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Pathology > Cardiovascular disease 24/10/22 > Flashcards

Cardiovascular disease 24/10/22 Flashcards

1
Q

What is cardiovascular disease?

A

It is an umbrella term that describes a range of conditions that affect the heart, the blood vessels, or both. It is caused by thrombosis (blood clots) or atheroslerosis.

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2
Q

What is atherosclerosis?

A

It is a condition where there is a build-up of fatty deposits (plaques) inside the artery that cause the artery to harden and narrow, restricting blood flow.

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3
Q

What conditions are caused by atherosclerosis?

A

Coronary heart disease (angina and myocardial infarction)
Stroke
Transient ischaemic attack
Peripheral arterial disease

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4
Q

What are the statistics for CVD?

A

It is a leading cause of morbidity and mortality and 1 in 3 deaths are related to CVD. It currently costs the NHS £29 billion and there are regional variants around the UK due to lifestyle, standards of care available, and standards of living.

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5
Q

What non-modifiable risk factors are associated with CVD?

A

Age
Gender (men more at risk)
Family history
Ethnic background (south Asian or African higher risk, south American or Chinese lower risk)
Menopause

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6
Q

What modifiable risk factors are associated with CVD?

A

Smoking
Low blood level of high-density lipoprotein (HDL) cholesterol
High blood level of non-HDL cholesterol
Sedentary lifestyle
Unhealthy diet
Alcohol intake high
Overweight and obesity

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7
Q

How many cases of CVD are due to modifiable risk factors?

A

Around 90% of cases the 1st heart attack is due to one of the modifiable risk factors.

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8
Q

What comorbidities can increase the risk of developing CVD?

A

Hypertension
Diabetes
Chronic kidney disease
Dyslipidaemia
Atrial fibrillation (a condition that causes an irregular and often fast heartbeat)
Arthritis, systemic lupus erythematous, and other systemic inflammatory disorders
Influenza
Mental health problems
Periodontitis (gum disease is where your gums are red and swollen)

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9
Q

Is there more CVD now than before?

A

There has been an improved access to healthcare, an increased life expectancy, and clinical recognition. This means people are living longer but are living with more disease, for example, more people are on CVD medication now than before.

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10
Q

What is aortic valve stenosis?

A

Progressive narrowing, stiffening, and thickening of the aortic valve (calcification). Normal value area is 3.5 – 4 cm2, it is considered critical if <0.8cm2.

Once symptoms develop there is a poor life expectancy of 2 to 5 years if untreated. Symptoms are chest pain (angina pectoris), fatigue, syncope, and congestive heart failure.

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11
Q

What are the risk factors of aortic valve stenosis?

A

Older Age
Congenital heart disease
Infection of the heart (rheumatic)
Degenerative (calcification)
Radiation therapy to the heart
CKD (normal > 90ml/min/1.73m2)
Having CVD risk factors (diabetes, high cholesterol, high blood pressure, obesity)

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12
Q

What is the treatment for aortic valve stenosis?

A

Aortic valve replacement (biological and mechanical).

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13
Q

What are the risks of aortic valve replacement?

A

*Heart Failure
* Arrhythmias
* Blood Clots
* Bleeding
* Endocarditis
* Stroke
* Death

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14
Q

How does the heart pump?

A

-Blood brought back from body into the right atrium through the superior and inferior vena cava (veins).
-Blood pumped from right atrium into the right ventricle and out pulmonary arteries to the lungs for gas exchange.
-Oxygenated blood returns in pulmonary veins to left atrium.
-Left atrium pumps blood into the left ventricle and out the aorta to the body. The process repeats.

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15
Q

What is diastole?

A

Diastole is when the heart muscle relaxes. When the heart relaxes, the chambers of the heart fill with blood, and a person’s blood pressure decreases.

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16
Q

What is atrial systole?

A

Atrial systole is when the left and right atria contract at the same time and push blood into the left and right ventricle, respectively.

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17
Q

What is ventricular systole?

