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Medicine 2 - Fourth Year BHMS

Contents

Medicine 2 - Fourth Year BHMS

Contents

CoursesBHMSMedicine 2 - Fourth Year BHMSCardiomyopathy

Cardiomyopathy

Content

Cardiomyopathy

1. Definition
Cardiomyopathy is a disease of the heart muscle in which the myocardium becomes enlarged, thickened or stiff, leading to impaired pumping ability. It is a common cause of failure and may result in sudden cardiac death.

2. Synonyms
Myocardial disease; heart‑muscle disease – terms used interchangeably in textbooks and clinical practice.

3. Causes / Etiology

  • Genetic mutations – inherited defects in sarcomeric proteins (e.g., MYH7, MYBPC3) produce abnormal muscle structure.
  • Ischemic injury – repeated episodes of coronary artery disease cause loss of viable myocardium and remodeling.
  • Hypertension – long‑standing high pressure forces the left ventricle to work harder, leading to hypertrophy and later dilation.
  • Diabetes mellitus – metabolic disturbances cause microvascular damage and fibrosis of the myocardium.
  • Infections (viral myocarditis) – Coxsackie B, adenovirus, etc., damage myocytes and trigger inflammation.
  • Toxins – chronic alcohol, cocaine, chemotherapeutic agents (e.g., doxorubicin), heavy metals produce direct myocyte injury.
  • Nutritional deficiencies – thiamine (beriberi) or selenium deficiency impair myocardial metabolism.

Each factor may act alone or combine with others to produce the various clinical forms.

4. Types / Classification

TypeOne‑line definitionMain causesTypical clinical featuresAcute vs chronic picture
Dilated cardiomyopathy (DCM)Ventricular chambers are enlarged with thin walls, systolic function reduced.Genetic, alcohol, viral myocarditis, post‑ischemic remodeling.Progressive dyspnoea, orthopnoea, peripheral oedema, reduced exercise tolerance.Chronic: gradual onset of heart‑failure signs. Acute decompensation: sudden pulmonary oedema, rapid weight gain, hypotension.
Hypertrophic cardiomyopathy (HCM)Asymmetric septal thickening, often with outflow obstruction.Autosomal dominant sarcomere gene mutations.Exertional chest pain, syncope, harsh systolic murmur, family history of sudden death.Chronic: intermittent symptoms, may be asymptomatic. Acute: sudden collapse during exertion, ventricular arrhythmia.
Restrictive cardiomyopathy (RCM)Ventricular walls become stiff, diastolic filling impaired, systolic function relatively preserved.Infiltrative diseases (amyloidosis, sarcoidosis), post‑radiation fibrosis, endomyocardial disease.Marked dyspnoea, ascites, jugular venous distension, normal‑size heart on X‑ray.Usually chronic; acute decompensation may present as rapid fluid overload.
Arrhythmogenic right ventricular cardiomyopathy (ARVC)Fatty‑fibrous replacement of right‑ventricular myocardium, prone to ventricular tachycardia.Desmosomal gene mutations (PKP2, DSG2).Palpitations, syncope, ventricular arrhythmias, sudden death in young athletes.Chronic: progressive arrhythmias. Acute: sustained VT/VF leading to cardiac arrest.
Takotsubo (stress) cardiomyopathy*Transient apical ballooning of left ventricle after emotional/physical stress.Catecholamine surge, microvascular spasm.Acute chest pain, ST‑segment changes, reversible LV dysfunction.Acute presentation mimics MI; recovery within weeks.

*Included because it fulfills the definition of a reversible myocardial disease.

5. Pathophysiology / Pathology – step by step

  1. Initial insult – genetic defect, toxin, ischemia or infection damages cardiomyocytes.
  2. Cellular injury – loss of contractile proteins, membrane leakage, calcium overload.
  3. Inflammation and necrosis – inflammatory cells infiltrate, cytokines released, scar tissue begins to form.
  4. Remodeling – surviving myocytes hypertrophy, extracellular matrix expands, ventricular geometry changes (dilation or thickening).
  5. Neuro‑hormonal activation – sympathetic nervous system and renin‑angiotensin‑aldosterone system become over‑active, worsening sodium retention and after‑load.
  6. Progressive dysfunction – systolic (DCM) or diastolic (HCM, RCM) failure develops, leading to clinical heart failure.

