Downloaded from http://heart.bmj.com/ on January 20, 2016 - Published by group.bmj.com
Editorial
Patient prosthesis mismatch in adult congenital heart disease Daniel Hernandez-Vaquero Patient prosthesis mismatch (PPM) was originally described by Rahimtoola almost four decades ago as follows: “the effective prosthetic valve area, after insertion into the patient, is less than that of a normal human valve”.1 That is, PPM is a situation in which the area of a perfectly functioning prosthetic valve is too small for the body surface area (BSA) of that patient. So, the indexed effective orifice area (IEOA) defined as the ratio between the effective orifice area (EOA) of a prosthetic valve and the BSA of that patient is the optimal parameter to calculate PPM. Due to its ability to maintain high transvalvular pressure gradients, the existence of PPM can lead to adverse outcomes and worse quality of life. After the aortic valve replacement (AVR), these high-pressure gradients result in a slowing or absence of LV mass regression, which hampers LV function recovery and favours myocardial ischaemia even with normal coronary arteries due to increased myocardial demand and decreased coronary flow reserve (figure 1).2 During these four decades, a huge number of articles and reviews on the prevalence and clinical impact of PPM have obtained different results. Several reasons are responsible for these controversial findings. First, different methods have been used for PPM calculation. Whereas the BSA can be easily calculated using the Dubois formula, the way to calculate the EOA and the cut-off point for the IEOA have been a matter of discussion. However, nowadays it is generally accepted that in vivo measurements must be present to calculate the prosthetic EOA since the ex vivo measurements given by the prosthetic manufacturers based on the internal diameter of the prostheses have been shown to overestimate the real EOA values.3 Moreover, there is a growing consensus to accept 0.85 cm2/m2 as the IEOA value below of which PPM comes into existence and 0.65 cm2/m2 to consider severe PPM.4 Second, there is not a perfect way to detect PPM. If we take the EOA value from published in vivo Correspondence to Dr Daniel Hernandez-Vaquero, Cardiac Surgery Department, Heart Area, Hospital Universitario Central de Asturias, Avenida de Roma S/N, Oviedo 33011, Spain; [email protected]
reference values, we are not taking into account possible variations between individuals. However, if we calculate the EOA performing an echocardiogram for each patient, we will not be able to evaluate those patients who previously died. And we have to know that some of these patients who died could have died due to a severe PPM, so prevalence of severe PPM may be undervalued. Third, the heterogeneity of the population previously studied. Some researchers have identified that the impact of PPM depends on baseline characteristics of the patient population. So, elderly population is more prone to develop PPM and young patients and those with LV dysfunctions are more vulnerable to its clinical consequences.5 Finally, AVR offers excellent outcomes with low incidences of adverse events, which makes it difficult to observe differences. In their Heart publication, Van Slooten and colleagues,6 circumventing all the aforementioned difficulties, study the prevalence and impact on exercise capacity of PPM. First, in vivo values of IEOA based on echocardiograms during follow-up after surgery are used to calculate PPM considering adequate cut-off points. Second and more importantly, they homogenise the sample studying, for the first time, the prevalence of PPM and its impact on exercise capacity in adult patients with left-sided congenital heart disease (ACHD).
Figure 1
The most important finding of this work6 is that the prevalence of severe PPM in these patients is 23%. But for those who were under 18 years old when they received their last AVR is 48%, which is more than four times the prevalence of severe mismatch in patients undergoing AVR due to adult heart disease.5 The increase in the BSA due to normal somatic growth associated with the same EOA value is likely the main reason for this difference. These authors also find that the presence of PPM results in worse exercise capacity, which can affect their quality of life and functional status for life. Moreover, they do not find an increase in mortality among patients with PPM. However, it is difficult to find differences when the number of patients and events is low, which is inherent to this kind of population. Several meta-analyses4 5 have shown that the presence of PPM is associated with long-term mortality especially in young patients, so ACHD is likely affected for this condition. In addition, we know that PPM is the main risk factor for developing early structural bioprosthesis deterioration, which can lead to reoperations and unpredictable life-threatening situations.7 In contrast to the majority of other risk factors affecting outcomes of patients who undergo AVR, PPM is a potentially modifiable parameter. In this population, the majority of patients received a mechanical prosthesis (71%). We have to be aware that some mechanical prostheses of 19 mm diameter, which is usually the smallest number, leave a mean EOA value of 1 cm2, whereas others provide 1.6 cm2.8 The choice of the appropriate
Pathophysiological mechanisms of patient prosthesis mismatch (PPM).
