Heart Arrhythmia

Also see:
Protect the Mitochondria
Thyroid Status and Cardiovascular Disease
“Normal” TSH: Marker for Increased Risk of Fatal Coronary Heart Disease
The Cholesterol and Thyroid Connection
High Blood Pressure and Hypothyroidism
A Cure for Heart Disease
Hypothyroidism and A Shift in Death Patterns
High Estrogen and Heart Disease in Men
Unsaturated Fats and Heart Damage
Estrogen Dominance and Magnesium Deficiency
Aldosterone as an endogenous cardiovascular toxin
Aldosterone and Thrombosis
Sodium Deficiency and Stress
Low Sodium Diet: High FFA, Insulin Resistance, Atherosclerosis
Sodium and Mortality: An Inverse Relationship
Ray Peat, PhD Quotes on Coconut Oil
Thyroid Hormones: The Ultimate Weapon Against Heart Disease?

All italic quotes by Ray Peat, PhD.

“Progesterone increases the heart’s pumping efficiency, and estrogen is antagonistic, and can produce cardiac arrhythmia.”

“Progesterone, which helps to maintain blood volume (partly by preventing vascular leakiness, preventing excessive sodium loss and by supporting albumin synthesis) antagonizes aldosterone. Aldosterone antagonists are now being recognized as effective treatments for hypertension, water retention, congestive heart failure, arrhythmia, diabetes, kidney disease, and a great variety of inflammatory problems.”

“Vitamins D and K, and calcium are important for stabilizing the heart rhythm. Estrogen tends to cause chemical hyperventilation (loss of carbon dioxide), which increases blood viscosity and the tendency toward atrial fibrillation. Progesterone and those other steroids have opposite effects (progesterone is a natural aldosterone antagonist, too). Thyroid is essential for helping cells to retain magnesium. A quart or two of milk, and a glass or two of orange juice every day helps with the main stabilizing minerals, but it’s good to have sea food once a week, especially shell fish, for the trace minerals.”

“A complete list of protective nutritional chemicals and natural drugs or analogs to our endogenous protective factors would be very long, but we should give special thought to certain ones, including succinic acid, which stimulates respiration and protective steroid synthesis; thyroid and vitamin E, which promote normal oxidation while preventing abnormal oxidation; magnesium; sodium and lithium, which help us to retain magnesium; tropical fruits, which contain GHB; coconut oil, which protects against cardiac necrosis, lipid peroxidation, hypothyroidism, hypoglycemia, and histamine damage; valium agonists, natural antihistamines; adenosine and uridine. Visits to higher elevations, and exposure’ to bright, long-wave light, can cause the body to optimize its own anti-stress chemistry. Avoiding the sense of being trapped is a high-level adaptive factor.”

“Albert Szent-Györgyi showed that the heart responds to progesterone, and more recently other researchers have presented evidence that DHEA is our “endogenous digitalis.”

Eur J Prev Cardiol. 2012 Nov 14. [Epub ahead of print]
Dehydroepiandrosterone sulfate levels and risk of atrial fibrillation: The Rotterdam Study.
Krijthe BP, de Jong FH, Hofman A, Franco OH, Witteman JC, Stricker BH, Heeringa J.
Background: High plasma dehydroepiandrosterone sulfate (DHEAS) levels have been associated with a reduced risk of cardiovascular disease and atherosclerosis. To our knowledge, no previous follow-up study has investigated the association between DHEAS and the development of atrial fibrillation. Our objective was to investigate the association between DHEAS levels and incident atrial fibrillation.Methods and results: The study was based on a random sample within the prospective population-based Rotterdam Study. The study population comprised 1180 participants without atrial fibrillation at baseline for whom baseline levels of DHEAS were measured in plasma. Atrial fibrillation was ascertained from centre visit electrocardiogram (ECG) assessments as well as medical records. During a mean follow-up period of 12.3 years, 129 participants developed atrial fibrillation. DHEAS levels were inversely associated with the risk of atrial fibrillation (hazard ratio (HR) per standard deviation (SD): 0.74, 95% confidence interval (CI): 0.58-0.94). Subjects in the highest DHEAS quartile had an almost three times lower risk of atrial fibrillation during follow-up, compared to those in the lowest DHEAS quartile (HR: 0.34, 95% CI: 0.18-0.64) adjusted for age, sex and cardiovascular risk factors.Conclusion: DHEAS can be regarded as an important indicator of future atrial fibrillation in both men and women, independent of known cardiovascular risk factors.

