Ischaemic Heart Disease

Ischaemic Heart Disease

1. Definition
   Ischaemic Heart Disease (IHD) is a condition in which the coronary blood supply to the myocardium is insufficient to meet its metabolic needs, producing chest pain or discomfort. It is one of the leading causes of death worldwide.

2. Synonyms (if any)

• Coronary Artery Disease – the term emphasizes the arterial involvement.
• Coronary Heart Disease – commonly used in epidemiological reports.

3. Causes / Etiology

• Atherosclerosis – progressive accumulation of lipid‑rich plaque in the coronary arteries; the main long‑term cause of reduced flow.
• Coronary artery spasm – transient, intense contraction of a coronary segment; may occur in younger patients without overt plaque.
• Thrombosis on a ruptured plaque – acute clot formation that suddenly occludes the lumen; responsible for most acute events.
• Rare causes (e.g., coronary emboli, vasculitis) – occasional contributors, especially in special clinical settings.

4. Types / Classification

Acute Coronary Syndrome (ACS) – includes unstable angina, NSTEMI and STEMI.
 • Causes – plaque rupture or erosion with superimposed thrombus, or severe spasm.
 • Clinical features – sudden, severe chest pressure, radiation to arm/jaw, dyspnoea, nausea; often at rest.
 • Duration – minutes to hours; may evolve over days if untreated.
 • Difference from chronic IHD – abrupt onset, marked ECG changes, rise in cardiac enzymes.

Chronic Ischaemic Heart Disease (stable angina).
 • Causes – fixed atherosclerotic narrowing that limits flow during increased demand.
 • Clinical features – predictable chest discomfort on exertion, relieved by rest or nitrates.
 • Duration – months to years; symptoms persist as long as the obstruction remains.
 • Difference from ACS – predictable pattern, no acute enzyme rise, stable ECG at rest.

5. Pathophysiology / Pathology

Step 1 – Plaque formation in the intima of coronary arteries.
 Plaque consists of lipids, foam cells, smooth‑muscle proliferation and a fibrous cap; it narrows the lumen.

Step 2 – Endothelial dysfunction and reduced nitric‑oxide production.
 Leads to vasoconstriction, increased platelet adhesion and a pro‑inflammatory state.

Step 3 – Myocardial ischaemia when oxygen demand exceeds supply.
 Ischaemia causes reversible metabolic disturbance and chest pain.

Step 4 – Prolonged ischaemia → necrosis (myocardial infarction).
 Cell death is irreversible, resulting in scar formation and loss of contractile function.

Step 5 – Remodelling of the ventricle and possible development of heart failure.
 Chronic changes may lead to dilatation, aneurysm formation or valvular dysfunction.

6. Clinical Features

General – central chest pressure, heaviness or squeezing; may be associated with breathlessness, sweating, nausea, and anxiety.

Acute IHD (ACS) – abrupt onset at rest, severe intensity, lasting > 5 min, often with ECG ST‑segment changes and troponin rise; indicates high risk of infarction.

Chronic IHD (stable angina) – discomfort triggered by exertion or emotional stress, lasting a few minutes, relieved by rest or sublingual nitrates; reflects fixed obstruction.

7. Complications

Acute complications – myocardial infarction, life‑threatening arrhythmias (ventricular tachycardia/fibrillation), acute left‑ventricular failure, cardiogenic shock. Early reperfusion reduces mortality.

Chronic complications – chronic heart failure, left‑ventricular aneurysm, papillary‑muscle dysfunction leading to mitral regurgitation, ventricular remodeling. Regular follow‑up helps to detect and treat these sequelae.

8. Investigations / Diagnosis

Routine –
 ECG: looks for ST‑segment depression/elevation, new Q‑waves, T‑wave inversion; provides immediate clue to ischaemia.
 Cardiac biomarkers (troponin I/T): rise indicates myocardial injury; helps differentiate ACS from stable angina.

Specific –
 Echocardiography: assesses wall‑motion abnormalities, ejection fraction and valvular function; useful for risk stratification.
 Exercise or pharmacologic stress test: demonstrates inducible ischaemia when baseline ECG is normal; guides need for angiography.

