cardiovasculer maret 2009.ppt...

CARDIOVASCULER

Dr.H.Delyuzar Sp.PA (K)

ISCHAEMIC HEART DIASEASE (±80%)

HYPERTENSIVE HEART DIASEASE ( 9%)

HEART RHEUMATIC HEART DIASEASE ( 2-3 %)

DISEASE CONGENITAL HEART DIASEASE (2 %)

ENDOCARDITIS BACTERIALIS ( 1 2 %)ENDOCARDITIS BACTERIALIS ( 1-2 %)

SYPHILLIS HEART DIASEASE ( 1%)

COR PULMONALE DIASEASE ( 1 %)

OTHERS ( 5%)2

CORONARY HEART DISEASE

CORONARY HEART DISEASECORONARY HEART DISEASE

ARTERIOSCLEROTIC HEART DISEASE

ANGINA PECTORISMYOCARDIAL INFARCTIONHEART DISEASE INFARCTION

8/24/20104 Departemen Pathology Anatomy - Cardiovascular

ARTERIOSCLEROTIC HEART DISEASE

Atherosclerotic coronary arteryDiffuse myocardial fibrotic occasionally cardiac valve fibrotic

MORPHOLOGY

Atherosclerotic Ischaemic Myocardial fibrotic

Marked as

Brownish-yellow granular diffusely (accumulates in the heart

Marked as Brown Atrophy

muscle) contained lipofuscin (complexes of lipid & protein)8/24/20105 Departemen Pathology Anatomy - Cardiovascular

ARTERIOSCLEROTIC HEART DISEASEOSC O C S S

The heart is become:

Small

Normal

Enlarged

Disorder of cardiac valve :

Mitral valve fibrotic

Ch d d f b l fChordae tendineae fibrotic or calcification


Gross appearance of heavily fibrotic and l ifi d di lcalcified cardiac valve


ANGINA PECTORISANGINA PECTORIS

Intermittent chest pain caused by transient, reversible myocardial ischaemic

TYPICAL / STABLE PRINZMETAL / UNSTABLETYPICAL / STABLEANGINA PECTORIS VARIANT,

ANGINAANGINA PECTORIS

(cressendo angina )


Pathogenesisg

Myocardial hypoxiay yp

Artherosclerotic coronary arteri

Syphilis heart diseaseSyphilis heart disease

Polyarthritis nodosa

Aorta valve insufficiency

Hypoxia caused of:

Anemia

Paroxismal myocadialypOcclusion of arteriesCoronary artery vasospasm

yhypoxia imposed by

exercise


MYOCARDIAL INFARCTIONMYOCARDIAL INFARCTION

Popularly called heart “attack “

Development of an area of myocardial necrosis caused by local

p y k

Development of an area of myocardial necrosis caused by local ischaemia

Coronary atherosclerosis (99%)Thrombosis & Emboli

Coroner insufficiency caused by :

Thrombosis & EmboliVascular diseases

Osteum occlusion caused by syphillisArteriosclerosis occlusion &

Hypotension8/24/201012 Departemen Pathology Anatomy - Cardiovascular

PathogenesisPathogenesis

• Basic : Coronary Arterial OcclusionBasic : Coronary Arterial Occlusion• Severe coronary atherosclerosis• Acute atherosclerotic plaque change (rupture)• S i d l t l t ti ti• Superimposed pletelet activation• Thrombosis & vasospasm

Consequence:

Myocardial Responsey p• Cessation of aerobic glycolysis anaerobic glycolysis

• Inadequate product of phosphate (Creatine phos & ATP)• acc lactid acid• acc lactid acid

Distribution of infarcts

Right coronary Left anterior g yartery

(30-40 %)descending artery

(40-50 %)

Left circumflexartery

(15-20 %)


