Cardiovascular Pathology

14 Products
Abdominal Aortic Aneurysm
Clinical HistoryThis 70-year-old man with a past history of mild gastro-oesophageal reflux presented to the Alfred Hospital with a sudden onset of severe upper abdominal pain, which radiated to the left shoulder tip. On examination, he was distressed and hyperventilating, pulse rate 87/min, and a blood pressure 140/90 mm Hg. Abdominal examination revealed board-like rigidity and diminished bowel sounds. At emergency laparotomy no evidence of a ruptured viscus was found; the pancreas appeared normal and an unruptured abdominal aortic aneurism was noted. Endoscopy on the following day showed a ruptured oesophageal ulcer and a Celestin tube was inserted. The patient developed localised infective complications, pulmonary oedema and congestion, and died 19 days after admission.Pathology The specimen consists of lower abdominal segment of aorta together with common iliac vessels and proximal portions of the internal and external iliac arteries. A large 10 x 7 cm aneurysm is situated below the origin of the renal arteries extending to the aortic bifurcation. The aneurysm with its severe thinning of the wall of the abdominal aorta is partly lined by a laminated thrombus, indicating the chronicity of the process. There is evidence of a recent thrombus on the luminal surface. There also appears to be some aneurysmal dilatation of the common iliac and (opened) proximal left external iliac artery. The abdominal aorta at the upper end of the specimen shows multiple focally ulcerated atheromatous plaques. There is no evidence of rupture.Further InformationAbdominal aortic aneurysm (AAA or triple A) represents a localized enlargement of the abdominal aorta (diameter >3 cm or more than 50% larger than normal)[1]. They are usually asymptomatic, except during rupture[1]. Large aneurysms may be palpable on abdominal examination. Occasionally, abdominal-, back-, or leg pain may occur depending on location and size. Rupture may result in pain in the abdomen or back, sudden low blood pressure with loss of consciousness, and often results in death[1]. AAA’s occur most commonly in those over 50 years of age, in men, and amongst those with a family history of this disease. Additional risk factors include smoking, high blood pressure, and other heart or blood vessel diseases. They are also found in genetic abnormalities, including Marfan’s syndrome and Ehlers-Danlos syndrome. AAAs are the most common form of aortic aneurysm, and about 85% occur below the kidneys.

Tetralogy of Fallot
Clinical HistoryA 21-month old boy was admitted with a history of exhaustion and exertional dyspnoea for the previous 2 to 3 months. During this time there had been several attacks of acute dyspnoea each lasting up to two minutes. Examination revealed central cyanosis, mild finger clubbing, and a harsh systolic bruit maximal at the left sternal edge. Cardiac catheterisation led to a diagnosis of Fallot‘s tetralogy and severe pulmonary oedema. A surgical correction was performed (Willis-Potts anastomosis between the aorta and the origin of the left pulmonary artery). The child developed acute dyspnoea and left lobar consolidation 12 hours post-operatively and died despite treatment.PathologyThe child‘s heart is viewed from the anterior aspect. The anterior wall of the right ventricle has been excised to reveal prominent right ventricular hypertrophy and a narrowed pulmonary outflow tract. The pulmonary valve ring is also small, with a bicuspid stenosed valve. There is a patch of endocardial fibrosis in the outflow tract below the pulmonary valve. The origin of the aorta overlies a high ventricular septal defect. A probe could be passes into the aorta from the hypertrophied right ventricle. The further probe was able to be passed from the narrowed pulmonary trunk into a dilated, thin-walled left pulmonary artery and through the surgical anastomosis into the descending aorta. Examination of the posterior aspect of the specimen reveals an opened right atrium and left ventricle. When viewed from the right side of the heart, there is a large atrial septal defect (ASD), 8 mm in diameter at the site of the foramen ovale (large arrow). Another tiny ASD (small arrow) 3 mm in diameter is present posterior to the upper border of the large ASD. Note that the wall of the left ventricle is slightly thinner than the wall of the right ventricle.Further Information The four features of tetralogy of Fallot are: 1. Ventricular septal defect (VSD); 2. An aorta that straddles the VSD with the latter communicating with both ventricles (over-riding aorta) instead of just the left ventricle; 3. Pulmonary stenosis or obstruction of the right ventricular overflow tract; 4. Right ventricular hypertrophy. This condition usually causes cyanosis early in life. Its severity depends on the degree of pulmonary outflow obstruction, which determines whether there is a left-to-right, or right-to-left shunt. In some patients, pulmonary blood flow is increased due to the presence of a patent ductus arteriosus. Patients with this condition may survive untreated into adult life, and a few may reach middle age. However, surgical correction is now possible and is desirable, as the disorder is ultimately fatal. Sometimes additional cardiac abnormalities may be present. (e.g. atrial septal defect, as was found in this case).In most cases of tetralogy of Fallot, the cause is not known although in some patients, genetic factors play a role. For example, the condition is more common in patients with Down syndrome (Trisomy 21; in association with AV canal defects) or DiGeorge syndrome (22q11 deletion).

