Cardiovasular Disease Flashcards
1
Q
What is the site and quality of pain in an ACS?
A
Location: central in the chest
Radiation: into jaw and arms
Quality: heavy
2
Q
What factors may lead to aggravation or relief of chest pain due to myocardial ischemia?
A
Aggravated: physical exertion, stress, emotion
Relieved: rest, sublingual nitrates
3
Q
What position typically relieves the pain of pericarditis?
A
Pericarditis pain is typically relieved by sitting up and learning forwards.
4
Q
What other symptoms may be associated with chest pain due to myocardial ischemia?
A
Diaphoresis Dyspnoea Nausea and vomiting Fatigue Pre-syncope
5
Q
What type of pain suggests aortic dissection?
A
Chest pain that radiates through to the back.
Tearing or ripping in sensation.
Reaches its peak intensity immediately.
6
Q
On examination, what do you find in a patient with MI?
(1) general inspection?
(2) vital signs?
(3) respiratory signs?
(4) heart signs?
A
(1) appear anxious, uncomfortable, in pain, pale, cyanotic, diaphoretic
(2) tachycardia, hypotension or hypertension both possible
(3) possibly crackles due to acute pulmonary oedema with left ventricular dysfunction as a result of MI
(4) possibly a 3rd or 4th heart sound, possibly a new murmur (as a result of mitral valve regurgitation developing, papillary muscle rupture, VSD)
7
Q
Give a differential diagnosis of chest pain. List 8 possible differentials.
A
Cardiac causes: myocardial ischemia - stable angina, unstable angina, NSTEMI, STEMI; pericarditis
Vascular causes: acute aortic syndrome
Pulmonary causes: PE, pneumonia, pneumothorax
GIT causes: oesophageal reflux, oesophageal spasm, peptic ulcer, cholecystitis, pancreatitis
Neuromuscular causes: costochondritis, trauma, herpes zoster
Psychological: anxiety
8
Q
What are the risks of coronary angiography?
A
Death Stroke Contrast nephropathy & AKI Bleeding Bruising Infection
9
Q
Define syncope.
A
Syncope is a transient loss of consciousness due to inadequate cerebral blood flow.
10
Q
What are the causes of syncope (neural, cardiac, orthostatic hypotension)?
A
NEURALLY-MEDIATED: Vasovagal (common faint) Situational Syncope - especially micturition syncope, but also Cough/Sneeze/Defectation/Swallowing syncope Carotid sinus syncope Cardiac - OBSTRUCTIVE: Aortic stenosis/Pulmonary stenosis Cardiac tamponade Hypertrophic cardiomyopathy PE Pulmonary hypertension Atrial myxoma Defective prosthetic valve Cardiac - ARRHYTHMIAS: Rapid tachycardias Profound bradycardias Significant pauses Pacemaker failure ORTHOSTATIC HYPOTENSION: Volume depletion Autonomic dysfunction Drugs - e.g. B blockers
11
Q
What other conditions may be mistaken for syncope? (give 3 conditions)
A
Seizures
Vertigo
Ataxia
12
Q
What investigations might be useful in a patient with syncope? (Give 5)
A
12 lead ECG Holter monitor Loop recorder Echocardiogram Exercise stress testing Electrophysiological studies EEG (if you suspect it was really a seizure)
13
Q
Give 6 causes of palpitations.
A
Cardiac arrhythmia Hyperthyroidism Pheochromocytoma Fever Dehydration Anaemia Hypoglycaemia Drugs - e.g. cocaine, caffeine Electrolyte disorders Panic attack
14
Q
Give 3 causes of bilateral leg swelling.
A
Congestive heart failure
Liver cirrhosis
Nephrotic syndrome
15
Q
Give 3 causes of unilateral leg swelling.
A
Venous insufficiency Thrombophlebitis Lymphoedema Ruptured Baker's cyst Ruptured gastrocnemius
16
Q
Give 8 common causes of fatigue.
A
ACTIVITY/SLEEP RELATED Prolonged exercise Inadequate sleep Sleep apnoea PSYCHOLOGICAL Stress Depression HEMATOLOGICAL Anaemia ENDOCRINE Hypo/hyper-thyroidism Addison's disease Diabetes mellitus CANCER CHF URAEMIA DRUGS/MEDICATIONS VITAMIN DEFICIENCY
17
Q
What investigations might be useful in investigating fatigue?
