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1 Source of Images Webpath- University of Utah Hypermedia Image Source Tables included
Conversion prepared and presented by Marc Imhotep Cray, M.D. Basic Medical Sciences Teacher
Webpath Hypermedia Source Tables
The purpose of this PowerPoint conversion is
1. To enable the learner to bring Webpath Cardiovascular Pathology image plates to their desktop for offline study 2. To contribute to mobile device viewing diversity 3. It serves as a part of the IVMS ANS and Cardiovascular
Pharmacology Sequenced Course Demonstration Open Demo
•Normal heart, gross •Normal aortic valve, gross •Normal tricuspid valve, gross •Normal coronary artery, microscopic •Normal myocardium, medium power microscopic
Normal heart, gross
• This 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
Normal tricuspid valve, gross
• This is the tricuspid valve. The leaflets and thin and delicate. • Just like the mitral valve, the leaflets have thin chordae tendineae that attach the leaflet margins to the papillary muscles of the ventricular wall below
Normal coronary artery, microscopic
• This is a normal coronary artery. • The lumen is large, without any narrowing by atheromatous plaque. The muscular arterial wall is of normal proportion
Normal myocardium, medium power microscopic
• This is the normal appearance of myocardial fibers in longitudinal section. • Note the central nuclei and the syncytial arrangement of the fibers, some of which have pale pink intercalated disks
Atherosclerotic Cardiovascular Disease
Atherosclerotic Cardiovascular Disease (1)
•Coronary artery with atherosclerotic narrowing, microscopic •Coronary artery with recanalized thrombosis, microscopic •Coronary artery with calcific atherosclerosis, microscopic •Coronary artery atherosclerosis, occlusive, microscopic •Coronary artery thrombosis, recent, microscopic •Atheromatous plaque, high power, microscopic •Aorta with rare lipid streaks, gross •Aorta with lipid streaks, gross •Aortas demonstrating various degrees of atherosclerosis, gross
Coronary artery with atherosclerotic narrowing, microscopic
• The coronary artery shown here has narrowing of the lumen due to build up of atherosclerotic plaque. • Severe narrowing can lead to angina, ischemia, and infarction
Coronary artery with recanalized thrombosis, microscopic
• This section of coronary artery demonstrates remote thrombosis with recanalization to leave only two small, narrow channels
Coronary artery with calcific atherosclerosis, microscopic
• There is a severe degree of narrowing in this coronary artery. • It is "complex" in that there is a large area of calcification on the lower right, which appears bluish on this H&E stain. • Complex atheroma have calcification, thrombosis, or hemorrhage. Such calcification would make coronary angioplasty difficult
Aortas demonstrating various degrees of atherosclerosis, gross
• These three aortas demonstrate mild, moderate, and severe atherosclerosis from bottom to top. • At the bottom, the mild atherosclerosis shows only scattered lipid plaques. • The aorta in the middle shows many more larger plaques. The severe atherosclerosis in the aorta at the top shows extensive ulceration in the plaques
Aorta, atherosclerotic aneurysm, gross
• Here is an example of an atherosclerotic aneurysm of the aorta in which a large "bulge" appears just above the aortic bifurcation. • Such aneurysms are prone to rupture when they reach about 6 to 7 cm in size. • They may be felt on physical examination as a pulsatile mass in the abdomen.Most such aneurysms are conveniently located below the renal arteries so that surgical resection can be performed with placement of a dacron graft
Atherosclerotic Cardiovascular Disease (2)
•Aorta, atherosclerotic aneurysm, gross [CT] •Aorta, atheroma, low power, microscopic •Aorta, atheroma, high power, microscopic •Aorta, ulcerative atherosclerosis with mural thrombosis, gross •Cholesterol emboli in kidney, medium power microscopic •Coronary artery, mild atherosclerosis, gross •Coronary artery, severe atherosclerosis, gross •Coronary artery, hemorrhage into plaque, gross •Coronary artery, occlusive atherosclerosis, gross •Heart and LAD coronary artery with recent thrombus, gross •Coronary artery with recent thrombus, longitudinal section, gross •Coronary artery with recent thrombus, cross section, gross
CT scan with contrast
• This abdominal high speed CT scan with contrast demonstrates an abdominal aortic aneurysm approximately 6 cm in diameter. • At this size, there is increased risk for rupture
Coronary artery, mild atherosclerosis, gross
• A coronary artery has been opened longitudinally. • The coronary extends from left to right across the middle of the picture and is surrounded by epicardial fat. Increased epicardial fat correlates with increasing total body fat. • There is a lot of fat here, suggesting one risk factor for atherosclerosis. • This coronary shows only mild atherosclerosis, with only an occasional yellow-tan lipid plaque and no narrowing
Coronary artery, severe atherosclerosis, gross
• This is the left coronary artery from the aortic root on the left. • Extending across the middle of the picture to the right is the anterior descending branch. • This coronary shows severe atherosclerosis with extensive calcification. At the far right, there is an area of significant narrowing
