Transcatheter Aortic Valve Replacement

Diagnosis Key Points ����The most common cause of valvular aortic stenosis (AS) in adults is calcification of a normal tricuspid or congenital bicuspid valve. ����Calcific AS typically presents in older individuals (ie, >75 years) in contrast to bicuspid AS, which presents a decade or more earlier. ����Stroke, the greatest risk accompanying aortic valve replacement (AVR), can be kept under 2% even in octogenerians by careful patient selection. ����Transcatheter aortic valve replacement (TAVR) offers new and potentially transformational technology for patients with severe aortic valvular stenosis who are either extremely high-risk candidates or inoperable for surgical AVR or who are inoperable by virtue of associated comorbidities. ����An estimated 40,000 patients have received TAVR worldwide. ������ Severe ������ Symptomatic Medical treatment including the potential for balloon valvuloplasty ������ Tricuspid valve ������ Prohibitive surgical risk ������ Severe ������ Hypotensive response to exercise ������ Moderate ������ Symptomatic ������ Need for related CV Surgery ������ Critical Aortic Stenosis TAVR OR High surgical risk ����In adults with valvular AS, the obstruction develops gradually, typically over many years during which the left ventricle (LV) adapts to the systolic pressure overload with progressive concentric hypertrophy that results in diastolic dysfunction, reduced coronary reserve, myocardial ischemia, and eventually, depressed contractility resulting in LV systolic dysfunction. Ultimately, in some patients, heart failure or sudden death occurs. Typically, patients with AS are free from cardiovascular symptoms (ie, angina, syncope, and heart failure) until late in the course of the disease. ������ Once symptoms manifest, the prognosis is poor, with the interval from the onset of symptoms to the time of death being approximately 2 years in patients with heart failure, 3 years in those with syncope, and 5 years in those with angina. ������ Echocardiography has largely replaced invasive cardiac catheterization as the standard for quantification of AS. ������ Echocardiographic diagnosis is made by observing a calcified valve with restricted leaflet opening by two-dimensional (2D) echocardiography with quantification of the peak and mean AV gradient made by applying the simplified Bernoulli equation (��p = 4v2) to the maximal velocity recorded through the aortic valve by continuous-wave Doppler. ����Severe stenosis is defined in the guidelines as a peak velocity >4.0 m/s (corresponding to a peak gradient of 64 mm Hg), a mean gradient >40 mm Hg, OR valve area <1.0 cm2 when LV systolic function is normal. Aortic Stenosis ������ Predicted survial ��� <12 months ������ Prohibitive TAVR risk Key Points AVR ������ To account for patient size, the valve area is often indexed to body surface area, ��� with 0.6 cm2/m2 considered to be the threshold for severe AS. ������ An important exception is when the gradient suggests less severe stenosis than the valve area, most commonly due to low stroke volume, either in dilated ventricles with low ejection fraction (EF) or small ventricles with normal EF. In this setting, a dobutamine stress study (maximum stress dose 20 mcg/kg/min), may be helpful. If the maximum jet velocity rises over 4 m/s with the dobutamine-induced increase in stroke volume while the aortic valve area (AVA) remains less than 1.0 cm2, then the valve is truly severely stenotic. On the other hand, if stroke volume increases with little rise in gradient (causing valve area to increase substantially), then the AS is only mild to moderate in severity, and the LV dysfunction is due to causes other than AS. ����Other adjunctive testing used in quantifying AS includes transesophageal echocardiography (TEE), computed tomography (CT) scanning (dynamic or gated during systole), cardiac magnetic resonance (CMR) and cardiac catheterization. ����In patients with equivocal symptoms, stress testing, and in particular stress echocardiography, can be very helpful.

• Cover