CARDIOVASCULER. Dr.H.Delyuzar Sp.PA (K)

Transcription

1 CARDIOVASCULER Dr.H.Delyuzar Sp.PA (K)

2 ISCHAEMIC HEART DIASEASE (±80%) HYPERTENSIVE HEART DIASEASE ( 9%) HEART DISEASE RHEUMATIC HEART DIASEASE ( 2-3 %) CONGENITAL HEART DIASEASE (2 %) ENDOCARDITIS BACTERIALIS ( 1-2 %) SYPHILLIS HEART DIASEASE ( 1%) COR PULMONALE DIASEASE ( 1 %) 2 OTHERS ( 5%)

3 CORONARY HEART DISEASE

4 CORONARY HEART DISEASE ARTERIOSCLEROTIC HEART DISEASE ANGINA PECTORIS MYOCARDIAL INFARCTION 4 Departemen Pathology Anatomy - Cardiovascular

5 ARTERIOSCLEROTIC HEART DISEASE Atherosclerotic coronary artery Diffuse myocardial fibrotic occasionally cardiac valve fibrotic MORPHOLOGY Atherosclerotic Ischaemic Myocardial fibrotic Brown Atrophy Marked as Brownish-yellow granular diffusely (accumulates in the heart muscle) contained lipofuscin (complexes of lipid & protein) 5 Departemen Pathology Anatomy - Cardiovascular

6 ARTERIOSCLEROTIC O C HEART DISEASE S The heart is become: Small Normal Enlarged Disorder of cardiac valve : Mitral valve fibrotic Chordae tendineae fibrotic or calcification 6 Departemen Pathology Anatomy - Cardiovascular

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8 Gross appearance of heavily fibrotic and calcified lifid cardiac valve 8 Departemen Pathology Anatomy - Cardiovascular

9 ANGINA PECTORIS Intermittent chest pain caused by transient, reversible myocardial ischaemic TYPICAL / STABLE ANGINA PECTORIS PRINZMETAL / VARIANT, ANGINA UNSTABLE ANGINA PECTORIS (cressendo angina ) 9 Departemen Pathology Anatomy - Cardiovascular

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11 Pathogenesis Myocardial hypoxia Artherosclerotic coronary arteri Syphilis heart disease Polyarthritis nodosa Aorta valve insufficiency Anemia Hypoxia caused of: Occlusion of arteries Coronary artery vasospasm Paroxismal myocadial hypoxia imposed by exercise 11 Departemen Pathology Anatomy - Cardiovascular

12 MYOCARDIAL INFARCTION Popularly called heart attack k Development of an area of myocardial necrosis caused by local ischaemia Coroner insufficiency caused by : 12 Departemen Pathology Anatomy - Cardiovascular Coronary atherosclerosis (99%) Thrombosis & Emboli Vascular diseases Osteum occlusion caused by syphillis Arteriosclerosis occlusion & Hypotension

13 Pathogenesis Basic : Coronary Arterial Occlusion Severe coronary atherosclerosis Acute atherosclerotic plaque change (rupture) Superimposed pletelet ltltactivation Thrombosis & vasospasm Consequence: Myocardial Response Cessation of aerobic glycolysis anaerobic glycolysis Inadequate product of phosphate (Creatine phos & ATP) acc lactid acid

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15 Distribution of infarcts Right coronary artery (30-40 %) Left anterior descending artery (40-50 %) Left circumflex artery (15-20 %) 15 Departemen Pathology Anatomy - Cardiovascular

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19 Evolution Of Morphologic Changes in Myocardial Infarction Time Gross Feature Light Microscopic Findings Reversible Injury Electron Microscopic Findings < ½ hr None None Relaxation of myofibrils; glycogen loss; mitochondrial swelling Irreversible Injury ½ -4 hr None Usually none; variable waviness of fibers at border 4-12 hr Occasionally dark mottling 19 Departemen Pathology Anatomy - Cardiovascular Beginning coagulation necrosis; edema; haemorrhage Sacrolemmal disruption; mitochondrial amorphous densities

