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184 Cards in this Set
- Front
- Back
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What is unique about Muscular arteries histologically?
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Internal elastic membrane in their intima
well structured wall with less adventitia compared to veins |
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What is unique about elastic arteries histologically?
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Elastic lamellae in their media
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What is unique about Large veins histologically?
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2-15 layers of smooth muscle in the media
longitudinal smooth muscle in the adventitia |
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What is unique about medium veins histologically?
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internal elastic membrane in their intima
'floppier' wall than an artery with higher amounts of adventitia |
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What nerves supply the coronary arteries and what do they do?
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PNS - Vagus nerve - constrict
SNS - T1-T4 sympathetic trunk - dilate |
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Name the sulci and arterial contents of the heart.
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-Anterior interventricular separates the RV/LV and contains the LAD
-Coronary sulcus separates the LA-RA/RA-RV and contains the RCA -Posterior interventricular separtes the LV/RV and contains the PDA |
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Name the coronary venous system components and their associated arteries.
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Coronary sinus - RCA
Small cardiac vein - RCA Middle cardiac vein - PDA Great cardiac vein - LAD |
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What are risk factors for atherosclerosis?
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Diabetes, hypercholesterolaemia, smoking, hypertension, male sex, increasing age, positive family history, sedentary lifestyle, obesity
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t/f... HDL is the primary lipoprotein involved in formation of atherosclerosis
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false, LDL is
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What modifications to LDL helps initiate atherosclerosis?
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oxidation, glycosylation, aggregation
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t/f... arterial branch points are predisposed to atherosclerosis
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true, due to increased turbulence
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How does the endothelium maintain vascular tone?
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releases prostacyclin (PGI2 - dilator), endothelin (constrictor), endothelium derived relaxing factor (EDRF - NO)
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What molecules cause adherence between endothelial cells and monocytes?
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VCAM and integrins
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t/f... fibrofatty lesions occur uniformally around the blood vessel lumen
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false, they are eccentric
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Describe the contents of a fibrofatty lesion.
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Thick smooth musle and CT cap overlying a core of lipid and necrotic cells. also contains matrix and CT from SMC and macrophage foam cells. T cells, mast cells, Ig, complement are also present
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t/f... coronary artery fibrofatty lesions contain more macrophages than smooth muscle foam cells
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false, they contain more SMC, aortic plaques contain more macrophages
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What is different about smooth muscle cells within an atherosclerotic plaque?
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Upon moving from the media to the intima, they have become synthetic/Matrix secreting instead of contractile, and some also ingest lipids to become foam cells.
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t/f... the depth of the fissure in an atherosclerotic plaque does not alter pathological outcomes
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false, a deeper fissure is more likely to be associated with vessel occlusion by thrombosis, and to allow necrotic core escape to occlude distal branches
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Does lowering cholesterol have any benefit in those with atherosclerosis?
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Yes, while it won't decrease stenosis by much and won't cause complete disappearance of the plaques, it induces regression of foam cell rish fatty streaks, and may decrease cellularity and lipid content of advanced plaques.
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What % of lumen obstruction is needed to limit coronary flow in exercise?
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70%
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What % of lumen obstruction is needed to limit coronary flow at rest?
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90%
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What is supply ischaemia?
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a significant fall in coronary blood flow
If slowly occuring, collaterals may develop. If longer than 30 minutes = infarction e.g. at rest when an artery has a 90% stenosis from atherosclerosis |
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What is demand ischaemia?
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increase in myocardial O2 demand in excess of the diseased coronary circulation's ability to increase flow e.g will occur with a 70% stenosis during exercise
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Briefly outline some of the events in the ischaemic cascade.
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metabolism switches to anaerobic, lactic acid is produced and less ATP, leads to failure of contraction = relaxation, resulting in elevated LVEDP and SOB
Less ATP = Na/K pump leaks K out of cells = raised membrane potential, reducing AP size and duration |
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What characteristic changes will you see in the ECG of a subendocardial ischaemia?
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ST depression (relative to TP/PQ lines)
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What characteristic changes will you see in the ECG of a transmural ischaemia?
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ST elevation (relative to TP/PQ lines)
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What is thought to cause pain in ischaemia?
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As a late ischaemic event, angina pectoris is though to be caused by adenosine stimulating sympathetic afferents that synapse with C8-T4 segments, produceing reffered pain to retrosternal area
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When you get peripheral limb pain at risk in peripheral vascular disease, what is the most likely cause?
