Echocardiography and monitoring patients receiving dopamine agonist therapy for hyperprolactinaemia: a joint position statement of the British Society of Echocardiography, the British Heart Valve Society and the Society for Endocrinology

in Echo Research and Practice

Correspondence should be addressed to R Steeds: Rick.Steeds@uhb.nhs.uk

This position statement has been externally peer-reviewed. This article is simultaneously published in Echo Research and Practice and Clinical Endocrinology.

R Steeds, V Sharma, J Chambers and G Lloyd are members of the editorial board of Echo Research and Practice. They were not involved in the review or editorial process for this article, on which they are listed as authors.

*(V Sharma is the Guidelines Chair)

This is a joint position statement of the British Society of Echocardiography, the British Heart Valve Society and the Society for Endocrinology on the role of echocardiography in monitoring patients receiving dopamine agonist (DA) therapy for hyperprolactinaemia. (1) Evidence that DA pharmacotherapy causes abnormal valve morphology and dysfunction at doses used in the management of hyperprolactinaemia is extremely limited. Evidence of clinically significant valve pathology is absent, except for isolated case reports around which questions remain. (2) Attributing change in degree of valvular regurgitation, especially in mild and moderate tricuspid regurgitation, to adverse effects of DA in hyperprolactinaemia should be avoided if there are no associated pathological changes in leaflet thickness, restriction or retraction. It must be noted that even where morphological change in leaflet structure and function may be suspected, grading is semi-quantitative on echocardiography and may vary between different machines, ultrasound settings and operators. (3) Decisions regarding discontinuation of medication should only be made after review of serial imaging by an echocardiographer experienced in analysing drug-induced valvulopathy or carcinoid heart disease. (4) A standard transthoracic echocardiogram should be performed before a patient starts DA therapy for hyperprolactinaemia. Repeat transthoracic echocardiography should then be performed at 5 years after starting cabergoline in patients taking a total weekly dose less than or equal to 2 mg. If there has been no change on the 5-year scan, repeat echocardiography could continue at 5-yearly intervals. If a patient is taking more than a total weekly dose of 2 mg, then annual echocardiography is recommended.

Abstract

This is a joint position statement of the British Society of Echocardiography, the British Heart Valve Society and the Society for Endocrinology on the role of echocardiography in monitoring patients receiving dopamine agonist (DA) therapy for hyperprolactinaemia. (1) Evidence that DA pharmacotherapy causes abnormal valve morphology and dysfunction at doses used in the management of hyperprolactinaemia is extremely limited. Evidence of clinically significant valve pathology is absent, except for isolated case reports around which questions remain. (2) Attributing change in degree of valvular regurgitation, especially in mild and moderate tricuspid regurgitation, to adverse effects of DA in hyperprolactinaemia should be avoided if there are no associated pathological changes in leaflet thickness, restriction or retraction. It must be noted that even where morphological change in leaflet structure and function may be suspected, grading is semi-quantitative on echocardiography and may vary between different machines, ultrasound settings and operators. (3) Decisions regarding discontinuation of medication should only be made after review of serial imaging by an echocardiographer experienced in analysing drug-induced valvulopathy or carcinoid heart disease. (4) A standard transthoracic echocardiogram should be performed before a patient starts DA therapy for hyperprolactinaemia. Repeat transthoracic echocardiography should then be performed at 5 years after starting cabergoline in patients taking a total weekly dose less than or equal to 2 mg. If there has been no change on the 5-year scan, repeat echocardiography could continue at 5-yearly intervals. If a patient is taking more than a total weekly dose of 2 mg, then annual echocardiography is recommended.

Introduction

It is more than ten years since the publication of a large population-based nested case-control study (1) and an echocardiographic prevalence study (2) reporting an association between the use of pergolide and cabergoline for the treatment of symptomatic Parkinson’s disease (PD) and an increased risk of restrictive valvular heart disease. These and other studies (3) led to the voluntary withdrawal of pergolide from the US market in 2007. While pergolide was used predominantly in PD, cabergoline is used more commonly in the treatment of hyperprolactinaemia. Dopamine agonists (DA) are first-line therapy for the treatment of hyperprolactinaemia because of excellent biochemical and tumoural control in the majority of patients, the alternative being surgery with or without radiotherapy, exposing patients to the risks of hypopituitarism (4). Cabergoline is generally the agent of choice because alternatives, such as bromocriptine, require multiple daily doses and have a less favourable side effect profile. The use of cabergoline in PD and hyperprolactinaemia differs considerably. Cabergoline is used in PD patients over a shorter period (months) at much higher dose (typically 3 mg a day) compared to a much longer period of treatment (years) at lower doses (typically 0.5–1 mg weekly) in hyperprolactinaemic patients (5). Moreover, while there are a number of effective alternative drugs in the treatment of PD, medical options for the treatment of hyperprolactinaemia are more limited. As a result of the studies documenting an increased risk of valvulopathy in PD patients, the Medicines and Healthcare products Regulatory Agency (MHRA) recommended that physicians in the United Kingdom should request baseline echocardiography to exclude valvular heart disease in all patients before starting cabergoline or bromocriptine, followed by a second echocardiogram performed 3–6 months after commencement and then at 6–12-month intervals while continuing on the medication. It was also recommended that treatment be stopped if echocardiography showed worsening or new valvular restriction, thickening or regurgitation. In the intervening years, much echocardiographic data from cabergoline-treated hyperprolactinaemic patients has been published. Most of these data suggest that the risk of developing significant valvular heart disease is negligible and not a cause for clinical concern. Despite this, constraints imposed by the working relationship between the MHRA and the EMA dictate that the published recommendations are unlikely to be revised. This position statement, endorsed by the British Society of Echocardiography, the British Heart Valve Society and the Society for Endocrinology has been written to provide endocrine and cardiac physicians with practical guidance in this area based on a contemporary review of the available literature.

