Peripartum Cardiomyopathy?
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You ever heard of Google????\n\nhttp://www.nlm.nih.gov/medlineplus/ency/article/000188.htm
138286
yes!\n\nhttp://www.medhelp.org/perl6/cardio/archive/14037.html\n\na number of ailments cause it. However you can get it to 50-60 or so with it being normal if you're an avid runner.
900709
Hard to diagnose people on here but could be post-partum depression, thyroid issues or hormonal challenges.\n\nSee your doctor; he/she can fix you up.
561397
Hi, I've had PVCs for many years and they come and go.  At first, I was scared to death and thought that something was seriously wrong with my heart.  After visiting the cardiologist and having a bunch of tests, I learned that my PVCs are totally harmless and most likely the result of stress.  I'm not a doctor, but I've had PVCs off and on for over 10 years and I can tell you that in the absence of other symptoms they're considered totally harmless.  Mine tend to come at night, right around bedtime, if at all.  Like you, I take vitamins (including all the ones you mentioned).  I would suggest you try taking some Magnesium, that seems to have helped me a great deal.  The other thing that helps is exercise -- cardio, and lots of it.  Oh, and by the way -- everyone gets skipped heartbeats, but not everyone notices them.  I think you can relax about your PVCs.  Mention them to your doctor at your next regular checkup, or if they return and suddenly get worse then by all means make that appointment sooner rather than later.  However, your PVCs are most likely just a nuisance.
1156820
Better visit a cardiologyst..
889124
Please get help!\n\nWhat are common symptoms?\nSymptoms of postpartum depression include extreme fatigue, loss of pleasure in daily life, sleeplessness (insomnia), sadness, tearfulness, anxiety, hopelessness, feelings of worthlessness and guilt, irritability, appetite change, and poor concentration.\n\nIt may be helpful to make a list of postpartum depression symptoms that you can take to your health professional. See a postpartum depression checklist  (What is a PDF document?) . \n\nAlthough any women with PPD can have fleeting, frightening thoughts of suicide or harming their babies, women with rare postpartum psychosis experience these thoughts as urges they feel compelled to act on. If you think you can't keep from hurting yourself, your baby, or someone else, see your health professional immediately or call 911 for emergency medical care. Other resources include: \n\nThe national suicide hotline, National Hopeline Network, at 1-800-784-2433.\nThe National Child Abuse Hotline at 1-800-422-4453.\nWhat causes postpartum depression?\nPPD seems to be triggered by the changes in hormone levels that occur after pregnancy. These hormonal changes are especially likely to lead to postpartum depression if you've had depression before, have poor support from your partner, friends, or family, or are under significant additional stress. 1 \n\nEvery woman has a risk of postpartum depression during the first several months after childbirth, miscarriage, or stillbirth. Women with a history of depression or postpartum depression have an even greater risk. A personal or family history of bipolar disorder , also known as manic-depression, increases the risk of postpartum psychosis.
