Evidence for Acute Myocardial and Skeletal Muscle Injury after Serial Transthoracic Shocks in Healthy Swine

Abstract

BackgroundPrevious serological studies have shown controversial results whether defibrillation or cardioversion can cause myocardial injury. Cardiovascular Magnetic Resonance (CMR) can be used to detect myocardial edema, hyperemia and capillary leak as features of acute myocardial injury. The aim of this study was to assess for myocardial and skeletal muscle injury in swine following transthoracic shocks.MethodsSeventeen anaesthetized swine were examined, with 11 undergoing five synchronized transthoracic shocks (200J). Myocardial and skeletal muscle injury were assessed at baseline and up to 5h post-shock employing T1 mapping, T2 mapping, early and late gadolinium enhancement. Serologic markers (cFABP, TnI, CK, and CK-MB) and myocardial tissue were assessed by standard histology methods.ResultsIn myocardial regions within the shock path, T1 and T2 were significantly increased compared to remote myocardium in the same animals. The early gadolinium enhancement ratio between the left-ventricular myocardium and the right pectoral muscle was also increased compared to control animals. After the shocks cFABP and CK were significantly elevated. After shock application, the regions identified as abnormal by CMR showed significantly increased interstitial and myocardial cell areas in histological analysis. This increased cell area suggests significant cellular and interstitial edema.ConclusionOur pilot study data indicate that serial defibrillator shocks lead to acute skeletal muscle and myocardial injury. CMR is a useful tool to detect and localize myocardial and skeletal muscle injury early after transthoracic shocks in vivo. In the future the technique could potentially be used as an additional tool for quality control such as verifying insufficient local shock application in non-responders after cardioversion or to develop safer shock forms.

Real‐Time Ventricular Fibrillation Amplitude‐Spectral Area Analysis to Guide Timing of Shock Delivery Improves Defibrillation Efficacy During Cardiopulmonary Resuscitation in Swine

“…Current defibrillators deliver biphasic electrical shocks, which are considered safer than monophasic electrical shocks for the myocardium . However, in a recent study—also in swine—synchronized biphasic electrical shocks delivered during spontaneous circulation (five 200‐J shocks in 5 minutes) were shown by cardiac magnetic resonance and histology to produce myocardial injury along the path of the electrical shock consistent with cell electroporation and capillary leakage leading to tissue edema . Functionally, there was reduction in left ventricular volumes indicative of diastolic dysfunction, an effect that we had previously reported after repetitive monophasic electrical shocks in an isolated rat heart model of VF .…”

“…12,13 However, in a recent study-also in swine-synchronized biphasic electrical shocks delivered during spontaneous circulation (five 200-J shocks in 5 minutes) were shown by cardiac magnetic resonance and histology to produce myocardial injury along the path of the electrical shock consistent with cell electroporation and capillary leakage leading to tissue edema. 42 Functionally, there was reduction in left ventricular volumes indicative of diastolic dysfunction, an effect that we had previously reported after repetitive monophasic electrical shocks in an isolated rat heart model of VF. 43 Our data suggest that shock burden could have been detrimental to the myocardium given its inverse relationship with both left ventricular function (modest association) and survival (weak association).…”

Targeted Delivery of Electrical Shocks and Epinephrine, Guided by Ventricular Fibrillation Amplitude Spectral Area, Reduces Electrical and Adrenergic Myocardial Burden, Improving Survival in Swine

“… 31 , 32 A previous study in swine showed that electrical shocks delivered during spontaneous circulation produced myocardial injury with functional reduction in left ventricular volume. 33 Histological analysis of these hearts revealed findings consistent with cell electroporation and capillary leakage, leading to tissue edema. A previous study in isolated rat hearts showed that repetitive monophasic shocks also resulted in decreased left ventricular volume and diastolic dysfunction.…”

Combined Analysis of Myocardial Deformation and Oxygenation Detects Inducible Ischemia Unmasked by Breathing Maneuvers in Chronic Coronary Syndrome

“…Accordingly, step-wise global deceleration of early diastolic strain across the breathing maneuvers was observed, and this was associated with increased T2 burden. Edema is also linked with ventricular stiffness and when myocardial edema aggravates, the rise of interstitial pressure reduces ventricular chamber compliance ( 34 , 35 ). While T2 is not often chronically elevated, edema at the time of CO 2 challenges may predispose cardiac patients to diastolic dysfunction.…”