Background: 

The prevalence of myocarditis in sudden cardiac death, especially in younger people ranges from 2 to 42%. Because of its variety of symptoms, the diagnosis remains challenging. T2 relaxation time has become the most important tool to diagnose active myocardial inflammation. However, some studies showed an impact of volume fluctuations on T2 relaxation time. Plasma volume status (PVS) is a good surrogate parameter for the patient´s volume status and is easy to calculate. 

The aim of this study was to determine the effect of PVS on the diagnostic value of T2 relaxation time in myocardial inflammation.

Methods: 

Between April 2017 and August 2021 patients with clinical indications for cardiac MRI were included in our study. Only patients with active inflammation and patients with normal findings were recognized. In every patient a blood sample was drawn and PVS was calculated. 

Patients were separated into PVS quartiles to explore T2 dependency.

Results: 

441 patients (47.27% female) were eligible for analysis. 347 patients were healthy (78.9%) while 93 (21.1%) showed signs of myocardial inflammation. T2 relaxation time was significantly elevated in patients with myocardial inflammation (37.83 (±3.00) vs 39.51 (±3.95), p<0.001). PVS showed no difference between the groups (-13.41 (±8.02) vs -12.33 (±10.25), p=0.283). PVS was correlated to T2 relaxation time with a beta of 0.19, p<0.001) (figure 1). In patients with pathological PVS values (above -4) T2 relaxation time was elevated (39.5ms [37ms – 42ms] vs 38ms [36ms – 40ms], p<0.01). There was a significant, non linear dose response relationship between PVS quartiles and T2  (37ms [ 35ms – 39ms] vs 38ms [36ms – 40ms] vs 39ms [37ms – 41ms] vs 39ms [ 37ms – 42ms], p < 0.001) (figure 2). Nevertheless T2 was a significant predictor of the presence of myocardial inflammation in logistic regression analysis (OR T2 1.18 [95% CI 1.09 – 1.27], p<0.001). Even after adjusting for PVS T2 remains an independent predictor for myocardial inflammation (OR T2 (adj. PVS) 1.18 [95% CI 1.09 – 1.28], p<0.001).

Conclusion: 

T2 predicts myocardial inflammation independent of the patients volumes status despite a significant dose response relationship of T2 and PVS.