8/24/2010Departemen Pathology Anatomy - Cardiovascular17

Evolution Of Morphologic Changes in Myocardial Infarction

Time Gross Feature Light Microscopic Findings

Electron Microscopic g p

Findings

Reversible Injury

< ½ hr None None Relaxation of myofibrils; glycogen loss; mitochondrial swelling

Irreversible Injury

½ -4 hr None Usually none; variable waviness of fibers at b d

Sacrolemmaldisruption;

h d l border mitochondrial amorphous densities

4 -12 hr Occasionally dark mottling

Beginning coagulation necrosis; edema; mottling necrosis; edema; haemorrhage


Evolution Of Morphologic Changes in Myocardial


18 24 h D k ttli C l ti i “ t ti

Infarction

18 – 24 hr Dark mottling Coagulation necrosis; “contraction band” necrosis at periphery of infarct; neutrophilic infiltrate

1 - 3 days Mottling with yellow-tan infarct center Complete coagulation necrosis of 1 - 3 days Mottling with yellow-tan infarct center Complete coagulation necrosis of myofibers; heavy neutrophilicinfiltrate

3 - 7 days Hyperemic border; central yellow-tan Beginning disintegration of dead y yp ; ysoftening

g g gmyofibers, with dying neutrophils; early phagocytosis of dead cells by macrophages at infarct border

7 - 10 days Maximally yellow-tan & soft, with depressed red-tan margins

Well-developed phagocytosis of dead cells; early formation of fibrovascular granulation tissue at marginsmargins



10 - 14 days Red-gray depressed infarct borders Well-established granulation tissue with new blood vessels & collagen deposition

2 – 8 wk Gray-white scar, progressive from border toward core of infarct

Increase collagen deposition, with decreased cellularity

> 2 month Scarring complete Dense collagenous scar


ComplicationsComplications

Papillary muscle dysfunction (infarcted papillary muscle may Papillary muscle dysfunction (infarcted papillary muscle may rupture)External rupture of the infarct cardiac tamponadeRupture of the intraventricular septumMural thrombi potential sources for systemic emboliVentricular fibrotic & aneurysmsVentricular fibrotic & aneurysms


HYPERTENSIVE HEART DISEASE

HYPERTENSIVE HEART DISEASEHYPERTENSIVE HEART DISEASEDiagnosis based on:

Left ventricular hypertrophy with a history of hypertension

A ti t i

Excluded

Aortic stenosis

Primary hypertropic cardiomyopathy


Morphology

Concentric hypertrophy (symetric, circumferential> 450 gm)

Size:E l N l dil t dEarly: Normal dilated

i iMicroscopic

• Myocytes >• Nuclei: large, hyperchrom, boxcar shaped


8/24/201027

VALVULAR HEART DISEASE

RHEUMATIC HEART DISEASE

Acute, immunologically mediated, multisystem inflammatory disease group A streptococcal pharyngitis

after an interval of a few weeks


Rheumatic Fever may cause

Chronic valvulardeformities

HD in acute phase

(A h i di i ) deformities(Acute rheumatic carditis)

Only 3% group A streptococcal pharyngitis RFInitial ↑ reactivation with subsequent pharyngeal infections

Ab >< M protein cross reaction with glycoprotein :H t Heart Joints & others

Onset : 2-3 weeks after infection Streptococci (-) in lesion8/24/201030 Departemen Pathology Anatomy - Cardiovascular

Morphology

Acute Rheumatic Fever

Inflammatory infiltrates in :

Acute Rheumatic Fever

ySynoviumJoint SkinHeart (most importantly) fibrosis deformitiesLung

Initial tissue reaction : focal fibrinoid necrosis


Acute Rheumatic Carditis (ARC)

Characteristic :

Inflammatory in 3 layers of heart (Pancarditis)

Hallmark of ARC : (Aschoff bodies)

Multiple foci of inflammation within connective tissue of heart C l f fib i id i Central focus fibrinoid necrosis Surrounded by :• Mononucleous• Anitschkow cells

(large histiocyte, vesicular nuclei, abundant basophilic cytoplasm)


Pericardial involment

Manifested grossly &

Fibrinous pericarditis

microscopically :

Fibrinous pericarditis

Serous/Sero-sanguineous effusion


Endocardium

Valvular inflammation tends to : mitral & aortic valves

Th l di The valve predisposes :

Small vegetations (valve closure) = verrucous endocarditis


Infective Endocarditis

Infection of the cardiac valve /mural surface of the endocardiumthrombotic (debris+organism) [term vegetation]

Caused by bacteria

Acute Sub-acute

High virulence

Previously abnormal valve

L i lHigh virulence(Staph. Aureus)

