Hypomagnesemia symptoms and causes list

Hypomagnesemia symptoms and causes – tables from [1, Slatoplosky, et al]

***This is an initial list of magnesium deficiency symptoms and causes. People with these conditions are at risk of chronic magnesium losses from bone stores and the resulting osteoporosis. Magnesium is used as a buffer by the kidneys and gastrointestinal tract when conditions are too acidic – frequently with our modern diet and beverages.

Magnesium supplements given orally during conditions of poor gastrointestinal absorption will be more likely to cause loose stools Magnesium ions can cause relaxation of the smooth muscles lining the intestines and watery bowel movements can occur – the common side effect is not similar to explosive diarrhea unless a very large dose is taken. Magnesium glycinate may be a better absorbed form. Lower more frequent doses are more likely to be absorbed well – 200 mg magnesium glycinate three times a day may result in more retention than 500 mg of a standard form two times a day. The RDA is lower and the UL – Upper Limit is a measly 325 mg but loose stools is really the only oral side effect. Intravenous use can be dangerous due to the rapid changes it can cause in the heart muscle that can trigger a stroke.Dosing Example for someone with a condition or medication that causes chronic wasting of magnesium stores:

“Maintenance therapy may require oral administration of Mg2+ oxide (400 mg twice daily or three times daily) for as long as the risk factors for Mg2+ deficiency exist. Oral Mg2+ gluconate (500 mg twice daily or three times daily) can also be used.” [1, p2293]

***This dosage is in reference to repletion needs for chronic magnesium deficiency typically due to decreased gastrointestinal absorption or increased renal losses.

Ideally our bodies expect a balance of magnesium in everything we eat and drink. Historically it was very rich in the water and soil and nature. An increase in insulin levels is the only main way the body can react to low magnesium levels. Historically an increased appetite would lead to increased magnesium levels because it was so common in the water and food supply. However it isn’t a primary fertilizer – the plants grow with minimal amounts and water softeners and bottling companies take it out along with the calcium and other ‘hard’ minerals. Our food supply and population is low in magnesium and when there is a high calcium intake the body loses more magnesium and preferentially absorbs the calcium. Calcium was never abundant directly in the soil and food supply – bird shells and tiny fish or animal bones would be rich sources and tiny amounts were available throughout the rest of the food and water supplies. Our bodies conserve calcium and waste magnesium because that is what used to work for us.Due to who knows what historical permutations, only sodium and potassium are officially considered electrolytes and have regulation standards for content in water supplies. The soil and everything consumed and drank was rich in magnesium ages ago as our bodies were adapting – before world flooding over the millennia washed nutrients to sea (brine pits are a source of many crucial nutrients and seaweed is a source of iodine because it filters it from the sea water – ocean vegetables for the next season are going to be contaminated from the nuclear accident).  Electrolyte beverages in our current market rarely have magnesium – the Glaceau brand of Smart Water does.

Magnesium can also be absorbed through the skin from Epsom salt baths, foot soaks or skin creams that have had it added (a compounding pharmacist can make it if prescribed). [35 B, 36 B,37 B] Magnesium has been successfully used within emergency inhalers for asthma.
____________________________________________________________________________
Clinical consequences of hypomagnesemia     [tables from 1,Slatoplosky, et al] ***symptom list
Electrolyte abnormalities
                Hypokalemia
                Hypocalcemia
Neuromuscular
                Carpopedal spasm
                Tetany
                Muscle cramps
                Muscle fasciculations
Neurologic
                Vertigo                 / dizziness
                Nystagmus           /  involuntary eye movement
                Aphasia                /  loss of speech abilities, may be temporary [12]
                Hemiparesis
                Depression
                Delirium
                Choreoathetosis    [10]
Cardiovascular
                Ventricular arrhythmias
                Torsade de points
                Supraventricular tachycardia
                Enhanced sensitivity to digoxin
Causes of Magnesium deficiency    [1]
***triggers and conditions that lead to magnesium wasting that may be genetic, pharmaceutical side effect related or possibly preventable –ie quit drinking too much alcohol –also smoking [14] needs to be added to this list [Bruerger’s vasculitis] and proton pump inhibitors for some people.
Gastrointestinal
                Malnutrition
                Malabsorption
                Chronic diarrhea
                Primary infantile hypomagnesemia
                Nasogastric suction
                Intestinal fistula
Renal
                Congenital magnesium wasting
                Bartter syndrome
                Gitelman syndrome
                Postobstructive diuresis
                Diuretic phase of ATN         [11]
                Loop and thiazide diuretics   [3,4, 5,6]
                Cisplatin
                Aminoglycosides   [7-drug names, 9 – kwashiorkor reference]
                Pentamidine
                Foscarnet
                Cyclosporin A
                Tacrolimus
Endocrine
                Hyperparathyroidism
                Hyperthyroidism
SIADH
                Hyperaldosteronism    [8 – edematous malnutrition reference]
Redistribution
                Hungry bone syndrome
                Acute pancreatitis
                Blood transfusions
                Insulin treatment
Miscellaneous
                Diabetes                   [59]
                Chronic alcoholism

