Wearable cardioverter defibrillator for peripartum cardiomyopathy patients
Duncker and colleagues1 have done us a great favour in looking so meticulously at their peripartum cardiomyopathy (PPCM) subjects for the risk of developing life-threatening ventricular tachyarrhythmias. It seems to me that this is an alarmingly high rate of ventricular fibrillation affecting one-third (3/9) of their PPCM subjects with diagnostic LVEF ≤0.35 and a quarter (3/12) of all their PPCM subjects followed prospectively in 2012/2013. This would be the highest rate of life-threatening arrhythmia ever reported for PPCM patients, although there have been some reports suggesting a higher rate than previously suspected.2,3 In view of what seems like a very high rate, although in relatively small numbers overall, there is some concern for any potential role of bromocriptine, as it appears that all subjects received bromocriptine in some dosage for some period of time, either to suppress lactation (n =4) or with the hope of benefit in outcomes (n =8).4,5 Despite the use of bromocriptine, the recovery rates to LVEF ≥0.50 by 12 months post-diagnosis is quite low, with only 1/9 in the diagnostic group with LVEF ≤0.35 and 2/3 in the diagnostic group with LVEF >0.35 reaching that level of recovery. However, all subjects experienced improvement in EF: the nine in the lowest diagnostic group gained
a mean of 26.8 EF points, with a range of 22.4–31.1 EF points. That is encouraging, although this is either a lower rate than or a comparable rate with that achieved in previous and ongoing studies in which no bromocriptine had been used.6 Does that suggest that the addition of bromocriptine has had relatively little if any impact on the outstanding evidence-based treatment with conventional treatment used in this group? Without a control group, one cannot know the answer to this. I had hoped to see a stronger influence with more recoveries to LVEF ≥0.50 by 12 months postpartum. Whether bromocriptine promotes recovery or not, it is important to be sure that it does not do harm in the peripartum setting.7,8 I hope it does not promote ventricular tachyarrhythmias in the peripartum period. However that works out, the most important message from this report is that we should continuously monitor heart rhythm for any PPCM patient who has an LVEF ≤0.35 at diagnosis until her LVEF moves above 0.35. The wearable cardioverter defibrillator (WCD) serves that purpose well as a temporary measure up to ∼5 or 6 months, when a permanent implantable cardioverter defibrillator (ICD) can be provided for the few in whom there has not yet been sufficient improvement. Conflict of interest: none declared.
References
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doi:10.1002/ejhf.215
...........................................................................................................................................
CORRESPONDENCE
1. Duncker D, Haghikia A, Konig T, Hohmann S, Gutieben KJ, Westenfield R, Oswald H, Klein H, Bauersachs J, Hilfiker-Kleiner D, Veltmann C. Risk for ventricular fibrillation in peripartum cardiomyopathy with severely reduced
2.
3.
4.
5.
6.
7.
8.
left ventricular function-value of the wearable cardioverter/defibrillator. Eur J Heart Fail 2014;16:1331–1336. Harper MA, Meyer RE, Berg CJ. Peripartum cardiomyopathy: population-based birth prevalence and 7-year mortality. Obstet Gynecol 2012;120:1013–1019. Fett JD. Earlier Detection can help avoid many serious complications of peripartum cardiomyopathy. Future Cardiol 2013;9:809–816. Hilfiker-Kleiner D, Kaminski K, Podewski E, Bonda T, Schaefer A, Sliwa K, Forster O, Quint A, Landmesser U, Doerries C, Luchtefeld M, Poli V, Schneider MD, Balligand JL, Desjardins F, Ansari A, Struman I, Nguyen NQ, Zschemisch NH, Klein G, Heusch G, Schulz R, Hilfiker A, Drexler H. A cathepsin D-cleaved 16 kDa form of prolactin mediates postpartum cardiomyopathy. Cell 2007;128:589–600. Haghikia A, Podewski E, Libhaber E, Labidi S, Tsikas D, Jordan J, Lichtinghagen R, von Kaisenberg CS, Struman I, Bovy N, Sliwa K, Bauersachs J, HilfikerKleiner D. Phenotyping and outcome on contemporary management in a German cohort of patients with peripartum cardiomyopathy. Basic Res Cardiol 2013;108:366. Cooper LT, Mather PJ, Alexis JD, Pauly DF, Torre-Amione G, Wkttstein IS, Dec GW, Zucker M, Narula J, Kip K, McNamara DM. IMAC2 Investigators. Myocardial recovery in peripartum cardiomyopathy: prospective comparison with recent onset cardiomyopathy in men and nonperipartum women. J Card Fail 2012; 18:28–33. Hopp L, Weisse AB, Iffy L. Acute myocardial infarction in a healthy mother using bromocriptine for milk suppression. Can J Cardiol 1996;12:415–418. Y-Hassan S, Jernberg T. Bromocriptine-induced coronary spasm caused acute coronary syndrome, which triggered its own clinical twin—Takotsubo syndrome. Cardiology 2011;119:1–6.
