The murmur is soft when stenosis is less severe, grows louder as stenosis progresses, and becomes longer and peaks in volume later in systole ie, crescendo phase becomes longer and decrescendo phase becomes shorter as stenosis becomes more severe.
As LV contractility decreases in critical AS, the murmur becomes softer and shorter. The intensity of the murmur may therefore be misleading in these circumstances. The murmur of aortic stenosis typically increases with maneuvers that increase LV volume and contractility eg, leg-raising, squatting, Valsalva release, after a ventricular premature beat and decreases with maneuvers that decrease LV volume Valsalva maneuver or increase afterload isometric handgrip. These dynamic maneuvers have the opposite effect on the murmur of hypertrophic cardiomyopathy, which can otherwise resemble that of AS.
The murmur of mitral regurgitation due to prolapse of the posterior leaflet may also mimic AS. Diagnosis of aortic stenosis is suspected clinically and confirmed by echocardiography Echocardiography This photo shows a patient having echocardiography.
This image shows all 4 cardiac chambers and the tricupsid and mitral valves. Echocardiography uses ultrasound waves to produce an image of Two-dimensional transthoracic echocardiography is used to identify a stenotic aortic valve and possible causes, to quantify LV hypertrophy and degree of systolic dysfunction, and to detect coexisting valvular heart disorders aortic regurgitation, mitral valve disorders and complications eg, endocarditis.
Doppler echocardiography is used to quantify degree of stenosis by measuring jet velocity, transvalvular systolic pressure gradient, and aortic valve area. Clinical judgment and critical review of the data are used to resolve any discordance among these parameters eg, moderate valve area but severe mean gradient.
Measurement of aortic valve area is least accurate when LV volume or systolic function is reduced, or if systemic hypertension is present. Two-dimensional echocardiogram, apical 4-chamber view. Video demonstrates limited excursion of the aortic valve cusps during systole. The gradient may be overestimated when aortic regurgitation Aortic Regurgitation Aortic regurgitation AR is incompetency of the aortic valve causing backflow from the aorta into the left ventricle during diastole.
The gradient may under-represent severity when the stroke volume is low, eg, in patients with systemic hypertension or LV systolic dysfunction low-gradient AS with reduced EF or a small, hypertrophied LV low-gradient AS with normal EF—see table Types of Severe Aortic Stenosis Types of Severe Aortic Stenosis Aortic stenosis AS is narrowing of the aortic valve, obstructing blood flow from the left ventricle to the ascending aorta during systole.
Sometimes LV systolic dysfunction results in low ventricular pressure that is inadequate to open nonstenotic valve leaflets, causing echocardiographic appearance of low valve area in the absence of stenosis pseudostenosis. Differentiation of pseudostenosis from low-gradient AS can be aided by calculation of the ratio of outflow tract to aortic velocity Doppler velocity index, DVI. Low-dose dobutamine stress echocardiography distinguishes low-gradient AS from pseudostenosis.
Cardiac catheterization Cardiac Catheterization Cardiac catheterization is the passage of a catheter through peripheral arteries or veins into cardiac chambers, the pulmonary artery, and coronary arteries and veins.
Cardiac catheterization Chest x-ray findings may include calcification of the aortic cusps seen on the lateral projection or on fluoroscopy and evidence of heart failure. Heart size may be normal or only mildly enlarged. In asymptomatic patients with severe aortic stenosis, closely supervised exercise ECG testing Stress Testing In stress testing, the heart is monitored by electrocardiography ECG and often imaging studies during an induced episode of increased cardiac demand so that ischemic areas potentially at risk Failure to normally increase BP and development of ST segment depression are less predictive of adverse prognosis.
Exercise testing is contraindicated in symptomatic patients. Circulation 5 :e35—e71, Aortic stenosis progresses faster as severity increases, but the wide variability in progression rates requires regular surveillance, particularly in sedentary older patients. In such patients, flow may become significantly compromised without triggering symptoms. The risk of surgery outweighs the survival benefit in asymptomatic patients, but with the onset of symptoms the mean survival plummets to 2 to 3 years, and prompt valve replacement is indicated to relieve symptoms and improve survival.
Risk of surgery increases for patients who require simultaneous coronary artery bypass graft CABG and for those with depressed systolic LV function. Nothing has yet been proved to slow the progression of aortic stenosis. In randomized trials, statin therapy has been ineffective. Drugs that can cause hypotension eg, nitrates should be used cautiously, although nitroprusside has been used as a temporizing measure to reduce afterload in patients with decompensated heart failure in the hours before valve replacement.