A
FBC Urinalysis EUC Fasting blood glucose Thyroid function tests ESR/CRP Chest x-ray Sleep study
18
Q
On an ECG, which leads correlate with the lateral aspect of the heart?
A
Lead I
V5, V6
aVL
19
Q
On an ECG, which leads correspond with the inferior aspect of the heart?
A
Lead II
Lead III
aVF
20
Q
On an ECG, which leads correspond to the IV septum?
A
V1
V2
21
Q
On an ECG, which leads correspond with the anterior aspect of the heart?
A
V3
V4
22
Q
Explain how you would determine cardiac axis.
A
Look at the QRS in lead I and aVF.
If they are both positive = normal axis
If lead I is positive but aVF is negative –> look at lead II. If lead II is positive, then the axis is normal, but if lead II is negative there is left axis deviation.
If lead I is negative and aVF is positive = right axis deviation.
23
Q
What is the PR interval? What is a normal PR interval?
A
PR interval is the time taken for a cardiac impulse to spread from the atria to the ventricles through the AV node and bundle of His.
It is measured from the BEGINNING of the P wave to the BEGINNING of the QRS complex.
A normal PR interval is 3-5 small squares.
24
Q
What is the definition of a wide QRS complex?
A
Greater than 3 small squares
25
In what leads is it normal to see T wave inversion?
aVR
| V1
26
Explain first degree heart block.
Delayed PR interval.
| There is a delay in the conduction, but each P wave conducts to the ventricles without dropping a beat.
27
Explain second degree heart block. What are the types?
Some P waves do not conduct to the ventricles.
Mobitz type I (aka Wenckeback) = progressive lengthening or PR and then failure to conduct, with PR interval then returning to normal and the cycle repeating
Mobitz type II = constant PR with occasional drop of a beat so that a P is not followed by a QRS
28
Explain third degree heart block.
P waves and QRS complexes are dissociated. Atrial conduction is not passing through to the ventricles. Ventricular contraction is maintained by an escape rhythm.
29
What does a right bundle branch block look like on ECG?
MaRRoW
R = right BBB
M = wide QRS in V1 appears like an M
W = wide QRS in V6 appears like a W
30
What does a left bundle branch block look like on an ECG?
WiLLiaM
L = left BBB
W = wide QRS in V1 appears like a W
M = wide QRS in V6 appears like a M
31
What is a 'hemiblock'?
The left bundle branch has two divisions - an anterior division and a posterior division. If one of these divisions is blocked it is called a hemiblock.
32
What does atrial fibrillation look like on ECG?
No P waves with an irregular baseline
Normal QRS
Irregularly irregular rhythm
33
What is Wolf-Parkinson-White Syndrome?
Normally, there is only one pathway between the atria and ventricles - i.e. through the AV node and the His bundles. In WPW syndrome, there is an accessory conducting bundle. In this situation, a re-entrant circuit can be established with the excitation passing down the His bundle and travelling back up the accessory pathway.
34
Give 3 causes of a wide QRS complex.
Ventricular extra-systole
Ventricular tachycardia
Wolf-Parkinson-White syndrome
Bundle branch block
35
What can cause a QRS complex of abnormal height?
Right or left ventricular hypertrophy
36
What is a pathological Q wave? What causes a pathological Q wave?
Q waves > 1 small square wide and > 2 mm deep are pathological.
These pathological q waves occur as the result of MI. Once developed, they are usually present permanently.
37
Give 4 causes of inverted T waves.
```
Normally, in aVR and V1.
Acute coronary syndromes
Ventricular hypertrophy
Bundle branch block
Digoxin treatment
```
38
Outline the changes on ECG that occur with a myocardial infarction. What is the timeline of these changes?
First, ST elevation.
Then there is: (1) T wave inversion and (2) Appearance of Q waves.
After this, within 24-48 hours: ST returns to baseline, but T wave inversion and Q waves are often permanently altered.
39
What ECG changes occur with hypokalaemia?
T wave flattening
| U waves
40
What ECG changes occur with hyperkalaemia?
Peaked T waves
41
What changes occur with hypercalcemia?
Shortened QT interval
42
What changes occur with hypocalcemia?
Prolonged QT interval
43
What blood tests would you order in someone with cardiac disease (give 5 that would be useful). Justify your decision.
FBC - anemia increases myocardial ischemia and can be the cause of palpitations.
