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Heart
Pathology Department,
Zhejiang University School of Medicine,
Zhu keqing 竺可青，
[email protected],
2011-5-9
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Atherosclerosis
Coronary atherosclerosis/CHD
Hypertension
Aneurysm
Rheumatism
Infective endocarditis
Chronic valvular vitium of the heart
Cardiomyopathy
Myocarditis
Pericarditis
Congenital heart disease
Five categories of disease account for nearly all cardiac mortality
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Congenital heart disease
Ischemic heart disease
Hypertensive heart disease (systemic and pulmonary)
Valvular heart disease
Nonischemic (primary) myocardial disease
Left ventricular hypertrophy
Schematic representation of the sequence of events in
cardiac hypertrophy and its progression to heart failure
1. Atherosclerosis,AS
• Arteriosclerosis动脉硬化:
• Arteriolosclerosis 细动脉硬化
• Atherosclerosis(AS)
• Medical calcification 动脉中层钙化
• 动脉硬化
• 指一组动脉壁增厚、变硬、弹性降低的疾病。包括动脉粥样硬化、动
脉中膜钙化、细动脉硬化等。
• 动脉粥样硬化
• 指动脉内膜由于脂质沉积、胶原纤维和平滑肌增生、伴有坏死和钙化，
引起动脉壁增厚变硬的疾病。主要侵犯大、中动脉
Risk factors for As
4高
• Hyperlipidemia
• Hypertension
• Smoking
• DM(Diabetes mellitus)
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Heritage
Age
Sex-Male
Lack of physical exercise
Obesity
Stress
Hyperlipidemia
BAD
• LDL/LDL-C
• sLDL—CHD
• VLDL/CM乳糜微粒
GOOD
HDL/HDL-C抗AS/CHD
• AS性脂蛋白表型—LDL(sLDL)\TG\VLDL\apoB异常升高与
HDL-C/apoA-I降低
The vascular wall
Endothelial cell response to environmental stimuli:
causes (activators) and consequences (induced genes).
Schematic diagram of the mechanism of intimal thickening, emphasizing smooth muscle
cell migration to, and proliferation and extracellular matrix elaboration in, the intima.
Evolution of
arterial wall
changes in the
response to injury
hypothesis
Schematic diagram of hypothetical sequence of
cellular interactions in atherosclerosis
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The response to injury hypothesis（损伤应答学说）, considers atherosclerosis to be
a chronic inflammatory response of the arterial wall initiated by injury to the
endothelium.
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Moreover, lesion progression is sustained by interaction between modified
lipoproteins（脂源性学说）, monocyte-derived macrophages, T lymphocytes, and the
normal cellular constituents of the arterial wall.
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脂质代谢障碍
高脂血症→脂蛋白（尤其β脂蛋白）↑→进入动脉内膜下沉积。
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动脉内膜损伤
内膜通透性增高→脂蛋白进入增多
内膜损伤因素：
1．高血压
2．吸烟
3．血管活性物质
Hypothetical sequence of cellular interactions in atherosclerosis
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Chronic endothelial injury内皮细胞损伤, usually subtle, with
resultant endothelial dysfunction, yielding increased
permeability, leukocyte adhesion, and thrombotic potential
Accumulation of lipoproteins, mainly LDL, with its high
cholesterol content, in the vessel wall 血脂异常
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Modification of lesional lipoproteins by oxidation 脂蛋白氧化修
饰ox-LDL
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Adhesion of blood monocytes (and other leukocytes) to the
endothelium, followed by their migration into the intima and
their transformation into macrophages and foam cells 泡沫细
胞
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Adhesion of platelets血小板黏附
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Release of factors from activated platelets, macrophages, or
vascular cells that cause migration of SMCs 平滑肌细胞迁徙
from media into the intima
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Proliferation of smooth muscle cells in the intima, and
elaboration of extracellular matrix, leading to the accumulation
of collagen and proteoglycans
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Enhanced accumulation of lipids both within cells
(macrophages and SMCs) and extracellularly.
Morphology
脂纹脂斑期
肉眼：黄色斑点（帽针大）、
黄色条纹。
镜检：泡沫细胞（单核细胞型、
平滑肌细胞型）
纤维斑块期
肉眼：内膜表面灰黄色→瓷白
色隆起斑块。
镜检：表层纤维帽、其下有平
滑肌细胞、巨噬细胞、泡沫细胞
和细胞外脂质（胆固醇）。
粥样斑块期
肉眼：表面斑块黄色或灰黄色，
切面深层有粥糜样黄色物。
镜检：表层纤维帽；深层无定
形坏死物，内有大量胆固醇；底
部和边缘肉芽组织和少量泡沫细
胞。
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The key processes in atherosclerosis
are intimal thickening and lipid
accumulation.
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Fatty streak:foam cells 脂纹期---泡沫细
胞
Fibrous plaque: fibrous cap 纤维斑块
（纤维帽）
Atheromatous plaque/atheroma 粥样
斑块（粥瘤）
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An atheroma粥瘤
consists of a raised focal lesion
initiating within the intima, having a
soft, yellow, grumous core of lipid
(mainly cholesterol and cholesterol
esters)胆固醇结晶, covered by a firm,
white fibrous cap纤维帽.
