Common cardiac conditions

Coronary blood supply

• Right coronary a.

• Left anterior descending a.

• Left circumflex a.

• Left ventricle is most metabolically active

• Subendocardial region of ventricle is watershed region

Myocardial ischaemia and infarction

• Block of coronary artery/arteries

  • localised region of ischaemia and infarction

  • transmural infarction (myocardial infarction that affects the full thickness of the heart wall — from the endocardium to the epicardium)

• Global (entire heart) decrease in blood flow

  • shock (BP + circulation ↓, not enough O2 to organs)

  • subendocardial ischaemia and infarction (damage/ death of endocardium due to reduced blood flow)

Clinical presentations of myocardial ischaemia and infarction

• Stable angina pectoris

  • central crushing chest pain on exertion → radiates to left arm, jar, neck + back

  • usually silent

• Unstable angina pectoris / myocardial infarction

  • central crushing chest pain at rest or on exertion → radiates to left arm, jaw, neck + back

  • syncope (fainting) + collapse

Pathology of myocardial infarction

depends on duration of infarction

Macroscopic pathology

• 0–4 hours: No visible changes yet.

• 4–24 hours: Dark mottling → patchy dark areas where tissue is dying.

• 1–3 days: Yellow centre → dead tissue accumulating.

• 4–7 days: Red rim around infarct → inflammation and increased blood flow around the dead area.

• 7–10 days: Soft centre → dead tissue breaking down.

• 10–14 days: Grey centre → healing tissue forming.

• 2–8 weeks: White fibrous scar → permanent scar tissue.

Microscopic pathology

• Early: No microscopic change yet

• After 4 hrs: Coagulative necrosis → heart muscle cells start dying but structure still visible

• 1–3 days: Neutrophils arrive → acute inflammation cleaning damaged tissue

• 3–7 days: Macrophages replace neutrophils → they digest dead tissue

• 7–14 days: Granulation tissue forms → new capillaries + healing tissue

• 2–8 weeks: Fibrous scar → permanent scar replaces muscle

Complications of myocardial infarction

• death

• myocardial rupture

• pericarditis

• arrhythmias

• ventricular aneurysm

• progressive heart failure

Acute rheumatic heart disease

Risk factors:

• low SES

• overcrowded living conditions

• poor nutrition

• high prevelance of group A β haemolytic Streptococci in the community

• predisposing genetic factors

Pancarditis

• Definition: Involves inflammation of all three layers of the heart (endocardium, myocardium, pericardium).

  Pericarditis: Fibrinous type, described as “bread and butter” appearance.

Myocarditis

• Timing: Occurs 10 days – 6 weeks after strep throat

• Pathognomonic feature: Aschoff bodies (diagnostic hallmark).

  • Components:

    • Swollen eosinophilic collagen

    • Plump macrophages

    • Caterpillar cells (Anitschkow cells)

    • Surrounding lymphocytes

Endocarditis

• Vegetations: Small (2–3 mm), non-friable.

• Composition: Fibrin deposition + Ab-Ag complexes.

• Location: Found at the lines of closure of valves.

• Result: Leads to fibrosis + valve changes

• Valve changes:

  • Leaflets thickened and fused.

  • Produces “fish mouth” stenosis of the mitral valve (MV).

  • Results in left atrial enlargement and wall thickening.

Chronic rheumatic heart disease

• Valve leaflets thickened + fused

• chordae tendinae shortened + thickened

• fibrosis + neovascularisation of valves

• Fish mouth stenosis MV, RA enlargement and RA thrombus

• Mitral valve always involved, >AV, >, rarely PV

Sequelae:

• stenosis: commissural adherence + fusion (thickening of cusps)

• regurgitation: shortening of cusps + chordae

Complications:

• Permanent risk of infective endocarditis

• atrial fibrillation

• thrombus and embolism

• cardiac failure

Management:

• Valvuplasty

• valve replacement

Endocardium contents

• true endocardium

• cardiac valves

• chordae tendinae

Infective endocarditis

• infection of endocardium by infective organisms

  • formation of bulky, friable vegetations

• aetiology = bacteria + fungi

• origin of infection = poor dental hygiene, IV drug use, recent surgery, systemic sepsis

Bacterial infective endocarditis

Classifications:

• acute bacterial infective endocarditis

  • highly virulent organisms

  • highly destrcctive

  • large and friable → easily dislodge and embolise

  • >90% mortality if not treated, 50% mortality even after treatment

  • vegetations at edges of defect

  • abscess formation (valve destruction, arrhythmias)

  • papillary muscle / chordae rupture

• subacute bacterial infective endocarditis

  • vegetations at lines of valves closure + edges of defect

  • large + friable (smaller than acute) → easily dislodge and embolise

  • fibrin + bacteria

  • valve damage

Clinical features of bacterial infective endocarditis

• acute = rapid onset, malaise, fever, chest pain, SOB, sudden death

• subacute = slow onset fever, malaise, fatigue

• clubbing

• murmurs

Pathological valvular lesions

• Stenosis: valve fails to open → blocks forward blood flow → pressure ↑ in chamber

• Regurgitation/Incompetence: valve fails to close → backward blood flow → blood volume ↑ in chamber

Complications of infective endocarditis

• systematic embolism

• valve/cord rupture

• septicaemia

• immune complex formation

Cardiac failure (congestive, left and right)

• congestive cardiac failure → fluid build up in lungs/ab.

• R sided failure (RV)

• L sided failure (LV)

LEFT HEART FAILURE

Aetiology:

• ischaemic heart disease

• systematic hypertension

• aortic + mitral valvular diseases

• primary myocardial diseases

Symptoms:

• cough and dyspnoea

• orthopnea

• PND (paradoxical nocturnal dyspnoea)

Pathology (condition)

• pulmonary oedema (lungs heavy + red)

• pleural effusions

• pale pink secretions in alveoli

RIGHT HEART FAILURE

Aetiology:

• underlying pulmonary disease

• pulmonary hypertension

• usually caused by left heart failure

Pathology:

• peripheral pedal oedema

• swollen liver (heptomegaly)

• enlarged spleen (splenomegaly)