Exp Gerontol. 2002 May;37(5):701-12.
Dehydroepiandrosterone-sulfate serum levels and common age-related diseases: results from a cross-sectional Italian study of a general elderly population.
Ravaglia G, Forti P, Maioli F, Sacchetti L, Nativio V, Scali CR, Mariani E,
Zanardi V, Stefanini A, Macini PL.
The association of low serum dehydroepiandrosterone sulfate (DHEAS) levels with age, lifestyle, general health status indicators, and specific diseases was investigated in 436 men and 544 women of 65-97 yr old. In both sexes low serum DHEAS levels were associated with age, alcohol intake, number of current medications, and decreased thyroid function. Low DHEAS was also associated with low serum albumin in men and low systolic blood pressure in women. Compared to healthy men (n=106) age-adjusted serum DHEAS levels were significantly lower in men with atrial fibrillation, chronic obstructive lung disease, dementia, parkinsonism, cancer, diabetes, hypothyroidism, and in institutionalized men. Compared to healthy women (n=100) age-adjusted serum DHEAS levels were significantly lower in women with occlusive arterial disease, chronic obstructive lung disease, and osteoporosis. After controlling for differences in lifestyle and general health status parameters, low DHEAS levels remained statistically associated only with atrial fibrillation in men and osteoporosis in women, and it cannot be excluded that these association were spurious, due to multiple comparisons. These data suggest that in elderly people low serum DHEAS levels are more a non-specific indicator of aging and health status than a risk indicator of specific diseases.

“Pregnenolone, progesterone, DHEA, testosterone, and thyroid all improve the stability of the heart.”

Reduced testosterone:
J Cardiovasc Electrophysiol. 2009 Sep;20(9):1055-60.
Deficiency of testosterone associates with the substrate of atrial fibrillation in the rat model.
Tsuneda T, Yamashita T, Kato T, Sekiguchi A, Sagara K, Sawada H, Aizawa T, Fu LT, Fujiki A, Inoue H.
Since the prevalence of atrial fibrillation (AF) increases progressively with aging, especially in men, we hypothesized that testosterone might affect the occurrence of AF.
We examined the electrophysiological properties of the atria in isolated-perfused hearts of sham-operated male (SM), female (SF), orchiectomized male with and without administration of testosterone (ORCH-T and ORCH), and ovariectomized female (OVX) Sprague-Dawley rats. An electrophysiological study revealed that repetitive atrial responses induced by electrical stimuli significantly increased in ORCH rats without changes in other electrophysiological properties and were abolished by administration of testosterone. To investigate the underlying mechanisms, we evaluated the expression level of calcium-handling proteins. In ORCH rats, the immunoreactive protein level of ryanodine receptor type 2 (RyR2) and sodium-calcium exchanger significantly increased as compared with SM and ORCH-T rats without alterations in the level of FK506-binding protein (FKBP12.6), sarcoendoplasmic reticulum Ca-ATPase, and phospholamban. Immunoprecipitation analysis demonstrated decreased binding of FKBP12.6 to RyR2 in ORCH rats, which was prevented by testosterone. In contrast, the expression levels of these proteins showed no significant differences between SF and OVX rats.
Deficiency of testosterone was arrhythmogenic in rat atria possibly through less binding of FKBP12.6 to RyR2, which could induce feasible calcium leakage from the sarcoendoplasmic reticulum. These results would explain, at least in part, the increase in the prevalence of AF in accordance with the decline of testosterone particularly in elderly men.

