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INTRODUCTION

ESSENTIALS OF DIAGNOSIS

  • Presentation dependent on the rapidity of onset of regurgitation: acute pulmonary edema or chronic dyspnea on exertion.

  • Wide pulse pressure with associated peripheral signs.

  • Diastolic decrescendo murmur at the left sternal border.

  • Left ventricular dilation and hypertrophy with preserved function.

  • Diagnosis confirmed and severity estimated by Doppler echocardiography, aortography, magnetic resonance imaging, or computed tomography angiography.

ETIOLOGY

Normally, the integrity of the aortic orifice during diastole is maintained by an intact aortic root and firm apposition of the free margins of the three aortic valve cusps. Aortic regurgitation (AR) may therefore be caused by a variety of disorders affecting the valve cusps, the aortic root, or the diastolic pressure in the proximal aorta (Table 18–1). With rheumatic heart disease becoming less common, nonrheumatic causes currently account for most of the underlying causes of AR, including congenitally malformed aortic valves, degenerative valve disease, and infective endocarditis. Disorders affecting the aortic root also account for many patients with AR. These conditions include Marfan syndrome, aortic dissection, and inflammatory diseases. Even in the absence of any obvious abnormality of the aortic valve or root, severe systemic hypertension has been reported to cause significant AR.

Table 18–1.Causes of Aortic Regurgitation

PATHOPHYSIOLOGY

The presentation and findings in patients with AR depend on its severity and rapidity of onset. The hemodynamic effects of acute severe AR are entirely different from the chronic type, and the two will be discussed separately.

A. Chronic Aortic Regurgitation

In response to the left ventricular volume overload associated with AR, progressive left ventricular dilation occurs. This results in a higher wall stress, which stimulates ventricular hypertrophy and which, in turn, tends to normalize wall stress. Patients with severe AR may have the largest end-diastolic volumes produced by any other heart disease and yet their end-diastolic pressures are not uniformly elevated. In keeping with the Frank-Starling mechanism, the stroke volume is also increased. Thus, despite the presence of regurgitation, a normal effective forward cardiac output can be maintained. This state persists for several years. Gradually, left ventricular diastolic properties and contractile function start to decline. The adaptive dilation and hypertrophy can no longer match the loading conditions. The left ventricular end-diastolic pressure begins to rise, and the ejection fraction drops ...

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