Objectives: Despite major advances in understanding of pathogenesis and treatment, the mortality associated with bronchial asthma has risen progressively since 1977. Analysis of contemporary medical history indicates that at least some excess deaths i...
Objectives: Despite major advances in understanding of pathogenesis and treatment, the mortality associated with bronchial asthma has risen progressively since 1977. Analysis of contemporary medical history indicates that at least some excess deaths in bronchial asthma is related to the use of inhaled beta-adrenergic agonists. So we undertook a study to examine the effects of inhaled beta-2 agonist in obstructive airway disease patients group whether it can produce abnormal cardiac function even in usual dosage. Methods: Heart rate, QTc interval, and serum potassium changes after inhalation of salbutamol were studied in 20 normal controls, 11 asthmatic patients, and 9 chronic obstructive pulmonary disease (COPD) patients. Base-line serum potassium level and electrocardiogram were taken just before and 60 minutes after 2 puffs(200㎍) inhalation of salbutamol. Three days later, repeated base-line serum potassium and electrocardiogram were taken just before and 60 minutes after 4 puffs(400 ㎍) inhalation of salbutamol. Results: The serum potassium concentraton was changed in normal control and COPD subjects, but statistical singificance was not found. Prolongation of the QTc interval was significant in asthma and COPD subjects after 4 puffs inhalation of salbutamol (p<0.05). Changes in QTc interval following 2 puffs inhalation of salbutamol was significant only in COPD subjects (p=0.05). Conclusion: Salbutamol causes QTc prolongation in bronchial asthma and COPD patients group in usual dosage. Futher studies are recommanded to evlauate the clinical significancy of QTc prolongation after inhaled beta-2 agonist use.