Hernandez-Vaquero D. Heart January 2016 Vol 102 No 2
89
Downloaded from http://heart.bmj.com/ on January 20, 2016 - Published by group.bmj.com
Editorial prosthesis for a young patient is likely the easiest way to avoid mismatch. Even when it is not expected to have PPM in that moment, many of them can develop it in the future. Procedures to enlarge the aortic annulus, the implantation of an autologous graft, which has the potential to grow with the patient or, when possible, repair the aortic valve, are other ways to avoid PPM, but decision-making for these techniques is more difficult since they may involve an increased surgical risk. Moreover, new devices as transcatheter aortic valve implantation or sutureless surgical valves play little role since the majority of these patients need combined procedures or aortic root replacement. Future research should work to establish the mortality pattern, the risk of sudden death and life-threatening situations during the follow-up of ACHD with severe PPM and its impact on their quality of life. We need to know whether we should be more focused on reducing the body mass index of ACHD in order to decrease as much as possible the BSA or, if necessary, those patients who develop severe PPM should be reoperated in order
90
to guarantee a valve area appropriate to their BSA.
3
Contributors DH-V have made this article in all terms. Provenance and peer review Commissioned; internally peer reviewed.
4
5
To cite Hernandez-Vaquero D. Heart 2016;102:89– 90. Accepted 5 October 2015 Published Online First 25 November 2015 6
▸ http://dx.doi.org/10.1136/heartjnl-2015-308013
7
Heart 2016;102:89–90. doi:10.1136/heartjnl-2015-308715 8
REFERENCES 1
2
Rahimtoola SH. The problem of valve prosthesis-patient mismatch. Circulation 1978;58:20–4. Rajappan K, Rimoldi OE, Dutka DP, et al. Mechanisms of coronary microcirculatory dysfunction in patients
with aortic stenosis and angiographically normal coronary arteries. Circulation 2002;105:470–6. Bleiziffer S, Eichinger WB, Hettich I, et al. Prediction of valve prosthesis-patient mismatch prior to aortic valve replacement: which is the best method. Heart 2007;93:615–20. Head SJ, Mokhles MM, Osnabrugge RL, et al. The impact of prosthesis-patient mismatch on long-term survival after aortic valve replacement: a systematic review and meta-analysis of 34 observational studies comprising 27 186 patients with 133 141 patient-years. Eur Heart J 2012;33:1518–29. Chen J, Lin Y, Kang B, et al. Indexed effective orifice area is a significant predictor of higher mid- and long-term mortality rates following aortic valve replacement in patients with prosthesis-patient mismatch. Eur J Cardiothorac Surg 2014;45: 234–40. Van Stoolen YJ, Van Melle JP, Freling HJ, et al. Aortic valve prosthesis-patient mismatch and exercise capacity in adult patients with congenital heart disease. Heart 2016;102:107–13. Sénage T, Le Tourneau T, Foucher Y, et al. Early structural valve deterioration of Mitroflow aortic bioprosthesis: mode, incidence, and impact on outcome in a large cohort of patients. Circulation 2014;130:2012–20. Pibarot P, Dumesnil JG. Prosthesis-patient mismatch: definition, clinical impact, and prevention. Heart 2006;92:1022–9.
Hernandez-Vaquero D. Heart January 2016 Vol 102 No 2
Downloaded from http://heart.bmj.com/ on January 20, 2016 - Published by group.bmj.com
Patient prosthesis mismatch in adult congenital heart disease Daniel Hernandez-Vaquero Heart 2016 102: 89-90 originally published online November 25, 2015
doi: 10.1136/heartjnl-2015-308715 Updated information and services can be found at: http://heart.bmj.com/content/102/2/89
These include:
References Email alerting service
Topic Collections
This article cites 8 articles, 7 of which you can access for free at: http://heart.bmj.com/content/102/2/89#BIBL Receive free email alerts when new articles cite this article. Sign up in the box at the top right corner of the online article.
