Coronary Heart Disease Overview

Coronary Heart Disease (Coronary Artery Disease)

• Coronary heart disease (CHD) encompasses ischemic heart disease, atherosclerosis, angina, and acute coronary syndrome (ACS).
• Ischemia is inadequate blood supply to an organ or part of the body, often the heart muscles.
• Infarction is tissue death due to a lack of blood supply.
• Coronary Circulation involves the right coronary artery (RCA), left main coronary artery (LCA), circumflex artery (CFX), left anterior descending artery (LAD), and acute marginal artery (supplying the right ventricle) and posterior descending/interventricular artery (PD) supplying the posterior septum.
• Causes of Coronary Heart Disease include atherosclerosis, embolus, vasospasm, and vasculitis.

Risk Factors for Atherosclerosis

• BMI greater than 30
• Age greater than 65
• Diabetes
• Hypertension
• Ethanol use
• Altered lipids (autoimmune)
• Relatives with history of cardiovascular disease
• Tobacco use

Atherosclerosis

• Atherosclerosis involves damage to endothelial cells, LDL accumulation in the tunica intima, attracting monocytes (via cytokines/adhesion molecules), foam cell production, and smooth muscle cell proliferation.
• LDL (low-density lipoprotein) contributes to plaque formation within the arteries.
• HDL (high-density lipoprotein) removes cholesterol from plaques.

Oxygen Demand and Supply

• Ischemia is an inadequate blood supply, resulting from an imbalance of oxygen demand and supply.
• Normal metabolism requires oxygen supply; Myocardial ischemia results from insufficient oxygen supply.

Acute Coronary Syndrome (ACS)

• Plaque disruption and platelet aggregation can lead to unstable plaques, unstable angina, and potentially NSTEMI (Non-ST-elevation Myocardial Infarction) or STEMI (ST-elevation myocardial infarction).

Pathophysiology of Symptoms

• Symptoms of CHD include chest pain, left arm, jaw pain, heavy weight on chest (elephant on chest), a feeling of impending doom.
• Diabetic patients may present with atypical symptoms masked by neuropathy; elderly individuals and post-heart transplant patients.
• Pain associated with Stable angina occurs only during exertion, linked to stable plaques and ischaemia in the subendocardial region (approx. 70% occlusion).

Acute Coronary Syndrome (ACS) - Unstable Angina

• Unstable angina is characterized by unstable plaques (approx. 90% occlusion), symptoms at rest, and ischaemia in the subendocardial region.

NSTEMI and STEMI

• NSTEMI (Non-ST-elevation myocardial infarction) represents subendocardial infarct with unstable plaques and thrombus formation (greater than 90% occlusion; long-term ischemia).
• STEMI (ST-elevation myocardial infarction) refers to transmural infarct resulting from total occlusion.

ECG Changes

• ECG (electrocardiogram) can assess the region affected. ST elevation (or depression) can help detect the presence of NSTEMI or STEMI..

Coronary Artery Bypass Grafting (CABG)

• CABG involves creating new pathways to improve blood flow, avoiding blocked arteries or sections with cholesterol plaques.

Complications Post MI

• Arrhythmias
• Heart failure
• Secondary MI
• Pericarditis
• Rupture
• Clot formation (embolus)

Diagnosis

• Diagnosis involves assessment of symptoms, ECG changes, blood biomarkers like troponins and CKMB, ECHO abnormalities, and catheterization/PCI.

Coagulation and Drugs

• Coagulation involves a complex cascade of factors leading to thrombus formation.
• Drugs targeting platelet activation (antiplatelet drugs like aspirin, clopidogrel), thrombin formation (anticoagulants like heparin and warfarin). Direct oral anticoagulants (DOACs like rivaroxaban, apixaban, dabigatran) affect specific factors.

Thrombus Formation

• Thrombi form (arterial or venous) due to rupture of atherosclerotic plaques (arterial) or altered vessel walls (venous).

Platelet Activation

• Platelet activation is a crucial step in thrombus formation triggered by exposed collagen, ADP, or thromboxane A2 releasing chemicals, leading to platelet aggregation.

Treatment

• Antiplatelet drugs like aspirin and clopidogrel inhibit platelet activation.
• Anticoagulant drugs like heparin and warfarin target various factors in the clotting cascade for preventive or treatment of thrombosis.
• Nitrates, CCBs, and beta-blockers are used to treat angina symptoms
• Thrombolytics like streptokinase and alteplase may be used to break down clots.

Angina Treatment

• For Stable Angina and secondary prevention, short-acting nitrates (sublingual GTN) for quick pain relief, preventative beta blockers/CCBs, long-acting nitrates, ivabradine, ranolazine. For atherosclerotic component, low-dose aspirin/statins are used.

Fibrinolysis

• Fibrinolysis is the breakdown of blood clots by enzymes like plasmin, which degrades fibrin clots and the core of a thrombus.

Invasive Methods

• Percutaneous coronary intervention (PCI) or angioplasty is a procedure that widens blocked coronary arteries to restore blood flow through the vessel.

Coronary Artery Bypass Grafting (CABG)

• CABG involves creating new passages to improve blood flow by bypassing blocked arteries through grafts from other blood vessels.

Nitrates Mechanism

• Nitrates relax smooth muscle via the NO-cGMP pathway.

Nicorandil Mechanism

• Nicorandil opens ATP-sensitive K+ channels, causing hyperpolarization and decreasing intracellular calcium levels to result in vasodilation.

Drug Mechanisms in Angina Therapy

• Drugs act on different systems influencing coronary blood flow and decreasing preload (e.g. by reducing heart rate, venous return, or afterload).

Secondary Prevention of Angina

• Secondary Prevention involves treatment of angina to reduce risk of further occurrences, and involves lifestyle changes, aspirin, statins and blood pressure control.