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Cardiovascular Disease Flashcards

1
Q

How many deaths in the UK does coronary heart disease cause in men and women?

A
  • 25% in men
  • 16% in women
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2
Q
A

Atheroma in a coronary artery

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3
Q

Define atherosclerosis.

A

An arteriosclerosis characterising by atheromatous deposits in and fibrosis of the inner layer of the arterioles

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4
Q

What its atherosclerosis characterised by?

A
  • There are intimal lesions (atheromatous plaques) that protrude into the vessel lumen
    • (1) Smooth endothelium is damaged, platelets stick to tissue, endothelium proliferates and a fibrous cap form

(2) There is deposition of cholesterol and the plaque enlarges blocking the artery

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5
Q
A

Top aorta has lots of atherosclerosis

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6
Q

What do atheromatous plaques look like?

A
  1. Raised lesion
  2. Soft lipid core
  3. White fibrous cap
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7
Q

What are the RFs of Artherosclerosis?

A
  • Risk factors:
    • Non-modifiable:
      • Age - Atherosclerosis progressive between 40->60 years incidence myocardial infarction (MI) X 5
      • Gender (premenopausal women protected → post-menopausal women = >risk than men)
      • Genetics (FHx, familial hypercholesterolaemia, polymorphisms)
      • Modifiable:
        • Hyperlipidaemia (LDL bad / HDL good, diet, statins inhibit HMG-CoA reductase)
        • Hypertension (increased IHD risk by 60%)
        • Smoking Definite risk in men, probable in women

Prolonged smoking doubles death rate from IHD

Stopping reduces risk considerably

  • Diabetes mellitus (induces hypercholesterolaemia and atherosclerosis)
  • Other risk factors: inflammation, hyperhomocyteinaemia, metabolic syndrome, lipoprotein a, haemostasis (pro-coagulation), lack of exercise, stress, obesity
  • Risk factors have a multiplicative effect – 2 risk factors increase the risk 4x (3 RFs = 7x increase risk)
  • 20% of CVD events occur in absence of RFs and 75% events in healthy women occur in LDL below the risk level
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8
Q

Describe the pathogenesis.

A
  • Pathogenesis – response to injury hypothesis:
  • Chronic inflammatory and healing response of arterial wall to endothelial injury
    • (1) endothelial injury → LDL accumulation
    • (2) monocyte adhesion to endothelium
    • (3) monocyte migration into intima → macrophages & foam cells
    • (4) platelet adhesion → factor release →smooth muscle cell recruitment
    • (5) lipid accumulation → extracellular and intracellular macrophages and smooth muscle cells
    • The early atheroma arises in intact endothelium however, endothelial dysfunction (see below for causes of endothelial dysfunction) is important which increases the permeability, alters gene expression and adhesion
    • Haemodynamic disturbance, hypercholesterolaemia and inflammation → dysfunction and vicious cycle
    • Factor release causes smooth muscle recruitment and lipid accumulation
      • Intimal smooth muscle proliferation
      • Some from circulating precursors (have synthetic & proliferative phenotype)
      • ECM matrix deposition
      • Fatty streak: mature atheroma and growth
      • PDGF, FGF, TGF-alpha implicated
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9
Q

What is role of infection?

A
  • Infection – no conclusive evidence
    • Herpes
    • CMV
    • Chlamydia pneumonia
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10
Q
A

Cracks - cholesterol

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11
Q
A

Fatty streak

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12
Q

What are fatty streaks?

A
  • (1) Fatty streak (these are tiny little streaks in the vessel wall)
    • Earliest lesion
    • Lipid filled foamy macrophages, no flow disturbance
    • In virtually all children <10y/o
    • Relationship to plaques is uncertain but in same sites as plaques
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13
Q
A

Atheroma

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14
Q

What are atherosclerotic plaque, what do they do?

A
  • Patchy: local flow disturbance
  • Only involve portion of the wall: rarely circumferential
  • Appear eccentric and composed of cells, lipid and matrix
  • Can rupture or obstruct
  • Occur in points of disturbed flow: carotids and coronary arteries
    • Bifurcations
    • Curvatures
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15
Q

What are the consequences of stenosis?

A
  • Critical stenosis is when demand > supply
  • Occurs at ~70% occlusion (or diameter <1mm)
  • Causes “stable” angina and can lead to chronic IHD
  • Acute plaque rupture can occur
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16
Q
A

Left to right : build up of atheroma form healthy to stable angina

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17
Q

Describe acute plaque changes.

A
  • Rupture: exposes prothrombogenic plaque contents
  • Erosion: exposes prothrombogenic subendothelial basement membrane
  • Haemorrhage into plaque (increases size)
  • Majority of plaques which show acute change only show mild to moderate luminal stenosis prior to acute change: therefore, there are numerous asymptomatic potential victims
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18
Q

What are the characteristic of vulnerable plaques?