Confirmatory –
 Coronary angiography (invasive or CT‑angiography): visualises the exact site and severity of stenosis; definitive for planning revascularisation.

9. Differential Diagnosis

• Unstable angina vs. stable angina: unstable angina presents with pain at rest, rapid progression and no enzyme rise; stable angina is exertional and predictable.
• IHD vs. pericarditis: pericarditis pain is sharp, improves when leaning forward, and shows diffuse ST elevation; IHD pain is pressure‑like and often localized.
• IHD vs. gastro‑oesophageal reflux disease: reflux pain is related to meals, improves with antacids, and lacks ECG changes; IHD pain is not food‑related and shows ischaemic ECG patterns.
• IHD vs. pulmonary embolism: PE causes sudden dyspnoea, pleuritic chest pain and may show right‑heart strain on ECG; IHD pain is more central and pressure‑type.

10. Management / Treatment

General management –
 Control of risk factors (stop smoking, control hypertension and diabetes, maintain healthy weight) reduces progression of atherosclerosis.
 Patient education on recognising warning symptoms and seeking prompt care improves outcomes.

Modern‑medicine treatment –
 Antiplatelet drugs (aspirin, clopidogrel) prevent further thrombus formation; essential in all ACS patients.
 Beta‑blockers lower heart‑rate and contractility, decreasing myocardial oxygen demand.
 Nitrates dilate coronary vessels and relieve angina; short‑acting for attacks, long‑acting for prophylaxis.
 Statins stabilise plaque by lowering LDL and exert anti‑inflammatory effects; indicated for primary and secondary prevention.
 ACE‑inhibitors or ARBs improve ventricular remodeling and are beneficial in heart‑failure or post‑MI patients.

Diet and lifestyle advice –
 Adopt a low‑saturated‑fat, low‑cholesterol diet rich in fruits, vegetables, whole grains and omega‑3 fatty acids; helps lower lipid levels and inflammation.
 Engage in moderate aerobic exercise (≥150 min/week) to improve endothelial function and cardiac fitness.
 Maintain stress‑reduction techniques (deep breathing, yoga) as stress can precipitate spasm and increase demand.
 Limit alcohol to ≤ 1 drink/day for women, ≤ 2 drinks/day for men; excessive intake worsens hypertension and arrhythmias.

11. Homeopathic Therapeutics (7 remedies, each with 7‑8 points)

Arnica montana

• Causation: physical trauma, over‑exertion, sudden strain on the heart.
• Characteristic symptoms: deep, bruising‑like chest soreness, feeling of heaviness.
• Modalities: pain worsens on exertion, improves with rest and gentle motion.
• Mental state: feels restless, wants to move despite pain.
• Thirst/appetite: normal thirst, reduced appetite when pain is severe.
• Discharges: occasional thin, watery sputum if pulmonary congestion develops.
• Physical generals: pale, cold extremities, rapid pulse at rest.
• Suitable constitution: active, outdoors‑type persons who push themselves hard.
• How it helps: relieves the bruised‑type chest discomfort that follows exertional ischaemia.

Crataegus monogyna

• Causation: chronic weakening of the cardiac muscle, often in the elderly.
• Characteristic symptoms: tight, squeezing chest pain with shortness of breath on minimal effort.
• Modalities: worse in cold weather, better in warm, open air.
• Mental state: anxious about heart health, fears collapse.
• Thirst/appetite: increased thirst, prefers cold drinks; appetite may be poor.
• Discharges: dry cough, scant sputum.
• Physical generals: weak, irregular pulse, mild peripheral oedema.
• Suitable constitution: frail, thin individuals with a family history of heart disease.
• How it helps: strengthens myocardial contractility and improves circulation.

Digitalis purpurea

• Causation: longstanding heart failure with reduced output.
• Characteristic symptoms: heaviness in the chest, feeling of “balloon” in the throat, palpitations.
• Modalities: worse after meals, better after lying down.
• Mental state: irritable, impatient, desires control.
• Thirst/appetite: diminished thirst, loss of appetite, especially for sweets.
• Discharges: thick, yellowish sputum if pulmonary congestion present.
• Physical generals: slow, thready pulse, cold hands, edema of ankles.
• Suitable constitution: older, sedentary persons with a history of rheumatic fever.
• How it helps: supports weak cardiac action and reduces dyspnoea.

