Aortic Valve Insufficiency

Presentation depends on whether the valvular insufficiency is an acute or a chronic process.

Patients with acute aortic insufficiency have severe dyspnea, signs of cardiogenic shock (tachycardia, hypotension), cyanosis, pulmonary edema, acute heart failure (fatigability and peripheral edema) and chest pain if coronary or aortic dissection is the cause of the regurgitation [1].

Chronic aortic insufficiency leads to palpitations and dyspnea which is initially exertional and afterward occurs with minimal efforts and chest pain if coronary perfusion is compromised. As the disease progresses, orthopnea and paroxysmal nocturnal dyspnea start to occur. Angina is predominantly nocturnal in these patients. As with all valvular diseases, aortic insufficiency is prone to endocarditis, manifesting as fever and central or peripheral embolism.

Auscultation reveals single S1 and S2 sounds and a diastolic descrescendo, high-pitched murmur that increases with squatting. Systolic blood pressure tends to increase, while the diastolic component is prone to decrease.

Chronic aortic insufficiency, but not the acute form, is accompanied by several peripheral signs, reflecting increased stroke volume and wide pulse pressure: pulsation of the liver (Rosenbach), spleen (Gerhardt), retinal arterioles (Becker), cervix (Shelly), uvula (De Musset), capillaries of the nail bed (Quincke), systolic contraction and diastolic dilation of the pupil (Landolfi). In aortic insufficiency, auscultation of the femoral artery reveals systolic and diastolic sounds (Traube) and bruits if the artery is slightly compressed (Duroziez). The "water-hammer" pulse is known as Corrigan's sign, while De Musset's sign describes a specific bobbing motion of the head with each cardiac cycle. When popliteal blood pressure is at least 60 mm Hg higher than the brachial one, Hill's sign is present and if diastolic brachial pressure decreases by at least 15 mm Hg when the arm is raised above the head, Mayne's sign should be noticed. As symptoms worsen, so does the prognosis [2].

Blood workup in aortic valve insufficiency should include complete blood count, inflammatory markers, and cultures if endocarditis is suspected, coagulation parameters like prothrombin time and activated partial thromboplastin time, electrolyte panel, renal and hepatic tests and lactate dehydrogenase.

Echocardiography is a valuable and accurate tool in aortic insufficiency, allowing morphological valvular description, vegetation identification, and ascending aorta evaluation for dissection or aneurysm. Cavity dimensions and ejection fraction should be evaluated, especially if surgical intervention is needed [3].

Severe aortic valvular insufficiency is defined by certain parameters, derived from color, continuous and pulsed wave Doppler studies: vena contracta > 6 mm, regurgitant volume > 60 mL/beat, regurgitation fraction > 50%, and holodiastolic flow reversal in the descending aorta. Left ventricle dilation and ejection fraction should also be investigated, as well as pulmonary hypertension, pericardial effusion and aortic dissection [4]. Transesophageal echocardiography is especially useful in patients with poor acoustic windows or valvular calcification which makes it difficult to identify valve anatomy. An enlarged aorta may need additional characterization using computer tomography [5] or magnetic resonance imaging [6], while radionuclide imaging may be useful in further investigating left ventricular ejection fraction if echocardiography results are disproportional to clinical status.

Electrocardiography can show cavity enlargement or hypertrophy or ischemia, while chest radiography shows cardiac dilatation with valvular insufficiency is chronic and a cardiac normal size if the problem is acute in character. In addition, X-ray helps to detect pulmonary edema.

Exercise testing is indicated in order to assess functional capacity of the heart in chronic aortic regurgitation [7].

Aortic angiography is indicated if dissection is suspected while coronary angiography is performed in all patients scheduled to undergo aortic valvular replacement, in order to assess the need for a concomitant coronary bypass [8].

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2. Dujardin KS, Enriquez-Sarano M, Schaff HV, et al. Mortality and morbidity of aortic regurgitation in clinical practice. A long-term follow-up study. Circulation 1999;99:1851 – 1857.
3. Friedman T, Mani A, Elefteriades JA. Bicuspid aortic valve: clinical approach and scientific review of a common clinical entity. Expert Rev Cardiovasc Ther. 2008;6(2):235-248.
4. Lancellotti P, Tribouilloy C, Hagendorff A, et al. European Association of Echocardiography recommendations for the assessment of valvular regurgitation. Part 1: aortic and pulmonary regurgitation (native valve disease). Eur J Echocardiogr. 2010;11(3):223-244.
5. Gaztanaga J, Pizarro G, Sanz J. Evaluation of cardiac valves using multidetector CT. Cardiol Clin. 2009;27(4):633-644.
6. Morello A, Gelfand EV. Cardiovascular magnetic resonance imaging for valvular heart disease. Curr Heart Fail Rep. 2009;6(3):160-166
7. Picano E, Pibarot P, Lancellotti P. The emerging role of exercise testing and stress echocardiography in valvular heart disease. J Am Coll Cardiol. 2009;54(24):2251-2260.
8. [Guideline] Nishimura RA, Otto CM, Bonow RO, et al. 2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2014;129 (23):e521-643.