EUC - many cardiac investigations require IV contrast and it is important to know their renal function as the contrast is nephrotoxic. Also, cardiac arrhythmia can be induced and exacerbated by electrolyte disturbance.
TFTs - thyroid disease can cause arrhythmia, and heart failure
Troponins - elevated troponin I and T indicates myocardial damage and is important in diagnosis of MI.
BNP - is elevated in CHF
44
Give 5 contraindications for cardiac catheterisation and angiography.
```
Patient refusal
Severe uncontrolled hypertension
Ventricular arrhythmia
Recent stroke
Active GI bleeding
Allergy to radiocontrast agents
Active infection
Acute kidney injury/acute renal failure
Severe coagulopathy
Uncompensated heart failure and the patient cannot lie flat
```
45
Give 6 complications of coronary catheterisation and angiography.
```
Death
Stroke
MI
Ventricular arrhythmia
Aortic dissection
Cardiac perforation and tamponade
Reaction to contrast, anaphylaxis
Nephrotoxicity and AKI
Haemorrhage
Infection
```
46
Give 8 risk factors for atherosclerotic disease.
NON-MODIFIABLE
Age
Male sex
Family history
```
MODIFIABLE
Hyperlipidaemia - low HDL, high LDL, high triglycerides, high total cholesterol
Cigarette smoking
Hypertension
DM
Lack of exercise
Obesity
```
47
Explain the steps in the formation of an atherosclerotic plaque.
1. Injury to the vessel wall
2. Injury causes endothelial dysfunction
3. This causes LDL to accumulate in the vessel wall
4. Monocytes migrate into the intima
5. Monocytes transform into macrophages and phagocytose lipid
6. Macrophages become foam cells
7. Smooth muscle cells are recruited into the intima from the vessel tunica media
48
Give 3 features of a 'vulnerable' atherosclerotic plaque.
Large areas of lipid
Thin fibrous cap
Large amount of inflammation
49
What might you see when examining a person with angina?
Often no abnormal findings
Possible 4th heart sound
Signs of atherosclerosis at other sites: carotid bruits, diminished peripheral pulses
Signs of predisposing conditions: anaemia (pallor of palmar creases and conjunctiva), thyrotoxicosis (tachycardia, tremor, eye signs)
Signs of risk factors: tendon xathomata, tendon xamthomata, hypertension
50
What is your approach to managing stable angina?
1. Identify and treat underlying/aggravating conditions - e.g. anaemia, hyperthryoidism
2. Identify and treat risk factors -
Control lipid levels
Control hypertension
Control DM
Weight loss is overweight
Smoking cessation
Increase physical activity
Healthy diet
3. Drug therapy to treat symptoms:
Nitrates for pain
If necessary for control of HTN - ACE-I
If necessary for control of lipids - Statin
If necessary for the control of DM - Metformin
4. Prevention of coronary events
Consider low-dose aspirin
5. Monitor
51
Explain the pathophysiology of a myocardial infarction.
MI usually occurs due to rupture of the fibrous cap of an atherosclerotic plaque in a coronary artery. This leads to platelet aggregation and formation of a fibrin clot that occludes the vessel lumen. As a result, there is blockage of blood supply to the heart in the area supplied by that artery. There is a lack of nutrients and oxygen being delivered --> this will cause infarction and death of myocytes if the blood supply is not promptly restored. other rarer causes of MI are spasm of a coronary artery, vasculitis and embolism to a coronary artery.
52
What might you see when examining a patient having a myocardial infarction?
```
General inspection: obviously unwell, distressed, in pain, anxious, diaphoretic
Vital signs: tachycardia or bradycardic, hypotensive or hypertensive
Cardiac examination: there may be -
Increased JVP
Dyskinetic apex beat
S3 and/or S4 heart sounds
New murmur
Development of arrhythmia
Pulmonary crackles
```
53
Patient is having an acute STEMI. What investigations are crucial?
ECG
Cardiac troponin level
```
Also useful:
FBC
Electrolytes
Glucose
Lipids
Echocardiogram
```
54
The patient is having a STEMI. What do you do?
1. Quickly perform a targeted history and examination.
2. ECG and troponins
3. Drugs: morphine, GTN, dual anti-platelet therapy (aspirin and ticagrelor)
4. Arrange for urgent cardiac revascularisation therapy
5. Thrombolysis if PCI is not available
55
Give 5 DDX for STEMI.