American Heart Association classification of human atherosclerotic
lesions from the fatty dot (type I) to the complicated type VI lesion
Fatty streak-a collection of foam cells in the intima
Schematic depiction of the major components of well-developed
intimal atheromatous plaque overlying an intact media.
Gross views of atherosclerosis in the aorta
• In the characteristic distribution of atherosclerotic plaques in
humans the abdominal aorta 腹主动脉瘤is usually much more
involved than the thoracic aorta,
• and lesions tend to be much more prominent around the
origins (ostia) of major branches.
Atherosclerotic plaques have three principal components:
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(1) cells, including SMCs, macrophages, and other leukocytes;
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(2) ECM, including collagen, elastic fibers, and proteoglycans;
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(3) intracellular and extracellular lipid.
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These components occur in varying proportions and configurations in
different lesions.
The advanced lesion并发症 of atherosclerosis:
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斑块破裂 Focal rupture, ulceration, or erosion of the luminal surface of
atheromatous plaques may result in exposure of highly thrombogenic substances that
induce thrombus formation or discharge of debris into the bloodstream, producing
microemboli composed of lesion contents (cholesterol emboli or atheroemboli).
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斑块内出血 Hemorrhage into a plaque, especially in the coronary arteries, may be
initiated by rupture of either the overlying fibrous cap or the thin-walled capillaries that
vascularize the plaque. A contained hematoma may expand the plaque or induce
plaque rupture.
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血栓形成 Superimposed thrombosis, the most feared complication, usually occurs
on disrupted lesions (those with rupture, ulceration, erosion, or hemorrhage) and may
partially or completely occlude the lumen.
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动脉瘤 Aneurysmal dilation may result from ATH-induced atrophy of the underlying
media, with loss of elastic tissue, causing weakness and potential rupture.
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血管腔狭窄
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钙化
View of the base of the brain, dissected to show the circle of Willis
with an aneurysm of the anterior cerebral artery
Dissected circle of Willis to show large aneurysm
Common sites of saccular (berry) aneurysms in the circle of Willis
Role of Acute Plaque Change.
In most patients the myocardial ischemia underlying unstable angina, acute MI, and (in
many cases) sudden cardiac death is precipitated by abrupt plaque change followed by
thrombosis
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Rupture/fissuring, exposing the
highly thrombogenic plaque
constituents.
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Erosion/ulceration, exposing the
thrombogenic subendothelial
basement membrane to blood.
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Hemorrhage into the atheroma,
expanding its volume.
2 Coronary artherosclerosis(CAS)
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凡因冠状动脉狭窄造成心肌供血不足引起的心脏病，简称冠心病。以冠状动
脉粥样硬化为最多见。
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冠状动脉病CAD
95%-99%CAS CAS=CAD CHD=IHD
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其余冠状动脉炎性疾病及畸形（风湿性/梅毒性主动脉炎）
Histologic features of atheromatous plaque in the coronary artery
A, Plaque rupture without superimposed thrombus, in patient who died suddenly.
B, Acute coronary thrombosis superimposed on an atherosclerotic plaque with focal disruption
of the fibrous cap, triggering fatal myocardial infarction.
•C, Massive plaque rupture with superimposed thrombus, also triggering a fatal myocardial
infarction (special stain highlighting fibrin in red).
In both A and B, an arrow points to the site of plaque rupture.
Estimated 10-year risk of coronary artery disease according to various
combinations of risk factor levels
The clinical manifestations of IHD can be divided into four syndromes:
1 Myocardial infarction (MI),
the most important form of IHD, in which the duration and severity of ischemia is sufficient to cause
death of heart muscle.
2 Angina pectoris,
in which the ischemia is less severe and does not cause death of cardiac muscle. Of the three
variants--stable angina,
Prinzmetal angina,
unstable angina-the latter is the most threatening as a frequent harbinger预兆 of MI.
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Chronic IHD with heart failure.
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Sudden cardiac death.
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冠心病的临床病理类型
（1）心绞痛
冠状动脉供血相对不足，发生急性暂时性心肌缺血缺氧的临床综合征。
（2）心肌梗死
冠状动脉供血绝对性不足，心肌持续性缺血缺氧，导致较大范围的心肌坏死。
发生原因：
⑴冠状动脉粥样硬化合并血栓形成或斑块内出血。
⑵冠状动脉痉挛。
⑶在冠状动脉粥样硬化的基础上，由于过度负荷，造成心肌供血不足
Pathogenesis
• The dominant influence in the causation of the IHD syndromes is
diminished coronary perfusion relative to myocardial demand,
• owing largely to a complex and dynamic interaction among:
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fixed atherosclerotic narrowing of the epicardial coronary arteries,
intraluminal thrombosis overlying a disrupted atherosclerotic plaque,
platelet aggregation,
and vasospasm.