Pathophysiology

The possibility that cabergoline might cause cardiac valvulopathy is pharmacologically and mechanistically plausible. Like other ergot-based drugs (e.g. methysergide and the weight loss drugs fenfluramine and dexfenfluramine), cabergoline binds to the serotonin receptor subtype 2B (5-HT2B) located on heart valves. Activation of these receptors induces valvular interstitial cell mitogenesis and proliferation, which in turn modifies the quantity and quality of the valvular extracellular matrix through actions on proteoglycans, collagen types I, III and IV, and matrix metalloproteinases (6). As a result, valve leaflets and chords become thickened, retracted and stiff, leading most commonly to valvular regurgitation (Videos 1 and 2). The histopathological appearance of valves affected by DA agonists is akin to that caused by carcinoid syndrome, with deposition of plaque-like material consisting of myofibroblasts within a fibromyxoid stroma (7). An association was found between higher cumulative doses of pergolide and cabergoline and the severity of cardiac valvular regurgitation in PD patients and, in particular, with the mitral valve tenting area, a subclinical index of leaflet stiffening and thickening (3). This quantitative method for measuring the impact of DA on valve function is important for the interpretation of the prolactinoma literature for a number of reasons. First, without careful blinding, there is evidence that subjective assessment tends to result in overestimation of valvulopathy (8). Secondly, most studies report only the degree of valve regurgitation and any assessment of leaflet thickening and retraction is subjective. Thirdly machine settings are not standardized, particularly the use of fundamental instead of second harmonic imaging. Harmonic imaging is a technique that employs the resonance characteristics of tissue to produce images with higher resolution and fewer artefacts than conventional (fundamental) imaging. Harmonic imaging is the principal technique now used in echocardiography, but overestimates leaflet thickness compared to fundamental imaging. Finally, most studies within the prolactinoma literature only reported on the prevalence of any valvular lesion as detected by echocardiography, without distinguishing cabergoline-associated valvulopathy from coincidental abnormalities that may often be found in patients in the United Kingdom of similar age to those studied (9).

Tilted parasternal long axis view of the tricuspid valve demonstrating thickening, retraction and fixation of the leaflets. View Video 1 at http://movie-usa.glencoesoftware.com/video/10.1530/ERP-18-0069/video-1.

Colour flow Doppler demonstrating severe tricuspid regurgitation. View Video 2 at http://movie-usa.glencoesoftware.com/video/10.1530/ERP-18-0069/video-2.

Current evidence

Following publication of the adverse effects of DA agonists at high dose in PD, several groups published single institution, cross-sectional case-control studies investigating the link between chronic DA therapy at low dose in hyperprolactinaemia and the presence of valvular abnormalities (10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23) (Table 1). These were all limited by small size. Moreover, the control groups in each study contained only healthy individuals or those referred for other cardiac symptoms, for example palpitations, who were then found to have normal echocardiography, rather than untreated patients with hyperprolactinaemia. One study in 50 patients found an increase in the prevalence of moderate (27/50; 54%) but not of mild tricuspid regurgitation (TR) among those treated with cabergoline at a median dose 280 mg for a median duration of 72 months compared to controls (9/50; 18%) (11). The distinction between mild and moderate TR was made in this article by the extent to which retrograde flow filled the atrium, which is a method known to be subject to error, and technical and haemodynamic variation. Furthermore, the difference in degree of TR was found in the absence of any changes to the thickness or restriction of the valve leaflets. In another study of 78 patients (mean cumulative dose 363 mg; mean treatment duration 60 months), mild TR was found more often (32/78, 41%) among those taking DA agonists than in controls (20/78, 26%), although there was no graded association with cumulative dose and there was no difference in ‘clinically significant’ valve disease (12). Again, the difference in degree of TR was found in the absence of any changes to the thickness or restriction of the valve leaflets. The same study also suggested an increase in aortic calcification, which is difficult to understand from a pathophysiological perspective and has not been replicated elsewhere. Thereafter, two more similar-sized case-controlled studies suggested other morphological changes (13, 17). In 102 patients (mean cumulative cabergoline dose 204 mg; mean treatment duration 79 months) (13), there was an increase in mitral valve tenting area but no difference in leaflet thickness and no change in any other valves. In 103 patients (mean cumulative cabergoline dose 174 mg; mean treatment duration 46 months) (17), there was a new category of ‘sub-clinical fibrosis’, defined by increased leaflet echogenicity and/or increased cusp thickness (>3 mm mitral; >2 mm other valves) but with no difference in the degree of regurgitation. These data also contrast with the results of ten similar-sized, single institution case-control studies that found no link between DA use and significant restrictive valve defects or regurgitation (10, 14, 15, 16, 18, 19, 20, 21, 22, 23). Finally, a large multi-centre cross-sectional study based in the United Kingdom of 747 patients taking DA agonists (median cabergoline dose 152 mg) showed no association between cumulative doses of cabergoline or bromocriptine and the age-corrected prevalence of valvular abnormalities (24). In summary, case-control studies investigating DA agonist valvulopathy in hyperprolactinaemia have provided poor quality data, using different diagnostic criteria, multiple testing in small groups and lack of standardized assessment of valve morphology. There are isolated case reports of restrictive valve disease after cabergoline but these have either been in cases treated with high dose (8, 25) or in patients with co-morbidity (26), and in one case developing bowel obstruction after diagnosis of DA valvulopathy without exclusion of coexisting neuroendocrine tumour (27).