Low virulence(α-Hemolytic Streptococcus)


MorphologyMorphology

V t ti Vegetations : Bacteria or other organism Single / multipleg pMay involved : > 1 valve

Most common : Aortic & Mitra

RV valve drug abuser

Fungal ↑↑


A t E d ditiAcute Endocarditis

Classic vegetation gBegins : small excrescences

indistinguishable from NBTE (Non Bacterial Thrombotic Endocarditis) Endocarditis)

Infection may extend through :Valve myocardium abscess peri-valvular (ring abscess)y p ( g )

Microscopic : B t i l fib i bl dBacterial, fibrin, bloodExtends beyond avasc valve neutrophil responseSystemic emboli brain, kidney, myocard infarct abscesses


Bacteriemia

EtiologyIV Drug Abuse

Dental Surgeryg y

Catheter

Brushung teeth

Risk Preexisting cardiac abnormal

• Prosthetic heart valves•I V drug abuser


PERICARDIAL DISEASE

PERICARDITISPERICARDITIS

Virus, pyogenic bacteria, mycobacteria, fungi

Cause :

, py g , y , g

Secondary to :

Acute myocard infarct

Cardiac surgery

Radiation to the mediastinum

Uremia

RF, SLE, metastatic malignancies


P i diti Pericarditis may :

1. Immediate hemodynamic complications

2 Resolve sequelae (-)2. Resolve sequelae (-)3. Progress to chronic fibrosing process


Morphology

Acute pericarditis

Patients with uremia / acute RF : fibrinous, shaggy (bread & butter pericarditis)

Viral : fibrinous

Acute Bacterial : fibrinopurulent

Tuberculous : caseous

Metastases : shaggy fibrinous

Acute fibrinous / fibrinopurulent resolve, sequelae (-)Extensive suppuration / caseation chronic pericarditisExtensive suppuration / caseation chronic pericarditis


Ch i i ditiChronic pericarditis

A Appearance ranges :

Delicate adhesions – dense, fibbrotic scars that obbliterate the pericardial spaceobbliterate the pericardial space

Constrictive pericarditis


ComplicationsCo p cat o s

1. Constrictive pericarditisp

2. Obliterate pericarditis (Focally / diffuse)

3. V. Cava compression, causes : AscitesHepatosphlenomegaly

4 DC4. DC


Pericardial Effusions

Serous Serosanguineous Chylous

CvHDHypoalbumiemia

Blunt chest traumaMalignancy

Mediastinallymphatic

obstruction


Hemopericardium

Separately from hemorrhagic pericardium effusion

Pure blood :Ruptured aortic aneurismaRuptured myocar infarctPenetrating trauma injPenetrating trauma inj

cardiac tamponade deathp


ATRIAL SEPTAL DEFECTATRIAL SEPTAL DEFECTIn the region of the foramen

l h l ovale on the interatrial septum is a small atrial septal defect, as seen in this heart ,opened on the right side. Here the defect is not closed b th t d by the septum secundum, so a shunt exists across from left to right.g

Congenital Heart DiseaseCongenital Heart DiseaseType of Defect Mechanism Ventricular Septal Defect (VSD)There is a hole within the membranous or muscular portions of the intraventricular septum that

d l f h h h l d f produces a left-to-right shunt, more severe with larger defects Atrial Septal Defect (ASD) A hole from a septum secundum or septum primum defect in the interatrial septum produces a modest left-to-right shunt Patent Ductus Arteriosus (PDA)The ductus arteriosus, which normally closes soon ( ) , yafter birth, remains open, and a left-to-right shunt develops Tetralogy of Fallot Pulmonic stenosis results in right ventricular hypertrophy and a right-to-left shunt across a VSD, which also has an overriding aorta Transposition of Great Vessels The aorta arises from the right ventricle and the Transposition of Great Vessels The aorta arises from the right ventricle and the pulmonic trunk from the left ventricle. A VSD, or ASD with PDA, is needed for extrauterine survival. There is right-to-left shunting. Truncus ArteriosusThere is incomplete separation of the aortic and pulmonary outflows, along with VSD, which allows mixing of oxygenated and deoxygenated blood , g , g yg ygand right-to-left shunting Hypoplastic Left Heart SyndromeThere are varying degrees of hypoplasia or atresia of the aortic and mitral valves, along with a small to absent left ventricular chamber Coarctation of Aorta Either just proximal (infantile form) or just distal (adult form) j p ( ) j ( )to the ductus is a narrowing of the aortic lumen, leading to outflow obstruction Total Anomalous Pulmonary Venous Return (TAPVR)The pulmonary veins do not directly connect to the left atrium, but drain into left innominate vein, coronary sinus, or some other site, leading to possible mixing of blood and right-sided overload