20 Evolution Of Morphologic Changes in Myocardial Infarction Time Gross Feature Light Microscopic Findings hr Dark mottling Coagulation necrosis; contraction ti band necrosis at periphery of infarct; neutrophilic infiltrate 1-3 days Mottling with yellow-tan infarct center Complete coagulation necrosis of myofibers; heavy neutrophilic infiltrate 3-7 days Hyperemic border; central yellow-tan Beginning gdisintegration of dead softening myofibers, 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 margins 20 Departemen Pathology Anatomy - Cardiovascular

21 Time Gross Feature Light Microscopic Findings 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 21 Departemen Pathology Anatomy - Cardiovascular

22 Complications Papillary muscle dysfunction (infarcted papillary muscle may rupture) External rupture of the infarct cardiac tamponade Rupture of the intraventricular septum Mural thrombi potential sources for systemic emboli Ventricular fibrotic & aneurysms 22 Departemen Pathology Anatomy - Cardiovascular

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24 HYPERTENSIVE HEART DISEASE

25 HYPERTENSIVE HEART DISEASE Diagnosis based on: Left ventricular hypertrophy with a history of hypertension Excluded Aortic stenosis Primary hypertropic cardiomyopathy 25 Departemen Pathology Anatomy - Cardiovascular

26 Morphology Concentric hypertrophy (symetric, circumferential > 450 gm) Size: Early: Normal dilated d Microscopic Myocytes > Nuclei: large, hyperchrom, boxcar shaped 26 Departemen Pathology Anatomy - Cardiovascular

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28 VALVULAR HEART DISEASE

29 RHEUMATIC HEART DISEASE Acute, immunologically mediated, multisystem inflammatory disease group A streptococcal pharyngitis after an interval of a few weeks 29 Departemen Pathology Anatomy - Cardiovascular

30 Rheumatic Fever may cause HD in acute phase Chronic valvular (Acute rheumatic carditis) i deformities Only 3% group A streptococcal pharyngitis RF Initial reactivation with subsequent pharyngeal infections Ab >< M protein cross reaction with glycoprotein : Heart Joints & others Onset : 2-3 weeks after infection Streptococci (-) in lesion 30 Departemen Pathology Anatomy - Cardiovascular

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33 Morphology Acute Rheumatic Fever Inflammatory infiltrates in : Synovium Joint Skin Heart (most importantly) fibrosis deformities Lung Initial tissue reaction : focal fibrinoid necrosis 33 Departemen Pathology Anatomy - Cardiovascular

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35 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 Central focus fibrinoidi id necrosis Surrounded by : Mononucleous Anitschkow cells (large histiocyte, vesicular nuclei, abundant basophilic cytoplasm) 35 Departemen Pathology Anatomy - Cardiovascular

36 Pericardial involment Manifested grossly & microscopically : Fibrinous pericarditis Serous/Sero-sanguineous effusion 36 Departemen Pathology Anatomy - Cardiovascular

37 Endocardium Valvular inflammation tends to : mitral & aortic valves The valve predisposes : Small vegetations (valve closure) = verrucous endocarditis 37 Departemen Pathology Anatomy - Cardiovascular

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39 Infective Endocarditis Infection of the cardiac valve /mural surface of the endocardium thrombotic (debris+organism) [term vegetation] Caused by bacteria Acute High virulence (Staph. Aureus) 39 Departemen Pathology Anatomy - Cardiovascular Sub-acute Previously abnormal valve Low virulence (α-hemolytic Streptococcus)

40 Morphology Vegetations ti : Bacteria or other organism Single / multiple May involved : > 1 valve Most common : Aortic & Mitra RV valve drug abuser Fungal 40 Departemen Pathology Anatomy - Cardiovascular

41 Acute Endocarditis diti Classic vegetation Begins : small excrescences indistinguishable from NBTE (Non Bacterial Thrombotic Endocarditis) Infection may extend through : Valve myocardium abscess peri-valvular (ring abscess) Microscopic : Bacterial, fibrin, i blood Extends beyond avasc valve neutrophil response Systemic emboli brain, kidney, myocard infarct abscesses 41 Departemen Pathology Anatomy - Cardiovascular

42 Etiology Bacteriemia IV Drug Abuse Dental Surgery Catheter Brushung teeth Risk Preexisting cardiac abnormal Prosthetic heart valves I V drug abuser 42 Departemen Pathology Anatomy - Cardiovascular

