Cardio Quiz 2a

eem8u's version from 2016-12-17 18:44

CV RISK Factors


Atherosclerosis Background / **review the progression slides 16.4-16.5
Question Answer
3 fx of normal endothelial cellsanti-inflammatory / promote vasodilation / resist thrombosis
2 fx of normal smooth musclevascular tone / produce ECM of collagen and elastin (that maintains vascular integrity)
vascular role of collagenstrength
define atherosclerosis— a SYSTEMIC DISEASE that manifests LOCALLY >>> disease of the ARTERIES characterized by the deposition of plaques of fatty material on their inner walls.
2 hallmarks of atherosclerosis1- LDL particles in subintmal space (due to endothelial c dysfx) 2- inflammation (T-cells, monocytes)
***Proatherogenic pathway - describe sequence to forming FATTY STREAK*endothelial c dysfx >> allows LDL into subintimal space >> inflammatory cell recruited >> ***LDL modified to mLDL (by Tcells and monocytes) >> mLDL taken up by foam cells (monocytes) >> apoptosis / necrosis / persistent inflammation
Proatherogenic pathway - describe sequence to forming PLAQUEinflammation >> smooth muscle migration into internal elastic lamina >> proliferation & collagen secretion >> fibrous cap
fibrous cap degraded byMMP, inflammatory cytokine (also inhibits sm.Muscle matrix synthesis)
‘stable’ vs. ‘vulnerable’ plaque determined bybalance between fibrous cap degradation & synthesis
vulernable plaques -lipid core / fibrous cap / inflammatory cellsLARGE core, thin cap, many inflammatory
stable plaques -lipid core / fibrous cap / inflammatory cellssmall core, thick cap, less inflammation (and preserved lumen)
thrombus forms whenfibrous cap of VULNERABLE plaque ruptures
thrombus consists offibrin, RBC, platelets


Atherosclerosis Risk Factors
Question Answer
3 “nontraditional” risk factorsapolipoprotein (a) , c-reative protein, homocysteine
4 modifiable risk factorsDyslipidemia, DM, smoking, inactivity
describe differential gender riskbefore menopause risk lower in women, after same or HIGHER for women
LDL vs HDL - compositionHDL = high density (low
fx of lipoproteinstransport cholesterol
role of cholesterol (2)cell membrane, make steroid hormone
external composition of lipoproteinsproteins, phospholipids, cholesterol
HDL-C function“good cholesterol” >> reverse transport from periphery to liver / removes HDL
LDL-C function“bad cholesterol” >> deposits cholesterol in arterial wall >> atherosclerosis
correlation b/t cholesterol and CVD mortality and AGEhigher cholesterol INCREASES risk ***independent of age***
HDL vs LDL - CAD riskLow LDL / High HDL = best outcome


Atherosclerosis Treatment
Question Answer
pharmacologic therapy - first line drugstatins
****pharmacologic therapy - second line drug (3)Niacin (B3), bile acid sequestrates, fibric acid
pharmacologic therapy - emergent therapyPCSK9 inhibitors (see below for mechanism)
Statins- benefit is proportional to ______degree of LDL- C lowering (also wee modest HDL-C increase)
****Statins- pleiotropic effects (3)vascular tone modulation (vasodilation) / plaque stabilization / reduce inflammation (pleiotropic = multiple effect from same gene)
****Statins - mechanismStatins = HMG-CoA Reductase Inhibitor (reduce cholesterol produced by liver) >>> more LDL-C receptors expressed >>> lower serum LDL-C levels
PCSK-9 inhibitors- mechanismPCSK-9 inhibitors are MONCLONAL antibodies that bind >> block PCSK-9, which usually degrades LDL-recptors causing increased LDL serum level
***LDL in serum - therapeutic goal levelbelow 70 mg/dL
****Who gets a statin? 3 factorsknown heart disease / high LDL (above 190) / diabetes (see 16.25 risk chart)
tx to raise serum HDLNONE proven / DIET and EXERCISE


Diabetes - Vascular effects
Question Answer
how does DM influence CV risk (2)1- accelerated atherosclerosis / 2- prothrombotic state (see 16.30) “like gas in a fire”
explain DM as Coronary Heart Dx “risk equivalent”same rate for survival as **prior MI***
Atherosclerosis & DM - microvascular complicationsnephropathy, neuropathy, retinopathy (prevented by good glycemic control)
****Atherosclerosis & DM - macrovascular complicationsstroke, MI, peripheral artery disease ***** (glycemic control may not prevent macrovasc.)