772616
The pages listed under this information section  contain summaries of relevant topics written by many different experts in the field for the Montgomery Heart Foundation for Cardiomyopathy. The information contained in these summaries was originally collected in 1997 to put together a printed brochure for patients, families and health care professionals.  Although these summaries are now 6 or 7 years old, they have been re-reviewed and we believe  contain basic and general information that is still helpful to patients and families today.\n\n \nWhile the entity of the "athlete's heart" has been recognized for over 100 years, only in the last two decades has the application of echocardiography and other noninvasive imagine techniques permitted definition with some precision of the alterations in cardiac dimensions associated with athletic conditioning.  Echocardiography has demonstrated that long-term athletic training leads to an increase in left ventricular (LV) mass due to increases in LV diastolic cavity dimension, wall thickness, or both.  These changes in cardiac morphology are relatively mild in absolute terms, and the differences between athlete and non-athlete populations are statistically significant but generally small.  Furthermore, cardiac alterations associated with training differ somewhat depending on the particular sporting discipline in which the individual athlete participates.  In particular, the changes in LV wall thickness, cavity dimensions, or both associated with long-term athletic training may be more striking in certain sports such as distance running, swimming, cycling and rowing/canoeing.  It is in athletes raining in such sports that the differential diagnosis is more likely to be raised.\n\nDifferential Diagnosis\n \nDilated Cardiomyopathy\nIn an important minority of athletes, the increase in LV end-diastolic cavity dimension that occurs with training overlaps that which is characteristic of certain pathologic entities.  While LV cavity dimension is athletes is usually in the range of 53 to 58 mm, in some individuals it may extend into what is regarded as the pathological range of >60 mm (up to 70 mm), and thereby resemble dilated cardiomyopathy.  However, the absence of LV systolic dysfunction is usually sufficient to distinguish such physiologic ventricular enlargement induced by training from dilated cardiomyopathy. \n\nArrhythmogenic Right Ventricular Dysplasia (ARVD)\nBecause highly trained athletes may demonstrate right ventricular enlargement and a variety of depolarization, repolarization and conduction abnormalities on the ECG, the differential diagnosis between athlete's heart and ARVD may arise.  Identification of ARVD by echocardiography may be exceedingly difficult because of technical limitations in imaging right heart morphology (and assessing right ventricular function), and also because the spectrum of disease is broad.  Demonstration of right ventricular segmental or global dysfunction or substantial cavity enlargement supports the diagnosis.  Magnetic resonance imaging, however, affords a more reliable noninvasive diagnosis of this condition.  In ARVD, ECG's frequently show T wave inversion in V1-V3.\n\nHypertrophic Cardiomyopathy\nThe dilemma of distinguishing clinically between athlete's heart and structural heart disease most frequently arises with respect to hypetrophic cardiomyopathy (HCM).  While at present there is no single approach that will definitively resolve this question in all such athletes, several strategies are described here that alone or in combination offer a large measure of clarification in most instances for this often compelling differential diagnosis.  The definition of HCM employed here is that of a patient (or athlete) with evidence of a hypertrophied and nondilated LV in the absence of another cardiac of systemic disease that could itself produce hypetrophy of the magnitude present in that individual.\n\nWall Thickness\nIn
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Here is an excerpt from the warning letter sent to physicians from the manufacturer of Herceptin:\n\n"Dear Healthcare Provider:\n\nGenentech, Inc. wishes to inform you of updated cardiotoxicity information related to the use of HERCEPTIN® (trastuzumab), obtained from the National Surgical Adjuvant Breast and Bowel Project (NSABP) study (B-31), a randomized, Phase III trial that was conducted in 2043 women with operable, HER2 overexpressing breast cancer (IHC 3+ or FISH+). \n\nThis study demonstrated a significant increase in cardiotoxicity in patients who were randomized to the HERCEPTIN-containing arm as compared to patients who received chemotherapy alone.