Heart and blood vessels- atheroma Flashcards Preview

Pathology > Heart and blood vessels- atheroma > Flashcards

Flashcards in Heart and blood vessels- atheroma Deck (20)
1

Atheroma

build-up of fatty material on the inside wall of an artery

2

Atherosclerosis

the progressive narrowing and hardening within an artery potentially resulting in a complete blockage

3

Where does atheroma affect?

Lower abdominal aorta, coronary arteries, popliteal arteries, internal carotid arteries and vessels of circle of Willis

4

Pathogenesis

Initiated by chronic injury to the endothelium (response to injury hypothesis) resulting in chronic inflammation
Causes of injury
Hyperlipidaemia, disturbed flow, smoking, hypertension
Progresses as white cells, fat and blood constituents infiltrate injury

5

Pathogenesis- Stages of atheroma

Type I: Initial lesion Isolated macrophage foam cells
Type II: Fatty streak lesion Mainly intracellular accumulation
Type III: Intermediate lesion Type II changes with small extracellular lipid pools
Type IV: Atheroma lesion Type II changes and core of EC lipid
Type V: Fibroatheroma lesion Lipid core and fibrotic layers, or mainly calcific, or mainly fibrotic
Type VI: Complicated lesion Surface defect, hematoma-hemorrhage, thrombus

6

Clinical manifestation of Atheroma

Can occur in any artery:
Coronary artery- heart attacks/angina(ischaemic heart disease
Aorta- aneurysm due to weakening of the wall
Carotid- narrowing causing strokes
Peripheral vascular disease

7

Atherosclerotic plaques

Atherosclerotic plaques develop slowly over decades but may acutely cause symptoms due to:
Aneurysm and Rupture
Thrombosis
Haematoma formation
Embolisation
Development of critical stenosis

8

Plaque rupture, thrombosis, and healing - Arterial remodeling during atherogenesis

A. Arterial remodeling during atherogenesis. During the initial part of the life history of an atheroma, growth is often outward, preserving the caliber of lumen. This phenomenon of “compensatory enlargement” accounts in part for the tendency of coronary arteriography to underestimate the degree of atherosclerosis.

9

Plaque rupture, thrombosis, and healing - Rupture of the plaque's fibrous cap

B. Rupture of the plaque's fibrous cap causes thrombosis. Physical disruption of the atherosclerotic plaque commonly causes arterial thrombosis by allowing blood coagulant factors to contact thrombogenic collagen found in the arterial extracellular matrix and tissue factor produced by macrophage-derived foam cells in the lipid core of lesions. In this manner, sites of plaque rupture form the nidus for thrombi. The normal artery wall possesses several fibrinolytic or antithrombotic mechanisms that tend to resist thrombosis and lyse clots that begin to form in situ. Such antithrombotic or thrombolytic molecules include thrombomodulin, tissue and urokinase-type plasminogen activators, heparan sulfate proteoglycans, prostacyclin, and nitric oxide.

10

Plaque rupture, thrombosis, and healing - Endogenous fibrinolytic mechanisms

C. When the clot overwhelms the endogenous fibrinolytic mechanisms, it may propagate and lead to arterial occlusion. The consequences of this occlusion depend on the degree of existing collateral vessels. In a patient with chronic multivessel, occlusive coronary artery disease, collateral channels have often formed. In such circumstances, even a total arterial occlusion may not lead to myocardial infarction, or it may produce an unexpectedly modest or a non-ST segment elevation infarct because of collateral flow. In the patient with less advanced disease and without substantial stenotic lesions to provide a stimulus to collateral vessel formation, sudden plaque rupture and arterial occlusion commonly produces ST-segment elevation infarction. These are the types of patients who may present with myocardial infarction or sudden death as a first manifestation of coronary atherosclerosis. In some cases, the thrombus may lyse or organize into a mural thrombus without occluding the vessel. Such instances may be clinically silent.

11

Plaque rupture, thrombosis, and healing - Fibroproliferative response

D. The subsequent thrombin-induced fibrosis and healing causes a fibroproliferative response that can lead to a more fibrous lesion, one that can produce an eccentric plaque that causes a hemodynamically significant stenosis. In this way, a nonocclusive mural thrombus, even if clinically silent or causing unstable angina rather than infarction, can provoke a healing response that can promote lesion fibrosis and luminal encroachment. Such a sequence of events may convert a “vulnerable” atheroma with a thin fibrous cap prone to rupture into a more “stable” fibrous plaque with a reinforced cap. Angioplasty of unstable coronary lesions may “stabilize” the lesions by a similar mechanism, producing a wound followed by healing.

12

Treatment for Atheroma

Revascularization

Secondary prevention

13

Ischaemic Heart Disease

Imbalance
between supply (perfusion) and demand of the heart for oxygenated blood

Important:
Not only ↓ oxygen but also ↓ nutrient substrates and inadequate removal of metabolites

14

Causes of Ischemic Heart Disease

>90% are caused by atherosclerotic obstruction of coronary arteries, coronary artery disease
Reduced/no flow of oxygenated blood --> Atheroma, Embolism & Spasm
increased demand for oxygenated blood --> Thyrotoxicosis, Myocardial hypertrophy (hypertension)

15

Risk Factors for Ischemic Heart Disease

Positive family history
Male
Age
Genetic (ACE gene deletion)
Hyperlipidaemia
cigarette smoking
Hypertension
Diabetes
Lack of exercise
obesity
Heavy alcohol consumption

16

Signs & Symptoms of Ischemic Heart disease

CHEST PAIN, often central, crushing, radiating to left arm or into jaw ***
SHORTNESS OF BREATH
PALPITATIONS
SYNCOPE
Nauseous, sweating, pale

17

Clinical presentation and diagnosis of ischemic heart disease

Stable angina
Unstable angina
NSTEMI (non-ST segment elevation myocardial infarction)
STEMI (ST segment elevation myocardial infarction)
Sudden death

18

Complications of myocardial infarctions

Cardiac arrest - Ventricular wall rupture
Arrythmias - Deep vein thrombosis
Pericarditis - Pulmonary embolus
Valvular defects

19

Treatment for ACS (acute coronary syndrome) and Angina

Immediate & common to all ACS and angina:
Oxygen
Pain relief
Aspirin
ANGINA: Lifestyle, Nitrates (dilates vasculature), B-blockers
ACS: thrombolytic therapy, PTCA (Percutaneous transluminal coronary angioplasty), CABG (coronary artery bypass graft), drugs

20

Hyperlipidaemia

LDL cholesterol – ‘bad cholesterol’, the form of cholesterol that is delivered to peripheral tissues
HDL cholesterol – ‘good cholesterol’, mobilizes cholesterol from the tissues and transports it to the liver to be excreted in bile.