Cardiology Flashcards
location of heart apex
used to palpate precordium to find apical impulse.
= in 4th or 5th intercostal spaces, along mid-clavicular line (in supine patient)
Jugular venous pressure
horizontal distance from sternal angle (aorta) to height of jugular distention (in neck).
Normal = 8 cm
Above normal –> CHF, tamponade, …
apical impulse
gentle pressure ("tap") felt at apex of heart,
= 1st 1/3 of systolediastolic murmur
low sound heard with bell,
= from mitral stenosis
sounds heard with bell of stethoscope
LOW sounds
- Rumble = diastolic murmur/mitral stenosis
- gallop = S3 and S4
sounds heard with diaphragm of stethoscope
HIGH pitched sounds,
- S1 and S2 (normal)
- ejection/mid-systolic clicks
- aortic regurgitation murmur
S1 heart sound
= mitral and tricuspid valves closing (AV valves),
normal. before carotid pulse. loudest at apex.
* changes w/ leaflet mobility & rate of L ventricular rise
Abnormal: short P-R interval, mitral stenosis
S2 heart sound
= semilunar valves closing (aortic and pulmonic)
normal. loudest at base. after carotid pulse.
* physiologic splitting: w/ exhale A closes before P closes
Abnormal:
- wide split w/ exhale: RBB block or pulm. valve stenosis
- wide, fixed split: atrial septal defect
- paradoxical/reverse splitting: LBBB, left ventricular failure, or hypertensive cardiovascular disease
Gallop heart sounds
abnormal. = S3 and S4,
S3 = rapid LV filling (LA P < LV P), after S2.
S4 = vigorous LA contraction, before S1, @ max. LA pressure.
* sign of heart failure.
C-reactive protein
non-specific serum marker of inflammation,
*hsCRP assay (high sensitivity) to ID risk of atherosclerosis
BUT CRP does not CAUSE IHD
** also high CRP if: lupus, rheumatiod arthritis **
(so not useful atherosclerosis test in these patients)
current biomarkers for MI
1. Troponins (I or T):
rise 2-3 hrs after, peak 24 hrs, stay for 10-14 days 2. creatine kinase (CK-MB). Also (older): Myoglobin, White cell count, AST
Forward heart failure
inability of the heart to pump blood forward sufficiently to meet metabolic demands of the body
Backward heart failure
inability of the heart to pump sufficient blood to body to meet metabolic demands EXCEPT when cardiac filling pressures are abnormally high.
preload
ventricular wall tension at the end of diastole.
= end diastolic Pressure
– if high => increased CO
afterload
degree of pressure to overcome during systole.
= wall stress during systole [= (P x r)/(2 x thickness)]
–> measure as systolic pressure
systolic Heart Failure
impaired ventricular contractility
- -> increased afterload
1. normal filling (but enlarged ventricles),
2. decreased % blood pumped out
diastolic heart failure
impaired ventricular filling;
- stiff ventricles –> reduced filling (less volume in)
- ~same % pumped out, but since total volume = less, still less blood out to body
concentric hypertropy
add muscle fibers in parallel, so get thick walls.
can be from:
- Aortic stenosis (HTN)
- pulmonary stenosis (pulm. HTN)
eccentric hypertrophy
add myocyte fibers in series, so dilate chambers (walls not thicker),
from: aortic insufficiency, mitral regurgitation, pulmonic insufficiency, tricuspid regurgitation, shunts
calcific aortic stenosis pathogenesis
increased LDL combines with inflammatory cells, and interacts w/ myocytes –> causes smooth muscle cell proliferation and ossification of cardiac tissue (by osteopontin).
aortic stenosis clinical picture
Sx: syncope, angina, dyspnea
Test findings:
- echo: reduced valve opening, dilated chambers, calcified valve
- ECG: ???
Tx: diuretics, inotropes, vasodilators;
* need surgery to replace valve if have Sx!
3 possible causes of aortic stenosis
- bicuspid stenosis
- calcific stenosis
- rheumatic stenosis
3 main types of lesions in congenital heart defects
- Left to right shunt - increased BF to lungs
- Right to Left shunt
- Obstruction(s)
Left to right shunt (a congenital heart defect)
shunt of oxygenated blood into pulmonary flow, => increase pulmonary BF
ie: ventricular septal defect, atrial septal defect, patent ductus arteriosus
Long-term: pulmonary HTN (w/ sm m hypertrophy) –> SWITCH to Right-Left Shunt (BAD!)