\n\nA preliminary analysis of the safety data from Study NSABP B-31 was presented at the annual meeting of the American Society of Clinical Oncology (ASCO) in May 2005, during the presentation of a joint analysis of Study NSABP B-31 and the North Central Cancer Treatment Group (NCCTG) study (N9831). Study NSABP B-31 was intended, in part, to characterize cardiotoxicity associated with HERCEPTIN use and to assess the value of serial cardiac monitoring during HERCEPTIN therapy as a predictor of cardiotoxicity and as an aid to early identification of cardiac toxicity.\n\nStudy NSABP B-31 evaluated the addition of HERCEPTIN to standard adjuvant chemotherapy. The chemotherapy regimen\nconsisted of four cycles of doxorubicin and cyclophosphamide (AC) followed by four cycles of paclitaxel every 3 weeks; patients were randomized to receive 1 year of HERCEPTIN, at the approved dose and schedule, during and following paclitaxel (Arm 2) or to paclitaxel alone (Arm 1). Patients in this study were required to have a baseline assessment of cardiac function with either multigated acquisition scan (MUGA) or echocardiogram and to have follow-up assessments at the completion of AC and at 6, 9, and 18 months after the initiation of paclitaxel with or without HERCEPTIN. \n\nEligible patients had a left ventricular ejection fraction (LVEF) measurement at baseline (prior to any therapy) that was within normal limits and no history of or active cardiac disease, including cardiomyopathy, congestive heart failure, prior myocardial infarction, or arrhythmia.\nPrior to initiation of HERCEPTIN (Arm 2), LVEF measurements were required to be at or above the radiology facility's lower limit of normal (LLN) and be no more than 15 points below baseline measurements. \n\nFor patients randomized to Arm 2 with asymptomatic decrease in LVEF, the following table lists the guidelines that were employed for dose modification of HERCEPTIN [table unable to be produced here].\n\nHERCEPTIN was permanently discontinued in patients with symptomatic cardiac toxicity. In the event that HERCEPTlN\nadministration was withheld or discontinued because of cardiotoxicity, paclitaxel was administered at the investigator's discretion.\n\nA total of 1019 patients were randomized to the HERCEPTIN-containing arm (Arm 2). Based on preliminary data and analyses through April 2005, 6.8% of patients were unable to initiate HERCEPTlN per the protocol because of decreased LVEF or symptoms of cardiac toxicity experienced during the AC portion of therapy. Among the evaluable patients who had adequate cardiac function and initiated HERCEPTIN, 30.5% required at least one dose delay because of asymptomatic decrease in LVEF or cardiac symptoms. \n\nIn 18.6% of patients, HERCEPTIN was discontinued prior to the completion of 1 year of therapy because of asymptomatic decrease in LVEF (14.3%) and symptomatic cardiac dysfunction/other cardiac toxicity (4.3%). \n\nIn addition, a statistically significant increase in the 3-year cumulative incidence of New York Heart Association Class III and IV congestive heart failure and cardiac death was observed in patients who received the HERCEPTIN-containing regimen (4.1%) compared with control (0.8%). \n\nThere were no cardiac deaths observed in patients who received the HERCEPTIN-containing reg
1014974
I' m not sure why at this point someone has not addressed surgery. Is she being followed by a cardiologist? Unless something else is the cause of what sounds to be heart failure, it seems like her regurg. is finally become symptomatic. Has no one approached her about surgery? Has she been told for some reason that she is inoperable? You definetely don't want to jump into surgery if you dont need to. I feel like I need more info to adequately answer your question though. What I would do is direct these questions towards her doctor, preferably a cardiologist. Has she had a heart cath yet?  If not, maybe see if its time. Email me if you find out more or if you have anymore questions. Im a RN in the cardiovascular ICU, I specialize in heart surgery. Good luck to you guys!
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May be HOCM (HypertrOphic Cardio Mypopathy)\n\nSudden Death Syndrome is the term, which is now used to describe unexpected and unexplained death occurring in apparently healthy young people. When the heart is examined by an expert pathologist a probable cardiac cause of death is found in the majority. Hypertrophic Cardiomyopathy (HCM) is the most common cause of sudden death in those under 30 years of age. It is a relatively uncommon heart disease although is estimated that ten thousand people in the United Kingdom have the condition.\n\nIn a healthy heart beat results from electrical signals starting at the top and passing down through the heart. HCM is a disease, which interrupts these vital electrical signals, which keep the heart beating. It is an incurable disease, which causes excessive thickening of the myocardium (the muscle in the heart). Heart muscle may thicken in individuals who have high blood pressure or who have prolonged athletic training, but in HCM patients the muscle thickens without an obvious cause.
