Unit 4 - Coronary Artery Disease Flashcards
(51 cards)
what kind of exams are coronary angiograms?
anatomical tests, not physiological; can visualize lesion but not discover if pathological or not
what is angina VS acute MI?
angina: larger artery that is slowly occluding
acute MI: smaller and fast artery occlusion
in who does angina usually occur?
- most commonly in patients with CAD involving at least one epicardial artery
- patients with valvular heart disease, hypertrophic cardiomyopathy, and uncontrolled HTN
- may have normal coronary arteries secondary to spasm or endothelial dysfunction
describe the metabolic effects of ischemia
- anaerobic glycolysis takes over, but cannot maintain
- ATP and creatine phosphate levels call
- intracellular and extracellular acidosis develops
- extracellular levels of K+, lactate, PO4, and FA levels rise
what is the most important contributor to electrophysiologic changes of ischemia? what else follows this?
elevated extracellular K+
- due to increased cell membrane permeability to K+ during plateau phase of AP (leak outwards)
- lactate and phosphate follow K+ out
what causes the increased circulating FFA in ischemia?
sympathetic activation from MI
- liposomal phospholipase is activated to break down membrane phospholipids
- LCFA accumulate in intracellular space
what is the gradient between ischemic cells and normal cells?
“injury current”
- partial depolarization
- shortened AP
what is the diastolic injury current?
phase 4 intracellular positive current flows from less negative ischemic cells to more negative normal cells
what is the systolic injury current?
during phase 2/3, shortening of AP causes intracellular potential of ischemic cells to be more negative than normal cells
-this causes intracellular positive current to flow from normal to ischemic cells –> ST-depression
which injury current should one focus on?
the systolic current (more negative ischemic flows to less negative healthy)
-in subendocardial injury –> ST depression
what is a noninvasive diagnosis of ischemia if one can exercise?
stress test on treadmill for 6-12 minutes (Bruce protocol)
-valid if patient reaches 85% of max predicted HR (220 - age)
what does an EKG diagnosis of ischemia look like? what if it is abnormal?
if normal baseline ECG to compare
- positive will have at least 1 mm of horizontal/downsloping ST depression
- use imaging if abnormal –> echocardiograph to look at induced wall motion abnormalities
what is a noninvasive diagnosis of ischemia if one cannot exercise?
pharmacologic stress test
- dobutamine (stimulate B1 receptors to increase contractility and HR)
- adenosine/dipyridamole (coronary vasodilators to inhibit cellular uptake and degradation of adenosine)
- -stenotic arteries don’t respond to these
what is coronary steal? what causes this?
pharmacological perfusion mismatch when healthy coronary arteries are dilated but unhealthy ones are constricted
- drugs cause more O2 to healthy, less to unhealthy
- occurs if use antiplatelet or pharmacologic stress test adeosine and dipyridamole
what do electron beam CT sans do?
identify Ca++ in coronaries
- use Ca++ score to correlate probability of significant coronary disease
- variable results
- most useful in predicting absence of CAD
what are the 2 objectives of medical management of CAD?
- prevent MI and death (increase quantity of life)
2. reduce symptoms of angina and occurence of ischemia (increase quality of life)
what should the first intervention of CAD treatment be?
identify and treat risk factors for CVD:
- lipid abnormalities
- smoking
- diabetes
- HTN
what is the only time you don’t use aspirin?
when someone is allergic
ticlopidine
- what is it?
- mechanism?
- use in angina?
- ASE?
thienopyridine derivative that inhibits platelet aggregation by adenosine phsophate (blocks ADP receptors)
- reduces blood viscosity by decreasing plasma fibrinogen
- increases RBC deformity
- has NOT shown a decrease in adverse events in patients with stable angina
- induces neutropenia and rarely TTP (require WBC monitoring)
clopidogrel
- what is it?
- mechanism?
- ASE?
thienopyridine derivative that inhibits platelet aggregation by adenosine phsophate (blocks ADP receptors)
- more potent than ticlopidine or aspirin; moreso used after stent placement
- selectively and irreversibly inhibits binding of adenosine diphosphate to platelet receptors –> blocks adenosine diphosphate-dependent activation of glycoprotein IIb/IIIa complex
- increased bleeding risk, so must monitor
Prasugrel
- what is it?
- mechanism?
- ASE?
thienopyridine class that inhibits platelet aggregation by adenosine phsophate (blocks ADP receptors)
- irreversibly binds to P2Y12 receptor (GPCR chemoreceptor for ADP)
- used to decrease thrombotic events in people w/ stents placed
- while less MI, more bleeding risk, thus limited to patients less than 75 yo and greater than 60 kg, w/o history of stroke or TIA
Ticagrelor
- what is it?
- mechanism?
- ASE?
adenosine derivative
- blocks ADP receptors like thienopyridines, but at different site from ADP; thus reversible blocckade
- doesn’t need hepatic activation, so can be used in liver dysfunction
- has faster onset of action, and faster elimination, thus needs more doses (less compliance)
- greater rates of non-lethal bleeding
- doses of aspirin above 100 mg decrease effectiveness of ticagrelor
dipyridamole
- what is it?
- mechanism?
- ASE?
pyrimido-pyrimidine derivative
- increases intracellular platelet cAMP
- -inhibits phosphodiesterase
- -activates adenylate cyclase
- -inhibits uptake of adenosine from vascular endothelium and RBCs
- limited use b/c vasodilates coronary arteries to enhance exercise-induced ischemia
cilostazol
- what is it?
- mechanism?
- ASE?
quinolinone derivative that inhibits cellular phosphodiesterase
- causes increase in CAMP to inhibit platelet aggregation
- causes vasodilation –> increased morbidity and mortality in HF patients
- used primarily as treatment for calduication with peripheral vascular disease
