Guest guest Posted February 10, 2005 Report Share Posted February 10, 2005 Hi All, See the discussion of the Love Hurts message after the CNN article. Lost love really can cause broken heart TRENTON, New Jersey (AP) -- Confirming the wisdom of the poets and philosophers, doctors say the sudden death of a loved one really can cause a broken heart. In fact, they have dubbed the condition " broken heart syndrome. " In a study published just in time for Valentine's Day -- February 14 - - doctors reported how a tragic or shocking event can stun the heart and produce classic heart attack-like symptoms, including chest pain, shortness of breath and fluid in the lungs. Unlike a heart attack, the condition is reversible. Patients often are hospitalized but typically recover within days after little more than bedrest and fluids and suffer no permanent damage to their hearts. In their study, published in Thursday's New England Journal of Medicine, doctors at s Hopkins University gave a name to the condition, demonstrated through sophisticated heart tests how it differs from a heart attack, and offered an explanation for what causes it. For centuries, doctors have known that emotional shocks can trigger heart attacks and sudden deaths. Broken heart syndrome, technically known as stress cardiomyopathy, is a different phenomenon. The s Hopkins doctors documented how a dayslong surge of adrenaline and other stress hormones can cause a decline in the heart's pumping capacity. The researchers theorized that the hormones probably cause tiny heart blood vessels to contract, but other explanations are possible. Until now, doctors " were trying to explain it away, but the pieces never quite fit, " said Dr. Hunter Champion, an assistant professor. " By our ability to recognize it, we've saved people from getting unnecessary (heart) procedures. " Champion and colleagues treated 19 emergency room patients with the syndrome between 1999 and 2003. Many were grieving over the death of a husband, parent or child. Other triggers included a surprise party, car accident, armed robbery, fierce argument, court appearance and fear of public speaking. MRIs and other tests showed they had not suffered heart attacks. Other doctors have since told Champion that they have seen the same thing, and researchers in Japan and Minnesota have reported similar cases. " This is probably something that happens all the time, " but most people do not seek treatment, Champion said. Dr. Shindler, director of the echocardiography lab at Wood Medical School in New Brunswick, New Jersey, said it apparently happened to his wife last week, when she was upset over her sister's death. The wife, who also is a doctor, sensed abnormalities in her heart. Testing showed abnormal rhythms, but she is fine now. Shindler said the researchers' conclusions make sense, given the well- known link between the brain and heart, and offer the first explanation he has heard for the phenomenon. Dr. Sidney , former American Heart Association president and director of University of North Carolina's Center for Cardiovascular Science and Medicine, said the study will lead more ER and heart doctors to consider the syndrome when examining patients with chest pain. " We'll definitely be paying more attention now than before " to patients who are grieving, Shindler said. On Sat, 11 Dec 2004 11:21:09 -0800, Al Pater <old542000@...> wrote: >Hi All, > > Stress costs us calories? This appears to me to be explained >in the pdf-available publication. See the Medline abstract and >pdf excerpts below. > > Here is a definition of a techincal term for our assistance: > > Adrenergic: Refers to neurons that use catecholamines >as neurotransmitters at a synapse when a nerve impulse >passes i.e. The sympathetic fibres. Also refers to neurones >that are activated by, characteristic of or secreting >adrenaline (adrenaline) or substances with similar activity. > > The descriptions of the role of energy in the cost of stress >are in the pdf text following the Medline abstract. See also, >the commended reading references at the bottom. > > Curr Opin Clin Nutr Metab Care. 2004 Mar;7(2):169-73. >Relationship between stress, inflammation and metabolism. >Seematter G, Binnert C, JL, Tappy L. > >PURPOSE OF REVIEW: Various threatening stimuli, such as pain, low blood >pressure, or infection, elicit a set of neuroendocrine responses that include an >increased secretion of catecholamines and glucocorticoid from the adrenal gland >and activation of the sympathetic nervous system. These hormonal secretions >allow a " fight or flight " response by mobilizing endogenous substrate. They also >exert anti-insulin actions, and may in the long term induce a state of insulin >resistance. In addition, stress stimulates inflammatory mediators in mononuclear >cells. Given the possible role of low-grade