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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The cause of hypothyroidism after subtotal thyroidectomy for primary thyrotoxicosis is not precisely understood. Activity is not just related to the size of the thyroid remnants, and ischemia of the remnants has been suggested as a factor which might contribute to the development of hypothyroidism. A prospective study has been carried out to look for evidence that ischemia is implicated. In 55 patients undergoing subtotal thyroidectomy for primary thyrotoxicosis, the inferior thyroid artery (ITA) was ligated on one side but preserved on the opposite side. All of the patients had postoperative isotope scans. We predicted that, if ITA ligation produced significant ischemia of the remnant, then the remnant with the intact ITA ought to show greater activity on the postoperative scan. This was not the case. The remnant with the intact ITA was dominant in only 15 of 55 patients, the remnant with the ligated ITA was dominant in the same proportion, 15 of 55 patients, while in the remaining 25 patients, activity was equally distributed between the two remnants. The results of this study provides no evidence to support the contention that nonligation of the inferior thyroid arteries will reduce ischemia of the thyroid remnants and thereby discourage postoperative hypothyroidism.
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PMID:The effect of ligation of the inferior thyroid artery upon thyroid remnant function. 336 61

In the absence of fixed coronary artery disease, thyrotoxicosis is rarely associated with acute myocardial infarction and/or ischemia. There are no known reports on the association of acute myocardial infarction with iatrogenic or factitious thyrotoxicosis in the absence of fixed coronary artery stenosis or coronary artery spasm. A 68-year-old woman, clinically in a state of thyrotoxicosis as a result of taking 0.3 g/d of exogenous thyroid replacement, sustained a severe, reversible myocardial ischemic event. Echocardiographic and scintigraphic evaluations demonstrated a large apical dyskinetic region. Subsequently, after the original dose of levothyroxine sodium was reduced to 0.15 mg and the patient became euthyroid, two-dimensional echocardiography and scintigraphic and cardiac catheterization studies demonstrated normal left ventricular contractility and normal coronary anatomy. Coronary artery spasm was not induced by ergonovine maleate therapy. Exogenous thyroid administration may directly influence myocardial oxygen supply and demand, exclusive of coronary artery disease and coronary spasm. A critical imbalance may then result in acute myocardial ischemia and reversible left ventricular segmental wall motion abnormalities.
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PMID:Myocardial infarction, severe reversible ischemia, and shock following excess thyroid administration in a woman with normal coronary arteries. 337 27

Acute heart insufficiency was simulated in dogs, rabbits and rats with experimental myocardial infarction, hypothyrosis, thyrotoxicosis, autoimmune cardiomyopathy, myocardium hypertrophy by exerting additional mechanical load on the heart (graded aortic stricture, swimming, running in a tread-ban). Irrespective of the basic pathological process the development of acute heart insufficiency was associated with generalized damage of plasmalemma of the majority of functioning cardiomyocytes, registered with colloid lanthanum. Plasmalemma damage precedes intracellular ultrastructural alterations and is reversible. Sarcolemma damages in non-functioning cardiomyocytes revealed in the focus of severe ischemia in experimental myocardial infarction is on the contrary indicative of irreversible cellular changes. The distinctions demonstrate that mechanisms causing damages in sarcolemma membrane can be different in conditions of preserved coronary blood flow and in severe ischemia.
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PMID:[Role of the sarcolemma in the morphogenesis of acute heart failure]. 623 4

Malignant exophthalmos or the ophthalmic component of Graves' disease is a functionally impairing and cosmetically deforming disorder of orbital tissue, separate from the sympathetic effects of thyrotoxicosis. The deposition of immune complexes of thyroglobulin and its antibodies within orbital muscles results in progressive exophthalmos, ophthalmoplegia, chemosis, and lid fullness. Increasing intraorbital edema and optic nerve tension may produce irreversible retinal ischemia. If unresponsive to medical treatment, patients exhibiting increasing loss of visual acuity are therefore candidates for emergency surgery. Early attempts at surgical correction of the mechanical aspect of Graves' ophthalmopathy were unsuccessful. The current technique of transantral orbital decompression, when done before extreme advancement of the ocular disease, is successful and meets the following objectives: It restores visual loss and prevents further deterioration of visual acuity, protects the cornea, restores extraocular muscle movements, decreases intraorbital pressure, produces a satisfactory cosmetic result, and avoids serious complications. Patients with persistent extraocular muscle imbalance or lid lag may ultimately require oculoplastic surgery.
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PMID:Ophthalmic surgery in malignant exophthalmos. 689 48

Myocardial ischemia is a rare but severe and possibly life threatening manifestation of hyperthyroidism, but does not usually result in persistent ischemia. We report on a 71-year-old woman who had undergone total thyroidectomy with subsequent irradiation because of follicular carcinoma 3 years ago. Since then, she had been maintained on oral levothyroxine replacement therapy at a dose of 0.15 mg alternating with 0.2 mg daily. When latent hypothyroidism became evident despite replacement therapy, the dose of levothyroxine was increased to 0.3 mg a day. Three weeks later, the patient suffered from an acute posterior myocardial infarction, although she had no previous history of coronary artery disease. Subsequent coronary arteriograms revealed no evidence of disease of the major vessels. Myocardial scintigraphy 3 weeks after infarction still revealed a persistent perfusion defect. Since it is known that thyroid hormones increase oxygen demand, the rapid elevation of oxygen utilization caused by thyrotoxicosis factitia is likely to be responsible for this patient's myocardial infarction. The case illustrates that a sudden increase in levothyroxine replacement dose should be avoided.
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PMID:Factitious hyperthyroidism causing acute myocardial infarction. 880 97