Clin Cardiol. 2009 Jan;32(1):43-6.
Reduced testosterone levels in males with lone atrial fibrillation.
Lai J, Zhou D, Xia S, Shang Y, Want L, Zheng L, Zhu J.
Sex hormones play an important role in the development of cardiovascular disease. Testosterone and estradiol have been reported to be down-regulated in subjects with coronary artery disease and heart failure, but has not been studied in atrial fibrillation (AF).
Levels of sex hormones may be associated with susceptibility to lone AF in men.
Fifty-eight male subjects who had electrocardiographic evidence of paroxysmal or chronic AF and a structurally normal heart on echocardiography were enrolled. Subjects were excluded if they had been taking angiotensin-converting enzyme inhibitors (ACEI), angiotensin receptor blockers (ARB), or statins within 3 mo or had a history of coronary artery disease, rheumatic heart disease, cardiomyopathy, significant valvular disease, hyperthyroidism, or hypertension. Fifty-eight controls were recruited from a healthy outpatient population. Serum total testosterone and estradiol levels were determined using a commercially available radioimmunoassay.
Mean levels of testosterone were significantly lower in subjects with lone AF when compared with controls (476 ng/dl versus 514 ng/dl, p = 0.005). No significant differences were found in the estradiol levels between the 2 groups (31.9 pg/ml versus 32.4 pg/ml, p = 0.789).
Reduced testosterone levels may be associated with susceptibility to lone AF in men.

Med Hypotheses. 2010 Aug;75(2):269-70.
Testosterone as an atrial fibrillation treatment and stroke preventative in aging
men: case histories and hypothesis.

Eby G.


“Broda Barnes showed that hypothyroidism causes heart disease, and also causes a tendency toward hypoglycemia. Low thyroid people compensate for the deficiency of energy and glucose (and of oxygen, for reasons similar to those mentioned above) by secreting an excess of adrenalin. Their 24 hour urine metabolites of adrenalin sometimes are 30 or 40 times normal. Recent studies that show that a moderate dose of thyroxin lowers lipid peroxidation confirm that thyroid has an antistress effect. The “conduction block” which occurs in hypothyroidism seems to be the same as the conduction block which develops in stress and predisposes to fibrillation.”

Neth Heart J. 2008 Feb;16(2):57-9.
Hypothyroidism as the cause of atrioventricular block in an elderly patient.
Schoenmakers N, de Graaff WE, Peters RH.
Department of Cardiology, Department of Internal Medicine, Tergooi Hospital
Blaricum, the Netherlands.
Syncope is a common problem in the older patient. Sometimes syncope is caused by
extreme bradycardia secondary to atrioventricular (AV) block. We describe a case
in which a 90-year-old woman presented with complete AV block due to severe
hypothyroidism. After suppletion with levothyroxine, AV conduction was restored.

(Neth Heart J 2008;16:57-9.).

Am J Med. 1990 Jun;88(6):638-41.
Recognition and management of cardiovascular disease related to thyroid dysfunction.
Ladenson PW.
Hypothyroidism and hyperthyroidism are both associated with clinically significant cardiovascular derangements. In hypothyroidism, these include pericardial effusion, heart failure, and the complex interrelationship between hypothyroidism and ischemic heart disease. Cardiovascular disorders associated with hyperthyroidism include atrial tachyarrhythmias, mitral valve dysfunction, and heart failure. Although these usually occur in individuals with intrinsic heart disease, thyroid dysfunction alone rarely causes serious but reversible cardiovascular dysfunction. Patients with commonly encountered cardiac disorders, e.g., idiopathic cardiomyopathy and atrial fibrillation, should be screened for potentially contributing subclinical thyroid diseases. In patients with heart failure and hypothyroidism, initial management should focus on diagnosis and optimal management of any primary cardiac disease, whereas in hyperthyroidism, aggressive measures to control excess thyroid hormone action should generally have the highest priority.