Coronary artery, hemorrhage into plaque, gross
• This is coronary atherosclerosis with the complication of hemorrhage into atheromatous plaque, seen here in the center of the photograph. • Such hemorrhage acutely may narrow the arterial lumen
Heart and LAD coronary artery with recent thrombus, gross
• The anterior surface of the heart demonstrates an opened left anterior descending coronary artery. • Within the lumen of the coronary can be seen a dark red recent coronary thrombosis. • The dull red color to the myocardium as seen below the glistening epicardium to the lower right of the thrombus is consistent with underlying myocardial infarction
•Heart, left ventricle, acute myocardial infarction, gross •Heart, left ventricle and septum, myocardial infarction, gross •Myocardium, contraction band necrosis, microscopic •Myocardium, acute myocardial infarction, 1 to 2 days, microscopic •Myocardium, acute myocardial infarction, 1 to 2 days, microscopic •Myocardium, acute myocardial infarction, 3 to 4 days, microscopic •Myocardium, intermediate myocardial infarction, 1 to 2 weeks, microscopic •Heart, transmural myocardial infarction with rupture and hemopericardium, gross •Heart, transmural myocardial infarction with rupture, gross •Heart, remote myocardial infarction, medium power microscopic •Heart, remote myocardial infarction, low power microscopic •Heart, remote myocardial infarction, gross •Heart, left ventricular aneurysm, gross •Heart, left ventricular aneurysm, gross •Heart, coronary artery bypass graft, gross 23
Heart, left ventricle, acute myocardial infarction, gross
• This is the left ventricular wall which has been sectioned lengthwise to reveal a large recent myocardial infarction. • The center of the infarct contains necrotic muscle that appears yellow-tan. • Surrounding this is a zone of red hyperemia. Remaining viable myocardium is reddishbrown
Heart, left ventricle and septum, myocardial infarction, gross
• This cross section through the heart demonstrates the left ventricle on the left. • Extending from the anterior portion and into the septum is a large recent myocardial infarction. • The center is tan with surrounding hyperemia. • The infarction is "transmural" in that it extends through the full thickness of the wall
Heart, transmural myocardial infarction with rupture and hemopericardium, gross
• 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. • The white arrow marks the point of rupture in this anterior-inferior myocardial infarction of the left ventricular free wall and septum. • Note the dark red blood clot forming the hemopericardium. The hemopericardium can lead to tamponade
Heart, left ventricular aneurysm, gross
• A cross section through the heart reveals a ventricular aneurysm with a very thin wall at the arrow. • Note how the aneurysm bulges out. The stasis in this aneurysm allows mural thrombus, which is present here, to form within the aneurysm
•Aorta, dissection with tear in arch, gross •Heart, dissection with tear through media, low power microscopic •Hemopericardium with cardiac tamponade, gross •Aorta, dissection, gross •Aorta, dissection, microscopic •Carotid artery, dissection with compression, gross •Aorta, dissection, microscopic •Aorta, dissection, Marfan's syndrome, gross •Floppy mitral valve with prolapse, Marfan's syndrome, gross •Floppy mitral valve with prolapse, Marfan's syndrome, gross •Aorta, cystic medial necrosis, Marfan's syndrome, Mucin stain, microscopic •Arachnodactyly, Marfan's syndrome, gross
Aorta, dissection with tear in arch, gross
• There is a tear (arrow) located 7 cm above the aortic valve and proximal to the great vessels in this aorta with marked atherosclerosis. • This is an aortic dissection
Hemopericardium with cardiac tamponade, gross
• An aortic dissection may lead to hemopericardium when blood dissects through the media proximally. • Such a massive amount of hemorrhage can lead to cardiac tamponade
Aorta, dissection, gross
• This aorta has been opened longitudinally to reveal an area of fairly limited dissection that is organizing. • The red-brown thrombus can be seen in on both sides of the section as it extends around the aorta. The intimal tear would have been at the left. • This creates a "double lumen" to the aorta. • This aorta shows severe atherosclerosis which, along with cystic medial necrosis and hypertension, is a risk factor for dissection
Aorta, dissection, microscopic
• Here, the dissection went into the muscular wall. In any case, an aortic dissection is an extreme emergency and can lead to death in a matter of minutes. • The blood can dissect up or down the aorta. • Blood dissecting up around the great vessels can close off the carotids. • Blood can dissect down to the coronaries and shut them off
Carotid artery, dissection with compression, gross
• The right carotid artery is compressed by blood dissecting upward from a tear with aortic dissection. • Blood may also dissect to coronary arteries. • Thus patients with aortic dissection may have symptoms of severe chest pain (for distal dissection) or may present with findings that suggest a stroke (with carotid dissection) or myocardial ischemia (with coronary dissection).