James D. Frett 2331 Mt. Hood Ct. SE Lacey WA 98520 USA Tel: +1 360 438 5270 E-mail: [email protected]
© 2015 The Authors European Journal of Heart Failure © 2015 European Society of Cardiology
Copyright of European Journal of Heart Failure is the property of John Wiley & Sons, Inc. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
Duncker and colleagues1 have done us a great favour in looking so meticulously at their peripartum cardiomyopathy (PPCM) subjects for the risk of developing life-threatening ventricular tachyarrhythmias. It seems to me that this is an alarmingly high rate of ventricular fibrillation affecting one-third (3/9) of their PPCM subjects with diagnostic LVEF ≤0.35 and a quarter (3/12) of all their PPCM subjects followed prospectively in 2012/2013. This would be the highest rate of life-threatening arrhythmia ever reported for PPCM patients, although there have been some reports suggesting a higher rate than previously suspected.2,3 In view of what seems like a very high rate, although in relatively small numbers overall, there is some concern for any potential role of bromocriptine, as it appears that all subjects received bromocriptine in some dosage for some period of time, either to suppress lactation (n =4) or with the hope of benefit in outcomes (n =8).4,5 Despite the use of bromocriptine, the recovery rates to LVEF ≥0.50 by 12 months post-diagnosis is quite low, with only 1/9 in the diagnostic group with LVEF ≤0.35 and 2/3 in the diagnostic group with LVEF >0.35 reaching that level of recovery. However, all subjects experienced improvement in EF: the nine in the lowest diagnostic group gained
a mean of 26.8 EF points, with a range of 22.4–31.1 EF points. That is encouraging, although this is either a lower rate than or a comparable rate with that achieved in previous and ongoing studies in which no bromocriptine had been used.6 Does that suggest that the addition of bromocriptine has had relatively little if any impact on the outstanding evidence-based treatment with conventional treatment used in this group? Without a control group, one cannot know the answer to this. I had hoped to see a stronger influence with more recoveries to LVEF ≥0.50 by 12 months postpartum. Whether bromocriptine promotes recovery or not, it is important to be sure that it does not do harm in the peripartum setting.7,8 I hope it does not promote ventricular tachyarrhythmias in the peripartum period. However that works out, the most important message from this report is that we should continuously monitor heart rhythm for any PPCM patient who has an LVEF ≤0.35 at diagnosis until her LVEF moves above 0.35. The wearable cardioverter defibrillator (WCD) serves that purpose well as a temporary measure up to ∼5 or 6 months, when a permanent implantable cardioverter defibrillator (ICD) can be provided for the few in whom there has not yet been sufficient improvement. Conflict of interest: none declared.
References
...........................................................................................................................................
doi:10.1002/ejhf.215
...........................................................................................................................................
CORRESPONDENCE
1. Duncker D, Haghikia A, Konig T, Hohmann S, Gutieben KJ, Westenfield R, Oswald H, Klein H, Bauersachs J, Hilfiker-Kleiner D, Veltmann C. Risk for ventricular fibrillation in peripartum cardiomyopathy with severely reduced
2.
3.
4.
5.
6.
7.
8.
left ventricular function-value of the wearable cardioverter/defibrillator. Eur J Heart Fail 2014;16:1331–1336. Harper MA, Meyer RE, Berg CJ. Peripartum cardiomyopathy: population-based birth prevalence and 7-year mortality. Obstet Gynecol 2012;120:1013–1019. Fett JD. Earlier Detection can help avoid many serious complications of peripartum cardiomyopathy. Future Cardiol 2013;9:809–816. Hilfiker-Kleiner D, Kaminski K, Podewski E, Bonda T, Schaefer A, Sliwa K, Forster O, Quint A, Landmesser U, Doerries C, Luchtefeld M, Poli V, Schneider MD, Balligand JL, Desjardins F, Ansari A, Struman I, Nguyen NQ, Zschemisch NH, Klein G, Heusch G, Schulz R, Hilfiker A, Drexler H. A cathepsin D-cleaved 16 kDa form of prolactin mediates postpartum cardiomyopathy. Cell 2007;128:589–600. Haghikia A, Podewski E, Libhaber E, Labidi S, Tsikas D, Jordan J, Lichtinghagen R, von Kaisenberg CS, Struman I, Bovy N, Sliwa K, Bauersachs J, HilfikerKleiner D. Phenotyping and outcome on contemporary management in a German cohort of patients with peripartum cardiomyopathy. Basic Res Cardiol 2013;108:366. Cooper LT, Mather PJ, Alexis JD, Pauly DF, Torre-Amione G, Wkttstein IS, Dec GW, Zucker M, Narula J, Kip K, McNamara DM. IMAC2 Investigators. Myocardial recovery in peripartum cardiomyopathy: prospective comparison with recent onset cardiomyopathy in men and nonperipartum women. J Card Fail 2012; 18:28–33. Hopp L, Weisse AB, Iffy L. Acute myocardial infarction in a healthy mother using bromocriptine for milk suppression. Can J Cardiol 1996;12:415–418. Y-Hassan S, Jernberg T. Bromocriptine-induced coronary spasm caused acute coronary syndrome, which triggered its own clinical twin—Takotsubo syndrome. Cardiology 2011;119:1–6.
James D. Frett 2331 Mt. Hood Ct. SE Lacey WA 98520 USA Tel: +1 360 438 5270 E-mail: [email protected]
© 2015 The Authors European Journal of Heart Failure © 2015 European Society of Cardiology
Copyright of European Journal of Heart Failure is the property of John Wiley & Sons, Inc. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