Table 1

Case-control studies and results.

Study, yearCases (male%)Controls (male%)Age cases ± s.d.Cumulative dose (mg) ± s.d.Duration Rx (months) ± s.d.Summary
Bogazzi 2008 (10)100 (21)100 (16)41 ± 13279 ± 30167 ± 39No effect
Boguszewski 2012 (21)51 (27)59 (27)42.3 ± 13.5239 ± 24338 ± 21↑ MV tenting

↑ mild TR (7.8% vs 0%)

↑ mild PR (no statistics presented)
Colao 2008 (11)50 (12)50 (12)36.5 ± 10.5414 ± 39081 ± 37↑ mod TR (54% vs 18%)

No other difference in VD
Cordoba-Soriano 2013 (23)8 (25)11 (34)38.8 ± 10.4158 (median)46No effect
Elenkova 2012 (17)103 (20)102 (21)38.6 ± 9.93174 (no SD)47 ± 286↑ subclinical fibrosis

(40% vs 23%)

No other difference in VD
Halperin 2012 (40)15 (40)58 (10)No data523 (median)No dataNo effect
Herring 2009 (18)50 (60)50 (60)51.2 ± 15.5443 ± 37579 ± 42No effect
Kars 2008 (12)47 (28)78 (26)46 ± 13363 ± 37762 ± 32↑ mild TR (41% vs 26%)

↑ AV calcification
Lancellotti 2008 (13)102 (28)51 (37)51 (median)184 ± 10579 (median)↑ MV tenting

No other difference in VD
Nachtigall 2010 (20)100 (48)100 (48)44 ± 13253 ± 52048 ± 40No effect
Tan 2010 (15)72 (26)72 (28)36 (median)126 (median)53 (median)No effect
Vallette 2009 (16)70 (47)70 (47)44 ± 13282 ± 27155 ± 22No effect
Wakil 2008 (14)44 (27)566 (32)41.8 ± 13.2279 ± 30144.8↑ OR mild TR; mild PR

No other difference in VD

Case-control studies in which patients were being treated for hyperprolactinaemia with cabergoline for a minimum of 6 months, a control group comparable to cases without history of DA therapy and had an echocardiogram after ≥6 months of cabergoline treatment. Values rounded to complete integer; mean ± s.d. unless stated.

In addition to the cross-sectional, case-control studies, there have been three studies with serial follow-up (Table 2). The first, small, single-centre study examined 45 patients receiving cabergoline for prolactinoma (mean cabergoline dose 401 mg) with baseline and then repeat echocardiography at 2 years, and found neither valve stenosis nor development of valvular regurgitation (28). In a follow-up of 192/747 patients from the original cross-sectional study by Drake et al., with median duration of cabergoline therapy 34 (24–42) months, no association was found between cumulative doses of cabergoline and clinically significant valvular abnormality (5). The third study followed 100 subjects for a median interval 62.5 (34.8–77) months between echocardiography following a median total duration of cabergoline therapy for 124.5 months (median dose 277.8 mg) and found no significant alterations in valve structure or function (29). One of these studies had a median follow-up of 10 years, although the potential expected duration of treatment with cabergoline can sometimes be longer.

Table 2

Serial follow-up studies and results.

Study, yearGender (male%)Age at first echo ± s.d.Cumulative dose at first echo (mg) ± s.d.Cumulative dose at second echo (mg) ± s.d.Duration Rx at first echo (months) ± s.d.Duration Rx at second echo (months) ± s.d.Summary
Auriemma 2013 (41)11 (28)38.7 ± 12.5No data149 (median)No data60 ± 0No effect
Delgado 2012 (28)13 (29)48 ± 12.1355 ± 369401 ± 36962.4 ± 32.486.4 ± 32.4↑ AV calcification (63% vs 38%)
Vroonen 2017 (29)30 (30)No data139.4 (median)278 (median)62.5 (median)124.5 (median)No effect

Meta-analyses have been performed however, that suggest a small effect may be present, although again there are limitations to these statistical studies (30, 31, 32). First, the meta-analyses have all been influenced by data from one early single-centre case-control study, in which 27/50 (54%) patients compared to 9/50 (18%) controls were reported as having moderate to severe TR (11). Interestingly, the same group subsequently reported a follow-up study in which there were no reported differences in the risk of TR between controls and cabergoline-treated patients. Secondly, although these meta-analyses indicated a possible increased risk of mild to moderate TR, they were not associated with the typical features of valve thickening and restriction, and no clinically significant valve lesions were identified. If, as is widely accepted, it is the interaction of cabergoline with 5HT2B receptors that mediates the abnormal valvular function then, by analogy with carcinoid heart disease, this should be accompanied by characteristic changes in valve morphology (leaflet thickening, restricted movement and calcification). A major barrier to progress in the field is the fact that long-term, detailed studies of the size sufficient to exclude an effect would be costly to perform and require considerable expertise to ensure consistent, reliable and quantitative echocardiographic assessment. It is important to note that in all studies performed, bromocriptine has not been implicated with any valvular abnormalities.

Alternative imaging modalities, for example cardiovascular magnetic resonance imaging, do not provide adequate spatial or temporal resolution to compete with echocardiography for detailed assessment of valve structure and function. Moreover, a prospective, placebo-controlled design among young women with hyperprolactinaemia and oligo-amenorrhoea would be unethical, and any effects of cabergoline would be impossible to separate from those caused by/associated with restoration of physiological oestrogen secretion. The expectation that existing clinical networks could produce accurate, large volume data by applying current MHRA guidelines on surveillance by echocardiography also appears unlikely, since adherence to current recommendations is poor. In a service evaluation performed by NHS Highland (North), only 2/45 patients started on a DA agonist had echocardiography prior to starting therapy (33).

