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Heart Pathology Department, Zhejiang University School of Medicin Zhu keqing 竺竺竺[email protected], 2011-5-9

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Heart. Pathology Department, Zhejiang University School of Medicine, Zhu keqing 竺可青, [email protected] , 2011-5-9. Atherosclerosis Coronary atherosclerosis/CHD Hypertension Aneurysm Rheumatism Infective endocarditis Chronic valvular vitium of the heart Cardiomyopathy - PowerPoint PPT Presentation


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Pathology Department, Zhejiang University School of Medicine, Zhu keqing 竺可青, [email protected], 2011-5-9

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1. Atherosclerosis2. Coronary atherosclerosis/CHD3. Hypertension4. Aneurysm5. Rheumatism6. Infective endocarditis7. Chronic valvular vitium of the heart8. Cardiomyopathy9. Myocarditis10. Pericarditis11. Congenital heart disease

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Five categories of disease account for nearly all cardiac mortality

• Congenital heart disease • Ischemic heart disease • Hypertensive heart disease (systemic and pulmonary) • Valvular heart disease • Nonischemic (primary) myocardial disease

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Left ventricular hypertrophy

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Schematic representation of the sequence of events in

cardiac hypertrophy and its progression to heart failure

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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


• 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,


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Risk factors for As

4 高• Hyperlipidemia• Hypertension• Smoking• DM(Diabetes mellitus)

• Heritage• Age• Sex-Male• Lack of physical exercise• Obesity• Stress

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• sLDL—CHD• VLDL/CM 乳糜微粒

• AS 性脂蛋白表型— LDL(sLDL)\TG\VLDL\apoB 异常升高与 HDL-C/apoA-I 降低

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The vascular wall

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Endothelial cell response to environmental stimuli:

causes (activators) and consequences (induced genes).

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Schematic diagram of the mechanism of intimal thickening, emphasizing smooth muscle

cell migration to, and proliferation and extracellular matrix elaboration in, the intima.

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Evolution of arterial wall

changes in the response to injury


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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.

• 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.

• 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。

• 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

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Hypothetical sequence of cellular interactions in atherosclerosis

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• The key processes in atherosclerosis are intimal thickening and lipid accumulation.

• 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)

• An atheroma 粥瘤 consists of a raised focal lesion initia

ting 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 .











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American Heart Association classification of human atherosclerotic

lesions from the fatty dot (type I) to the complicated type VI lesion

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Fatty streak-a collection of foam cells in the intima

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Schematic depiction of the major components of well-developed intimal atheromatous plaque overlying an intact media.

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Gross views of atherosclerosis in the aorta

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• 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.

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Atherosclerotic plaques have three principal components:

• (1) cells, including SMCs, macrophages, and other leukocytes;

• (2) ECM, including collagen, elastic fibers, and proteoglycans;

• (3) intracellular and extracellular lipid.

• These components occur in varying proportions and configurations in different lesions.

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The advanced lesion 并发症 of atherosclerosis: • 斑块破裂 Focal rupture, ulceration, or erosion of the luminal surface of atheromat

ous 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).

• 斑块内出血 Hemorrhage into a plaque, especially in the coronary arteries, may be in

itiated 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.

• 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.

• 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.

• 血管腔狭窄

• 钙化

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View of the base of the brain, dissected to show the circle of Willis

with an aneurysm of the anterior cerebral artery

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Dissected circle of Willis to show large aneurysm

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Common sites of saccular (berry) aneurysms in the circle of Willis

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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

• Rupture/fissuring, exposing the highly thrombogenic plaque constituents.

• Erosion/ulceration, exposing the thrombogenic subendothelial basement membrane to blood.

• Hemorrhage into the atheroma, expanding its volume.

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2 Coronary artherosclerosis(CAS)

• 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。

• 冠状动脉病 CAD


• 其余冠状动脉炎性疾病及畸形(风湿性 / 梅毒性主动脉炎)

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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.

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Estimated 10-year risk of coronary artery disease according to various

combinations of risk factor levels

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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 caus

e 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 vari

ants--- stable angina, Prinzmetal angina, unstable angina-the latter is the most threatening as a frequent harbinger 预兆 of MI.

3 Chronic IHD with heart failure.

4 Sudden cardiac death.

• 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

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Pathogenesis• The dominant influence in the causation of the IHD syndromes is di

minished coronary perfusion relative to myocardial demand,

• owing largely to a complex and dynamic interaction among:

• fixed atherosclerotic narrowing of the epicardial coronary arteries, • intraluminal thrombosis overlying a disrupted atherosclerotic plaque, • platelet aggregation, • and vasospasm.