A
  • Lots of foam cells and extracellular lipid
  • Thin fibrous cap
  • Few smooth-muscle cells
  • Clusters of inflammatory cells
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19
Q

What is the mechanism behind rupture of vulnerable plaques?

A
  • Mechanism
    • Adrenaline increases BP and causes vasoconstriction
    • Increases physical stress on plaque
    • Hence emotional stress increases risk of sudden death
    • Circadian periodicity to sudden death (6am-noon)
      • Not all rupture → occlusion – plaque disruption with platelet aggregation/thrombosis common
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20
Q

What is role off vasoconstriction in CVD?

A
  • Vasoconstriction adds to the problem
    • Reduces luminal size
    • Increases local mechanical forces
    • Occurs due to adrenergic agonists, platelet contents, reduced endothelial relaxing factors and mediators from perivascular cells
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21
Q
A

Human coronary atherosclerotic plaque with a yellow core of lipid separated from the lumen by a fibrous cap. Opposite the plaque is an arc of normal vessel wall

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22
Q
A

Cross section of LV - white area is myocardial infarction

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23
Q

What is the epidemiology go IHD? What is it?

A
  • Imbalance of supply to demand for oxygenated blood: less nutrients and less waste removal [2 main features]
    • Therefore, less well tolerated than pure hypoxia
    • 90% of myocardial ischaemia due to reduced blood flow due to atherosclerosis
    • 75%+ stenosis needed to cause symptoms precipitated by exercise (stable angina) → 90% = pain at rest
    • Long silent progression prior to symptoms
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24
Q
A

