1. Coronary atherosclerosis and coronary heart disease
Lesson 3
Coronary atherosclerosis and coronary heart disease

2. (Ⅰ) Coronary atherosclerosis
Coronary AS is narrowing of the lumina of the coronary artery and accounts for the vast majority of coronary artery disease, and is most marked in the proximal parts of the coronary arteries.

3. (Ⅰ) Coronary atherosclerosis
1. Distribution ：
①Left >right，large branch>small branch，
proximal segment > distant segment
② Left anterior descending coronary A
>right CA>left CA>left circumflex CA

4. Occlusion CA
Infarction zone

5. 2. Features：cutface crescent plaque of myocardial side， stenosis
4 grades Ⅰ < 25% Ⅱ 26-50%
Ⅲ 51-75% Ⅳ >76%

6. Normal CA
Mild coronary AS
severe Calcification of CA

8. Thrombus of CA LM
Thrombus of CA EYE

9. (Ⅱ)Coronary heart disease (CHD)
CHD： ischemic heart disease(IHD)
a group of closely related syndromes
resulting from myocardial ischemia

10. Etiology and pathogenesis：
① Insufficient blood supply: AS, spasm
② Increase in cardiac energy demand:
BP↑↑，overworked，excite
→work load of heart↑
An imbalance between the perfusion and demand of the heart for oxygenated blood

11. cardiac oxygen demand↑↑ 1. Angina pectoris
Acute , temporarily, comparatively coronary A blood supply
cardiac oxygen
demand↑↑
A symptom complex of IHD characterized by paroxysmal and usually attacks of substernal or precordial chest discomfort (constricting, squeezing, chocking or knifelike)

12. Clinical types :
(1) Stable or typical angina：
relived by rest or nitroglycerin,
stenosis of coronary AS >75%
(2) Prinzmetal or variant angina:
episodic angina, occure at rest
due to coronary vasospasm
ECG：S-T elevated

13. （3）Unstable angina： occure with progressively increasing
frequency tend to be of more prolonged duration induced by rupture of AS plaque with superimposed partial thrombosis and embolization or vasospasm (preinfarction angina)

14. 2. Myocardial infarction，(MI)
Concept：acute ischemic necrosis due
to severe sustained ischemia
Types：95% LV, trnasmural or
subendocardial infarction

15. (1) Subendocardial myocardial infarction
① Concept：an area of ischemic necrosis limited
to the inner 1/3 and involve papillary muscle,
trabeculae carnae
② Lesion：multi different in size focal necrosis
③ Circumferential infarction:
entire LV endocardium

16. Subendocardial myocardial infarction

17. (2) Transmural myocardial infarction
① The ischemic necrosis involves the full or
nearly full thickness of the ventricular
wall in the distribution of a single
coronary artery.
>2/3→thick layer infarct

18. Transmural myocardial infarction
LV posterior wall infarction

19. The progression of myocardial necrosis

20. ② Favorite sites： LAD 40-50% RCA 30-40% LCX 15-20%
Anterior wall of LV near
apex,anterior portion of
ventricular septrm, apex
circumferentially
RCA 30-40%
Inferior-posterior wall of LV, posteriole portion of ventricular septum, inferior-posterior RV free wall
LCX 15-20%
Lateral wall of LV except at apex

21. Lesion：
anemic infarct，yellow or gray-red，dry
irregular
2hr LM
change
6hr naked eye

22. Gross ½-4hr None 4-12hr Occasionally dark motting 12-24hr Dark motting
Motting with yellow-tan infarct center
3-7d
Hyperemic border, center yellow-tan softing
7-10d
Maximally yellow-tan and soft with depressed red-tan margins
10-14d
Red-gray depressed infarct borders
2-8w
Gray-white scar, progressive from border to core of infarct
>2m
Scarring complete

23. LM ½-4hr Variable waviness of fibers at border 4-12hr
Beginning coagulation necrosis,edema,hemorrhage
12-24hr
Ongoing coagulation necrosis,myocyte hypereosinophilia, marginal contraction band necrosis
1-3d
Coagulation necrosis,with loss of nuclei and striation,interstitial infiltrate of neutrophils
3-7d
Beginning disintegratin of dead myofibers,early phagocytosis
7-10d
Well-developed phagocytosis of dead cells,early formation of fibrovascular granulation at margin
10-14d
Well-estabished granulation and collagen deposition
2-8w
Increased collagen deposition
>2m
Dense collagenous scar LM

24. Coagulative necrosis of myocardial, outline the organizational structure can still be saved
After 48hr, nuclears disappear, many inflamatory cells infiltrate the space between myocardial

25. After 7d, nucleus is almost completely disappeared, granulation tissue proliferates

26. Lab：
CPK↑
AST ↑
LDH↑
GPT↑
GOP↑
Infarction of LAD

27. Complication ① Papillary muscle dysfunction or rupture：
② Myocardial rupture：
◆acute,severe，1-3days or 1week（within 2weeks）

28. Favorite site
Results
Ventricular free wall
Hemopericardium and cardiac tamponade
Ventricular septum
Left-to-right shunt
Papillary muscle
Severe mitral regurgitation

29. ③ Ventricular aneurysm：
from a large transmural anteroseptal infarct

30. ④ Mural thrombosis：
⑤ Post-myocardial infarct syndrome
Acute pericarditis：
acute fibrinous inflammation
Acute left heart failure
Cardiogenic shock: >40%→output↓
Arrhythmias: conduction disturbance

31. Mural thrombosis

32. 3. Myocardial fibrosis (1) Cause：moderate-severe stenosis
of the coronary A. or total occlusion
(2) Gross：LV hypertrophy and dilation,
discrete, gray-white scars
(3) LM : Diffuse myocardial fibrosis
myocardial hypertrophy or atrophy
(4) Clinical features：heart failure

33. Van Gieson stain
Fibrosis(red) , myocardium (yellow)

34. 4. Sudden coronary death (1) Risk factors： alcohol , strain , smoking
athlete, some at nigh
(2) Lesion：
major vessel severe stenosis