Eisenmenger Syndrome
Central cyanosis, exercise and risk of sudden death
bc de-oxygenated blood is being pumped into systemic circulation (w/ congenital R-L shunt)
Long term complications of Cyanotic Heart Disease
- Failure to thrive (low O2 perfusion to body)
- Polycytemia (too many RBCs)
- Digital clubbing (chronic hypoxemia)
- Cerebral hypoxemia (poor neuro f(x))
Right to Left Shunt (congenital defects)
- Problem - Causes
Problem: mix deoxygenated blood in LV, pump to systemic circ., --> hypoxemia, cyanotic heart disease Causes = "terrible T's" - Transposition of the Great Vessels - Tetralogy of Fallot - Truncus Arteriosus
Common causes of Congenital Heart Obstruction
- Aortic atresia
- Aortic coarctation
- Pulmonary stenosis
- often occur w/ shunt (structural “defect”) which allows for circulation & survival! (ie: VSD, ASD, patent ductus)
Ductus Arteriosus (normal)
in the fetus, connects RV/Pulm. artery to aorta
–> shunts blood into systemic circulation bc all blood is oxygenated by mom (enters via placenta), so no need to go to lungs
Closure of ductus arteriosus
stimulated by decrease in prostaglandin levels.
–> when placenta cut (placenta secretes prostaglandins)
–> when take NSAIDs
*may be dangerous if need the shunt to provide blood to body!
=> prevent closure by giving exogenous prostaglandins
Ductus-dependent Lesions (congenital)
(when ductus shunt provides most or all oxygenated blood for body)
- neonatal emergency, MUST give prostaglandin E until fixed!
- transposition w/ intact septa
- aortic atresia
- interrupted aortic arch
- hypoplastic left heart
Ventricular Septal Defect (congenital)
L to R shunt, (bc LV has higher P)
- Large –> heart failure @ birth; => failure to thrive bc can’t meet metabolic need (from high work of breathing).
- Small –> holosytolic murmur w/ mid-diastolic rumble only after 2-6 wks bc pulm. vascular resistance changes; LA & LV hypertrophy; heart failure @ 3 mo.
Atrial Septal Defect
L to R shunt btwn atria, w/ diastolic flow murmur & fixed wide splitting of S2, classic RSR’ on ECG.
- may be asymptomatic in adults,
- secundum: incomplete closure of foramen ovale (gap persists)
- primum
- sinus venosus defect
- flow determined by ventricular compliance
Atrioventricular canal (aka atrioventricular septal defect)
failure of endocardial cushions to fuse.
Complete = 3 problems:
- atrial septal defect
- ventricular septal defect/membranous ventricular septum
- AV valve abnormalities
** 50% of Down syndrome (trisomy 21) pts have AV canal**
“Conotruncal” abnormalities
= defects in arterial outflow tracts; cause cyanotic heart disease.
- transposition of great arteries
- truncus arteriosus
- strong connection w/ Del 22q11 syndrome**
transposition of the great arteries
defect where connections to aorta & pulmonary artery = switched
(R ventricle to aorta, L ventricle to pulmonary artery)
* NEED shunt to survive!
- 40% stable VSD,
- 60% UNstable patent foramen ovale OR ductus arteriosus)
Tx: arterial switch surgery
Truncus Arteriosus
(aka: common arterial trunk)
failure of aorta and pulmonary artery to separate;
* often underlying VSD or other anomaly
–> cyanosis & high pulmonary blood flow
Del 22q11 syndrome
abnormal migration of neural crest cells to neck & upper thorax;
can cause conotruncal defects:
- transposition of great vessels
- tetralogy of Fallot
- Interrupted aortic arch
Also: thymic hypoplasia/aplasia, parathyroid defects
Tetralogy of Fallot
4 main features
most common cyanotic congenital heart defect
problems bc displaced “infundibular” (outflow) septum;
4 features:
1. pulmonary outflow tract stenosis
2. overriding aorta
3. Ventricular septal defect (VSD)
4. R ventricular hypertrophy
Tetralogy of Fallot symptoms
- cyanotic episodes (“Tet spells,” bc of RV outflow tract spasms)
- R to L shunt in 1st 6 months if “classic” (moderate/severe)
- systolic ejection murmur
- 2/3 pts also have valvar pulmonary stenosis, fewer pts: pulmonary atresia, NO associated CHF
Aortic Coarctation
= narrowing of the aorta, near ductus arteriosus;
=> infant heart failure, & BP higher in upper extremities than lower extremities
Often w/: bicuspid aortic valve, VSD (ventricular septal defect), other lesions
** some association w/ Turner’s Syndrome (monosomy X, aka 45X)
incidence of congenital heart disease
in live births
8/1000! (fairly common)
– most common = VSD
heart response to increasing metabolic demands
- near maximal O2 extraction from coronary vessels at rest!
