Treatment with pioglitazone induced significant, reversible mitral regurgitation
© Dorkhan et al; licensee BioMed Central Ltd. 2008
Received: 05 March 2008
Accepted: 30 April 2008
Published: 30 April 2008
There has in recent years been great concern about possible cardiac side effects of thiazolidinediones (TZDs). We present a case-report of a 60 year-old male who developed significant mitral regurgitation during six months treatment with pioglitazone in parallel with laboratory indications of fluid retention. Echocardiography six months after discontinuation of medication showed regression of mitral regurgitation and the laboratory parameters were also normalized. It is noteworthy that six months treatment with pioglitazone could induce significant valve dysfunction, which was reversible, and this underlines the importance of carefully monitoring patients when placing them on treatment with TZDs.
There is an ongoing discussion concerning the possible effects of thiazolidinediones (TZDs) on the heart. In a recent meta/teleo-analysis Singh et al concluded that heart failure might occur at both high and low doses, usually weeks to months after initiating TZDs and in patients without a history of heart failure .
Descriptive statistics of anthropometrical, echocardiography and laboratory data.
LV diastolic vol (ml)
LV systolic vol (ml)
LA vol (ml)
Mitral regurgitation (1–3)
This case-report highlights the importance of careful monitoring of patients under treatment with TZDs. In this case, changes in haemoglobin and BNP indicated fluid retention in the absence of clinical signs or symptoms of cardiopulmonary stress or oedema. What caused the mitral regurgitation? One plausible hypothesis is that the fluid retention caused left ventricular dilatation which in turn resulted in mitral annular dilatation and to altered papillary muscle orientation, which then leads to inadequate mitral leaflet coaptation. Mitral regurgitations that are caused by left ventricular dilatation tend to have a central jet, as in our patient. It is, however, possible that there was some structural weakness in the mitral valve apparatus that was not detected on the transthoracic echocardiography examinations and that this could in part be contributing to the regurgitation. There is a need for tools to help clinicians to identify subsets of patients for whom this kind of therapy is likely to have particularly favourable/unfavourable effect, using readily identifiable clinical and laboratory factors. BNP, being a peptide hormone released from the cardiac ventricles in response to myocyte stretch have generated a lot of attention in recent years and have been proposed as potential diagnostic and prognostic marker for cardiac disease but currently there are no clear algorithms on how this should be implemented into clinical practice. However, the knowledge is increasing in this field and hopefully the results will enable clinicians to select proper therapy for individual patients in future.
Brain natriuretic peptide
Left ventricular end-diastolic diameter
Left ventricular end-systolic diameter
End-diastolic inter-ventricular septum
End-diastolic posterior wall
Left atrial end-systolic diameter
- LV diastolic:
Left ventricular end-diastolic volume
- LV systolic vol:
Left ventricular end-systolic volume
- LA vol:
Left atrial volume
Indices of left ventricular diastolic function
estimation of left ventricular filling pressure.
The patient described in this case report has given permission to publish this case report.
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