Ischemic Heart Disease Flashcards
How does atherosclerosis progress?
- usually asymptomatic
- how lumen narrows: low density lipoproteins (cholesterol) go into sub endothelial layer and are phagocytoses by monocytes which then rupture causing more LDL and more monocytes and foam cells -> more plaque
- often impedes blood flow -> ischemia typically in people above 40 and are often chronic and intermittent (worse with exertion of target organ)
- lumen keeps narrowing until there is an injury to the blood vessel so blood cells react to it as an injury so hate2felo b thrombus , said thrombus blocks the rest of the lumen
Leading to ischemic and possibly infarction
If this happens in the coronary artery then it will lead to angina on exertion or if it happens in superficial femoral artery leads to calf pain specifically intermittent claudication (cramping pain) on exertion
What is angina pectoris?
Pain due to myocardial ischemia, tightness or heaviness of the chest radiating to the jaw (shabah irreversible pulpitis) and left arm and may cause epigastric pain
Exertional chest pain that goes away with rest
Spectrum of IHD?
Acute coronary syndromes:
1. Stable angina ( have triggers such as stress)
2. Unstable angina ( more serious , may not have a trigger more unpredictable , may not go away after rest)
3. Myocardial infarction , shabah unstable angina but here law 3amal ecg hayban eno heart attack
Comparison between angina and myocardial infarction
- Site: both the same , chest , left arm , jaw , epigastrum
- Trigger; angina has a trigger such as emotion while myocardial infarction has no obvious trigger
- Angina is relieved by sublingual nitrates while MI is not
- Mild severity , MI is severe
- Anxiety in angina is absent or mild while in MI severe
- No nausea or vomiting while it is common in MI
- Sympathetic activity; increased only in MI
Who’s at risk of IHD?
- males ( females protected by oestrogen and progesterone)
- increased age
- predisposing factors : hypertension, diabetes, obesity, genetics , family history
How to investigate IHD?
- symptoms + ECG can tell if there’s ischemia or myocardial infarction
- Cardiac enzymes; only elevated in a myocardial infarction, CK - MB bas it takes up to 6-8 hours to enter blood stream so I ace of emergency test for troponin because it is rapidly released into circulation within 1 hours of infarction.
( if there’s chest pain but enzymes are normal then it is ischemia) - Echo and cardiac catherization: both diagnostic and therapeutic emergency and elective. Can identify site, severity of vascular occlusion and state of collaterals
- Stress ECG , if ECG is normal at rest but there is chest pain, hatdakhalo f stress 3ashan yeban reason el Exertional chest pain. ( important law had dashed ya3mel operation and you don’t know if they have IHD or not.
- Stress echo , same fekra but instead of ecg probes hanhot electrodes
- Isotopic scanning , radionuclide myocardial perfusion imaging ( rMPI) beteh2en radio isotope w betersem el blood so that you can tell wher the reduced blood flow is
- Catherization: hateh2en sabgha in radial or femoral artery w ya3mel ask mapping l kol el circulation so that you can see , site , severity, f kam artery
Treatment of IHD?
- Urgent: sublingual nitrates for immediate relief ( only feel ischemia not myocardial infarction)
Fel MI give aspirin daily to stop propagation of platelets so that the thrombus mayehsaloosh progression, aspirin 75 - 162 mg - Medical treatment,
A) control risk factors ( diabetes, hypertension , dyslipidimia)
B) lipid lowering drugs/ statins
C) anti platelets eg aspirin
Other…
Ultimate treatment: catheterization/ revascularization, with balloon to cause dilation and to prevent collapse then insert stent
If stent fails (maybe be due to excessive atheroscelrosis or diabetic weak blood vessels) only solution would be,
Coronary artery bypass grafting (CABG) ha2os artery wageeb graft men vein or replace el artery khales
