Tehran University Medical Journal

Background: The use of synchronized intermittent mandatory ventilation (SIMV) and pressure support ventilation (PSV) have been used for older children and adults. The purpose of this study was to compare PSV and SIMV modes in weaning from mechanical ventilation in neonate with respiratory failure.

Methods: A randomized clinical trial study carried out in NICU ward of Valiasr hospital Imam Khomeini Hospital complex, Tehran, Iran. Thirty neonates enrolled in two groups of 15. At the weaning time they randomly assigned to SIMV or PSV. They compared for tidal volume (V_T), peak inspiratory pressure (PIP), incidence of pneumothorax, weaning failure and duration of weaning. For two groups to be homogeneous, maternal disease during pregnancy were also considered.

Results: In this study, V_T, PIP, incidence of pneumothorax and weaning failure did not differ between groups duration of ventilation of the two methods (hours) and duration of hospitalization (days) were separately calculated. The only meaningful difference in two groups were due to weaning duration. The neonates weaned by PSV mode experienced shorter weaning time. (6.05 hours). The weaning time in SIMV mode was longer (45 hours) (P=0.006). There were no other meaningful differences between the two groups

Conclusions: According to the results of this study there were no advantage using PSV over SIMV except that the weaning time were shorter in PSV. This decrease in weaning time causes less dependence of the neonate to the ventilator and as a result secure them from complications.

Background: Various therapeutic protocols have been recommended for treating dyslipidemia, particularly in patients with coronary artery disease. The purpose of this study was to assess the efficacy of statin use with or without fenofibrate on echocardiographic findings of patients with coronary artery disease and dyslipidemia.
Methods: This clinical trial was conducted on 124 patients with coronary artery disease and dyslipidemia in Baqiyatallah Hospital in Tehran, Iran during 2008 to 2010. The first group of patients (64) received simvastatin (20 mg) and fenofibrate (200 mg) with low lipid diet and exercise while the second group (60) only received simvastatin with low lipid diet and exercise for one year.
Results: The mean age of the participants was 54.3±6.5 years. The first group showed significant changes in lipid profile and left ventricular ejection fraction (LVEF), (P<0.05). Left ventricular diastolic function parameters showed no significant changes in both groups upon 12 months of treatment.
Conclusion: The results of this study show, one-year treatment by simvastatin and fenofibrate can be effective on lipid profiles, and improve LVEF with resultant positive effect on heart function.

Background: The 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhi-bitors (statins) have revolutionized the treatment of hypercholesterolemia. Some evide-nce indicated the role of nodal refractoriness and concealed conduction in anticipating the ventricular rate during atrial fibrillation. Recent evidence has indicated that statins can reduce the incidence of both supraventricular and ventricular arrhythmias. The aim of the present study is to investigate adenosine A1 receptor role on simvastatin protecti-ve effects on atrioventricular nodal properties in isolated atrial fibrillation model of rabbit heart.
Methods: The present study was performed in cardiovascular research center of Golestan University of Medical Sciences in 2012. Recovery and atrial fibrillation protoc-ols were used to study electrophysiological properties of atrioventricular node in 5 groups of male Newsland rabbits (n=40). Extracellular recording was carried out from transitional cells of posterior and anterior extension of AV-node and upper part of atrium and its bundle. All stimuli protocols repeated in the presence of adenosine A1 receptor agonist and antagonist (dipridamole and CPX) alone or with simvastatin on isolated perfused atrio-nodal preparation. Extracellular field potential recording was sampled during specific stimulation protocols.
Results: Significant inhibition was observed in basic node properties such as wencke-bach prolongation, functional refractory period, effective refractory period and atriove-ntricular node conduction time with simvastatin (P<0.05). Simvastatin prolonged His-His interval and increased number of concealed beat in atrial fibrillation protocol (P<0.05). The simvastatin protective effects on atrioventricular nodal properties were intensified by dipridamole as an adenosine A1 receptor agonist (P<0.05), but CPX as an adenosine A1 receptor antagonist could only dampen them (P>0.05).
Conclusion: Our results showed that the use of adenosine agonist increased simvastatin effects on electrophysiological properties of atrioventricular node, but its antagonist could not prevent these effects. This may indicate simvastatin protective mechanism on atrioventricular node electrophysiological properties without adenosine direct involve-ment.