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Aortic regurgitation: Clinical Presentation, Disease Stages, and Management
Key points
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Aortic regurgitation (AR) may be caused by abnormalities of the aortic leaflets, aortic root, or ascending aorta. Evaluation of AR should include valve morphology, regurgitation mechanism, and severity and aortic dilation assessment.
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Color Doppler proximal jet width with measurement of the vena contracta and diastolic flow reversal in the descending aorta are the most useful echocardiographic methods to assess AR severity in clinical practice. The flow convergence method (i.e., proximal isovelocity surface area [PISA] method) is less sensitive to loading conditions but more technically demanding.
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Cardiac magnetic resonance (CMR) may be used in the quantitative assessment of regurgitant severity and left ventricular (LV) function when echocardiography is suboptimal. CMR and computed tomography provide accurate ascending aorta measurements, which are important for understanding functional AR mechanisms, follow-up of aorta size, and targeting the optimal time and strategy for ascending aorta surgery.
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Symptoms are the indication for surgical intervention in most patients with chronic AR; but some patients have impaired ventricular contractility in the absence of symptoms. LV ejection fraction less than 50% and/or LV end-systolic diameter greater than 50 mm (>21 mm/m 2 ) are the most useful parameters for clinical decision making. Indexed end-systolic diameter is recommended when the body surface area is less than 1.65 m 2 .
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Conservative aortic valve surgery, including valve-sparing operations, and aortic cusp repair should be considered in the management of severe AR. Intraoperative transesophageal echocardiography is mandatory after repair to assess the functional result and identify patients at risk for early AR recurrence.
Aortic regurgitation (AR) is characterized by diastolic reflux of blood from the aorta into the left ventricle (LV). The overall prevalence of AR detected by color Doppler echocardiography in an adult population was 4.9% in the Framingham Heart Study and 10% in the Strong Heart Study. Most cases were trace or mild AR; moderate or severe AR is less common (0.5%–2.7%).
Etiology
AR causes fall into two broad categories: primary abnormalities of the aortic valve leaflets and abnormalities of the aortic root and ascending aorta ( Table 10.1 ). The most frequent causes include congenital abnormalities of the aortic valve (most notably bicuspid valves, but also unicuspid, and quadricuspid valves), rheumatic disease, infective endocarditis, calcific degeneration, and myxomatous degeneration ( Fig. 10.1 ). Other common causes of AR represent diseases of the aorta without direct involvement of the aortic valve, as in patients with aorta dilation secondary to genetic disorders such as Marfan syndrome, idiopathic annulo-aortic ectasia, degenerative aneurysms (more frequent in patients with systemic hypertension), and aortic dissection. ,
TABLE 10.1
Causes of Aortic Regurgitation.
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With the development and clinical adoption of transcatheter aortic valve replacement (TAVR) techniques, TAVR has emerged as a common and potentially important cause of acute and chronic AR. AR may also develop as a complication of balloon aortic valvuloplasty or after LV assist device implantation. However, in many cases of AR, the precise cause is unclear. In a pathologic study of a surgical series of excised aortic valves, up to 34% of pure AR cases, the cause was unclear. In the Euro Heart Survey for Valvular Diseases, AR represented 13.3% of patients with single native left-sided disease: 15.2% had a congenital origin, and the same percentage was observed for rheumatic origin.
Most of these lesions produce chronic AR, with slow, insidious LV dilation and a prolonged asymptomatic phase. Other lesions, particularly infective endocarditis, aortic dissection, and trauma, more often produce acute severe AR with sudden elevation of LV filling pressures, pulmonary edema, and reduced cardiac output.
Acute aortic regurgitation
Diagnosis
Acute severe AR may be misdiagnosed as another acute condition. Many of the characteristic physical findings of chronic volume overload are modified or absent when valvular regurgitation is acute, and the severity of AR can be underestimated. Due to acute hemodynamic deterioration, patients with acute AR are often tachycardic, tachypneic, and in pulmonary edema. However, LV size may be normal on physical examination, and cardiomegaly may be absent on the chest radiograph. Pulse pressure may not be increased because systolic pressure is reduced in relation to the decrease in forward stroke volume, and diastolic pressure equals the elevated LV diastolic pressure. In the absence of a widened pulse pressure, the characteristic peripheral signs of AR are absent. Although a diastolic murmur is usually present, it can be soft and short because the rapidly rising LV diastolic pressure reduces the aortic-ventricular pressure gradient. The murmur is often difficult to hear.