```
Aortic dissection
Pericarditis
Pulmonary embolism
Oesophageal spasm
GI reflux
Peptic ulcer
Acute cholecystitis
Pancreatitis
```
56
Give 6 complications of STEMI.
```
Cardiogenic shock
Aneurysmal dilation of the infarcted area
Rupture of the ventricular free wall
Rupture of the ventricular septum forming a VSD
Arrhythmia - VT, VF, AF, AV block
Embolism
Papillary muscle dysfunction/rupture
Heart failure
Dressler syndrome
```
57
What are the 3 main causes of congestive heart failure?
Ischemic heart disease
Dilated cardiomyopathy
Hypertension
58
Explain the pathophysiology of heart failure.
Heart failure occurs when disease (e.g. IHD, HTN, valvular disease, arrhythmia, cardiomyopathy) causes structural and/or functional changes in the heart that means the heart is unable to fill or contract effectively. These changes are called 'cardiac remodelling'. The remodelling is the result of activation of systems such as the RAAS, the SNS and various cytokines/mediators.
SNS Activation: Decreased CO in heart failure activates the SNS via the baroreflex. The SNS stimulates the heart, increasing contractility and HR, which in the short term is compensatory but in the long term contributes to remodelling.
RAAS Activation: The RAAS is activated by (1) reduced effective circulating blood volume leading to hypoperfusion of the kidneys --> decreased GFR --> altered delivery of sodium to the macula densa --> renin release; (2) SNS activates renin release directly. Through this pathway there is production of angiotensin II and aldosterone. In the short term these also help compensate for heart failure, but in the long term contribute to cardiac remodelling.
59
Give 5 pathological changes with ventricular remodelling.
```
Altered excitation-contraction coupling in myocytes
Altered expression of myosin heavy chain genes
Hypertrophy of myocytes
Fibrosis
Apoptosis
Necrosis
Dilation of the ventricles
Thinning of the ventricular wall
```
60
How is heart failure classified?
Heart failure is divided into:
1. Heart failure with reduced ejection fraction (HFrEF) - previously known as systolic heart failure
2. Heart failure with preserved ejection fraction (HFpEF) - previously known as diastolic heart failure
61
What are common symptoms of left heat failure?
Cough
Dyspnoea
Orthopnoea
Paroxysmal nocturnal dypsnoea
62
What are the signs of left heart failure?
```
Cardiac cachexia
Tachypnoea
Peripheral cyanosis
Sinus tachycardia
Hypotension
Apex beat - displaced, dyskinetic
Possible S3
Possible murmur due to mitral regurgitation (functional regurgitation due to dilation of the ventricle)
Pulmonary crackles
```
63
What are common symptoms of right heart failure?
Peripheral oedema
Abdominal swelling
Anorexia and nausea
64
What are the signs of right heart failure?
```
Cardiac cachexia
Peripheral cyanosis
Raised JVP
Right ventricular heave
Possible S3
Possible murmur due to tricuspid regurgitation
Tender hepatomegaly
Pulsatile liver
Ascites
Sacral oedema
Pitting ankle oedema
Possible signs of the underlying cause, especially lung disease and left heart failure.
```
65
What investigations would you order to diagnose heart failure?
```
Blood tests: BNP, LFTs
CXR: looking for cardiomegaly
ECG
Echocardiogram: used to assess chamber size, heart function and ejection fraction, wall motion abnormalities, valvular dysfunction
Other possibly useful tests:
Stress echocardiogram
Nuclear imaging: SPECT, PET
Cardiac MRI
Cardiac catherisation
Cardiac biopsy
Holter monitor
```
66
What medications are prescribed routinely to treat heart failure?
ACE-Inhibitor
B-blocker
Spironolactone
Diuretic
If this combination is not tolerated/effective, consider:
Combined ARB + Neprilysin inhibitor - Sacubitril
Digoxin
67
What are the three mechanism of tachycardia?
1. Accelerated automaticity
2. Triggered activity - i.e. after-depolarisations
3. Re-entry circuits
68
What is the main cause of accelerated automaticity?
Excessive sympathetic nervous system stimulation
69
What is 'triggered activity'? How does it lead to arrhythmia?
Triggered activity refers to 'after-depolarisations' that occur when the transmembrane potential oscillates at the action potential. If the potential reaches threshold, another action is generated. Triggered activity is usually the result of myocardial damage, and is increased by catecholamines, electrolyte disturbance, hypoxia and acidosis.