Recent Prog Horm Res. 2004;59:31-50.
Effects of thyroid hormone on the cardiovascular system.
Fazio S, Palmieri EA, Lombardi G, Biondi B.
Increased or reduced action of thyroid hormone on certain molecular pathways in the heart and vasculature causes relevant cardiovascular derangements. It is well established that overt hyperthyroidism induces a hyperdynamic cardiovascular state (high cardiac output with low systemic vascular resistance), which is associated with a faster heart rate, enhanced left ventricular (LV) systolic and diastolic function, and increased prevalence of supraventricular tachyarrhythmias – namely, atrial fibrillation – whereas overt hypothyroidism is characterized by the opposite changes. However, whether changes in cardiac performance associated with overt thyroid dysfunction are due mainly to alterations of myocardial contractility or to loading conditions remains unclear. Extensive evidence indicates that the cardiovascular system responds to the minimal but persistent changes in circulating thyroid hormone levels, which are typical of individuals with subclinical thyroid dysfunction. Subclinical hyperthyroidism is associated with increased heart rate, atrial arrhythmias, increased LV mass, impaired ventricular relaxation, reduced exercise performance, and increased risk of cardiovascular mortality. Subclinical hypothyroidism is associated with impaired LV diastolic function and subtle systolic dysfunction and an enhanced risk for atherosclerosis and myocardial infarction. Because all cardiovascular abnormalities are reversed by restoration of euthyroidism (“subclinical hypothyroidism”) or blunted by beta-blockade and L-thyroxine (L-T4) dose tailoring (“subclinical hyperthyroidism”), timely treatment is advisable in an attempt to avoid adverse cardiovascular effects. Interestingly, some data indicate that patients with acute and chronic cardiovascular disorders and those undergoing cardiac surgery may have altered peripheral thyroid hormone metabolism that, in turn, may contribute to altered cardiac function. Preliminary clinical investigations suggest that administration of thyroid hormone or its analogue 3,5-diiodothyropropionic acid greatly benefits these patients, highlighting the potential role of thyroid hormone treatment in patients with acute and chronic cardiovascular disease.

Pol Arch Med Wewn. 1983 Sep;70(3):81-5.
[Functional disorders of the heart conduction system as a symptom of thyroid hormone deficiency].
[Article in Polish]
Jonderko G, Kocot E, Marcisz C.

Nouv Presse Med. 1975 Jun 21;4(25):1859-62.
[Disorders of intra-cardiac conduction and hypothyroidism in adults. A systematic
study of 42 cases].

[Article in French]
Lardoux H, Cénac A, Perlemuter L, Bernheim R, Hazard J.
The rate of occurrence of disturbances of intracardiac conduction in association with adult hypothyroidism is not well known. On the basis of routine study of the electrocardiograms of 42 non-treated patients, disturbances of conduction were found in almost one third. Left anterior hemiblock (6/42) and first degree atrioventricular block (5/42) are the commonest. Bifascicular involvement is rare. Neither a trifascicular lesion nor complete AV dissociation were seen. There was no evident effect of hormone therapy on conduction disturbances. Their prognosis is good but they should perhaps be taken into consideration when the indications for beta-blockers are weighed.

Magnesium retention compromised in hypothyroidism.

“Simply eating an adequate amount of calcium and magnesium can alleviate many problems related to stress and aging that are considered serious, such as heart arrhythmia, pancreatitis, and tissue calcification.”

“In hypothyroidism, the brain exciting hormones adrenaline, estrogen, and cortisol are usually elevated, and the nerve-muscle relaxant magnesium is low.”

“Low-thyroid cells are unable to retain magnesium efficiently, and a magnesium deficiency prevents muscle relaxation, wasting energy. Adequate sodium prevents urinary magnesium loss.”

“Magnesium, retained in the cell largely under the influence of ATP and thyroid, is our basic “calcium blocker,” or calcium antagonist.”

“Magnesium, which is protective against excitatory damage and is a calcium antagonist, tends to be retained in proportion to the activity of thyroid hormone.”

Am J Vet Res. 1978 Jan;39(1):159-61.
Effect of thyroid state on magnesium concentration of rat tissues.
Oliver JW.
The effect of alteration of thyroid status by thiouracil (0.1% concentration in drinking water for 60 days) or exogenous thyroxine (25 mg/dg of body weight administered SC from days 30 to 60) on magnesium content of rat tissues following exogenous magnesium was evaluated. Treatment of rats with magnesium solution (25 mg of magnesium sulfate/dg of body weight) resulted in increased magnesium concentration in most tissues of hypothyroid and hyperthyroid rats, with the mesenchymal-derived tissues (aorta, trachea, and ear cartilage) exhibiting the greatest increases (respectively, 154, 130, and 133% of control group values for hypothyroid rats, and 115, 108, and 107% of control group values for the hyperthyroid group). Magnesium concentration in skeletal and cardiac muscle was similar for hyperthyroid and control rats, but magnesium concentration in these same tissues of hypothyroid rats was decreased. Magnesium distribution and retention in rat tissues is altered considerably, depending on the functional status of thyroid gland.