Moyamoya syndrome is the secondary form of intracranial arterial occlusive diseases that produces collateral vessels from the base of brain. We report a case of Moyamoya syndrome developing in association with Graves thyrotoxicosis; as a result of its rapid progression and severe global ischemia, it was ultimately fatal. Because of the rarity of this association, we reviewed the literature in an attempt to establish possible demographic and clinical characteristics that may suggest putative mechanisms of pathogenesis.
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PMID:Rapidly progressive fatal bihemispheric infarction secondary to Moyamoya syndrome in association with Graves thyrotoxicosis. 1655 9

Impaired microcirculation with evolving sludge phenomenon and thrombosis underlie placental changes in maternal thyroid disease. Capillary blood circulatory defect is largely due to villous immaturity. Placental tissue ischemia gives rise to fibrinoid, sclerosis, and alternative processes. Dysadaptive changes are mostly observed in thyrotoxicosis and hypothyroidism. Adaptive processes evolving at the ultrastructural level are best pronounced in euthyroid goiter.
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PMID:[Impact of maternal thyroid disease on the formation of relationships in the maternal-placental-fetal system]. 1698 91

The cross-sectional epidemiological studies investigating hyperthyroidism as a risk factor for hypertension and stroke are not conclusive. Several case studies, however, indicate that persistent thyrotoxicosis aggravates neurological damage subsequent to a stroke. To test the hypothesis, we measured physiological and biochemical parameters in a model of transient focal ischemia in rats with prior induction of thyrotoxicosis to investigate its effects. Age- and weight-matched rats were made hyperthyroid prior to middle cerebral artery (MCA) occlusion and killed after 3 days of reperfusion. We then estimated neurological deficit scores, body temperature, circulating total and free thyroxine (fT(4)) levels, lipid peroxide and thiol levels, and lactate dehydrogenase activity. While the standard 2-h occlusion of MCA resulted in very high mortality in hyperthyroid animals, the 30-min MCA occlusion resulted in a significant increase in neurological deficits compared with sham-operated animals. We observed a twofold or more increase in circulating fT(4) levels in rats receiving thyroxine. The increase in infarct size directly correlated with the increased dose of thyroxine. A significant thyroxine dose-dependent increase in lipid peroxide (malondialdehyde levels, P<0.05), lactate dehydrogenase activity (P<0.01), and a significant decrease in protective thiol levels (P<0.05) were observed. The data support our hypothesis that thyrotoxicosis is an independent risk factor which contributes to the aggravation of post-stroke injury and death. The study results indicate a need to control thyrotoxicosis in elderly populations to reduce the risk.
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PMID:Pathophysiological basis for thyrotoxicosis as an aggravating factor in post-ischemic brain injury in rats. 1825 57

Atrial fibrillation (AF) is a complex condition with several possible contributing factors. The rapid and irregular heartbeat produced by AF increases the risk of blood clot formation inside the heart. These clots may eventually become dislodged, causing embolism, stroke and other disorders. AF occurs in up to 15% of patients with hyperthyroidism compared to 4% of people in the general population and is more common in men and in patients with triiodothyronine (T3) toxicosis. The incidence of AF increases with advancing age. Also, subclinical hyperthyroidism is a risk factor associated with a 3-fold increase in development of AF. Thyrotoxicosis exerts marked influences on electrical impulse generation (chronotropic effect) and conduction (dromotropic effect). Several potential mechanisms could be invoked for the effect of thyroid hormones on AF risk, including elevation of left atrial pressure secondary to increased left ventricular mass and impaired ventricular relaxation, ischemia resulting from increased resting heart rate, and increased atrial eopic activity. Reentry has been postulated as one of the main mechanisms leading to AF. AF is more likely if effective refractory periods are short and conduction is slow. Hyperthyroidism is associated with shortening of action potential duration which may also contribute to AF.
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PMID:The mechanisms of atrial fibrillation in hyperthyroidism. 1934 75

Right ventricular failure can be secondary to right ventricular ischemia, pulmonary or tricuspid valvular disease, myocardial shunts, cardiomyopathy, acute and chronic pulmonary hypertension, myocarditis and pericardial disease and it generally carries a poor prognosis. Thyrotoxicosis is a clinical state resulting from high thyroid hormone action in tissues generally due to high thyroid hormone levels. The association between severe hyperthyroidism and high-output heart failure is well-known. Less widespread is the concept that hyperthyroid patients, irrespective of coexisting diseases and through mechanisms not fully elucidated, are at higher risk for pulmonary hypertension and right heart failure, both reversible with the achievement of euthyroidism and associated with a good prognosis. We describe the case of a 44-year-old woman with right ventricular failure and moderate pulmonary hypertension in the setting of thyrotoxicosis, which resolved rapidly after antithyroid treatment. The potential mechanisms underlying this condition will also be discussed.
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PMID:Acute Right Ventricular Heart Failure: An Uncommon Case of Thyrotoxicosis. 3013 80


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