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بسم الله الرحمن الرحيم
Cardiac Diseases Dr. Samar Al H akeem Department of pathology Faculty of Medicine University of Mosul


Congestive Heart Failure Cardiac output not adequate for body needs Mainly due to inability of the heart to eject the blood that receives from the venous system (pumping failure) Less frequently due to Blood loss Low venous return Increase demands in tissue as in pregnancy


Causes of CHF (Congestive heart failure) 1/ Left heart failure: 1- Ischemic heart disease 2- Hypertension 3- Aortic & mitral valve disease 4- Myocardial disease


Manifestations of heart failure 1/ LHF 1- Dyspnea: exertional, orthopnia, paroxysmal nocturnal dyspnea due to congestion & edema of the lungs 2- Hypoxic/ ischemic encephalopathy: due to CNS hypoxia

2/ Right heart failure: 1- LHF 2-Primary disease of pulmonary vasculature 3- Pulmonary or tricuspid valve disease 4- Cardiomyopathies & myocarditis 5- Primary lung diseases


Manifestations of heart failure 1/ RHF Peripheral edema Effusion in body cavities (ascitis, pleural effusion) Dusky face, engorged veins of the neck Chronic liver congestion & congestive splenomegaly

CONGENITAL HEART DISEASES

most common types of heart diseases among children occur in about 1% of live births, higher incidence in prematures and stillborns


clinical features
-left to right shunt -right to left shunt -flow obstruction shunt is an abnormal communication between chambers or blood vessels


left to right shunt -Non cyanotic heart disease -cyanosis appears later on due to reversing of shunt from right to left and development of (Eisenmenger syndrome) -conditions .atrial septal defect (ASD) .ventricular septal defect (VSD) .patent ductus arteriosus (PDA) .atrioventricular septal defect

Ventricular septal defect

Right to left shunt
cyanosis, chronic cyanosis causing clubbing of the fingers and toes (hypertrophic osteo-arthropathy) and polycythemia conditions .tetralogy of fallot .transposition of the great arteries .persistent truncus arteriosus .tricuspid atresia .total anomalous pulmonary .venous connection

Congenital heart disease, transposition of the great arteries

obstructive congenital heart diseases examples .coarctation of the aorta .aortic valvular stenosis .pulmonary valvular stenosis

Ischemic Heart disease (IHD)

Ischemic Heart Disease (IHD)
A group of closely related syndromes caused by an imbalance between the myocardial oxygen demands & blood supply Most common underlying cause is atherosclerosis of coronary arteries Clinical syndrome of IHD includes: Angina pectoris Myocardial infarction Sudden cardiac death Chronic IHD & CHF

Acute coronary syndromes

Pathogenesis of ischemic heart disease


Symptomatic IHD is typically associated with a critical stenosis (75% or more) reduction in the lumen of 1 or more coronary arteries by atherosclerotic plaque Other that play in IHD 1/ Acute change in plaque morphology: Fissuring, hemorrhage & rupture embolization of debris into distal coronary artery Increase platelet aggregation increase risk of thrombosis Platelet aggregation causes mechanical occlusion vasospasm coronary artery thrombosis


2/Non atherosclerotic lesion of coronary artery Emboli from vegetation on valves Vasaculitis Severe hypotension Spasm of coronary artery 3/increase myocardial demands Hypertrophy Cardiomyopathies

Angina Pectoris

Angina Pectoris
A clinical syndrome characterized by paroxysmal attacks of chest pain usually situated retrosternal, radiating to precordium & left upper limb & other sites caused by transient, (15 seconds- 15 minutes) myocardial ischemia1/ Classical AP2/ Vasopastic (prinzmetal’s) angina

3/ Unstable angina (preinfarction angina) More frequent Provoked by less effort or emotion Lasts longer Nitroglycerine is required more & less effective Carries a bad prognostic implication Caused by acute plaque lesion with superimposed partial thrombosis


Myocardial Infarction

Acute Myocardial Infarction

An area of ischemic necrosisAcute MI is the most common cause of death in West 1.5 mil of MI / yr in USA with Ѕ mil deaths. Large number of which don’t reach hospital2 types of MI1/Transmural MI: full thickness infarction caused by severe atheroma with acute plaque changes leading to complete occlusion2/Subendocardial MI: limited to inner 1/3rd or Ѕ of wall thickness caused by global ischemia due to atheroma with increased demand often super-imposed on chronic non-critical coronary stenosis

Progression of myocardial necrosis following coronary artery occlusion

Distribution of myocardial infarction in relation to coronary artery occlusion


Morphology of MI Gross pathology: MI fewer than 12 hr old are usually unapparent on gross examination. However; it is possible to outline the area of necrosis after 2-3 hr by impression tissue slices in solution of triphenile tetrazlium, the dye impart a brick-red color to non infarct area

Transmural myocardial infarction, staining by tripheniletetrazolium chloride solution

Histology: Necrosis start after 20-40 min of ischemia Coagulative necrosis become apparent microscopically by about 4-12 hrs

Myocardial Infarction

Histology
Grossly


Slight pallor area Central pallor with hyperemic border Yellow soft shrunken center with purple border Firm gray fibrous tissue
Few wavy fibers at the margin of infarct Early coagulative necrosis, edema, occasional polymorph Established coagulative necrosis, heavy polymorph Macrophages appear, disintegration of muscle fibers & phagocytosis, granulation tissue at border Granulation tissue maximum Fibrosis
Time
1-2 hr
4-12 hr
12-24 hr
4-7 days

7-10 days

7-10 weeks

Myocardial infarction, 1 day, 3-4 days, 7-10 days, granulation tissue, scar

Infarction modification after reperfusion Reperfusion sufficiently early (within the first 15-20 min) may prevent all necrosis If delay after 15-20 min might limit the size of infarction & induced some changes includes: Hemorrhage into ischemic area due to vascular injury Contraction band necrosis in fibers at periphery of infarct caused by hypercontraction of myofibrils in dying cells which induced by influx of calcium from plasma into the cells after the damage of cell membrane by free radicals formed by reperfusion

Reperfusion injury


Laboratory Diagnosis of MI Cardiac enzymes & proteins Creatinine kinase-MB: rise within 2-4 hr, peak at 18 hr & disappear after 48 hr lactic dehydrogenase(Ld1): rises within 24 hr, peaks at 72 hr & persist for 1 week Troponines (I & T): most specific, appear similar to CK but remain 7-10 days c-reactive protein serves as a marker to predict the risk of MI in patients with angina and the risk of new infarcts in patients who recover from infarcts ECG changes: q wave, ST elevation & T inversion

Consequences and complications of MI

Half of the deaths occur within one hour of onset of symptoms

Factors associated with poor prognosis; -advanced age -female gender -diabetes mellitus -previous MI

Complication of MI

After infarction about 25% of patients experience sudden death due to fetal arrhythmias If patient survive the acute event, 80-90% develop complications 1-Arrhythmias (75-95%) 2- CHF (60%) 3- Cardiogenic shock (10%) if > 40% of LV infarction 4- Rarely papillary muscle infarction with or without rupture leading to mitral valve dysfunction

5- Mural thrombosis with thromboembolic phenomena (15-40%) 6- Ventricular rupture (1-5%) During the 1st 10 days, maximum (4-5) days Free wall rupture causing pericardial hemorrhage & cardiac temponade IVS rupture causing left to right shunt & right ventricular overload 7-Venticular aneurysm 8- Fibrinous or hemorrhagic pericarditis


Complications of myocardial infarction, rupture, pericarditis, expansion, aneurysm

Sudden Cardiac Death

Unexpected death from cardiac cause within 1 hour of onset of symptoms Majority are complication of IHD 75-95% have marked atheromas Other causes Marked aortic stenosis Abnormalities of conductive system Myocarditis Mitral valve prolapsed Cardiomyopathies Ruptured aortic aneurysm

Left ventricular hypertrophy

Hypertensive heart disease, systemic, pulmonary

Rheumatic Fever & Rheumatic Heart Disease


R F is an acute recurrent immunological mediated multisystemic inflammatory disease mainly affecting children following pharyngitis with group A beta hemolytic streptococci & characterized by Jones Criteria
Major Criteria:1-Pancarditis2-migratory polyarthritis3-Subcutaneous nodules4-Sydenham’s chorea 5-Erythema marginatum of the skin Minor Criteria: 1-Fever 2-Arthralgia 3-Elevated Antistreptolysin O(ASOT) 4-Elevated acute phase reactant C protein 5-Prolongation of PR intervals


