I. Epidemiology and Incidence of ACS in Critically Ill Patients

ACS remains the leading cause of cardiovascular death globally. In the ICU, stressors such as sepsis and hemodynamic instability amplify coronary risk and often yield atypical presentations.

• Global burden: Ischemic heart disease causes over 9 million deaths per year worldwide; age-adjusted mortality is declining in high-income countries but rising in low-resource settings.
• ICU prevalence: Sepsis, hypoxemia, hypotension, and tachyarrhythmias precipitate Type 2 MI; troponin elevations occur in up to 40% of septic patients.
• High-risk comorbidities: Diabetes (increases silent ischemia), Chronic Kidney Disease (CKD) (increases vascular calcification, chronic troponin elevation), prior Myocardial Infarction (MI) (residual plaque burden, remodeling).

II. Pathophysiology of Acute Coronary Syndromes

Atherosclerotic plaque instability and thrombosis underpin ACS. The extent and duration of coronary occlusion dictate clinical severity from unstable angina to STEMI.

Plaque Evolution and Disruption

• Thrombus burden: Partial occlusion often leads to unstable angina or NSTEMI; complete occlusion typically results in STEMI. Microvascular obstruction can worsen reperfusion injury even after epicardial flow is restored.
• Ischemia continuum: Myocyte injury may be reversible within the first few minutes of ischemia. However, irreversible necrosis typically begins after approximately 20–30 minutes of severe hypoperfusion.

III. Impact of Chronic Diseases on ACS Presentation

Diabetes, CKD, and prior MI alter pathobiology and symptom patterns, complicating ACS recognition and management.

• Diabetes mellitus:
  • Accelerates atherosclerosis; causes autonomic neuropathy leading to silent or atypical ischemia.
  • Patients may present more often with dyspnea, fatigue, or gastrointestinal discomfort than classic chest pain.
• Chronic kidney disease (CKD):
  • Baseline troponin is often elevated due to chronic myocardial stress and reduced clearance. Use a significant change (delta, e.g., ≥ 20% if baseline elevated, or absolute changes per local lab protocol) over serial testing to define acute MI.
  • Uremia-related platelet dysfunction alters the balance between bleeding and thrombosis.
• Prior MI:
  • Scar tissue and ventricular remodeling can blunt ischemic pain perception.
  • Increased risk of ventricular arrhythmias and heart failure development or exacerbation.

IV. Social Determinants of Health as Risk Modifiers

Socioeconomic factors, health literacy, and cultural barriers significantly influence ACS risk, timely diagnosis, and long-term outcomes.

• Medication access: Cost and insurance gaps can lead to poor adherence to essential cardiovascular medications like antiplatelets, statins, and antihypertensives.
• Health literacy/cultural factors: Delayed symptom recognition, language barriers, and mistrust of healthcare systems can significantly delay presentation and treatment.
• Socioeconomic status: Patients from low-income backgrounds often present with more advanced disease and experience higher in-hospital mortality rates.

V. Clinical Presentation: Typical and Atypical Symptoms

Classic ACS manifests as substernal chest pressure with autonomic signs. High-risk groups, including women, the elderly, and individuals with diabetes, often lack typical pain, requiring vigilance for alternative presentations.

Typical Symptoms:

• Central chest pressure, tightness, squeezing, or heaviness, typically lasting more than 20 minutes. Pain may radiate to the left arm (or both arms), neck, jaw, or back.
• Associated autonomic symptoms: Diaphoresis (sweating), nausea, vomiting, dyspnea (shortness of breath), and anxiety or a sense of impending doom.

Atypical Presentations (more common in women, elderly, and patients with diabetes):

• Isolated dyspnea, syncope (fainting) or presyncope, profound fatigue or weakness.
• Epigastric pain or discomfort (may be mistaken for indigestion), nausea, and/or vomiting.
• Minimal or no chest discomfort; pain may be described as aching, stabbing, or pleuritic.

Associated Signs:

• Hypotension or hypertension.
• Tachyarrhythmias or bradyarrhythmias.
• Signs of heart failure (e.g., S3 gallop, pulmonary rales, jugular venous distension).

VI. ECG Criteria for ACS Recognition

Rapid ECG interpretation is essential to distinguish STEMI from NSTEMI and to detect STEMI equivalents that mandate urgent reperfusion therapy.

STEMI Diagnosis:

• New ST-segment elevation at the J-point in at least two contiguous leads:
  • ≥1 mm (0.1 mV) in all leads other than V2-V3.
  • For leads V2-V3: ≥2 mm (0.2 mV) in men ≥40 years, ≥2.5 mm (0.25 mV) in men <40 years, or ≥1.5 mm (0.15 mV) in women regardless of age.
• New or presumed new left bundle branch block (LBBB) in the context of ischemic symptoms is considered a STEMI equivalent (though Sgarbossa criteria or modified Sgarbossa criteria can aid in diagnosing MI in LBBB).

Posterior MI Recognition:

• Often presents with ST-segment depression ≥0.5 mm in leads V1-V3 (especially V2-V3).
• Tall R waves (R/S ratio >1) in V1-V2 may be present.
• Confirm with ST-segment elevation ≥0.5 mm in posterior leads (V7-V9). (Note: ≥1mm for men <40 years in V7-V9).

Other STEMI Equivalents (indicate acute coronary occlusion):

• Hyperacute T waves: Broad-based, peaked, and symmetrical T waves, often an early sign of STEMI.
• de Winter pattern: Upsloping ST-segment depression ≥1 mm at the J-point in precordial leads, followed by tall, positive, symmetrical T waves.
• Wellens syndrome: Deeply inverted or biphasic T waves in leads V2-V3, indicating critical stenosis of the left anterior descending (LAD) artery. This is typically seen in a pain-free interval and signals high risk of impending large anterior MI.

VII. Biomarker Algorithms and MI Classification

High-sensitivity cardiac troponin (hs-cTn) assays enable rapid 0/1-hour or 0/2-0/3-hour rule-in/rule-out protocols. Distinguishing Type 1 MI from Type 2 MI is crucial as it guides antithrombotic therapy decisions.

High-Sensitivity Troponin Protocols:

Specific thresholds vary by assay. The following are conceptual examples:

Chronic elevations: Common in CKD and heart failure. A significant rise and/or fall (delta) from the patient’s baseline, often defined as ≥ 20% if the baseline is elevated, is used to define acute myocardial injury in this context.

Myocardial Infarction Classification:

Clinical implications: Antiplatelet and anticoagulant therapies are the cornerstone for Type 1 MI but may be unnecessary or even harmful in Type 2 MI if the bleeding risk is high and there’s no evidence of acute plaque rupture.