Treatable risk factors for CAD
smoking
hypertension
Dyslipidemia/cholesterol
Treatable questionable risk factors for CAD:
diabetes obesity inflammation psychological stress sedentary lifestyle
Not treatable risk factor for CAD
male gender
age
genetics
Smoking causes a ______ tendency, promotes _____ by aryl hydrocarbon
thrombogenic
atherosclerosis
Smoking causes adverse effect on ____, ___ decrease O2 delivery, and causes ___dysfunction
lipoproteins (decrease DHL)
CO
Endothelial
HTN increases shear stress on arterial wall that cause direct ____
endothelial cell injury
HTN: Increased arterial wall stress initiates pathologic cell signaling program causing ____
oxidant stress, cellular proliferation
Diabetes and insulin resistance are associated with ________
inflammation, oxidative stress, dyslipidemia that predispose to atherosclerosis.
dyslipidemic triad includes ___
high LDL
low HDL
high Triglycerides
Oxided LDL becomes ___
pro inflammatory/atherogenic
Oxidized LDL effects:(4)
- injure vascular endothelium = impaired endothelial function
- Deposite in arterial wall = plaque volume/foam cell
- Activate inflammatory cell = progression/instability of lesion
- Activates platelet/prothrombotic
Roles of HDL (5)
- inhibit LDL oxidation
- Inhibit TF
- Enchance reverse cholesterol transport
- Stimulate endothelial NO production
- Inhibit endothelial adhesion molecules
DHL Overall function is to oppose ____
atherothrombosis
Inflammation plays a key role in ___ and ___
initiation and progression of atherosclerosis
Lipid laden macrophages in arterial walls are highly ____
pro-inflammatory
Extravascular inflammation (ex: ____) increase risk of _____ ____events
dental diseases
atherosclerotic CV events
Circulating markers of inflammation provides _____ about CV ___; ie: ___ (which is released by liver upon ___signal)
info
risk
C-reactive protein
IL6
stable CAD causes _____
myocardial ischemia
myocardial ischemia is:
tissue blood flow insufficient to meet oxygen requirement
Cardinal symptoms of myocardial ischemia is ___
chest pain/agina pectoris
coronary circulation is unique in ___ metabolism for energy supply, extract ___% of O2, perfused during ____
aerobic
near 100%
diastole ony
If O2 demands increase, supply will increase by ___ in heart
increase blood flow
Myocardial O2 supply determined by:
Coronary blood flow rate
Oxygen content of blood
Coronary blood flow rate determined by (4)
- perfusion pressure
- perfusion time
- vascular resistance
Autoregulation range implies
heart will provide constant coronary flow within moderate change in perfusion pressure
_____ can compromise coronary flow by intramural coronary vessel compression
tachycardia
O2 supply compromised by:
anemia (less hemoglobin)
Hypoxemia (incomplete O2 sat)
Treatment of:
- perfusion pressure
- Diastolic time
- Coronary resistance
- O2 content
- prevent HTN
- rate control drugs
- Vasodilator/coronary agnioplasy/bypass surgery
- treat anemia/hypoxemia
Determinants of Mycoardial O2 demand
- heart rate
- wall tension
- inotropic state
Treatment of:
- systolic pressure
- HR
- Wall tension
- Inotropic state
- antihypertensive drug
- rate slowing drug
- limit LV - diuretic/nitrate
- negative inotropes (beta/Ca blocker)
stable CAD caused by:
obstructive coronary lesion limits coronary flow
Causes of unstable CAD (8)
inflammation weakening fibromuscular cap plaque fissue/rupture thrombogenic component to blood Thrombosis partial/complete vessel occlusion MI Cardiac dysfcn
unstable angina is caused by a ______ occlusion of vessel that ____ heart attack with biomarkers ___
near complete
threatened
negative
Acute MI is a ___ CAD
unstable
AMI is caused by ______ coronary flow reduction, thrombus with ___vessle occlusion, wavefront with ______, biomakers ____
persistent/severe
complete
myocardial necrosis
elevated
AMI ______ is key to treatment but can also cause ___ injury
early reperfusion
reperfusion
AMI high early mortality ___; late mortality ___
1/3 pt don’t get to hospital
Extent of LV dysfunction
Timeline of acute MI
- diastolic dysfunction
- systolic dysfunction
- ECG sign of M. injury
- symptoms
hour:
mycardial necrosis/infarction
time: ____ = no harm; ____ 50% infarct
0-30 min
2 hours
3-4 hr = near complete necorsis
inflamed arterial atheroma releases ___ markers (ie ___; downstream myocardial injury shows ___ markers (ie__)
Inflammatory (markers)
CRP
cardiac (markers)
Troponin/creatine kinase