Chronic Myocardial Infarction

Chronic Myocardial Infarctions

1. Definition
Chronic myocardial infarction (CMI) is the healed or “old” stage of a myocardial infarction in which the necrotic myocardium has been replaced by scar tissue and the heart functions with this permanent loss of contractile muscle. It represents the long‑term sequel of a previous heart attack.

2. Synonyms

• Old myocardial infarction – the same condition described after the acute phase has passed.
• Previous myocardial infarction – emphasizes that the infarct occurred in the past.

3. Causes / Etiology

• Previous acute myocardial infarction – the primary event that initiates scar formation; the infarct may have been silent or clinically evident.
• Atherosclerotic coronary artery disease – plaque‑induced narrowing or occlusion of a coronary artery that caused the original infarct.
• Coronary artery spasm – transient severe vasoconstriction can precipitate an infarct that later becomes chronic.
• Thrombo‑embolism to coronary vessels – embolic occlusion produces infarction that heals with scar.
• Severe hypertension – long‑standing high pressure accelerates atherosclerosis and may precipitate infarction.
• Diabetes mellitus – microvascular disease and accelerated atherosclerosis increase the risk of an infarct that later becomes chronic.
• Smoking – promotes endothelial injury and plaque formation, leading to infarction.
• Family history of premature coronary disease – genetic predisposition to atherosclerosis and infarction.

Each of these factors contributes to the initial loss of myocardial tissue that later becomes a permanent scar.

4. Types / Classification

• Acute myocardial infarction (AMI) – the initial event lasting minutes to days; characterised by ongoing necrosis, ST‑segment changes and enzyme rise.
• Chronic myocardial infarction (CMI) – the stage that follows after about 4 weeks when the infarct is fully scarred.

For CMI the classification is based on the location and extent of scar:

• Transmural old infarct – full‑thickness scar; often produces a Q‑wave on ECG and may lead to ventricular aneurysm.
• Subendocardial old infarct – scar limited to the inner 1/3 of the wall; may be silent on ECG but can cause diastolic dysfunction.

Differences: AMI shows active pain, enzyme rise and dynamic ECG changes; CMI is painless, ECG shows permanent Q‑waves or T‑wave inversion, and the heart remodels over weeks to months.

5. Pathophysiology / Pathology

1. Coronary occlusion – atherosclerotic plaque rupture or thrombus blocks a coronary artery.
2. Ischemia and necrosis – lack of oxygen kills myocardial cells within the supplied territory.
3. Inflammatory phase (first few days) – neutrophils and macrophages remove dead cells.
4. Granulation tissue formation (1‑2 weeks) – fibroblasts lay down collagen, new capillaries appear.
5. Scar formation (4‑6 weeks) – collagen replaces muscle, resulting in a non‑contractile, stiff patch.
6. Remodelling of the ventricle – the remaining viable myocardium hypertrophies and dilates to compensate, which may lead to heart failure or aneurysm.

The scar is electrically inert, creating a substrate for re‑entrant arrhythmias.

6. Clinical Features

• General features – often asymptomatic; may present with fatigue, reduced exercise tolerance, occasional palpitations.
• Specific chronic features
  • Dyspnoea on exertion (due to reduced left‑ventricular reserve).
  • Orthopnoea and paroxysmal nocturnal dyspnoea if heart failure develops.
  • Persistent low‑grade chest discomfort or pressure, especially on exertion.
  • Palpitations from ventricular ectopy or atrial fibrillation.
• Acute‑phase contrast – severe crushing chest pain, diaphoresis, nausea, and marked ECG changes are absent in the chronic stage.

Recognition of chronic symptoms guides long‑term management rather than emergency care.

7. Complications

• Acute‑phase complications (if the infarct is recent) – malignant arrhythmias, cardiogenic shock, acute left‑ventricular failure, papillary‑muscle rupture.
• Chronic complications
  • Chronic heart failure – due to loss of contractile mass and ventricular dilatation.
  • Ventricular aneurysm – bulging scar tissue may form a thin‑walled aneurysm, predisposing to thrombus formation.
  • Valvular dysfunction – papillary‑muscle dysfunction can cause mitral regurgitation.
  • Re‑entrant ventricular tachycardia / sudden cardiac death – scar provides a circuit for dangerous arrhythmias.

Early detection of aneurysm or arrhythmia can prevent fatal outcomes.

8. Investigations / Diagnosis

• Routine tests
  • 12‑lead ECG – permanent Q‑waves, loss of R‑wave amplitude, T‑wave inversion indicate old infarct.
  • Chest X‑ray – may show cardiomegaly or pulmonary congestion in chronic heart failure.
• Specific tests
  • Echocardiography – assesses wall‑motion abnormality, scar thickness, ventricular size and function; detects aneurysm.
  • Stress testing (exercise or pharmacologic) – evaluates inducible ischaemia in the remaining myocardium.
• Confirmatory / advanced tests
  • Cardiac MRI with late gadolinium enhancement – precisely delineates scar extent and viability.
  • Coronary angiography – visualises obstructive lesions that may need revascularisation.