“In general, Magnesium deficiency is the result of either gastrointestinal or renal losses. If no cause is readily apparent, then one can distinguish between gastrointestinal and renal losses by measuring the 24-H urinary MG²+ excretion or fractional excretion of Mg2+. The normal response of the kidney to Mg2+ depletion is to reduce Mg2+ excretion to low levels. The measurement of 24-H urinary Mg2+ excretion of  more than 30 mg in a person with normal renal function and hypomagnesemia indicates renal Mg2+ wasting. If Mg2+ deficiency is suspected in the absence of hypomagnesemia, then one might consider evaluating the renal excretion of Mg2+ in response to an intravenous Mg2+ load. [20,21] this, however, is rarely done in clinical practice. In the presence of unexplained hypocalcemia or hypokalemia, a trial of Mg2+ administration is more commonly performed.” (Slatoplosky, et al, p2292 ) [1]

/Disclaimer: Opinions are my own and  the information is provided for educational purposes within the guidelines of fair use. While I am a Registered Dietitian this information is not intended to provide individual health guidance. Please see a health professional for individual health care purposes./

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Bibliography
1.   1.   [jasn.asnjournals.org/content/20/11/2291.long]  Kevin J. Martin,  Esther A. González and Eduardo Slatopolsky, Clinical Consequences and Management of Hypomagnesemia,  doi: 10.1681/ASN.2007111194 (JASN November 1, 2009 vol. 20 no. 11 2291-2295)
3.       Michael E. Ernst and Marvin Moser, “Use of Diuretics in Patients with Hypertension,” New England Journal of Medicine 361, no. 22 (2009): 2153-2164.

“However, thiazides are now used in substantially smaller doses, and the term low-dose thiazide has become synonymous with hydrochlorothiazide at a dose of 12.5 to 25 mg per day (or the equivalent dose of another thiazide). Approximately 50% of patients will respond initially to these low doses. In the Systolic Hypertension in the Elderly Program (SHEP),34 chlorthalidone given at a dose of 12.5 mg per day controlled blood pressure, for several years, in more than 50% of patients. Increasing the dose of hydrochlorothiazide from 12.5 to 25 mg per day may result in a response in an additional 20% (approximately) of patients; at 50 mg per day, 80 to 90% of patients should have measurable decreases in blood pressure.35 Increased electrolyte losses at the higher doses of diuretics may preclude their routine use.” [3]                      (***diabetes after a year of use is also a risk)

List of Thiazide and Thazide-like Diuretics (water pills) used in the Treatment of High Blood Pressure     4.   [infobloodpressure.com/drugs/thiazide-list.html ]
  • Bendroflumethiazide (Naturetin)
  • Benzthiazide               (Exna)
  • Chlorothalidone          (Hygroton, Thalitone)
  • Chlorothiazide            (Diurigen, Duril)
  • Hydrochlorothiazide   (Esidrix, Hydrodiuril, Hydro-Par, Microzide, Oretic)
  • Hydroflumethiazide    (Diucardin, Saluron)
  • Indapamide                 (Lozol)
  • Metolazone                 (Mykrox, Zaroxolyn, Diulo)
  • Methychothiazide       (Aquatensen, Enduron)
  • Polythiazide                (Renese)
  • Quinethazone             (Hydromax)
  • Trichlormethiazide      (Diurese, Metahydrin, Naqua)