Recommendations on surveillance

Echocardiography is accepted as the gold standard technique for assessment of native valve structure and function (34). The detection of changes in structure and function in native valves may be subtle and echocardiography should be performed by properly trained, accredited professionals (35). In each case, a standard transthoracic study should be performed following minimum standards (36). In addition to this, however, careful attention should be taken to perform semi-quantitative assessment of valve structure and function to detect the changes typical of DA agonist therapy. Although there are no methods validated for assessment in DA agonist therapy per se, the changes to be detected are the same as those in patients with carcinoid heart disease, for which there are validated scoring systems with high feasibility and discriminatory value (37). Of these, the most sensitive and specific is an echocardiographic scoring system that assesses leaflet thickening, mobility and morphology, severity of valvular regurgitation and stenosis, and the haemodynamic effects on (right) ventricular size and function with good inter-observer agreement (38). Moreover, this incorporates assessment of all four cardiac valves, although focusses on haemodynamically significant right-sided valvular lesions through secondary effects on right ventricular size and function, which have been most frequently identified in the literature in DA agonist therapy (Table 3). Although tenting area has been used to quantify stiffening, this has not been validated in large studies and repeatability and reproducibility are not known, so that this is not a recommended feature for screening and follow-up.

Table 3

Scoring system for patients receiving dopamine agonist therapy. Some data from Bhattacharyya et al. (38).

Normal = 0Mild = 1Moderate = 2Severe = 3
Leaflet thickening0++++++
Leaflet mobility0↓↓↓↓↓
Leaflet morphologyNormalStiff and straightMild retractionModerate–severe retraction
Stenosis0MildModerateSevere
Regurgitation0MildModerateSevere
RV dimension0>42 mmRV = LVRV forming the LV apex
RV function0↓↓↓↓↓

Given that one of the major difficulties with the existing literature is the separation of valve disease due to DA agonist therapy from pre-existing changes in valve structure and function, it is recommended that all patients starting DA agonist therapy should undergo a transthoracic echocardiogram before drug therapy is commenced (Table 4). An increase in valve score may then be interpreted in the clinical context, considering the age and sex of the patient, the impact of other factors on valve leaflet thickening, mobility and morphology (e.g. ageing, chronic kidney disease), and likely impact of DA agonist (total dosage and exposure). The main problem in clinical practice will be the use of such a score in patients who were on a DA agonist for some time and in whom there may be changes identified on echocardiography. There have been no prospective validation studies of a scoring system and therefore, it is not possible to give a value or ‘score’ above which a patient should be categorized as affected by DA valvopathy. The sensitivity of the scoring system for identifying changes in patients with carcinoid increases with increasing score, with a median score in those affected 12 (range 8–21) and in those not affected 2 (IQR 1–3) (37). It could be argued that routinely performing a transthoracic echocardiogram before drug therapy is commenced may be unnecessary and that doing an echocardiogram if the dose is increased above 2 mg per week may be sufficient. The approach in this guideline is conservative, since the existing case-control and longitudinal follow-up studies cannot definitively exclude a small effect in the longer term. Moreover, given the semi-quantitative nature of echocardiographic evaluation of the changes described in DA valvulopathy and the fact that some of these changes can be seen in other conditions, assessment before initiation of drug therapy is considered a pragmatic solution pending further data.

Table 4

Summary of recommendations for patients receiving dopamine agonist therapy in hyperprolactinaemia.

Recommendations
  1. All patients should undergo echocardiography before commencing DA therapy.
  2. Patients taking a dose of cabergoline of ≤2 mg/week should undergo surveillance echocardiography at 5 years.
  3. Patients taking a dose of cabergoline of >2 mg/week should undergo annual echocardiography.
  4. Patients taking a dose of ≤2 mg/week who develop a change in valve function should undergo annual echocardiography if treatment is to continue.
  5. Decisions regarding discontinuation of medication should only be made after review of serial imaging by an echocardiographer experienced in analysing drug-induced valvulopathy or carcinoid heart disease.

Given the worst-case scenario for potential progression based on the largest cohort with serial follow-up (5), it is recommended that repeat transthoracic echocardiography should be performed at 5 years after starting cabergoline in patients taking a total weekly dose ≤2 mg. If there has been no change on the 5-year scan, repeat echocardiography could continue at 5-yearly intervals. Within this time interval, there has been no evidence of major clinical change affecting patient outcome. There is an option for annual surveillance with auscultation, although there are no data regarding accuracy of this approach relative to the use of echocardiography (39). If a patient is taking a total weekly dose of more than 2 mg, then annual echocardiography is recommended, although the number of these patients is small (Table 4). Once cabergoline has been stopped, no further echocardiography is warranted assuming that no moderate or severe valve abnormality has been identified.

Given that grading is semi-quantitative, with subjective assessment of leaflet thickening, mobility and morphology, it is vital that follow-up studies are cross-checked by a different observer blinded to the initial echocardiographic score. Specifically, where there is a discrepancy >2 points in score, an echocardiographer with experience of patient monitoring for DA valvulopathy or with experience in patients who have carcinoid heart disease should analyse the serial studies available in the patient before any decision is made regarding discontinuation of medication. It is critical to understand that changes in degree of regurgitation alone, for example from mild to moderate TR, should not on its own be sufficient to alter clinical management, especially without morphological change in leaflet motion, thickness or retraction.

