Ischemic Heart Disease Lecture Flashcards
Myocardial ischemia is due to what
due to atherosclerosis which is a progressive inflammatory disease of the arterial walls
this process of inflammation and healing leads to deposition of extracellular matrix and proliferation of smooth muscle–> fibermuscular cap
in myocardial ischemia atherosclerosis of the coronary arteries decreases blood flow to the myocardium
the risk of IHD is similar to atherosclerosis and its incidence increases with age
what are the consequences of atherosclerosis and what diffuse organs are affected
Cardiac–> coronary arteries, aorta
Neurologic–> CVA, TIA, Stroke
Renal–> renal artery stenosis
Peripheral vascular–> claudication, limb ischemia
list the stages of the atherosclerosis timeline
foam cells–> fatty streak–> intermediate lesion–> atheroma–>complicated lesion/rupture–>fibrous plaque
what are the risk factors for CVD
Age-most powerful independent: greater than 55 for men and greater than 65 for women
Family history: premature CVD/hypertension, hyperlipid, diabetes–>genetic
Hypertension
Smoking- dose dependent
Hyperlipidemia–> LDL high and low HDL and High triglycerides
Diabetes –> CAD equivalent
what are the markers that used for CVD
Elevated hsCRP and urine microalbumin
what are the clinical presentations of Cardiovascular disease
Silent
Stable anina
Unstable angina
Myocardial Infarction
Sudden death
Stable Angina
- Chest pain that arises with exertion or emotional stress (slow reduction of luminal diameter and slow progressive symptoms)
- Pain radiates to the left arm or lower jaw(not upper jaw)
- this is reversible injury to myocytes; must last beyond 20 minutes to have irreversible damage
- athersclerosis must produce a stenosis greater than 70%
- dereased blood flow is not able to meet the metabolic demands of the myocardium during exertion.
- ST segment on EKG is depressed due to subendocardial ischemia.
- relieve occurs after rest or nitroglycerin
72 yr old gentlemen with history of Diabetes Mellitus, Hypertension, hypercholesteremia complains of chest pains climbing 1/2 of stairs over the past few days
stable angina
what are some of the clinical presentation of stable angina
upon exertion you get chest pains, heaviness, squeezing
Pain radiates to the left arm, lower jaw and neck
patient will have dsypnea/shortness of breath, diaphoresis, nausea/vomiting
what is the therapy for stable angina?
- fix coronary flow with a stent
- risk factor modification
- aspirin
- nitrates for systemic vasodilation and coronary vasodilation
- beta and alpha blockers
- ranolazine like nitrate can vasodilate by inhibing late sodium channel
what are the categories for acute coronary syndrome
unstable angina
non st elevation mi
st elevation mi
what is the presenation of acute coronary syndrome
rapidly worsening angina
minimal exertion or rest
increased intensity and duration
acute coronary syndrome pathogenesis
Unstable plaque–>fibrous cap compromised–>Lipid core exposed–>cascade–>Thrombosis and Thrombolysis
stable plaque abruptly converts to unstable atherothrombotic lesion
rupture, erosion, ulceration, fissuring, hemorrhage
flow in unstable vs ST eveleation MI vs Non ST elevation MI
everything depends on how stable the clot is. There is still flow in Unstable angina, there is complete obstruction in ST eleveation MI, and Non ST elevation is somewhere in between
unstable angina findings and cardiac enzymes
Ischemia but no infarction
EKG has a deep t wave inversion, ST depression, or normal
cardiac enzymes- biochemical markers infarct the tissue they should be negative in this case(CK-MB and troponins)
NSTEMI vs STEMI
NSTEMI: same EKG as unstable
STEMI: ST elevation or LBBB
NSTEMI and STEMI both have positive Troponins and CK-MB and infarction
what would be the acute management of anginas?
imediate: EKG and cardiac enzymes and aspirin to chew plus oxygen
Medications: Anticoagulants(heparin), +/- oral B blockers- Tx myocardial demand, ventricular arrythmias, and ace inhibitors- in the setting of LV dysfunction(prevents negative remodeling)
Reperfusion: Dual Antiplatelet measures- 1)Aspirin 2)clopidogrel(because you are putting metal inside the body) 3) More antiplatelets 4)Thrombolytics- i.e fibrinolytics (STEMI) 5)Mechanical-coronary intervention/CABG(coronary bypass grafting) sometimes there are too many occlusions
what are some secondary preventions?
Aspirin
Statins to stablize the blacks
Ace inhibitor
Smoking cessation
Beta blockers-not long term
Peripheral Arterial Disease
intermittent claudication
burning sensation in leg after exertion
therapy: walking program and statin
this is due to cholesterol filled plaques
critical limb ischemia
diabetic vascular disease
The first 2-3 hours after a myocardial infarction?
you have dehydrogenase stained in infarcted regions of the heart
Microscopic changes after 4-12 hrs
you will see contraction bands, myocytolysis, wavy fibers
contraction bands occurs due to the abnormality of the ischemic cardiac muscle to contract
Myocytolysis- is leaking and swelling in the middle
Early coagulative necrosis, hemorrhage, edema
12-24 hours following a myocardial infarction
hemorrhaging, coagulative necrosis(no nuclei), and edema in between cells, and eosinophilia
1-3 days after infarction
the infarcted area begins to turn soft and yellow due to the influx of neutrophils. Coagulative necrosis continues. Nuclei and striations disappear. The bottom right shows the massive amounts of neutrophils that have entered the infarct. This time period represents the maximum inflammation post-infarct.
1-2 weeks after an infarction
we begin to see a depressed red/tan/grey border surrounding the yellow/tan inner part of the infarct. The border comes from the ingrowth of new vessels from the outside forming granulation tissue.
2 weeks – 2 months
after an MI, gray/white scarring forms. It progresses from the border to the center of the infarct. The top left shows an example of an older white collagenous scar.
myocardial rupture
rupture is also a possible complication of MI. 3-7 days post-MI, the infarct is in its soft yellow phase. If this soft heart muscle ruptures, blood will poor out of the heart and cause rapidly fatal hemopericardium and cardiac tamponade! Risk factors include being female, over 60 y/o, or having hypertension. The antero-lateral wall is the most common site! If an MI occurs in the ventricular septum, rupture here will lead to VSD, causing a left-to-right shunt