Atrial septal defect
Clinical HistoryA 10-year-old girl with a known congenital heart was admitted for surgical repair because of the recent onset of cyanosis and cardiac failure. On examination, she was breathless with a blood pressure of 105/60mm/Hg and a pulse rate of 140/min. There was a loud heart murmur in the fourth left intercostal space adjacent to the sternum. The jugular venous pressure was elevated, and there were bilateral pulmonary basal crepitations but no peripheral oedema. At operation, the defect was repaired; however, death followed a sudden post-operative deterioration of unknown cause.Pathology The heart is viewed from the left side. The left atrium has been opened to display a large ovoid defect 3.5 cm in greatest diameter in the inter-atrial septum. Only a small postero-inferior crescentic rim of septum remains. The left ventricle is small, and the right ventricle is hypertrophied (see posterior aspect of specimen where part of the right postero-lateral wall of the right ventricle has been cut away to demonstrate the thickened wall). The pulmonary artery, seen to the left of the atrial cavities, is greatly enlarged. The smaller vessel seen lying above the cut end of the pulmonary artery is the aortic arch. The cut edge of a lumen 8 mm in diameter immediately below the cut end of the pulmonary artery is the left auricular appendage.Further InformationAtrial septal defect is usually asymptomatic early in life, even when large. Symptoms may not develop until adult life. The onset of symptoms is due to reversal of the initial left-to-right shunt as a result of increasing right ventricular hypertrophy and pulmonary hypertension. The ensuing right-to-left shunt is associated with cyanosis and dyspnoea, and ultimately leads to congestive cardiac failure.There are several types of atrial septal defects, including:Secundum - This is the most common type of ASD and occurs in the middle of the wall between the atria (atrial septum). Primum - This defect occurs in the lower part of the atrial septum and might occur with other congenital heart problems.Sinus venosus - This rare defect usually occurs in the upper part of the atrial septum and is often associated with other congenital heart problems.Coronary sinus - In this rare defect, part of the wall between the coronary sinus — which is part of the vein system of the heart — and the left atrium is missing.It is not known why all atrial septal defects occur, but some congenital heart defects appear to be familial and sometimes occur with other genetic problems, such as Trisomy 21 (Down’s syndrome). Some conditions during pregnancy can increase the risk of having a baby with a heart defect, including acute infections such as Rubella infection; drug, tobacco or alcohol use, or exposure to certain substances (such as cocaine) during the first trimester of pregnancy; and underlying systemic conditions, such as diabetes or systemic lupus erythematosus.