Etiology & Pathogenesis of RF RF is an immune reaction secondary to streptococcus infection Antibodies against strept. antigen cross react with tissue antigens including cardiac antigens

Morphology of RF

1/ Acute attack The pathognomic lesion is a disseminated focal inflammatory foci known as Aschoff bodies
Aschoff body: focus of fibrinoid necrosis surr. by a collagen, lymphocytes, macrophages & few plasma cells plus modified histiocytes known as Antischow cells & multinucleated cells known as Aschoff giant cells. Typically seen in myocardium esp. around blood vessels

2/ Chronic attack

Fibrosis & deformities of the heart esp. the valves Mitral valve most commonly affected followed by aortic valve, tricuspid valve & lastly pulmonary valve


Endocarditis: Small nodular or warty vegetations (platelets & fibrin) along lines of closure of the valve cusps, chorda tendeni & mural endocardium (verrucous or rheumatic endocarditis) Healing either by minimal fibrosis or may end in severe valve deformity


Chronic Rheumatic Heart Disease More likely to occurs in: 1-First attack in early childhood 2-Severe initial attack of RF 3-Recurrent attacks Mitral valve alone most commonly involved in 65-70 % of cases, then mitral & aortic valves in combination in 25 %, less affection is aortic valve alone Pulmonary & tricuspid valves are rarely affected


Chronic Rheumatic Heart Disease Mitral Valve: 1-Fibrous thickening & calcification of leaflets 2-Fusion of commissaries result in fish mouth or button hole deformity & stenosis 3-Chorda tendeni are thickened, fused & shortened 4-Mitral stenosis or combined stenosis & incompetence 5- More common in female Aortic Valve: 1-Similar to MV with prominent nodular calcification in the sinuses-bind the leaflets 2-Aortic stenosis or combined stenosis & incompetence 3-More common in male

Complication of acute & chronic RHD 1-Mural thrombi & thromboembolism 2-Infective endocarditis superimposed deformed valve 3-Heart failure 4-Cardiac arrhythmia

Endocarditis

Endocarditis: Inflammation of valves &/or mural endocardium It classified into:
1/ Infective endocarditis: Bacterial Viral fungal Chlymadial Recticeal (Q fever)
2/ Non-infective endocarditis: Rheumatic endocarditis Non-bacterial thrombotic endocarditis (Marantic endocarditis) Libman-Sacks endocarditis (SLE ass endocarditis)


1/ Infective endocarditis: Infection & colonization of cardiac valves or mural endocardium by microbiological agents leading to formation of bulky friable & destructive vegetation Most are caused by bacteria (bacterial endocarditis It is classified into acute & subacute endocarditis depending on clinical course of the disease & virulence of microorganism & the underlying valve status


Etiology & pathogenesis: Colonization of the valves by bacteria in episodes of bacteremia both obvious & occult Intravenous drug abuse Source of infection in the body Surgical or oral procedures Predisposing factors in IE: Rheumatics heart disease Congenital heart disease Mitral valve prolapsed Artificial valve Neutropenia, immunodeficiency & immunosuppression



Causative bacterial organisms Streptococcus viridians Staphylococcus aureus Oral commensals (HACEK) Haemophilus species, Aggregatibacter species, Cardiobacterium hominis, Eikenella corrodens, and Kingella species Coagulase negative staphylococcus. (staphylococcus epidermidis)

Non bacterial thrombotic endocarditis (Marantic)

Precipitation of small masses of fibrin, platelets & other blood elements on valve leaflets usually single, resemble the vegetations of rheumatic endocarditis (small non destructive, non inflammatory, sterile) most cases seen in patients died of debilitating disease as in cancer, sepses, extensive burn Hypercoagulable state causing embolic phenomena no local effect

Valvular Heart Diseases

Valvular Heart Diseases It may congenital or acquired Most frequent acquired stenosis of mitral & aortic valves which account for 2/3rd of all valve lesion Incompetence may appear either Acutely as in IF & ruptured cords Chronically as in leaflet scaring Valvular stenosis almost always a chronic process