Examples of loop diuretics include:

  • Bumetanide
  • Ethacrynic acid (Edecrin)
  • Furosemide (Lasix)
  • Torsemide (Demadex)
Aminoglycosides are a group of antibiotics including at least eight drugs: amikacin, gentamicin, kanamycin, neomycin, netilmicin, paromomycin, streptomycin, and tobramycin.
7. Read more on aminoglycoside antibiotics: [healthline.com/galecontent/aminoglycosides#ixzz1HdHbebJf]
Healthline.com – Connect to Better Health

8. [icmr.nic.in/ijmr/2009/November/1128.pdf ] Tahmeed Ahmed, Sabuktagin Rahman & Alejandro Cravioto, Oedematous malnutrition,  Indian J Med Res 130, November 2009, pp 651-654

Hyperaldosteronism may be occurring in edematous malnutrition:

Anti-diuretic factor in the urine of children with nutritional oedema: Nutritional oedema is associated with an increased secretion of an anti-diuretic substance (probably anti-diuretic hormone) which prevents the normal excretory response to water administration. Gopalan and Venkatachalam15 in a study furnished indirect proof of the effect of posture on the urinary response to water load in normal subjects and in cases of nutritional oedema. The normal subjects were found to excrete over 100 per cent of ingested water within 4 h of ingestion in the recumbent posture, while in the erect posture they excreted only 80 per cent. In case of nutritional oedema, the urinary excretion was found to be much lower than in the normal subjects in both recumbent and erect postures. The effect of dietary protein deficiency on the hepatic inactivation of ADH in rats has also been investigated. It was found that the rats maintained on low-protein, low-calorie diets showed a delayed and incomplete response to a water load, and that the livers of these animals showed a reduced capacity for inactivating ADH (Gopalan & Srikantia, unpublished).

Role of ferritin and aldosterone: Srikantia observed presence of ferritin in children with kwashiorkor16. With a view to reveal the precise role of ferritin in the pathogenesis of nutritional oedema, Gopalan and Srikantia17 investigated the sequence of changes occurring in induced protein and calorie under-nutrition with focus on oedema formation in monkeys. O n the basis of the findings, they suggested that calorie-protein undernutrition leads to structural and functional changes in the liver, further leading to defective inactivation of ADH. Active ferritin is released from damaged liver leading to increased secretion of ADH. The net result is water retention. Among other factors, aldosterone, the salt retaining hormone, which is known for influencing water metabolism by altering renal tubular reabsorption of sodium, is also known to be inactivated by the liver. Altered aldosterone metabolism has been reported in diseases of the liver. Associated hyperaldosteronism could account for the sodium retention18. In oedematous children aldosterone secretion becomes higher during loss of oedema19.

“In a clinical trial, the administration of N-acetylcysteine, a glutathione precursor, resulted in more rapid resolution of oedema in kwashiorkor31. These associations between oxidative stress and kwashiorkor indicate that antioxidant depletion may cause kwashiorkor which can therefore be prevented with antioxidant supplementation.”

9. [ajcn.org/content/89/2/592.long]
Reduced production of sulfated glycosaminoglycans occurs in Zambian children with kwashiorkor but not marasmus also good –

10. Excerpt from wikipedia / Choreoathetosis 
10. [en.wikipedia.org/wiki/Chorea_%28disease%29]

Choreia is characterized by brief, quasi-purposeful, irregular contractions that are not repetitive or rhythmic, but appear to flow from one muscle to the next.These ‘dance-like’ movements of choreia (from the same root word as “choreography”) often occur with athetosis, which adds twisting and writhing movements.Choreia can occur in a variety of conditions and disorders.

