![]() TAVI also requires a shorter hospital stay, causes less pain, and permits more rapid return to activity however, it also increases vascular complications and paravalvular regurgitation and increases the need for permanent pacemaker implantation and early repeat valve intervention.Degenerative calcific aortic stenosis (AS) is one of the most common valvular heart diseases, affecting >3% of those aged >65 years in the West. Compared with SAVR, transfemoral TAVI has lower short-term mortality, and less risk of stroke, major bleeding, and atrial fibrillation. In patients with a life expectancy of < 1 year even with a successful procedure, intervention is not recommended. If the patient’s arteries are not suited to the transfemoral route, then SAVR is preferred as long as surgical risk is not prohibitive. Causes include a congenital bicuspid valve, idiopathic. 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. Guidelines to inform shared decision-making suggest SAVR for patients 80 years or who have a life expectancy of < 10 years. The choice is between the up-front risk and morbidity of SAVR versus the unknown durability of TAVI valves beyond 5 years. Low-dose dobutamine stress echocardiography distinguishes low-gradient AS from pseudostenosis. It is very likely when the calcium score is > 3000 (men) and > 1600 (women). Differentiation of pseudostenosis from low-gradient AS can be aided by calculation of the ratio of outflow tract to aortic velocity (Doppler velocity index ). 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). 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 ). Causes include valvular degeneration and aortic root dilation. 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 intensity of the murmur may therefore be misleading in these circumstances. As LV contractility decreases in critical AS, the murmur becomes softer and shorter. 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. But in older patients, vibration of the unfused cusps of calcified aortic valve leaflets may transmit a louder, more high-pitched, “cooing” or musical sound to the cardiac apex, with softening or absence of the murmur parasternally (Gallavardin phenomenon), thereby mimicking mitral regurgitation. The murmur typically radiates to the right clavicle and both carotid arteries (left often louder than right) and has a harsh or grating quality. ![]() ![]() The hallmark finding is a crescendo-decrescendo ejection murmur, heard best with the diaphragm of the stethoscope at the right and left upper sternal borders when a patient who is sitting upright leans forward. read more are at increased risk for atherosclerosis, and more recently, psoriasis has been tied to an increased risk of aortic stenosis. Patients with psoriasis Psoriasis Psoriasis is an inflammatory disease that manifests most commonly as well-circumscribed, erythematous papules and plaques covered with silvery scales. Elevated lipoprotein (a) levels also predict faster hemodynamic progression of AS. Lipoprotein (a) is implicated in the pathogenesis of both aortic stenosis and atherosclerosis. Over years, aortic sclerosis progresses to stenosis in as many as 15% of patients. Lipid deposition and inflammation lead to thickening of aortic valve structures by fibrosis and calcification initially without causing significant obstruction. Genetic, anatomic, fluid dynamic, and environmental risk factors include hypertension, smoking, high cholesterol, and presence of a bicuspid valve. The cause of aortic sclerosis and stenosis is not yet known but is mediated by an inflammatory process that is similar to but distinct from atherosclerosis.
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