Aortic Valve Replacement

Excerpt

The aortic valve is a semilunar valve with three leaflets, which lies at the junction of left ventricle and aorta. It allows unidirectional blood flow from the left ventricle to the aorta and the rest of the body. Because of the highly complex and sophisticated cellular and molecular functions, the thin valve leaflet can withstand extreme mechanical and hemodynamic forces with every cardiac cycle. Various factors including age and congenital defects can compromise the normal valvular function leading to a wide variety of complications.

Although bicuspid aortic valves (BAV) are the most common congenital abnormality, congenital valve defects can range from aortic atresia (missing or incomplete closure of aortic valves) to a sub or supra-valvular stenosis. BAV is reported to have an incidence of 1 to 2% with a male predominance. Lack of microfibrillar proteins during valvulogenesis has been reported to affect the leaflet development where two leaflets are fused to form one large leaflet. It frequently correlates with aortic abnormalities such as aortic dilation (root, ascending and arch) and coarctation of the aorta. The bicuspid aortic valve leaflets can undergo accelerated calcific degeneration because of abnormal hemodynamic forces.

Congenital abnormalities including BAV can lead to various valvular complications including aortic stenosis and aortic regurgitation leading to an increased risk to infective endocarditis, which has a reported incidence of 12 to 39% in BAV. Unless severe, BAV generally remains asymptomatic until the age of 50 to 60 years.

Aortic stenosis (AS) is a narrowing of the valve aperture reducing the aortic valve area. Increased resistance to blood flow and transvalvular pressure gradient causes increased left ventricle workload causing hypertrophy. Its prevalence increases with age and can be as high as 4.6% in people greater than age 75 years. Being the most common valvular disease in Europe and America, estimates are that 3.5 million people in England alone will have AS by the year 2020. Calcific degeneration leading to stiffening and restriction motion of valve leaflet is the most common cause of AS. Disruption of endothelium lining on the aortic side caused by increased mechanical stress seem to be the inciting event. Posterior leaflets are reported to be affected the most. Rheumatic fever causing inflammation of the leaflets is still the leading cause of AS in developing countries.

AS can be asymptomatic or can cause symptoms of syncope, angina and heart failure. Severe AS is fatal with a 50% mortality at 2 years. As per The American College of Cardiology/American Heart Association (ACC/AHA) guidelines, AS is graded severe when the orifice area is less than 1.0 cm, the mean gradient is greater than 40 mmHg or the jet velocity is greater than 4 m/s. Prognosis is poor in symptomatic or severe cases unless the valve is replaced. Up to 30% of patients aged > 75 do not undergo surgical valve replacement either because of technical reasons; this may include porcelain aorta, general frailty, refusal to undergo surgery, and serious comorbid conditions. The operative death risk for surgical aortic valve replacement (SAVR) is as high as 10% in patients with LV dysfunction, chronic renal disease, and advanced age. Trans-catheter aortic valve replacement and trans-catheter aortic valve implantation (TAVR/TAVI) have emerged as a more feasible and less risky option for patients not suitable for surgery.

Aortic regurgitation (AR) is the backflow of blood from the aorta to the left ventricle when the valve leaflets fail to coapt. Common causes include congenital defects, calcific degeneration, infective endocarditis, rheumatic fever, and trauma. Ventricular hypertrophy in chronic cases accommodates increased volume to maintain the normal stroke volume and end-diastolic pressure; hence, chronic AR can be asymptomatic for decades. In contrast, with acute cases of AR, ventricles do not have enough time to undergo the needed changes such as hypertrophy to accommodate increased volumes. Because of decreased stroke volume, the heart rate increases to maintain cardiac output but is insufficient to meet the demand resulting in increased left atrial pressure, pulmonary edema and cardiogenic shock.

On physical examination, AR murmur is blowing, high-pitched, diastolic, and decrescendo, beginning soon after the aortic component of S (A); it is loudest at the 3rd or 4th left parasternal intercostal space. It also has associations with various other murmurs including: