Atherosclerosis and Ischemic Heart Disease: Utline
Atherosclerosis and Ischemic Heart Disease: Utline
Atherosclerosis and Ischemic Heart Disease: Utline
B. MYOCARDIAL ISCHEMIA
• A reduction of coronary blood flow caused by fixed and/or
Figure 2. Ischemic Heart Disease. Atherosclerosis limits dynamic epicardial coronary artery (i.e. conductive vessel)
appropriate increase in the perfusion when the demand for flow stenosis, an abnormal constriction or deficient relaxation of
is augmented, e.g. exertion or excitement.
GUIDE QUESTIONS
1. A 65 year old male with coronary artery disease, post
coronary artery bypass grafting, was rushed to the ER
due to shortness of breath, easy fatigability, and pedal
edema for two days. BP was 100/60 mmHg and HR was
Figure 10. Angioplasty. Insert a catheter with a balloon in it 60 bpm. Auscultation of lungs revealed bilateral mid to
and if it is able to pass the atheroma then it is a way of bringing basal rales and wheezes. The following medications
in the balloon which will be used to dilate the artery. After may be given:
inserting the balloon you remove the endoplasmic catheter a. Captopril, Spironolactone, Furosemide
leaving behind an open artery. However, today we just do not b. B. Enalapril, Metoprolol succinate, Digoxin
leave an open artery after balloon dilatation since soon it will be c. Losartan, Carvedilol, Furosemide
thrombosed again since 1) the artery is already diseased and 2)
Answer Key:
1) A – Beta blockers are not needed for a patient
presenting with pulmonary edema secondary to
impending heart failure , you need following diuretics
to lessen the load of the heart.
2) C
3) C – Typical angina is typically described by exertional
pain that is relieved by nitroglycerin (NTG). Unstable
angina is pain at rest that is unrelieved by NTG.
Prinzmetal angina (also called variant angina) is pain
at rest that is relieved by NTG.
REFERENCES
1. Lecture Notes
2. Recording
3. 2016 Transcription
4. 2017 Transcription
5. Harrison’s Principle of Internal Medicine
APPENDIX
Figure 1. Formation of Atherosclerosis. ! 1) LDL is present in the arterial bloodstream 2) along with monocytes and cell adhesion
molecules. 3) The monocytes will phagocytize LDL, adhere to the endothelium then 4) enter the tunica media and intima layer of the
arteries. 5) There, the macrophages will be engulfed by the scavenger receptors, which 6) will trigger an inflammation cascade, 7)
forming foam cells, fibrosis and apoptosis.
Table 1. LDL cholesterol goals and culprits for therapeutic lifestyle changes (TLC) drug therapy in different risk categories.