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

(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.

(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

Occlusion CA Infarction zone

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

Normal CA Mild coronary AS severe Calcification of CA

Thrombus of CA LM Thrombus of CA EYE

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

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

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)

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

（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)

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

(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

Subendocardial myocardial infarction

(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

Transmural myocardial infarction LV posterior wall infarction

The progression of myocardial necrosis

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

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

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

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

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

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

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

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

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

③ Ventricular aneurysm： from a large transmural anteroseptal infarct

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

Mural thrombosis

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

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

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