The Heart

Normal Structure

1. Anatomy and Physiology

Heart Function: Muscular pump that circulates blood through the body.
Weight:
- Adult Male: 300-350 gm
- Adult Female: 250-300 gm
Chambers:

Right Atrium and Left Atrium (superior)
Right Ventricle and Left Ventricle (inferior and larger)

Septa:

Interatrial septum: Thin wall between atria.
Interventricular septum: Thick wall between ventricles.

Wall Thickness:

Right Ventricle: 0.3–0.5 cm
Left Ventricle: 1.3–1.5 cm

2. Blood Flow Pathway

Systemic veins → Right atrium → Right ventricle → Pulmonary arteries → Lungs → Pulmonary veins → Left atrium → Left ventricle → Aorta → Systemic arteries

3. Cardiac Valves

Atrioventricular (AV) Valves:
- Tricuspid valve (right)
- Mitral/Bicuspid valve (left)
Semilunar Valves :
- Pulmonary valve
- Aortic valve

4. Wall Layers of the Heart

Epicardium (Visceral Pericardium): Outer covering
Myocardium: Muscle layer
Endocardium: Inner lining

5. Myocardium Structure

Muscle Fibers: Branching, striated (pattern of light and dark bands seen in certain muscle tissues under a microscope. These bands are caused by the regular arrangement of actin and myosin filaments), arranged in parallel.
Intercalated Discs: Connections for ion and action potential movement.
Mitochondria: Abundant for ATP production.
Sarcoplasmic Reticulum: Stores calcium ions.
Sarcomere Structure:
- A-band: Thick myosin filaments
- I-band: Thin actin filaments
- Tropomyosin: Covers actin
- Troponin Complex:
  - Troponin-I, Troponin-T, Troponin-C (regulate contraction)

6. Conduction System of the Heart

Controls heart rate and rhythm:

SA Node (Sinoatrial Node): Pacemaker (Right atrium wall)
AV Node (Atrioventricular Node): Top of interventricular septum
AV Bundle (Bundle of His): Carries impulse down the septum (facilitating the transmission of electrical impulses from the atrioventricular (AV) node to the ventricles)
Bundle Branches: Right and left bundles to ventricles

7. Pericardium

Visceral Pericardium (Epicardium): Inner layer
Parietal Pericardium: Outer fibrous sac
Pericardial Cavity: Space containing 10–30 ml serous fluid (lubricates and protects heart)

8. Endocardium

Inner smooth lining of heart chambers, valves, chordae tendineae (fibrous cords that connect the papillary muscles to the tricuspid and mitral valves in the heart), and papillary muscles (pillar-like muscle projections located within the ventricles of the heart).
Made of endothelium, connective tissue, and elastic fibers.

9. Heart Valves

Thin, translucent structures.
Strengthened by collagen and elastic tissue.
Covered by endothelium (valvular endocardium).

10. Myocardial Blood Supply

Supplied by coronary arteries originating just above the aortic valve.
Most blood flow happens during diastole (relaxation phase) ?.

Major Coronary Arteries:

Left Anterior Descending Artery:
- Apex, anterior left ventricle, part of right ventricle, and septum (2/3rd).
Circumflex Artery:
- Left atrium and lateral left ventricle.
Right Coronary Artery:
- Right atrium, anterior right ventricle, part of left ventricle, and posterior septum (1/3rd).

12. Venous Drainage

Coronary veins collect blood after oxygen is used.
Drain into the coronary sinus.

HEART FAILURE

Definition

Heart failure is a pathophysiological condition where the heart is unable to pump enough blood to meet the metabolic demands of the body.

