BackgroundOxygenation-sensitive (OS) Cardiovascular Magnetic Resonance (CMR) is a promising utility in the diagnosis of heart disease. Contrast in OS-CMR images is generated through deoxyhemoglobin in the tissue, which is negatively correlated with the signal intensity (SI). Thus, changing hematocrit levels may be a confounder in the interpretation of OS-CMR results. We hypothesized that hemodilution confounds the observed signal intensity in OS-CMR images.MethodsVenous and arterial blood from five pigs was diluted with lactated Ringer solution in 10 % increments to 50 %. The changes in signal intensity (SI) were compared to changes in blood gases and hemoglobin concentration. We performed an OS-CMR scan in 21 healthy volunteers using vasoactive breathing stimuli at baseline, which was then repeated after rapid infusion of 1 L of lactated Ringer’s solution within 5–8 min. Changes of SI were measured and compared between the hydration states.ResultsThe % change in SI from baseline for arterial (r = -0.67, p < 0.0001) and venous blood (r = -0.55, p = 0.002) were negatively correlated with the changes in hemoglobin (Hb). SI changes in venous blood were also associated with SO2 (r = 0.68, p < 0.0001) and deoxyHb concentration (-0.65, p < 0.0001). In healthy volunteers, rapid infusion resulted in a significant drop in the hemoglobin concentration (142.5 ± 15.2 g/L vs. 128.8 ± 15.2 g/L; p < 0.0001). Baseline myocardial SI increased by 3.0 ± 5.7 % (p = 0.026) following rapid infusion, and in males there was a strong association between the change in hemoglobin concentration and % changes in SI (r = 0.82, p = 0.002). After hyperhydration, the SI response after hyperventilation was attenuated (HV, p = 0.037), as was the maximum SI increase during apnea (p = 0.012). The extent of SI attenuation was correlated with the reduction in hemoglobin concentration at the end of apnea (r = 0.55, p = 0.012) for all subjects and at maximal SI (r = 0.63, p = 0.037) and the end of breath-hold (r = 0.68, p = 0.016) for males only.ConclusionIn dynamic studies using oxygenation-sensitive CMR, the hematocrit level affects baseline signal intensity and the observed signal intensity response. Thus, the hydration status of the patient may be a confounder for OS-CMR image analysis.

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.

In conclusion, a voluntary long breathhold after hyperventilation leads to an increase of the myocardial perfusion reserve index. This may impact findings from current practice of first-pass perfusion imaging. The clinical utility of breathing maneuvers as a vasodilatory stimulus for first-pass perfusion imaging may warrant further research. J. MAGN. RESON. IMAGING 2016;44:947-955.

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