Obesity & smoking - Vascular effects
Question Answer
obesity - describe vascular effects (4)1- inflammation (adipose release pro-inflammatory cytokines) 2-HTN (increased CO for high metabolic demands of excess body weight) 3- endothelial dysfx 4- insulin resistance
overweight vs obesity BMI Overweight = 25.0-29.9 / Obese ≥ 30.0
current AHA recommendations- Physical activity30 minutes/5 day moderate activity OR 25 minutes/3 dayvigorous activity AND High Intensity/2 day muscle strength
in young smokers,____ and ____ found in abdominal aortafatty streaks, raised lesions
****smoking - mechanisms of injury (4)endothelial damage / ***prothrombotic effect / coronary vasoconstriction / oxidation of LDL-C (leads to more inflammation)
****relative risk of CHD death from smoking2.1 (<24 cigarettes/day) / risk of three 3 ( > 25 /day)


Additional Makers of CADx
Question Answer
homocysteine - defineamino acid , byproduct in protein metabolism
homocysteine - level in CVDelevated (perhaps a parker of disease), no evidence that reduction improves outcomes
****Lipoprotein (a) - define and 2 functionsvariant of LDL w/ apolipoprotein apo(a) // may impair endogenous thrombolysis & promotes inflammation
Lipoprotein (a) - level in CVDhigher level >> higher risk (no therapy available) to lower)
****C-reactive protein (CRP) - defineacute phase reactant (such as infection, atherosclerosis) released by liver
CRP - level in CVD>> marker of inflammation / assc w/ increased cardiac risk (unclear if it is also mediator of dx)

Stable Coronary Artery Disease I



Question Answer
underlying mechanism of ischemic heart diseaseimbalance of myocardial o2 demand/supply
2 components of myocardial o2 supply1- coronary flow (perfusion) 2- blood o2 content
calculate coronary flowQ = dP/ R (directly related to pressure gradient, inversely related to resistance) ***Resistance is key mediator of flow
****minimum diastolic pressure to ensure coronary flow60-65 mmHg (ensures a pressure gradient with LV end DIASTOLIC P)
normal diastolic pressure~80mmHG
2 determinants of coronary vascular resistance1- tone / 2- degree of stenosis (EPICARDIAL VESSELS)
most important mediator of coronary vascular tone (AND MECHANISM)ADENOSINE > produced during hypoxemia > binds to smooth muscle >> vasodilation


Question Answer
vasodilators produced by endothelium (3)NO, prostacyclin, EDHF
vasoconstrictors produced by endothelium (1)endothelia 1
endothelial response to Achnormal >> vasodilation (via NO) // dysfunction >> vasoconstriction (indicates dysfx)
3 determinants of Myocardial oxygen demandwall stress (b/c causes hypertrophy) / increase HR / increased contractility
calculate ventricular wall stressP x r / 2 h (r= ventricular dimension, h = thickness of myocytes/hypertrophy)
Ventricular pressure overload states (2)aortic stenosis / HTN >> increased wall stress
volume overload statemitral regorge >>> increased wall stress
calculate vessel resistanceR ~ L/r^4 (decrease in r >>> big increase in R
Maximal coronary flow under stress reduced at ___ % stenosis70% stenosis
resting coronary flow reduced at ___% stenosis90%
stenotic lesions manifestCONDUIT vessels = epicardial arteries (macrovasculature of heart)


Question Answer
role of endothelial c dysfx in ischemia (2)decreased vasodilator release (prostacyclin/NO), loss of antithrombotic effects
low 02 supply - non-Atherosclerotic causes (2)1- aortic regurge (decrease diastolic P >> decreased coronary perfusion P) 2- acute blood loss (GI bleed)
increase o2 demand - non-Atherosclerotic causes (3)tachyarrhythmia (increase HR), hypertensive crisis (increase afterload), aortic stenosis (causes increased wall stress)


