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Pathology
Arterial disease
Angina pectoris
Stable angina
Unstable angina
Myocardial infarction
Prinzmetal angina
Coronary steal syndrome
Peripheral artery disease
Subclavian steal syndrome
Aneurysms
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Long QT syndrome and Torsade de pointes
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Acyanotic congenital heart defects: Pathology review
Cyanotic congenital heart defects: Pathology review
Atherosclerosis and arteriosclerosis: Pathology review
Coronary artery disease: Pathology review
Peripheral artery disease: Pathology review
Valvular heart disease: Pathology review
Cardiomyopathies: Pathology review
Heart failure: Pathology review
Supraventricular arrhythmias: Pathology review
Ventricular arrhythmias: Pathology review
Heart blocks: Pathology review
Aortic dissections and aneurysms: Pathology review
Pericardial disease: Pathology review
Endocarditis: Pathology review
Hypertension: Pathology review
Shock: Pathology review
Vasculitis: Pathology review
Cardiac and vascular tumors: Pathology review
Dyslipidemias: Pathology review
Aortic valve disease
0 / 26 complete
0 / 5 complete
of complete
of complete
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2021
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aortic stenosis p. 298
presentation p. 716
ejection click and p. 728
heart murmurs p. 298
macroangiopathic anemia p. 417
paradoxical splitting in p. 296
presentation p. 716
pulse pressure in p. 292
S4 heart sound and p. 728
systolic murmur in p. 297
Williams syndrome p. 306
aortic stenosis p. 298
aortic stenosis p. 716
The aortic valve is typically made up of three leaflets: the left, the right, and the posterior leaflet and it opens during systole to allow blood to be ejected to the body. During diastole, it closes to allow the heart to fill with blood and get ready for another systole. If the aortic valve doesn’t open all the way, it gets harder to pump out to the body and this is called aortic stenosis. If it doesn’t close all the way, then blood leaks back into the left ventricle called aortic valve regurgitation or aortic insufficiency.
Usually, the aortic valve opens to about 3-4 cm2, but with stenosis it can become less than 1 cm2. This is usually caused by mechanical stress over time, which damages endothelial cells around the valves, causing fibrosis and calcification, which hardens the valve and makes it more difficult to open completely. This type usually shows up in late adulthood, with patients over 60 years old.
Similarly, patients that have a bicuspid valve — with two leaflets — as opposed to a tricuspid — with three — are more at risk of fibrosis and calcification because the mechanical stress that’s usually distributed between three leaflets is now being split by two leaflets and therefore, they see more stress per leaflet. Another important cause of aortic stenosis is chronic rheumatic fever, which can cause repeated inflammation and repair, leading to fibrosis. In this case, the leaflets can actually fuse together — called commissural fusion — which is an important distinction from the type caused by mechanical stress over time.
When the valve fuses together or hardens, it doesn’t open as easily, right? And so as the left ventricle contracts, it creates this high pressure that eventually pushes on the valve until it finally snaps open, causing a characteristic “ejection click.” Since the blood has to flow through a narrow opening, there’s turbulence which creates noise, or a murmur, which gets initially louder as more blood flows past the opening, and then quieter as the amount of blood flowing subsides because less remains in the ventricle. This is called a crescendo-decrescendo murmur.
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