inflammation in chronic metabolic >disorders, this suggests that stress may be a factor in the development of >insulin resistance and the metabolic syndrome. RECENT FINDINGS: Studies reviewed >in this article cover: (1) the metabolic and haemodynamic effects of stress in >healthy and insulin-resistant individuals; (2) the relationship between stress >and inflammation and the role of the autonomic nervous system; and (3) some >factors known to modulate the neuroendocrine responses to stress. Future >perspectives, together with some hints regarding the role of neurotrophins such >as brain-derived neurotrophic factor, are delineated. SUMMARY: Recent work >performed in the field has indicated that stress may be a significant factor in >the pathogenesis of metabolic disorders. Nutritional intervention or >pharmacological agents targeted at modulating stress should be investigated. > PMID: 15075708 [PubMed - indexed for MEDLINE] > > ... Introduction >The human body has developed an intricate set of >neural and endocrine mechanisms that aim at maintain- >ing a constant `internal milieu':a process called `home- >ostasis '.In order to be able to cope with special >situations,the organism has,however,to alter the >internal milieu.This occurs for instance during physical >exercise when endogenous substrates are mobilized from >the adipose tissue,the liver,and skeletal muscles,to >ensure sufficient energy provision to the working >muscle.It has been recognized for more than 50 years >that the human body,when under acute aggression, >elicits a set of rather stereotyped neuroendocrine >responses.This set of responses is triggered by infection >and trauma,but also by fear or psychological stress.It >involves activation of the sympathetic nervous system >and secretion of epinephrine from the adrenal medulla >and activation of the hypothalamo –pituitary adrenal axis, >the latter resulting in the secretion of glucocorticoids >from the adrenal cortex.The combined effects of these >neuroendocrine alterations are the mobilization of lipids >from the adipose tissue and of glucose from hepatic >glycogen,to ensure ample energy availability together >with the development of an acute state of insulin >resistance,which diverts glucose away from skeletal >muscle to ensure glucose supply to the brain.Simulta- >neously,vasoconstriction occurs in the splanchnic area >and vasodilation takes place in skeletal muscle,allowing >an ample supply of oxygen and energy substrates to the >muscle [1 ].These coordinated responses allow a fiight or >flight response essential to avoid or to survive predators. >These responses to threat or stress constitute a >controlled deviation from homeostasis,which has been >called `allostasis '[2,3 ].The stress response was probably >essential in ancient times to survive when predators were >roaming around.This threat has now essentially >disappeared in our industrialized societies.The stress >responses,however,remain an important defence against >acute trauma or severe infection. >Stress responses occur not only in response to severe >physical aggression,but can be elicited by emotional >stimuli or professional stress.Furthermore,stress re- >sponses show considerable interindividual variability, >and some people may suffer more important and long- >lasting stress responses than others when subjected to >the same stress [4 ]. [snip] Hi All, The above introduction is maybe an appropriate prelude to the below, suggesting that emotional stress, to which CRers may be less susceptible, cause heart problems. Both references (1, 2) below are pdf-available. Nature 10 Feb 2005 433 (7026) A broken heart harms your health Ebert Emotional stress causes an unusual type of heart disease. Being 'broken-hearted' as a result of emotional trauma may be a more apposite turn of phrase than we imagined. US researchers have shown how sudden emotional stress can release hormones that stun the heart into submission, resulting in symptoms that mimic a typical heart attack. People suffering from stress cardiomyopathy, or 'broken-heart syndrome', seem to be having a heart attack: they have chest pain, fluid in the lungs, shortness of breath and heart failure. But although the ability of the heart to pump is significantly reduced and the heart muscle is weakened, it is not killed, or infarcted, as in a classic attack. " The tissue is alive, " says Hunter Champion of s Hopkins Hospital in Baltimore, land, who led the study. " It's just not moving. " In 1999, Champion and a fellow s Hopkins cardiologist, Ilan Wittstein, noticed something unusual about certain heart-attack patients. They were particularly struck by results from postmenopausal women who had experienced an intense emotional event before their attack, such as the loss of a loved one or a court appearance. These patients had unique electrocardiogram