Author + information
- Published online February 3, 2020.
- Federico M. Asch, MD∗ ( and )
- Diego Medvedofsky, MD
- ↵∗Address for correspondence:
Dr. Federico M. Asch, MedStar Health Research Institute at MedStar, Washington Hospital Center, 100 Irving Street, NW, Suite EB 5123, Washington, DC 20010.
- global longitudinal strain
- right ventricle
- stress-induced cardiomyopathy
- subarachnoid hemorrhage
Although ejection fraction (EF) is still the reference standard for evaluation of left ventricular (LV) function, concerns over reproducibility and accuracy have challenged its use in clinical practice. Moreover, the idea that a fall in EF is not a sensitive marker of subtle LV dysfunction has shifted attention to more novel approaches. Among them, myocardial deformation analysis by strain is a more direct form of evaluating the myocardium itself throughout the cardiac cycle, as opposed to EF, which relies on LV volumes and endocardial inward traction based only on the end-diastolic and end-systolic frames. Therefore, a subtle myocardial dysfunction that does not significantly affect endocardial movement or does not affect the end-systolic frame may not reflect an impaired EF but could be detected by strain analysis. LV longitudinal strain has been suggested to be superior to EF in cardiomyopathies of different causes, including primary cardiomyopathies or those secondary to the use of toxic drugs such as oncologic treatments (1,2). Despite significant limitations related to its reproducibility (mostly among different vendors), global longitudinal strain (GLS) is an interesting concept that is being well received by physicians beyond cardiology and helps to build bridges among cardiologists and neurologists, oncologists, and specialists in other disciplines.
The relationship between acute neurological events and LV dysfunction has been described for years. Indeed, electrocardiographic changes described as “neurological T waves” became part of our everyday medical glossary. Over the last 20 years, stress-induced cardiomyopathy has been the subject of major research and clinical interest. The focus has been to understand how emotional or post-surgical stress or even the modulation caused by the use of adrenergic drugs could induce characteristic forms of wall motion abnormalities. The typical apical ballooning form in which the apex is akinetic or dyskinetic and basal segments are normal or hyperdynamic (i.e., Takotsubo cardiomyopathy, named after a fishing pot used in ancient Japan to trap octopi) is the pathology most commonly found. However, a variety of phenotypes for this syndrome have been described, so-called atypical or reversed Takotsubo, in which the wall motion abnormalities present with a different distribution. A 2-dimensional echocardiographic pattern consistent with “reversed Takotsubo” in patients with subarachnoid hemorrhage (SAH) was described 20 years ago by Zaroff et al. (3) and was suggested to be a “neurally-mediated” cardiac injury based on the fact that adrenergic terminals are more prominent in the affected regions of myocardium. The link between adrenergic surge and stress-induced cardiomyopathy was later demonstrated by Wittstein et al. (4) through correlations between serum catecholamine levels and the typical wall motion abnormalities.
In this issue of iJACC, Kagiyama et al. (5) add an extra relevant piece to the landscape of neurocardiology by analyzing LV myocardial deformation in a large population of patients with acute SAH detected using speckle tracking technology. Their findings suggest that GLS can detect subtle myocardial dysfunction with higher sensitivity than LVEF or electrocardiograms and, most importantly, that the presence of abnormal GLS carries a worse prognosis in the setting of a neurological condition that is per se high risk. The regional abnormalities followed a pattern similar to that described by Zaroff et al. (3), consistent with reversed Takotsubo cardiomyopathy. Interestingly, abnormal right ventricular GLS had additive value to LV GLS results in predicting in-hospital mortality, suggesting that the neurocardiac injury in SAH cases could indeed be mediated by a systemic condition such as an adrenergic surge. Possibly, we are in the presence of one more cause (along with emotional, post-surgical, and psychiatric drugs, and so forth) in the spectrum of stress-induced cardiomyopathies. Although much remains to be understood about the interaction between the neurological system, acute subarachnoid hemorrhage, stress, catecholamines, and the myocardium, the report by Kagiyama et al. (5) provides an important new piece to filling in the neurocardiologic puzzle. Some immediate questions arise. If the catecholamine surge occurring in acute SAH induces stress-induced cardiomyopathy and increases the risk for in-hospital death, is there a role for beta- and alpha-blockers in the acute treatment of these patients? Should every patient undergo an echocardiogram study with strain analysis?
Whether by proving prognostic value, detecting subclinical disease, or improving interdisciplinary medical care, the clinical value of myocardial deformation and strain keeps growing. We look forward to further progress in neurocardiology and to further understanding cardiac diseases and myocardial injury with the development of strain technologies.
↵∗ Editorials published in JACC: Cardiovascular Imaging reflect the views of the authors and do not necessarily represent the views of iJACC or the American College of Cardiology.
Dr. Asch has received research grants from TomTec, GE Healthcare, and Ultromics. Dr. Medvedofsky has reported that he has no relationships relevant to the contents of this paper to disclose.
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