946461
To be brutal it is pretty much impossible to completely recover. True CHF is weakening of the heart muscle to the point where it can no longer pump enough volume to keep the blood from backing up. The weakening itself is going to be there. It is very possible you were diagnosed very early and with proper diet and medication you are able to keep the area beating strong enough to not have problems. If you stopped taking care of yourself, however, it would return as it was. This is mostly a conjecture since I don't have any history or medication or what the MD actually told you but, no a complete disappearance of the disease isn't possible.
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Dilated cardiomyopathy. This is the most common form of cardiomyopathy. In this disorder, the left ventricle — your heart's main pumping chamber — becomes enlarged (dilated) and its pumping ability becomes less forceful. Although this type can affect people of all ages, it occurs most often in middle-aged people, with an incidence greater among men than women. Some people with dilated cardiomyopathy may have inherited the condition. \n\nHypertrophic cardiomyopathy. This type involves abnormal growth or thickening of your heart muscle, particularly affecting the muscle of the left ventricle. As thickening occurs, the heart tends to stiffen and the size of the pumping chamber may shrink, interfering with your heart's ability to deliver blood to your body. Hypertrophic cardiomyopathy can develop at any age, but the condition tends to be more severe among those diagnosed during childhood. Researchers have identified abnormal genes that predispose people to hypertrophic cardiomyopathy. Most affected people have a family history of the disease. \n\nRestrictive cardiomyopathy. The heart muscle in people with restrictive cardiomyopathy becomes rigid and less elastic, interfering with the expansion and filling of the heart's ventricles with blood between heartbeats or contractions. While restrictive cardiomyopathy can occur at any age, it tends to affect older people most often. It's much less common than the other types of cardiomyopathy. Restrictive cardiomyopathy can occur for no known reason (idiopathic) or may result from diseases elsewhere in the body that affect the heart. One example is amyloidosis, a rare condition in which abnormal proteins present in the blood are deposited into the heart. \n\nIn most people, the cause of cardiomyopathy is unknown. In some people, however, doctors are able to identify a cause or contributing factors, including some that affect the heart and cardiovascular system. For example, any of the following conditions may cause or contribute to a dilated and poorly functioning heart:\n\nSustained high blood pressure \nHeart valve problems \nHeart tissue damage from a previous heart attack \nChronic rapid heart rate \nMetabolic disorders, such as thyroid disease or diabetes \nNutritional deficiencies of essential vitamins and minerals, such as thiamin (vitamin B-1), selenium, calcium and magnesium \nPregnancy \nExcessive use of alcohol over many years \nAbuse of cocaine or antidepressant medications, such as tricyclic antidepressants \nUse of some chemotherapy drugs to treat cancer \nCertain viral infections, which may injure the heart and trigger cardiomyopathy \nHemochromatosis is a disorder in which your body doesn't properly metabolize iron, causing the accumulation of iron in your heart muscle. This can lead to a weakening of the heart muscle, resulting in the appearance of dilated cardiomyopathy.\n\nI hope this helps.  Good luck.
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You need to have her checked for Wolff-Parkinson-White Syndrome, spontaneous rapid heartbeat associated with an extra pathway in her heart.  There are treatments and medications available.\n\nIt can also be quite dangerous, so you want to make sure this is not what she has.
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Heart disease\nHigh blood pressure
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Heart failure is a common problem and any competent physician (especially a cardiologist) can deal with it.  It is a chronic problem that will require much medication optimization over the years and thus having someone local to care for her is probably better than trying to travel very far for an opinion. All of these big hospitals function as consultative centers anyway...they will expect you to have a doctor at home to follow their recommendations and again, the heart failure management goes way beyond one visit recommendation.  If you do take her places, obviously the Mayo Clinic is one of the best.
725852
Probably best to check with a medical doctor or a lactation consultant.
378755
be sure to let your MD know.  Could be dependent edema from the increased fluid loads given during the post op time, but could be signs of worse problems, such as a deep vein thrombosis- this could be lethal.  Also you might have CHF congestive heart failure, once again talk with your MD.  After that is done, you should be on a cardio rehab program that teaches proper eating, exercise and medication regiment.