Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151814 (coronary occlusion)
 3,687 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Brain stimulation can provoke a variety of arrhythmias and lower the ventricular vulnerable threshold. In the animal with acute myocardial ischemia such stimuli suffice to provoke ventricular fibrillation. Vagal neural traffic or adrenal catecholamines are not the conduits for this brain-heart linkage. Accompanying increases in heart rate or blood pressure are not prerequisites for the changes in cardiac excitability. Increased sympathetic activity, whether induced by neural or neurohumoral action, predisposes the heart to ventricular fibrillation. Protection can be achieved with surgical and pharmacologic denervation or reflex reduction in sympathetic tone. With acute myocardial ischemia, augmented sympathetic activity accounts for the early surge of ectopic activity frequently precipitating ventricular fibrillation. Asymmetries in sympathetic neural discharge may also contribute to the genesis of serious arrhythmias. The vagus nerve, through its muscarinic action, exerts an indirect effect on cardiac vulnerability, the consequence of annulment of concomitant adrenergic influence, rather than of any direct cholinergic action on the ventricles. There exist anatomic, physiologic as well as molecular bases for such interactions. Available experimental evidence indicates that environmental stresses of diverse types can injure the heart, lower the threshold of cardiac vulnerability to ventricular fibrillation and, in the animal with coronary occlusion, provoke potentially malignant ventricular arrhythmias. Available evidence indicates that in man, as in the experimental animal, administration of catecholamines can induce ventricular arrhythmia, whereas vagal activity exerts an opposite effect. Furthermore, in certain subjects diverse stresses and various psychologic states provoke ventricular ectopic activity.
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PMID:Neural and psychologic mechanisms and the problem of sudden cardiac death. 86 Jun 97

Takotsubo cardiomyopathy is classically stress induced and characterized by regional wall motion abnormalities in the absence of coronary occlusion. It predominantly affects postmenopausal women; emotional and physical stressors can trigger the classic cardiomyopathic findings. These changes are likely mediated by catecholamines, which cause a distinctive pattern of ventricular dysfunction with a unique pathologic phenotype of apical ballooning. Underlying mood disorders increase the risk for developing takotsubo cardiomyopathy after a triggering event. Takotsubo cardiomyopathy is one of several brain-heart disorders; its unique pathology can shed light on the complex interactions between the brain, sympathetic nervous system, and the cardiovascular system.
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PMID:Brain-heart interaction in takotsubo cardiomyopathy. 2356 22