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Life has many unexpected surprises. Sometimes the surprises are so profound and shocking that it is traumatic and very stressful. These stressful events may include the sudden loss of a loved one, a severe heated argument, a break-up with a spouse, a surprise party, an unexpected job loss, a natural disaster, a frightening medical diagnosis or others. Sometimes the surprise and shock of the event is so powerful it affects the heart and can lead to Broken Heart Syndrome.
Broken Heart Syndrome (BHS) also known as Takotsubo cardiomyopathy (TTS) or stress cardiomyopathy is a temporary heart condition that is triggered by severe stressful situations. Individuals respond to the stress with symptoms similar to a heart attack with chest pain, shortness of breath, congestive heart failure, and low blood pressure. The symptoms begin within a few minutes to hours after the severe, unexpected stress. The condition often quickly improves over days to a few weeks.
There are key differences between Broken Heart Syndrome and a heart attack, but it requires astute health care to differentiate between the conditions. In Broken Heart Syndrome, the coronary arteries are usually normal and do not have severe blockages or clots. Heart attacks caused by blood clots cause heart cells to die. This is not seen in BHS/TTS. The sudden burst of stress hormones and adrenaline causes the heart cells in the left ventricular area of the heart to become stunned or jolted, but the cells do not die. The heart cells recover from this jolt and there is no long-term damage, unlike a heart attack where there is permanent damage to the heart cells.
The preponderance and mechanisms for Broken Heart Syndrome are still being discovered and understood as it is a relatively newly recognized disorder first described in 1990. Medical literature shows that it occurs most commonly in postmenopausal middle-age or elderly women with the average age about 60. It can happen in men and younger women too, but is considerably less common.
Causes of Broken Heart Syndrome
The cause for Broken Heart Syndrome is still unclear. However, research suggests that some of the causes include hyperactivity of the sympathetic nervous system, i.e. the fight-flight part of the autonomic nervous system is in overdrive, along with problems with coronary vasospasm, microcirculation and estrogen deficiency.
Researchers in the December 2014 International Journal of Cardiology stated that BHS/TTS is one of the cardiac abnormalities most frequently induced by central nervous system disorders. They found a link with how some brain disorders can directly or indirectly affect the heart (brain-heart disorders). Brain disorders that can trigger the BHS/TTS include subarachnoid bleeding, epilepsy, ischemic stroke, intracerebral bleeding, migraine, encephalitis, traumatic brain injury, PRES syndrome, or ALS. They recommended that neurological support be provided when treating Broken Heart Syndrome.
Mitochondria and Heart Cells
Researchers are also looking at a different mechanism for the BHS or stress-induced cardiomyopathy. In a study published last month, researchers caused rats to experience BHS or stressed-induced cardiomyopathy. The rats were given an overdose of the medication isoproterenol. This medication is often used in cases of asthma, slow heart beat, or ventricular fibrillation to stimulate the heart and make it go faster. The experiment forced the rodents’ hearts into overdrive which caused the BHS/TTS cardiomyopathy. It caused heart muscle injury and blood pressure symptoms for a few weeks post challenge, but then the heart cells recovered from the damage. They were able to measure how the mitochondria within the heart cells functioned after the initial chemical jolt to the system. The results showed that the mitochondria and their function faltered. They went into a state of uncoupling of the mitochondria oxidative phosphorylation process, the process that mitochondria use to make ATP or energy.
The stress response induced by the medication essentially caused the heart cells’ energy generator to stall out and need repair. The mitochondria showed poor metabolic function, had weak, fragile membranes and high levels of oxidative stress. The mitochondria were bruised and battered, but not gone. One other factor seen was that calcium inside of the heart cells was misused for heart muscle contractions. This interfered with both systolic and diastolic blood pressure regulation; proper calcium function is needed for heart muscles to rhythmically contract.
A study entitled Mending a Broken Heart: The Role of Mitophagy in Cardioprotection offers further information about the breakdown of mitochondria health in heart cells. Heart cells have a clean up process when the mitochondria are damaged and need replacing. The mitochondria are removed through a process called mitochondrial autophagy or mitophagy. The damaged mitochondria are selectively removed to keep the undamaged parts of the cell healthy. Rather than the whole cell being removed from the workforce, only the damaged mitochondria are removed. This process of mitophagy occurs with regular cycles of breakdown of old, damaged mitochondria and the birth of new mitochondria. This is great news for those with sudden stress jolts to the heart. It gives further credence to the innate restorative process found in our bodies.
