Aa
what's with females having babies and heart problems
Pretty much every single female I talked to that had kids has weird heart rhythm episodes...i'm really bothered by this because i think there should be more information on pregnancy and how it affects your heart during and after pregnancy....i started getting frequent one minute heart-pace-went faster episode after my first...and then after my second child i got SVT and PAC constant...i tired of doctors saying it's anxiety....no no no because pregnancy puts a big strain on your body and after you have the baby your body is trying to get back to normal and that unfortuntely includes your heart...but what causes this??? hormones? digestive system? not having enough blood volume?
just tired of the lack of information that's all... :(
just tired of the lack of information that's all... :(
this is so weird that I came across this! my daughter is 9 months old and I have been having PVCs and SVT. Allie is my second child and started noticing my heart while pregnant but was told it was normal, never had this problem when pregnant with my first. I also had a uterine infection after allie which they think effected 2 of my valves, I am now suffering from a high heart rate and am headed to cleavland heart clinic of wed to see if they can help me. Doctors kept telling me it was anxiety I HATE THAT every time I would go in with a genuine health concern they would say are you sure your not just having some anxiety!!!! I swear I had had it...my doctor would not order any heart test and I had to beg to have anything done and sure enough there was somthing wrong and it was not anxiety. Doctors want to chuck up everything to depression and anxiety which does exist and can cuase problems but so many things are going untreated and its being used as a catch 22......pregnancy can take a tole on your body thats for sure with my daughter I found out I was pregnant and had gallstones same day...I was sick for 4 months only thing I put in my body was gatoraide and beef broth until they could safley take it out and I wouldnt lose the baby so pregnancy is also a very amazing thing aswell and totally worth it. I just wish doctors werent so quick to call it anxiety!!!! that really pisses me off! I swear I had a doc try to tell me I didnt have bronchitis ....IT WAS ANXIETY now that takes the cake!
I don't know if the development of PPCM is affected by nursing. If the prolactin theory does prove to be true I would imagine that anyone could get PPCM. As far as I know everyone gets a surge of prolactin whether they breastfeed or not. I'm not sure though as it's not my area.
The work published so far is only the starting point for a long line of research and unfortunately in molecular biology the picture almost always turns out to be way complex than originally thought. The more research that is done the more questions are raised and the more complicated the whole puzzle gets. The human body is just so complex that it's rarely anything is ever fully understood. There are probably multiple factors at work in PPCM.
The work published so far is only the starting point for a long line of research and unfortunately in molecular biology the picture almost always turns out to be way complex than originally thought. The more research that is done the more questions are raised and the more complicated the whole puzzle gets. The human body is just so complex that it's rarely anything is ever fully understood. There are probably multiple factors at work in PPCM.
so women who don't nurse never get PPCM? Oh, from the last trimester? There must be much more going on, because I got DCM, and I have had a few kids with no problem, and nursed them all.
Ok sorry, just read that back again. the mutation is not in the prolactin gene itself but in an upstream regulator and affects the way the prolactin protein is cleaved.
There's a good chance that, as with most things, there are multiple factors involved; genetic, environmental etc.
As anacyde said the study published in cell regarding the role of prolactin was conducted in rats (apart form the small bromocriptine trial which was in women aswell). To further invetigate the prolactin theory they need to sequence the prolactin genes of a large number of PPCM women. The abstract is below.
A cathepsin D-cleaved 16 kDa form of prolactin mediates postpartum cardiomyopathy.
Department of Cardiology and Angiology, MHH, 30625 Hannover, Germany. hilfiker.
Postpartum cardiomyopathy (PPCM) is a disease of unknown etiology and exposes women to high risk of mortality after delivery. Here, we show that female mice with a cardiomyocyte-specific deletion of stat3 develop PPCM. In these mice, cardiac cathepsin D (CD) expression and activity is enhanced and associated with the generation of a cleaved antiangiogenic and proapoptotic 16 kDa form of the nursing hormone prolactin. Treatment with bromocriptine, an inhibitor of prolactin secretion, prevents the development of PPCM, whereas forced myocardial generation of 16 kDa prolactin impairs the cardiac capillary network and function, thereby recapitulating the cardiac phenotype of PPCM. Myocardial STAT3 protein levels are reduced and serum levels of activated CD and 16 kDa prolactin are elevated in PPCM patients. Thus, a biologically active derivative of the pregnancy hormone prolactin mediates PPCM, implying that inhibition of prolactin release may represent a novel therapeutic strategy for PPCM.
As anacyde said the study published in cell regarding the role of prolactin was conducted in rats (apart form the small bromocriptine trial which was in women aswell). To further invetigate the prolactin theory they need to sequence the prolactin genes of a large number of PPCM women. The abstract is below.
A cathepsin D-cleaved 16 kDa form of prolactin mediates postpartum cardiomyopathy.
Department of Cardiology and Angiology, MHH, 30625 Hannover, Germany. hilfiker.
Postpartum cardiomyopathy (PPCM) is a disease of unknown etiology and exposes women to high risk of mortality after delivery. Here, we show that female mice with a cardiomyocyte-specific deletion of stat3 develop PPCM. In these mice, cardiac cathepsin D (CD) expression and activity is enhanced and associated with the generation of a cleaved antiangiogenic and proapoptotic 16 kDa form of the nursing hormone prolactin. Treatment with bromocriptine, an inhibitor of prolactin secretion, prevents the development of PPCM, whereas forced myocardial generation of 16 kDa prolactin impairs the cardiac capillary network and function, thereby recapitulating the cardiac phenotype of PPCM. Myocardial STAT3 protein levels are reduced and serum levels of activated CD and 16 kDa prolactin are elevated in PPCM patients. Thus, a biologically active derivative of the pregnancy hormone prolactin mediates PPCM, implying that inhibition of prolactin release may represent a novel therapeutic strategy for PPCM.
Hi Anacyde. Just saw your post. I will have a look at some of the other papers on the subject. I just came across the Hilfiker-Kleiner Cell paper when it came out in 2007. It's one of the hundreds I've had to read as part of my job and I must admit I haven't had a chance to read the paper properly or look at it since but it really stuck in my mind.
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