Each stage reinforces the next, creating a vicious cycle of worsening cardiac performance.

6. Clinical Features

  • General – fatigue, reduced exercise tolerance, dyspnoea on exertion, orthopnoea, paroxysmal nocturnal dyspnoea, peripheral oedema, palpitations, chest discomfort.
  • Specific to type
    • DCM: displaced apical impulse, third heart sound, pulsatile liver.
    • HCM: harsh systolic ejection murmur that increases with Valsalva, systolic anterior motion of mitral valve.
    • RCM: signs of right‑sided failure dominate, Kussmaul’s sign, normal‑size heart on chest X‑ray.
    • ARVC: frequent premature ventricular beats, epsilon wave on ECG.
  • Acute features – sudden pulmonary oedema, hypotension, rapid weight gain, arrhythmic storm.
  • Chronic features – gradual worsening of NYHA class, cachexia, chronic atrial fibrillation.

Recognition of the pattern helps to differentiate the type and stage.

7. Complications

  • Heart failure – progressive pump failure, pulmonary congestion, systemic congestion.
  • Life‑threatening arrhythmias – ventricular tachycardia/fibrillation, atrial fibrillation with rapid ventricular response.
  • Thrombo‑embolism – left‑ventricular thrombus in DCM, systemic emboli, stroke.
  • Sudden cardiac death – especially in HCM and ARVC.
  • End‑organ damage – renal dysfunction, hepatic congestion, cachexia.

Early detection and prophylactic therapy (e.g., ICD implantation) can reduce mortality.

8. Investigations / Diagnosis

  • Electrocardiogram – low voltage, Q‑waves, LVH, ST‑T changes, epsilon wave (ARVC).
  • Chest X‑ray – cardiomegaly in DCM, normal size in HCM/RCM, pulmonary congestion.
  • Echocardiography – gold standard for chamber size, wall thickness, systolic/diastolic function, outflow obstruction.
  • Cardiac MRI – detailed tissue characterization, detection of fibrosis, fatty infiltration (ARVC).
  • Holter / event monitor – documentation of arrhythmias, burden of ectopy.
  • Blood tests – BNP/NT‑proBNP (severity marker), troponin (acute injury), metabolic panel, viral serology if myocarditis suspected.
  • Genetic testing – when familial disease is suspected, to guide counseling and screening.

Each test adds a piece of the puzzle, confirming the type and severity.

9. Differential Diagnosis

  1. Coronary artery disease (ischemic cardiomyopathy) – chest pain with exertion, regional wall motion abnormalities on echo; distinguished by coronary angiography.
  2. Hypertensive heart disease – concentric LV hypertrophy without outflow obstruction; blood pressure history is key.
  3. Valvular heart disease – murmurs of stenosis/regurgitation, valve morphology on echo; cardiomyopathy lacks primary valve pathology.
  4. Pericardial disease (constrictive pericarditis) – signs of right‑sided failure, pericardial thickening on CT/MRI; differentiate by pericardial calcification and equalization of diastolic pressures.

Correct differentiation directs appropriate therapy.

10. Management / Treatment

General management – patient education, regular follow‑up, monitoring of weight and symptoms, avoidance of excessive alcohol and illicit drugs, vaccination against influenza and pneumococcus.

Modern medicine –

  • ACE inhibitors / ARBs – reduce after‑load, improve survival in systolic failure.
  • Beta‑blockers – control heart rate, improve remodeling, especially in HCM and DCM.
  • Mineralocorticoid receptor antagonists – limit fibrosis, lower mortality.
  • Diuretics – relieve congestion (loop diuretics first line).
  • Anti‑arrhythmic drugs – amiodarone or sotalol for ventricular arrhythmias; anticoagulation for atrial fibrillation.
  • Device therapy – ICD for primary/secondary prevention of sudden death; CRT for selected DCM with dyssynchrony.
  • Advanced options – cardiac transplantation or ventricular assist devices in end‑stage disease.