Conclusions

Evidence that DAs cause valvulopathy akin to carcinoid heart disease in patients with hyperprolactinaemia is limited to a very small number of isolated case reports in which the cumulative doses used were very high and not dissimilar to those reported in the original studies on PD patients. The finding of valvular regurgitation in a patient taking cabergoline for hyperprolactinaemia does not, in the absence of typical valvular structural changes, mandate discontinuation of the drug. Any decision about discontinuation of the drug should be a multidisciplinary one, in discussion with the patient, and consideration should be given to the replacement with bromocriptine. Ongoing collection of high-quality data, via collaborative audit and study initiatives, together with post-marketing reporting (e.g. ‘yellow card’ reports in the United Kingdom) of independently confirmed cases, is strongly encouraged.

Declaration of interest

Vishal Sharma is Co-Editor-in-Chief, Richard Steeds and John Chambers are strategic editors, and Guy Lloyd is an associate editor of Echo Research and Practice. They were not involved in the review or editorial process for this article, on which they are listed as an author. The other authors have nothing to disclose.

Funding

This work did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector.

Author contribution statement

R P S and W D conceived the work and wrote the text, C S collaborated and contributed for the text and the manuscript was reviewed and conclusions drawn with V S, G L and J C.

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  • 19

    LafeberMStadesAMValkGDCramerMJTeding van BerkhoutFZelissenPM. Absence of major fibrotic adverse events in hyperprolactinemic patients treated with cabergoline. European Journal of Endocrinology 2010 162 667675. (https://doi.org/10.1530/EJE-09-0989)

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 20

    NachtigallLBValassiELoJMcCartyDPasseriJBillerBMKMillerKKUtzAGrinspoonSLawsonEAet al. Gender effects on cardiac valvular function in hyperprolactinaemic patients receiving cabergoline: a retrospective study. Clinical Endocrinology 2010 72 5358. (https://doi.org/10.1111/j.1365-2265.2009.03608.x)

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 21

    BoguszewskiCLdos SantosCMCSakamotoKSMariniLCde SouzaAMAzevedoM. A comparison of cabergoline and bromocriptine on the risk of valvular heart disease in patients with prolactinomas. Pituitary 2012 15 4449. (https://doi.org/10.1007/s11102-011-0339-7)

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 22

    DoğanBAArducATunaMMBerkerDDemirciNDemirtaşSÇiçekcioğluHGülerS. Autoimmune fibrotic adverse reactions in one-year treatment with cabergoline for women with prolactinoma. Endocrine Metabolic and Immune Disorders 2016 16 4755. (https://doi.org/10.2174/1871530316666160229120142)

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 23

    Córdoba-SorianoJGLamas-OliveiraCHidalgo-OlivaresVMTercero-MartínezABarambio-RuízMSalas-NietoJ. Valvular heart disease in hyperprolactinemic patients treated with low doses of cabergoline. Revista Española de Cardiología 2013 66 410412. (https://doi.org/10.1016/j.rec.2012.10.016)

    • Search Google Scholar
    • Export Citation
  • 24

    DrakeWMStilesCEHowlettTAToogoodAABevanJSSteedsRP. A cross-sectional study of the prevalence of cardiac valvular abnormalities in hyperprolactinemic patients treated with ergot-derived dopamine agonists. Journal of Clinical Endocrinology and Metabolism 2014 99 9096. (https://doi.org/10.1210/jc.2013-2254)

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 25

    D’AloiaAPiovanelliBRovettaRBonadeiIVizzardiECurnisAMetraM. A case of iatrogenic severe mitral regurgitation. Monaldi Archives for Chest Disease 2013 80 133136. (https://doi.org/10.4081/monaldi.2013.75)

    • Search Google Scholar
    • Export Citation
  • 26

    IzgiCFerayHCevikCSaltanYMansurogluDNugentK. Severe tricuspid regurgitation in a patient receiving low-dose cabergoline for the treatment of acromegaly. Journal of Heart Valve Disease 2010 19 797800.

    • Search Google Scholar
    • Export Citation
  • 27

    CawoodTJBridgmanPHunterLColeD. Low-dose cabergoline causing valvular heart disease in a patient treated for prolactinoma. Internal Medicine Journal 2009 39 266267. (https://doi.org/10.1111/j.1445-5994.2009.01920.x)

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 28

    DelgadoVBiermaszNRvan ThielSWEweSHMarsanNAHolmanERFeeldersRASmitJWBaxJJPereiraAM. Changes in heart valve structure and function in patients treated with dopamine agonists for prolactinomas, a 2-year follow-up study. Clinical Endocrinology 2012 77 99105. (https://doi.org/10.1111/j.1365-2265.2011.04326.x)

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 29

    VroonenLLancellottiPGarciaMTDulgheruRRubio-AlmanzaMMaigaIMagneJPetrossiansPAuriemmaRDalyAFet al. Prospective, long-term study of the effect of cabergoline on valvular status in patients with prolactinoma and idiopathic hyperprolactinemia. Endocrine 2017 55 239245. (https://doi.org/10.1007/s12020-016-1120-5)

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 30

    De VecchisREspositoCArianoC. Cabergoline use and risk of fibrosis and insufficiency of cardiac valves. Meta-analysis of observational studies. Herz 2013 38 868880. (https://doi.org/10.1007/s00059-013-3816-0)

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 31

    BogazziFManettiLRaffaelliVLombardiMRossiGMartinoE. Cabergoline therapy and the risk of cardiac valve regurgitation in patients with hyperprolactinemia: a metaanalysis from clinical studies. Journal of Endocrinological Investigation 2008 31 11191123. (https://doi.org/10.1007/BF03345662)

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 32

    StilesCETetteh-WayoeETBestwickJSteedsRPDrakeWM. A meta-analysis of the incidence of cardiac valvulopathy in hyperprolactinemic patients treated with cabergoline. Journal of Clinical Endocrinology and Metabolism 2018 104 523538. (https://doi.org/10.1210/jc.2018-01071)