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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).

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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

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Coronary Artery Pathology in Ischemic Heart Disease

• Syndrome Stenoses Plaque Disruption Plaque-Associated Thrombus

• Stable angina >75% No No

• Unstable angina Variable Frequent Nonocclusive, often with thromboemboli • Transmural myocardial infarction Frequent Occlusive

• Subendocardial myocardial infarction Variable Widely variable, may be absent, partial/complete, or lysed

• Sudden death Usually severe Frequent small platelet aggregates / thrombi / thromboemboli


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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.

• 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

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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.

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Prinzmetal variant angina

• An uncommon pattern of episodic angina that occurs at

rest and is due to coronary artery spasm.

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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).

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In the typical case of MI, the following sequence of events can be proposed:

• 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.

• 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.

• Vasospasm is stimulated by platelet aggregation and the release of mediators.

• Other mediators activate the extrinsic pathway of coagulation, adding to the bulk of the thrombus.

• Frequently within minutes, the thrombus evolves to completely occlude the lumen of the coronary vessel.

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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 involvin

g the posterior left and right ventricles.

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The precise location, size, and specific morphologic features of an acute myocardial infarct depend on:

• The location, severity, and rate of development of coronary atherosclerotic obstructions

• The size of the vascular bed perfused by the obstructed vessels • The duration of the occlusion

• The metabolic/oxygen needs of the myocardium at risk • The extent of collateral blood vessels • The presence, site, and severity of coronary arterial spasm

• Other factors, such as alterations in blood pressure, heart rate, and cardiac rhythm.

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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

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Schematic representation of the progression of myocardial necrosis after coronary artery occlusion

• Subendocardial myocardial infarction 心内膜下心肌梗死

• Circumferential infarction 环状梗死

• Transmural myocardial infarction 透壁性心肌梗死

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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。

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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.

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Dense polymorphonuclear leukocytic infiltrate in area of acute myocardial

infarction of 3 to 4 days' duration

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Nearly complete removal of necrotic myocytes by phagocytosis (approximately 7 to 10 days)

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Granulation tissue characterized by loose collagen and abundant capillaries

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Well-healed myocardial infarct with replacement of the necrotic fibers by

dense collagenous scar

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Microscopic features of myocardial infarction and its repair.

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Temporal sequence of early biochemical, ultrastructural, histochemical, and histologic finding

s after onset of severe myocardial ischemia

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Consequences of myocardial ischemia followed by reperfusion

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Appearance of myocardium modified by reperfusion

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合并症 Consequences and Complications of Myocardial Infarction

• 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

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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.

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Fibrinous pericarditis showing a dark, roughened epicardial surface overlying an acute infarct.

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Early expansion of anteroapical infarct with wall thinning and mural thrombus

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Large apical left ventricular aneurysm

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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

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• 1 ) Angina pectoris• 2) Myocardial infarction

• 3) Myocardial fibrosis =Ischemic cardiomyopathy =Chronic ischemic heart disease

• 4) Sudden coronary death

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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 syste

m • Isolated hypertrophy, hypertensive or unknown cause.

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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)

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发病因素• Genetic predisposition

• Salt sensitivity

• Stress

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The critical roles of cardiac output and peripheral resistance in blood pressure regulation

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Blood pressure regulation by the renin-angiotensin system and the central roles of sodiu

m metabolism in specific causes of inherited and acquired forms of hypertension

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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. Th

e resultant increases in cardiac output and peripheral resistance contribute to hypertension.

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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.

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• 1 Chronic/Benign hypertension

• 2 Accelerated/malignant hypertension

• 3 Hypertensive heart disease

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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

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• 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


• 3 .弹力肌型及弹力型动脉:可伴发粥样硬化病变。

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器官病变期(三期)• 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。

• 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。

• 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

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Hypertensive heart disease with marked concentric thickening of

the left ventricular wall causing reduction in lumen size

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Accelerated/malignant hypertension

• Young• 230/130mmHg• Hyperplastic arteriolosclerosis• Necrotizing arteriolitis (内膜中膜纤维素样坏死)• Renal failure ( 1年)

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• 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。

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Chronic cor pulmonale

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4. True and false aneurysms 动脉瘤

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Abdominal aortic aneurysm

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• 1 True aneurysm• 2 False aneurysm/Pseudoaneurysm• 3 Arterial dissection /Dissecting aneurysm/Aortic dissection

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Aortic dissection

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Medial degeneration

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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.

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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.