Diet and lifestyle –

  • Low‑salt diet (≤2 g Na⁺/day) to prevent fluid retention.
  • Moderate fluid restriction (1.5–2 L/day) if severe congestion.
  • Balanced diet rich in fruits, vegetables, whole grains, lean protein; avoids saturated fats and trans‑fats to reduce atherosclerotic risk.
  • Regular aerobic exercise (as tolerated) improves functional capacity; avoid extreme exertion in HCM/ARVC.
  • Smoking cessation and control of diabetes/hypertension are essential preventive steps.

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

Remedy 1 – Arnica montana

  • Causation: trauma, over‑exertion, sudden strain on the heart.
  • Characteristic symptoms: soreness, bruised feeling in the chest, fear of being touched.
  • Modalities: worse from pressure, movement, cold; better from rest and warm applications.
  • Mental state: anxious, anticipatory fear, feels “shaken”.
  • Thirst/appetite: increased thirst, appetite may be reduced when pain dominates.
  • Discharges/secretions: occasional scant, watery sputum if pulmonary congestion present.
  • Physical generals: muscular stiffness, tender palpation points, rapid pulse.
  • Suitable constitution: active, outdoorsy persons, athletes who push limits.
  • How it helps: diminishes inflammatory response in the myocardium and relieves painful over‑stretch.

Remedy 2 – Crataegus oxyacantha

  • Causation: chronic heart‑muscle weakness, hereditary predisposition.
  • Characteristic symptoms: palpitations with irregular rhythm, feeling of “flutter” in the chest.
  • Modalities: better from lying on left side, warm drinks; worse from emotional stress, cold air.
  • Mental state: nervous, easily startled, anticipates doom.
  • Thirst/appetite: normal thirst, appetite may be poor when fatigue is severe.
  • Discharges: scant, thin sputum if mild pulmonary congestion.
  • Physical generals: weak pulse, low blood pressure, slight edema of ankles.
  • Suitable constitution: timid, delicate individuals, often women with family history of heart disease.
  • How it helps: strengthens myocardial contractility and stabilises rhythm.

Remedy 3 – Digitalis purpurea

  • Causation: advanced heart failure, long‑standing dilatation, use of digitalis‑like drugs.
  • Characteristic symptoms: slow, weak pulse; visual disturbances (yellow‑green halos).
  • Modalities: worse from cold, exertion; better from warmth, lying on left side.
  • Mental state: confused, irritable, feels “heavy” in the head.
  • Thirst/appetite: decreased thirst, loss of appetite.
  • Discharges: frothy, pink‑tinged sputum if pulmonary oedema.
  • Physical generals: cold extremities, cyanosis of lips, swollen abdomen.
  • Suitable constitution: elderly, frail patients with chronic decompensation.
  • How it helps: improves contractility and reduces ventricular filling pressures.

Remedy 4 – Kali carbonicum

  • Causation: hereditary cardiomyopathy, exposure to cold, over‑work of the heart.
  • Characteristic symptoms: sudden palpitations, feeling of “tightness” in the chest.
  • Modalities: worse from cold, damp weather; better from warm drinks, open air.
  • Mental state: anxious, anticipates catastrophe, restless at night.
  • Thirst/appetite: normal thirst, appetite may be diminished by nausea.
  • Discharges: scant, clear sputum; occasional bitter taste.
  • Physical generals: weak, thready pulse; slight peripheral oedema.
  • Suitable constitution: thin, nervous individuals, often with a family history of sudden death.
  • How it helps: restores electrical stability and eases ventricular stiffness.