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peripheral nerve ischaemia
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Who is indicated for laboratory tests to define vessel patency at lower levels?
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severe claudicant, with rest pain with limb-threatening ischaemia
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What investigative procedure would you use to assess peripheral vessel patency?
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Doppler ultrasound, coupled with treadmill exercise
Angiography before surgical intervention Arterial duplex |
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What are the 'big five' personality traits?
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Openness (inventive/curious vs. consistent/cautious)
Conscientiousness (efficient/organized vs. easy-going/careless) Extraversion (outgoing/energetic vs. solitary/reserved) Agreeableness (friendly/compassionate vs. cold/unkind) Neuroticism |
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What are the key features of the Type A behaviour pattern?
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insecurity, hostility, time urgency, impatience and competetiveness
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t/f... Type A personality is a robust predictor of CHD
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false
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What psychological traits are found in people with a poorer prognosis for CHD?
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expressive hostility, particularly in interactions with others, cynical mistrust, suppressed resentment
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What is Type D personality?
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distress personality - negative affectivity and social inhibition
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What type of infarcts are particularly likely to result in a bradyarrhythmia?
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transmural infarcts in the posterior wall of the left ventricle
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What % of the wall would you think would at least be involved in a transmural infarct to cause pump failure?
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40%
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Where are three sites where myocardium softening can occur after infarction and cause a pathological effect?
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External ventricular wall = haemopericardium
Interventricular septum = L>R shunt Papillary muscle = mitral regurgitation, acute pulmonary oedema |
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What is a common occurence within a few days of a transmural myocardial infarction?
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acute fibrinous percarditis
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t/f... necrosis may extend to adjoining areas weeks following the infarct
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true. called infarct extension
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t/f... infarct expansion is synonymous with infarct extension
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false. Infarct expansion is when an area of infarct dilatates by 'cell slippage', but no extra tissue undergoes necrosis, whereas infarct extension is when the bordering area to an infarct undergoes necrosis
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What are the major modifiable risks in preventing vascular disease?
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cigarette smoking, poor diet, inactivity
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t/f... vascular disease is best treated using a multidisciplinary approach
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true
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What are the major determinants of myocardial oxygen demand?
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HR
Wall stress contractility |
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t/f... tachycardia can limit coronary blood flow
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true, as diastole as a % of cardiac cycle is shortened with increased HR
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What are some the general principles behind treating stable angina?
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Treat the ischaemia, not the pain.
Reduce O2 demand by blocking the heart rate increase when exercising, reducing afterload and ventricular volume with a vasodilator. |
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What is an invasive treatment for stable angina?
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balloon angioplasty with stenting
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Which drugs reduce the risk of coronary disease?
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aspirin, statins, ACEI, fishoil
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What are the antianginal drug groups?
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Nitrates
Beta blockers Ca entry blockers Perhexiline Ivabradine |
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How do nitrates treat angina?
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Vasodilation (at low doses just venous, at high arterial as well) through cGMP, reducing afterload and ventricular dimension, decreasing the metabolic needs of the heart so that it doesn't get ischaemic
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t/f... short acting nitrates produce tolerance
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false, long acting nitrates produce tolerance wi 24 hours unless a nitrate -free period of 10 hours/overnight is provided.
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What is the main side effect of Nitrates?
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headache from vasodilation
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How do beta blockers assist in reducing angina?
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decrease HR, which decreases myocardial O2 demand, decreasing ischaemia.
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What are the side effects of beta blockers?
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fatigue, loss of libido, impotence, bad dreams
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How do Ca channel blockers assist in angina?
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Cause arterial dilation, decreasing BP and afterload (some also slow HR)
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What are the side effects of Ca channel blockers?
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flushing, hypotension, oedema
(hypotension, brachycadia, heart block and heart failure can occur if used with beta blockers - be wary) |
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What is a contraindication of Ca channel blockers?
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Heart failure
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How does perhexiline reduce angina?
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reduces myocardial requirement for aerobic metabolism through system effects
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What is a side effect of perhexiline?
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A significant proportion or the population are slow metabolisers who get hepatotoxic and neurotoxic side effects.
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How does Ivabradine reduce angina?
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Blocks the If channel in the sinus node that helps produce the spontaneously depolarisint current. This delays the next AP and heart beat, decreasing the energy/O2 demand of the heart and preventing ischaemia
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How many people die prematurely every year around the world from air pollution?
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2 million, according to WHO estimates
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What % of deaths is air pollution thought to be a factor in, in Australia?