Consequences of magnesium deficiency on the heart.

Int J Biochem Cell Biol. 1997 Nov;29(11):1273-8.
Magnesium deficiency enhances oxidative stress and collagen synthesis in vivo in the aorta of rats.
Shivakumar K, Kumar BP.
Magnesium deficiency has been shown to produce vascular lesions in experimental animals, but the underlying mechanisms of vascular injury are not clear. It has been reported that in rodents, magnesium deficiency enhances circulating levels of factors that promote free radical generation and are mitogenic. In pursuance of these observations, the present study tested the hypothesis that magnesium deficiency may enhance oxidative stress and trigger an accelerated growth response in vivo in the aorta of rats. Oxidative stress was evaluated in terms of levels of thiobarbituric acid-reactive substances in the serum and aorta and activity of superoxide dismutase and catalase in the aorta; fractional rates of collagen synthesis were assessed using [3H]-proline. Serum and tissue levels of magnesium and calcium were determined by atomic absorption spectrophotometry. The present study demonstrated for the first time that magnesium deficiency significantly (P < 0.001) increases levels of thiobarbituric acid-reactive substances in the aorta of rats. Other changes in the aorta of animals on the Mg-deficient diet included a significant reduction (54%, P < 0.001) in the activity of superoxide dismutase and catalase (37%, P < 0.01) and a 19% increase in net fractional rates of collagen synthesis (P < 0.05). While serum magnesium was significantly reduced in these animals (P < 0.001), aortic tissue levels of magnesium in these animals remained unaltered throughout the duration of the study, suggesting the existence of other control mechanisms, apart from reduced tissue levels of magnesium, mediating the observed effects. These findings suggest that magnesium deficiency may trigger a wound healing response, involving oxidative injury and growth stimulation, in the vascular system.

Int J Biochem Cell Biol. 1997 Jan;29(1):129-34.
Magnesium deficiency-related changes in lipid peroxidation and collagen metabolism in vivo in rat heart.
Kumar BP, Shivakumar K, Kartha CC.
Magnesium deficiency is known to produce a cardiomyopathy, characterised by myocardial necrosis and fibrosis. As part of the ongoing investigations in this laboratory to establish the biochemical correlates of these histological changes, the present study probed the extent of lipid peroxidation and alterations in collagen metabolism in the heart in rats fed a magnesium-deficient diet for 28, 60 or 80 days. While lipid peroxidation was measured by the thiobarbituric acid reaction, collagen turnover rates and fibroblast proliferation were assessed using [3H]-proline and [3H]-thymidine, respectively. Tissue levels of magnesium and calcium were determined by atomic absorption spectrophotometry. A 39% increase in the cardiac tissue level of thiobarbituric acid reactive substances was observed on day 60 of deficiency (p < 0.001). A marked drop in collagen deposition rate (59%, p < 0.001%) on day 28 but a significant rise in fractional synthesis rate (12%, p < 0.001) and collagen deposition rate (24%, p < 0.001) on day 60 were observed. A fibroproliferative response in the heart was evident on day 80 but not at earlier time-points. Thus, the present study provides evidence of increased lipid peroxidation and net deposition of collagen in the myocardium in response to dietary deficiency of magnesium. These changes were, however, not directly related to alterations in the tissue levels of Mg. It is suggested that the increase in cardiac collagen synthesis and fibroplasia associated with Mg deficiency may represent reparative fibrogenesis, upon oxidative damage to the cardiac muscle, and is mediated by a mechanism independent of changes in cardiac tissue levels of Mg.