Etiology (Causes)

1. Intrinsic Pump Failure

These conditions directly impair the contractile function of the heart muscle.

a. Ischemic Heart Disease (IHD)

Mechanism:
- Atherosclerosis in coronary arteries → reduced oxygen supply → myocardial ischemia or infarction.
- Infarcted myocardium is replaced by non-contractile fibrous tissue.
- Leads to ventricular remodeling, thinning, dilation → ↓ ejection fraction.
Type of HF: Systolic heart failure

b. Myocarditis

Etiology: Viral (e.g., coxsackievirus B), bacterial, autoimmune, toxins.
Mechanism:
- Inflammation damages myocytes
- Weakens contractility; can evolve into dilated cardiomyopathy.
Type of HF: systolic heart failure.

c. Cardiomyopathies

Heart muscle (myocardium) is structurally and functionally abnormal in the absence of coronary artery disease

Dilated Cardiomyopathy:
- Thin, stretched ventricles → poor systolic contraction.
- Cause: Idiopathic, alcohol, genetic, toxins, post-viral.
- HF Type: Systolic.
Hypertrophic Cardiomyopathy:
- Thickened myocardium → impaired filling.
- Often genetic; causes diastolic dysfunction.
Restrictive Cardiomyopathy:
- Stiff walls due to infiltration (amyloidosis).
- Impaired filling.
- HF Type: Diastolic.

d. Metabolic Disorders (e.g., Beriberi)

Beriberi: Thiamine (B1) deficiency.
Mechanism:
- Thiamine needed for ATP generation.
- Deficiency impairs myocardial energy metabolism → weak contractility.
HF Type: High-output failure → progresses to systolic HF.

e. Arrhythmias

Mechanism:
- Irregular, rapid contraction → poor ventricular filling and output.
HF Type: Both systolic and diastolic, depending on duration and severity.

2. Increased Workload on Heart

These conditions overload the heart either by pressure or volume, leading to hypertrophy and eventual failure.

a. Pressure Overload

i. Hypertension (Systemic or Pulmonary)

Systemic HTN → Left ventricular hypertrophy → diastolic dysfunction → eventual systolic failure.
Pulmonary HTN (e.g., due to COPD) → Right ventricular hypertrophy → right-sided HF.

ii. Valvular Stenosis (Aortic, Mitral, Pulmonary)

Mechanism:
- Obstruction to outflow (aortic/pulmonary).
- Increases pressure load on ventricles or atria.
- Long-term hypertrophy → ↓ compliance and eventual failure.
HF Type: Initially diastolic, progresses to systolic.

iii. Chronic Lung Disease

Mechanism:
- Hypoxia → pulmonary vasoconstriction → ↑ pulmonary artery pressure.
- Right ventricular pressure overload → hypertrophy → right-sided HF.

b. Volume Overload

i. Valvular Insufficiency (Regurgitation)

Mechanism:
- Retrograde flow increases volume.
- Volume overload leads to dilation → systolic dysfunction.
Examples: aortic regurgitation.

ii. Anaemia

Mechanism:
- Decreased oxygen-carrying capacity → increased cardiac output demand.
- Chronic high-output state strains heart.

iii. Thyrotoxicosis

Mechanism:
- Increased metabolism and O2 demand.
- Increases heart rate and contractility → chronic strain.

iv. Chronic Hypoxia (e.g., from lung disease)

Mechanism:
- Pulmonary vasoconstriction → right ventricular overload.
- Leads to right heart failure.

3. Impaired Filling of Chambers

These conditions restrict diastolic filling, leading primarily to diastolic heart failure.

a. Cardiac Tamponade

Mechanism:
- Fluid accumulation in pericardial sac → ↑ pericardial pressure.
- Prevents ventricular filling → ↓ stroke volume and output

b. Constrictive Pericarditis

Mechanism:
- Rigid, thickened pericardium (post-infectious, TB) restricts diastolic filling.
- Leads to elevated venous pressures, ↓ output

Types of heart failure

Acute vs Chronic Heart Failure

A. Acute Heart Failure

Definition: Rapid onset of heart failure symptoms due to sudden cardiac event.
Causes:
- Myocardial infarction (MI)
- Valve rupture (e.g., papillary muscle rupture)
- Cardiac tamponade (fluid accumulation in pericardium compressing the heart)
Pathophysiology:
- Sudden decline in cardiac output
- Inadequate time for compensatory mechanisms to activate
Clinical Features:
- Hypotension: Due to reduced stroke volume
- Cardiogenic shock: Life-threatening failure of heart to maintain adequate perfusion
- Hypoxia: Poor oxygen delivery to tissues
- Absence of peripheral oedema: Due to insufficient time for fluid accumulation