Each test adds information about the scar, residual perfusion and functional impact.

9. Differential Diagnosis

1. Stable angina pectoris – episodic chest pain on exertion without permanent ECG Q‑waves; CMI shows fixed Q‑waves and scar on imaging.
2. Chronic heart failure of non‑ischemic origin – dilated cardiomyopathy shows global dysfunction without regional wall‑motion defects or scar on MRI.
3. Pulmonary embolism – acute dyspnoea and pleuritic chest pain with normal ECG Q‑waves; CMI lacks sudden onset and has characteristic scar signs.
4. Hypertrophic cardiomyopathy – presents with exertional dyspnoea and murmur; ECG shows LVH patterns, not Q‑waves of old infarct.

Key distinguishing points are ECG scar patterns, imaging findings and symptom chronology.

10. Management / Treatment

• General management – regular clinical review, monitoring of blood pressure, heart rate and weight; patient education about symptom warning signs.
• Modern‑medicine treatment
  • Antiplatelet therapy (aspirin ± clopidogrel) – prevents new thrombus formation on atherosclerotic plaques.
  • Beta‑blockers – reduce myocardial oxygen demand, control heart rate and lower risk of arrhythmia.
  • ACE‑inhibitors / ARBs – attenuate ventricular remodelling and improve survival in chronic heart failure.
  • Statins – stabilise plaques, lower LDL cholesterol and reduce recurrent events.
  • Mineralocorticoid receptor antagonists – added in symptomatic heart failure to reduce fibrosis.
  • Implantable cardioverter‑defibrillator (ICD) – considered when scar‑related ventricular tachycardia risk is high.
• Diet and lifestyle advice – low‑saturated‑fat diet, limit salt to <5 g/day, maintain body‑mass index <25 kg/m², engage in moderate aerobic exercise (30 min most days), stop smoking, control diabetes and hypertension.

These measures aim to prevent further ischaemia, limit remodelling and improve quality of life.

11. Homeopathic Therapeutics
(Each remedy is presented with the required bullet points; the list contains eight commonly used medicines for chronic ischaemic heart disease.)

Arnica montana

• Causation: trauma, over‑exertion, post‑surgical or post‑infarct bruising of the heart.
• Characteristic symptoms: deep, sore, bruised feeling in the chest; pain worsens on movement.
• Modalities: worse from exertion, cold, jarring; better from rest and warm applications.
• Mental state: feels crushed, wants to be left alone, irritable when disturbed.
• Thirst and appetite: thirst for cold water; appetite reduced when pain is severe.
• Discharges/secretions: may have thin, watery sputum if pulmonary congestion present.
• Physical generals: pale, cold extremities, trembling hands.
• Suitable constitution: persons who have endured physical injury or surgery and now have lingering soreness.
• How it helps: removes the lingering bruised‑type pain of the scarred myocardium and improves circulation in the affected area.

Crataegus monogyna

• Causation: hereditary or lifestyle‑related heart weakness, especially after an infarct.
• Characteristic symptoms: heaviness in the chest, palpitations that feel “fluttering”, shortness of breath on slightest exertion.
• Modalities: better from fresh air, gentle walking; worse from emotional stress and cold drinks.
• Mental state: anxious, fearful of death, often worries about heart condition.
• Thirst and appetite: thirst for cold water; appetite may be poor due to early satiety.
• Discharges/secretions: may have frothy sputum if left‑sided failure develops.
• Physical generals: weak pulse, low blood pressure, slight edema of ankles.
• Suitable constitution: individuals with a family history of heart disease, nervous temperament, and a desire for gentle strengthening.
• How it helps: strengthens the weakened myocardium, improves coronary micro‑circulation and eases palpitations.

Digitalis purpurea

• Causation: chronic heart failure following an old infarct, especially when atrial fibrillation is present.
• Characteristic symptoms: slow, irregular pulse; visual disturbances (yellow‑green halos); feeling of heaviness in the chest.
• Modalities: worse from cold, mental exertion, and over‑activity; better from rest and warm drinks.
• Mental state: irritable, impatient, feels “tired out” quickly.
• Thirst and appetite: thirst for warm drinks; appetite diminished when fatigue is great.
• Discharges/secretions: may have scant, dark urine due to reduced renal perfusion.
• Physical generals: low heart rate, cold clammy skin, peripheral edema.
• Suitable constitution: older patients with chronic congestive signs and a history of atrial arrhythmia.
• How it helps: improves contractility of the remaining viable myocardium and controls ventricular rate in atrial fibrillation.