- -> MUST increase coronary blood flow to increase oxygen supply to heart.
3 factors influencing blood flow to heart
- basal viscous resistance (blood quality)
- autoregulatory resistance (resistance vessels dilate)
- compressive resistance (increase R w/ activity, highest in systole)
Effect of systole on heart tissue perfusion
In Systole: endocardium gets disproportionately LOW perfusion
(in diastole, all layers ~equal perfusion)
endogenous triggers for coronary vasodilation
Metabolic: hypoxia, high pH, high PaCO2, high adenosine
Neurologic: a-adrenergic and beta-adrenergic innervation
Endothelial factors (NO, adenosine indirectly)
Coronary stenosis (physiology, consequences)
coronary vessels become thickened –> increase resistance,
—> vessels dilate to compensate (even at rest).
=> worse w/ exercise (get ischemia) bc vessels are already @ max dilation.
* no significant Sx until 70%+ lumen narrowing!
2 main treatment strategies for ischemic heart disease
- Limit heart’s oxygen demand (beta blockers)
- Increase dilation capacity (nitrates, angioplasty/re-vascularization)
* Re-vascularization treats Sxs, but does NOT change mortality rate.
4 determinants of O2 demand
- Wall tension
- heart rate
- contractility
- basal cost
equation for calculating wall tension
wall tension = P*d/h
= (systolic LV pressure x LV chamber diameter)/wall thickness
path to angina
- ischemia
- ATP loss
- impaired relaxation (requires O2)
- systolic dysfunction
- ST depression
- angina
locating ischemic tissue w/ ECG
- ST Depression if: ischemic tissue is behind healthy tissue
(electrode on other side of healthy tissue from ischemia) - ST Elevation if: ischemic tissue = closest to the electrode
Utility of exercise stress testing
- Diagnosis of angina/ischemic heart disease
- evaluating Prognosis of diagnosed CAD
- Monitor efficacy of treatment
- Screen for CAD/heart disease
mechanism of action of nitrates (for angina/ischemic heart disease)
- coronary vasodilation (& coronary collaterals)
2. dilate systemic veins (–> decrease LV size = decrease wall tension)
Classical Angina Pectoris
(= stress-induced endocardial ischemia, stops w/ rest bc return to fully compensated O2 perfusion)
Sx: diffuse visceral chest discomfort/pressure, 1-10 min., w/ stress & esp. in AM or after meals
Dx: exercise stress test (also: rales, S4, mitral regurg, tachycardia)
Tx: nitroglycerine & beta-blockers; + stop smoking, ASA…
physical exam findings for angina & why
- S4: stiff L ventricle
- Mitral Regurgitation: papillary m. dysfunction
- Rales: pulmonary congestion
- Tachycardia (perfusion compensation)
variant angina (“prinzmetal”)
angina @ rest, = ischemia due to coronary artery spasm;
Dx: ST elevation
Tx: nitroglycerine, beta-blockers, ASA
common causes of myocardial infarction
atherosclerosis, aortic dissection, vasculitis, congenital anomaly, embolism, trauma, increased blood viscosity…
main pathogenic recipe for MI
- endothelial injury
- platelet activation & clotting cascade
- failure of anti-thrombotic mechanisms
steps involved in endothelial injury for MI
= Plaque rupture caused by stressors (infection, surgery, emotional/physical stress, hormones…) => decrease vessel diameter.
- macrophages/foam cells: degrade collagen of fibrous cap & make TF (pro-coagulant)
- T cells: increase macrophage synth, decrease collagen synth, & induce sm. m. cell apoptosis!
Steps of platelet activation for MI
When blood is turbulent and endothelial collagen is exposed:
- platelets stick to endothelial integrins –> change formation
- secrete alpha granules
- aggregate (w/ more platelets)
steps in coagulation cascade (causing MI)
- TF from macrophages/foam cells triggers activation of thrombin and fibrinogen.