Cross section - fatty plaques

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25
Complete block → death from MI
26
Presentation of IHD?
27
IHD epidemiology.
28
IHD pathogenesis
29
What is acute coronary syndrome?
* Acute coronary syndromes = stable becomes unstable (i.e. rupture, erosion, haemorrhage) → superimposed thrombus
30
What is angina pectoris?
* Transient ischaemia not producing myocyte necrosis * Plaques form in first parts of _LAD or LCx_; or entire length of _RCA_ * **Stable**, **Prinzmetal** or **unstable** * Stable comes on with exertion, relieved by rest, no plaque disruption * Prinzmetal is uncommon but due to artery spasm
31
What is unstable angina?
* **Unstable** is when is becomes more frequent, longer, onset with less exertion or at rest * Disruption of plaque * Superimposed thrombus * Possible embolisation or vasospasm * Warning of impending infarction
32
What is a myocardial infarction? What is the epidemiology?
* Death of cardiac muscle due to prolonged ischaemia * Incidence 5/1000 per year UK (ST elevation) * 10% less than 40yrs; 45% less than 65yrs; blacks and whites equal; men greater risk than women throughout life IHD most common cause death postmenopausal women
33
What is the pathogenesis of MI?
* Pathogenesis * (1) Artery occlusion: * Sudden change of plaque Platelet aggregation Vasospasm * Coagulation Thrombus evolves * (2) Myocardial response * Myocardial blood supply compromised leading to ischaemia * Loss of contractility within 60 seconds * Therefore, heart failure can precede myocyte death * **Potentially reversible but irreversible after 20-30 minutes** * **LAD**: **50**%, anterior wall left ventricle, anterior septum, apex * **RCA**: **40**%, posterior wall left ventricle, posterior septum, posterior right ventricle * ![]()**LCx**: **20**%, lateral left ventricle, not apex
34
Describe the evolution of MI
* **\<6 hours**: normal by histology (CK-MB also normal) * **6–24 hours**: coagulative necrosis, loss of nuclei and striations * **1-4 days**: infiltration of **neutrophils**  **macrophages** (clear up debris) * **5-10 days**: removal of debris (**macrophages**) * **10-14 days**: granulation, angiogenesis, collagen synthesis (**myofibroblasts**, **macrophages**, **angioblasts**) * **Weeks to months**: strengthening, decellularising scar
35
MI 1-3 days Coagulation necrosis, loss nuclei & striations, neutrophils +++
36
MI 10-14 days granulation tissue, macrophages
37
MI \> 2 month sold
38
What are the clinical features of MIs?
* 10-15% asymptomatic: elderly and DM * Cardiac enzymes (CK, troponin) * Subendocardial infarct may not cause usual ST changes
39
MI consequences
* General Points: * In hospital death rate is 7% * Half of deaths occur **within 1 hour of onset** (most of these do not reach hospital) * Age, female, DM and previous MI = worse prognosis
40
What is reperfusion injury?
* **Reperfusion injury**: due to **oxidative stress**, **Ca2+ overload**, **inflammation** * Arrhythmias common * Biochemical abnormalities last days to weeks * Thought to **cause “stunned myocardium”**: reversible cardiac failure lasting several days
41
What is hibernating myocardium?
chronic sublethal ischaemia causes lowered metabolism in myocytes is reversed with revascularisation
42
What are the complication of MI?
* D Death V Valvular disease * A Arrhythmia A Aneurysm of ventricle * R Rupture (papillary muscle) D Dressler’s syndrome (pericarditis; 2nd or 3rd day) * T Tamponade E Embolism (i.e. bowel ischaemia) * H Heart Failure R Recurrence * Total mortality is 30% in one year but 3-4% after this due to complications
43
Dressler Syndrome
44
Normal LV and aneurysm
45
Papiillary muscle rupture
46
What is Chronic IHD?
* Progressive heart failure due to ischaemic myocardial damage: **_may not be prior infarction_** * Can arise with severe obstructive coronary artery disease: enlarged heavy heart, hypertrophied, dilated LV * Atherosclerosis; maybe mural thrombi * Fibrosis (microscopic)
47
What is sudden cardiac death? What is the epidemiology?
* “Unexpected death from cardiac causes in individuals without symptomatic heart disease or early (1 hour) after onset of symptoms”; usually due to lethal arrhythmia (from **_ischaemia-induced electrical instability_**) * Usually on background of IHD (90%) although drugs such a cocaine may be the cause * **Acute myocardial ischaemia** is usual trigger * Usually causes electrical instability at sites distant from conduction system (near scars from old MIs) * Other conditions also associated (aortic stenosis, mitral valve prolapse, pulmonary hypertension)
48
What is cardiac failure? What are the types?
* The end point of many conditions * Types: * Left: SOB, pulmonary oedema (CXR = ABCDE) * Right: peripheral oedema (_nutmeg liver_) * Left and right = congestive heart failure
49
What are the causes of cardiac failure?
•***_Causes_*** –Ischaemic heart disease –Valve disease –Hypertension –Myocarditis –Cardiomyopathy – Left sided heart failure (Right)
50
What are the complications of cardiac failure?
* **Complications**: sudden death, arrhythmias, systemic emboli, pulmonary oedema with superimposed infection
51
What is the pathology of cardiac failure?
* **Pathology**: * Dilated heart, scarring and thinning of the walls * Microscopy: fibrosis and replacement of the ventricular myocardium
52
What is cardiomyopathy?
too thin, too thick, too stiff
53
What are the causes of dilated cardiomyopathy?
* Progressive loss of myocytes * Dilated heart * Causes: * Idiopathic * Infective: viral myocarditis * Toxic: alcohol, chemotherapy (adriamycin, daunorubicin) * Cobalt, iron * Hormonal: hyper/hypothyroid, diabetes, peri-partum * Genetic: haemochromatosis, Fabry’s, McArdle’s * Immunological: myocarditis; inc. viral
54
What are the causes of hypertrophic cardiomyopathy?
* Left ventricular hypertrophy * Familial in 50% (autosomal dominant, variable penetrance) * Beta-myosin heavy chain * Thickening of septum narrows left ventricular outflow tract
55
What is restrictive cardiomyopathy?
* Impaired ventricular compliance * Idiopathic or secondary to myocardial disease (amyloid, sarcoidosis) * Normal heart size but big atria
56
What is chronic rheumatic valvular disease?
* Sequelae of earlier rheumatic fever * Predominantly left-sided valves (almost always **_mitral stenosis_**) * Mitral \> Aortic \> Tricuspid \> Pulmonic * Mitral alone 48%; mitral and aortic 42% * Thickening of valve leaflet, especially along lines of closure * Fusion of commissures * Thickening, shortening and fusion of _chordae tendineae_
57
What his calcific aortic stenosis?
* Commonest cause of aortic stenosis (esp. in elderly; 70s or 80s) * Calcium deposits in outflow side cusp which impair opening or orifice is compromised * Outflow tract obstruction
58
What causes aortic regurgitation?
* **Rigidity**: RHD * **Destruction**: IE * Left-sided normally (as it is often the more ‘damaged valve’) * Right-sided in IVDU (as it is the first valve the bacterium come across) * **Disease of aortic valve ring**: dilatation means that valve is insufficient to cover increased area * Marfan's Syndrome Dissecting aneurysm * Syphilitic aortitis Ankylosing spondylitis
59
Endocarditis
60
What are the types of aneurysms? What causes them?
* True: all layers of the wall * False: extravascular haematoma → aortic dissections * Causes: weak wall of large arteries * Marfan’s * Atherosclerosis * Hypertension
60
What are the types of aneurysms? What causes them?
* True: all layers of the wall * False: extravascular haematoma → aortic dissections * Causes: weak wall of large arteries * Marfan’s * Atherosclerosis * Hypertension

Histopathology (14 decks)

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