Non-infective Endocarditis •Non-bacterial thrombotic endocarditis, gross •Non-bacterial thrombotic endocarditis, gross •Non-bacterial thrombotic endocarditis, microscopic •Libman-Sacks endocarditis (and mitral rheumatic valvulitis), gross •Mitral valve, acute rheumatic vegetations, gross •Mitral valve, rheumatic mitral stenosis, gross
Aortic valve, infective endocarditis, gross
• This is infective endocarditis. The aortic valve demonstrates a large, irregular, reddish tan vegetation. • Virulent organisms, such as Staphylococcus aureus, produce an "acute" bacterial endocarditis, while some organisms such as Streptococcus viridans produce a "subacute" bacterial endocarditis
Infective endocarditis spreading to myocardium, gross
• In this case, the infective endocarditis demonstrates how the infection tends to spread from the valve surface. • Here, vegetations can be seen on the endocardial surfaces, and the infection is extending into to underlying myocardium
Infective endocarditis, microscopic
• Microscopically, the valve in infective endocarditis demonstrates friable vegetations of fibrin and platelets (pink) mixed with inflammatory cells and bacterial colonies (blue). • The friability explains how portions of the vegetation can break off and embolize
Pericarditis •Serous pericarditis, diagram •Fibrinous pericarditis, diagram •Fibrinous pericarditis, gross •Fibrinous pericarditis, gross •Fibrinous pericarditis, gross •Fibrinous pericarditis, microscopic •Hemorrhagic pericarditis, gross •Hemorrhagic pericarditis, gross •Purulent pericarditis, gross
Fibrinous pericarditis, gross
• A 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 pericarditis, gross
• The 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
•Heart, microabscesses, gross •Heart, microabscess, gross •Heart, microabscess, microscopic •Acute rheumatic carditis, microscopic •Acute rheumatic carditis, microscopic •Acute rheumatic carditis, microscopic •Chronic rheumatic valvulitis, gross •Interstitial viral myocarditis, microscopic
Heart, microabscesses, gross
The epicardial surface of the heart is smooth and glistening, but there are small scattered pinpoint yellowish microabscesses. (Higher magnification in next photo).
Heart, microabscess, gross
This magnification of the preceding photograph shows the small yellowish pinpoint microabscesses on the epicardial surface. Microabscesses may appear in persons who are septic. They may also represent emboli from an infective endocarditis in which small portions of a vegetation have embolized out the coronary arteries.
Heart, microabscess, microscopic
The microscopic appearance of a microabscess is shown here. The center consists of blue bacterial colonies and is surrounded by acute inflammatory cells.
Acute rheumatic carditis, microscopic (1)
Microscopically, acute rheumatic carditis is marked by a peculiar form of granulomatous inflammation with so-called "Aschoff nodules" seen best in myocardium. These are centered in interstitium around vessels as shown here. The myocarditis may be severe enough to cause congestive heart failure.
Acute rheumatic carditis, microscopic (2)
Here is an Aschoff nodule at high magnification. The most characteristic component is the Aschoff 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.
Acute rheumatic carditis, microscopic (3)
Another peculiar cell seen with acute rheumatic carditis is the Anitschkow myocyte. This is a long, thin cell with an elongated nucleus.
Chronic rheumatic valvulitis, gross
In time, chronic rheumatic valvulitis may develop by organization of the acute endocardial inflammation along with fibrosis, as shown here affecting the mitral valve. Note the shortened and thickened chordae tendineae.
Interstitial viral myocarditis, microscopic
The 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.
•Heart, rhabdomyoma, gross •Heart, atrial myxoma, gross •Heart, atrial myxoma, microscopic •Heart, epicardium, metastases, gross •Heart, myocardium, metastatic melanoma, microscopic
Heart, rhabdomyoma, gross
• This two year old child died suddenly. At autopsy, a large firm, white tumor mass was found filling much of the left ventricle. • This is a cardiac rhabdomyoma. Such primary tumors of the heart are rare
Heart, atrial myxoma, gross
• The left atrium has been opened to reveal the most common primary cardiac neoplasm--an atrial myxoma. • 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
Heart, epicardium, metastases, gross
• Primary tumors of the heart are uncommon. • Metastases to the heart are more common, but rare overall (only about 5 to 10% of all malignancies have cardiac metastases). • Seen over the surface of the epicardium are pale white-tan nodules of metastatic tumor. Metastases may lead to a hemorrhagic pericarditis.