Atherosclerotic plaque rupture.
A, Plaque rupture without superimposed thrombus, in patient who died
suddenly.
B, Acute coronary thrombosis superimposed on an atherosclerotic plaque with
focal disruption of the fibrous cap, triggering fatal myocardial infarction.
C, Massive plaque rupture with superimposed thrombus, also triggering a fatal
myocardial infarction (special stain highlighting fibrin in red).
Schematic representation of sequential progression of coronary artery lesion morphology, beginning with
stable chronic plaque responsible for typical angina and leading to the various acute coronary syndromes
Coronary Artery Pathology in Ischemic Heart Disease
Syndrome
Stenoses
Plaque Disruption
Stable angina
Unstable angina
>75%
Variable
No
Frequent
Plaque-Associated Thrombus
No
Nonocclusive, often with thromboemboli
Transmural myocardial infarction
Subendocardial myocardial infarction
Frequent
Variable
Occlusive
Widely variable, may be absent, partial/complete, or lysed
Sudden death
Frequent
small platelet aggregates / thrombi / thromboemboli
Usually severe
Angina pectoris
• A symptom complex of IHD characterized by
paroxysmal and usually recurrent attacks of substernal or precordial
chest discomfort (variously described as constricting, squeezing,
choking, or knifelike) caused by transient (15 seconds to 15 minutes)
myocardial ischemia that falls short of inducing the cellular necrosis
that defines infarction.
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There are three overlapping patterns of angina pectoris:
(1) stable or typical angina, 稳定型
(2) Prinzmetal or variant angina,变异型
(3) unstable or crescendo angina. 不稳定型/恶化型
Stable angina
The most common form and therefore called typical angina pectoris,
appears to be caused by the reduction of coronary perfusion to a
critical level by chronic stenosing coronary atherosclerosis.
Prinzmetal variant angina
• An uncommon pattern of episodic angina that occurs at
rest and is due to coronary artery spasm.
Unstable angina
• Refers to a pattern of pain that occurs with progressively increasing
frequency, is precipitated with progressively less effort, often occurs
at rest休息, and tends to be of more prolonged duration.
• In most patients, unstable angina is induced by disruption of an
atherosclerotic plaque with superimposed partial (mural) thrombosis
and possibly embolization or vasospasm (or both).
In the typical case of MI, the following sequence of events can be proposed:
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The initial event is a sudden change in the morphology of an atheromatous plaque,
that is, disruption-manifest as intraplaque hemorrhage, erosion or ulceration, or
rupture or fissuring.
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Exposed to subendothelial collagen and necrotic plaque contents, platelets undergo
adhesion, aggregation, activation, and release of potent aggregators including
thromboxane A2, serotonin, and platelet factors 3 and 4.
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Vasospasm is stimulated by platelet aggregation and the release of mediators.
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Other mediators activate the extrinsic pathway of coagulation, adding to the bulk of
the thrombus.
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Frequently within minutes, the thrombus evolves to completely occlude the lumen of
the coronary vessel.
Postmortem angiogram showing the posterior aspect of the heart of a patient who died during
the evolution of acute myocardial infarction, demonstrating total occlusion of the distal right
coronary artery by an acute thrombus (arrow) and a large zone of myocardial hypoperfusion
involving the posterior left and right ventricles.
The precise location, size, and specific morphologic features of an
acute myocardial infarct depend on:
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The location, severity, and rate of development of coronary atherosclerotic
obstructions
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The size of the vascular bed perfused by the obstructed vessels
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The duration of the occlusion
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The metabolic/oxygen needs of the myocardium at risk
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The extent of collateral blood vessels
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The presence, site, and severity of coronary arterial spasm
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Other factors, such as alterations in blood pressure, heart rate, and cardiac
rhythm.
冠状动脉粥样硬化：占95%
最常见左前降支、其次右主干、再其次左旋支。斑块病变多发生于血管
的心壁侧，呈新月形，使管腔呈偏心性狭窄。
• 左前降支 Left anterior descending coronary artery (40% to 50%):
infarct involves anterior wall of left ventricle near apex; anterior
portion of ventricular septum; apex circumferentially
• 右冠 Right coronary artery (30% to 40%): infarct involves
inferior/posterior wall of left ventricle; posterior portion of ventricular
septum; inferior/posterior right ventricular free wall in some cases
• 左旋支 Left circumflex coronary artery (15% to 20%): infarct involves
lateral wall of left ventricle except at apex
Schematic representation of the progression of myocardial necrosis after coronary artery occlusion
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Subendocardial
myocardial
infarction 心内膜下
心肌梗死
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Circumferential
infarction 环状梗死
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Transmural
myocardial
infarction 透壁性心
肌梗死
Acute myocardial infarct
• 肉眼所见：梗死灶形状不规则呈
地图状，其颜色随梗死时间而变
化。梗死后6小时颜色苍白，9时
土黄色，4天充血带，2-3周边红
色，5周灰白色。
• 镜检：凝固性坏死，边缘充血和
中性粒细胞浸润。
One-day-old infarct showing coagulative necrosis along with wavy fibers (elongated
and narrow), compared with adjacent normal fibers (at right).