- PAI (plasminogen activator inhibitor) stops plasmin from degrading clot.
major reason for anti-thrombotic mech failure in MIs
Endothelial dysfunction –> less prostacyclin, EDRF, & NO
==> less vasodilation and platelet inhibition.
pathological findings of MI & their molecular causes
- intracellular edema: low ATP production –> increased intracellular Ca2+ and extracellular K+
- chromatin clumping: lactic acidosis (low pH)
- PMN infiltration of tissue (= acute inflammatory response)
time intervals to tissue damage
20 minutes of ischemia: IRReversible damage
18 hrs - 4 days: coagulative –> total necrosis
2-3 weeks: fibrosis
* 3-6 weeks: healing
partial vs. complete occlusion from coronary thrombosis
- Partial: NSTEMI, w/ ST depression & T wave inversion
(= subendocardial MI), OR Unstable angina - Complete: STEMI / Q wave MI = transmural (all layers affected)
stunned myocardium
injured but not necrotic myocardial tissue that remains dysfunctional after blood flow is restored; recovers over time.
Mech: Ca2+ overload from mitochondia, ROS accumulation, or disrupted excitation coupling.
Hibernating myocardium
hypocontractile myocardium due to chronic hypOperfusion (not MI); ~immediately reversed when restore full blood flow.
ie: from severely (& chronically) atherosclerotic coronary artery
Ventricular remodeling
changes in shape & thickness of the L ventricle due to MI
–> expand & hypercontract either infarcted or opposite wall.
==> decreased systolic f(x) & high risk of LV aneurysm!
TIMI score
used to quantify risk of MI (points if yes for each question) Patient Hx: 1. age > 65; 2. 3+ CAD risk factors; 3. prior coronary stenosis > 50%, 4. 2+ anginal events in past 24 hrs 5. took ASA in last 7 days Test results: 6. ST shift on ECG; 7. + biomarkers (troponin, Ck-MB, etc.)
treatments for MI
1: Re-perfusion (surgical angioplasty > thrombolytics)
- anti-platelet Tx (ASA, P2Y12 inhibitors, GP2b3a inhibitors)
- anti-thrombolytic Tx: (heparin, Xa inhibitors)
- cardioprotective (beta blockers, ACE Is/ARBs, nitrates)
Common complications of MI
- Decreased contractility –> LV aneurysm, CHF
- Electrical instability –> Arrhythmias
- Tissue necrosis –> papillary m rupture, ventricular-septal rupture, myocardial rupture
Cardiogenic shock
systemic hypoperfusion due to low CO; (w/ multi-vessel CAD)
Sx: systemic hypOtension, acidosis, cool extremities
Tx: use permanent balloon pump to hold coronary vessel open during diastole (so won’t collapse)
cause of Recurrent Ischemia/Infarction after MI
= due to damage/injury of tissue from using balloon pump for re-perfusion.
Arrhythmias due to electrical failure
(= ventricular)
- PVCs - V-fib.
- ventricular tachycardia
- accelerated idioventricular rhythm
Consequences of tissue necrosis (from MI)
- Papillary muscle rupture
- Ventricular Septal rupture
- Myocardial rupture
Arrhythmias due to pump failure
- sinus tachycardia
- A-fib or Atrial flutter
- paroxysmal supraventricular tachycardia
Arrhythmias due to damaged conduction
(aka: increased parasympathetic tone)
- sinus bradycardia
- junctional escape rhythm
- atrioventricular block
* * these ppl need catheterization IMMEDIATELY & pacemakers**
Common causes of heart failure
MI/CAD, HTN, valve disease, congenital heart disease, cardiomyopathies.