Congenital Heart Disease
Congenital Heart Disease
•Congenital heart disease, table •Heart, probe patent foramen ovale, and paradoxical embolus, gross •Heart, atrial septal defect, gross •Heart, atrial septal defect, Eisenmenger's complex, gross •Heart, ventricular septal defect, gross •Heart, atrial septal defect and ventricular septal defect, gross •Aorta, coarctation, gross •Aorta, coarctation, gross •Pulmonic valve, quadricuspid, gross •Aortic valve, bicuspid, gross •Aortic valve, senile calcific aortic stenosis, gross •Heart, tetralogy of Fallot, diagram •Heart, persistent truncus arteriosus, diagram •Heart, transposition of great vessels, diagram
Congenital Heart Disease
Type of Defect Mechanism
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
Type of Defect Mechanism
• 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-toleft 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
Type of Defect Mechanism
• Hypoplastic Left Heart Syndrome There 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
Heart, atrial septal defect, gross
• 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
Heart, ventricular septal defect, gross
• This is the heart of a premature 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.
Aorta, coarctation, gross
• This portion of aorta was resected from a patient with a coarctation. • The aorta narrows postductally here to about a 3 mm opening
Aorta, coarctation, gross
• 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.
Heart, tetralogy of Fallot, diagram
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.
Heart, transposition of great vessels, diagram
• In the diagram, transposition of the great vessels is shown • occurs when the trunco-conal septum does not spiral down. Instead, it descends straight down. As a result, outflow of right ventricle is into aorta and outflow from left ventricle is into the pulmonic trunk. • In order for this system to work, there must be a connection between 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
•Cardiomyopathies, table •Heart, dilated cardiomyopathy, gross [XRAY] •Heart, dilated cardiomyopathy, gross •Heart, cardiomyopathy, microscopic •Heart, hypertrophic cardiomyopathy, explanted heart, gross •Heart, restrictive cardiomyopathy from hemochromatosis, microscopic •Heart, restrictive cardiomyopathy from amyloidosis, microscopic •Myocardium, amyloidosis, apple-green birefringence with polarized light, Congo red stain, microscopic •Heart, hypertension with left ventricular hypertrophy, gross •Heart, hypertrophy with hypertension, gross
Type of CMP Findings
• Dilated (Congestive) All four chambers are dilated, and there is also hypertrophy. The most common cause is chronic alcoholism, though some may be the end-stage of remote viral myocarditis. •
Hypertrophic The most common form, idiopathic hypertrophic subaortic stenosis (IHSS) results from asymmetric interventricular septal hypertrophy, resulting in left ventricular outflow obstruction.
Restrictive The myocardium is infiltrated with a material that results in impaired ventricular filling. The most common causes are amyloidosis and hemochromatosis.
Heart, dilated cardiomyopathy, gross
• This very large heart has a globoid shape because all of the chambers are dilated. • It felt very flabby, and the myocardium was poorly contractile. • This is an example of a cardiomyopathy. • This term is used to denote conditions in which the myocardium functions poorly and the heart is large and dilated, but there is no specific histologic finding
Heart, dilated cardiomyopathy, [XRAY]
• This chest radiograph demontrates marked cardiomegaly, with the left heart edge appearing far to the left
Heart, cardiomyopathy, microscopic
• Microscopically, the heart in cardiomyopathy • demonstrates hypertrophy of myocardial fibers (which also have prominent dark nuclei) along with interstitial fibrosis
Heart, hypertrophic cardiomyopathy, explanted heart, gross
• There is marked left ventricular hypertrophy, with asymmetric bulging of a very large interventricular 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).
Heart, hypertension with left ventricular hypertrophy, gross
• This left ventricle is very thickened (slightly over 2 cm in thickness), but the rest of the heart is not greatly enlarged. • This is typical for hypertensive heart disease. • The hypertension creates a greater pressure load on the heart to induce the hypertrophy
Heart, hypertrophy with hypertension, gross
• The left ventricle is markedly thickened in this patient with severe hypertension that was untreated for many years. • The myocardial fibers have undergone hypertrophy
Arterial and Venous Diseases
Renal arteriole, fibrinoid necrosis with malignant hypertension, microscopic
• One complication of hyperplastic arteriolosclerosis with malignant hypertension is fibrinoid necrosis, as seen here in a renal arteriole
Varicose veins, gross
• The prominent veins shown here on the lower leg are varicosities. Varicose veins are a common problem with aging. The venous valves become incompetent. • There may be muscular atrophy with less tone to provide a massage effect on the large superficial veins, and skin becomes less elastic with time. • Hydrostatic pressure from standing for long periods exacerbates the problem
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