and ultrasound patterns, lacked coronary artery disease and recovered quickly. Between November 1999 and September 2003, Champion and Wittstein gathered biochemical and imaging data for 19 patients suffering from stress cardiomyopathy and compared them with 7 classic heart-attack patients. The researchers found that initial levels of hormones called catecholamines (particularly adrenaline) in the patients with broken heart syndrome were 2 to 3 times greater than those in classic heart-attack patients, and between 7 and 34 times greater than in healthy people. " This is the first time the strong association of elevated catecholamine levels and this syndrome has been shown, " says Champion. Japan ahead Stress cardiomyopathy has been known for ten years in Japan, where it is called takotsubo cardiomyopathy, after an octopus trap with a round bottom that resembles the appearance of a stunned heart. The disease has so far gone relatively unrecognized in the West, but studies such as Champion's are bringing it to the fore, says Barry Maron, a cardiologist at the Minneapolis Heart Institute Foundation, Minnesota. Maron describes the disease in this month's Circulation1 and Champion's study is being published online by the New England Journal of Medicine2. It will be important that doctors appreciate the difference between broken-heart syndrome and classic heart disease when examining patients, says Maron. " It is a separate disease entity that has to be distinguished in differential diagnosis. " By spotting broken-heart sufferers, " unnecessary procedures could be averted " , says Champion, referring to defibrillator implants. What's more, as doctors learn to recognize the syndrome's unique features, more cases are likely to be documented. " This may be the tip of the iceberg, " says Champion. " It may occur much more frequently than we think. " The next step for the s Hopkins team is to work out the mechanism by which stress hormones stun the heart. They also aim to set up a stress cardiomyopathy registry to gather information from broken-hearted patients. This, Champion hopes, could reveal whether there is a genetic predisposition for the disease, and why older women seem to be more vulnerable. References 1. Sharkey SW, Lesser JR, Zenovich AG, Maron MS, Lindberg J, Longe TF, Maron BJ. Acute and reversible cardiomyopathy provoked by stress in women from the United States. Circulation. 2005 Feb 1;111(4):472-9. PMID: 15687136 [PubMed - in process] http://tinyurl.com/4q7y7 2. I. S. Wittstein and Others N Engl J Med 352, 539-548 (2005). ABSTRACT Background Reversible left ventricular dysfunction precipitated by emotional stress has been reported, but the mechanism remains unknown. Methods We evaluated 19 patients who presented with left ventricular dysfunction after sudden emotional stress. All patients underwent coronary angiography and serial echocardiography; five underwent endomyocardial biopsy. Plasma catecholamine levels in 13 patients with stress-related myocardial dysfunction were compared with those in 7 patients with Killip class III myocardial infarction. Results The median age of patients with stress-induced cardiomyopathy was 63 years, and 95 percent were women. Clinical presentations included chest pain, pulmonary edema, and cardiogenic shock. Diffuse T-wave inversion and a prolonged QT interval occurred in most patients. Seventeen patients had mildly elevated serum troponin I levels, but only 1 of 19 had angiographic evidence of clinically significant coronary disease. Severe left ventricular dysfunction was present on admission (median ejection fraction, 0.20; interquartile range, 0.15 to 0.30) and rapidly resolved in all patients (ejection fraction at two to four weeks, 0.60; interquartile range, 0.55 to 0.65; P<0.001). Endomyocardial biopsy showed mononuclear infiltrates and contraction-band necrosis. Plasma catecholamine levels at presentation were markedly higher among patients with stress-induced cardiomyopathy than among those with Killip class III myocardial infarction (median epinephrine level, 1264 pg per milliliter [interquartile range, 916 to 1374] vs. 376 pg per milliliter [interquartile range, 275 to 476]; norepinephrine level, 2284 pg per milliliter [interquartile range, 1709 to 2910] vs. 1100 pg per milliliter [interquartile range, 914 to 1320]; and dopamine level, 111 pg per milliliter [interquartile range, 106 to 146] vs. 61 pg per milliliter [interquartile range, 46 to 77]; P<0.005 for all comparisons). Conclusions Emotional stress can precipitate severe, reversible left ventricular dysfunction in patients without coronary disease. Exaggerated sympathetic stimulation is probably central to the cause of this syndrome. Al Pater. Quote Link to comment Share on other sites More sharing options...
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