Remedy 5 – Lycopus europaeus

  • Causation: stress‑induced cardiac strain, over‑use of stimulants.
  • Characteristic symptoms: rapid, irregular heartbeat, feeling of “fluttering” in the throat.
  • Modalities: worse from mental strain, loud noises; better from quiet, fresh air.
  • Mental state: irritable, impatient, feels “on edge”.
  • Thirst/appetite: normal thirst, appetite may be reduced by anxiety.
  • Discharges: thin, watery sputum if mild congestion.
  • Physical generals: tremulous hands, slight tremor of the chest wall.
  • Suitable constitution: high‑energy, ambitious persons who neglect rest.
  • How it helps: calms the autonomic nervous system and reduces ectopic beats.

Remedy 6 – Spigelia anthelmia

  • Causation: sudden chest pain after emotional upset, acute decompensation.
  • Characteristic symptoms: sharp, stabbing pain in the left side of the chest, radiating to the back.
  • Modalities: worse from movement, pressure on the area; better from lying still, warm compresses.
  • Mental state: angry, irritable, feels “bitter” about the situation.
  • Thirst/appetite: increased thirst, appetite often suppressed by pain.
  • Discharges: scant, sometimes blood‑tinged sputum if pulmonary congestion present.
  • Physical generals: rapid, bounding pulse; sweating of the forehead.
  • Suitable constitution: persons with a history of sudden emotional outbursts, often middle‑aged men.
  • How it helps: relieves acute chest pain and reduces sympathetic over‑drive.

Remedy 7 – Strophanthus hispidus

  • Causation: chronic heart failure with low output, often after long‑standing DCM.
  • Characteristic symptoms: feeling of heaviness in the chest, faintness on standing.
  • Modalities: worse from exertion, cold drinks; better from warm fluids, lying down.
  • Mental state: apathetic, indifferent, “doesn’t care” about surroundings.
  • Thirst/appetite: decreased thirst, poor appetite, early satiety.
  • Discharges: frothy, pink sputum when pulmonary oedema worsens.
  • Physical generals: weak, thready pulse; peripheral cyanosis; swollen ankles.
  • Suitable constitution: elderly, frail individuals with long‑standing fatigue.
  • How it helps: supports myocardial contractility and improves peripheral circulation.

Remedy 8 – Nux vomica

  • Causation: over‑indulgence in stimulants (caffeine, alcohol), chronic stress on the heart.
  • Characteristic symptoms: irritability, burning sensation in the epigastrium, palpitations after meals.
  • Modalities: worse from cold, late‑night meals; better from warm drinks, fresh air.
  • Mental state: irritable, impatient, feels “pressed” by obligations.
  • Thirst/appetite: increased thirst, appetite for spicy, salty foods.
  • Discharges: scant, sometimes acidic sputum if reflux present.
  • Physical generals: rapid pulse, dry mouth, constipation.
  • Suitable constitution: work‑aholics, night‑owls, people who ignore regular meals.
  • How it helps: reduces stimulant‑induced tachycardia and eases digestive‑related cardiac stress.

12. Prognosis
The outlook depends on type, stage, and response to therapy. HCM patients with good risk stratification may live a normal lifespan, whereas untreated DCM often progresses to end‑stage heart failure. Presence of sustained ventricular arrhythmias, advanced NYHA class, and co‑existing renal or hepatic dysfunction worsen prognosis. Early diagnosis, optimal medical therapy and device implantation improve survival markedly.

13. Prevention

  • Screen high‑risk families – echocardiography and genetic testing in relatives of known cardiomyopathy patients.
  • Control modifiable risk factors – maintain blood pressure <130/80 mmHg, tight glycaemic control, limit alcohol (<30 g/day) and avoid illicit drugs.
  • Vaccinations – influenza and pneumococcal vaccines reduce infection‑related decompensation.

Preventive actions reduce the incidence of decompensated episodes and delay progression.

14. Diet

  • Recommended foods – fresh fruits, leafy vegetables, whole‑grain cereals, lean fish or poultry, low‑fat dairy; these provide antioxidants, omega‑3 fatty acids and adequate protein for myocardial health.
  • Foods to avoid – excess salt (>2 g/day), saturated and trans fats, sugary drinks, heavy alcohol; these aggravate hypertension, promote atherosclerosis and increase myocardial workload.

A heart‑friendly diet supports optimal cardiac function and complements pharmacologic therapy.