Nux vomica

• Causation: over‑indulgence in stimulants (caffeine, tobacco) and stress.
• Characteristic symptoms: sharp, burning chest pain radiating to the back, aggravated by anger.
• Modalities: worse after midnight, better after warm drinks.
• Mental state: irritable, impatient, easily annoyed.
• Thirst/appetite: great thirst for hot water, appetite for spicy food.
• Discharges: scant, clear sputum; occasional nausea.
• Physical generals: rapid pulse, flushed face, constipation.
• Suitable constitution: work‑aholic, high‑pressure individuals.
• How it helps: counteracts the stimulant‑induced coronary spasm.

Lycopodium clavatum

• Causation: chronic digestive disturbances leading to low‑grade cardiac strain.
• Characteristic symptoms: vague, left‑sided chest heaviness, worse after a large meal.
• Modalities: worse in the evening, better in open air.
• Mental state: self‑critical, lacks confidence, fears failure.
• Thirst/appetite: prefers warm drinks, appetite for sweets, but feels bloated.
• Discharges: dry, rattling cough if bronchial irritation present.
• Physical generals: weak pulse, cold feet, mild constipation.
• Suitable constitution: timid, introverted persons with a history of dyspepsia.
• How it helps: eases the low‑grade ischaemia that follows overeating.

Phosphorus

• Causation: constitutional weakness with a tendency to fatigue and respiratory irritation.
• Characteristic symptoms: burning chest pain that improves when sitting up, worsens at night.
• Modalities: worse in cold, damp weather; better with fresh air and warm drinks.
• Mental state: anxious, fearful of death, loves music.
• Thirst/appetite: great thirst for cold water, appetite variable.
• Discharges: thin, frothy sputum, especially after exertion.
• Physical generals: rapid, weak pulse, pallor, trembling hands.
• Suitable constitution: young, active individuals with a family predisposition to heart disease.
• How it helps: improves oxygen utilisation and reduces nocturnal anginal attacks.

Sulphur

• Causation: constitutional predisposition to inflammation and metabolic imbalance.
• Characteristic symptoms: burning, itching sensation in the chest, worse after eating rich foods.
• Modalities: worse in warm rooms, better in cool, fresh air.
• Mental state: intellectual, restless, often feels “over‑heated”.
• Thirst/appetite: great thirst for cold water, appetite for spicy, fried foods.
• Discharges: yellowish sputum if bronchial irritation present.
• Physical generals: warm skin, dilated pupils, frequent belching.
• Suitable constitution: individuals with a history of skin eruptions and digestive upset.
• How it helps: reduces inflammatory mediators that aggravate coronary plaque.

12. Prognosis
    Outcome depends on the extent of coronary obstruction, left‑ventricular ejection fraction and presence of comorbidities such as diabetes or chronic kidney disease. Early diagnosis, risk‑factor control and appropriate revascularisation markedly improve survival and quality of life.

13. Prevention

Primary prevention – aggressive modification of smoking, hypertension, dyslipidaemia and sedentary lifestyle; this can halt plaque formation and delay disease onset.

Secondary prevention – continued antiplatelet therapy, statins, beta‑blockers and lifestyle adherence after an event; reduces recurrence and mortality.

14. Diet

Recommended foods –
 Whole‑grain cereals, oats and brown rice (provide fibre that lowers cholesterol).
 Fresh fruits and vegetables (rich in antioxidants that stabilise plaque).
 Legumes and low‑fat dairy (source of plant protein and calcium without saturated fat).
 Fish rich in omega‑3 fatty acids (anti‑inflammatory, improve endothelial function).

Foods to avoid –
 Red meat, butter and ghee (high in saturated fat, raise LDL).
 Fried snacks, pastries and sugary drinks (increase triglycerides and promote obesity).
 Processed meats with added salts (raise blood pressure and contribute to endothelial injury).