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Massachusetts General Hospital, 55 Fruit St, Boston, MA 02114
(Email: rkaple{at}partners.org).
This retrospective study by Khandhar and colleagues [1] evaluates the effect of aortic valve replacement (AVR) for severe aortic regurgitation (AR) in the setting of pulmonary hypertension (PHT). In this cohort of patients, AVR is safe and translates into a survival benefit at 5 years. Although the study is small, it offers a timely opportunity to reconsider indications for AVR and the underlying pathophysiology of left-heart causes of PHT.
Current American College of Cardiology/American Heart Association recommendations for AVR do not include PHT. We know that untreated AR results in left ventricular dilation, dysfunction, and eventually, PHT [2]. Severe AR also results in endothelial injury within the pulmonary vasculature, interstitial edema, and fibrosis, all of which contribute to increased pulmonary artery vascular tone. Furthermore, severe right ventricular dysfunction can result in chronic small emboli to the lungs and worsen the disease process, and likely blunt postoperative recovery. Indeed, these pulmonary insults are the consequences of prolonged disease.
The reality of prolonged disease before surgical intervention raises two questions: whether PHT should be an indication for AVR and whether we are waiting too long to perform AVR in this population. At present, there is a class IIa recommendation to perform AVR in asymptomatic patients with evidence of severe left ventricular dysfunction, defined as end-diastolic dimension exceeding 75 mm or end-systolic dimension exceeding 55 mm. For women, in particular, this degree of left-heart dysfunction may be too severe to expect AVR to improve the clinical outcome.
Further clarification of the effect of mitral valve function will also be helpful. Mitral stenosis and regurgitation both result in increased pulmonary vascular resistance and contribute to elevated pulmonary artery pressures. The mitral effective regurgitant orifice and mitral deceleration time have been shown to strongly correlate with elevated pulmonary artery pressures [3]. Khandhar and associates [1] appropriately call our attention to mitral valve function in this cohort: 16 of the 32 patients receiving AVR had mitral valve repair (n = 8) or replacement (n = 8). Definitive aortic and mitral valve procedures may be necessary to restore left-sided hemodynamics and filling pressures. In fact, the lack of mitral regurgitation may suggest secondary causes of PHT at work.
As we reconsider our indications for AVR in the setting of PHT, new screening variables and closer attention to mitral valve function will be essential.
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