Aortic Stenosis Flashcards
main causes of valvular heart disease (VHD)
- degenerative disease (like aortic stenosis)
- ischemic coronary disease (mitral regurgitation)
- endocarditis (triscuspid or mitral valve regurgitation)
- rheumatic fever and disease (like mitral stenosis)
- congenital valvular disease (like pulmonic stesosis)
the vast majority of valve disease involves which side of the heart?
- left
* diseases of the right valves are far less common
most common valve disease of the pulmonic valve
•congenital pulmonic stenosis
the most common valve disease of the tricuspid valve
•regurgitation due to right ventricular failure and dilatation
the two most common causes of aortic stenosis
- aortic sclerosis involving a normal tricuspid valve
2. congenital bicuspid aortic valve
bicuspid aortic valve
- more often seen in males
- more susceptible to calcification and endocarditis
- thought to be a collagen disorder - thus dilatation of the ascending aorta is often seen with bicuspid aortic valves - can lead to aneurysm (must screen for this)
- bicuspid valves are often stenotic and regurgitant at the same time if aortic dilation is associated
- a non calcified valve may show no symptoms
- symptomatic AS in patients younger than 60 is usually due to a bicuspid valve instead of sclerosis
aortic sclerosis
- a process that causes thickening and calcification of the aortic leaflets which can lead to immobilization of the leaflets with resultant stenosis of the valve
- aortic sclerosis and atherosclerosis have the same risk factors and are very similar pathophysiologically
physical findings in a patient without significant stenosis or a bicuspid valve with minimal obstruction
- grade 1 or 2 systolic ejection murmur in the right intercostal space
- the murmur peaks early in systole
- no thrill, and the murmur does not radiate
- PMI normal
- carotid pulses have a normal upstroke and normal amplitude
- these patients are asymptomatic
physical findings in a patient with severe AS
- murmur becomes grade 3+
- peaks in late systole
- may radiate to the carotids
- the aortic second sound may be absent
- may be a thrill over the RICS
- may be a decrescendo diastolic murmur in the 2nd RICS, which can be due to aortic insufficiency
- PMI may be laterally displaced and can be of increased amplitude
- carotid pulses have a delayed upstroke and decreased amplitude (parvus et tardus)
chest X-ray findings
- subtle
- LV may appear prominent or enlarged
- may be dilatation or prominence of the ascending aorta
- on the lateral film, there can be calcification in the area of the aortic valve (calcification best detected by fluoroscopy)
EKG findings
- the increased systolic pressure in the LV causes LVH, which is detected as LVH on the EKG
- normal sinus rhythm
- if a fib develops, there is a significant decrease in cardia output
echocardiography
•transthoracic echocardiography confirms diagnosis
•calcification seen as echo-bright density
•velocity of flow is measured by using Doppler echocardiography
-normal < 1m/sec
-as the severity of stenosis increases, velocity increases (smaller hole, greater velocity - hose)
-most patienmts with severe AS have a velocity of > 4 m/sec
•valve area calculated using pressure gradient
-mean pressure of > 40 mmHg and aortic area <1 cmsquared = severe AS
•left ventricular ejection fraction measured
•presence or absence of LVH assessed
cardiac catheterization
- usually performed when AS is severe on echo and there is a planned cardiothoracic aortic valve replacement OR if there is a discrepency on echocardiogram and physical exam
- key finding is a pressure gradient across the aortic valve
- by measuring the flow and the gradient, the area can be measured using the Gorlin formula
- when the gradient is approx 30 mmHG or more and the valve area approaches 1 sq cm, symptoms may occur
- coronary arteriography determines if there is associated coronary artery disease
symptoms and natural course of AS
•no symptoms with minimal obstruction •gradient across aortic valve increases by about 7 mmHg per year and aortic valve area decreases by 0.12 sq m/year •syncope •angina •dyspnea •more severe AS -orthopnea -paroxysmal dyspnea -possibly acute pulmonary edema •without surgery, 50% patients die within 5 years of the onset of angina, 3 years after syncope and within 2 years after onset of dyspnea
therapy
•no medical therapy
•surgery! valve replacement
-mechanical
-bioprosthetic
•can be replaced percutaneously - Transcutaneous Aortic Valve Replacement (TAVR)
•survivors of surgery have a normal life expectancy