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44 PERICARDIAL DISEASE

45 PERICARDITIS Cause : Virus, pyogenic bacteria, mycobacteria, fungi Secondary to : Acute myocard infarct Cardiac surgery Radiation to the mediastinum Uremia RF, SLE, metastatic malignancies 45 Departemen Pathology Anatomy - Cardiovascular

46 Pericarditis may : 1. Immediate hemodynamic complications 2. Resolve sequelae (-) 3. Progress to chronic fibrosing process 46 Departemen Pathology Anatomy - Cardiovascular

47 Morphology Acute pericarditis Patients with uremia / acute RF : fibrinous, shaggy (bread & butter pericarditis) Viral : fibrinous Acute Bacterial : fibrinopurulent Tuberculous Metastases : caseous : shaggy fibrinous Acute fibrinous / fibrinopurulent resolve, sequelae (-) Extensive suppuration / caseation chronic pericarditis 47 Departemen Pathology Anatomy - Cardiovascular

48 Chronic pericarditis Appearance ranges : Delicate adhesions dense, fibbrotic scars that obbliterate the pericardial space Constrictive pericarditis 48 Departemen Pathology Anatomy - Cardiovascular

49 Complications o 1. Constrictive pericarditis 2. Obliterate pericarditis (Focally / diffuse) 3. V. Cava compression, causes : Ascites Hepatosphlenomegaly 4. DC 49 Departemen Pathology Anatomy - Cardiovascular

50 Pericardial Effusions Serous Serosanguineous Chylous CvHD Hypoalbumiemia Blunt chest trauma Malignancy Mediastinal lymphatic obstruction 50 Departemen Pathology Anatomy - Cardiovascular

51 Hemopericardium Separately from hemorrhagic pericardium effusion Pure blood : Ruptured aortic aneurisma Ruptured myocar infarct Penetrating trauma inj cardiac tamponade death 51 Departemen Pathology Anatomy - Cardiovascular

52 ATRIAL SEPTAL DEFECT In the region of the foramen 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 by the septum secundum, so a shunt exists across from left to right.

53 Congenital Heart Disease Type of Defect Mechanism Ventricular Septal Defect (VSD)There is a hole within the membranous or muscular portions of the intraventricular septum that 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 after 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 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 and 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) 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

54 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 pressures rise with pulmonary hypertension (as with pulmonary embolus), the foramen may open and even allow a thrombus to go from right to left. This is a "paradoxical embolus", rare (seen on the left here), and so called because a thromboembolus arising from the venous circulation can end in the systemic circulation.

55 VETRICULAR SEPTAL DEFECT This is the heart of a premature stillborn with Trisomy 13 in which h 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.

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

57 COARTIO AORTA The aorta is opened longitudinally here 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 from a patient with a coarctation. The aorta narrows postductally here to about a 3 mm opening.

58 The diagram above depicts the findings with a persistent truncus arteriosus. This occurs when there is failure of fusion and descent of the spiral ridges of the truncus and conus that would ordinarily divide into aorta and pulmonic trunck respectively. When the spiral septum fails to completely descend, the aortic and pulmonic trunks are left undivided at their outflow. The truncus overrides both ventricles. The persistent truncus is always accompanied by a membranous ventricular septal defect.

59 This diagram depicts the features of Tetralogy of Fallot 1. Ventricular septal defect; 2. Overriding aorta; 3. Pulmonic stenosis; 4. Right ventricular hypertrophy. The obstruction to right ventricular outflow creates a right-to-left shunt that leads to cyanosis.

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

61 Here is a congenital bicuspid aortic valve. Most bicuspid valves are prone to calcification. Patients can remain relatively asymptomatic until the stenosis reaches a critical point when congestive heart failure rapidly ensues. The dense white nodules of calcification are present on either valve surface. The valve here has been opened with the aortic outflow above and the left ventricular myocardium below.

62 In the diagram above, transposition of the great vessels is shown. This occurs when the trunco-conal 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 be a connection between bt the system and pulmonic circulations. Sometimes this is through a ventricular septal defect or an atrial septal defect. In the diagram at the left, this is through a patent ductus arteriosus.

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