Aortic stenosis gross pathology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Pathological Findings

Images shown below are courtesy of Professor Peter Anderson DVM PhD and published with permission. © PEIR, University of Alabama at Birmingham, Department of Pathology

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  Aortic Stenosis, Bicuspid valve: Gross; excellent image of bicuspid and calcific valve showing a false raphe.

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  Aortic Stenosis, Bicuspid valve: Gross; good example of bicuspid valve

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  Aortic Stenosis, Bicuspid valve: Gross; image of bicuspid aortic valve, an excellent example

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  Aortic Stenosis, Bicuspid valve: Gross; close-up image of bicuspid aortic valve.

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  Aortic Stenosis, Bicuspid valve: Gross; close-up image of bicuspid aortic valve.

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  Bicuspid aortic valve

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  Gross natural color opened first portion aortic arch with bicuspid aortic valve shows stenosis and aortic root is dilated

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  Aortic Stenosis Bicuspid: Gross; natural color opened left ventricular outflow tract with calcific masses on valve as well as anterior leaflet mitral valve probably did not cause significant stenosis

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  Bicuspid Aortic Valve with Repaired Aorta Coarctation: Gross natural color opened left ventricular outflow tract with uncomplicated bicuspid aortic valve repaired coarctation barely visible ruptured postoperative young female with ovaries Turner mosaic not ruled out

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  Bicuspid Aortic Stenosis: Gross; fixed tissue

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  Aortic Stenosis, Bicuspid: Gross; fixed tissue view of stenotic valve through ventricular outlet track

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  Aortic Stenosis Bicuspid: Gross; fixed tissue. Bicuspid valve and false raphe classical

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  Bicuspid aortic valve

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  Bicuspid aortic valve

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  Bicuspid aortic valve

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  Left ventricular hypertrophy due to bicuspid aortic valve

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  Congenital aortic stenosis: Gangrene toe In Infant: Gross, natural color, 1 month old child with congenital aortic stenosis

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  Unicuspid aortic stenosis

An Autopsy Report

A 68-year-old man initially sought medical advice five years prior to his death. His symptoms at that time were exercise intolerance and occasional peripheral edema. He gave a history of a "heart murmur" that was diagnosed 25 years ago during an employment physical. No follow up care had been given for this murmur.

The patient's terminal admission was for signs of severe heart failure--the patient had marked peripheral edema and shortness of breath and chest x-ray revealed significant cardiac enlargement and pulmonary edema with bilateral pleural effusions. He sustained a cardiac arrest shortly after admission and could not be resuscitated.

Autopsy Findings

Autopsy disclosed a markedly enlarged heart weighing 650 grams and having dilated chambers. The aortic valve was calcified and showed evidence of stenosis and insufficiency. The coronary arteries were narrowed 60 to 70% by atherosclerosis. No acute coronary occlusions were found and there was no evidence of myocardial infarction.

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  This is a gross photograph of a cross section of a normal human heart taken at autopsy (right) and the heart from this case, which demonstrates concentric hypertrophy of the left ventricular wall. Note the marked thickening of the left ventricular wall. There is also moderate thickening of the right ventricular wall.

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  This low-power photomicrograph shows normal myocardium (left) compared to hypertrophied myocardium (right).

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  Normal myocardium (left) is compared here to hypertrophied myocardium (right). The muscle fibers are thicker and the nuclei are larger and darker in the hypertrophied myocardium.The clear spaces between the muscle fibers are due to processing artifacts and are not present during life.

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  Normal myocardium (left) is compared to hypertrophied myocardium (right). This high power view demonstrates the large dark nuclei (arrow) found in hypertrophied cardiac muscle cells. Polyploidy is a common feature in cardiac hypertrophy. Also note the increased size (thickness) of the individual cardiac muscle cell on the right compared to normal cardiac myocytes (left).