Patients who develop heart failure but are too high risk for valve intervention benefit from cautious treatment with digoxin , diuretics, and angiotensin-converting enzyme ACE inhibitors. Thus, patients should have periodic clinical evaluations, including echocardiography and sometimes exercise testing, to determine the optimal time for valve replacement. Valve replacement is recommended when aortic stenosis is severe and there is any one of the following:. When cardiac surgery is being done for other reasons, concomitant aortic valve surgery is indicated regardless of symptoms if the AS is moderate or greater.
Balloon valvotomy is used primarily in children and very young adults with congenital AS. In older patients who are not candidates for surgery, balloon valvuloplasty has been used as a bridge to valve replacement but this procedure has a high complication rate and provides only temporary relief. It is being replaced by transcatheter valve implantation, which can be done with similar procedural risk, even in sick, high-risk patients.
Transcatheter percutaneous aortic valve implantation TAVI sometimes called transcatheter aortic valve replacement, or TAVR is a less invasive method of aortic valve replacement for which the indications continue to expand. In patients aged 65 to 80 years who are suitable for transfemoral TAVI, the decision regarding SAVR or TAVI is determined based on individual patient characteristics 1 Treatment reference Aortic stenosis AS is narrowing of the aortic valve, obstructing blood flow from the left ventricle to the ascending aorta during systole.
In patients with a life expectancy of Preoperative evaluation for CAD is indicated so that CABG and valve replacement, if indicated, can be done during the same procedure. An aortic bioprosthetic valve requires anticoagulation for 3 to 6 months postoperatively, but a mechanical valve requires lifetime anticoagulation using warfarin.
Newer direct-acting oral anticoagulants DOAC are ineffective and should not be used see also Anticoagulation for patients with a prosthetic cardiac valve Anticoagulation for patients with a prosthetic cardiac valve Any heart valve can become stenotic or insufficient also termed regurgitant or incompetent , causing hemodynamic changes long before symptoms.
The most common cause of aortic stenosis AS in patients Untreated AS ultimately results in exertional syncope, angina, and dyspnea; sudden death may occur. The bell is used to hear low-pitched sounds. Use for mid-diastolic murmur of mitral stenosis or S3 in heart failure. The diaphragm , by filtering out low-pitched sounds, highlights high-pitched sounds. Use for analyzing the second heart sound, ejection and midsystolic clicks and for the soft but high-pitched early diastolic murmur of aortic regurgitation.
You can relate the auscultatory findings to the cardiac cycle by simultaneously palpating the carotid artery while listening to the heart:.
If anything abnormal is found, move the stethoscope around until the abnormality is heard most clearly. Earpieces should be angled forwards to match the direction of the practitioner's external auditory meati. Pericardial sounds are sometime best heard with the patient on hands and knees. Auscultate the heart at various sites At the apex. A Holodiastolic Murmur The duration and quality of murmur are directly proportional to the severity of AR.
Marked Peripheral Signs There are only few data about the predictive value of peripheral signs in diagnosing the severity of AR. The Austin Flint Murmur The murmur typically begins in mid-diastole, often has a presystolic accentuation, and terminates at the end of diastole. Signs of LV Dilation and Dysfunction The systolic apical impulse is laterally and inferiorly displaced, the intensity of the S1 is decreased due to the elevated LVED pressure and the early closure of the mitral valve and a protodiastolic gallop S3 gallop is usually heard at the apex.
Conclusion If we are aware of its limitations and strengths and we succeed in keeping our expertise and proficiency in cardiac auscultation, then clinical examination remains a valuable and cost-effective tool that often enables a rapid, integrative, accurate and patient-orientated diagnosis of aortic valve disease.
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Am Heart J. JAMA Cardiol. A systolic murmur is a common presentation of aortic regurgitation detected by echocardiography. Clin Cardiol. Usefulness of peripheral arterial signs in the evaluation of aortic regurgitation. J Cardiol. About the ESC. Press and Media. Follow us. Help centre Contact us. The intensity of the murmur reflects the velocity and turbulence of blood flow across the valve.
Difficult to be assessed clinically, especially in patients with tachycardia, atrial fibrillation, low grade murmur. The aortic cusps are immobile, so the A2 is faint or even not audible. S2 is increased in associated pulmonary hypertension, other valve heart diseases, hypertensive heart. In LV dysfunction the ejection time does not correlate to the AV area.
It occurs at the moment of maximal opening of the AV, when the valve is bicuspid, still flexible. Forceful atrial contraction into a hypertrophied, non-compliant left ventricle. Other causes of LV hypertrophy Absent in atrial fibrillation.
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