    • Search Google Scholar
    • Export Citation
  • 33

    GambleDFairleyRHarveyRFarmanCCantleyNLeslieSJ. Screening for valve disease in patients with hyperprolactinaemia disorders prescribed cabergoline: a service evaluation and literature review. Therapeutic Advances in Drug Safety 2017 8 215229. (https://doi.org/10.1177/2042098617703647)

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 34

    BaumgartnerHFalkVBaxJJDe BonisMHammCHolmPJIungBLancellottiPLansacERodriguez MuñozDet al. 2017 ESC/EACTS guidelines for the management of valvular heart disease. European Heart Journal 2017 38 27392791. (https://doi.org/10.1093/eurheartj/ehx391)

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 35

    MonaghanM. Training in echocardiography. Heart 1994 71 (4 Supplement) 25. (https://doi.org/10.1136/hrt.71.4_Suppl.2)

  • 36

    WhartonGSteedsRAllenJPhillipsHJonesRKanagalaPLloydGMasaniNMathewTOxboroughDet al. A minimum dataset for a standard adult transthoracic echocardiogram: a guideline protocol from the British Society of Echocardiography. Echo Research and Practice 2015 2 G9G24. (https://doi.org/10.1530/ERP-14-0079)

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 37

    DobsonRCuthbertsonDJJonesJValleJWKeevilBChadwickCPostonGPBurgessMI. Determination of the optimal echocardiographic scoring system to quantify carcinoid heart disease. Neuroendocrinology 2014 99 8593. (https://doi.org/10.1159/000360767)

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 38

    BhattacharyyaSToumpanakisCCaplinMEDavarJ. Usefulness of N-terminal pro-brain natriuretic peptide as a biomarker of the presence of carcinoid heart disease. American Journal of Cardiology 2008 102 938942. (https://doi.org/10.1016/j.amjcard.2008.05.047)

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 39

    CaputoCPriorDInderWJ. The need for annual echocardiography to detect cabergoline-associated valvulopathy in patients with prolactinoma: a systematic review and additional clinical data. Lancet Diabetes and Endocrinology 2015 3 906913. (https://doi.org/10.1016/S2213-8587(14)70212-8)

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 40

    HalperinIAllerJVarelaCMoraMAbadADoltraASantosAEBatistaEGarcía-PavíaPSitgesMet al. No clinically significant valvular regurgitation in long-term cabergoline treatment for prolactinoma. Clinical Endocrinology 2012 77 275280. (https://doi.org/10.1111/j.1365-2265.2012.04349.x.)

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 41

    AuriemmaRSPivonelloRPeroneYGrassoLFFerreriLSimeoliCIacuanielloDGasperiM & ColaoA. Safety of long-term treatment with cabergoline on cardiac valve disease in patients with prolactinomas. European Journal of Endocrinology 2013 169 359366. (https://doi.org/10.1530/eje-13-0231)

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation

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  • 1

    SchadeRAndersohnFSuissaSHaverkampWGarbeE. Dopamine agonists and the risk of cardiac-valve regurgitation. New England Journal of Medicine 2007 356 2938. (https://doi.org/10.1056/NEJMoa062222)

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  • 2

    ZanettiniRAntoniniAGattoGGentileRTeseiSPezzoliG. Valvular heart disease and the use of dopamine agonists for Parkinson’s disease. New England Journal of Medicine 2007 356 3946. (https://doi.org/10.1056/NEJMoa054830)

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    • Export Citation
  • 3

    Van CampGFlamezACosynsBWeytjensCMuyldermansLVan ZandijckeMDe SutterJSantensPDecoodtPMoermanCet al. Treatment of Parkinson’s disease with pergolide and relation to restrictive valvular heart disease. Lancet 2004 363 11791183. (https://doi.org/10.1016/S0140-6736(04)15945-X)

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  • 4

    CasanuevaFFMolitchMESchlechteJAAbsRBonertVBronsteinMDBrueTCappabiancaPColaoAFahlbuschRet al. Guidelines of the Pituitary Society for the diagnosis and management of prolactinomas. Clinical Endocrinology 2006 65 265273. (https://doi.org/10.1111/j.1365-2265.2006.02562.x)

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    • PubMed
    • Search Google Scholar
    • Export Citation
  • 5

    DrakeWMStilesCEBevanJSKaravitakiNTrainerPJReesDARichardsonTIBaldewegSEStojanovicNMurrayRDet al. A follow-up study of the prevalence of valvular heart abnormalities in hyperprolactinemic patients treated with cabergoline. Journal of Clinical Endocrinology and Metabolism 2016 101 41894194. (https://doi.org/10.1210/jc.2016-2224)

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  • 6

    ElangbamCS. Drug-induced valvulopathy: an update. Toxicologic Pathology 2010 38 837848. (https://doi.org/10.1177/0192623310378027)

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    PineroAMarcos-AlbercaPFortesJ. Cabergoline-related severe restrictive mitral regurgitation. New England Journal of Medicine 2005 353 19761977. (https://doi.org/10.1056/NEJM200511033531822)

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  • 8

    GuHLuckSCarrollPVPowrieJChambersJ. Cardiac valve disease and low-dose dopamine agonist therapy: an artefact of reporting bias? Clinical Endocrinology 2011 74 608610. (https://doi.org/10.1111/j.1365-2265.2010.03973.x)

