Objective Pathophysiological mechanisms and pathways linking cardiovascular mortality and morbidity with air pollution were recently hypothesized. The present study evaluated association between air pollution and changes in heart rate variability as a marker of cardiac autonomic function in healthy individuals, and also determined the frequency of cardiac arrhythmias and QT interval changes on polluted compared to unpolluted days. Methods Continuous Holter electrocardiography (ECG) monitoring was conducted on 21 young healthy individuals in the two episodes of clean air and elevated air pollution in Tehran. All subjects underwent a medical history review, a physical examination and echocardiography in order to rule out structural heart diseases. Measured pollutants and parameters included NO 2 , CO 2 , O 3 , SO 2 , and PM10, which all showed significantly higher concentrations on polluted days. Holter parameters were measured for 24-h time segments and compared. Results Maximum heart rate was significantly lower in polluted air conditions in comparison with clean air conditions (115.1 ± 32.2 vs. 128.9 ± 17.7), and the square root of the mean of squared differences between adjacent NN intervals (r-MSSD) was higher in polluted air compared to clean air (99.0 ± 58.2 vs. 58.5 ± 26.4). Also, the occurrence of nonsustained supraventricular tachycardia was reported in 42.9% of participants in air pollution episodes, whereas this arrhythmia was not seen in clear air conditions (p = 0.001).Conclusion Changes in air pollution indices may lead to the occurrence of nonsustained supraventricular tachycardia, a slight reduction in maximum heart rate, and an increase in r-MSSD in healthy individuals. Air quality monitoring in cities associated with a high exposure to air pollutants is recommended in order to prevent such events.

In this study the severity of aspirin-induced gastric mucosal damage was investigated in rats with obstructive cholestasis. Cholestasis was induced by ligation and resection of the bile duct under general anesthesia. Two weeks after operation, the rats were fasted for 24 hours. Aspirin was administered orally in doses of 0, 128, 192, 266 and 335 mg/kg, and the animals were killed four hours after dosing. The dose of 266 mg/kg was chosen for a study of the time-dependency; other groups of animals were killed at time intervals of one, three, five, seven and nine hours after aspirin administration. The results showed that aspirin induces more severe gastric damage in bile duct resected rats compared with sham-operated and control animals. Salicylate levels of serums were also measured but there was no significant difference in serum salicylate levels between bile duct resected, sham-operated and control rats. It can be concluded that cholestasis can potentiate aspirin-induced gastric damage in rats.

A low-watt, low-temperature RF current application into the slow pathway area can be a provocative method for the induction of AVNRT probably by AV-junction warming and conduction-velocity augmentation.

The rate of dislodgement of atrial pacing leads is approximately 3%. To solve this problem, reoperation and repositioning of these leads is one of the solutions. Some operators have reported repositioning these leads with snare systems or deflectable catheters. In this communication, we present a new method using a specially designed urological basket to solve this problem.

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