A

Ventricular systole is where the left and right ventricles contract at the same time and pump blood into the aorta and pulmonary trunk, respectively.

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18
Q

What is the ejection fraction?

A

Ejection fraction (EF) is a measurement, expressed as a percentage, of how much blood the left ventricle pumps out with each contraction. An ejection fraction of 60 percent means that 60 percent of the total amount of blood in the left ventricle is pushed out with each heartbeat. An ejection of 55% is normal.

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19
Q

What is cardiomyopathy?

A

A disease of the heart muscle, where the walls of the heart chambers have become stretched, thickened, or stiff. This affects the heart’s ability to pump blood around the body.

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20
Q

What are the three types of cardiomyopathies?

A

Hypertrophic cardiomyopathy
Dilated cardiomyopathy
Arrhythmogenic right ventricular cardiomyopathy

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21
Q

What is the other type of cardiomyopathy?

A

Takotsubo cardiomyopathy - is caused by extreme stress and is not passed on through families and can often disappear with time.

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22
Q

What is hypertrophic cardiomyopathy?

A

This is an autosomal dominant inherited disease of the heart muscle caused by a mutation. This mutation affects the myofilament components of the sarcomere and the most common is the beta-myosin heavy chain myosin binding protein. This affects 1 in 500. Diagnosis often via Echocardiography and treated by pharmacotherapy (symptoms), cardiac resynchronisation therapy (for arrhythmia), septal ablation, and surgical myectomy.

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23
Q

What is dilated cardiomyopathy?

A

Dilated cardiomyopathy is a disease of your heart muscle where it becomes stretched, thin, and floppy. It is inherited genetically and diagnosis is often via patient symptoms and echocardiography. Treatments are pharmacotherapy (symptoms), cardiac resynchronisation, therapy (for arrhythmia), and ablation.

24
Q

What is arrhythmic right ventricular cardiomyopathy?

A

Primarily autosomal dominant. Some heart proteins do not develop properly and cannot keep the muscle cells together. Desmosomes keep the myocytes together, providing strength.
Myocytes detach with fatty deposits build up to repair the damage, and the muscle becomes progressively thin and stretched.

Some acquired cases (viral myocarditis) and it normally affects RV but can also affect LV leading to bi-ventricular HF.
Diagnosis often via ECG, echocardiography, CMRI, and myocardial biopsy. Treatments are
pharmacotherapy (symptoms), cardiac resynchronisation, therapy (for arrhythmia), ablation, and heart transplant.

25
Q

What are the two different types of heart failure?

A

Reduced ejection fraction - heart muscle is weak and not pumping properly, and the left ventricle does not eject sufficient blood.

Preserved ejection fraction - heart muscle is stiff and not able to relax, and the left ventricle does not fill with enough blood. The heart pumping function is preserved.

26
Q

How is heart failure caused and diagnosed?

A

Diagnosis often via symptoms, ECG, echocardiography, and CMRI.

Causes are:
Obesity
CKD
Sleep apnoea
Long-term (particularly poorly controlled) hypertension
Ischemia associated with coronary artery disease
Myocardial infarction
Valvular heart disease
Myocarditis
Congenital malformations
Familial cardiomyopathies

27
Q

How does the electrical system work in the heart?

A

An electrical stimulus is generated by the sinus node. Located in the atria of the heart. The sinus node generates an electrical stimulus regularly, 60 to 100 times per minute under normal conditions. The atria are then activated. The electrical stimulus travels down through the atrioventricular node via the bundle of His into the ventricles. The bundle of His divides into right and left pathways, called bundle branches, to stimulate the right and left ventricles. This causes the heart’s ventricles to contract and pump out blood. The 2 upper chambers of the heart (atria) are stimulated first and contract for a short period of time before the 2 lower chambers of the heart (ventricles).

28
Q

What is atrial fibrillation?

A

In atrial fibrillation, the SA node isn’t directing your heart’s electrical rhythm. Instead, many different impulses rapidly fire at the same time, causing a fast, chaotic rhythm in your atria. As a result, your atria can’t contract or pump blood effectively into your ventricles.

