adventitia
UNSTABLE CORONARY ARTERY DISEASE
Thrombus forms a extends into the lumen and the plaq
thrombus
lipilidpicdocroere
adventitia
Atherothrombosis:
A Generalized and Progressive Process
②ST段抬高性心肌梗塞( STEMI )
如果斑块受损导致血栓完全闭塞冠脉, 则可导致STEMI；如血栓使冠脉不完 全闭塞，则导致UA或NSTEMI。
ACS with persistent ST-segment elevation
ACS without persistent ST-segment elevation
↓Extracellular Components
↑ ↑MMPs Expression
From Vulnerable plaque to Vulnerable patient
目前的研究，已由过去单纯重视局部（易损斑块，易损血液和易损 心肌）转为重视整体（易损病人）
AMI分为两大类
①非ST段抬高性心肌梗塞( NSTEMI )
Normal
Fatty streak
Fibrous plaque
Atherosclerotic plaque
Plaque rupture/ fissure & thrombosis
Unstable
} angina ACS
MI
Ischemic stroke/TIA
Clinically silent
Stable angina Intermittent claudication
急性心肌梗死治疗与进展
定义
急性心肌梗死是指在冠状动脉病变的基 础上,发生冠状动脉供血急剧减少或中断， 使相应的心肌严重而持久地急性缺血， 并导致心肌坏死。
AMI的发病机制
AMI的主要发病机制是在冠状动脉粥样 斑块破裂的基础上,发生急性血栓形成。 血管壁损伤,粥样斑块出现裂隙、糜烂、 溃疡或破裂，使内皮下组织暴露于血循 环，促使血小板与内皮下胶原、组织因 子及脂质等接触，并迅速被激活、破裂， 由此导致了凝血系统的启动，最终形成 血栓。
CK- MB or Troponin
Troponin elevated or not
AMI分类的演变
80年代以前 透壁/非透壁（心内膜下）
foam cells
lipid
6
Cytokines and growth factors produced by activated macrophages induce smooth muscle cell migration
into the intimal
Migrating smooth muscle cells change from
Critical leg ischemia
Cardiovascular death
Increasing age
ACS, acute coronary syndrome; TIA, transient ischemic attack
动脉粥样斑块破裂的危险因素
Local Factors
Cap Fatigue
inflammatory cells, predominantly monocyt
பைடு நூலகம்
lipid
EARLY ATHEROSCLEROSIS
Monocytes migrat into intimal,
differentiate into macrophages and ingest lipid to form
Impaired Fibrinolysis
Plaque Rupture
Fuster V, et al. N Engl J Med. 1992;326:310-318. Falk E, et al. Circulation. 1995:92:657-671.
动脉粥样血栓形成基质:破裂斑块
Adapted from Falk E, et al. Circulation. 1995;92:657-671.
EARLY ATHEROSCLEROSIS
3
Lipid accumulates in the intimal space and
is associated with abnormal endothelial
cell function
lipid
EARLY ATHEROSCLEROSIS
4
Activated endothelial cells express adhesion molecules and recruit
contractile to repair phenotype
8
STABLE ATHEROSCLEROTIC PLAQUE
endothelial cells
fibrous cap
(smooth muscle cells & matrix)
intimal smooth muscle c (repair phenotype)
Atheromatous Core (size/consistency)
Cap Thickness/ Consistency
Cap
Inflammation
Smoking
Systemic Factors
Cholesterol
Diabetes Mellitus
Fibrinogen
Homocysteine
lipid core
adventitia
medial smooth muscle cells (contractile phenotype)
UNSTABLE CORONARY
ARTERY DISEASE
Platelets aggregate at
site of rupture/erosion
lilpipiidd ccoorree
促使斑块破裂及血栓形成的诱因
6Am～12Am 交感活性增加时 饱餐 重体力活动,情绪激动或用力大便时 休克、脱水、出血等 AMI可发生在无心绞痛病史的患者
NORMAL ARTERY WALL
Endothelial cells
Contractile vascular smooth muscle cells