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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。

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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:


• ( 3 )硬化期(愈合期):

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Rheumatic heart disease1 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

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• 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。

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• 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。

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Aschoff body• During acute RF, focal inflammatory lesions are found in various tiss

ues. 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 round-t

o-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 As

choff giant cells.

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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.

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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.

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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).

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Surgically removed specimen of rheumatic aortic stenosis, demonstrating thi

ckening and distortion of the cusps with commissural fusion

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Acute and chronic rheumatic heart disease

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• 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

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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。

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• Acute Infective endocarditis/ acute bacterial endocarditis, ABE• Subacute Infective endocarditis/subacute bacterial endocarditi

s, 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.

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ABE/SBE区别• Acute endocarditis describes a destructive, tumultuous infection, fr

equently 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.

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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.

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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).

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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.

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Nonbacterial thrombotic endocarditis (NBTE)

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Complications of artificial heart valves

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7. Chronic valvular vitium of the heart

• Vavular stenosis

• Valvular insufficiency

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• 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.

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• 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).

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Mitral stenosis

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Calcific valvular degeneration

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Myxomatous degeneration of the mitral valve

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8. Cardiomyopathy

• Dilated Cardiomyopathy

• Hypertrophic Cardiomyopathy

• Restrictive Cardiomyopathy

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Graphic representation of the three distinctive and predominant

clinical-pathologic-functional forms of myocardial disease

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Cardiomyopathy and Indirect Myocardial Dysfunction: Functional Patterns and Causes

• Functional Pattern Left Ventricular Ejection Fraction Mechanisms of Heart Failure Causes Indirect Myocardial Dysfunction (Not Cardiomyopathy)

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

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Conditions Associated with Heart Muscle Diseases(1)

Cardiac Infections• Viruses• Chlamydia• Rickettsia• Bacteria• Fungi• Protozoa Toxins• Cobalt• Alcohol• Catecholamines• Carbon monoxide• Lithium Hydrocarbons• Arsenic• Cyclophosphamide Doxorubicin (Adriamycin) and daunorubicinMetabolic• Hyperthroidism• Hypothyroidism• Hyperkalemia• Hypokalemia• Nutritional deficiency (protein, thiamine, other avitaminoses)• Hemochromatosis

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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


• Leukemia

• Carcinomatosis

• Sarcoidosis

• Radiation-induced fibrosis


• Myocarditis (several forms)

• Post-transplant rejection

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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 four-chamber 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).

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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).

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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).

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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.

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Pathways of dilated and hypertrophic cardiomyopathy

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9. Myocarditis

• Viral Myocarditis

• Bacterial Myocarditis

• Isolated Myocarditis

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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 rejectionUnknown• Sarcoidosis• Giant cell myocarditis

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Lymphocytic myocarditis, with mononuclear inflammatory cell infi

ltrate and associated myocyte injury

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Hypersensitivity myocarditis, characterized by interstitial inflammatory infiltrate composed largely of eosinophils and mononuclear inflammatory cells, predominantly localized to perivascular and large interstitial spaces. T

his form of myocarditis is associated with drug hypersensitivity

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Giant cell myocarditis, with mononuclear inflammatory infiltrate containing lymphocytes and macrophages, extensive loss of muscl

e, and multinucleated giant cells

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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.

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10. Pericarditis• Acute PericarditisSerious PericarditisFibrinous and serofibrinous PericarditisPurulent or suppurative PericarditisHemorrhagic Pericarditis

• Chronic PericarditisNon-specific typeAdhesive mediastinopricarditisConstrictive Pericarditis

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Causes of PericarditisInfectious Agents• Viruses• Pyogenic bacteria• Tuberculosis• Fungi• Other parasitesPresumably Immunologically Mediated• Rheumatic fever• Systemic lupus erythematosus• Scleroderma• Postcardiotomy• Postmyocardial infarction (Dressler) syndrome• Drug hypersensitivity reactionMiscellaneous• Myocardial infarction• Uremia• Following cardiac surgery• Neoplasia• Trauma• Radiation

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Acute suppurative pericarditis as an extension fro

m a pneumonia

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Left atrial myxoma

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Complications of heart transplantation

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11. Congenital heart disease

• Atrial septal defect

• Ventricular septal defect

• Tetralogy of Fallot

• Patent ductus arteriosus

• Coarctation of aorta

• Transposition of the great arteries

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Cardiac defects related to neural crest abnormalities

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Schematic diagram of congenital left-to-right shunts

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Gross photograph of a ventricular septal defect (membranous type)

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Schematic diagram of the most important right-to-left

shunts (cyanotic congenital heart disease)

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Transposition of the great arteries

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Diagram showing coarctation of the aorta with and

without PDA