HEART

HEARTBY DR ABIODUN MARK AKANMODE.

CONTENT.Normal heart physiology and anatomy.Heart failure.Congenital heart diseases.Ischemic heart diseases.Hypertensive heart diseases.Valvular heart diseases.Endocarditis.Cardiomyopaties.Myocarditis.Miscellaneous.

Normal heartThis is the external appearance of a normal heart.The epicardial surface is smooth and glistening. The amount of epicardial fat is usual.The left anterior descending coronary artery extends down from the aortic root to the apex.

Myocardial(NORMAL)This is the normal appearance of myocardial fibers in longitudinal section. Note thecentral nucleiand the syncytial arrangement of the fibers, some of which have pale pinkintercalated disks.Heart failure(HF)Congestive heart failure(CHF) orcongestive cardiac failure(CCF), occurs when theheartis unable to provide sufficient pump action to maintainblood flowto meet the needs of the body.The condition is diagnosed by patient physical examination and confirmed withechocardiography. In a chronic patient already in a stable situation, treatment commonly consists of lifestyle measures such assmoking cessation, light exercise, dietary changes, and medications.Generally CCF can be divided into RHF and LHF.

RSF.RSF is mostly caused by LSF.

Isolated RSF is caused by intrinsic conditions that increase the pressure within the lungs also tricuspid or pulmonary valvular diseases can lead to increase pressure on lungs ultimately causing pulmonary HTN.

This is referred to as cor pulmonale.(i.e. RSF due to pulmonary hypertension)

DISTENDED JVP.

LHF.The major causes of LHF are ischemic heart diseases, hypertension, aortic and mitral valve diseases etc.LHF is manifested classically by pulmonary edema & congestion.Reduced renal perfusion due to decreased cardiac output.Reduced CNS perfusion causing hypoxic encephalopathy which could range from mare irritability to severe coma.

CONGENITAL HEART DISEASES.CHD.CHD refers to cardiac or great vessel abnormalities that are present at birth.Most of the CHD are attributed to faulty embryogenesis between the 3rd and 8th week of gestation when major organs like the heart develops.CHD are of 2 types.-Shunts.-obstructions.CHD-SHUNTS.Shuts can be of 2 types.Left to right shunts(late cyanosis or blue kids)e.g.: ASD(atrial septal defects)VSD(ventricular septal defect)PDA(patent ductus arteriosus)Right to left shunts(early cyanosis or blue babies)e.g.: TOF(tetralogy of fallot)TG(transposition of great vessels)PTA.(persistent truncus arteriosus)TAVPR.(total anomalous venous pulmonary return) TA.(tricuspid atresia)LEFT TO RIGHT SHUNT: ASD.

RIGHT TO LEFT SHUNT:TOF.

CHD-OBSTRUCTION.Obstructive congenital diseases include:Aortic coarctation which can either be preductal or postductal.Valvular stenosis and atresias.Obstructive congenital diseases are generally not associated with cyanosis.ISCHEMIC HEART DISEASES.IHD(ISCHEMIC HEART DISEASES)This refers to a group of closely related heart diseases resulting from ischemia.Ischemia here is not just oxygen insufficiency but nutrients and metabolites also.Basically there is a mismatch between cardiac demands and vascular supply.The 4 basic IHD are: Myocardial infarction. Angina pectoris. Chronic ischemic HD Sudden cardiac death.MYOCARDIAL INFARCTION.MI the most important form of IHD generally occurs when the duration and severity of ischemia is sufficient to cause the death of cardiac muscle cells.

MI can be of 2 types.-transmural MI: involves all layers of the heart.

-Subendocardial infact: does not involve all layers.

Contraction band necrosis in MI.The earliest change histologically seen with acute myocardial infarction in the first day iscontraction bandnecrosis. The myocardial fibers are beginning to lose cross striations and the nuclei are not clearly visible in most of the cells seen here. Note the many irregular darker pink wavy contraction bands extending across the fibers.Complications of MI.Fatal arrytmias.CHF.Cardiogenic shock.Ventricular free wall rupture causing pericardial tamponade.Fibrinous pericarditis.Dresslers syndrome.

Ventricular wall Rupture.One complication of a transmural myocardial infarction is rupture of the myocardium. This is most likely to occur in the first week between 3 to 5 days following the initial event, when the myocardium is the softest. Note the dark red blood clot forming the hemopericardium. The hemopericardium can lead to tamponade.

Coronary artery bypass graftingThis patient underwent coronary artery bypass grafting with autogenous vein (saphenous vein) grafts. The largest of these runs down the center of the heart to anastomose with the left anterior descending artery distally.The internal mammary artery can also be harvested for CABG. The internal mammary artery has a better 10 yr prognosis as compared to the saphenous vein.Hypertensive heart disease.HHD.Hypertensive heart diseases mostly affects the left ventricle.In the setting of chronic hypertension the workload on the ventricles is increases and since he heart muscles cannot divide or replicate(permanent cells) they undergo hypertrophy so as to maintain cardiac function.

Here the ventricular wall is thickened (>2cm) and the heart weight is greater than 550gm.HHDLeft ventricular hypertrophy.

VALVULAR HEART DISEASES.VHD in adults is typically caused by degeneration(e.g calcific aortic stenosis, mitral anular calcification, mitral valve prolapse),immunologic inflammatory processes (e.g rheumatic heart diseases etc) or infections.Degenerative calcific aortic valve stenosis.Mitral valve prolapse.ENDOCARDITIS.Endocarditis.Endocarditisis aninflammationof the inner layer of theheart, theendocardium. It usually involves theheart valves(native or prosthetic valves). Other structures that may be involved include theinterventricular septum, thechordae tendineae, the mural endocardium, or even the surfaces of intracardiac devices. Endocarditis is characterized by a prototypic lesion, thevegetation, which is a mass ofplatelets,fibrin, microcolonies of microorganisms, and scant inammatory cellsTypes of Endocarditis.Infective endocarditis: here microbes colonize the heart valves and forms friable vegetations. The 2 types of infective endocarditis are acute and subacute.Diagnosis is via the Dukes criteria.