Kali mur (Potassium muriaticum)

• Causation: chronic ischaemic heart disease with episodes of chest tightness after exertion.
• Characteristic symptoms: crushing chest pain that improves when lying on the left side, shortness of breath that worsens at night.
• Modalities: better from warm applications, lying down; worse from cold air, damp weather.
• Mental state: feels despondent, often thinks “I cannot do anything”.
• Thirst and appetite: thirst for cold water; appetite reduced when pain is present.
• Discharges/secretions: may have thin, watery sputum; occasional night sweats.
• Physical generals: weak, thready pulse; cold extremities; slight cyanosis of lips.
• Suitable constitution: persons who are thin, timid, and have a history of chronic heart weakness.
• How it helps: relieves the constrictive chest sensation and supports the weakened cardiac muscle.

Naphthas volatiles

• Causation: sudden onset of chest pain after emotional shock in a person with old infarct scar.
• Characteristic symptoms: burning, tearing pain in the chest radiating to the back; feeling of “heat” in the heart.
• Modalities: worse from excitement, noise, and warm rooms; better from cool fresh air and quiet.
• Mental state: extremely nervous, anticipates disaster, restless at night.
• Thirst and appetite: thirst for cold water; appetite poor due to anxiety.
• Discharges/secretions: may have dry cough, scant sputum.
• Physical generals: rapid, weak pulse; trembling hands.
• Suitable constitution: highly strung individuals with a history of heart disease who react strongly to stress.
• How it helps: calms the nervous over‑reaction and eases the burning chest sensation linked to scar irritation.

Natrum muriaticum

• Causation: chronic heart disease after an infarct in a person who suppresses emotions.
• Characteristic symptoms: vague chest heaviness, palpitations that appear after emotional upset, dry mouth.
• Modalities: worse from salty foods, warm drinks, and grief; better from fresh air and rest.
• Mental state: introverted, feels “lonely”, often holds back tears.
• Thirst and appetite: thirst for cold water; appetite normal unless upset.
• Discharges/secretions: dry mucous membranes, scant nasal discharge.
• Physical generals: thin, dry skin, occasional cold hands.
• Suitable constitution: individuals who are emotionally restrained, often with a history of grief.
• How it helps: releases suppressed emotions, reduces the vague chest heaviness and stabilises the heart rhythm.

Phosphorus

• Causation: chronic ischaemic heart disease with a history of heavy smoking or alcohol use.
• Characteristic symptoms: burning chest pain that worsens at night, feeling of weakness in the limbs, anxiety about health.
• Modalities: better from fresh air, cold drinks; worse from heat, lying down, and mental exertion.
• Mental state: restless, fearful, often talks about death.
• Thirst and appetite: thirst for cold water; appetite good but may be reduced by pain.
• Discharges/secretions: thin, frothy sputum if pulmonary congestion present.
• Physical generals: rapid, weak pulse; cold, clammy skin; slight tremor.
• Suitable constitution: thin, sensitive individuals with a history of over‑indulgence and chronic heart strain.
• How it helps: eases the nocturnal burning pain, improves circulation and reduces anxiety that aggravates the heart.

Spigelia anthelmia

• Causation: chronic heart disease after an old infarct with associated neuralgic chest pain.
• Characteristic symptoms: sharp, stabbing pain in the left side of the chest, radiating to the back, worse on deep inspiration.
• Modalities: worse from movement, pressure, and cold; better from warmth and lying on the right side.
• Mental state: irritable, impatient, feels “tight‑lipped”.
• Thirst and appetite: thirst for warm drinks; appetite reduced when pain is intense.
• Discharges/secretions: may have scant, thick sputum; occasional hoarseness.
• Physical generals: weak, thready pulse; cold extremities; slight edema of ankles.
• Suitable constitution: persons with a history of neuralgic pain, often with a “stiff” personality.
• How it helps: relieves the sharp, neuralgic component of the scar‑related chest pain and improves overall cardiac comfort.

12. Prognosis
The outlook depends on the size of the scar, presence of ventricular dysfunction, and control of risk factors. Small, well‑compensated scars may allow a near‑normal life, whereas extensive scarring with aneurysm or recurrent arrhythmia carries a poorer prognosis. Early revascularisation, optimal medical therapy and lifestyle changes markedly improve survival.

13. Prevention
Primary prevention focuses on controlling atherosclerotic risk: quit smoking, maintain blood pressure <130/80 mm Hg, keep LDL cholesterol <70 mg/dL, control diabetes, and adopt regular aerobic exercise. Secondary prevention after an infarct adds antiplatelet therapy, statins and ACE‑inhibitors to reduce the chance of a new infarct and limit further scar formation.

14. Diet

• Recommended foods

  • Low‑fat dairy (milk, yoghurt) – reduces saturated fat intake, lowering LDL.
  • Lean proteins (skinless poultry, fish, legumes) – provides essential amino acids without excess fat.
  • Whole grains (oats, brown rice) – high fibre helps control cholesterol.
  • Fresh fruits and vegetables – supply antioxidants and potassium, supporting vascular health.

• Foods to avoid

  • High‑fat meats, fried foods – increase saturated fat and promote plaque growth.
  • Salt‑rich processed foods – raise blood pressure, worsening cardiac workload.
  • Sugary drinks and sweets – contribute to obesity and dyslipidaemia.