Mitochondrial Toxins
The study of mitochondria is a hot button in cardiology and may be the key powerful link for the development of Broken Heart Syndrome. Cardiovascular disease is indeed started or worsened with things that disrupt mitochondrial function, leading to heart problems including BHS/TTS. It is also important to learn that there are several chemicals and drugs that contribute to cardiac weakening by poisoning the mitochondria. This increases the susceptibility to Broken Heart Syndrome. Compounds identified so far include anthracyclines (particularly doxorubicin), mitoxantrone, cyclophosphamide, cisplatin, fluorouracil, imatinib, bortezomib, trastuzumab, arsenic trioxide, cyclosporine-A, zidovudine, lamotrigine, glycosides, lidocain, isoproterenol, nitroprusside, pivalic acid, alcohol, cocaine, pesticides, cadmium, mycotoxins, cyanotoxins, meat meal, or carbon monoxide. Mercury and arsenic are two of the most toxic pollutants to mitochondria. Even more agents exhibit cardiac abnormalities due to mitochondrion-toxicity only in animals or tissue cultures. Other drugs known to interfere with mitochondria health in various parts of the body include valproic acid, antiretrovirals, statins, aspirin, aminoglycoside antibiotics and chemotherapeutic agents, acetaminophen (Tylenol), metformin, beta blockers, and steroids. Researchers are insisting that “medicine, which has traditionally focused on organ pathophysiology, may well have to adjust its focus to include organelle pathology as an aspect of human disease”. Just looking at this list of medications makes one cringe for those heart patients who are on daily intake of statins and aspirin and use Tylenol periodically. How are their mitochondria functioning? What risk do they have for BHS or stress-induced cardiomyopathy?
Mitochondrial Support
It is impossible to forecast the future and know when a severe overwhelming stressor will occur, but we can be proactive in removing as many chemical exposures and stressors to the mitochondria as possible. We can also work to ensure proper nourishment for these energy generators. Just like a car engine needs proper maintenance so does a well-tuned body. Mitochondria are everywhere in the body but especially in the brain and heart. They require many different nutrients in order to function and to protect themselves. These nutrients include coenzyme Q10, thiamine, riboflavin, niacin, folate, vitamins C, D, and E, the amino acid acetyl-L-carnitine, lipoic acid, grape seed extract, quercetin, and omega 3 fatty acids. In a fast-paced, highly stressed world with nutrition-compromised diets, these nutrients are rapidly used up on a daily basis and must be thoroughly replenished to maintain health. In an effort to fortify the body to withstand things that inevitably occur, make sure that your mitochondria have fortification and a buffer to protect themselves against the shocking events of life. These nutrients provide vital life sustaining nourishment to mitochondria that are rapidly depleted during high levels of stress and output. Are you prepared for that time?
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Broken Heart Syndrome (BHS) also known as Takotsubo cardiomyopathy (TTS) or stress cardiomyopathy is a temporary heart condition that is triggered by severe stressful situations. Individuals respond to the stress with symptoms similar to a heart attack with chest pain, shortness of breath, congestive heart failure, and low blood pressure. The symptoms begin within a few minutes to hours after the severe, unexpected stress. The condition often quickly improves over days to a few weeks.
There are key differences between Broken Heart Syndrome and a heart attack, but it requires astute health care to differentiate between the conditions. In Broken Heart Syndrome, the coronary arteries are usually normal and do not have severe blockages or clots. Heart attacks caused by blood clots cause heart cells to die. This is not seen in BHS/TTS. The sudden burst of stress hormones and adrenaline causes the heart cells in the left ventricular area of the heart to become stunned or jolted, but the cells do not die. The heart cells recover from this jolt and there is no long-term damage, unlike a heart attack where there is permanent damage to the heart cells.
The preponderance and mechanisms for Broken Heart Syndrome are still being discovered and understood as it is a relatively newly recognized disorder first described in 1990. Medical literature shows that it occurs most commonly in postmenopausal middle-age or elderly women with the average age about 60. It can happen in men and younger women too, but is considerably less common.
Causes of Broken Heart Syndrome
The cause for Broken Heart Syndrome is still unclear. However, research suggests that some of the causes include hyperactivity of the sympathetic nervous system, i.e. the fight-flight part of the autonomic nervous system is in overdrive, along with problems with coronary vasospasm, microcirculation and estrogen deficiency.
Researchers in the December 2014 International Journal of Cardiology stated that BHS/TTS is one of the cardiac abnormalities most frequently induced by central nervous system disorders. They found a link with how some brain disorders can directly or indirectly affect the heart (brain-heart disorders). Brain disorders that can trigger the BHS/TTS include subarachnoid bleeding, epilepsy, ischemic stroke, intracerebral bleeding, migraine, encephalitis, traumatic brain injury, PRES syndrome, or ALS. They recommended that neurological support be provided when treating Broken Heart Syndrome.