Bicuspid Aortic Valve
Clinical HistoryA 64-year old woman presented with a story of chest pain for 5 months, associated with breathlessness and wheezing for 4 months. On examination, she was dyspnoeic, with an expiratory wheeze, left-sided crepitations and signs of a right pleural effusion. The pulse rate and blood pressure were normal. There was a precordial systolic murmur and a heaving apex beat in the 5th left intercostal space 10 cm from the midline. There was no peripheral oedema. The patient died 4 days after admission.PathologyThe heart has been opened to display the left ventricle and associated valves. The aortic valve has 2 cusps instead of the usual three. The valves are otherwise normal apart from patchy slight thickening. The aortic origins of the left and right coronary arteries are widely patent, as is the left circumflex coronary artery, seen cut transversely in the atrio-ventricular groove at the right hand lower edge of the specimen. There is dense pericardial fibrosis and adhesions on the posterior side of the specimen, suggestive of a constrictive pericarditis. The cause of this is not apparent from the history. At autopsy, there was ascites, a small shrunken cirrhotic liver, bilateral pleural effusions (R>L), and right pulmonary collapse. The cause of death was liver cirrhosis and failure, possibly consequential to the above-described constrictive pericarditis. The bicuspid aortic valve was an incidental finding.Further InformationBicuspid aortic valve is a more common congenital anomaly than widely appreciated as it may remain asymptomatic till later in life. The condition predisposes to the development of calcific aortic stenosis, usually in the 5th to 7th decades of life. They may occur alone or as part of a congenital syndrome, such as Tetralogy of Fallot. The latter is a combination of four congenital abnormalities, including a ventricular septal defect, pulmonary valve stenosis, a misplaced aorta and a right ventricular hypertrophy.Bicuspid aortic valves have unequal cusp sizes usually as a result of two or the three normal cusps being fused together. This can lead to greater valvular dysfunction. Patients with bicuspid aortic valves are at high risk of aortic dilatation and dissection.Bicuspid aortic valves are more likely to become calcified in older age than tricuspid aortic valves, and this is due to abnormal motion and turbulence caused by the unequal leaflet sizes.With increasing age, patients can develop aortic stenosis or aortic regurgitation. When these become severe, symptoms associated with dyspnoea and reduced exercise tolerance may develop. This may be the first sign of a bicuspid aortic valve. Diagnosis of bicuspid aortic valves is confirmed using transthoracic echocardiogram.

Acute Bacterial Endocarditis
Clinical HistoryA 15-year old boy with cough and sputum developed a hectic (spiking) fever and chest pain a few days before being admitted in a comatosed condition. Examination revealed an early diastolic murmur at the aortic area, which radiated down the left sternal edge. He deteriorated very quickly and died, despite antibiotic chemotherapy. Blood cultures grew Staphylococcus aureus.Pathology This small heart displays the left ventricle and associated valves. The non-coronary cusp of the aortic valve is ulcerated and perforated and has friable vegetations attached. Immediately below this cusp a perforation extends into the right atrium just above the tricuspid valve (see back of specimen. The other aortic cusp is also thickened. This is an acute bacterial endocarditis with aortic cusp and atrioventricular perforations.Further InformationAcute bacterial endocarditis is a form of infective endocarditis. Endocarditis due to fungal infections can also occur although they are rare.In normal circumstances, the endothelial lining of the heart and valves is relatively resistant to infection by most bacteria or fungi. Therefore, in order for infective endocarditis to occur, there needs to be initial damage or injury to the endocardial tissue. This often results in aggregation of platelets and fibrin, which then become infected, resulting in vegetation formation (i.e. an infective nidus). Staphylococcus aureus, however, is highly virulent and can sometimes infect normal heart valves.After the initial platelet-fibrin aggregation, there is further activation of the coagulating system via the extrinsic clotting pathway and initiation of the inflammatory response via monocytes, resulting in further growth of the vegetation/thrombus. The microbial growth tends to occur within the fibrin matrix, which makes it difficult for the immune responses to eradicate the infection. An additional problem is that these infected thombi can also embolise causing distant sites of infection in smaller capillaries (e.g. in the kidney).Risk factors for developing an infective endocarditis include valvular heart disease, such as previous rheumatic heart disease, congenital heart disease (e.g. ventricular septal defect or bicuspid aortic valve), prosthetic heart valves or any previous invasive cardiac procedures. Anti-thrombotic medications – e.g. heparin or aspirin – may have to be administered in patients at risk. Diagnosis is initially made by clinical examination followed by pathology (blood cultures) and diagnostic imaging. Transthoracic echocardiogram is often first line, followed by transoesophageal echocardiogram. Treatment includes antimicrobial therapy, anti-coagulants, and in some complicated cases, surgical intervention such as valve surgery.