Widened spaces between the dead fibers contain edema fluid and scattered neutrophils.
Dense polymorphonuclear leukocytic infiltrate in area of acute myocardial
infarction of 3 to 4 days' duration
Nearly complete removal of necrotic myocytes by phagocytosis
(approximately 7 to 10 days)
Granulation tissue characterized by loose collagen and abundant capillaries
Well-healed myocardial infarct with replacement of the necrotic fibers by
dense collagenous scar
Microscopic features of myocardial infarction and its repair.
Temporal sequence of early biochemical, ultrastructural, histochemical, and histologic findings
after onset of severe myocardial ischemia
Consequences of myocardial ischemia followed by reperfusion
Appearance of myocardium modified by reperfusion
合并症Consequences and Complications of Myocardial Infarction
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Contractile dysfunction 收缩损伤—急性左心衰
Arrhythmias 心律失常
Myocardial rupture 心脏破裂
Pericarditis 心包炎
Right ventricular infarction
Infarct extension /Infarct expansion
Mural thrombus 附壁血栓形成
Ventricular aneurysm 室壁瘤
Papillary muscle dysfunction 乳头肌功能失调
Progressive late heart failure
Complications of myocardial infarction. Cardiac rupture syndromes. Cardiac rupture
syndromes (A, B, and C). A, Anterior myocardial rupture in an acute infarct (arrow). B,
Rupture of the ventricular septum (arrow). C, Complete rupture of a necrotic papillary
muscle.
Fibrinous pericarditis
showing a dark, roughened epicardial surface overlying an
acute infarct.
Early expansion of anteroapical infarct with wall thinning and mural thrombus
Large apical left ventricular aneurysm
心肌梗死的合并症和死因
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1．心脏破裂
2．室壁瘤
3．附壁血栓形成→栓塞
4．心功能不全
5．心源性休克
6．心律不整
7．机化疤痕形成
8．急性心包炎
CHD
• 1）Angina pectoris
• 2) Myocardial infarction
• 3) Myocardial fibrosis
=Ischemic cardiomyopathy
=Chronic ischemic heart disease
• 4) Sudden coronary death
SUDDEN CARDIAC DEATH (SCD)
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Congenital structural or coronary arterial abnormalities
Aortic valve stenosis
Mitral valve prolapse
Myocarditis
Dilated or hypertrophic cardiomyopathy
Pulmonary hypertension
Hereditary or acquired abnormalities of the cardiac conduction
system
• Isolated hypertrophy, hypertensive or unknown cause.
3. Hypertension
• 人体体循环动脉血压持续升高，称为高血压。我
国规定标准：成年人血压，在安静休息状态下，
收缩压超过140mmHg（18.4 kpa），舒张压超过
90 mmHg（12.0 kpa），即为高血压。
• Hypertension 140mmHg/90mmHg
• Secondary/ Symptomatic hypertension
• Primary/Essential hypertension 5-10%
(3大原因：肾性/血管性/内分泌性）
发病因素
• Genetic predisposition
• Salt sensitivity
• Stress
The critical roles of cardiac output and peripheral resistance in blood pressure regulation
Blood pressure regulation by the renin-angiotensin system and the central roles of
sodium metabolism in specific causes of inherited and acquired forms of hypertension
Hypothetical scheme for the pathogenesis of essential hypertension,
implicating genetic defects in renal excretion of sodium, functional regulation of vascular tone, and
structural regulation of vascular caliber.
Environmental factors, especially increased salt intake, may potentiate the effects of genetic factors.
The resultant increases in cardiac output and peripheral resistance contribute to hypertension.
The minimal criteria for the diagnosis of systemic HHD are the following:
• (1) left ventricular hypertrophy (usually concentric) in the absence of
other cardiovascular pathology that might have induced it
• (2) a history or pathologic evidence of hypertension.