70
What symptoms might a person with an arrhythmia have? Give 4.
```
Palpitations
Syncope
Chest pain
Dizziness
Sudden death
No symptoms
```
71
What are the (1) extrinsic and (2) intrinsic factors that can lead to sinus bradycardia?
```
EXTRINSIC
Hypothyroidism
Hypothermia
Raised ICP
B-blockers
Increased vagal tone - e.g. vasovagal syncope
INTRINSIC
Ischemia/infarction of the SA node
Sick sinus syndrome
```
72
What are 5 common causes of AF?
```
Hypertension
Heart failure
Hyperthyroidism
Rheumatic heart disease
Heart surgery
```
73
What is the pathophysiology of AF?
AF is due to continuous, rapid activation of the atria by multiple re-entry wavelets. These wavelets predominantly originate in the pulmonary veins.
74
Why is AF a problem? Give 2 reasons.
1. There is stasis of blood in the atrium (left atrial appendage specifically). This can lead to embolism and stroke.
2. There is loss of the atrial contribution to ventricular filling. This can cause a decreased stroke volume and cardiac output, causing or worsening heart failure.
75
What are the two approaches to managing AF? What drugs are used in each of these approaches?
Rate control and rhythm control.
RATE CONTROL
B-Blocker used to slow HR. Other drug options are a Ca channel blocker or amiodarone.
RHYTHM CONTROL
An antiarrhythmic and cardioversion is used. Flecainide (Na channel blocker) is the drug commonly used.
+ ANTICOAGULATION if the patient is at high risk of stroke (determined by the CHA2DS2-VASc score). Options are warfarin or a NOAC.
76
What CHA2DS2-VASc score indicates the need for oral anticoagulation?
A score of 2 or more = anticoagulant recommended
77
What is the most common cause of mitral valve stenosis?
Rheumatic heart disease
78
Explain rheumatic fever.
Rheumatic fever is an acute, immune-mediated, multisystem disorder that occurs a few weeks after an episode of group A streptococcus pharyngitis. The disorder is the result of a host immune response to the Group A streptococci. The antibodies and T cell response against the bacteria also recognise cardiac self-antigens --> the host attacks its own heart.
79
What are the valves most commonly affected by rheumatic heart disease?
Mitral valve is the main valve affected.
| Also commonly affected is the aortic valve.
80
What are the symptoms and signs of an acute rheumatic fever?
```
Migratory polyarthritis in large joints
Pancarditis
Subcutaneous nodules
Rash: erythema marginatum
Syndenham chorea
```
81
What factors predispose to development of infective endocarditis? Give 5 risk factors.
```
IVDU
Poor dental hygiene/dental procedure
IV cannula
Indwelling urinary catheter
Heart surgery
Prosthetic heart valve
```
82
What are 3 organisms that commonly cause IE?
Staph aureus
Staph epidermidis
Strep viridans
83
What are common symptoms of IE?
Fever
Chills
Sweats
Malaise
84
What are common signs of IE?
Fever
Hands: splinter haemorrhage, Janeway lesions, Osler's nodes, clubbing
Arms: track marks
Eyes: retinal or conjunctival haemorrhages, Roth's spots
Heart: new murmur, mechanical heart valve
Peripheral evidence of embolisation
Urinalysis: heamaturia
85
What investigations would be useful in investigation of infective endocarditis? Give 5.
```
Blood cultures
Urinalysis
ECG
Chest x-ray
Echocardiogram: TTE or TOE
```
86
What is the name of the criteria used to diagnose infective endocarditis?
DUKE criteria
87
Give 3 complications of infective endocarditis.
Death
Abscess formation
Septic emboli
88
Give 5 clinical features that can be caused by an arrhythmia.
```
Palpitations
Syncope
Dizziness
Lightheadedness
Chest pain
Asymptomatic
Sudden death
```
89
What are the features of first degree heart block?
A prolonged PR interval, with every P being followed by a QRS.
90
What are the features of second degree heart block?
Some P waves conduct to the ventricles, but some are dropped.
91
What are the two types of second degree heart block?
Mobitz type I (Wenckeback) = PR progressively prolongs until a P wave fails to conduct to the ventricles. The cycle is then reset and the PR progressively prolongs again.