Syphilitic Aneurysm
Clinical HistoryA 61-year old male presents with exertional anginal chest pain and dyspnoea. He has had these symptoms for 6 years with increasing severity. On examination, he is cyanotic and tachycardic with a collapsing pulse. A swelling was noted on the right side of his neck. There was a thrill in his carotid artery. The apex beat was displaced inferolaterally. A loud systolic and diastolic murmur was auscultated in the aortic area. Chest X-rays showed cardiomegaly with a large rounded lesion in the right upper mediastinum continuous with the heart shadow with radiographic evidence of cardiac failure. Blood tests were positive for anti-treponemal antibodies. The patient‘s condition deteriorated and he died of cardiac failure.PathologyThis specimen is the patient‘s enlarged heart, including the aortic arch and descending aorta. The ascending aorta is dilated up to 7 cm in diameter, and is expanded superiorly by a large aneurysmal bulge 11 x 13 cm in diameter. This has been opened to display the wrinkled scarred intimal surface. There is also marked atheroma of the intima. The innominate, left common carotid and subclavian arteries have been displaced towards the patients left by the aneurysm. On the internal surface of the aneurysm there is a ridge-like thickening 5 mm high. This is the site of attachment of the pericardial sac externally. There is marked congestion of small blood vessels in the adventitia of the aorta. This is a syphilitic aneurysm of the arch of the aorta.Further InformationSyphilis is a chronic infection caused by the spirochete Treponema pallidum. Sexually transmitted infection is most common but it may also be congenitally acquired by transplacental transmission of the bacteria. Those who have the higher risk of syphilis infection include those of a sexually active age, intravenous drug user, HIV-infected patients and male same sex relationships. Syphilis infection rates decreased significantly with the introduction of penicillin in 1943; it remains the main treatment today. However, the infection rate has been increasing since the early 2000s.Syphilis is divided into three clinical stages with distinct clinical and pathological features with characteristic proliferative endarteritis affecting small vessels.Primary syphilis occurs usually 3 weeks after initial infection. This manifests typically as a single, painless and erythematous lesion called a chancre at the site of inoculation. The syphilis spreads throughout the body from this chancre which then heals spontaneously after 3 to 6 weeks.Secondary syphilis occurs weeks to a few months after the primary chancre resolves in 75% of untreated patients. During this stage patients commonly have generalised symptoms, such as malaise and lymphadenopathy and skin rashes. Palmar/plantar rashes are the most frequent site but rashes can be diffuse. These rashes can be maculopapular, scaly or putular.Condylomata lata are elevated gray plaques that arise on the moist mucous membranes such as oral or genital regions. Other less common manifestations include hepatitis, gastrointestinal invasion or ulceration and neurosyphilis - discussed below.Tertiary syphilis has three main characteristics: cardiovascular syphilis, neurosyphilis and gummatous syphilis. These occur after a latent period of 5 years or more in ? of untreated patients. Cardiovascular syphilis involves an aortitis for which the exact pathophysiology is unclear. The vasculitis involves the ascending thoracic aorta leading to progressive dilation of the aortic root. This can lead to aortic valve insufficiency from dilation of the aortic valve ring. Endarteritis of the vasa vasorum leads to scarringof the media with loss of muscle and elastic tissue leading to the formation of aneurysms. Clinical manifestation usually happens 15-30 years post initial infection.Neurosyphilis can be symptomatic or asymptomatic. It occurs in 10% of untreated patients. Early clinical manifestations include headaches, meningitis, hearing loss and ocular involvement, most commonly uveitis, causing vision loss. Late manifestations can occur up to 25 years post initial infection. Main features are meningovascular neurosyphilis, paretic neurosyphilis and tabes dorsalis. Meningovascular involvement involves chronic meningitis and endarteritis which can lead to strokes. Tabes dorsalis is caused from degeneration of the posterior columns within the spinal cord. This causes loss of proprioception, ataxia, loss of pain sensation, and loss of reflexes. Paretic neurosyphilis is caused by invasion and damage of the brain parenchyma, most commonly the frontal lobes. This leads to progressive cognitive impairment and mood disturbance.Gummatous syphilis is characterised by the formation of nodular lesions most commonly bone, skin and mucosa of the upper airway and mouth called gummas. These can occur anywhere including viscera. The formation of gummas is rare but occurs more frequently in HIV-infected patients. Skeletal involvement causes pain and pathological fractures.

