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Aortic Valve Regurgitation

  • Aortic Valve Regurgitation occurs due to incomplete closure of the aortic valve, thus allowing inappropriate retrograde movement of blood from the aorta to the left ventricle during diastole.
  • Overview
    • Insufficiency of the aortic valve may be due to primary disease of the valve leaflets preventing their full closure; alternatively, several primary diseases of the aortic root result in widening of the valvular annulus and thus prevent full closure of otherwise healthy aortic valve leaflets.
  • Primary Leaflet Disease
    • Congenital Bicuspid Aortic Valve: Interferes with full valvular coaptation.
    • Infective Endocarditis: Can cause perforation or physical destruction of the valve leaflets
    • Rheumatic Fever: In some patients Rheumatic Heart Disease results in sclerosis and deformation of the aortic valve
  • Primary Aortic Root Disease
    • Aortic Dissection: Specifically Type A dissections which extend into the aortic root
    • Syphilitic Aneurysm: Can occur during Tertiary Syphilis
    • Aortic Aneurysms: Aneurysmal dilation of the aorta is sometimes seen in patients with Marfan Syndrome and some other familial diseases.
  • Overview
    • Aortic Regurgitation allows a portion of the forward volume output of the heart to return to the left ventricle. Consequently, the left ventricle is filled with the normal volume it receives from the left atria in addition to the regurgitant volume, resulting in elevation of the Left Ventricular End Diastolic Volume (VEDV). Because of the Frank-Starling Relationship, this substantial increase in left ventricular preload improves ventricular ejection and consequently cardiac output is initially not compromised. However, several pathophysiological sequelae result which can lead to severe clinical consequences. The subsequent pathophysiological progression is largely dependent on the timescale, acute or chronic, in which regurgitation develops.
  • Acute Aortic Regurgitation
    • Acute Aortic Regurgitation primarily occurs in the context of aortic dissection and in some cases of infective endocarditis. Regurgitation into an otherwise normal left ventricle results in substantial increases in diastolic ventricular pressures. These pressures in turn necessitate higher left atrial pressures to maintain sufficient ventricular filling. Greater left atrial pressures are in turn retrogradely transmitted into the pulmonary circulation, ultimately resulting in sudden and severe pulmonary edema.
  • Chronic Aortic Regurgitation
    • The chronic presence of aortic regurgitation allows for significant compensatory remodeling of the left ventricle. The left ventricle compensates for chronic volume overload by undergoing eccentric ventricular hypertrophy and thus chamber dilation. This allows the regurgitant volume to enter the left ventricle without significantly increasing diastolic filling pressures, thus avoiding backward transmission of that pressure to the pulmonary circulation and in turn preventing pulmonary edema. However, when regurgitatant volumes are large, the systemic arterial pressure rapidly falls during diastole as much of the ejected blood returns to the dilated left ventricle.
    • Because the majority of cardiac blood flow occurs during diastole, reduced diastolic pressure can significantly reduce coronary perfusion to the point that transient episodes of myocardial ischemia are encountered. Furthermore, as the left ventricle dilates, the Law of Laplace dictates that the myocardial tension required to achieve ventricular ejection increases, thus effectively increasing the left heart's afterload. In consequence, the dilating left ventricle encounters a situation of chronically increased preload and afterload, an unsustainable hemodynamic burden which ultimately leads to Left Heart Failure in many patients.
Clinical Consequences
  • Acute Aortic Regurgitation
    • As described above, rapid development of severe pulmonary edema results in intense dyspnea. In many cases, Cardiogenic Shock develops.
  • Chronic Aortic Regurgitation
    • Chronic Aortic Regurgitation can be well-tolerated for many years without significant symptomology. Patients often present only once signs and symptomology of Left Heart Failure have developed such as dyspnea, orthopnea, and Paroxysmal Nocturnal Dyspnea. In some cases, patients manifest with anginal chest pain due to episodes of myocardial ischemia, as described above.
  • Heart Murmur:
    • The prototypical auscultory finding of aortic regurgitation is a blowing, decrescendo diastolic murmur caused by the dissipating jet of regurgitating blood.
  • Widened Pulse Pressure:
    • In cases of severe chronic aortic regurgitation the rapid dissipation of systemic diastolic pressure results in a significant widening of the pulse pressure. This manifests as a number of different physical findings but most prominently as "Water-hammer" pulses which fall rapidly during diastole (Also known as Corrigan's Pulse). In addition, pulses in the carotids may be so widened that a patients head may bob to-and-fro, known as de Musset Sign.