29
Q

What is ventricular fibrillation?

A

Ventricular fibrillation is a type of irregular heart rhythm (arrhythmia). During ventricular fibrillation, the lower heart chambers contract in a very rapid and uncoordinated manner. As a result, the heart doesn’t pump blood to the rest of the body.

30
Q

What are the consequences of an electrical defect?

A

A cardiac thrombi (clot in the heart).

31
Q

What is the treatment for people with CVD?

A
  1. Statins – cholesterol-lowering medications that inhibit HMA-CoA reductase (the enzyme responsible for the production of cholesterol in
    the liver). Nice recommendations in patients with > 20% 10-year CVD risk. Can decrease CVD risk by up to 60%.
  2. Cardioinhibitory - beta-adrenergic blocking agents (Beta Blockers). Negative chronotropic and inotropic influences (decrease HR and CO).
    Can reduce blood pressure. Calcium channel blockers can inhibit Ca movement in and out of cells (heart and blood vessels). Direct negative inotropic influences and reduce blood pressure.
    Diuretics - relieve the heart’s workload by lowering blood volume and reducing blood
    pressure.
  3. Vasodilators - ACE inhibitors/ARBs, NO donors (GTN in angina/acute cardiac ischemia).
  4. Cardio-stimulatory - positive inotropes (Digitalis).
  5. Anti-coagulants - thrombolytics (alteplase), anti-platelets (aspirin, clopidogrel), anti-coagulants (Vitamin K inhibitors (warfarin), DOACs (apixaban, rivaroxaban).. Antiarrhythmic drugs
  6. Amiodarone and flecainide.
  7. Ablation.
  8. Ablation + Cardiac resynchronisation therapy (pacemakers/pacemakers + defibrillators).
  9. Lifestyle changes such as diet, exercise, weight loss, and stress reduction.
32
Q

What is vascular disease?

A

Vascular disease includes any condition that affects your circulatory system or the system of blood vessels.

33
Q

What is the endothelium?

A

Endothelial cells form the innermost lining (single cell layer thick) of the blood vessel.

34
Q

What is the function of the endothelium?

A

*Mechanosensitive (responsive to the direction of blood flow and the pressure on them)
* Actively help regulate vascular tone
(vasodilate and vasoconstrict)
*Key regulator of vascular homeostasis
* Responsive to physical and chemical
signals and produces a wide range of
factors that help regulate the processes that are involved in CVD.

35
Q

How does the endothelium play a role in CVD?

A
  1. Processes involved in smooth muscle relaxation hyperpolarization can increase or decrease vasodilation and vascular tone.
  2. Processes involved in anti-fibrinolysis regulation of clotting cascade can increase or decrease platelet adhesion, fibrinolysis, and clotting cascade.
  3. Processes involved in anti-inflammatory actions oxidative stress can cause leukocyte adhesion.
36
Q

What is pulse wave velocity?

A

Arterial stiffness (using ultrasound), measures the speed of arterial pressure waves traveling along the aorta and large arteries. It is calculated by dividing the distance by pressure wave transit time at the two points of recording arteries. If ts slow the blood vessels are healthy, if its fast they’re unhealthy.

37
Q

What is atherosclerosis?

A

A lipoprotein-driven disease that leads to plaque formation at the specific sites of the arterial tree though endothelial (intimal) activation, inflammation, necrosis, fibrosis, and calcification
Leads to narrowing of the blood vessels which makes them more susceptible to formation of thrombi and plaque rupture. Obstruction of blood flow to peripheral organs, including the heart, brain and/or lower extremities.

38
Q

What is a fatty streak?

A

A fatty streak develops between the intima and the media.

39
Q

What is a vulnerable plaque?

A

An unstable plaque develops with a fatty core and a thin fibrous outer shell.

40
Q

What is a plaque rupture?

A

A plaque can sometimes rupture into the bloodstream.

41
Q

What is an occlusion?

A

If the blood clot enlarges to completely block the artery, all tissues supplied by that artery begin to die below the blockage.

42
Q

What is ischaemic heart disease (angina)?

A

Angina is where you have attacks of chest pain caused by reduced blood flow to your heart.

43
Q

How does atherosclerosis cause damage to the endothelium?

A

Low oscillatory sheer at branch points leads to an injury to the endothelial layer.

44
Q

What is a carotid artery plaque?

A

Carotid artery disease is caused by a buildup of plaques in arteries that deliver blood to your brain. Plaques are clumps of cholesterol, calcium, fibrous tissue, and other cellular debris that gather at microscopic injury sites within the artery.

45
Q

How does the endothelium respond to shear stress?

A

Disturbed flow results in:
* Increase in response to inflammatory stimuli
* Increase in reactive oxygen species (ROS)
production
* Increase in permeability
* Increase in apoptosis and proliferation
* Decrease in bioavailability of nitric oxide (NO)
and prostacyclin (PGI2)

Laminar flow results in the opposite (decrease and increase) of the same things seen in disturbed flow.

46
Q

What is vascular calcification?

A

Most individuals age 60+ have calcium deposits within their arterial wall (intimal or medial). Increasingly recognised as a serious problem as it leads to vessel stiffness and increased blood pressure.

47
Q

What causes vascular calcification?

A

Vascular calcifications are mineral deposits on the walls of your arteries and veins. These mineral deposits sometimes stick to fatty deposits, or plaques, that are already built up on the walls of a blood vessel.

48
Q

What are the characteristics of medial vascular calcification?

A

Clinical complications - arterial stiffness, increased pulse pressure, increased pulse wave velocity, surgical complications, and increased all-cause mortality
Associated pathologies - age, diabetes, renal failure, and aortic aneurism
VSMC phenotypes - osteocytic, and chondrocytic
Known drivers - oxidative stress, apoptosis, mitochondrial dysfunction, mechanical stress, loss of inhibitors, uraemia, senescence

49
Q

What are the characteristics of intimal vascular calcification?

A

Clinical complications - plaque rupture, stroke, myocardial infarction
Associated pathologies - atherosclerosis, hyperlipidemia, metabolic syndrome
VSMC phenotypes - osteocytic, and chondrocytic, foam cells
Known drivers - oxidative stress, apoptosis, mitochondrial dysfunction, mechanical stress, inflammation

50
Q

Characteristics of a stable plaque?

A

Thick fibrous cap, smaller lipid pool, few inflammatory cells, dense extracellular matrix.

51
Q

Characteristics of unstable plaque?

A

Thin fibrous cap, large lipid pool, many inflammatory cells, few smooth muscle cells.

52
Q

What leads to the erosion of a plaque?

A

Endothelial dysfunction, leukocyte activation, modification of sub-endothelial matrix by endothelial or SMCs, leading to loss of adhesion to the ECM or apoptosis.

53
Q

What are the consequences of atherosclerosis?

A

Angina
Acute myocardial infarction - occurs when one of the coronary arteries becomes occluded by an embolus leading to heart muscle ischaemia
In-stent restenosis - the narrowing of a stented coronary artery lesion
Ischaemic stroke - occurs when the blood supply to a part of the brain is compromised
Carotid plaques - patients referred for check up after displaying symptoms including dizziness, visual disturbances, and memory loss

54
Q

What are the treatments for atherosclerosis using bypass?

A

Coronary artery bypass graft (CABG) - this is performed in patients with advanced atherosclerosis and/or multi-vessel disease. The procedure involves grafting a vessel from another part of the body (often the vein or IMA) to bypass the CA blockage. The increased blood flow to the heart muscle reduces the chance of myocardial infarction. Grafting can be performed as a single, double, triple, or even quadruple procedure.

55
Q

What are the treatments for atherosclerosis using carotid endarterectomy surgery?

A

During a carotid endarterectomy, the plaque will be surgically removed (plaque that builds up inside the carotid artery). A cut (incision) on the side of the neck over the affected carotid artery will be made and the artery is opened and the plaque removed.

Pathology (5 decks)

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