  • Choreia is a primary feature of Huntington’s disease, a progressive neurological disorder.
  • Twenty percent of children and adolescents with rheumatic fever develop Sydenham’s chorea as a complication.
  • Choreia gravidarum is rare type of choreia which is a complication of pregnancy.
  • Choreia may also be caused by drugs (levodopa, anti-convulsants, anti-psychotics), metabolic disorders, endocrine disorders, and vascular incidents.
  • Ataxia telangiectasia
  • Wilson’s disease, a genetic disorder that leads to toxic levels of copper in the body
  • McLeod syndrome,is a genetic disorder that may affect the blood, brain, peripheral nerves, muscle and heart. Common features include peripheral neuropathy, cardiomyopathy and hemolytic anemia. Other features include limb chorea, facial tics, other oral movements (lip and tongue biting), seizures, a late-onset dementia and behavioral changes.
11. Diseases of the kidney and urinary tract  By Robert W. Schrier  page 2303 hypophosphatemia, diuretic phase of ATN, acute tubule nephropathy

Aphasia is a total or partial loss of the ability to speak correctly or to understand or comprehend what is being said. It may be caused by brain injury or disease. It’s most often caused by a stroke that injures the brain’s language center, located on the left side of the brain in most people. Some people with aphasia recover quickly and completely after a stroke. Others may have permanent speech and language problems.

  • Speech problems can range from trouble finding words to being unable to talk at all. Some stroke patients describe it as “having trouble getting words out.”
  • Some people have problems understanding what others are saying or have trouble with reading, writing or math.
  • In other cases, a person with aphasia may have trouble talking but can understand what others say perfectly.
Each person’s speech and language problem is unique. A language professional (speech therapist) can help set up a treatment plan and help others understand the needs of a person with aphasia.
For stroke information, call the American Stroke Association at 1-888-4-STROKE.
 
13. Garrison M. Tong and Robert K. Rude, “Magnesium Deficiency in Critical Illness,” Journal of Intensive Care Medicine 20, no. 1 (January): 3 -17.

14. Satoru Torii et al., “Magnesium Deficiency Causes Loss of Response to Intermittent Hypoxia in Paraganglion Cells,” Journal of Biological Chemistry 284, no. 28 (July 10, 2009): 19077 -19089. (free article)[jbc.org/content/284/28/19077.full]
*** Magnesium deficiency is found to reduce the normal response to hypoxia (lack of oxygen) of increasing adrenal gland production of erthyopoietin and endothelial vascular growth factor. This could suggest fewer red blood cells and weaker capillary and blood vessel structure in the magnesium deficient individual with breathing issues or other reduced oxygen situations (smokers).

15. “Possible Interactions with: Magnesium,” [umm.edu/altmed/articles/magnesium- 000968.htm.]

16. B Grimaldi, “The central role of magnesium deficiency in Tourette’s syndrome: causal relationships between magnesium deficiency, altered biochemical pathways and symptoms relating to Tourette’s syndrome and several reported comorbid conditions,” Medical Hypotheses 58, no. 1 (1, 2002): 47-60.

17. G Eby, “Rescue treatment and prevention of asthma using magnesium throat lozenges: Hypothesis for a mouth–lung biologically closed electric circuit☆,” Medical Hypotheses 67, no. 5 (2006): 1136-1141.

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22. P Chambers, “Lone atrial fibrillation: Pathologic or not?,” Medical Hypotheses 68, no. 2 (2007): 281-287.

23. “Complementary vascular-protective actions of magnesium and taurine: A rationale for magnesium taurate,” [medical-hypotheses.com/article/S0306-9877(96)90007-9/abstract.]

24. Abe E. Sahmoun and Brij B. Singh, “Does a higher ratio of serum calcium to magnesium increase the risk for postmenopausal breast cancer?,” Medical Hypotheses 75, no. 3 (9, 2010): 315-318.

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29. E Planells et al., “Effect of magnesium deficiency on vitamin B2 and B6 status in the rat,” Journal of the American College of Nutrition 16, no. 4 (August 1997): 352-356.

30. Sivan Ben-Avraham et al., “Dietary strategies for patients with type 2 diabetes in the era of multi-approaches; review and results from the Dietary Intervention Randomized Controlled Trial (DIRECT),” Diabetes Research and Clinical Practice 86 Suppl 1 (December 2009): S41-48.

31. “Utility of magnesium as antiarrhythmic agent reviewed. – Health & Medicine Week | HighBeam Research – FREE trial,” [highbeam.com/doc/1G1-121345520.html.]

32. Barbara Chipperfield and JohnR. Chipperfield, “Relation of Myocardial Metal Concentrations to Water Hardness and Death-Rates from Ishchaemic Heart Disease,” The Lancet 314, no. 8145 (October 6, 1979): 709-712.