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2.3%
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What air pollutants are most likely to cause CVS impacts?
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particles, carbon monoxide, lead
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How do particles taken into the body from the environment cause CVS pathology?
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triggering system infalmmation and altering clotting/stability of atheromatous plaues
neural reflex effects leading to arrythmias |
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What are the adverse effects of lead exposure?
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Hypertension
Neurodevelopment effects in children |
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What are the resistance vessels of the systemic circulation?
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arterioles (pressure drops from 90 - 40 over the arterioles)
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What is the ~ pressure of the venules?
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15 >10 mmHg (from distal to proximal circulation to the heart)
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What is the ~ pressure of the veins?
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10>5 mmHg (from distal to proximal circulation to the heart)
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What is the ~ pressure of the capillaries?
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40>15 mmHg (from proximal to distal circulation to the heart)
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What is the pressure drop from the beginning to the end of the arteries (start of the arterioles)?
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10mmHg (from 100 - > 90)
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t/f... pressures in the pulmonary system are 10 times lower than systemic
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false, 4 times lower
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What keeps arterial BP constant?
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baroreceptor/SNS
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t/f...in vessels in parallel, flow is inversely related to resistance
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true
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t/f... sympathetic nerves always cause vasodilation
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false, vasoconstrictor nerves are tonically active and induce vasoconstriction in arterioles. vasodilation can be caused by both sympathetic dilator nerves to muscle and PNS nerves
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What organs have the lowest density of sympathetic vasoconstrictor nerves?
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heart brain they have local regulators of blood flow
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What receptor and transmitter are used in vasoconstriction?
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NA, alpha adrenergeic receptors
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What tissue in the body has Beta1 adrenergic receptors?
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coronary arterioles (vasodilation)
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Where is adrenaline released from?
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Adrenal medulla by SNS activity
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What does Angiotensin do to bv?
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vasoconstricts
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What does ADH do to bv?
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vasoconstrictor, promotes water retention in the kidneys
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How does histamine effect bv?
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vasodilator, increase capillary permeability
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What is the basal vascular tone?
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a degree of intrinsic tone in blood vessels, caused by spontaneous vascular smooth muscle activity and induced by stress/high blood pressure.
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What local factors are used to increase local blood flow to a tissue? How are they removed?
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hypoxia, increase CO2, lactic acid and adenosine accumulate in metabolising tissue, cause vasodilation, which then increases blood flow and washes away these metabolites
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What are some endothelial derived blood flow factors?
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NO - relax
endothelin - constrictor PGL EDHRF |
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When is NO produced by endothelial cells?
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in response to shear stress
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What is the main mechanism for matching local blood flow to local tissue needs?
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Intrinsic regulation/local factors
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What causes reactive hyperaemia after a cuff placement?
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accumulation of local tissue metabolites, which cause vasodilation etc and are washed away when blood flow returns
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t/f... sympathectomy is an effective treatment of local atheromatous blockage
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false
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What causes smooth muscle contraction triggered?
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transmitter (adrenaline) binds to receptor (alpha), activates G protein which increases channel allowing positive ions in = depolarisation = VOCC open = Ca in and contraction
OR activated receptor causes G protein to activate PLC, which activates IP3, which causes SR Ca release (no depolarisation) |
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How does smooth muscle contract?
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Phosphorylated Myosin light chain and actin produce force. Myosin light chain is phosphorylated by Calcium, calmodulin and MLCK.
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What is the MOA of nitrates in causing vasodilation?
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increases cGMP, which activates PK, which phosphorylates to deactivate MLCK. This prevents MLCK, Calcium and calmodulin from phosphorylating MLC, which with actin would otherwise induce contraction
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How does viagra work?
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It inhibits a phosphodiesterase which breaks down cGMP. This allows it to activate PK, which phosphorylates to deactivate MLCK, disallowing MLC phosphorylation and susequent contraction. The blood in the penis is then allowed to pool in the corpus cavernosa to induce erection.
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t/f... hydrophobic sterol rings stabilise intracellular plasma membranes
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true, found within cholesterol and cholesterol ester
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How are lipids able to be dispersed in blood?
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amphipathic apolipoproteins attach, and act like detergents, forming a sphere called a lipoprotein
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What are the contents of a lipoprotein?
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hydrophobic core - triglyceride and chloesterol ester, surrounded by a more hydrophilic coat of phospholipd and apoliprotein (can act as a receptor ligand)
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What are the triglyceride rich lipoproteins?
