Untitled Quiz

ACS encompasses a range of clinical presentations, from ST-segment elevation myocardial infarction (STEMI) to non-ST-segment elevation myocardial infarction (NSTEMI) or unstable angina.
It's almost always associated with rupture of an atherosclerotic plaque and partial or complete thrombosis of the infarct-related artery.
The primary cause of ACS is diminished myocardial blood flow due to an occlusive or partially occlusive coronary artery thrombus.

ACS is categorized based on electrocardiogram (ECG) changes.
ST-segment elevation ACS (STE ACS or STEMI)
Non-ST-segment elevation ACS (NSTE ACS), including non-ST-segment elevation myocardial infarction (NSTE MI) and unstable angina (UA).
Pathologic Q waves on the ECG after a STEMI typically indicate transmural MI.

Endothelial dysfunction, inflammation, and fatty streak formation contribute to atherosclerotic coronary artery plaque development.
Plaque rupture and subsequent thrombus formation significantly reduce myocardial blood flow and oxygen supply, leading to ischemia and potential infarction.
Thin fibrous caps in atherosclerotic plaques are often non-obstructive (<70% lumenal diameter) and so may not cause angina before rupture due to adequate autoregulation. Increased catecholamines during physical/emotional stress increase rupture likelihood.
Platelet adhesion and activation occur at injured plaque sites. Collagen in the damaged plaque activates platelet glycoprotein (GP) VI receptors, initiating platelet aggregation (via thrombin, thromboxane A2, ADP, epinephrine, and serotonin). This forms a platelet plug which the clotting cascade further traps cells in a thrombus. This dramatically reduces myocardial blood flow and oxygen supply.

MI is based on etiology:
- Rupture, fissure, or erosion of plaque (90%)
- Reduced myocardial oxygen supply or increased demand without coronary artery process
- MI without measurable biomarkers
- MI associated with PCI (percutaneous coronary intervention) or stent thrombosis, or CABG (coronary artery bypass graft) surgery.

After MI, there are acute and chronic adaptations to prevent hemodynamic collapse.
The SNS (sympathetic nervous system) and RAAS (renin-angiotensin-aldosterone system) are stimulated to compensate for reduced cardiac output. Chronic overactivation can lead to ventricular hypertrophy and reduced contractility.
Inflammatory mediators and collagen deposition cause myocardial fibrosis.
Possible complications include ventricular/bradyarrhythmias, heart block, heart failure, cardiogenic shock, LV (left ventricular) free-wall or septal rupture, thromboembolism, aneurysm, and pericarditis.

Patients typically present with acute distress.
The classic symptom is abrupt substernal chest pain or discomfort (squeezing, heaviness, tightness), lasting 10 minutes or more.
Symptoms may radiate to the arms, shoulders (especially the left), back, abdomen, or jaw. Other accompanying symptoms can include nausea, vomiting, diaphoresis or shortness of breath.
Many patients (especially older adults, women, and those with DM [diabetes mellitus], renal impairment, or dementia experience atypical symptoms — epigastric pain, indigestion, pleuritic chest pain, increasing exertional dyspnea.
Physical exam findings are not specific to ACS.

Obtain 12-lead ECG within 10 minutes of presentation (detecting ischemia: ST-segment elevation (STE), depression, or T-wave inversion).
New LBBB (left bundle-branch block) strongly suggests acute MI.
Cardiac troponin (T or I) measured at presentation and repeated in 3-6 hrs (myocardial injury; elevated within 2–4 hours, & elevated up to 2 weeks).
Serial troponin with a rise and/or fall of 20% confirms acute myocardial injury. Elevated troponin values in setting of ischemic changes on ECG or other evidence of ischemia confirms MI diagnosis.
Patients with atypical ACS symptoms and negative troponin may have non-ACS etiology.

Short-term goals include restoring infarct-artery blood flow (prevent expansion in MI; prevention of complete occlusion/MI in UA) to prevent complications/death, relieving chest discomfort, and maintaining normoglycemia.
Long-term goals after MI focus on controlling modifiable CHD (coronary heart disease) risk factors, preventing systolic heart failure, recurrent MI/stroke, and death.

Stratification of patients based on presentation, past medical history, ECG, and biomarkers is crucial in deciding on low, medium, or high-risk approaches: reperfusion therapy (early invasive approach), or medical management.
For STEMI, emergent referral for primary PCI (percutaneous coronary intervention) is the priority for its highest-risk of death potential.
For patients presenting with NSTE-ACS, early pharmacotherapy involves intranasal oxygen, sublingual nitroglycerine, aspirin, and either a β-blocker (Ca Channel Blocker), or an anticoagulant (UFH, LMWH).
General measures (hospital admission, oxygen, ECG, vital signs, pain relief, and antithrombotic therapy) are employed.
Non-pharmacologic options include fibrinolysis or primary PCI for STEMI.
ACS pharmacotherapy includes aspirin, β-blockers, nitrates, and use of fibrinolytics for selected patients. Antiplatelet agents and anticoagulants are administered concurrently.
General measures, medications, and clinical assessments are all critical.