33. Barbara Chipperfield et al., “Magnesium and Potassium Content of Normal He3art Muscle in Areas of Hard and Soft Water,” The Lancet 307, no. 7951 (January 17, 1976): 121-122.

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37. “Magnesium Treatment for Sudden Hearing Loss – The Annals of Otology, Rhinology & Laryngology | HighBeam Research – FREE trial,”[highbeam.com/doc/1P3-679636211.html#.]

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42. Yuhei Kawano et al., “Effects of Magnesium Supplementation in Hypertensive Patients : Assessment by Office, Home, and Ambulatory Blood Pressures,” Hypertension 32, no. 2 (August 1, 1998): 260-265.

43. Robert E. Kleiger et al., “Effects of chronic depletion of potassium and magnesium upon the action of acetylstrophanthidin on the heart,” The American Journal of Cardiology 17, no. 4 (April 1966): 520-527.

44. Andrew D Hershey, “Current approaches to the diagnosis and management of paediatric migraine,” The Lancet Neurology 9, no. 2 (2, 2010): 190-204.

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[59.  todaysdietitian.com/newarchives/td_1104p37.shtml]

Victoria Shanta-Retelny, RD, LD, The Magnesium-Diabetes Connection, Today’s Dietitian, Vol. 6, No. 11, p. 37, November 2004

 