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chylomicrons (dietary triglycerides) and very low density lipoproteins (VLDL - endogenous triglycerides)
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t/f... chylomicrons transport mainly endogenous triglycerides
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false, VLDL transport mainly endogenous triglycerides. chylomicrons transport dietary triglycerides
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What is an IDL?
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Intermittent density lipoprotein, the remnant of a triglyceride depleted VLDL, which is used as a precursor for LDL
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What is LDL?
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Low density lipoprotein, transports cholesterol to periphery
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What is HDL?
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one of the smallest lipoproteins, cholesterol and phospholipid rich High Density Lipoprotein used to transport cholesterol away from the periphery.
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What apolipoprotein is most involved in atherosclerosis, and what lipoproteins is it found in?
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Apolipoprotein B, found in LDL, IDL, VLDL
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How do bile acid sequestrants lower cholesterol?
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inhibit bile salt reabsoprtion in ileum by inhibiting Intestinal Bile Acid Transporter (this induces synthesis of new bile acid instead of usual recycling, increasing LDL clearance by the liver)
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How do plant sterols lower cholesterol?
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displace cholesterol from micelles in the GIT lumen, preventing GIT absorption (this reduces cholesterol that is transported to liver, increasing LDL clearance by the liver)
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How does Ezetimibe reduce cholesterol?
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inhibits uptake of micellar cholesterol in GIT by inhibiting NPC1L1 (this reduces cholesterol that is transported to liver, increasing LDL clearance by the liver)
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What form is cholesterol in as it travels from an enterocyte to the liver?
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found within chylomicron lipoprotein, travels in lymph
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What does DHA (22:6) do in cholesterol up take?
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inhibits cholesterol trafficking to the ER by suppressing NPC1L1, which normally transports chloesterol into the cell
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Where is the highest absorption of cholesterol in the GIT?
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Proximal small intestine, the duodenum and jejunum, where NPCL1L1 transporter expression is highest
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What 2 things can happen to cholesterol after it is taken up by an enterocyte?
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some is exported back by ABC, remaining is esterified and packaged into chylomicron lipoproteins
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What happens to chylomicrons that reach the liver?
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they are used to synthesis bile salts
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What does orlistate do with regards to cholesterol metabolism?
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It is an intestinal lipase inhibitor which blocks dietary fat digestion
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What in the circulation stops/binds to chylomicrons?
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lipoprotein lipase on endothelial surfaces in tissues that require fatty acids (muscle and adipose tissue)
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What happens to a chylomicron after the triglycerides have been depleted from within it?
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It becomes a chylomicron remnant which contains apoB and apo E that bind to LDL receptors and LRP receptors in the liver for uptake.
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t/f... Apo C always enhances LipoProtein Lipase activity on endothelial surface membranes
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false. there are different types of ApoC, Apo C-II enhances, but Apo C-III inhibits activity of LPL
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What do LDL-receptors do?
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bind to apo B and E in LDL, IDL, LDL and chylomicron remnants to uptake in the liver
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What are SREBPs?
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TF released by hepatocytes in low cholesterol levels. Cause increase in LDL uptake by increasing LDL-R expression, while also increasing the degradation of LDL-R, leading to limited LDL clearance from the blood
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How do statins reduce cholesterol?
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They inhibit HMGCoA Reductase, needed to synthesise cholesterol. This stimulates SREBP, which upregulates LDL-R, which removes more LDL from the circulation.
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Name three effects in the hepatocyte after its uptake of cholesterol via LDL-R?
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reduces cholesterol synthesis via HMGCoA, reduces LDL-R synthesis, increases cholesterol storage as esters, increases STREBP
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What are membrane lipid rafts?
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areas in the cell membrane which accumulate excess free cholesterol
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What substance in the blood do lipid rafts interact with to form HDL?
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Apo A1 (lipid poor apoprotein derived from liver, intestine and catabolised lipoproteins)
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What causes HDL to mature into spherical, cholesterol ester enriched particles?
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LCAT (lecithin)
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What causes macrophages to give up their cholesterol to nascent HDL particles?
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ABCA1
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How does the HDL get cholesterol to the liver?
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Directly - through SR-BI scavengers
Indirectly - transferring to VLDL and LDL via CETP |
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What drives the movement of LDL into arterial intima at the very beginning of fatty streak formation?
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gradient - high lumenal LDL goes to area of low LDL in the intima
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What keeps LDLs in arterial intima once there?
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binding to proteoglycans which oxidise and modify them
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What draws LDLs into arterial intima, even when their is already a high concentration found in the intima?