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    • PubMed
    • Search Google Scholar
    • Export Citation
  • 9

    d’ArcyJLCoffeySLoudonMAKennedyAPearson-StuttardJBirksJFrangouEFarmerAJMantDWilsonJet al. Large-scale community echocardiographic screening reveals a major burden of undiagnosed valvular heart disease in older people: the OxVALVE Population Cohort Study. European Heart Journal 2016 37 35153522. (https://doi.org/10.1093/eurheartj/ehw229)

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 10

    BogazziFBuralliSManettiLRaffaelliVCigniTLombardiMBoresiFTaddeiSSalvettiAMartinoE. Treatment with low doses of cabergoline is not associated with increased prevalence of cardiac valve regurgitation in patients with hyperprolactinaemia. International Journal of Clinical Practice 2008 62 18641869. (https://doi.org/10.1111/j.1742-1241.2008.01779.x)

    • Crossref
    • PubMed
    • Search Google Scholar
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  • 11

    ColaoAGalderisiMDi SarnoAPardoMGaccioneMD’AndreaMGuerraEPivonelloRLerroGLombardiG. Increased prevalence of tricuspid regurgitation in patients with prolactinomas chronically treated with cabergoline. Journal of Clinical Endocrinology and Metabolism 2008 93 37773784. (https://doi.org/10.1210/jc.2007-1403)

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    • Search Google Scholar
    • Export Citation
  • 12

    KarsMDelgadoVHolmanERFeeldersRASmitJWARomijnJABaxJJPereiraAM. Aortic valve calcification and mild tricuspid regurgitation but no clinical heart disease after 8 years of dopamine agonist therapy for prolactinoma. Journal of Clinical Endocrinology and Metabolism 2008 93 33483356. (https://doi.org/10.1210/jc.2007-2658)

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 13

    LancellottiPLivadariuEMarkovMDalyAFBurlacuMCBeteaDPierardLBeckersA. Cabergoline and the risk of valvular lesions in endocrine disease. European Journal of Endocrinology 2008 159 15. (https://doi.org/10.1530/EJE-08-0213)

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    • PubMed
    • Search Google Scholar
    • Export Citation
  • 14

    WakilARigbyASClarkALKallvikbacka-BennettAAtkinSL. Low dose cabergoline for hyperprolactinaemia is not associated with clinically significant valvular heart disease. European Journal of Endocrinology 2008 159 R11R14. (https://doi.org/10.1530/EJE-08-0365)

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    • Search Google Scholar
    • Export Citation
  • 15

    TanTCabritaIZHensmanDGrogonoJDhilloWSBaynesKCEliahooJMeeranKRobinsonSNihoyannopoulosPet al. Assessment of cardiac valve dysfunction in patients receiving cabergoline treatment for hyperprolactinaemia. Clinical Endocrinology 2010 73 369374. (https://doi.org/10.1111/j.1365-2265.2010.03827.x)

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    • PubMed
    • Search Google Scholar
    • Export Citation
  • 16

    ValletteSSerriKRiveraJSantagataPDelormeSGarfieldNKahtaniNBeauregardHAris-JilwanNHoudeGet al. Long-term cabergoline therapy is not associated with valvular heart disease in patients with prolactinomas. Pituitary 2009 12 153157. (https://doi.org/10.1007/s11102-008-0134-2)

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 17

    ElenkovaAShabaniRKalinovKZacharievaS. Increased prevalence of subclinical cardiac valve fibrosis in patients with prolactinomas on long-term bromocriptine and cabergoline treatment. European Journal of Endocrinology 2012 167 1725. (https://doi.org/10.1530/EJE-12-0121)

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 18

    HerringNSzmigielskiCBecherHKaravitakiNWassJAH. Valvular heart disease and the use of cabergoline for the treatment of prolactinoma. Clinical Endocrinology 2009 70 104108. (https://doi.org/10.1111/j.1365-2265.2008.03458.x)

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 19

    LafeberMStadesAMValkGDCramerMJTeding van BerkhoutFZelissenPM. Absence of major fibrotic adverse events in hyperprolactinemic patients treated with cabergoline. European Journal of Endocrinology 2010 162 667675. (https://doi.org/10.1530/EJE-09-0989)

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 20

    NachtigallLBValassiELoJMcCartyDPasseriJBillerBMKMillerKKUtzAGrinspoonSLawsonEAet al. Gender effects on cardiac valvular function in hyperprolactinaemic patients receiving cabergoline: a retrospective study. Clinical Endocrinology 2010 72 5358. (https://doi.org/10.1111/j.1365-2265.2009.03608.x)

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 21

    BoguszewskiCLdos SantosCMCSakamotoKSMariniLCde SouzaAMAzevedoM. A comparison of cabergoline and bromocriptine on the risk of valvular heart disease in patients with prolactinomas. Pituitary 2012 15 4449. (https://doi.org/10.1007/s11102-011-0339-7)

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 22

    DoğanBAArducATunaMMBerkerDDemirciNDemirtaşSÇiçekcioğluHGülerS. Autoimmune fibrotic adverse reactions in one-year treatment with cabergoline for women with prolactinoma. Endocrine Metabolic and Immune Disorders 2016 16 4755. (https://doi.org/10.2174/1871530316666160229120142)

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 23

    Córdoba-SorianoJGLamas-OliveiraCHidalgo-OlivaresVMTercero-MartínezABarambio-RuízMSalas-NietoJ. Valvular heart disease in hyperprolactinemic patients treated with low doses of cabergoline. Revista Española de Cardiología 2013 66 410412. (https://doi.org/10.1016/j.rec.2012.10.016)

    • Search Google Scholar
    • Export Citation
  • 24

    DrakeWMStilesCEHowlettTAToogoodAABevanJSSteedsRP. A cross-sectional study of the prevalence of cardiac valvular abnormalities in hyperprolactinemic patients treated with ergot-derived dopamine agonists. Journal of Clinical Endocrinology and Metabolism 2014 99 9096. (https://doi.org/10.1210/jc.2013-2254)

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 25

    D’AloiaAPiovanelliBRovettaRBonadeiIVizzardiECurnisAMetraM. A case of iatrogenic severe mitral regurgitation. Monaldi Archives for Chest Disease 2013 80 133136. (https://doi.org/10.4081/monaldi.2013.75)

    • Search Google Scholar
    • Export Citation
  • 26

    IzgiCFerayHCevikCSaltanYMansurogluDNugentK. Severe tricuspid regurgitation in a patient receiving low-dose cabergoline for the treatment of acromegaly. Journal of Heart Valve Disease 2010 19 797800.