Mitochondria and Heart Cells
Researchers are also looking at a different mechanism for the BHS or stress-induced cardiomyopathy. In a study published last month, researchers caused rats to experience BHS or stressed-induced cardiomyopathy. The rats were given an overdose of the medication isoproterenol. This medication is often used in cases of asthma, slow heart beat, or ventricular fibrillation to stimulate the heart and make it go faster. The experiment forced the rodents’ hearts into overdrive which caused the BHS/TTS cardiomyopathy. It caused heart muscle injury and blood pressure symptoms for a few weeks post challenge, but then the heart cells recovered from the damage. They were able to measure how the mitochondria within the heart cells functioned after the initial chemical jolt to the system. The results showed that the mitochondria and their function faltered. They went into a state of uncoupling of the mitochondria oxidative phosphorylation process, the process that mitochondria use to make ATP or energy.
The stress response induced by the medication essentially caused the heart cells’ energy generator to stall out and need repair. The mitochondria showed poor metabolic function, had weak, fragile membranes and high levels of oxidative stress. The mitochondria were bruised and battered, but not gone. One other factor seen was that calcium inside of the heart cells was misused for heart muscle contractions. This interfered with both systolic and diastolic blood pressure regulation; proper calcium function is needed for heart muscles to rhythmically contract.
A study entitled Mending a Broken Heart: The Role of Mitophagy in Cardioprotection offers further information about the breakdown of mitochondria health in heart cells. Heart cells have a clean up process when the mitochondria are damaged and need replacing. The mitochondria are removed through a process called mitochondrial autophagy or mitophagy. The damaged mitochondria are selectively removed to keep the undamaged parts of the cell healthy. Rather than the whole cell being removed from the workforce, only the damaged mitochondria are removed. This process of mitophagy occurs with regular cycles of breakdown of old, damaged mitochondria and the birth of new mitochondria. This is great news for those with sudden stress jolts to the heart. It gives further credence to the innate restorative process found in our bodies.
Mitochondrial Toxins
The study of mitochondria is a hot button in cardiology and may be the key powerful link for the development of Broken Heart Syndrome. Cardiovascular disease is indeed started or worsened with things that disrupt mitochondrial function, leading to heart problems including BHS/TTS. It is also important to learn that there are several chemicals and drugs that contribute to cardiac weakening by poisoning the mitochondria. This increases the susceptibility to Broken Heart Syndrome. Compounds identified so far include anthracyclines (particularly doxorubicin), mitoxantrone, cyclophosphamide, cisplatin, fluorouracil, imatinib, bortezomib, trastuzumab, arsenic trioxide, cyclosporine-A, zidovudine, lamotrigine, glycosides, lidocain, isoproterenol, nitroprusside, pivalic acid, alcohol, cocaine, pesticides, cadmium, mycotoxins, cyanotoxins, meat meal, or carbon monoxide. Mercury and arsenic are two of the most toxic pollutants to mitochondria. Even more agents exhibit cardiac abnormalities due to mitochondrion-toxicity only in animals or tissue cultures. Other drugs known to interfere with mitochondria health in various parts of the body include valproic acid, antiretrovirals, statins, aspirin, aminoglycoside antibiotics and chemotherapeutic agents, acetaminophen (Tylenol), metformin, beta blockers, and steroids. Researchers are insisting that “medicine, which has traditionally focused on organ pathophysiology, may well have to adjust its focus to include organelle pathology as an aspect of human disease”. Just looking at this list of medications makes one cringe for those heart patients who are on daily intake of statins and aspirin and use Tylenol periodically. How are their mitochondria functioning? What risk do they have for BHS or stress-induced cardiomyopathy?
Mitochondrial Support
It is impossible to forecast the future and know when a severe overwhelming stressor will occur, but we can be proactive in removing as many chemical exposures and stressors to the mitochondria as possible. We can also work to ensure proper nourishment for these energy generators. Just like a car engine needs proper maintenance so does a well-tuned body. Mitochondria are everywhere in the body but especially in the brain and heart. They require many different nutrients in order to function and to protect themselves. These nutrients include coenzyme Q10, thiamine, riboflavin, niacin, folate, vitamins C, D, and E, the amino acid acetyl-L-carnitine, lipoic acid, grape seed extract, quercetin, and omega 3 fatty acids. In a fast-paced, highly stressed world with nutrition-compromised diets, these nutrients are rapidly used up on a daily basis and must be thoroughly replenished to maintain health. In an effort to fortify the body to withstand things that inevitably occur, make sure that your mitochondria have fortification and a buffer to protect themselves against the shocking events of life. These nutrients provide vital life sustaining nourishment to mitochondria that are rapidly depleted during high levels of stress and output. Are you prepared for that time?
More...
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