Non bacterial thrombotic endocarditis aka marantic endocarditis: this variant characteristically occurs in the settings of cancers e.g. adenocarcinomas

Libman sacks endocarditis: occurs with systemic diseases like SLE and antiphospholipid syndrome.

Marantic endocarditis/NBTE.The small pink vegetation on the rightmost cusp margin represents the typical finding with non-bacterial thrombotic endocarditis (or so-called "marantic endocarditis").

This is non-infective. It tends to occur in persons with a hypercoagulable state and in some malignancies.41

Verrucous vegetations in LBE.The smallverrucous vegetationsseen along the closure line of this mitral valve are associated with SLE LIBMAN SACKS ENDOCARDITIS.

These warty vegetations average only a few millimeters and form along the line of valve closure over areas of endocardial inflammation. Such verrucae are too small to cause serious cardiac problems.CARDIOMYOPATIES.

Dilated cardiomyopathyHere is a large, dilated left ventricle typical of a dilated, or congestive, cardiomyopathy. Many of these have no known etiology (so-called "idiopathic dilated cardiomyopathy") while others may be associated with chronic alcoholism. The heart is very enlarged and flabby.Microscopically, the heart in cardiomyopathy demonstrates hypertrophy of myocardial fibers (which also have prominent dark nuclei) along with interstitial fibrosis.

Hypertrophic cardiomyopathyThere is marked left ventricular hypertrophy, withasymmetric bulging of a very large inter-ventricular septum into the left ventricular chamber.

This is hypertrophic cardiomyopathy. About half of these cases are familial, though a variety of different genes may be responsible for this disease. Both children and adults can be affected, and sudden death can occur. Seen here is the explanted heart. Pacemaker wires enter the right ventricle. The atria with venous connections, along with great vessels, remained behind to connect to the transplanted heart (provided by someone who cared enough to make transplantation possible).PERICARDITIS.

Purulent pericarditisThis is a purulent pericarditis. Note the yellowishexudatethat has pooled in the lower pericardial sac that has been opened here. A bacterial organism is usually implicated in this process, and the infection typically spreads from the lungs.

fibrinous pericarditisA window of adherent pericardium has been opened to reveal the surface of the heart. There are thin strands of fibrinous exudate that extend from the epicardial surface to the pericarial sac. This is typical for a fibrinous pericarditis.

Hemorrhagic pericarditisThe surface of the heart with hemorrhagic pericarditis demonstrates a roughened and red appearance.

Hemorrhagic pericarditis is most likely to occur with metastatic tumor and with tuberculosis (TB).

TB can also lead to a granulomatous pericarditis that may calcify and produce a "constrictive" pericarditis.

Hemorrhagic pericarditisThe pericarditis here not only has fibrin, but also hemorrhage. Thus, this is called a "hemorrhagic pericarditis". It is really just fibrinous pericarditis with hemorrhage. Without inflammation, blood in the pericardial sac would be called "hemopericardium".RHEUMATIC FEVER & RHEUMATOID HEART DISEASES.RHD( RHEUMATIC HEAR DISEASE)This is an acute inflammatory disease classically occuring in children between the ages of 5-15.RHF ussually follows an episode of infection with the GAS bacteria.Diagnosis is based on clinical history and 2 of 5 Jones criteria.( erythema marginatum, syndehams chorea, carditis, subcutaneous nodules and migratory pilartheitis)Minor criteria includes fever, leukocytosis and athralgias.

Aschoff nodulesMicroscopically, acute rheumatic carditis is marked by a peculiar form of granulomatous inflammation with so-called "Aschoff nodules" seen best in myocardium. They are foci of fibrinoid necrosis found in the myocardium.The myocarditis associated with RHD may be severe enough to cause congestive heart failure.

Aschoff giant cellHere is an Aschoff nodule at high magnification. The most characteristic component is theAschoff giant cell. Several appear here as large cells with two or more nuclei that have prominent nucleoli. Scattered inflammatory cells accompany them and can be mononuclears or occasionally neutrophils.

Anitschkow myocyteAnother peculiar cell seen with acute rheumatic carditis is the Anitschkow myocyte. This is a long, thin cell with an elongated nucleus.Anitschklow cells are basically activated histocytes.MYOCARDITIS.Myocarditis.Typically refers to inflammation of the myocardial layer.

Causes include: Cox B virus T.cruzi (chagas disease)Alcohol Amylodosis Iron overload etc.

Viral myocarditisThe interstitial lymphocytic infiltrates shown here are characteristic for a viral myocarditis, which is probably the most common type of myocarditis. Many of these cases are probably subclinical. Some may be a cause for sudden death in young persons. There is usually little necrosis. The most common viral agent is Coxsackie B.

CARDIAC TUMORS.

AtrialmyxomaThe left atrium has been opened to reveal the most common primary cardiac neoplasm--an atrialmyxoma. These benign masses are most often attached to the atrial wall, but can arise on a valve or in a ventricle. They can produce a "ball valve" effect by intermittently occluding the atrioventricular valve orifice. Embolization of fragments of tumor may also occur. Myxomas are easily diagnosed by echocardiography. They may also be seen with chest CT scan and with magnetic resonance angiography.Muchas gracias..Al final.