Right Ventricular Hypertrophy
Clinical HistoryThis 56-year old female suffered from emphysema and gave a 2-year history of increasing shortness of breath on exertion associated with recurrent attacks of bronchitis. On examination, she had a BP 160/90 mm Hg, pulse rate of 96 beats/min, and 6 cm of jugular venous congestion. The apex beat was impalpable, bilateral crepitations were heard and pitting oedema was present peripherally. Special investigations: ECG showed right heart strain pattern. Arterial blood examination showed respiratory acidosis. Despite treatment there was steady deterioration and death.Pathology The specimen is of the external surface of the heart viewed from the anterior aspect. The right ventricle is greatly enlarged and hypertrophied. All appears to be normal otherwise. This is an example of right ventricular hypertrophy (RVH) in a patient with emphysema.Further informationRVH usually occurs due to chronic lung disease or structural defects in the heart. One of the most common causes of RVH is pulmonary hypertension (PH), which leads to increased pulmonary artery pressure. As the right ventricle tries to compensate for this increased pressure it changes its shape and size causing hypertrophy and right ventricular wall thickness. The global incidence of PH is 4 per 1M people: RVH occurs in approximately 30% of these cases. Common causes of PH include chronic obstructive pulmonary disease (COPD), pulmonary embolism, and other restrictive lung diseases. RVH also occurs in response to structural defects in the heart, such as tricuspid insufficiency, which allows the backward flow of blood into the ventricle. Other structural defects that lead to RVH include tetralogy of Fallot, ventricular septal defects, pulmonary valve stenosis, and atrial septal defects. RVH is also associated with abdominal obesity and high systolic blood pressure.

Congenital Pulmonary Stenosis

Hydatid Disease Affecting the Heart and Aorta
Clinical HistoryThis 11-year-old female had an 18-month history of hydatid disease (see below). In total, 17 cysts were removed from the child’s brain at craniotomy on three occasions, and subsequently cysts were found in the kidneys, mesentery, and abdominal aorta at its bifurcation. X-ray of the heart showed a calcified cyst, and the patient was referred to a tertiary hospital for its removal. The patient deteriorated and died following open-heart surgery during which a dead hydatid cyst was found in the left ventricle.Pathology The specimens are of the heart, with the left ventricle being laid open, and of the aorta at its common iliac bifurcation. The aorta shows some atheromatous depositions in the upper portion. There is a large mass of antemortem clot at the point of iliac bifurcation with extension down both common iliac arteries.The heart shows hypertrophy of the left ventricular wall, and an abnormal communication between the left ventricle and atrium running through the posterior cusp of the mitral valve via the papillary muscle into the left ventricular cavity. This channel is surrounded by thickened fibrous-looking tissue. The posterior cusp of the valve has been split. Sutured surgical incisions are visible on the posterior aspect of the specimen and the ventricular wall and in the left atrial appendage. Hydatid cysts occupy the abdominal aorta at its bifurcation, and the channel joining the left ventricle and left atrium.Histology demonstrated cysts within the aorta wall comprised of 3 layers: an outermost pericyst fibrous layer; a middle ectocyst layer that was laminated, hyaline and acellular; and the inner endocyst in the germinative layer, consisting of daughter cysts and brood capsules with scolices. A focal granulomatous palisading reaction was also present within the aorta wall.Further InformationHydatid cyst is a human parasitic disease caused by the larval stage of the cestode tapeworm Echinococcus granulosus, which infests the gut of dogs—its definitive hosts. Human beings may serve as incidental hosts by the ingestion of ova in vegetables or water contaminated with dog faeces. Humans become infected by the ingestion of eggs passed in dog faeces. Oncospheres released from the eggs penetrate the intestinal mucosa and, via the portal system, lodge in the liver, lungs, muscle or other organs, where the hydatid cysts form.Hydatid disease is endemic in cattle-raising areas of the world, notably in the Mediterranean countries, the Middle East, South America, Australia, and New Zealand. Although no body part can be spared from hydatid cysts, they mostly affect the liver and lungs. Cardiac involvement is much rarer, yet potentially fatal condition and comprises 0.5–2% of all hydatid cases. Cardiac complications and presentation vary depends on the location, size and integrity of the cyst(s). The myocardium of the left ventricle more frequently involved. Pericardial involvement occurs mostly in multifocal cardiac echinococcosis. Growth of the cyst leads them being pushed toward a weaker side of the cardiac wall, either the epicardium or the endocardium. LV HCs are usually located subepicardially, therefore rarely rupture into the pericardial space. However, if rupture happens, it may be silent or it may cause acute pericardial tamponade, constrictive pericarditis or secondary pericardial cysts[1].Although E. granulosus is still found in sheep and rural dogs in Australia, the prevalence of transmission is less common than it was. The marked reduction in prevalence in rural domestic dogs, and also sheep, is the result of the highly effective cestocidal drug, praziquantel, being included inreadily available, cheap, generic, all-wormers for dogs and the development of inexpensive commercial dry dog food[2].References1. Oraha et al. Ann Med Surg (Lond). 2018 18–212. Jenkins et al. Int J Parasitol Parasites Wildl. 2019: 256–259.

