Ann Thorac Surg 2017;103:1359–62
Kamal Khalil, MD Division of Cardiothoracic and Vascular Surgery University of Texas Health Science Center in Houston 6400 Fannin St, Ste 2850 Houston, TX 77030 email:
[email protected]
References 1. Oncel M, Sunam GS, Yildiran H. Pain control with bupivacaine after lung resections (letter). Ann Thorac Surg 2017;103:1360. 2. Khalil KG, Boutrous ML, Irani AD, et al. Operative intercostal nerve blocks with long-acting bupivacaine liposome for pain control after thoracotomy. Ann Thorac Surg 2016;100:2013–8. 3. Bergese SD, Rammamoorthy S, Patou G, Bramlett K, Gorfine SR, Candiotti KA. Efficacy profile of liposome bupivacaine, a novel formulation of bupivacaine for post surgical analgesia. J Pian Res 2012;5:107–16. 4. Woolf CJ, Chong MS. Preemptive analgesia-treating postoperative pain by preventing the establishment of of central sensitization. Anesth Analg 1993;77:362–79.
Prosthesis Size Selection for Patients With Severe Mitral Stenosis To the Editor:
Ó 2017 by The Society of Thoracic Surgeons Published by Elsevier Inc.
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Zhi-Wei Zhang, MD, PhD Tian-Xiang Gu, MD, PhD Department of Cardiovascular Surgery 1st Affiliated Hospital of China Medical University 155 Nanjing St Shenyang, China email:
[email protected]
References 1. Hwang HY, Kim YH, Kim KH, Kim KB, Ahn H. Patientprosthesis mismatch after mitral valve replacement: a propensity score analysis. Ann Thorac Surg 2016;101:1796–803. 2. Rajbanshi BG, Suri RM, Nkomo VT, et al. Influence of mitral valve repair versus replacement on the development of late functional tricuspid regurgitation. J Thorac Cardiovasc Surg 2014;148:1957–62. 3. Crawford FA. Residual pulmonary artery hypertension after mitral valve replacement: size matters. J Am Coll Cardiol 2005;45:1041–2. 4. Xu ZY, Zhang BR, Zhu JL, et al. Valve replacement in rheumatic mitral stenosis with small left ventricle. Zhonghua Xiong Xin Wai Ke Za Zhi 1997;13:1–4.
Reply To the Editor: We greatly appreciate the letter by Zhang and colleagues [1] about our recent study [2]. We agree with the authors’ concern that a left ventricle with long-standing severe mitral stenosis (MS) might be vulnerable to a sudden increase in influx after mitral valve replacement (MVR). We have also observed a substantial number of MS patients who have experienced hemodynamic collapse after MVR. In our opinion, however, using small valves does not seem to help prevent this adverse event, and the valves should be as large as possible for optimal long-term results after operation. Other important factors could affect the postoperative outcomes after MVR in patients with MS; as the authors commented [1], long-lasting inflammation itself could affect myocardial function. In addition, tricuspid regurgitation (TR) combined with right ventricular failure caused by longstanding left-sided pressure overload could result in an undesirable postoperative course. When performing MVR, we always try to preserve papillary–annular continuity, not only to prevent ventricular rupture but also to preserve left ventricular function [3]. After MVR, pulmonary artery and capillary wedge pressures, cardiac output, and systemic vascular resistance are monitored continuously, and inhaled nitric oxide, inotropic agents, and afterload-lowering agents are used accordingly. To provide more objective evidence, we evaluated the data from 340 patients who underwent first-time MVR for rheumatic mitral stenosis and were enrolled in our recent study [2]; 57 patients were included in the patient–prosthesis mismatch (PPM) group, and the remaining 283 patients were in the nonPPM (NPPM) group. Overall, 25 patients (7.4%) experienced low cardiac output syndrome (LCOS) after MVR, and no statistically significant difference in the LCOS rate was found between the PPM group (4 of 57 patients, 7.0%) and the NPPM group (21 of 283 patients, 7.4%), p > 0.999. In a multivariable analysis, preoperative grades of TR (odds ratio ¼ 1.668; 95% confidence interval 1.173–2.371; p ¼ 0.004) and worse New York Heart Association functional class (odds ratio ¼ 2.272; confidence interval 1.218–4.236; p ¼ 0.010) were identified as risk factors for LCOS after MVR. These data also support that placement of a large prosthesis in the mitral position does not result in a poor postoperative course in rheumatic MS patients. 0003-4975/$36.00
MISCELLANEOUS
We read the article by Hwang and colleagues [1] with great interest. In their report, the authors found that long-term survival and freedom from cardiac death were worse in the patientprosthesis mismatch group than in the non–patient-prosthesis mismatch group for as long as 20 years after the operation. It is known that the natural mitral orifice is larger than its artificial substitutes. The hemodynamic superiority of mitral valve repair over mitral valve replacement (MVR) with any size or type of prosthesis has been documented [2]. MVR may be associated with residual gradients resulting from a relatively small effective orifice area, and residual pulmonary hypertension should be expected rather than surprising [3]. Nevertheless, all cardiac surgeons should attempt to implant the largest prosthesis that fits comfortably during MVR. Because of economic reasons, rheumatic heart disease is still prevalent in some parts of China. In clinical practice, there are some patients with a long history of severe mitral stenosis. In these patients, the size of the left ventricle becomes smaller than normal, with a left ventricular volume index less than 60 mL/m2. There has been discrepancy in prosthesis size selection for these patients domestically. Some surgeons have suggested that smaller-sized prostheses should be selected for these patients [4]. The hypothesis is that the “atrophied” left ventricle cannot accommodate the sudden massive influx of blood volume from the left atrium when a larger valve is used. The clinical manifestation is hemodynamic compromise immediately after MVR, and certain forms of circulatory support may be needed, resulting in higher mortality compared with those who receive smaller prostheses, usually a No. 25 valve. Opponents argue that the postoperative course just mentioned is caused by myocardial damage from the long-lasting rheumatic history in these very sick patients. For better long-term results, larger valves should be selected; otherwise it is replacing a stenotic mitral valve with a stenotic prosthetic valve. We are frustrated about this issue sometimes too, although we have been performing mitral valve operations for decades. We would like to know the authors’ advice and experience on this issue.
CORRESPONDENCE