3.2 Acute Coronary Syndromes & Heart Failure

3.2 Acute Coronary Syndromes & Heart Failure

Acute Coronary Syndromes (ACS): Pathophysiology and Classification

Acute Coronary Syndromes (ACS) represent a continuum of myocardial ischemic conditions resulting from an imbalance between myocardial oxygen demand and supply. The primary underlying pathophysiology is the rupture or erosion of an atherosclerotic plaque in a coronary artery, leading to subsequent platelet aggregation, thrombus formation, and varying degrees of vascular occlusion. ACS is broadly classified into three categories based on clinical presentation, ECG findings, and cardiac biomarker levels:

1. Unstable Angina (UA): Characterized by ischemic chest pain occurring at rest, new-onset severe angina, or increasing frequency/intensity of prior angina. Crucially, in UA, cardiac biomarkers (such as high-sensitivity troponin) remain negative, indicating no significant myocardial necrosis. ECG may show ischemic changes (ST depression or T-wave inversion) but no ST elevation.
2. Non-ST-Segment Elevation Myocardial Infarction (NSTEMI): The clinical presentation and ECG findings are similar to those of UA; however, cardiac biomarkers are elevated, signifying that myocardial necrosis has occurred. The coronary occlusion in NSTEMI is typically partial or transient.
3. ST-Segment Elevation Myocardial Infarction (STEMI): This is the most severe form of ACS, resulting from a complete, prolonged occlusion of a major epicardial coronary artery. The hallmark ECG finding is ST-segment elevation in two or more contiguous leads. Cardiac biomarkers will be elevated, and prompt reperfusion therapy is mandatory to salvage myocardium and prevent transmural infarction.

Initial Management of ACS

The immediate management of a patient presenting with suspected ACS aims to relieve ischemia, prevent further thrombosis, and stabilize the patient hemodynamically. The classic mnemonic "MONA" (Morphine, Oxygen, Nitroglycerin, Aspirin) has evolved to reflect current evidence-based guidelines:

• Aspirin: Administer 162-325 mg (typically 324 mg) chewed immediately to achieve rapid antiplatelet effect via inhibition of thromboxane A2.
• Nitroglycerin: Sublingual nitroglycerin (0.4 mg every 5 minutes up to 3 doses) promotes coronary vasodilation and reduces preload. It is contraindicated in patients with right ventricular infarction, severe hypotension, or recent use of phosphodiesterase inhibitors (e.g., sildenafil).
• Oxygen: Only administer supplemental oxygen if the patient is hypoxic (oxygen saturation <90%) or in respiratory distress. Hyperoxia can cause coronary vasoconstriction and may worsen outcomes.
• Morphine: Use is now restricted to patients with unacceptable pain unresponsive to nitroglycerin, as it may delay the absorption and efficacy of oral antiplatelet agents.
• P2Y12 Inhibitors: Dual antiplatelet therapy (DAPT) is the standard of care. Agents like clopidogrel, ticagrelor, or prasugrel should be loaded early, especially if percutaneous coronary intervention (PCI) is planned.
• Anticoagulation: Intravenous unfractionated heparin, enoxaparin, or bivalirudin should be initiated to inhibit further thrombus propagation.

Reperfusion Strategies in STEMI

For patients with a confirmed STEMI, time is muscle. The primary goal is prompt restoration of coronary blood flow.

• Primary PCI: The preferred reperfusion strategy. The goal is a door-to-balloon time of less than 90 minutes.
• Fibrinolytic Therapy: Administered if PCI is not available within 120 minutes of first medical contact. The goal is a door-to-needle time of less than 30 minutes. Absolute contraindications include prior intracranial hemorrhage, known structural cerebral vascular lesion, suspected aortic dissection, and active bleeding.

Heart Failure Classification and Phenotypes

Heart Failure (HF) is a complex clinical syndrome characterized by the heart's inability to pump adequate blood to meet the metabolic demands of the body. It is broadly classified by the Left Ventricular Ejection Fraction (LVEF):

• Heart Failure with Reduced Ejection Fraction (HFrEF): LVEF ≤ 40%. Characterized by systolic dysfunction and impaired contractility.
• Heart Failure with Preserved Ejection Fraction (HFpEF): LVEF ≥ 50%. Characterized by diastolic dysfunction, impaired ventricular relaxation, and increased stiffness.

Acute Decompensated Heart Failure (ADHF) is a sudden worsening of HF symptoms requiring urgent intervention. Patients present along a continuum of congestion (wet vs. dry) and perfusion (warm vs. cold).

ADHF Clinical Profiles and Management Table

Guideline-Directed Medical Therapy (GDMT) for HFrEF

The cornerstone of chronic management for HFrEF focuses on neurohormonal blockade to prevent maladaptive cardiac remodeling and improve survival. The "four pillars" of modern GDMT include:

1. Beta-Blockers: Specifically carvedilol, metoprolol succinate, or bisoprolol. They reduce sympathetic overactivation and risk of arrhythmias.
2. Renin-Angiotensin System Inhibitors: An Angiotensin Receptor-Neprilysin Inhibitor (ARNI), such as sacubitril/valsartan, is preferred over ACE inhibitors or ARBs for superior mortality benefits.
3. Mineralocorticoid Receptor Antagonists (MRAs): Spironolactone or eplerenone. They block aldosterone, reducing fibrosis and sodium retention.
4. SGLT2 Inhibitors: Dapagliflozin or empagliflozin. Originally diabetes medications, they profoundly reduce HF hospitalizations and cardiovascular mortality across the LVEF spectrum.

In advanced stages or cardiogenic shock, Mechanical Circulatory Support (MCS) devices, including Intra-aortic Balloon Pumps (IABP), Impella devices, or Extracorporeal Membrane Oxygenation (ECMO), may be employed as a bridge to recovery, destination therapy, or cardiac transplantation.