B. Chronic Heart Failure

Definition: Slow progression of heart failure over weeks to years
Causes:
- Ischemic heart disease (IHD)
- Chronic hypertension
- Valvular heart diseases (e.g., aortic stenosis, mitral regurgitation)
Pathophysiology:
- Sustained pressure/volume overload
- Cardiac remodeling: Dilatation and hypertrophy
Clinical Features:
- Edema: Due to sodium and water retention
- Fatigue and dyspnea: Progressive tissue hypoperfusion

II. Left-Sided vs Right-Sided Heart Failure

A. Left-Sided Heart Failure

Causes:
- Systemic hypertension
- Aortic or mitral valve diseases
- Ischemic heart disease (IHD)
- Myocarditis, cardiomyopathy
Pathophysiology:
- Left ventricular dysfunction → blood backs up into lungs
Clinical Manifestations:
- Pulmonary congestion:
  - Dyspnea
  - Orthopnea (dyspnea when lying flat)
- Hypoperfusion:
  - Renal dysfunction (↓ GFR)
  - Cerebral hypoxia (confusion, dizziness)
  - General fatigue

B. Right-Sided Heart Failure

Causes:
- Secondary to left-sided failure (most common)
- Due to chronic lung disease
- Pulmonary/tricuspid valve disease
- Pulmonary embolism (PE)
Pathophysiology:
- Right ventricular dysfunction → systemic venous congestion
Clinical Manifestations:
- Systemic venous congestion:
  - Peripheral oedema (pitting edema)
  - Hepatomegaly (congestive hepatopathy)
  - Ascites (fluid in abdomen)

I. Overview of Heart Failure Terminology

Forward Failure: Inadequate cardiac output to perfuse tissues.
Backward Failure: Venous congestion due to impaired ventricular emptying.

II. Forward Heart Failure

Definition

Inability of the heart to pump sufficient blood forward into the arterial circulation to meet the metabolic demands of tissues.

Pathophysiology

↓ Cardiac output → ↓ perfusion of vital organs
Triggers neurohormonal responses (e.g., RAAS activation) → vasoconstriction and fluid retention, which can worsen the problem
Common in left-sided failure

Causes

Systolic dysfunction (↓ ejection fraction)
Acute myocardial infarction
Severe cardiomyopathies
Advanced aortic stenosis

Clinical Features

Fatigue and weakness: ↓ muscle perfusion
Hypotension: ↓ stroke volume and systemic output
Cold extremities: Peripheral vasoconstriction + low flow
Renal dysfunction: ↓ renal perfusion → ↓ urine output (oliguria)
Cerebral hypoxia: Dizziness, confusion

III. Backward Heart Failure

Definition

Failure of the heart to effectively eject blood → leads to increased venous pressures behind the affected chamber → congestion in pulmonary or systemic circulation.

Pathophysiology

Blood “backs up” behind the failing ventricle
↑ Hydrostatic pressure in veins and capillaries
Fluid transudation → edema and effusions

Types

Left-sided backward failure: Pulmonary venous congestion
Right-sided backward failure: Systemic venous congestion

Causes

Diastolic dysfunction (impaired filling)
Valvular regurgitation (e.g., mitral or tricuspid)
Chronic hypertension (causing stiff ventricles)

Clinical Features

Left-Sided Backward Failure:

Pulmonary congestion: Dyspnea, orthopnea, paroxysmal nocturnal dyspnea
Pulmonary edema: Frothy sputum
Cough

Right-Sided Backward Failure:

Peripheral pitting edema
Hepatomegaly
Ascites

Compensatory Mechanisms

Cardiac hypertrophy and dilatation
Tachycardia due to neurohumoral activation (norepinephrine, ANP, RAAS)
Starling’s Law: Dilated heart increases sarcomere length to maintain stroke volume — eventually fails

Cardiac Hypertrophy

Definition: ↑ Myocardial size and weight
Stimuli: Mechanical stretch, hypoxia, hormonal factors

A. Left Ventricular Hypertrophy Causes:

Systemic hypertension, aortic/mitral disease, CAD, coarctation, thyrotoxicosis, anaemia

B. Right Ventricular Hypertrophy Causes:

Pulmonary hypertension, tricuspid disease, mitral stenosis, chronic lung disease, left heart failure