Factors influencing Cardiac Output
- Heart Rate
- Stroke Volume
- preload, afterload, & contractility
Use of beta blockers for Heart Failure
YES: bc interrupts compensatory neurohormonal cycle (prevent pulm. edema & peripheral hypOperfusion)
BUT: careful not to use too much –> causes Na+ retention & myocyte hypertrophy/death (=> ischemia, arrhythmias)
Compensatory endogenous responses to Heart Failure
- increase Renin-Ang-Aldosterone system (increase blood volume)
- increase sympathetic signaling (increase HR, vasoconstrict)
- ventricular hypertrophy
Pathologic changes w/ Heart Failure
- decrease contractility (bc chronic volume overload)
- increase afterload –> systolic dysf(x)
- impair LV filling & relaxation –> diastolic dysf(x)
problems associated w/ systolic dysfunction from Heart Failure
Systolic dysf(x):
- decrease contractility –> MI/ischemia, mitral/aortic regurg., dilated cardiomyopathy
- increase afterload –> aortic stenosis, HTN
problems associated w/ diastolic dysfunction from Heart Failure
= impaired LV filling & relaxation;
–> LV hypertrophy, trannsient ischemia, hypertrophic OR restrictive cardiomyopathies.
NYHA classification of Heart Failure
Class I: no physical limitations
Class II: Sx (dyspnea, fatigue) w/ moderate activity
Class III: Sx w/ normal daily activities (minimal exertion)
Class IV: symptoms present @ rest
Normal hemodynamic values (from catheterization)
R atrium: 0-6 mmHg R ventricle: 15-30/0-6 Pulmonary a: 15-30/6-12 L atrium: 6-12 L ventricle: 100-140/6-12 Aorta: 100-140/60-80
Phases of hemodynamic changes in heart failure
- warm & dry = normal perfusion, no edema
- warm & wet = edema/congestion from bc increase preload to maintain CO
- cold & wet = edema, no longer able to compensate for perfusion (cold extremities)
- cold & dry = end-stage. low perfusion (cold extremities) and loss of volume & CO (no edema)
Common exam signs for congestion
orthopnea, edema, rales, systolic murmur & S3
Common signs of poor perfusion
(= from low CO)
sleepy, cool extremities, pulsus alternans, hypotension when on ACE Inhibitor
Goals of treatment for Heart Failure
- Identify and treat cause of heart failure
- manage symptoms (congestion & limit neurohormonal response)
- increase long term survival (*not possible for diastolic dysfunction)
Recommended drug treatment for Congestive Heart Failure
1: ACE inhibitor & beta blocker
- not b-blocker if volume overload*
2nd line: ARB (if can’t tolerate ACE I)
3rd: Nitrates & Hydralazine combo (if can’t tolerate 1st 2 options, OR esp. if african-american)
Contraindications for ACE inhibitors in CHF
- = 1st line therapy, but can’t use if:
- pregnant
- renal stenosis
- asthma
- DM (only if unable to ID drops in glucemia)
Dilated Cardiomyopathy (DCM)
enlarged L ventricular chamber, may also have enlarged L atrium;
usually in ages 20-60, = #1 reason for heart transplant.
Symptoms and tests for diagnosing Dilated cardiomyopathy
Sx: CHF, arrhythmias, sudden death; may be asymptomatic.
Dx: cardiac catheterization, ECG, echocardiogram, CMP (blood), thyroid & drug screens, genetic testing.
causes of Dilated Cardiomyopathy (4 types)
- familial/genetic (sarcomere proteins)
- inflammatory (viral, sarcoidosis, peripartum, CT disorders)
- toxic (EtOH, chemotherapy - ie: adriamycin)
- neuromuscular
Treatment for dilated cardiomyopathy
- alter diet - fluid and Na+ restriction
- ACE inhibitor & beta-blockers (if symptomatic)
- may also use ARBs or diuretics
- anti-coagulants (if experience thromboembolic events)
Hypertrophic cardiomyopathy
disease of the heart muscle –> enlarged intraventricular septum and/or L ventricular hypertrophy (not from CHF).
Sx: dyspnea, angina, syncope.
* most common age: ~20s
exam findings for diagnosing Hypertrophic cardiomyopathy
S4 w/ systolic murmur.
* murmur: LOUDer w/ valsalva (when increase preload)
treatment for hypertrophic cardiomyopathy
If…
- No/mild Sx: no drugs
- CHF: beta blockers, +/- diuretics (decrease afterload)
- A-fib: cardioversion, rate control, & anti-coagulation
- NO sports participation (= contraindicated for disease!)
Restrictive Cardiomyopathy
rare disease of heart muscle => rigid ventricles & atria may be larger than ventricles.
Caused by infiltrates into muscle fibers OR muscle tissue fibrosis.
=> Normal contraction, but poor filling.
Symptoms of restrictive cardiomyopathy
R heart failure, ascites, edema;
*must be distinguished from constrictive pericarditis!