Articles on similar topics can be found in the following collections Interventional cardiology (2849) Drugs: cardiovascular system (8530) Congenital heart disease (718)
Notes
To request permissions go to: http://group.bmj.com/group/rights-licensing/permissions To order reprints go to: http://journals.bmj.com/cgi/reprintform To subscribe to BMJ go to: http://group.bmj.com/subscribe/
Editorial
Patient prosthesis mismatch in adult congenital heart disease Daniel Hernandez-Vaquero Patient prosthesis mismatch (PPM) was originally described by Rahimtoola almost four decades ago as follows: “the effective prosthetic valve area, after insertion into the patient, is less than that of a normal human valve”.1 That is, PPM is a situation in which the area of a perfectly functioning prosthetic valve is too small for the body surface area (BSA) of that patient. So, the indexed effective orifice area (IEOA) defined as the ratio between the effective orifice area (EOA) of a prosthetic valve and the BSA of that patient is the optimal parameter to calculate PPM. Due to its ability to maintain high transvalvular pressure gradients, the existence of PPM can lead to adverse outcomes and worse quality of life. After the aortic valve replacement (AVR), these high-pressure gradients result in a slowing or absence of LV mass regression, which hampers LV function recovery and favours myocardial ischaemia even with normal coronary arteries due to increased myocardial demand and decreased coronary flow reserve (figure 1).2 During these four decades, a huge number of articles and reviews on the prevalence and clinical impact of PPM have obtained different results. Several reasons are responsible for these controversial findings. First, different methods have been used for PPM calculation. Whereas the BSA can be easily calculated using the Dubois formula, the way to calculate the EOA and the cut-off point for the IEOA have been a matter of discussion. However, nowadays it is generally accepted that in vivo measurements must be present to calculate the prosthetic EOA since the ex vivo measurements given by the prosthetic manufacturers based on the internal diameter of the prostheses have been shown to overestimate the real EOA values.3 Moreover, there is a growing consensus to accept 0.85 cm2/m2 as the IEOA value below of which PPM comes into existence and 0.65 cm2/m2 to consider severe PPM.4 Second, there is not a perfect way to detect PPM. If we take the EOA value from published in vivo Correspondence to Dr Daniel Hernandez-Vaquero, Cardiac Surgery Department, Heart Area, Hospital Universitario Central de Asturias, Avenida de Roma S/N, Oviedo 33011, Spain; [email protected]
reference values, we are not taking into account possible variations between individuals. However, if we calculate the EOA performing an echocardiogram for each patient, we will not be able to evaluate those patients who previously died. And we have to know that some of these patients who died could have died due to a severe PPM, so prevalence of severe PPM may be undervalued. Third, the heterogeneity of the population previously studied. Some researchers have identified that the impact of PPM depends on baseline characteristics of the patient population. So, elderly population is more prone to develop PPM and young patients and those with LV dysfunctions are more vulnerable to its clinical consequences.5 Finally, AVR offers excellent outcomes with low incidences of adverse events, which makes it difficult to observe differences. In their Heart publication, Van Slooten and colleagues,6 circumventing all the aforementioned difficulties, study the prevalence and impact on exercise capacity of PPM. First, in vivo values of IEOA based on echocardiograms during follow-up after surgery are used to calculate PPM considering adequate cut-off points. Second and more importantly, they homogenise the sample studying, for the first time, the prevalence of PPM and its impact on exercise capacity in adult patients with left-sided congenital heart disease (ACHD).
Figure 1
The most important finding of this work6 is that the prevalence of severe PPM in these patients is 23%. But for those who were under 18 years old when they received their last AVR is 48%, which is more than four times the prevalence of severe mismatch in patients undergoing AVR due to adult heart disease.5 The increase in the BSA due to normal somatic growth associated with the same EOA value is likely the main reason for this difference. These authors also find that the presence of PPM results in worse exercise capacity, which can affect their quality of life and functional status for life. Moreover, they do not find an increase in mortality among patients with PPM. However, it is difficult to find differences when the number of patients and events is low, which is inherent to this kind of population. Several meta-analyses4 5 have shown that the presence of PPM is associated with long-term mortality especially in young patients, so ACHD is likely affected for this condition. In addition, we know that PPM is the main risk factor for developing early structural bioprosthesis deterioration, which can lead to reoperations and unpredictable life-threatening situations.7 In contrast to the majority of other risk factors affecting outcomes of patients who undergo AVR, PPM is a potentially modifiable parameter. In this population, the majority of patients received a mechanical prosthesis (71%). We have to be aware that some mechanical prostheses of 19 mm diameter, which is usually the smallest number, leave a mean EOA value of 1 cm2, whereas others provide 1.6 cm2.8 The choice of the appropriate
Pathophysiological mechanisms of patient prosthesis mismatch (PPM).
