Coronary Artery Disease (CAD) Flashcards
Coronary artery disease
- mostly due to atherosclerosis
- cardiac disease due to impaired cardiac perfusion
- coronary arteries (supplying heart tissue with blood) narrowing & occlusion causes impaired coronary blood flow
Angina =
chest pain
Types
Chronic ischemic heart disease: -stable angina -microvascular angina (induced by exercise, angiogram shows normal) -variant angina -silent myocardial ischemia (ischemia without pain "silent") Acute Coronary Syndromes (ACS): -unstable angina -MI
Ischemia
an inadequate blood supply to an organ or part of the body, especially the heart muscles
Angina pectoris
- pain is not a disease it’s a manifestation–angina pectoris is a manifestation of CAD
- inadequate perfusion to meet cardiac metabolic demand
Angina pectoris etiology
- mostly due to atherosclerosis
- also due to vasospasm (=acute constriction of blood vessel, stays constricted for awhile)
- thrombosis
Patho of Angina pectoris
- coronary arteries need to dilate on demand–atherosclerosis prevents dilation because unable to dilate because already dilated fully or cannot dilate
- inadequate perfusion – Ischemia –chest pain
Mnfts of angina pectoris
chest pain
Stable angina
lesion is a fixed plaque within wall
Stable angina is triggered by
- exertion (needs extra perfusion)
- cold (cold causes vasoconstriction, decrease size of lumen blood unable to move through causing ischemia and then angina
- stress (increase in HR, pumps more blood, unable to pump blood)
stable angina ______ at rest and
doesn’t present with pain at rest, but an increase in activity causes ischemic pain
stable angina is brief ____ chest pain
transient (not permanent)
stable angina is relived by
rest
variant angina also called
vasospastic or prinzmetals angina
variant/vasospastic/prinzmetals angina
- due to spasm of coronary artery
- nocturnal, at rest
- ECG changes during episode
variant/vasospastic/prinzmetals angina________ etiology
unclear etiology
- endothelial?
- Ca?
- Sympathetic nervous system?
- Nitric oxide?
suspected etiology for variant/vasospastic/prinzmetals angina
endothelial: drugs that might impact endothelial may cause vasospasm of vessel
Ca+: calcium enters muscle cells in order to contract –inappropriate Ca+ — causing vasospasm
Sympathetic nervous system: parts become hyperactive–triggers vasospasm
nitric oxide: (various fx in body 2 are: triggers vasodilation + acts as mediator for vs fx) May cause inappropriate trigger of vasodilation cause spasm
Unstable angina
- UNSTABLE PLAQUE
- thrombosis & agglutination of platelets
- if disrupted, will cause platelet aggregation (thrombosis)
- when platelets aggregate they degranulate
- prostoglandin (local hormone) release causing vessel spasm - platelets, plaque & prostaglandins restricting vessel (triple whammy)
- plaque collects platelets, fibrin, cellular debris
- the more angina experinced the greater the chance of having MI
mnfts of angina in general
- transient, mild to moderate chest pain
- squeezing, burning (heartburn/indigestion)–
- usually radiates to left shoulder & upper arm
treatment of angina in general
- cease activity (avoid trigger)
- nitro-glycerin (a vasodilator) causing systemic vasodilation
- prevention in order to decrease risk of MI
Degranulation
is a cellular process that releases antimicrobial cytotoxic or other molecules from secretory vesicles called granules found inside some cells. It is used by several different cells involved in the immune system, including granulocytes (neutrophils, basophils, and eosinophils) and mast cells
what is the pain like with unstable angina
severe, longer, at rest and nocturnal