• 1 Chronic/Benign hypertension
• 2 Accelerated/malignant hypertension
• 3 Hypertensive heart disease
Chronic/benign hypertension
1 机能紊乱期—细小动脉痉挛
2 动脉系统病变期
Arteriolosclerosis/细动脉玻璃样变—肾入球动脉和视网膜动脉
3 内脏病变期(大心小肾脑出血）
HHD:concentric hypertrophy/eccentric hypertrophy
Arteriolar nephrosclerosis/Primary granulo-contracted kidney
Hypertensive encephalopathy/Hypertensive crisis
/Softening of brain(microinfarct)/Microaneurysm
良性高血压病的病变特点
• 又称缓进型高血压病。起病缓慢，呈慢性经过，病程可长
达10-20年，其病理过程分三期：
• 机能改变期（一期）全身细、小动脉痉挛→血压↑。无器
质性改变。
• 动脉系统病变期（二期）
• 1．细动脉：动脉痉挛→动脉壁玻璃样变→细动脉硬化
• 2．小动脉：动脉痉挛→中膜平滑肌增生、肥大，胶原弹
性纤维增加。内膜平滑肌增生，产生胶原和弹性纤维→小
动脉硬化。
• 3．弹力肌型及弹力型动脉：可伴发粥样硬化病变。
器官病变期（三期）
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1．心脏 左室代偿性向心性肥大→左室失代偿性肌源性扩张→心力衰竭。
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2．肾脏 原发性颗粒性固缩肾→肾功能不全→尿毒症。
肉眼：肾体积缩小、变硬，表面均匀细颗粒状。
镜检：
（1）部分肾入球、出球细动脉玻璃样变，引起肾小球玻璃样变和纤维化。
（2）部分肾单位代偿性肥大和扩大。
（3）间质纤维化和淋巴细胞浸润。
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3．脑 脑出血和脑软化
（1）脑出血：最严重的并发症常致死。出血常位于基底节、内囊。
出血区脑组织被破坏，呈囊腔状，囊内为坏死和凝血块，出血量多时，破入侧脑室，
常昏迷死亡。
出血灶累及内囊时，发生对侧肢体偏瘫和感觉消失。
脑出血机理：细小动脉硬化血压突升致血管破裂；多发性细小动脉瘤破裂性出血；豆
纹动脉从大脑中动脉直角分支承受高压而破裂。
（2）脑软化：缺血性小灶性坏死。一般无严重后果。
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Vascular pathology in hypertension
Hypertensive heart disease with marked concentric thickening of
the left ventricular wall causing reduction in lumen size
Accelerated/malignant hypertension
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Young
230/130mmHg
Hyperplastic arteriolosclerosis
Necrotizing arteriolitis（内膜中膜纤维素样坏死）
Renal failure（1年）
• 恶性高血压病的病变特点
• 又称急进型高血压病。病程短，进展迅速，多数
一年内死亡。
• 其病变特点为：
• 1.细动脉纤维素样坏死+血浆内渗→动脉壁极度增
厚，动脉腔狭窄 肾小球毛细血管节段性坏死→血
压明显增高。
• 2.小动脉增生性动脉内膜炎→闭塞性动脉内膜炎
→动脉腔高度狭窄→血压明显上升。
• 死亡原因：尿毒症、脑出血、心力衰竭。
Chronic cor pulmonale
4. True and false aneurysms 动脉瘤
Abdominal aortic aneurysm
Aneurysm
• 1 True aneurysm
• 2 False aneurysm/Pseudoaneurysm
• 3 Arterial dissection /Dissecting aneurysm/Aortic dissection
Aortic dissection
Medial degeneration
Classification of dissection into types A and B. Type A (proximal) involves the
ascending aorta, whereas type B (distal) does not. The serious complications
predominantly occur in the region from the aortic valve through the arch.
5. Rheumatism
• 风湿病的概念:与A型溶血性链球菌感染有关的结缔组织变态反应性炎。
常累及心脏、关节，其次为皮肤、动脉和中枢神经等。
• Rheumatic fever (RF) is an acute, immunologically mediated,
multisystem inflammatory disease that occurs a few weeks following
an episode of group A streptococcal pharyngitis溶血性链球菌.
• Acute rheumatic carditis during the active phase of RF may progress
to chronic rheumatic heart disease (RHD).
• The most important consequence of RF are chronic valvular
deformities, characterized principally by deforming fibrotic valvular
disease (particularly mitral stenosis), which produces permanent
dysfunction and severe, sometimes fatal, cardiac problems decades
later.
The pathogenetic sequence and key morphologic features of acute rheumatic heart disease
• 风湿病的病因发病机理
• （1）风湿病与A型溶血
性链球菌感染有关。
• （2）风湿病不是A型溶
血性链球菌直接引起。
• （3）风湿病是A型溶血
性链球菌感染后引起的自
身免疫性疾病。
1 非特异性炎
2（肉牙肿性炎）3 stages
• 变质渗出期---黏液样变/纤维素样坏死---1月
• 增生期/肉牙肿期---风湿细胞/Aschoff cell/ Aschoff body---2/3月
• 纤维化期/愈合期---4/6月
•
•
•
•
基本病变
（1）变质渗出期：结缔组织粘液样变性和纤维素样坏死, 浆液、纤维素、淋巴细胞、
单核细胞渗出。
（2）增生期（肉芽肿期）：形成风湿小结（Aschoff小结）。风湿小结的构成细胞有：
风湿细胞、纤维细胞、单核细胞和淋巴细胞以及纤维素样坏死物。风湿细胞胞浆丰富、
嗜硷、核大、卵圆、染色质集中核中央，似枭眼或毛虫状。
（3）硬化期（愈合期）：
Rheumatic heart disease
1 Rheumatic endocarditis
valvulitis---vegetations---verrucous endocarditis---McCallum斑
2 Rheumatic myocarditis ---Aschoff body
3 Rheumatic pericarditis---绒毛心Cor villosum ---constrictive
pericarditis
4 Rheumatic pancarditis
风湿性心内膜炎
• 部位：二尖瓣、二尖瓣和主动脉瓣。
• 肉眼：瓣膜肿胀，白血流面闭锁缘形成单行排列疣状赘生
物、灰白、小而坚实。
• 镜检：赘生物为白色血栓，瓣膜水肿、纤维素样坏死和少
量风湿小结。
• 结果：病灶反复发作，赘生物机化，瓣膜纤维化→慢性风
湿性心瓣膜病。左心房心内膜增厚、粗糙、皱缩，称
McCallum斑。
• 风湿性心肌炎
• 镜检：心肌间质风湿小结
• 结果：影响心肌收缩力、严重者心力衰竭。后期疤痕形成，无害。
• 风湿性心外膜炎
• 肉眼：浆液性纤维素性炎，心包腔大量浆液，心外膜纤维素渗出→绒
毛心。
• 镜检：心外膜纤维素样坏变、大量纤维素渗出。
• 结果：
• 1．渗出液吸收痊愈。
• 2．纤维素部分不吸收而机化→缩窄性心包炎。
Aschoff body
• During acute RF, focal inflammatory lesions are found in various
tissues. They are most distinctive within the heart, where they are
called Aschoff bodies.