    • Search Google Scholar
    • Export Citation
  • 27

    CawoodTJBridgmanPHunterLColeD. Low-dose cabergoline causing valvular heart disease in a patient treated for prolactinoma. Internal Medicine Journal 2009 39 266267. (https://doi.org/10.1111/j.1445-5994.2009.01920.x)

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 28

    DelgadoVBiermaszNRvan ThielSWEweSHMarsanNAHolmanERFeeldersRASmitJWBaxJJPereiraAM. Changes in heart valve structure and function in patients treated with dopamine agonists for prolactinomas, a 2-year follow-up study. Clinical Endocrinology 2012 77 99105. (https://doi.org/10.1111/j.1365-2265.2011.04326.x)

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 29

    VroonenLLancellottiPGarciaMTDulgheruRRubio-AlmanzaMMaigaIMagneJPetrossiansPAuriemmaRDalyAFet al. Prospective, long-term study of the effect of cabergoline on valvular status in patients with prolactinoma and idiopathic hyperprolactinemia. Endocrine 2017 55 239245. (https://doi.org/10.1007/s12020-016-1120-5)

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 30

    De VecchisREspositoCArianoC. Cabergoline use and risk of fibrosis and insufficiency of cardiac valves. Meta-analysis of observational studies. Herz 2013 38 868880. (https://doi.org/10.1007/s00059-013-3816-0)

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 31

    BogazziFManettiLRaffaelliVLombardiMRossiGMartinoE. Cabergoline therapy and the risk of cardiac valve regurgitation in patients with hyperprolactinemia: a metaanalysis from clinical studies. Journal of Endocrinological Investigation 2008 31 11191123. (https://doi.org/10.1007/BF03345662)

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 32

    StilesCETetteh-WayoeETBestwickJSteedsRPDrakeWM. A meta-analysis of the incidence of cardiac valvulopathy in hyperprolactinemic patients treated with cabergoline. Journal of Clinical Endocrinology and Metabolism 2018 104 523538. (https://doi.org/10.1210/jc.2018-01071)

    • Search Google Scholar
    • Export Citation
  • 33

    GambleDFairleyRHarveyRFarmanCCantleyNLeslieSJ. Screening for valve disease in patients with hyperprolactinaemia disorders prescribed cabergoline: a service evaluation and literature review. Therapeutic Advances in Drug Safety 2017 8 215229. (https://doi.org/10.1177/2042098617703647)

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 34

    BaumgartnerHFalkVBaxJJDe BonisMHammCHolmPJIungBLancellottiPLansacERodriguez MuñozDet al. 2017 ESC/EACTS guidelines for the management of valvular heart disease. European Heart Journal 2017 38 27392791. (https://doi.org/10.1093/eurheartj/ehx391)

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 35

    MonaghanM. Training in echocardiography. Heart 1994 71 (4 Supplement) 25. (https://doi.org/10.1136/hrt.71.4_Suppl.2)

  • 36

    WhartonGSteedsRAllenJPhillipsHJonesRKanagalaPLloydGMasaniNMathewTOxboroughDet al. A minimum dataset for a standard adult transthoracic echocardiogram: a guideline protocol from the British Society of Echocardiography. Echo Research and Practice 2015 2 G9G24. (https://doi.org/10.1530/ERP-14-0079)

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 37

    DobsonRCuthbertsonDJJonesJValleJWKeevilBChadwickCPostonGPBurgessMI. Determination of the optimal echocardiographic scoring system to quantify carcinoid heart disease. Neuroendocrinology 2014 99 8593. (https://doi.org/10.1159/000360767)

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 38

    BhattacharyyaSToumpanakisCCaplinMEDavarJ. Usefulness of N-terminal pro-brain natriuretic peptide as a biomarker of the presence of carcinoid heart disease. American Journal of Cardiology 2008 102 938942. (https://doi.org/10.1016/j.amjcard.2008.05.047)

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 39

    CaputoCPriorDInderWJ. The need for annual echocardiography to detect cabergoline-associated valvulopathy in patients with prolactinoma: a systematic review and additional clinical data. Lancet Diabetes and Endocrinology 2015 3 906913. (https://doi.org/10.1016/S2213-8587(14)70212-8)

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 40

    HalperinIAllerJVarelaCMoraMAbadADoltraASantosAEBatistaEGarcía-PavíaPSitgesMet al. No clinically significant valvular regurgitation in long-term cabergoline treatment for prolactinoma. Clinical Endocrinology 2012 77 275280. (https://doi.org/10.1111/j.1365-2265.2012.04349.x.)

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 41

    AuriemmaRSPivonelloRPeroneYGrassoLFFerreriLSimeoliCIacuanielloDGasperiM & ColaoA. Safety of long-term treatment with cabergoline on cardiac valve disease in patients with prolactinomas. European Journal of Endocrinology 2013 169 359366. (https://doi.org/10.1530/eje-13-0231)

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation