This study provides Class I evidence that in ED patients with acute migraine, IV valproate is inferior to metoclopramide or ketorolac in improving headache outcomes.
Heart failure (HF) is a systemic illness with grave implications for bodily functions. The brain, among other vital organs, often suffers insults as a result of HF, and both anatomic and functional brain abnormalities were found in the HF population. This injury was demonstrated across a wide range of clinical conditions and cardiac functions and was shown to affect patients' outcomes. Although reduced cardiac output and high burden of cardiovascular risk factors are the prevailing explanations for these findings, there are data showing the involvement of neurohormonal, nutritional, and inflammatory mechanisms in this complex process. Here, the authors review the suggested pathophysiology behind brain injury in HF, describe its effect on patients' outcomes, offer a diagnostic approach, and discuss possible therapeutic options.
Myocardial ischemia, which results from emotional provocation, occurs in as many as 30–50% of patients with CAD during the discourse of their daily lives. This emotionally provoked or mental stress ischemia is associated with the poor prognosis, with emerging treatment strategies. This chapter will outline the conceptual constructs which support the pathophysiologic underpinnings, and biobehavioral aspects associated with this mental stress ischemia. We will review a biobehavioral model where cognitive stress is transduced in the brain. The response of the brain to psychosocial stress is a highly sophisticated and integrated process by which sensory inputs are evaluated and appraised for its importance in relation to previous experience and current goals. The biologic consequences of such stress transduced in the CNS has its effect upon the cardiovascular flow and function through changes in autonomic balance, which result in various biologic processes that culminate in the perturbation of flow and function of the heart.
beta-blocker therapy does not diminish the ability of vasodilator stress MPI to detect clinically significant CAD, nor hide the mortality risk of patients with normal studies not referred for catheterization.
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