• They consist of foci of swollen eosinophilic collagen surrounded by
lymphocytes (primarily T cells), occasional plasma cells, and plump
macrophages called Anitschkow cells.
• These distinctive cells have abundant cytoplasm and central roundto-ovoid nuclei in which the chromatin is disposed in a central,
slender, wavy ribbon (hence the designation "caterpillar cells").
• Some of the larger macrophages become multinucleated to form
Aschoff giant cells.
Acute and chronic rheumatic heart disease
A, Acute rheumatic mitral valvulitis superimposed on chronic rheumatic heart disease. Small
vegetations (verrucae) are visible along the line of closure of the mitral valve leaflet (arrows). Previous
episodes of rheumatic valvulitis have caused fibrous thickening and fusion of the chordae tendineae.
B, Microscopic appearance of Aschoff body in a patient with acute rheumatic carditis. The myocardial
interstitium has a circumscribed collection of mononuclear inflammatory cells, including some large
histiocytes with prominent nucleoli and a prominent binuclear histiocyte, and central necrosis.
Mitral stenosis with diffuse fibrous thickening and distortion of the valve
leaflets, commissural fusion (arrows), and thickening and shortening of
the chordae tendineae. Marked dilation of the left atrium is noted in the
left atrial view (C). D, Opened valve. Note neovascularization of anterior
mitral leaflet (arrow).
Surgically removed specimen of rheumatic aortic stenosis, demonstrating
thickening and distortion of the cusps with commissural fusion
Acute and chronic rheumatic heart disease
•
•
•
•
•
Rheumatic arthritis –游/大/无-舔关节咬心脏
Erythema annullare 环形红斑-非特异性渗出性炎
Subcutaneous nodules 皮下结节-风湿小体
Rheumatic arteritis-风湿小体
Chorea minor 小舞蹈症- Rheumatic arteritis/皮质下脑炎
基底结黑质时，面肌及肢体不自主运动
心外器官风湿病变
•
•
•
（1）风湿性关节炎
部位：膝、踝、肩、腕、肘大关节。
病变：浆液性炎。关节周围有风湿小结。
•
•
•
•
（2）风湿性皮肤病变
⑴环形红斑：非特异性渗出性炎。
⑵皮下结节：增生性炎，风湿小结。
均在急性风湿时出现，有诊断意义。
•
•
•
（3）风湿性动脉炎
部位：冠状动脉、肾动脉、脑动脉、肺动脉。
病变：呈风湿病三期改变，后期疤痕形成，动脉壁增厚，腔狭窄。
•
•
（4）中枢神经系统风湿
主要由于风湿性脑动脉炎引起脑神经细胞坏变、胶质细胞增生。如发生在锥
体外系，则出现小舞蹈症。
6. INFECTIVE ENDOCARDITIS (IE)
ABE/SBE
• Acute Infective endocarditis/ acute bacterial endocarditis, ABE
• Subacute Infective endocarditis/subacute bacterial endocarditis,
SBE
• Infective endocarditis, one of the most serious of all infections,
is characterized by colonization or invasion of the heart valves
or the mural endocardium by a microbe, leading to the
formation of bulky, friable vegetations composed of thrombotic
debris and organisms, often associated with destruction of the
underlying cardiac tissues.
ABE/SBE区别
• Acute endocarditis describes a destructive, tumultuous infection,
frequently of a previously normal heart valve, with a highly virulent
organism, that leads to death within days to weeks of more than
50% of patients despite antibiotics and surgery.
• In contrast, organisms of low virulence can cause infection in a
previously abnormal heart, particularly on deformed valves. In such
cases, the disease may appear insidiously and, even untreated,
pursue a protracted course of weeks to months (subacute
endocarditis). Most patients with subacute IE recover after
appropriate antibiotic therapy.
Infective (bacterial) endocarditis.
