A 70-year-old woman was admitted to the hospital with chest discomfort after quarreling with her neighbors. Electrocardiography revealed ST-segment elevation in leads I, II, III, aVL, aVF, and V2 through V6. Coronary angiography demonstrated normal arteries, but left ventriculography showed apical akinesis and basal hyperkinesis. Takotsubo cardiomyopathy was diagnosed on the basis of these characteristic findings. The creatine kinase and creatine kinase-MB concentrations were elevated at admission and reached maximum levels 6 hours after admission. The plasma level of brain natriuretic peptide was 10.7 pg/mL (reference range, <18.4 pg/mL) on the first hospital day. ST-segment elevation in leads I, II, III, aVL, aVF, and V2 through V6 persisted at 72 hours after admission. On the third hospital day, sudden rupture of the left ventricle occurred, and despite extensive resuscitation efforts, the patient died. Takotsubo cardiomyopathy presents in a manner similar to that of acute myocardial infarction, but ventricular systolic function usually returns to normal within a few weeks. To our knowledge, this is the first reported case of fatal left ventricular rupture associated with takotsubo cardiomyopathy. We suggest that takotsubo cardiomyopathy may be a newly recognized cause of sudden cardiac death.

No abstract

In the ears of anaesthetized rabbits cutaneous efferent sympathetic nerve activity (SkNA) and blood flow (Q) to capillaries have been measured during various thermal treatments. Warming the spinal cord or skin of the body midside caused a marked decrease in SkNA but capillary Q increased only slightly. Exposure to a warm environment or localized warming of the ear alone induced either a decrease, an increase, or no change in SkNA, but capillary Q always increased markedly. The usual slight increase in capillary Q during spinal warming, was abolished by preventing the usual marked increase in skin temperature. When the spinal cord of the conscious rat was warmed, a marked increase in temperature of the tail (which contains arteriovenous anastomoses, AVA's) indicated dilatation, whereas there was no change in ear temperature (where there are no AVA's). When these results are considered together with recently defined differential influences of reflex and direct effects of temperature on blood flow through cutaneous AVA's and capillaries, it is concluded: (1) That thermally-induced reflex changes in skin blood flow are mediated via sympathetic nervous action on AVA's; (2) Changes in blood flow evoked by direct heating take place through the capillaries, not the AVA's, quite independently of SkNA.

The effect of intracerebroventricular infusion of compound 48/80 (C48/80), a mast cell secretagogue, on adrenal cortisol secretion was investigated in dogs under pentobarbital sodium anesthesia. A marked increase in adrenal cortisol secretion was elicited by C48/80 along with a concomitant increase in the plasma levels of cortisol and immunoreactive ACTH, but neither arterial blood pressure and heart rate nor the plasma histamine level altered significantly. Pretreatment with either anti-CRF antiserum or pyrilamine maleate (H(1) histamine-receptor antagonist) significantly attenuated the C48/80-evoked increase in cortisol secretion, but pretreatment with metiamide (H(2)-receptor antagonist) significantly potentiated it. Significant attenuation of the C48/80-evoked increase in cortisol also occurred in dogs given ketotifen, a mast cell stabilizing drug, before pharmacologic challenge. In the pars tuberalis and median eminence (ME), mast cells were highly concentrated in close association with the primary plexus of the hypophysial portal system. Degranulated mast cells were extensively found in the ME of C48/80-treated animals. These results suggest that mast cells located in these regions liberated histamine within the brain as a result of degranulation induced by C48/80 and that this led to activation of the hypothalamic-pituitary-adrenocortical axis.

Objective High-density lipoprotein cholesterol (HDL-C)