Aortic Valvopathy

Aortic Stenosis – Etiology and Pathophysiology

Aortic valve stenosis, as previously mentioned, is the valve change that leads to the emergence of a transvalvular systolic gradient. This is due to a reduction in the aortic valve area during left ventricular systole, for several reasons.

Valve obstruction leads to side effects on the left ventricle, peripheral vasculature and coronary blood flow, which affect the clinical manifestations to varying degrees.

Etiology

Aortic stenosis can be caused by several reasons, but here are the main ones. The congenital etiology can be manifested as uni, bi or quadricuspid. In general, they do not produce significant valve disease in childhood, with degeneration occurring throughout life. As it is a separate etiology, we will address it further in a specific post.

The stereotype of aortic stenosis is the senile calcification etiology, which has been at the center of discussions since the advent of TAVR and, mainly, due to the aging population witnessed in developed countries. Another etiology is rheumatic disease, still very prevalent in developing countries where the fusion of the aortic valve commissures leads to the formation of a gradient and advanced deterioration.

Calcific Aortic Stenosis

Currently, it is the most common cause of aortic stenosis in adults and the elderly worldwide. Approximately 2% of individuals over 65 years of age have severe stenosis, while 30% already experience minor sclerosis. Even though sclerosis does not have significant hemodynamic repercussions, it points to the beginning of the process and increases the risk of cardiovascular death by up to 50%.

Pathophysiological studies of the development of this valve involvement point to a degenerative process, with proliferative and inflammatory changes, leading to the accumulation of lipids and subsequent deposition of calcium. We also found a high prevalence of calcific valve stenosis in patients with Paget’s disease and terminal stages of chronic kidney disease.

These patients share risk factors with those traditionally referred to in coronary artery disease and Mitral Annular Calcification (MAC).

Rheumatic Aortic Stenosis

Although the aortic valve is not the most affected by rheumatic disease, in underdeveloped countries, the prevalence ends up being high due to the very high number of rheumatic heart diseases present in young individuals. It is not uncommon to find young adults with multivalvular disease secondary to rheumatic involvement.

As the commissures fuse and calcified nodules appear, in many cases we find a double aortic lesion, which makes management a little more challenging. With the reduction of cases of rheumatic fever in developed populations, the prevalence of this etiology has been reduced worldwide, but it is still a matter of concern in poor nations.

Pathophysiology

As almost the absolute majority of patients experience progressive and gradual reduction of the valve area over years, we see the maintenance of cardiac output at the expense of a compensatory hypertrophy that makes it possible to tolerate the appearance of high gradients, balancing the wall stress (read it here).

As the contraction of the hypertrophied left ventricle becomes more and more isometric (due to the increased mass), the left ventricular pressure pulse exhibits a rounded apex and the velocity curves on the echocardiographic doppler show a late peak and also roundness of the top of the curve. Speed vs. Time.

Contraction of the left atrium plays a fundamental role in cases of major aortic stenosis with due concentric hypertrophy. It works as an accessory pump, raising the diastolic pressure of the left ventricle at the end of diastole without the pressure being reflected retrograde to the pulmonary capillary, preventing the appearance of symptoms of pulmonary congestion. Loss of atrial contraction as in cases of atrial fibrillation can lead to rapid clinical deterioration in patients with significant aortic stenosis.

Here is a note: Patients presenting decompensated arterial hypertension can hinder the proper assessment of aortic stenosis. The situation of high afterload due to the presence of hypertension above the values considered normal causes problems in measuring the systolic gradient, since the gradient is a pressure difference. Thus, if the pressure on the periphery of the organism is high, a lower gradient between the LV and the periphery is expected, which may hinder the adequate measurement of gravity. In addition, concentric hypertrophy is influenced by uncontrolled SAH, which further hinders the compensatory mechanisms of high afterload.

The physiology of sport is altered in these patients, even in those asymptomatic. In the early stages, physical activity leads to a small increase in the valve area (0.2 cm2), but in advanced stages this mechanism is lost, with the appearance of a fixed valve area. This means that the stroke volume does not increase, leaving cardiac output dependent almost exclusively on heart rate. In this scenario, the elevated heart rate leads to a transient increase in speed and flow rate and in the systolic gradient. Elevation less than 10 mmHg in systolic pressure during physical activity, in general, points to significant aortic valve stenosis.

In patients with aortic stenosis, the coronary flow is increased at rest, but when corrected for the mass, it is within normal limits. There is an imbalance in the flow reserve that leads to the onset of ischemia, even in the absence of obstructive coronary artery disease (read it here), caused in summary by muscle hypertrophy, elevated intracavitary systolic pressure, prolonged ejection and increased oxygen consumption .

Suggested literature:

            1 – Otto CM, Bonow RO. A Valvular Heart Disease – A companion to Braunwald’s Heart Disease. Fourth Edition, 2014.

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