LAUSR

Objectives The most perfect example of the mind-body interaction in all of medicine is provided by stress cardiomyopathy. In stress cardiomyopathy, what is initially a purely emotional event may become rapidly fatal. Prolongation of the QT interval is a cardinal feature of the condition, but the mechanism of the prolongation is unknown. We undertook a randomised controlled trial of stress with a cross-over design, comparing the cardiac response of women with a history of stress cardiomyopathy to age-matched controls to explore the mind-body interaction. Our hypothesis is that the hearts of women with a history of stress cardiomyopathy will respond differently to emotional stress than those of the controls. Method This is a randomised cross-over study. Each patient underwent two separate 24-hour Holter monitors performed at least 5 days apart. Baseline recording was followed by either the stress intervention (hyperventilation) or control (diaphragmatic breathing). Our primary endpoint is change in QTc interval over the first hour. Secondary endpoints were change in QTc over 24 hours, and change in SDNN, a measure of heart rate variability. As a secondary stressor, each participant was telephoned four times during their stressed recording and asked to complete a questionnaire. Results Twelve stress cardiomyopathy patients and twelve control patients were recruited. Baseline characteristics did not differ between cases and controls. With hyperventilation, there was a significant initial difference in anxiety (p<0.001), heart rate response (p<0.0001), and QTc (p<0.0002) compared to diaphragmatic breathing, but no differences between the cases and controls. Only first phone call caused an increase in QTc in cases and controls (p = 0.0098). SDNN increased with hyperventilation (p<0.0001) but did not differ between cases and controls. Conclusions QTc response in women with a history of stress cardiomyopathy does not differ from controls. The relevance of QT prolongation and sensitivity in the autonomic response to the pathogenesis of stress cardiomyopathy remains uncertain.