Magnesium references From Bibliography for Dietitian Recommends Stop Vitamin D and Calcium ASAP 
8B. http://www.ijkd.org/index.php/ijkd/article/view/140 Assadi, F., Hypomagnesemia, An Evidence-Based Approach to Clinical Cases, (Iranian Journal of Kidney Diseases, Vol 4, No 1 (2010)
18 B. http://www.ncbi.nlm.nih.gov/pubmed/20081245 Magdalena Bujalska, Helena Makulska-Nowak, Stanis³aw W. Gumuka Magnesium ions and opioid agonistsin vincristine-induced neuropathy , Department of Pharmacodynamics, Medical University of Warsaw, Krakowskie Przedmieoecie 26/28, PL 00-927 Warszawa, Poland
19 B. Magnesium: an emerging drug in anaesthesia, , Editorial I, M. F. M. James, British Journal of Anaesthesia, 103 (4): 465-7 (2009) DOI:10.1093/bja/aep242
23 B. http://www.ncbi.nlm.nih.gov/pubmed/17823441 Dai Q, Shrubsole MJ, Ness RM, Schlundt D, Cai Q, Smalley WE, Li M, Shyr Y, Zheng W., The relation of magnesium and calcium intakes and a genetic polymorphism in the magnesium transporter to colorectal neoplasia risk. ( Am J Clin Nutr. 2007 Sep;86(3):743-51)
24 B. Joan L Caddell, Geriatric cachexia: a role for magnesium deficiency as well as for cytokines?, Letter to the Editor, , (Am J Clin Nutr 2000;;71:844-53. pp 851-853)
25 B. Carl J Johnson, M.D., Donald R. Peterson, M.D., Elizabeth K. Smith, PhD, Myocardial tissue concentrations of magnesium and potassium in men dying suddenly from ischemic heart disease, (Am J Clin Nutr 32: MAY 1979, pp 967-970)
29 B. Geeta Sharma and Charles f Stevens, A mutation that alters magnesium block of N-methyl-D-aspartate receptor channels, Pub: Proceedings of the National Academy of Sciences of The United States 93.n17 (August 20, 1996): pp9259+. InfoTrac General Science Collection.
30 B. Beasley R, Aldington S, Magnesium in the treatment of asthma..Medical Research Institute of New Zealand, Wellington, New Zealand., Richard.Beasley@mrinz.ac.nz, Curr Opin Allergy Clin Immunol. 2007 Feb;7(1):107-1
32 B. Maged M. Costantine, MD, Steven J. Weiner, MS, Effects of Antenatal exposure to Magnesium Sulfate on Neuroprotection and Mortality in Preterm Infants: A Meta Analysis, Obstet Gynecol. 2009 August; 114(2 Pt 1): 354-364 DOI:10.1097/AOG0b013e3181ae98c2
33 B. Burton M. Altura, Bella T. Altura and Anthony Carella., Magnesium deficiency-induced spasms of umbilical vessels: relation to preeclampsia, hypertension, growth retardation. Pub:Science, 221 (July 22, 1983): pp376(2)
34 B. Burton M. Altura, Bella T. Altura, Asefa Gebrewold, Harmut Ising and Theo Gunther, Magnesium deficiency and hypertension: correlation between magnesium-deficient diets and microcirculatory changes in situ.,. Pub: Science, 223.(March 23, 1984): pp1315(3).
37 B. [ahavaus.com/site/dead_sea_wonders.html] Line of skin care products containing magnesium.
42 B. Magnesium intake from food and supplements is associated with bone mineral density in healthy older white subjects. (elderly health), Kathryn M. Ryder, Ronald I Shorr, Andrew J. Bush, Tamara Harris, Katie Stone and Frances A Tylavsky. Journal of the American Geriatrics Society, 53.11 (Nove 2005): p1875-1881. Academic One File. Web. 13 Dec. 2010
43 B. DASH Diet May Cut Heart Disease Risk, – source John Hopkins Medicine, Today’s Dietitian, Vol . 12, No. 10, Oct. 2010, p 25
44 B. Christine Feillet-Coudray, Charles Coudray, Zjean-Claude Tressol, Denise Pepin, Andrzej Mazur, Steven A Abrams, Exchangeable magnesium pool masses in healthy women: effects of magnesium supplementation, Yves Rayssiguier, Am J Clin Nutr 2002;75;72-8
45 B. [.highbeam.com/doc/1P3-2180507851.html] “Researchers Identify Protein that Regulates Magnesium and Can Restart Stem Cells.” Targeted News Service. Targeted News Service LLC. 2010. HighBeam Research. 16 Feb. 2011 . “An international team led by researchers at the University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School has published new findings that demonstrate how a specific protein controls the body’s ability to balance magnesium levels. Magnesium is an essential element for good health and is critical to more than 300 biochemical reactions that occur in the body. “Currently more than half of the US population does not consume an adequate amount of magnesium in their diet,” said Alexey G. Ryazanov, Ph.D., one of the study’s authors and a professor of pharmacology and member of The Cancer Institute of New Jersey at UMDNJ-Robert Wood Johnson Medical School. “Magnesium deficiency may be associated with many medical disorders including hypertension, atherosclerosis, anxiety, asthma and a host of other disorders.” “The team of researchers from the United States, France and Poland demonstrated for the first time that a protein called TRPM7 plays a key role in the maintenance of magnesium homeostasis (balance within the body) and is essential for proliferation of embryonic stem cells.”
77 B. Neuromed Phamaceuticals and Merck and Co., Inc. Announce Agreement for Novel N-type Calcium channel Compounds, from Business Wire, March 20, 2006, High Beam Research – **Neuromed is a pharmaceutical company focusing on calcium channel blockers. “blocking pain signaling through the N-type calcium channel is a novel approach for the treatment of pain” said Christopher Gallen,MD, PhD, President and Chief Executive Officer of Neuromed. **Providing adequate magnesium would be a less novel way to block nerve pain caused by overexcitation by excess calcium. Citation #9 demonstrated that diabetic neuropathy pain could be reduced by magnesium injection alone – why bother with the opioid or the synthetic calcium channel blocker. They are an expensive and dangerous class of pharmaceuticals that would be pretty much not necessary if we weren’t being drained of magnesium reserves by excessive calcium and acidity intakes.
95 B [also 3/PPI article].     [jasn.asnjournals.org/content/20/11/2291.long]  Kevin J. Martin,  Esther A. González and Eduardo Slatopolsky, Clinical Consequences and Management of Hypomagnesemia,  doi: 10.1681/ASN.2007111194 (JASN November 1, 2009 vol. 20 no. 11 2291-2295)
96 B.    [.ncbi.nlm.nih.gov/pmc/articles/PMC2639130/?tool=pubmed] Karl T. Weber, William B. Weglicki, and Robert U. Simpson, Macro- and micronutrient dyshomeostasis in the adverse structural remodelling of myocardium,  (Cardiovasc Res. 2009 February 15; 81(3): 500–508.) Published online 2008 October 3. doi: [10.1093/cvr/cvn261].