At the right is a probe patent foramen ovale in an adult. A metal probe lifts the septum secundum and reveals the opening. Normally, the left atrial pressure keeps the foramen closed, but if right atrial gpressures rise with pulmonary hypertension (as with pulmonary embolus), the foramen may open and even allow a thrombus to go gfrom right to left. This is a "paradoxical embolus", rare (seen on the left here), and so called because a thromboembolus arising gfrom the venous circulation can end in the systemic circulation.

VETRICULAR SEPTAL DEFECTVETRICULAR SEPTAL DEFECT

This is the heart of a premature illb i h T i 13 i hi h stillborn with Trisomy 13 in which a

ventricular septal defect is visible in the membranous septum. About 90% of VSD's are in the membranous septum and 10% in the muscular septum.

Here is a heart with both an atrial septal defect (ASD) and a muscular septal defect (ASD) and a muscular ventricular septal defect (VSD). The heart is opened on the left side. Such small defects do not produce psignificant left-to-right shunting, but they do increase the risk for infective endocarditis.

COARTIO AORTACOARTIO AORTAThe aorta is opened longitudinally here to reveal a coarctation. In the region of to reveal a coarctation. In the region of the narrowing, there was increased turbulence that led to increased atherosclerosis.

This portion of aorta was resected This portion of aorta was resected from a patient with a coarctation. The aorta narrows postductally here to about a 3 mm opening.p g

The diagram above depicts the findings with a persistent truncus arteriosus.

This occurs when there is failure of fusion and descent of the spiral pridges of the truncus and conus that would ordinarily divide into aorta and pulmonic trunck respectively.When the spiral septum fails to When the spiral septum fails to completely descend, the aortic and pulmonic trunks are left undivided at their outflow.Th t id b th The truncus overrides both ventricles.The persistent truncus is always accompanied by a membranous ventricular septal defect.

This diagram depicts the features of Tetralogy of Fallot

1 Ventricular septal defect; 1. Ventricular septal defect; 2. Overriding aorta; 3. Pulmonic stenosis; 4 Ri ht t i l 4. Right ventricular

hypertrophy.

The obstruction to right ventricular outflow creates a right-to-left shunt that g

leads to cyanosis.

This large atrial septal defect with left-to-right shunt gresulted in pulmonary hypertension with increased pulmonary arterial pressures that eventually led to reversal yand right-to-left shunt, resulting in marked right ventricular hypertrophy. This result from a cardiac septal pdefect is known as Eisenmenger's complex. The finger at the left is holding a markedly thickened right y gventricular free wall below the tricuspid valve, and the finger at the right is holding the interventricular septum. p

Here is a congenital bicuspid aortic valve. Most bicuspid valves are prone to are prone to calcification. Patients can remain relatively asymptomatic until the y pstenosis reaches a critical point when congestive heart failure

idl Th rapidly ensues. The dense white nodules of calcification are present on either valve surface on either valve surface. The valve here has been opened with the aortic outflow above and the left ventricular myocardium below.

In the diagram above, transposition of th g t l i h the great vessels is shown.

This occurs when the trunco-conal septum does not spiral down septum does not spiral down. Instead, it descends straight down. As a result, the outflow of right ventricle is into the aorta and the outflow from the left ventricle is into the pulmonic trunk.In order for this system to work, there must b ti b t th t be a connection between the system and pulmonic circulations. Sometimes this is through a ventricular septal defect or an atrial ventricular septal defect or an atrial septal defect. In the diagram at the left, this is through a patent ductus arteriosus.

cardiovasculer maret 2009.ppt...

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