Echocardiography is indispensable in confirming the presence and severity of AR, assessing its cause, and determining whether there is a rapid equilibration of aortic and LV diastolic pressure. Evidence for rapid pressure equilibration includes a short AR diastolic half-time (<300 ms) and a short mitral deceleration time (<150 ms) ( Fig. 10.2 ). Premature mitral valve closure is a specific and sensitive, noninvasive indicator of acute severe AR, and the extent of premature mitral valve closure correlates with the degree of increase in LV diastolic pressure. In severe AR, the LV end-diastolic pressure can exceed the left atrial pressure and cause premature, presystolic closure of the mitral valve.
Transesophageal echocardiography (TEE) is indicated when aortic dissection, acute endocarditis, or trauma is suspected ( Fig. 10.3 ). Computed tomography (CT) or cardiac magnetic resonance (CMR) can be used in some settings when it can yield a more rapid diagnosis of aortic dissection than can be achieved by TEE. , Intraoperative TEE is indispensable for demonstrating the mechanism of AR in aortic dissection and can facilitate the choice of aortic valve surgical procedure (i.e., resuspension or replacement). Mechanisms include aortic root dilation, false lumen–produced annulus pressure on a cusp that causes asymmetric cusp coaptation, flail of an aortic cusp attributable to annular support disruption, and prolapse of a mobile intimal flap through the aortic valve.
Pathophysiology
In acute severe AR, the abrupt development of a large regurgitant volume is imposed on a LV of normal size that has not had time to adapt to the volume overload. The acute increase in diastolic flow into the nondilated LV leads to a marked elevation in end-diastolic pressure due to a rightward shift along the normal LV diastolic pressure-volume curve. In severe cases, the increased ventricular pressures during the diastolic filling period in conjunction with the decrease in the aortic diastolic pressure leads to a rapid equalization of aortic and LV pressures at end-diastole. , With acute regurgitation, forward cardiac output is decreased because the total stroke volume of the nondilated ventricle includes the regurgitant and forward stroke volume. Compensatory tachycardia may partially correct this decline in forward stroke volume, but it is often insufficient to maintain cardiac output, and patients may present in cardiogenic shock. Pulmonary edema results from the markedly elevated LV end-diastolic pressure and concomitant elevation of pulmonary venous pressure. Acutely-diminished coronary flow reserve may lead to subendocardial ischemia. In patients with preexisting LV hypertrophy due to arterial hypertension or aortic stenosis, acute moderate AR (as may develop after TAVR) can cause severe hemodynamic changes due to a noncompliant LV with a reduced preload reserve.
Management
Death due to pulmonary edema, ventricular arrhythmias, electromechanical dissociation, or circulatory collapse is common in acute, severe AR. Patients often require emergency or urgent aortic valve replacement (AVR) for correction of the underlying disease process and relief of the acute volume overload. Intraaortic balloon counterpulsation is contraindicated. In patients with acute AR due to an ascending aortic dissection, prompt surgical intervention with a composite replacement of the aorta along with aortic valve or a valve-sparing reimplantation technique is required. , In cases of severe acute AR due to infective endocarditis, patients need immediate antibiotics and aggressive medical treatment. If the hemodynamic situation does not improve immediately, emergent AVR may be lifesaving. If the clinical situation stabilizes, surgery may be postponed for a few days so that the patient, under strict medical supervision, can be treated with antibiotics before surgical correction. ,
Chronic aortic regurgitation
Clinical presentation
Clinical history
Many patients with AR are diagnosed before symptom onset based on the finding of a diastolic murmur on physical examination, discovery of an enlarged cardiac silhouette on the chest radiograph, or evidence of LV hypertrophy on electrocardiography. The most common initial symptom of patients with chronic severe AR is exertional dyspnea, most likely due to an elevated LV end-diastolic pressure with exercise.
Because chronic AR has a slowly progressive course, the gradual decrease in exercise capacity may not be recognized as abnormal by the patient, and very careful questioning is often needed to elicit evidence of a subtle decline in functional status. In cases of doubtful or equivocal symptoms, exercise testing may be valuable for assessing functional capacity. In more advanced cases with severe LV dysfunction, patients can have symptoms of overt heart failure, including dyspnea at rest, orthopnea, and pulmonary edema. The acute onset of heart failure symptoms can occur in patients with chronic disease due to an acute increase in regurgitation severity, such as patients with infective endocarditis or aortic dissection.
Angina may occur, even in the absence of atherosclerotic coronary artery disease, due to lower myocardial perfusion pressure, increased myocardial oxygen demand, and a decreased ratio of coronary artery size to myocardial mass. Syncope or sudden death, albeit rare, can occur in AR. Sudden death has been associated with extreme degrees of LV dilation. Some patients may be uncomfortably aware of their heart beat or palpitations related to increased pulse pressure, which is the earliest symptom leading to the diagnosis of AR.
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