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modified/oxidised LDLs are inflammatory and attract circulating LDLs
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How are macrophages involved in atherosclerotic plaque formation?
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oxidised LDLs are inflammatory, and attract monocytes via induction of adhesion molecules on the endothelium. Monocytes differentiate into macophages which via scavenger receptors uptake the ox-LDL to form foam cells. These foam cells then attract T-cells which secrete IFN-gamma to further stimulate macrophage activity.
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How does obesity and insulin resistance cause atheroma?
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overproduction of triglyceride rich VLDL, which have enhanced CETP activity, promoting triglyceride exchange with LDL and HDL. This causes small dense LDL, whilst making small unstable HDL which are catabolised. This imbalance favours atherosclerosis
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What are the predisposing factors in the atheroma to causing plaque rupture?
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lipid accumulation, increase in lipid laden macrophages, disruption in reparative smooth muscle proliferation in the cap
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What are treatable classical risk factors in atherosclerosis development?
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smoking, hypertension, diabeties, dyslipidaemia
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How do you assess lipids and lipoproteins in the laboratory?
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Measure total cholesterol (VLDL, LDL, HDL), HDL and fasting TG, measure LDL level
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What are some secondary causes of dyslipidaemia?
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Cholesterol - hypothyroidism, nephrotic syndrome, cholestasis. Triglyceride - diabetes, obesity, renal impairment, alcohol, drugs
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What are the goals in lipoprotein levels in treating people with atherosclerosis?
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LDL <2.5 mmol/L, HDL >1 mmol/L, TG <2.0 mmo/L
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What is familial hypercholesterolaemia?
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mutation of the LDL-R gene, causing increased LDL and reduced clearance of remnants. This leads to CHD, CVD, aortic stenosis, xanthomas, corneal arcus etc
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What is the therapy for hypercholesterolaemia? (High LDL)
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Diet, manage secondary causes, statins***, ezetimibe, niacin, bile acid resins
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What is the therapy for hypertriglyceridaemia? (High triglycerides)
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lifestyle modification and management of 2* causes, fibrates, statins, fish oil, Niacin
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What is the effect of statins in hypertriglyceridaemia?
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statins (mildly decreases TG, increases HDL)
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What is the effect of fish oil in hypertriglyceridaemia?
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fish oil (decreases TG, no effect on HDL)
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What is the effect of Niacin in hypertriglyceridaemia?
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Niacin (mildly decreases TG, increases HDL, side effect is that it incresases glucose and insulin resistance)
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What type of hypertriglyceridaemia are fibrates effect in treating?
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fibrates are effective in High TG, low HDL. They increase HDL, decrease VLDL production and increase its clearance, and decrease TG levels
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t/f... bile acid resins are 2nd line treatment for hypertriglyceraemia.
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false. bile acids resins are used in hypercholesteraemia, but are contraindicated in hypertriglyceridaemia as they increase TG
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What causes the ST elevation in the ECG of someone with transmural ischaemia?
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actually a T-Q depression. The ischaemic zone is more + so current flows out of it into a scattered but backward direction, (away from electrode) especially in diastole. This leads to a TQ depression, which makes ST appear elevated
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What causes the ST depression in the ECG of someone with subendocardial ischaemia?
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Actually a T-Q elevation. the ischamic inner wall zone is more positive, so current flows out of it towards the outer of the wall and towards the electrode, especially in diastole. This elevates TQ, making ST appear depressed.
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t/f... you can localise the area of ischaemia from what leads show ST depression in a stress test
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false. ST depression is endocardial ischaemia. You can only localise transmural ischaemia from which leads show ST elevation.
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If an ECG is showing ST elevation in V1-V5, what does this indicate?
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Transmural ischaemia of the anterior wall, most likely due to LAD issue
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If an ECG is showing ST elevation in V6 or aVL, what does this indicate?
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Transmural ischaemia of the lateral wall, most likely due to circumflex coronary artery issue
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If an ECG is showing ST elevation in II, III or aVF, what does this indicate?
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Transmural ischaemia of the inferior wall, most likely due to a right coronary artery issue
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What results would you need to establish a diagnosis of CAD in an exercise stress test?
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1+ angina chest pain, ST segment depression, fall in BP, or failure to rise
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What are the indications for exercise stress testing for CAD?
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diagnosis of chest pain, assess prognosis of CAD, assess efficacy of therapy, screen high risk asympto pts, aid in cardiac rehab
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What do you do to induce stress in a nuclear perfusion scanning test for CAD?