Cardiac Dilatation

Due to volume overload → elongation of fibres

Causes:

Valvular insufficiencies (mitral/aortic/tricuspid/pulmonary)
Left-to-right shunts (e.g., VSD)
High-output states (thyrotoxicosis, AV shunts)
Cardiomyopathies, hypertension

Morphological Features

Hypertrophy Types:
- Concentric: Pure hypertrophy → ↑ wall thickness, ↓ lumen
- Eccentric: With dilatation → ↑ lumen size
Gross: Heart weight >500 gm; LV wall >15 mm
Microscopy:
- ↑ fibre size
- Foci of necrosis
- Relative hypoxia in deep myocardium
- ↑ RNA/DNA ratio, ↑ myofilaments, multiple intercalated discs

Summary

Left-sided failure: Pulmonary symptoms (dyspnea, fatigue)
Right-sided failure: Systemic congestion (oedema, hepatomegaly)
CHF = Combination of both sides
Long-term compensation leads to hypertrophy, then decompensation

Congenital Heart Disease (CHD)

Definition

Structural abnormalities of the heart present at birth.
Most common heart disease in infants (~0.5% of newborns); higher in preterm infants (before 37 weeks).

Etiology

Largely unknown; multifactorial (genetic + environmental).
Risk factors:
- Maternal rubella infection
- Drugs and alcohol during pregnancy
- Fetal injury during gestation (These injuries can disrupt normal cardiac embryogenesis, especially during the first trimester when the heart is forming (3rd to 8th weeks of gestation)

Classification of Congenital Heart Diseases

Group	Examples
I. Malpositions	Dextrocardia (± situs inversus)
II. Shunts	A. Left-to-Right Shunts (Acyanotic or late cyanotic) VSD, ASD, PDA B. Right-to-Left Shunts (Cyanotic) Tetralogy of Fallot, Transposition of great arteries, Persistent truncus arteriosus, Tricuspid atresia/stenosis
III. Obstructions	Coarctation of aorta, Aortic stenosis/atresia, Pulmonary stenosis/atresia

I. Malpositions of the Heart

Dextrocardia

Heart apex points to the right.
May be isolated or part of situs inversus.
Isolated dextrocardia often linked with severe anomalies like transposition of great vessels.

II. Shunts

A. Left-to-Right Shunts (Acyanotic → Late Cyanosis)

1. Ventricular Septal Defect (VSD)

VSD changes how blood flows through the heart and lungs. Oxygen-rich blood gets pumped back to the lungs instead of out to the body. The oxygen-rich blood mixes with oxygen-poor blood. These changes may increase blood pressure in the lungs and require the heart to work harder to pump blood.

Most common CHD (30%)
Types:

Membranous septum (Upper portion of the interventricular septum, near the atrioventricular (AV) node and valves (aortic and tricuspid)) (90%)
Subpulmonic (Just below the pulmonary valve), subaortic (Just below the Aortic valve, muscular septum (In the muscular (trabeculated) part of the septum, anywhere from mid to lower septal regions) - 10%

Effects:

↑ Pulmonary blood flow
Right ventricular volume hypertrophy
Left atrial and ventricular hypertrophy (In VSD, blood from the left ventricle flows into the right ventricle. This shunted blood is sent to the lungs, oxygenated, and then returns to the left atrium via the pulmonary veins. Result: Extra blood volume enters the LA and LV, increasing their workload and then hypertrophy)
Valve changes (tricuspid, pulmonary, mitral, aortic); Left-to-right shunting increases pulmonary blood flow, returning excess volume to the left atrium and ventricle. This causes chamber dilation, especially of the left-sided chambers. As the ventricular and atrial walls stretch, the valve annuli (rings) stretch too.