Serotonin and heart arrhythmia:

Res Commun Chem Pathol Pharmacol. 1990 Jun;68(3):383-6.
5-Hydroxytryptamine (serotonin) enhances ventricular arrhythmias induced by acute
coronary artery ligation in rats.

el-Mahdy SA.
Ventricular arrhythmias were induced by acute coronary artery ligation in anesthetized rats. 5-Hydroxytryptamine (5-HT) in doses of 100-200 micrograms kg-1, given i.v. 5 minutes before coronary artery ligation, enhanced the severity of ventricular arrhythmias as shown by a significant dose-dependent increase in the number of ventricular ectopic beats, duration of ventricular tachycardia (VT) and ventricular fibrillation (VF). This effect was antagonized by pretreatment with the selective 5-HT2-receptor antagonist ritanserin (1 mg kg-1, i.p.) given 15 minutes before 5-HT. Ritanserin when used alone was observed to produce a significant reduction in the number of ventricular ectopic beats and duration of VT and VF. 5-HT significantly lowered the heart rate and produced initial rise of the systolic blood pressure (SBP). These effects were antagonized by ritanserin. Ritanserin significantly lowered the heart rate but did not alter the SBP. It was postulated that 5-HT might be implicated in the genesis and determination of severity of ventricular arrhythmias induced by acute myocardial ischemia, and that this effect is mediated via 5-HT2-receptors. 5-HT2-receptor antagonists may provide potential useful therapeutic agents for the management of these arrhythmias.

J Cardiovasc Electrophysiol. 2003 Feb;14(2):209-14.
5-hydroxytryptamine and atrial fibrillation: how significant is this piece in the puzzle?
Yusuf S, Al-Saady N, Camm AJ.
5-Hydroxytryptamine, a recent addition to the list of hormonal triggers for atrial fibrillation (AF), may play a pivotal role in the induction of AF related not only to cardiac surgery but also to acute coronary syndromes, valvular heart disease, cardiomyopathies, alcoholism, aging, and conducting tissue disease. This review examines the supporting laboratory and clinical evidence and provides a comprehensive insight into the basic underlying mechanisms involved. It also delves into the potential benefits and limitations of 5-HT4 antagonists in the prevention and management of this arrhythmia.

Psychosomatics. 2006 Nov-Dec;47(6):533-6.
Cardioversion of persistent atrial arrhythmia after treatment with venlafaxine in successful management of major depression and posttraumatic stress disorder
Finch SJ, van Zyl LT.
There is increasing evidence linking depression and cardiovascular disease. However, the authors could find no literature directly linking depression with atrial fibrillation or atrial flutter. The authors report the case of a patient with uncontrolled atrial arrhythmia who cardioverted to normal sinus rhythm after treatment of major depressive disorder (MDD) and posttraumatic stress disorder (PTSD) with venlafaxine. The authors discuss comorbidity of MDD and atrial fibrillation, and explore evidence of venlafaxine as an antiarrhythmic agent. Further research is needed to establish the clinical role of venlafaxine as a Class 1 antiarrhythmic agent and any association between atrial arrhythmias and MDD and PTSD.

Clin Res Cardiol. 2007 Feb;96(2):114-8.
Atrial fibrillation in carcinoid heart disease: The role of serotonin. A review of the literature.
Langer C, Piper C, Vogt J, Heintze J, Butz T, Lindner O, Burchert W, Kersting C,
Horstkotte D.

J Mol Cell Cardiol. 2007 Jan;42(1):51-3.
5-hydroxytryptamine and atrial arrhythmogenesis: a “culprit mechanism” or bystander in patients with chronic atrial fibrillation?
Dobrev D.

43. Indian J Physiol Pharmacol. 1973 Apr-Jun;17(2):111-6.
Influence of 5-hydroxytryptamine on experimentally induced atrial arrhythmias in dogs.
Kuruvilla A, Aiman R.

Sov Med. 1972 Oct;35(10):30-3.
[Some aspects of the metabolism of biogenic monoamines (catecholamines and serotonin) in fibrillation arrhythmia treated by electrical impulses].
[Article in Russian]
Berestov AA, Safronova VI.

Klin Med (Mosk). 1971 Jan;49(1):25-9.
[Blood serotonin content during auricular fibrillation and its treatment by defibrillation].
[Article in Russian]
Panchenko VM, Kucherenko IA.

