The cardinal manifestations of aortic stenosis are 3 and reflect the hemodynamic repercussions that valve disease causes. They are:
- Dyspnea on exertion (up to heart failure)
In a seminal publication from the 1960s, Eugene Braunwald exposed the correlation between the appearance of symptoms and the prognosis of the patient with aortic stenosis. So, for over 50 years, we know that while the patient is asymptomatic, his evolution is very similar to that of a patient without the pathology, with rare acute events.
From the point at which he develops angina, in general, in 5 years there is a negative outcome, such as death or stroke. When developing syncope, this time is reduced to 3 years and when developing dyspnea or advanced degrees of heart failure, this time drops to 2 years, if there is no adequate intervention.
Symptoms usually appear in the fifth or sixth decade of life, with little variety if the underlying disease is bivalvular aortic valve, with earlier onset. The most common presentation is the progressive reduction in exercise tolerance, initially marked by diastolic dysfunction caused by ventricular hypertrophy. More advanced conditions lead to more exuberant symptoms, such as paroxysmal nocturnal dyspnea or orthopnea and the intervention must precede this stage.
Angina occurs in up to 60% of patients, half of whom have concomitance with significant coronary obstruction, since they are diseases that share a series of comorbidities considered as risk factors. In the absence of obstruction, the explanation was given before and can also be checked here.
Syncope is the main cause of poor cerebral perfusion during physical activity. This occurs because the patient with significant aortic stenosis has a relative fixed cardiac output due to valve obstruction and experiences, in physical activity, a physiological peripheral vasodilation. As a final route of this combination, there is a drop in diastolic blood pressure and a transient deficit in the perfusion of the CNS. Other associated causes are dysfunction of baroreceptors, as well as inadequate vasopressor response in the face of high intraventricular pressure on exertion.
Pictures that occur at rest are more related to the sudden loss of atrial contraction due to atrial fibrillation or atrioventricular block caused by the extensive calcification of the annulus that invades the conduction system. Malignant ventricular arrhythmias are uncommon and occur in patients with extensive myocardial fibrosis and the presence of advanced systolic dysfunction.
Patients with severe aortic stenosis may experience a series of bleedings in the gastrointestinal tract. This occurs due to the formation of angiodysplasias, mainly in the right colon. This complication comes from the platelet aggregation induced by shear stress, with a reduction in von Willebrand’s multimers, when passing through the stenotic valve. These hemorrhagic events are ended with valve repair.
In summary, the physical examination directed at the patient with aortic stenosis should assess:
Carotid pulse palpation
Auscultation of precordium
Investigation of HF signs
The carotid pulse corresponds to the formation of the pulse wave. The change with high specificity is expected for severe conditions with slow increase and low amplitude, which has the pulse designation “parvus et tardus”. However, situations of double aortic injury or uncontrolled hypertension mask this characteristic on physical examination. Thus, the absence of this finding does not exclude the severity of aortic stenosis. In cases of intense murmur, we may have irradiation to the carotid arteries, including a thrill, which can be palpable in the examination of the carotid arteries.
Precordium inspection may provide some information, with the presence of a muscular and propulsive ictus, compatible with major concentric hypertrophy. In cases of left ventricular systolic dysfunction, an ictus deviated to the left and downwards can be found. Situations of hyperdynamic precordium signal the involvement of another valve disease such as aortic or even mitral regurgitation.
Cardiac auscultation is classic in these patients. They present an ejection systolic murmur, shaped like a diamond or growing and decreasing. It can radiate to the vessels of the base, being better audible with the patient seated and slightly leaning forward. A characteristic that helps to differentiate from the murmur of mitral regurgitation is that the auscultation of the second sound is well marked. The murmur of aortic stenosis ends before component A2 of the second sound, facilitating differentiation.
In patients with advanced conditions and with intense calcification, a harsh murmur is heard at the base and high-frequency components can radiate to the tip of the heart. This is called the Gallavardin effect or phenomenon, but it must be kept in mind that the sound perceived at the tip of the heart maintains the original diamond shape and at that point, the second sound is also clearly heard. So the difference is only in the tone and not in other characteristics.
Another characteristic that may suggest the severity of the condition is the late peak of the murmur. The later the peak occurs, the greater the severity of valve stenosis. Likewise, high intensity murmurs are more associated with severe conditions, with the maximum degree almost exclusive in cases with the presence of thrill. The opposite cannot be said, as several patients experience severe aortic stenosis and on auscultation do not present such a semiological depth.
The physiological breakdown of the second heart sound in the elderly virtually excludes severe involvement of aortic stenosis, as this points to the presence of not very calcified leaflets. This may not occur in young people who have a congenital etiology and little calcification.
The auscultation of aortic stenosis can be dynamic according to the heart rate. Patients with atrial fibrillation may have variable murmur due to different diastolic time from cycle to cycle. Longer diastolic times lead to greater ejection volume and, therefore, more intense murmurs. The same occurs after a postextrasystolic pause, in which we see greater diastolic time and a more intense murmur. This does not occur in mitral regurgitation and thus can also be used as a tool for differentiation.
The examiner may use some maneuvers to confirm the diagnosis by auscultating the precordium. Semiology maneuvers exist to temporarily change the pre and post-load situations. A classic example is the Handgrip maneuver in which the peripheral muscles contract for about 5 seconds. This transiently raises the afterload with which the ventricle has to work.
By raising the afterload with the maneuver, the transvalvular gradient is reduced, as we now have increased peripheral capillary pressure. The effect of this maneuver on auscultation is to reduce the intensity of the murmur after the 5 seconds of muscle contraction. Thus, it is much easier to differentiate murmur from aortic stenosis from murmur from mitral regurgitation, since the latter rises with the same maneuver.
1 – Otto CM, Bonow RO. A Valvular Heart Disease – A companion to Braunwald’s Heart Disease. Fourth Edition, 2014.