Ischemic Heart Disease Flashcards
low density lipoproteins
bad cholesterol, atherogenic, carries lipids from liver to tissues
high density lipoproteins
good cholesterol, carries excess lipids to the liver for elimination
triglycerides
type of fat transported in bloodstream and stored in fat, some association with risk of cv disease
manifestations of atherosclerosis
ischemic stroke, coronary artery disease, carotid artery stenosis (stroke), renal artery stenosis, peripheral artery disease (PAD)
smoking effect on atherosclerosis
reduces hdl, impacts cholesterol retrieval, increases oxidation of lipoproteins, cytotoxic effects to endothelium, increases thrombogenesis
diabetes effect on atherosclerosis
major source of oxidative stress
htn effect on atherosclerosis
increases atherosclerotic cv disease
non-modifiable atherosclerotic risk factors
male >45, female >55
family history of CAD event: male> 55, female<65
history of family ischemic stroke or MI –> increased risk due to genetics
modifiable atherosclerotic risks
smoking (primary), htn dyslipidemia, diabetes, obesity, physical inactivity
ischemia
inadequate blood supply to an organ or tissue that leads to tissue damage and necrosis
arterial response to ischemia
arterial vasodilation to increase oxygen delivery
coronary arteries
starts just above the aortic root and supplies blood and oxygen to the myocardium
cardiac chest pain (angina)
described as a heavy weight or pressure on chest (not sharp pains) in substernal area (rarely radiates)
can be worsened by exercise, cold weather, postprandial and emotional stress
typical angina
occurs with characteristic quality, location, and duration, provoked by exertion or emotional stressm relieved by nitroglycerin or rest
atypical angina
meets only 2 or 3 typical angina criteria
women, older adults and individuals with diabetes may present with different symptoms including: anxiety, sob, weakness, fatigue, and indigestion, this often leads to misdiagnosis
non-cardiac chest pain
meets one or no criteria for typical angina
ischemic heart disease can be presented as
acute coronary symptoms (ACS) or chronic coronary disease (CCD)
chronic coronary disease (CCD) can present as
stable angina, patients discharged after ACS, patients diagnosed with CCD based on screening
acute coronary symptoms (ACS) presents as
ubstable angina, non-ST MI (NSTEM), ST MI (STEMI)
stable angina
chronic angina precipitated by activity or upset, relieved at rest
atherosclerotic plaque is reducing blood flow, there is no plaque rupture/hemostasis
discharged after ACS
patients are considered to have CCD after they are discharged for an ACS event
CCD diagnosed after screening
patients may have risk factors of or symptoms consistent with CCD for which a screening test is completed and CCD is identified
unstable angina
increased frequency or duration of angina episodes produced at a lower level of exertion or at rest
acute change in level of what is causing patient to have chest pain
non-ST elevation MI (NSTEMI)
myocardial necrosis resulting from prolonged interruption of the blood supply, generally results in acute thrombosis, but no ECG changes
partial occlusion
atherosclerotic plaque ruptures leading to primary and secondary hemostasis
ST elevation MI (STEMI)
myocardial necrosis resulting from prolonged interruption of the blood supply generally results from an acute thrombus with ECG changes
complete occlusion
atherosclerotic plaque ruptures leading to primary and secondary hemostasis
diagnosed with positive troponins and a 1 mm elevation in at least 2 contiguous leads on ECG
primary hemostasis
first step in plaque rupture- more relevant for arterial clots
forms a platelet plug in 3 steps
1. adhesion
2. activation
3. aggregation
first line of hemostatic defense, begins in seconds of vessel injury and is mediated by circulating agents
secondary hemostasis
main driver of venous clots.
forms fibrin clots through clotting cascade
plasma coagulation cascade initiated by exposure of tissue factor from the vascular injury –> thrombin activation –> clot stabilizes and strengthens the platelet plug
primary hemostasis adherence
adhere to collagen in the vascular sub endothelium, exposed collagen releases von Willebrand factor
primary hemostasis activation
releases adp, ca, and thomboxane a2 to activate further platelets, GP IIb/IIIa receptors are exposed to platelets
primary hemostasis activation
platelets aggregate through GP IIb/IIIa fibrinogen to form a platelet plug
clotting cascade
surface activation –> XIIa __> XIa –> IXa –> factor XA –> converts prothrombin to thrombin –> converts fibrinogen to fibrin
vascular injury –> VIIa –> factor XA –> prothrombin to thrombin –> fibrinogen to fibrin
left coronary artery
supplies left ventricle (major heart attack if occluded)
right coronary artery
supplies the right side of the heart
circumflex artery
supplies back side of left heart (minor heart attack if occluded)
presence of cardiac enzymes in ACS
UA: no cardiac enzymes
NSTEMI: cardiac enzymes
STEMI: cardiac enzymes
ECG ST elevation in ACS
UA: no st elevation
NSTEMI: no st elevation
STEMI: st elevation
troponin
primary biomarker for ACS- takes 6 hrs to show up
ST elevation on ECG
only present in STEMI (complete occlusion), take about 5 minutes to show up- needs to be tested in that window
functional CAD testing
exercise stress tests, pharmacologic stress test
anatomical CAD testing
coronary artery angiography, coronary artery ca scoring
stress test
often initial recommended test, can be done with pharmacologic agents if patient is unable to exercise –> sent to angiogram if abnormal results
coronary artery CT scqn
looking for calcification of the coronary arteries – abnormal results? –> coronary angiogram
coronary artery calcium testing
used in asymptomatic patients, uses ct scan- no dye, calculates mass of Ca, score per age
Peripheral artery disease
atherosclerosis that occurs in periphery, usually in lower extremities, can lead to pain on exertion, tissue damage, ulcers, and infection
most common in aortoiliac, femoral, popliteal, and tibeal
intermittent claudication
Presentation of PAD pain when walking in the buttocks, thighs or calves, often relieved with rest, severe cases will have pain at rest
chronic limb threatening disease
Presentation of PAD chronic decreased flow that can lead to ulcerations, gangrene, infections
patients with diabetes and smokers are at the highest risk
acute limb threatening disease
presentation of PAD medical emergency, requires immediate revascularization to prevent limb loss
Normal ABI levels
1-1.4 - no PAD