“Selye’s demonstration of corn oil’s toxicity to the heart is an important link in the general picture of stress injury and adrenalin toxicity. The protective effects of saturated fats are not surprising when seen against the background of the toxic effects of adrenalin, causing the mobilization of fatty acids and the resulting lipid peroxidation.”

PUFA and arrhythmia:
Cardiovasc Res. 2007 Jan 15;73(2):386-94. Epub 2006 Oct 13.
Dietary n-3 fatty acids promote arrhythmias during acute regional myocardial ischemia in isolated pig hearts.
Coronel R, Wilms-Schopman FJ, Den Ruijter HM, Belterman CN, Schumacher CA, Opthof T, Hovenier R, Lemmens AG, Terpstra AH, Katan MB, Zock P.
Dietary supplementation with fish oil-derived n-3 fatty acids reduces mortality in patients with myocardial infarction, but may have adverse effects in angina patients. The underlying electrophysiologic mechanisms are poorly understood. We studied the arrhythmias and the electrophysiologic changes during regional ischemia in hearts from pigs fed a diet rich in fish oil.
Pigs received diets rich in fish oil, in sunflower oil, or a control diet for 8 weeks. Hearts were isolated and perfused. Ischemia was created by occluding the left anterior descending artery. Diastolic stimulation threshold, refractory period, conduction velocity, activation recovery intervals and the maximum downstroke velocity of 176 electrograms were measured in the ischemic zone. Spontaneous arrhythmias during 75 min of regional ischemia were counted.
More episodes of spontaneous ischemia-induced sustained ventricular tachycardia and ventricular fibrillation occurred in the fish oil and sunflower oil group than in the control group. More inexcitable myocardium was present in the ischemic zone in the group fed fish oil or sunflower oil than in the control group after 20 min of ischemia. After 40 min of ischemia, more block occurred in the control group than in the other groups. The downstroke velocity of the electrograms in the ischemic border zone was lower in the fish oil group and sunflower oil group than in the control after 20 min.
A diet rich in fish oil results in proarrhythmia compared to a control diet during regional ischemia in pigs. Myocardial excitability is reduced in the fish oil and sunflower oil group during the early phase of arrhythmogenesis. In the late phase of arrhythmogenesis, excitability is more reduced in the control group than in the fish oil and sunflower oil group.

Progesterone protects against hemorrhagic shock, improves cardiovascular responses:

Crit Care Med. 2003 Jun;31(6):1786-93.
Progesterone administration after trauma and hemorrhagic shock improves cardiovascular responses.
Kuebler JF1, Jarrar D, Bland KI, Rue L 3rd, Wang P, Chaudry IH.
Studies have shown that female rats during the proestrus stage have significantly improved cell and organ functions after trauma-hemorrhage compared with male and ovariectomized females. This study investigated the hypothesis that progesterone can improve the depressed cardiovascular function in sex steroid-deficient female rats (i.e., ovariectomized females) after trauma-hemorrhage and resuscitation.
Prospective study.
University laboratory.
Ovariectomized female Sprague-Dawley rats (weight, 250-300 g).
Rats underwent a 5-cm midline laparotomy (i.e., soft-tissue trauma), were bled to a mean arterial pressure of 35 mm Hg for approximately 90 mins, and were then resuscitated using Ringer’s lactate. A single dose of progesterone (25 mg/kg of body weight) or vehicle was administered subcutaneously during resuscitation.
At 20 hrs after trauma-hemorrhage or sham operation, cardiac output and heart performance and the circulating blood volume were assessed using the indocyanine green dilution technique and a left ventricular catheter. Furthermore, the binding activity of progesterone receptors in nuclear extracts of left ventricular tissue was determined.
Cardiac output, heart performance, and circulating blood volume were significantly decreased in vehicle-treated animals after trauma-hemorrhage. Administration of progesterone significantly improved cardiac output and heart performance and increased the circulating blood volume. This was associated with an increased progesterone receptor activity in the left ventricular nuclear extracts.

Because administration of progesterone after trauma-hemorrhage in sex steroid-deficient females improved cardiovascular responses, this hormone seems to be a useful adjunct for the treatment of cardiovascular depression in postmenopausal and ovariectomized female trauma patients.

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