Hypertrophic Subaortic stenosis
Clinical HistoryA thin 42-year-old American tourist was found dead in his hotel bedroom. A coroner’s autopsy was performed.PathologyThis is a longitudinal section through the heart displaying the left and right ventricles and interventricular septum. The outstanding abnormality is a grossly thickened interventricular septum and left ventricular hypertrophy. The aortic cusps that are visible appear unremarkable, as does the mitral valve. The ventricular septum is so large that it encroaches on the lumen of the left ventricle.DiagnosisIdiopathic hypertrophic subaortic stenosis, also known as hypertrophic cardiomyopathy.Further InformationSubaortic stenosis is considered to be acquired rather than congenital and is suggested to result from an underlying defect in the architecture of the left ventricular outflow tract (LVOT). The defect may be such that the resulting turbulent blood flow leads to progressive thickening and fibrosis of the LVOT and the aortic valve. Progression of the disease will often lead to a hypertrophic cardiomyopathy secondary to the increased aortic pressure needed to be overcome by the left ventricle. Mild or moderate stenosis is often asymptomatic. As disease progresses and the stenosis becomes severe, symptoms such as exertional dyspnoea and syncope may become apparent. Investigation and subsequent diagnosis are often prompted by the presence of an ejection systolic murmur on physical examination. Echocardiography is used to confirm diagnosis.These days, definitive treatment of subaortic stenosis consists of surgical correction of the obstruction.