Hernandez-Vaquero D. Heart January 2016 Vol 102 No 2
89
Downloaded from http://heart.bmj.com/ on January 20, 2016 - Published by group.bmj.com
Editorial prosthesis for a young patient is likely the easiest way to avoid mismatch. Even when it is not expected to have PPM in that moment, many of them can develop it in the future. Procedures to enlarge the aortic annulus, the implantation of an autologous graft, which has the potential to grow with the patient or, when possible, repair the aortic valve, are other ways to avoid PPM, but decision-making for these techniques is more difficult since they may involve an increased surgical risk. Moreover, new devices as transcatheter aortic valve implantation or sutureless surgical valves play little role since the majority of these patients need combined procedures or aortic root replacement. Future research should work to establish the mortality pattern, the risk of sudden death and life-threatening situations during the follow-up of ACHD with severe PPM and its impact on their quality of life. We need to know whether we should be more focused on reducing the body mass index of ACHD in order to decrease as much as possible the BSA or, if necessary, those patients who develop severe PPM should be reoperated in order
90
to guarantee a valve area appropriate to their BSA.
3
Contributors DH-V have made this article in all terms. Provenance and peer review Commissioned; internally peer reviewed.
4
5
To cite Hernandez-Vaquero D. Heart 2016;102:89– 90. Accepted 5 October 2015 Published Online First 25 November 2015 6
▸ http://dx.doi.org/10.1136/heartjnl-2015-308013
7
Heart 2016;102:89–90. doi:10.1136/heartjnl-2015-308715 8
REFERENCES 1
2
Rahimtoola SH. The problem of valve prosthesis-patient mismatch. Circulation 1978;58:20–4. Rajappan K, Rimoldi OE, Dutka DP, et al. Mechanisms of coronary microcirculatory dysfunction in patients
with aortic stenosis and angiographically normal coronary arteries. Circulation 2002;105:470–6. Bleiziffer S, Eichinger WB, Hettich I, et al. Prediction of valve prosthesis-patient mismatch prior to aortic valve replacement: which is the best method. Heart 2007;93:615–20. Head SJ, Mokhles MM, Osnabrugge RL, et al. The impact of prosthesis-patient mismatch on long-term survival after aortic valve replacement: a systematic review and meta-analysis of 34 observational studies comprising 27 186 patients with 133 141 patient-years. Eur Heart J 2012;33:1518–29. Chen J, Lin Y, Kang B, et al. Indexed effective orifice area is a significant predictor of higher mid- and long-term mortality rates following aortic valve replacement in patients with prosthesis-patient mismatch. Eur J Cardiothorac Surg 2014;45: 234–40. Van Stoolen YJ, Van Melle JP, Freling HJ, et al. Aortic valve prosthesis-patient mismatch and exercise capacity in adult patients with congenital heart disease. Heart 2016;102:107–13. Sénage T, Le Tourneau T, Foucher Y, et al. Early structural valve deterioration of Mitroflow aortic bioprosthesis: mode, incidence, and impact on outcome in a large cohort of patients. Circulation 2014;130:2012–20. Pibarot P, Dumesnil JG. Prosthesis-patient mismatch: definition, clinical impact, and prevention. Heart 2006;92:1022–9.
Hernandez-Vaquero D. Heart January 2016 Vol 102 No 2
Downloaded from http://heart.bmj.com/ on January 20, 2016 - Published by group.bmj.com
Patient prosthesis mismatch in adult congenital heart disease Daniel Hernandez-Vaquero Heart 2016 102: 89-90 originally published online November 25, 2015
doi: 10.1136/heartjnl-2015-308715 Updated information and services can be found at: http://heart.bmj.com/content/102/2/89
These include:
References Email alerting service
Topic Collections
This article cites 8 articles, 7 of which you can access for free at: http://heart.bmj.com/content/102/2/89#BIBL Receive free email alerts when new articles cite this article. Sign up in the box at the top right corner of the online article.
Articles on similar topics can be found in the following collections Interventional cardiology (2849) Drugs: cardiovascular system (8530) Congenital heart disease (718)
Notes
To request permissions go to: http://group.bmj.com/group/rights-licensing/permissions To order reprints go to: http://journals.bmj.com/cgi/reprintform To subscribe to BMJ go to: http://group.bmj.com/subscribe/
