Ischemic Heart Disease Lecture

Question 1

Myocardial ischemia is due to what

Answer 1

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

Question 2

what are the consequences of atherosclerosis and what diffuse organs are affected

Answer 2

Cardiac–> coronary arteries, aorta

Neurologic–> CVA, TIA, Stroke

Renal–> renal artery stenosis

Peripheral vascular–> claudication, limb ischemia

Question 3

list the stages of the atherosclerosis timeline

Answer 3

foam cells–> fatty streak–> intermediate lesion–> atheroma–>complicated lesion/rupture–>fibrous plaque

Question 4

what are the risk factors for CVD

Answer 4

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

Question 5

what are the markers that used for CVD

Answer 5

Elevated hsCRP and urine microalbumin

Question 6

what are the clinical presentations of Cardiovascular disease

Answer 6

Silent

Stable anina

Unstable angina

Myocardial Infarction

Sudden death

Question 7

Stable Angina

Answer 7

• 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

Question 8

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

Answer 8

stable angina

Question 9

what are some of the clinical presentation of stable angina

Answer 9

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

Question 10

what is the therapy for stable angina?

Answer 10

• 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

Question 11

what are the categories for acute coronary syndrome

Answer 11

unstable angina

non st elevation mi

st elevation mi

Question 12

what is the presenation of acute coronary syndrome

Answer 12

rapidly worsening angina

minimal exertion or rest

increased intensity and duration

Question 13

acute coronary syndrome pathogenesis

Answer 13

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

Question 14

flow in unstable vs ST eveleation MI vs Non ST elevation MI

Answer 14

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

Question 15

unstable angina findings and cardiac enzymes

Answer 15

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)

Question 16

NSTEMI vs STEMI

Answer 16

NSTEMI: same EKG as unstable

STEMI: ST elevation or LBBB

NSTEMI and STEMI both have positive Troponins and CK-MB and infarction

Question 17

what would be the acute management of anginas?

Answer 17

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

Question 18

what are some secondary preventions?

Answer 18

Aspirin

Statins to stablize the blacks

Ace inhibitor

Smoking cessation

Beta blockers-not long term

Question 19

Peripheral Arterial Disease

Answer 19

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

Question 20

The first 2-3 hours after a myocardial infarction?

Answer 20

you have dehydrogenase stained in infarcted regions of the heart

Question 21

Microscopic changes after 4-12 hrs

Answer 21

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

Question 22

12-24 hours following a myocardial infarction

Answer 22

hemorrhaging, coagulative necrosis(no nuclei), and edema in between cells, and eosinophilia

Question 23

1-3 days after infarction

Answer 23

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.

Question 24

1-2 weeks after an infarction

Answer 24

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.

Question 25

2 weeks – 2 months

Answer 25

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.

Question 26

myocardial rupture

Answer 26

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