2. Atrial Septal Defect (ASD)

~10% of CHDs
Types:

Ostium secundum (90%) – fossa ovalis (opening in the fetal heart that allows blood to bypass the lungs, which are not yet functional. It connects the right atrium directly to the left atrium, allowing oxygen-rich blood from the placenta to go directly to the systemic circulation)
Ostium primum (5%) – lower septum; may involve mitral valve cleft
Sinus venosus (5%) – upper septum

Effects:
- Right atrial and ventricular hypertrophy (the right atrium receives excess blood from both the systemic veins and the left atrium via the shunt, leading to increased volume load. The right atrium dilates and hypertrophies over time. The overloaded right atrium then pumps more blood into the right ventricle, increasing its preload, which causes the right ventricle to hypertrophy)
- Small left heart chambers and orifices (In Atrial Septal Defect (ASD), blood shunts from the left to the right atrium, reducing the amount of blood reaching the left heart. As a result, the left atrium and ventricle receive less blood, leading to smaller left heart chambers and narrower orifice).

3. Patent Ductus Arteriosus (PDA)

PDA occurs when the opening between the aorta (the artery that carries oxygen-rich blood to the body) and the pulmonary artery (the artery that carries oxygen-poor blood to the lungs) does not close as it should.

Ductus fails to close by 3 months
Often isolated (90%), may coexist with other defects
Causes: Persistent PGE₂ synthesis
Effects:
- ↑ Pulmonary flow (more oxygenated blood from the left side of the heart to flow into the right side (right atrium and right ventricle), which is then pumped to the lungs via the pulmonary artery)
- Left heart hypertrophy (increased pulmonary blood flow, the left atrium receives more blood than normal. As the left atrium enlarges, the left ventricle also begins to take in excess blood and has to work harder to accommodate the increased volume)
- Aortic and mitral valve enlargement (increased volume can cause stretching of the mitral valve annulus

B. Right-to-Left Shunts (Cyanotic)

1. Tetralogy of Fallot

Most common cyanotic CHD (10%)
Four components:

VSD
Overriding aorta
Pulmonary stenosis
Right ventricular hypertrophy

Forms:

Cyanotic: Severe stenosis → R-to-L shunt
Acyanotic: Large VSD, mild stenosis → L-to-R shunt

Some babies with tetralogy of Fallot suddenly develop deep blue or gray skin, nails, and lips. This usually happens when the baby cries, eats or is upset. These episodes are called tet spells.

2. Transposition of Great Arteries

Regular: Aorta from RV, pulmonary trunk from LV → cyanosis at birth
Corrected: Both great arteries and veins transposed → physiological correction

3. Persistent Truncus Arteriosus

Single arterial trunk from both ventricles
Often with VSD
Early cyanosis; poor prognosis

4. Tricuspid Atresia/Stenosis

Absence or malformation of tricuspid valve
Associated interatrial defect → R-to-L shunt
Cyanosis at birth, short survival

III. Obstructive Congenital Heart Diseases

These involve impeded outflow of blood from the heart chambers.

1. Coarctation of the Aorta

Narrowing of the aorta, usually near the ductus arteriosus.

Types:
- Preductal (infantile).
- Postductal (adult-type).
May present with:
- Upper limb hypertension.
- Lower limb hypotension.

2. Aortic Stenosis / Atresia

Obstruction of left ventricular outflow.
May range from valvular narrowing to complete atresia.
Leads to:
- LV hypertrophy.
- Possible hypoplastic left heart syndrome in severe cases.

3. Pulmonary Stenosis / Atresia

Obstruction of right ventricular outflow.
May occur alone or with other defects (e.g., TOF).
Can cause:
- RV hypertrophy.

Summary Chart: Clinical and Pathological Features

Defect	Shunt Direction	Cyanosis	Key Features
VSD	Left to Right	No (early)	RV, LA, LV hypertrophy
ASD	Left to Right	No	RA, RV enlargement
PDA	Left to Right	No	Machine-like murmur, bounding pulses
Tetralogy of Fallot	Right to Left	Yes (early)	Cyanosis, squatting, boot-shaped heart
TGA	Right to Left	Yes (birth)	Requires surgical correction
Persistent Truncus Arteriosus	Mixed	Yes (early)	Single trunk, early CHF
Tricuspid Atresia	Right to Left	Yes (birth)	Hypoplastic RV, short survival
Coarctation of Aorta	None (Obstructive)	No	BP differential in limbs, rib notching
Aortic Stenosis	None (Obstructive)	No	LV hypertrophy
Pulmonary Stenosis	None (Obstructive)	Possible	RV hypertrophy, may cause cyanosis if severe

Ischemic Heart Disease (IHD)

Definition: IHD is heart damage due to imbalance between oxygen supply and demand to heart muscle.
Main cause: Narrowing or blockage of coronary arteries (usually from atherosclerosis).
Also called Coronary Artery Disease (CAD).
Most common cause of death in developed countries; increasing globally.

