W3: atherosclerosis Flashcards
Which main cardiac veins are anterior and which ones are posterior?
Anterior:
anterior cardiac vein
great cardiac vein
small cardiac vein
Posterior:
posterior cardiac vein
Middle cardiac vein
(Small loops around skins on both sides?)
What vessel do most of the coronary veins drain into?
Coronary sulcus
Which vein does not drain into the coronary sulcus? Where does it drain into?
Anterior cardiac vein - drains directly into the right atrium
What type of adrenergic receptors are found in the heart and which one is most prevalent?
Beta 1 and Beta 2. the most predominant one is BETA 1
Describe the cardiovascular changes that occur during exercise
Increased: Force of contractility Heart Rate Stroke Volume Cardiac Output MAP Blood flow
Decreased:
Total peripheral resistance
Explain the role that the ANS plays in in the increases in heart rate and blood pressure during exercise
Increases sympathetic activity release Noradrenaline which binds to the Beta receptors on the heart. This increases rate of conduction, contraction and heart rate.
This increase in force of contraction of the heart increases cardiac output and blood pressure.
Decrease in sympathetic activity also contributes to increased HR.
Sympathetic activity also induces vasoconstriction in skeletal muscle arterioles and increase blood flow here. (Adrenaline binds to alpha receptors)
Define atherosclerosis
Atherosclerosis is chronic inflammatory disease of the arterial wall resulting in the hardening and narrowing of (medium and large) arteries due to plaque formation.
describe the pathophysiology of atherosclerosis
Damage to endothelium occurs due to cigarette smoke, toxins, viruses, hyperlipidaemia, diabetes, hypertension, high LDL levels.
This damages stimulates an inflammatory response and endothelial cells generate inflammatory mediators and cytokines to increase adhesion of WBCs. This generates oxidant stress.
The endothelium increases its permeability to lipids and this causes LDLs to deposit in the tunica Intima.
LDLs become oxidised and there is transmigration of WBCs, including monocytes. Monocytes move in and become macrophages. Macrophages engulf the oxidised LDLs and become lipid-laden foam cells.
These foam cells aggregate on the blood vessel to form a fatty streak. They also release chemokines attract more monocytes.
Foam cells release cytokines to trigger migration of SMCs from tunica media to tunica Intima and growth factors to induce their proliferation.
SMC proliferation and formation of a dense ECM results in superficial fibrous cap covering the fatty streak. Foams cells become so full with lipid that they burst/die and release their lipid contents. This lipid debris contributes to the necrotic, lipid core below the fibrous cap.
Presence of MMPs and oxidant stress thin the fibrous cap making the plaque unstable. If the plaque ruptures, there is thrombus formation and vessel occlusion resulting in myocardial ischemia.
what makes a plaque vulnerable?
Large lipid core
Thin fibrous cap
Abundance of inflammatory cells
Smaller number of SMCs so fibrous cap is less thick
Risk factors of Coronary artery disease?
Age
Gender (male)
Genetic factors
Obesity Diabetes Hypertension High LDL levels Infection Lack of exercise High saturated fat diet Excessive alcohol Stress
Describe how coronary artery stenosis results in myocardial ischaemia
CA stenosis is narrowing of the artery either due to atherosclerosis or a blood clot. This reduces the blood flow to the heart and causes myocardial ischaemia where there is an insufficient oxygen supply to the heart.
Explain the production, character and distribution of cardiac chest pain
Myocardial schema results in angina pectoris. this occurs when myocardial oxygen demand is higher than the supply.
The chest pain is produced by a build up of metabolites (adenosine, K, Co2, lactate) which activate sensory neurons.
Character of chest pain: tight, pressurised. It occurs centrally and can radiate to the left arm/shoulder and jaw.
What are associated symptoms of angina pectoris?
Breathlessness Sweating Pallor Nausea Vomiting
Describe the difference between stable and unstable angina and their origins?
Stable:
Chest pain is predictable.
Occurs due to physical exertion, exercise, cold weather, strong emotion.
Lasts up to 15 minutes
Origin: atherosclerosis plays a role as oxygen demand is not met
Unstable:
Unpredictable chest pain
Occurs randomly, even when at rest
Pain is more severe and lasts for 30 minutes or longer.
Origin: temporary coronary artery occlusion - Small plaque rupture and platelet aggregation which temporarily occludes the coronary arteries. Clot is then washed away.
Indicative of a future bigger heart attack.
What is variant angina caused by and is it common and predictable?
Caused by vasospasm of coronary artery.
Uncommon
Unpredictable
Describe what occurs during thrombus formation? When does it lead to myocardial infarction
when a plaque ruptures, there is thrombus formation to stop the lipid contents spilling into the lumen.
This involves platelet aggregation, migration of inflammatory cells, vasoconstriction and clot formation.
If the vessel is completely occluded then myocardial infarction occurs and there is death of cardiac myocytes.
Describe the investigations of angina pectoris
Laboratory tests: to check for presence of high troponin levels (troponin leaks into blood after angina attack)
ECG: check for heart abnormalities
Chest Xray to rule out other causes of chest pain.
Stress echo: Echocardiogram taken before and after exercise. Patient performs a physical activity usually on a treadmill. Speed and resistance increases with time. Checks for abnormalities in wall motion of heart.
Exercise stress test (ECG): same as above but ECG is recorded.
Nuclear stress test: radioactive substance is injected into patient and their coronary blood flow is measured before and after stress.
CT coronary angiogram: contrast dye is injected into vein and special Xray images are taken to view coronary blood flow.
Invasive coronary angiogram: contrast dye is injected, catheter is inserted into artery and passed up into coronary artery. X ray images are used to check for narrowing.
Describe the coronary steal phenomenon
Downstream of an occlusion, the arteries are maximally vasodilated. This is because the narrowing causes a reduction in the blood and oxygen supply. There is active hyperaemia and the blood vessel compensates by vasodilating to its maximal dilation.
So vasodilators have no effect on these occluded areas as they cannot dilate them further. Instead, they vasodilate already well-perfused areas and blood is stolen from occluded areas.