A, Endocarditis of mitral valve (subacute, caused by Strep. viridans). The large, friable vegetations are
denoted by arrows.
B, Acute endocarditis of congenitally bicuspid aortic valve (caused by Staph. aureus) with extensive
cuspal destruction and ring abscess (arrow).
C, Histologic appearance of vegetation of endocarditis with extensive acute inflammatory cells and
fibrin. Bacterial organisms were demonstrated by tissue Gram stain.
D, Healed endocarditis, demonstrating mitral valvular destruction but no active vegetations.
Morphology.
• In both the subacute and acute forms of the disease, friable, bulky,
and potentially destructive vegetations containing fibrin,
inflammatory cells, and bacteria or other organisms are present on
the heart valves.
• Osler小结-皮下小动脉炎
• Systemic emboli may occur at any time because of the friable
nature of the vegetations, and they may cause infarcts in the brain,
kidneys, myocardium, and other tissues.
• Because the embolic fragments contain large numbers of virulent
organisms, abscesses often develop at the sites of such infarcts
(septic infarcts).
Four major forms of vegetative endocarditis.
The rheumatic fever phase of RHD (rheumatic heart disease) is marked by a row of
small, warty vegetations along the lines of closure of the valve leaflets.
IE (infective endocarditis) is characterized by large, irregular masses on the valve
cusps that can extend onto the chordae.
NBTE (nonbacterial thrombotic endocarditis) typically exhibits small, bland
vegetations, usually attached at the line of closure. One or many may be present.
LSE (Libman-Sacks endocarditis) has small or medium-sized vegetations on either
or both sides of the valve leaflets.
Nonbacterial thrombotic endocarditis (NBTE)
Complications of artificial heart valves
7. Chronic valvular vitium of the heart
• Vavular stenosis
• Valvular insufficiency
• Stenosis is the failure of a valve to open
completely, thereby impeding forward flow.
• Insufficiency, in contrast, results from
failure of a valve to close completely,
thereby allowing reversed flow.
• Aortic stenosis: calcification of anatomically
normal and congenitally bicuspid aortic valves.
• Aortic insufficiency: dilation of the ascending
aorta, related to hypertension and aging.
• Mitral stenosis: rheumatic heart disease.
• Mitral insufficiency: myxomatous degeneration
(mitral valve prolapse).
Mitral stenosis
Calcific valvular degeneration
Myxomatous degeneration of the mitral valve
8. Cardiomyopathy
• Dilated Cardiomyopathy
• Hypertrophic Cardiomyopathy
• Restrictive Cardiomyopathy
Graphic representation of the three distinctive and predominant
clinical-pathologic-functional forms of myocardial disease
Cardiomyopathy and Indirect Myocardial Dysfunction: Functional
Patterns and Causes
•
Functional Pattern
Left Ventricular Ejection Fraction
Indirect Myocardial Dysfunction (Not Cardiomyopathy)
Mechanisms of Heart Failure Causes
Dilated
•
<40%
•
Impairment of contractility (systolic dysfunction)
•
Idiopathic; alcohol; peripartum; genetic; myocarditis; hemochromatosis; chronic anemia;
doxorubicin (Adriamycin); sarcoidosis
•
Ischemic heart disease; valvular heart disease; hypertensive heart disease; congenital heart
disease
Hypertrophic
•
50-80%
•
Impairment of compliance (diastolic dysfunction)
•
Genetic; Friedreich ataxia; storage diseases; infants of diabetic mothers
•
Hypertensive heart disease; aortic stenosis
Restrictive
•
45-90%
•
Impairment of compliance (diastolic dysfunction)
•
Idiopathic; amyloidosis; radiation-induced fibrosis
•
Pericardial constriction
Conditions Associated with Heart Muscle Diseases(1)
Cardiac Infections
•
Viruses
•
Chlamydia
•
Rickettsia
•
Bacteria
•
Fungi
•
Protozoa
Toxins
•
Cobalt
•
Alcohol
•
Catecholamines
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Carbon monoxide
•
Lithium Hydrocarbons
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Arsenic
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Cyclophosphamide Doxorubicin (Adriamycin) and daunorubicin
Metabolic
•
Hyperthroidism
•
Hypothyroidism
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Hyperkalemia
•
Hypokalemia
•
Nutritional deficiency (protein, thiamine, other avitaminoses)
•
Hemochromatosis
Conditions Associated with Heart Muscle Diseases(2)
Neuromuscular Disease
•
Friedreich ataxia
•
Muscular dystrophy
•
Congenital atrophies
Storage Disorders and Other Depositions
•
Hunter-Hurler syndrome
•
Glycogen storage disease
•
Fabry disease
•
Amyloidosis
Infiltrative
•
Leukemia
•
Carcinomatosis
•
Sarcoidosis
•
Radiation-induced fibrosis
Immunologic
•
Myocarditis (several forms)
•
Post-transplant rejection
Dilated cardiomyopathy.
