Hid

• Ischemic Heart Disease (IHD) or Coronary Artery Disease (CAD) is a condition where there is an inadequate supply of blood and oxygen to a portion of the myocardium, often caused by atherosclerotic disease of a coronary artery
• Disease of the coronary arteries is mainly due to atheroma and its complications, particularly thrombosis; occasionally, other disorders like Aortitis, Polyarteritis, and other connective tissue disorders can also be involved
• Patients with IHD fall into two large groups: Chronic CAD (stable angina) and Acute coronary syndromes (ACSs), which encompass unstable angina and myocardial infarction (MI)
• The two main coronary arteries, branches of the ascending aorta, are the Left coronary arteries supplying LA, LV, and the anterior wall of the RV, and the Right coronary arteries supplying RA, RV, and the SA node
• Over 60% of the global burden of IHD occurs in developing countries, with the risk increasing with age; men are more affected than women, but CAD is the leading cause of death in both genders
• Risk factors for IHD include hypertension, elevated LDL/VLDL cholesterol, reduced HDL cholesterol, smoking, excess angiotensin II, obesity, insulin resistance, and diabetes mellitus
• The pathophysiology of IHD starts with atherosclerosis, a low-grade inflammatory state of the intima of medium-sized arteries, which progresses for decades before acute events, accelerated by risk factors like hypertension, hyperlipidemia, smoking, diabetes, and genetics
• Clinical features of stable angina include central chest pain, radiating to the shoulder/arm/neck/jaw, precipitated by exertion, relieved by rest or nitrates, lasting less than 10-15 minutes, and associated with breathlessness, diaphoresis, nausea, and anxiety
• The diagnosis of IHD relies heavily on the patient's history; investigations like ECG and coronary arteriography provide detailed anatomical information about the extent and nature of coronary artery disease
• Specific treatments for IHD include antiplatelet therapy with aspirin or clopidogrel, and anti-anginal drug treatments like nitrates, beta-blockers, calcium antagonists, and potassium channel activators
• Nitrates act directly on vascular smooth muscle to produce venous and arteriolar dilatation, reducing myocardial oxygen demand and increasing supply; side effects include headache, hypotension, and syncope
• Beta-blockers lower myocardial oxygen demand by reducing heart rate, BP, and myocardial contractility; they may provoke bronchospasm in asthma patients, so cardioselective preparations are preferred
• Calcium channel antagonists lower myocardial oxygen demand by reducing BP and myocardial contractility; dihydropyridine calcium antagonists may cause reflex tachycardia, best used in combination with a beta-blocker
• Dihydropyridine calcium antagonists like nifedipine and nicardipine can cause reflex tachycardia, best used in combination with a β-blocker
• Verapamil and diltiazem are suitable for patients not receiving a β-blocker, as they slow SA node firing, inhibit conduction through the AV node, and tend to cause bradycardia
• Percutaneous coronary intervention (PCI) involves passing a fine guidewire across a coronary stenosis under radiographic control, using it to position a balloon that is then inflated to dilate the stenosis
• Coronary artery bypass grafting can use internal mammary arteries, radial arteries, or reversed segments of the patient’s own saphenous vein to bypass coronary artery stenoses
• Acute coronary syndrome (ACS) encompasses unstable angina (UA) and myocardial infarction (MI) (NSTEMI and STEMI), characterized by new-onset or rapidly worsening angina, angina on minimal exertion, or angina at rest in the absence of myocardial damage
• Myocardial infarction (MI) occurs when symptoms occur at rest, with evidence of myocardial necrosis demonstrated by an elevation in cardiac biomarkers like troponin or CK-MB isoenzyme
• NSTEMI is established if a patient with the clinical features of UA develops evidence of myocardial necrosis, reflected in elevated cardiac biomarkers like CKMB or Troponin
• Clinical features of ACS include chest pain, breathlessness, vomiting, collapse, diaphoresis, pale and cool skin, sinus tachycardia, hypotension, and a third and/or fourth heart sound with basilar rales
• The diagnosis of ACS heavily depends on the analysis of chest pain character and its associated features, evaluation of the ECG, and serial measurements of biochemical markers of cardiac damage
• Electrocardiography (ECG) is central to confirming the diagnosis of ACS, with ST-segment elevation seen in proximal occlusion of a major coronary artery, and development of a Q wave in transmural infarction
• In NST segment elevation, there is partial occlusion of a major vessel or complete occlusion of a minor vessel, causing unstable angina or partial-thickness (subendocardial) MI, usually associated with ST-segment depression and T-wave changes
• Plasma cardiac biomarkers like Creatine Kinase (CK), CK-MB, and Troponins T and I are used in diagnosing ACS, with no detectable rise in cardiac biomarkers or enzymes in unstable angina (UA)
• Plasma cardiac biomarkers include:

  • Creatine kinase (CK)
  • CK-MB (a more sensitive and cardio-specific isoform of CK)
  • Troponins T and I (the cardio-specific proteins)
• In unstable angina (UA), there is no detectable rise in cardiac biomarkers or enzymes, and the initial diagnosis is made from the clinical history and ECG only
• In contrast, myocardial infarction (MI) causes a rise in plasma cardiac biomarkers or enzymes that are normally concentrated within cardiac cells, confirming the diagnosis
• CK starts to rise at 4–6 hours, peaks at about 12 hours, and falls to normal within 48–72 hours; it is also present in skeletal muscle
• The most sensitive markers of myocardial cell damage are troponins T and I, released within 4–6 hours and remaining elevated for up to 2 weeks
• Chest X-ray may demonstrate pulmonary oedema not evident on clinical examination, and echocardiography is useful for assessing ventricular function and detecting complications like mural thrombus, cardiac rupture, ventricular septal defect, mitral regurgitation, and pericardial effusion
• Immediate treatment for myocardial infarction includes analgesia to relieve distress, lower adrenergic drive, reduce vascular resistance, BP, infarct size, and susceptibility to ventricular arrhythmias, along with oxygen therapy
• Antithrombotic therapy involves antiplatelet therapy with aspirin and clopidogrel, reducing the risk of ischaemic events
• Anticoagulants like unfractionated heparin or low-molecular-weight heparin reduce the risk of thromboembolic complications and prevent re-infarction
• Anti-anginal therapy includes nitrates for pain relief, β-blockers to reduce arrhythmias and improve mortality, and calcium channel antagonists like verapamil and diltiazem
• Fibrinolytic therapy aims for prompt restoration of full coronary arterial patency using tissue plasminogen activator (tPA), streptokinase, tenecteplase (TNK), or reteplase (rPA)
• Long-term treatment for coronary artery disease involves risk factor modification, lipid-lowering drugs, ACE inhibitors for plaque stabilization, and antiplatelet therapy with aspirin and clopidogrel