Stress-induced cardiomyopathy in the perioperative setting

Abstract

In their report in this issue of the Journal, Suk et al. describe the case of a 37-year-old female who developed anaphylaxis in response to cefotiam administration during a laparoscopic surgical procedure. A prolonged period of profound hypotension was followed by appropriate resuscitative maneuvers, but the patient subsequently developed a cardiomyopathy requiring ongoing medical treatment. The authors highlight a rather unusual presentation of Tako-Tsubo cardiomyopathy which occurred in the perioperative setting. Increasingly, we are recognizing that Tako-Tsubo cardiomyopathy, also commonly referred to as stress-induced cardiomyopathy, transient cardiomyopathy, or apical ballooning syndrome, is a condition which may be more frequent in the perioperative setting than commonly appreciated. What is unusual about this case and somewhat unsettling is the observation that antibiotic-induced anaphylaxis or the treatment of anaphylaxis could, in turn, be associated with a potentially life-threatening cardiomyopathy. Interestingly, the pathophysiology of this cardiomyopathy may be similar to that of other disease entities that may be associated with acute cardiac dysfunction, including subarachnoid hemorrhage. Based on the underlying etiology, stress-induced cardiomyopathy can be divided into two categories. The first category is related to emotional distress, leading to catecholamine surges and resulting in cardiac dysfunction. The second category is related to physical-pathological distress secondary to disease entities, including pneumonia, severe acute asthma, or anaphylaxis, where catecholamine surges are secondary to the underlying disease process, which secondarily induces this unique cardiomyopathy. For both categories of stress-induced cardiomyopathy, there is an associated release of large quantities of epinephrine and norepinephrine, which are thought to be the primary mediators of the cardiomyopathy. The catecholamines temporarily disrupt the cardiac microvasculature resulting in myocardial dysfunction. In their report, Suk et al. infer that excess catecholamine surges may have occurred, either in response to the primary anaphylactic event or secondarily to the administration of exogenous epinephrine and norepinephrine given to treat the acute event. The original report of stress-induced cardiomyopathy originates from Japan in 1991. The authors reported on five cases from a series of 415 patients who presented with symptoms of acute myocardial infarction (AMI). Two of these patients had evidence of vasospasm at the time of angiography; two others developed vasospasm in response to the injection of ergonovine as a provocative test. There are numerous other reports in the literature of ambulatory patients presenting with stress-induced cardiomyopathy. The most comprehensive of these reports is from a systematic review of published case series. From the published series, it is inferred that up to 2% of patients presenting with AMI have a stress-induced cardiomyopathy, and furthermore, 27% of the presentations are secondary to emotional stress only, with 38% of patients having some type of physical stressor. The underlying causes in the remainder of cases were unreported. The associated mortality is reported to be 1.1%. While many case reports have documented an emotional trigger prior to the onset of symptoms, the few perioperative case reports have typically described events occurring intraoperatively under general anesthesia. D. Bainbridge, MD (&) D. Cheng, MD Department of Anesthesia & Perioperative Medicine, London Health Sciences Center-University Hospital & St. Joseph’s Health Care, University of Western Ontario, 339 Windermere Road, London, ON N6A 5A5, Canada e-mail: daniel.bainbridge@lhsc.on.ca