Epidemiology

More common in men than women (until menopause).
By 2020s, predicted to be #1 cause of death worldwide.

Causes of IHD

I. Coronary Atherosclerosis (90%)

Major cause of IHD due to "fixed" blockages in coronary arteries.
Common sites:
- Left anterior descending (most common)
- Right coronary artery
- Left circumflex artery
Significant blockage: >75% reduction in lumen.

II. Superadded Changes on Atherosclerosis

Plaque rupture or ulceration → triggers clot formation.
Coronary thrombosis → causes complete artery blockage.
Platelet aggregation & spasm → worsens blockage and reduces blood flow.

III. Non-Atherosclerotic Causes (Less than 10%)

Vasospasm (e.g., from drugs or unknown causes)
Coronary artery inflammation (e.g., Kawasaki, Takayasu, infections)
Embolism (e.g., from infective endocarditis)
Blood disorders (e.g., sickle cell, polycythemia)
Trauma
Aneurysms or tumors compressing the artery

Effects of Myocardial Ischemia

Depends on severity, location, and duration of blood supply interruption.

1. Asymptomatic

Minor narrowing; no symptoms

2. Angina Pectoris

Chest pain on exertion due to temporary ischemia

3. Myocardial Infarction (MI)

Heart attack due to complete blockage

4. Chronic IHD / Ischemic Cardiomyopathy

Long-standing poor blood flow → heart muscle damage, fibrosis

5. Sudden Cardiac Death

Sudden heart stop, usually from arrhythmia

🔺Acute Coronary Syndromes = MI + Unstable Angina + Sudden Cardiac Death

ANGINA PECTORIS

A clinical syndrome of Ischemic Heart Disease (IHD) caused by transient myocardial ischemia, presenting as paroxysmal chest pain. Common in men over 50 years.

Pain Characteristics:

Location: Substernal/precordial
Radiation: Left arm, neck, jaw, or right arm
Triggered by exertion/emotion
Relieved by rest or nitroglycerin

Types of Angina:

Type	Features
Stable (Typical) Angina	Most common; triggered by exertion; due to chronic atherosclerosis; ST depression, no enzyme rise
Prinzmetal’s (Variant)	Occurs at rest; due to coronary vasospasm; ST elevation; responds to vasodilators
Unstable (Crescendo)	Occurs at rest, more frequent and severe; warning of impending MI; ECG: NSTEMI or STEMI possible

ACUTE MYOCARDIAL INFARCTION (MI)

Irreversible myocardial necrosis due to prolonged ischemia; the most serious consequence of coronary artery disease.

Epidemiology:

Accounts for 10–25% deaths in developed nations
5% occur in <40 years (especially with risk factors)
More common in males
Oestrogen is protective in females (incidence ↑ after menopause)

Etiopathogenesis:

Coronary atherosclerosis (>75% narrowing) – major cause (90%)
Platelet aggregation → thrombosis
Plaque rupture/haemorrhage
Non-atherosclerotic causes (10%): Vasospasm, embolism, arteritis
Transmural vs Subendocardial infarcts
- Transmural: Full wall thickness, common (95%), usually due to thrombosis
- Subendocardial: Inner wall only; due to hypoperfusion without critical stenosis

CLASSIFICATION OF INFARCTS

Classification	Types/Examples
Anatomic Site	Anterior, Posterior, Septal, Lateral, Combinations
Wall Thickness	Transmural (full), Subendocardial (partial)
Age of Infarct	Acute (fresh), Chronic (healed/organized)

Common Arterial Involvements:

Artery	Area Affected
Left Anterior Descending	Anterior LV, apex, anterior 2/3 septum (40–50%)
Right Coronary Artery	Posterior LV, posterior 1/3 septum (30–40%)
Left Circumflex Artery	Lateral wall of LV (15–20%)

MORPHOLOGICAL CHANGES IN MI

Early Changes (within 30 min):