Ischemic Syndromes
Question Answer
define stunned myocardiumsystolic dysfx after transient ischemia (recovers)
define hibernating myocardiumchronic ventricular dysfx due to multi vessel CAD
stable angina relieved by (2)rest or NTG
threshold for stable angina70% stenosis
prinzmetal angina - define**occurs at rest** due to coronary spasm
prinxmetal angina -mechanismendothelial cell dysfx and increased sympathetic activity >> spasm
Syndrome X- definechest pain, + stress test, NORMAL coronary arteries
Syndrome X- mechanismmicrovascular dysfx >> abnormal adenosine response (no vasodilation) >> ischemia
Silent ischemia more common in (3)DM, women, elderly (think about who experiences pain differently)


chronic stable angina
Question Answer
durationusually few minutes (few seconds ~ non cardiac cause)
locationdiffuse > focal
associated sx (4)dyspnea, fatigue, diaphoresis, nausea
know the differential !see 17.18 (Cardiac, GI, MSK-costochondritis)
ECG(signs of ischemia) ST segment depression and/or T wave inversion /// can be normal!!!!
stress testingwill show ABNORMAL blood intake at peak stress (see 17.20)
gold standard tool of CAD diagnosisangiography

Stable Coronary Artery Disease II - TREATMENT

*******Medical Treatment - given to ALL patients
Question Answer
Nitrates-mechanismvasodilation > reduce LV volume (reduce preload) > lower wall stress & myocardial o2 demand
nitrates - SE’s (2)lightheaded, headache
B-Blocker - heart SE’sbradycardia, SHOCK in decompensated LV, heart block
B-blocker - systemic SE’ssexual dysfx, fatigue, *bronchospasm
***medications that reduce cardiac eventsB-blocker, Statins, ACE-I, ASA (for prior MI and HF) (nitrate, ranolazine, CCB DO NOT)
drug useful for patient with spasmnitrates, Dihydropyridine Ca+ blocker - mechanism
drug w/ primary benefit in SYMPTOMATIC patientsb-blocker
Dihydropyridine Ca+ blocker - effectvasodilation > reduce wall stress > reduce myocardial o2 demand , the DIhydro is DI-lating
amlodipine - typeDihydropyridine Ca+ blocker
nifedipine - typeDihydropyridine Ca+ blocker
verapamil - typenondihydropyridine Ca+ blocker
****diltiazem - typenondihydropyridine Ca+ blocker
nondihydropyridine Ca+ blocker - effectcardiac depressant >> reduce HR/contractility >> lower o2 demand
***Ranolazine - effectdecrease angina frequency & improve exercise tolerance
***Aspirin - tx effectAntiplatelet >> reduce risk of thrombosis
clopidogrel / thienopyridineAntiplatelet >> reduce risk of thrombosis (are potent than ASA)
clopidogrel / thienopyridine - mechanismplatelet P2Y12 receptor >> antiplatelet
statins - effectlower LDL (HMG co-a reductase)
ACE-I especially good for _____ underlying conditions (4)LV dos fiction, DM, CKD, hypertension


Question Answer
best tx for prophylaxisCABG (b/c it bypasses both stenotic & nonstenotic lesions
PCI must be administered w/ANTIPLATELET therapy (b/c induces trauma) - eg Aspirin, clopidogrel
SE of PCI w/ bare metal stentneointimal proliferation due to smooth muscle cell migration
SE of drug-eluting stentdelays normal endothelialization b/c of drugs > must take with APTx
who gets PCI vs medical therapy (2)refractory despite tx / intolerant to medical tx
arterial graft - patency~ 90% at 10 years)
venous great - potencyby 10 years ~ 50%
know the anatomic subsets that benefit from revascularization > medical interventionsee 18-18
PCI vs CABG outcomesSAME in low risk pts. / CABG confers greater advantage in HIGH risk pts
PCI - advantages (2)low procedural risk / outpatient
PCI - disadvantages (2)needs APT (bleeding risk!) / revascularization rates higher than CABG
CABG - advantages (3)complete revascularizaiton and no DAPT necessary
CABG - disadvantages (2)high procedural risk, longer healing time