Causes of Restrictive Cardiomyopathy
Infiltrates (4): amyloidosis, sarcoidosis, hemochromatosis, glycogen storage disease.
Fibrosis (3): metastatic tumors, hypereosinophilic syndrome, radiation therapy.
incidence of congenital heart disease in live births (in USA)
8/1000 (fairly common)
congenital heart diseases that may NOT cause cyanosis
- VSD
- PDA
- ASD
treatment for Restrictive Pericarditis
- Poor prognosis, but:
1. treat underlying disease
2. diuretics
True Anuerysm
bulging of vessel wall involving all 3 vessel wall layers,
> 50% increase in diameter.
2 types: fusiform (symmetrical) or saccular (localized)
causes of aneurysm in ascending aorta
due to cystic medial necrosis, from:
- bicuspid aortic valve
- HTN
- Connective tissue disease (Marfans, Ehlers-Danlos)
False Aneurysm
Bulging of vessel wall only lined by adventitial layer
- -> high risk of rupture!
causes: infection, trauma
classes of aortic dissection (2)
A = occurring before/up to aortic arch B = occurring AFTER (distal to) the aortic arch
treatment for aortic dissection
1: reduce BP & ejection force to limit progression of dissection
- type A: surgical treatment (early = best)
- type B: Percutaneous catheter repair
- –> surgery ONLY if major branch occlusion or imminent rupture
path of fetal blood circulation
placenta –> ductus venosus –> IVC;
R atrium –> foramen ovale –> L atrium (… -> aorta, body…)
*R ventricle –> pulmonary artery –> ductus arteriosus –> aorta
(to body, umbilical arteries –> back to mom)
clinical appearance of Left-sided obstruction lesions (congenital defect)
cause anterograde conduction problems –> poor/no systemic perfusion!
* appear mottled & gray (like newborn strep) BUT have NO/weak femoral pulse!
Key observation to Dx ductal-dependent coarctation of the aorta
systolic BP in legs LOWER than in arms (when supine)
[should be same or higher if healthy]
transposition of great vessels vs. Tetralogy of Fallot
Transposition: cyanotic RIGHT AWAY at birth, no murmur usually,
“Big blue, happy tachypnic newborn,” w/ cardiomegaly.
Tetralogy: cyanotic 1 month AFTER birth,
atherosclerosis
thickening of the inner layer of the aorta and muscular arteries w/ fatty deposits and fibrous tissue
normal function of endothelium (4)
- barrier to large molecs
- modulate sm. muscle action
- resist leukocyte adhesion
- antithrombotic mechanisms
steps of atherosclerosis formation (5)
- endothelial dysfunction (from oxidative & shear stress)
- lipid accumulation
- recruit leukocytes
- form foam cells
- deposit extracellular plaque
layer of vessel wall which produces inflammatory molecs
Smooth muscle cells in media
* sm. muscle cell proliferation/hyperplasia in atherosclerosis
characteristics of activated endothelium
(activated by irritants)
- leaky - decreased NO & prostaglandin production
- produce cell surface adhesion molecs
- release inflammatory cytokines
Causes of acute limb ischemia
- Embolic (A-fib, MI, cardiomyopathy)
- paradoxical embolism (if patent foramen w/ bearing down)
- thrombosis in situ (atherosclerosis or trauma)
- atheroembolism
atheroembolism
crystals from plaque break off and obstruct SMALL vessles,
ie: after cardiac catheterization
“Blue toe syndrome”
Reynauld’s Phenomenon
digital artery vasospasm induced by cold or vibration
- triphasic: 1. blanch, 2. cyanosis (blue), 3. “rubor” (red & sting)
may be primary or secondary
Tx: Ca channel blockers, alpha adrenergic antagonists
types of primary vasculitis
- Takayasu’s arteritis (“pulseless disease,” -> in carotid or limb pulses)
- Giant cell arteritis (in temporal or opthalmic arteries)
- Buerger’s disease (in male smokers, Tx: stop smoking!)
modifiable risk factors for HTN
smoking, dyslipidemia, diabetes, obesity/sedentary lifestyle
2 growth patterns for atherosclerosis
- stable plaque – steady rate, w/ fibrous cap.
- vulnerable plaque – growth spurts, w/ high risk of rupture (not well attached to wall)
- rupture may be asymptomatic,
- plaque hemorrhage will cause more growth
