How Heart Rate Should Be Controlled in Patients with Atherosclerosis and Heart Failure.

PURPOSE OF REVIEW: Resting heart rate is an independent risk factor for all-cause and cardiovascular mortality in patients with heart failure. The main objectives are to discuss the prognosis of heart rate, its association with coronary atherosclerosis, and the modalities of control of the heart rate in sinus rhythm and in the rhythm of atrial fibrillation in patients with chronic heart failure. RECENT FINDINGS: As a therapeutic option for control heart rate, medications such as beta-blockers, digoxin, and finally ivabradine have been studied. Non-dihydropyridine calcium channel blockers are contraindicated in patients with heart failure and reduced ejection fraction. The influence of the magnitude of heart rate reduction and beta-blocker dose on morbidity and mortality will be discussed. Regarding the patients with heart failure and atrial fibrillation, there are different findings in heart rate control with the use of a beta-blocker. Patients eligible for ivabradine have clinical benefits and increased ejection fraction. Vagal nerve stimulation has low efficacy for the control of heart rate. Complementary therapies such as tai chi and yoga showed no effect on heart rate. In this review, we discuss the main therapeutic options for the control of heart rate in patients with atherosclerosis and heart failure. More research is needed to examine the effects of therapeutic options for heart rate control in different population types, as well as their effects on clinical outcomes and impact on morbidity and mortality.

Effects of acute prenatal exposure to ethanol on the postnatal morphology of the prefrontal cortex in wistar rats

Prenatal exposure to ethanol is frequently associated with micronecephaly, hypomyelinization, delayed cell migration, and impaired neuronal and glial maturation in the offspring. The mechanism by which ethanol induces its effects on the development of the nervous system is still not fully understood. In this study, the influence of acute prenatal exposure to ethanol on the prefrontal cortex cells of rats were examined. Three doses of ethanol (3g/kg of body weight) were administered intraperitoneally to pregnant female rats on the 12th day of pregnacy, at 8 hours intervals. Control rats received the same treatment but with a saline solution. Cells in the synthesis phase (S) of the cell cycle were labeled with bromodeoxyuridine. Six controls and 12 ethanol-treated neonates were sacrificed on the 8th day of postnatal life. The distance between nuclear cores in immunohistochemically labeled cells was determined by image analysis. Control rats had a normal neocortex, with six layers in the prefrontal region. Rats treated with ethanol showed ectopia of pyramidal neurons in layers I and II, heterotopia in the basal area of the prefrontal fissure, and a decrease in cellular density in layers I and VI of the cerebral prefrontal cortex. These alterations could help to explain some of the dysfunctions reported in patients with fetal alcohol syndrome.