Mitral stenosis

Causes: Rheumatic heart disease Congenital Large vegetation of IE Complication Thrombosis in LA Systemic embolization Arrhythmias
Mitral regurgitation
Causes: Abnormalities of the leaflets Rheumatic heart disease IE Mitral valve prolapsed Abnormalities of tensor apparatus Ruptured of papillary muscle or chordae tendenea Fibrosis of papillary muscle Abnormalities of the LV cavity LV enlargement Calcification of mitral ring

Mitral valve prolapsed (Floppy mitral valve)

A congenital disorder characterized by ballooning of the valve leaflets, particularly the posterior leading to functional incompetence A common condition, more in females 20-40 yr of age affect 3% of population May be a feature of Marfans syndrome

Aortic stenosis

Causes: Rheumatic heart disease Calcification Congenital
Aortic regurgitation
Causes: Intrinsic valvular diseases Rheumatic heart disease IE Disease of Aorta: Syphilitic aortitis Ankylosing spondylitis Rheumatoid arthritis Marfans syndrome


Calcific Aortic stenosis Degenerative, age related lesions occurring more frequently & earlier (6th-7th decades) in congenital bicuspid valves Heaped up calcified masses within the sinus of valsalva + thickening & fibrosis of the aortic cusps with narrowing of the orifice

Myocarditis

Myocarditis
Inflammation of the myocardium in which the inflammatory cells are associated with myocyte necrosis & degeneration


Causes of myocarditis 1- Infectious: viral, bacterial, fungal (candida), protozoal (Toxoplasmosis & Trypanosome cruzi), helminthes (Trichinosis) 2- Non infectious: rheumatic fever, SLE, drug hypersensitivity 3- Others: Sarcodosis, giant cell myocarditis Most common is viral & esp. Coxackie-B& A viruses, other are HIV & CMV Bacterial by Corynebacterium diphtheria & Neisseria meningococcus)

Cardiomyopathies Heart muscle disease of unknown cause Pathophysiologic categories of CMP Dilated (congested) CMP Hypertrophic (obstructive) CMP Restrictive (infiltrative) CMP



Dilated (congestive) CMP Occurs at any age esp. between 20-60 yr Slowly developing CHF Causes Unknown (idiopathic) Pregnancy induced Alcoholism & drugs Myocarditis Genetic in 20-30% Heart is always increase in weight, dilation may mask hypertrophy Causes of death CHF Embolic phenomena Fatal arrhythmias


Hypertrophic (obstructive) CMP (idiopathic Hypertrophic subaortic stenosis) Characterized by increased wall thickness, mainly LV esp. the interventicular septum particularly upper portion Reduced compliance Reduced volume capacity of LV Low stroke volume

Hypertrophic (obstructive) CMP (idiopathic Hypertrophic subaortic stenosis)

Hypertrophic (obstructive) CMP (idiopathic Hypertrophic subaortic stenosis) Major complication Atrial fibrillation Mural thrombi with embolization Sudden cardiac death

Restrictive (infiltrative) CMPLeast common type, characterized by restriction of ventricular filling during diastole & thus reduced cardiac output due to decrease compliance of ventricleDiastolic dysfunctionCausesAmyloidosis, both systemic or localizedRadiation, sarcoidosisMetastatic trEndomyocardial fibrosisLoffler’s endocarditisEndocardial fibroelastosis: diffuse cartilage-like fibroelastic thickening of the endocardium most commonly seen in childrenDeath is usually due to emboli or CHF

Pericarditis Causes Infectious: viral, pyogenic bacterial, Tb, fungal Immune mediated: RF, SLE, scleroderma Miscellaneous: MI, uremia, malignancies Types Serous Fibrinous & serofibrinous Most common type Purulent (suppurative) pericarditis Bacterial, fungal and parasitic Hemorrhagic pericarditis Tb, malignancy Caseous pericarditis Tb Constrictive pericarditis

TUMORS OF THE HEART

Primary tumors are rare. Myxoma: most common primary tumor, benign, mostly located in the atria as solitary sessile or pedunculated mass of 1-10cm. Rhabdomyoma: Benign tumor seen in children

Metastatic tumors to the heart occur in about 5% of patients dying of cancer




رفعت المحاضرة من قبل: Omar Almoula
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