A, Gross photograph. Four-chamber dilatation and hypertrophy are evident. There is
granular mural thrombus at the apex of the left ventricle (on the right in this apical fourchamber view). The coronary arteries were unobstructed.
B, Histology demonstrating variable myocyte hypertrophy and interstitial fibrosis (collagen
is highlighted as blue in this Masson trichrome stain).
Arrythmogenic right ventricular cardiomyopathy.
A, Gross photograph, showing dilation of the right ventricle and near transmural
replacement of the right ventricular free-wall myocardium by fat and fibrosis. The left
ventricle has a virtually normal configuration.
B, Histologic section of the right ventricular free wall, demonstrating replacement of
myocardium (red) by fibrosis (blue, arrow) and fat (collagen is blue in this Masson
trichrome stain).
Hypertrophic cardiomyopathy with asymmetric septal hypertrophy.
A, The septal muscle bulges into the left ventricular outflow tract, and the left atrium is
enlarged. The anterior mitral leaflet has been moved away from the septum to reveal a
fibrous endocardial plaque (arrow).
B, Histologic appearance demonstrating disarray, extreme hypertrophy, and characteristic
branching of myocytes as well as the interstitial fibrosis characteristic of hypertrophic
cardiomyopathy (collagen is blue in this Masson trichrome stain).
Schematic structure of the sarcomere of cardiac muscle, highlighting proteins in which
mutations cause defective contraction, hypertrophy, and myocyte disarray in hypertrophic
cardiomyopathy. The frequency of a particular gene mutation is indicated as a percentage of all
cases of HCM; most common are mutations in β-myosin heavy chain. Normal contraction of
the sarcomere involves myosin-actin interaction initiated by calcium binding to troponin C, I,
and T and α-tropomyosin. Actin stimulates ATPase activity in the myosin head and produces
force along the actin filaments. Myocyte-binding protein C modulates contraction.
Pathways of dilated and hypertrophic cardiomyopathy
9. Myocarditis
• Viral Myocarditis
• Bacterial Myocarditis
• Isolated Myocarditis
Major Causes of Myocarditis
Infections
• Viruses (e.g., coxsackievirus, ECHO, influenza, HIV, cytomegalovirus)
• Chlamydiae (e.g., C. psittaci)
• Rickettsiae (e.g., R. typhi, typhus fever)
• Bacteria (e.g., Corynebacterium diphtheriae, Neisseria meningococcus, Borrelia
(Lyme disease)
• Fungi (e.g., Candida)
• Protozoa (e.g., Trypanosoma Chagas disease, toxoplasmosis)
• Helminths (e.g., trichinosis)
Immune-Mediated Reactions
• Postviral
• Poststreptococcal (rheumatic fever)
• Systemic lupus erythematosus
• Drug hypersensitivity (e.g., methyldopa , sulfonamides)
• Transplant rejection
Unknown
• Sarcoidosis
• Giant cell myocarditis
Lymphocytic myocarditis, with mononuclear inflammatory cell
infiltrate and associated myocyte injury
Hypersensitivity myocarditis, characterized by interstitial inflammatory
infiltrate composed largely of eosinophils and mononuclear inflammatory
cells, predominantly localized to perivascular and large interstitial spaces.
This form of myocarditis is associated with drug hypersensitivity
Giant cell myocarditis, with mononuclear inflammatory infiltrate
containing lymphocytes and macrophages, extensive loss of
muscle, and multinucleated giant cells
The myocarditis of Chagas disease. A myofiber is distended with
trypanosomes锥形虫 (arrow). There is a surrounding inflammatory
reaction and individual myofiber necrosis.
10. Pericarditis
• Acute Pericarditis
Serious Pericarditis
Fibrinous and serofibrinous Pericarditis
Purulent or suppurative Pericarditis
Hemorrhagic Pericarditis
• Chronic Pericarditis
Non-specific type
Adhesive mediastinopricarditis
Constrictive Pericarditis
Causes of Pericarditis
Infectious Agents
• Viruses
• Pyogenic bacteria
• Tuberculosis
• Fungi
• Other parasites
Presumably Immunologically Mediated
• Rheumatic fever
• Systemic lupus erythematosus
• Scleroderma
• Postcardiotomy
• Postmyocardial infarction (Dressler) syndrome
• Drug hypersensitivity reaction
Miscellaneous
• Myocardial infarction
• Uremia
• Following cardiac surgery
• Neoplasia
• Trauma
• Radiation
Acute suppurative pericarditis as an extension
from a pneumonia
Left atrial myxoma
Complications of heart transplantation
11. Congenital heart disease
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•
•
•
•
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Atrial septal defect
Ventricular septal defect
Tetralogy of Fallot
Patent ductus arteriosus
Coarctation of aorta
Transposition of the great arteries
Cardiac defects related to neural crest abnormalities
Schematic diagram of congenital left-to-right shunts
Gross photograph of a ventricular septal defect (membranous type)
Schematic diagram of the most important right-to-left
shunts (cyanotic congenital heart disease)
Transposition of the great arteries
Diagram showing coarctation of the aorta with and
without PDA