI, the next best step after ECG confirmation is emergent reperfusion. Primary percutaneous coronary intervention (PCI) is the preferred reperfusion strategy if it can be performed within 90 minutes of first medical contact (door-to-balloon time). If PCI is not available within 120 minutes, fibrinolytic therapy must be administered within 30 minutes (door-to-needle time). Absolute contraindications to fibrinolytics include active internal bleeding, suspected aortic dissection, prior intracranial hemorrhage, ischemic stroke within 3 months, and known intracranial neoplasm.
For NSTEMI and unstable angina, the initial approach is medical stabilization with antiplatelet, anticoagulation, beta-blocker, and statin therapy. Invasive coronary angiography is then performed based on risk stratification. High-risk features (ongoing chest pain, hemodynamic instability, new heart failure, sustained ventricular tachycardia, very high troponin, dynamic ECG changes) warrant an early invasive strategy within 24 hours.
Beta-blockers reduce myocardial oxygen demand by lowering heart rate and contractility. They are contraindicated in patients with acute decompensated heart failure, cardiogenic shock, significant bradycardia (HR <60), heart block greater than first degree, or systolic blood pressure below 100 mmHg. In cocaine-induced ACS, beta-blockers are avoided because blocking beta-receptors leaves alpha-mediated vasoconstriction unopposed, worsening coronary spasm; benzodiazepines are used instead.
ACE inhibitors are started within 24 hours for patients with anterior STEMI, heart failure, or reduced ejection fraction. They reduce adverse remodeling and mortality. They are contraindicated in bilateral renal artery stenosis, hyperkalemia, and pregnancy.
Nitroglycerin provides symptom relief through venodilation (reducing preload) and coronary vasodilation. It must be avoided in right ventricular infarction because these patients are preload-dependent; reducing preload with nitrates or diuretics can cause severe hypotension. Always check right-sided ECG leads (V4R) when you see an inferior STEMI before giving nitroglycerin. Also contraindicated if the patient has taken a phosphodiesterase-5 inhibitor (sildenafil, tadalafil) within 24-48 hours, as the combination can cause life-threatening hypotension.
Long-term management after discharge includes indefinite aspirin, P2Y12 inhibitor for 12 months, high-intensity statin, beta-blocker (especially if reduced EF), ACE inhibitor (if indicated), lifestyle modification (smoking cessation, dietary changes, exercise, weight management), and cardiac rehabilitation.

05Differential Diagnosis and Distractors

06Traps and High-Yield Pearls

The most common way students lose points on ACS questions is by failing to recognize the management pathway split between STEMI and NSTEMI. When the vignette describes ST-elevation on ECG, the next best step is always emergent reperfusion (PCI or fibrinolytics), not serial troponins. Waiting for troponin results in a STEMI delays reperfusion and is a classic wrong answer.
Another frequent trap involves right ventricular infarction. When you see an inferior MI (ST-elevation in leads II, III, aVF), always think about RV involvement. The vignette will describe hypotension, clear lung fields, and elevated JVP. The tested concept is that nitroglycerin and diuretics are contraindicated because these patients need volume (IV normal saline) to maintain preload. If you give nitrates to an RV infarct patient, you drop their blood pressure further.
Cocaine-associated chest pain is another high-yield scenario. The tested principle is that beta-blockers are contraindicated. The correct management is benzodiazepines (to reduce sympathetic drive), nitroglycerin, and aspirin. If beta-blockade is needed later, use a combined alpha-beta blocker like labetalol only after the acute phase.
Distinguishing NSTEMI from unstable angina rests entirely on troponin. The clinical presentation and ECG may be identical. If troponin is elevated, it is NSTEMI. If troponin remains normal on serial measurements, it is unstable angina. This distinction does not change acute management, but it does affect prognosis (NSTEMI carries higher risk).
Finally, be alert for the aortic dissection masquerading as STEMI. The vignette gives tearing chest pain radiating to the back with a blood pressure difference between arms. If you administer fibrinolytics to this patient, you cause catastrophic hemorrhage. The test is evaluating whether you can identify the dissection before reflexively treating the ST-elevation. Always look for red flags of dissection before choosing reperfusion therapy.