Rheumatic endocarditis
Clinical HistoryThe patient was a 52-year old female with increasing dyspnoea. She gave a past history of fever with flitting joint pains in childhood following a sore throat. On examination: cyanotic, pulse showed atrial fibrillation, jugular venous pulse elevated, pan-systolic murmur at apex, hepatomegaly, and dependent oedema. She was being treated with digoxin, lasix (furosemide) and penicillin but died after cardiac arrest.Pathology The specimen is that of a heart opened to show the left atrium and left ventricle. The mitral valve has been cut, but those visible parts show significant thickening. The left atrial wall shows deposition of blood and fibrin. The left auricular appendage is filled with blood clot, caused by atrial fibrillation. The mural thrombus on the atrial wall is in the typical site:- the deep layers of the endocardium forming irregular thickenings, called MacCallum’s plaques (arrows).Further InformationIn this patient, the history of fever and joint pains following a sore throat is very suggestive of a history of rheumatic fever. Rheumatic fever is an inflammatory disease that can involve the heart, joints, skin, and brain. Typical symptoms include fever, multiple painful joints, involuntary muscle movements (chorea), and occasionally a characteristic non-itchy rash known as ‘erythema marginatum’.Rheumatic fever may occur 2-4 weeks following an infection of the throat by the bacterium Streptococcus pyogenes. If the infection is left untreated (with pencillin), rheumatic fever occurs in up to three percent of people. The underlying mechanism is believed to involve the production of antibodies against a person‘s own tissues (autoimmune disease). Due to their genetics, some people are more likely to get the disease when exposed to the bacteria than others. Other risk factors include malnutrition and poverty, occurring more commonly in low to middle income countries and particularly in Indigenous communities.The heart is involved in about half of the cases. Damage to the heart valves, known as rheumatic heart disease (RHD), usually occurs after repeated attacks (carditis) but can sometimes occur after one. Carditis can progress to chronic rheumatic heart disease, usually affecting cardiac valves. The mitral valve is the most commonly affected valve, with fibrosis leading to mitral valve stenosis and this specimen highlights the thickening of the mitral valve. Stenosis is thought to occur due to Aschoff nodules, which are granulomatous lesions with a central area of fibrinoid necrosis and surrounded by an infiltration of autoreactive T cells. The Aschoff nodules also contain ‘giant cells’, which are thought to be some type of degenerative connective or endothelial tissue.Stenosis may progress through the years and as it worsens, the left atrium will become increasingly dilated. Consequentially, atrial fibrillation may develop and mural thrombi can be formed. Further, tight mitral stenosis can result in severe cardiac failure.

Traumatic Oesophageal-aortic fistula
Clinical HistoryA woman who swallowed a chop bone during lunch collapsed later in the afternoon and suffered a massive haematemesis. At laparotomy, the stomach was filled with fresh blood but the cause was not identified. She died one day later and necropsy revealed a communication between aorta and oesophagus. The stomach was distended with blood and contained a few fragments of bone.PathologyThe specimen is a block dissection of distal trachea (posterolateral on right margin), aortic arch (opened in coronal plane and viewed from anterior aspect) and oesophagus (posteriorly and opened longitudinally). The oesophageal mucosa is ulcerated and haemorrhagic. A small blue probe identifies a fistula between the oesophagus and posterior wall of the thoracic descending aorta.NoteWhile this scenario was a traumatic cause of oesophageal-aortic fistula, it should be noted that there are non-traumatic causes of the same. In fact, these fistulae can be caused by compression of the aorta from an aneurysm, advanced gastrointestinal malignancies or erosion of an aortic graft into adjacent gastrointestinal tract and can occur anywhere along the length of the aorta.Aorto-enteric fistulas are life-threatening. The most common presentation is gastrointestinal bleeding and can present as either minor bleeding or a large life-threatening bleed that results in haemodynamic compromise. Patients can present with melaena (dark sticky faeces containing partly digested blood) or frank bleeding in stools. In smaller fistulas with slow, minor bleeds, patients can present with malaise or ischaemia of lower limbs due to less blood flow from the aortic bleed. Other presentations include haematemesis as occurred in this case.Diagnoses of these fistulas can be difficult, depending on the cause, size and location of the fistula. In a stable patient, endoscopic exploration or CT angiography may be first line options for diagnosis. However, diagnosis in hemodynamically unstable patients is more time critical and may require laparotomy as well stabilisation with blood transfusions.

