Cardiovascular Pathology Overview

This presentation covers cardiovascular pathology, focusing on atherosclerosis, aneurysms, aortic dissection, vasculitis (giant cell arteritis & polyarteritis nodosa), myocardial infarction (MI), and heart failure.

Students will be able to list two microscopic changes in atherosclerosis.
Students will be able to list two types of aneurysm.
Students will be able to define aortic dissection and describe its microscopic features.
Students will be able to list two differences between giant cell arteritis and poly arteritis nodosa.
Students will be able to list two microscopic changes in MI on day one and day three.

A specific type of arteriosclerosis, the most common and clinically important vascular disease.
Primarily affects large elastic and medium-sized muscular arteries.
Grossly appears as white to yellow raised lesions; may be red-brown if ulcerated and thrombus is superimposed.
Atherosclerosis is an intima-based lesion, with key features being intimal thickening and lipid accumulation.
Lesions are patchy, affecting only portions of the arterial wall, appearing eccentric on cross-section.
Microscopic examination reveals soft lipid cores covered by fibrous caps containing smooth muscle cells (SMCs), collagen, inflammatory cells, variable degrees of neo-angiogenesis, lipid, and necrotic debris.
The media can be attenuated and fibrotic with smooth muscle atrophy.
Atherosclerosis can cause serious consequences like ulceration, rupture, hemorrhage, embolism, and aneurysm formation.

Congenital or acquired dilatation of blood vessels or the heart, involving the entire wall thickness.
Typically occurs in the abdominal portion distal to the renal arteries.
Extensive atherosclerosis with thinning and focal destruction of the underlying media are commonly associated with aortic aneurysms.
Aneurysms are classified by shape:
- Saccular: discrete outpouching
- Fusiform: circumferential dilatation
Rupture of the aneurysm is a major complication.

Arterial blood penetrates the intima and splays apart the media, forming a blood-filled channel within the aortic walls.
Usually found in the ascending aorta within 10 cm of the aortic valve.
Grossly characterized by an intimal tear with subsequent splitting of the aortic wall, leading to massive hemorrhage into the adventitia and surrounding soft tissue.
May be associated with small oblique intimal tear and intramural hematoma.
Two lumens may be observed, one true and one false.
The false lumen displays irregular surface and blood clots while the true lumen exhibits endothelial lining.

A general term for vessel wall inflammation.
Two common pathogenic mechanisms are immune-mediated inflammation and direct vascular invasion by infections.
Example: Giant cell arteritis.

Chronic inflammatory disorder, typically with granulomatous inflammation.
Primarily affects large to medium-sized arteries in the head.
Grossly characterized by tender and thickened scalp veins.
Histopathological features include chronic inflammation, granuloma formation, and destruction of the media and elastic lamina with intimal remodelling and hyperplasia, leading to lumen occlusion.

A systemic vasculitis of medium-sized muscular arteries.
Typically involves renal and visceral vessels but usually spares the lungs.
Acute lesions are characterized by fibrinoid necrosis of the vessel wall and infiltrating neutrophils.
Chronic lesions are fibrotic and associated with chronic inflammation.

Right-side heart failure leads to chronic venous congestion of the liver.
Liver shows alternating pale and dark areas resembling a nutmeg appearance due to passive congestion.
Hepatic parenchyma with a faintly nodular pattern.
Central liver lobules show congestion and dilatation of central veins and blood sinusoids, with atrophy and necrosis of liver cells.
Left-side heart failure results in chronic venous congestion of the lung. The lungs are distended and reddish, with congestion. Normal lung tissue is present on the edges. Microscopic examination reveals thickened alveolar walls with dilated and engorged capillaries, with red blood cells (RBCs) present in the alveolar spaces.

Necrosis of heart muscle resulting from ischemia (lack of blood flow).
Elevated enzymes in ischemia include troponin, CK-MB, LDH, and myoglobin.
Grossly, soft hemorrhagic areas are consistent with MI.
MI can result in arrhythmia, ventricular rupture, papillary muscle rupture, aneurysm, heart failure, and other complications.
Microscopic features of MI vary depending on the time post-infarction:
- Day 1: coagulative necrosis with wavy fibers; necrotic cells separated by edema fluid.
- Days 2-3: dense neutrophilic infiltrate.
- Days 7-10: nearly complete removal of necrotic myocytes by phagocytic macrophages.
- Healed MI: dense collagenous scar tissue.