Effect of Pain on Cardiac Twist Mechanics: A Preliminary Study

Introduction: The sympathetic nervous system (SNS) is known to respond to various stresses that the body encounters. Stimulation of the SNS is associated with increases in heart rate, blood pressure, myocardial contractility and work of the heart. While it is universally accepted that pain causes excitation of the SNS, the relationship between the two is not completely understood due to its complicated nature. Moreover, in patients with impaired pump function, pain may further compromise pump function of the heart, yet this has not been previously investigated. As a preliminary study, we hypothesized that acute pain will increase the demand of the pump, and hence decrease myocardial strain indices, with a resultant increase in myocardial stiffness in healthy subjects. Methods: IRB approval was obtained and each subject gave informed consent according to the Declaration of Helsinki. Each subject (N=3) underwent a standard medical history and physical prior to participation. Subjects each completed two cold pressor stimuli (CPS) by submerging a hand in two different water temperatures (4° C, and 16°) in duplicate for a total of 4 CPS exposures. After the subject’s hand had been submerged for one minute, echocardiographic measurements were recorded. Images taken during this time included a 4-chamber, 2-chamber, and AP long axis view. A period of 20 minutes between each test was allotted to allow the subject’s physiologic variables to return to baseline values. After completion of each study, echocardiographic data, including strain and strain rate was analyzed to calculate cardiac strain indices. Results: It was found that the 4°C CPS was associated with a decreased in cardiac strain (5% change in strain from baseline), correlating with increased chamber stiffness and increased sympathetic stimulation. There was little change in cardiac strain indices during the 16°C CPT trials (2% change in strain from baseline). Conclusions: These preliminary results suggest that perceived acute pain is at least partially responsible for increasing myocardial wall stiffness, as evidenced by cardiac strain indices. This study will be continued to fully address the hypotheses and eventually be implemented in a patient population to determine whether the effects are more significant in a diseased heart.