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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 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

Mental and emotional stress can provoke transient ischemia and acute coronary syndrome in vulnerable patients. Furthermore, those patients so provoked are at increased risk for recurrent cardiac events and early death. Viable psychological treatments to improve prognosis exist, and preliminary trials demonstrate their efficacy with regard to short- and long-term outcomes, as well as economic savings. These findings heighten the need for efforts directed toward the complete identification of the differential pathophysiology of mental stress-induced ischemia, with an eye toward development of diagnostic tests and establishment of risk stratification algorithms that can be applied in the clinical setting. Ongoing research in this vein is identifying unique aspects of the brain-heart relationship during mental stress that underlie the cognitive and emotional aspects of mental stress, and the "dow nwind" pathways by which distinct patterns of brain activity during mental stress can provoke otherwise silent myocardial ischemia. This research is making important contributions to the larger clinical goals associated with diagnostic testing, risk stratification, and treatment of patients at risk for mental stress-induced ischemia and poorer prognosis.
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PMID:The heart-brain interaction during emotionally provoked myocardial ischemia: implications of cortical hyperactivation in CAD and gender interactions. 1745 47

Acute cardiac complications in critical brain disease should be understood as a clinical condition representing an intense brain-heart crosstalk and might mimic ischemic heart disease. Two main entities (neurogenic stunned myocardium [NSM] and stress cardiomyopathy) have been better characterized in the neurocritically ill patients and they portend worse clinical outcomes in these cases. The pathophysiology of NSM remains elusive. However, significant progress has been made on the early identification of neurocardiac compromise following acute critical brain disease. Effective prevention and treatment interventions are yet to be determined.
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PMID:Acute Cardiac Complications in Critical Brain Disease. 2896 13

Acute cardiac complications in critical brain disease should be understood as a clinical condition representing an intense brain-heart crosstalk and might mimic ischemic heart disease. Two main entities (neurogenic stunned myocardium [NSM] and stress cardiomyopathy) have been better characterized in the neurocritically ill patients and they portend worse clinical outcomes in these cases. The pathophysiology of NSM remains elusive. However, significant progress has been made on the early identification of neurocardiac compromise following acute critical brain disease. Effective prevention and treatment interventions are yet to be determined.
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PMID:Acute Cardiac Complications in Critical Brain Disease. 2950 18