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exercise, give dipyridamole/dobutamine for those who can't exercise (increases HR)
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What finding in a test is the most powerful predictor of cardiac events in asymptomatic population?
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a High Coronary Calcium score in an electron beam CT scan.
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What are some disadvantages of CT scanning of coronary arteries?
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cannot assess stent stenosis, requires a slow/even pulse
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What are the advantages of a coronary angiography in investigating CAD?
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direct visualisation, guides appropriate therapy
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What are the disadvantages of a coronary angiography in investigating CAD?
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Invasive, complication risk e.g. stroke, local bruising, MI, arrhythmia, death, allergy to contrast
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What is sensitivity?
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capability of a test to detect an abnormality (i.e. proportion of pts with disease correctly identified as abnormal)
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What is specificity?
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ability of a test to recognise a normal subject (i.e. % of pts without disease correctly identified as normal)
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What is accuracy?
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ability of a test to yield true results
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What is predictive value?
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clinical significance of a positive test result
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How do you investigate LV function?
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Echocardiography, Gated Blood Pool Scanning, Left ventricular angiograms
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How do you assess myocardial viability?
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PET (FDG takeup?), Delayed Thallium (gated blood pool scan?), cardiac MRI
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What risk factors are addressed in the first line strategy of IHD treatment?
|
cholesterol, smoking, diabetes, obesity, hypertension
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What drugs are used to improve the prognosis, or decrease the mortality, of IHD?
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Aspirin, beta blocker, statin, ACE-I
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What drugs are used purely to improve the symptoms, or decrease the morbidity, of IHD? (but don't decrease mortality)
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Nitrates, Beta blockers, Ca Antagonist
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What are the adverse effects of aspirin?
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GIT upset/ulcer, sensitivity, asthma
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When is Aspirin indicated, wrt IHD?
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Primary prevention of high risk pts, Secondary prevention in those with disease, those with acute coronary syndromes
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What is clopidogrel?
|
Antagonist of ADP receptor on platelets to prevent aggregation
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When is clopidogrel indicated?
|
coronary stent placement (at least for 12 months with drug-eluting stent), 2nd prevention in the aspirin intolerant (those with recurrent acute attakes, cerebro ischamia)
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What are the adverse effects from statins?
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muscle pain, increasing CK levels (indicator of muscle injury) , hepatic dysfunction
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What is the aetiology of obstructive vascular disease?
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atherosclerosis, diabetes, thrombosis, congenital, trauma
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What can be the pathophysiological consequences of vascular disease?
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ulcer, gangrene, infarct, pain on when exercising or at rest, stroke, TIA, ruptured aneurysm
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What is the clinical presentation of lower limb ischaemia?
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Pulslessness, Perishingly cold, Painful, Paralysis, Parasthesia, Pale; skin ulcers, gangrene, impotence
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What does the body do to compensate for stenosis or obstruction to flow in peripheral vascular disease?
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By developing a collateral blood supply
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What is intermittent claudication?
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In the limb, when circulation is adequate at rest, but on exercise, arterial occlusion prevents increased flow, allowing the build up of anaerobic metabolites that produce pain
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How many people with intermittent claudication die?
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20%
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How many people need amputations related to their intermittent claudication?
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5%
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t/f... most people with intermittent claudication manage without an operation
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true, it is generally benign and 85% manage without operation by responding to an exercise program
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What is the treatment for claudication?
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Exercise program *******, arterial bypass(using saphenous/upper limb vein, synthetic artery as last resort), balloon angioplasty and stenting
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What is the commonest cause of stroke and Transient Ischaemic Attack?
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thromboembolic disease, arising from extra cranial vessels (internal carotid, carotid bifurcation, vertebral artery, subclavian, aortic arch)
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What % of people are dead within 1 year of having a stroke?
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33%
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What is a way to prevent embolus when doing a carotid stent?
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while doing the procedure, have in place a protectve device which traps embolic material
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How should patients with symptomatic carotid stenosis of >60% be treated?
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endarterectomy = lower rates of stroke or death than stenting (which does however decrease chance of MI)
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What % of untreated lower limb ischaemia will need amputation?
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50%
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What does motor neuopathy in a diabetic foot cause?
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calluses, corns, pressure ulcers, deep seated tissue necrosis
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What is the mortality rate associated with an abdominal aortic aneurysm rupture?
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<50%
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What is the treatment for AAA?
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endoluminal tube graft through the aneurysm, usually with bifurcation
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