Ruptured Thoracic Aortic Aneurysm
Clinical HistoryNo clinical details are available for this specimen.Pathology The heart displays both ventricles from the posterior aspect. There is a prominent saccular dilatation of the thoracic ascending aorta, which shows several atherosclerotic plaques and posteriorly is seen to be ruptured (identified by the dark staining). Both ventricles are hypertrophied. The coronary arteries together with the aortic and tricuspid valves are normal. This is an example of a ruptured aneurysm of the ascending aorta.Further informationThe dilation of the ascending aorta is a common incidental finding on transthoracic echocardiography performed for unrelated indications.The thoracic aorta is divided into 3 parts: ascending, arch and descending. The ascending aorta originates beyond the aortic valve and ends right before the innominate artery (brachiocephalic trunk). It is approximately 5 cm long and is composed of two distinct segments. The lower segment, known as the aortic root, encompasses the coronary sinuses and sinotubular junction (STJ). The upper segment, known as the tubular ascending aorta, begins at the STJ and extends to the aortic arch (innominate artery). More than 50% of thoracic aortic aneurysms are localized to the ascending aorta, which may affect either the aortic root or tubular aortic segment.An aneurysm is defined as a localized dilation of the aorta that is more than 50% of predicted (ratio of observed to expected diameter = 1.5). Aneurysm should be distinguished from ectasia, which represents a diffuse dilation of the aorta less than 50% of normal aorta diameter. The incidence of ascending thoracic aortic aneurysms is estimated to be around 10 per 100,000 person-years[1].Reference1. Saliba et al. (2015). Int J Cardiol Heart Vasc. 6: 91–100.

Calcified Aortic Valvular Stenosis Bicuspid Aortic Valve
Clinical HistoryThere is no clinical history for this specimen.PathologyThe specimen is partial horizontal 1.5cm slice through the plane of the left atrium whose smooth internal lining together with the left auricular appendage and part of the left ventricle are visible on the inferior aspect. On the superior aspect the pulmonary trunk (and part of the pulmonary tricuspid valve) and aorta, including the affected abnormal bicuspid valve, are clearly discernible. Calcified aggregations or thickenings on the opposing margins of the valve can be seen from this upper perspective. There is also a region of calcification on one of the cusps of the pulmonary valves.Further informationBicuspid aortic valve is a common congenital abnormality that is often not detected into adulthood. Indeed, it is the most common congenital anomaly of the heart. Aortic valve stenosis can range from mild to severe, and signs and symptoms generally develop when narrowing of the valve is severe. Some people with aortic valve stenosis may not experience symptoms for many years. Signs and symptoms may include abnormal heart sound (heart murmur), radiating chest pain (angina), shortness of breath and chest pain, especially during times of increased activity, heart palpitations — sensations of a rapid, fluttering heartbeat. The heart-weakening effects of aortic valve stenosis may lead to heart failure. Heart failure signs and symptoms include fatigue, shortness of breath, and swollen ankles and feet.When the aortic valve is narrowed, the left ventricle has to work harder to pump a sufficient amount of blood into the aorta and onward to the rest of the body. This can cause the left ventricle to thicken and enlarge. Eventually the extra work of the heart can weaken the left ventricle and the heart overall, with it ultimately not being able to function properly (heart failure), causing other downstream problems.Calcium deposits build up on the valve particularly those with a congenitally abnormal aortic valve, such as a bicuspid aortic valve resulting in stiffening of the valve cusps. This stiffening narrows the aortic valve lumen and thereby increases the blood flow.


Human body replicas to improve teaching!

Erler-Zimmer's groundbreaking Anatomy Series features a unique and unrivalled collection of colourised human body replicas specifically designed to enhance teaching and learning. This premium collection of highly accurate human anatomy has been created directly from radiological data or real specimens using the latest imaging techniques. The 3D Human Anatomy Series offers a cost-effective way to meet your specific teaching and demonstration needs across the curriculum in medicine, health sciences and biology. A detailed description of the anatomy represented in each 3D printed specimen is included. What are the advantages of the Monash 3D Anatomy Series compared to plastic models or real human plastinates? Each body replica has been carefully developed from selected radiological patient data or dissected human bodies of the highest quality, chosen by a highly skilled team of anatomists at Monash University's Human Anatomy Teaching Centre, to represent clinically important areas of anatomy in a quality and detail not possible with conventional models - it is real anatomy, not stylised. Each body replica has been rigorously checked by the highly qualified team of anatomists at Monash University's Human Anatomy Teaching Centre to ensure the anatomical accuracy of the final product. The body replicas are not real human tissue and are therefore not subject to any restrictions on transport, import or use in educational institutions that do not have permission to use cadavers. The exclusive 3D Anatomy Series avoids these and other ethical issues that arise when dealing with plastinated human remains.

Your last viewed products