Mobitz type II = occasionally a P wave fails to conduct to the ventricles, but without preceeding PR prolongation.
92
What are the features of third degree heart block?
There is complete dissociation between atria and ventricles with no relationship between P waves and QRS. P waves do not conduct to the ventricles.
93
What does CHA2DS2-VASc stand for? What is use used for?
```
This scoring system is used to decide whether a patient with AF requires oral anticoagulation.
C = congesitve heart failure (1 point)
H = hypertension (1 point)
A= age 75 or greater (2 points)
D = diabetes (1 point)
S = prior stroke, TIA or thromboembolism (2 points)
V = vascular disease (1 point)
A = age 65-74 years (1 point)
S = female sex (1 point)
```
94
At what CHA2DS2-VASc score is anticoagulation recommended?
2 or more
95
What arrhythmia does Brugada syndrome cause?
Ventricular fibrillation
96
What are the four features of a Tetralogy of Fallot?
VSD
Over-riding aorta
Pulmonary stenosis
Right ventricular hypertrophy
97
What is considered to be a normal blood pressure?
Systolic 120-129 and
| Diastolic 80-84
98
What is the threshold at which hypertension is diagnosed?
140/99
99
Give 8 causes of secondary hypertension (include at least 1 of each category: renal, endocrine, neurological, cardiovascular)
```
RENAL:
- renal artery stenosis
- CKD
- polycystic kidney disease
ENDOCRINE:
- pheochromocytoma
- Conn's syndrome
- Cushing's syndrome
- Acromegaly
- Hyperthyroidism/hypothyroidism
CARDIOVASCULAR:
- Coarctation of the aorta
NEUROLOGICAL:
- Obstructive sleep apnoea
- Acute stress
- Increased ICP
```
100
What is a hypertensive urgency?
A severe elevation in BP (>180/110) that is not immediately life-threatening but is associated with symptoms and damage to organs.
101
What is a hypertensive emergency?
A severe blood pressure elevation (>220/140) with acute organ damage/dysfunction.
102
What factors determine BP?
BP = CO x peripheral resistance.
103
Outline the RAAS.
Angiotensinogen is released by the liver into the systemic circulation. Renin is then produced by the JGA cells of the kidney in response to decreased effective circulating blood volume. Renin cleaves a bond in angiotensinogen to form angiotensin I. ACE is present on the endothelial cells of the lung, and converts angiotensin I to angiotensin II. The ATII stimulates Na+ resorption by the kidneys, aldosterone release from the adrenal cortex, vasoconstriction, thirst and release of ADH.
104
What is the action of aldosterone?
Aldosterone acts in the kidneys to cause upregulation of the sodium channels (ENaC) and their translocation to the apical membrane of principal cells in the collecting ducts. This leads to an increased uptake of Na+ and increased secretion of K+ by these cells.
105
In a patient with hypertension, what are 5 lifestyle factors that it would be useful to address?
- Physical activity
- Weight control
- Diet
- Smoking cessation
- Limit alcohol intake
106
What are the 4 first line antihypertensive medications?
ACE-I
ARBs
Ca channel blocker
Thiazide diuretics
107
What is the most common cause of myocarditis in Australia?
Viral infection
108
How do you tell apart ST segment elevation caused by a MI and ST segment elevation caused by pericarditis?
In STEMI, the ST elevation is limited to the leads representing the infarcted region; in pericarditis, the elevation is widespread through the leads.
109
Give 5 risk factors for DVT.
```
Immobilisation
HRT
OCP
Pregnancy
Obesity
Past history of DVT
Cancer
```
110
You examine a patient lower leg. What features would make you suspect DVT? (5 features)
```
Calf pain/tenderness
Calf swelling
Calf erythema
Warmth
Enrgorged superficial veins
```
111
What are 3 investigations that you could use to diagnose PE?
D-Dimer
CTPA
V/Q Scan
112
Give 6 factors that predispose to AAA.
```
DEGENERATION OF VESSELS CAUSED BY:
- Age
- Smoking
- Hyperlipidemia
- Hypertension
- Atherosclerosis
GENETIC/DEVELOPMENTAL CAUSES:
- Marfan's syndrome
- Ehlers-Danlos syndrome
- Turner's syndrome
- Bicuspid aortic valve
AORTITIS:
- Vasculitis
- RA
- Infective: syphilis, TB
TRAUMA
```