Electron Microscopy:
- Glycogen loss (5 min)
- Mitochondrial swelling (20–30 min)
- Sarcolemma disruption
Biochemical:
- ↑ Lactic acid, ↓ K⁺, ↑ Na⁺, ↑ Ca²⁺ → irreversible injury

CLINICAL FEATURES OF ACUTE MI

Pain: Severe, crushing, prolonged, radiating; not relieved by rest
GI symptoms: Nausea, vomiting, heartburn-like
Apprehension: Fear, anxiety
Shock signs: Low BP, tachy/bradycardia, cyanosis
Oliguria: <20 mL/hr urine
Fever: Mild, begins in 24h, lasts a week
Pulmonary edema: Due to LV failure – dyspnea, orthopnea

DIAGNOSIS OF ACUTE MI

1. ECG Changes (STEMI):

ST Elevation: Key marker
T wave inversion
Pathologic Q waves

2. Serum Cardiac Markers:

Marker	Notes
CK-MB	Cardiac-specific; rises in 3–12 hrs, peaks in 24 hrs
Troponin I/T	Most specific; rises in 3–6 hrs, remains elevated for 7–10 days
LDH, Myoglobin	Less specific; earlier rise for myoglobin

CHRONIC ISCHAEMIC HEART DISEASE (IHD)

Also known as:

Ischaemic cardiomyopathy
Myocardial fibrosis

Definition:

A long-term condition in which parts of the heart muscle are replaced by fibrous tissue (scarring) due to reduced blood supply (ischaemia). It is commonly seen in elderly patients with a history of angina (chest pain) or heart attacks (MI).

What Happens:

The heart slowly becomes weak and less efficient.
Patients may develop chronic heart failure (CHF) over years.
Sometimes, sudden arrhythmias (abnormal heart rhythms) or another heart attack can occur, leading to sudden death.

CAUSES (Etiopathogenesis):

Main cause: Coronary atherosclerosis – gradual narrowing and hardening of coronary arteries due to plaque buildup.
Less common causes:
- Emboli – blood clots blocking arteries
- Coronary arteritis – inflammation of the coronary arteries
- Myocarditis – infection or inflammation of heart muscle

How Fibrosis Develops:

There are two main theories:

Healing of small, unnoticed heart attacks (microinfarcts).
Slow degeneration (myocytolysis) of small areas of heart muscle due to poor oxygen supply. These dead muscle cells are removed and replaced by fibroblasts and collagen, forming scar tissue.

MORPHOLOGY (What the heart looks like):

Gross Features (visible to the naked eye):

Heart may be normal or enlarged (hypertrophied)
Fibrotic (scarred) areas appear as grey-white patches in the heart muscle
Previous healed heart attacks may be visible
Left heart valves may be thickened and calcified
Coronary arteries show severe atherosclerosis

Microscopic Features:

Scattered areas of fibrosis, especially around small blood vessels
Myocardial cells vary in size; some show myocytolysis (breakdown)
Brown atrophy – age-related pigment (lipofuscin) in muscle cells. Lipofuscin is a "wear-and-tear" or "aging pigment". It consists of oxidized lipids, proteins, and metals that accumulate inside lysosomes of long-living cells. It is not harmful but is a sign of cellular aging and oxidative stress.
Coronary arteries have atherosclerotic plaques, sometimes with thrombi (clots)

SUDDEN CARDIAC DEATH

Definition:

Unexpected death within 24 hours of developing heart symptoms, most often due to a fatal arrhythmia.

Main Cause:

Coronary atherosclerosis (major cause)
Other causes include:
- Coronary artery spasm
- Calcific aortic stenosis (narrow aortic valve)
- Myocarditis
- Hypertrophic cardiomyopathy (thickened heart muscle)
- Mitral valve prolapse
- Endocarditis (heart valve infection)
- Conduction system disorders (inherited or acquired)

Mechanism:

Usually due to sudden arrhythmias, like:
- Ventricular asystole (heart stops beating)
- Ventricular fibrillation (heart quivers instead of pumping)

Autopsy Findings:

Severe narrowing (≥75%) of one or more major coronary arteries
May show:
- Thrombosis (clot)
- Plaque rupture or bleeding (plaque hemorrhage)
- Signs of new or healed infarcts