Response to: myositis after SARS-CoV-2 vaccination occurs more frequently than assumed and is probably causally related.

We thank Finsterer et al. for the attention paid to our publication; we recognize the validity of the points mentioned in their letter to the editor and will try to answer the observations made.

Idiopathic inflammatory myopathies linked to vaccination against SARS-CoV-2: a systematic review.

The COVID-19 pandemic represents a global health problem, which has been mitigated by the opportune introduction of vaccination programs. Although we already know the benefit that vaccines provide, these are not exempt from adverse events which can be mild to deadly, such as idiopathic inflammatory myopathies, in which a temporal association has not been defined. It is for this reason that we carried out a systematic review of all reported cases of vaccination against COVID-19 and myositis. To identify previously reported cases of idiopathic inflammatory myopathies associated with vaccination against SARS-CoV-2 we registered this protocol on the website of PROSPERO with identification number CRD42022355551. Of the 63 publications identified in MEDLINE and 117 in Scopus, 21 studies were included, reporting 31 cases of patients with vaccination-associated myositis. Most of these cases were women (61.3%); mean age was 52.3 years (range 19-76 years) and mean time of symptom onset post-vaccination was 6.8 days. More than half of the cases were associated with Comirnaty, 11 cases (35.5%) were classified as dermatomyositis, and 9 (29%) as amyopathic dermatomyositis. In 6 (19.3%) patients another probable trigger was identified. Case reports of inflammatory myopathies associated with vaccination have heterogeneous presentations without any specific characteristics: as a consequence, it is not possible to ensure a temporal association between vaccination and the development of inflammatory myopathies. Large epidemiological studies are required to determine the existence of a causal association.

Polyunsaturated ω3 fatty acids prevent the cardiac hypertrophy in hypertensive rats.

It has been demonstrated that supplementation with the two main omega 3 polyunsaturated fatty acids (ω3 FAs), docosahexaenoic acid (DHA), and eicosapentaenoic acid (EPA), leads to modifications in the cardiac physiology. ω3 FAs can affect the membrane's lipid composition, as well as proteins' location and/or function. The Na+/H+ exchanger (NHE1) is an integral membrane protein involved in the maintenance of intracellular pH and its hyperactivity has been associated with the development of various cardiovascular diseases such as cardiac hypertrophy. Our aim was to determine the effect of ω3 FAs on systolic blood pressure (SBP), lipid profiles, NHE1 activity, and cardiac function in spontaneously hypertensive rats (SHR) using Wistar rats (W) as normotensive control. After weaning, the rats received orally ω3 FAs (200 mg/kg body mass/day/ 4 months). We measured SBP, lipid profiles, and different echocardiography parameters, which were used to calculate cardiac hypertrophy index, systolic function, and ventricular geometry. The rats were sacrificed, and ventricular cardiomyocytes were obtained to measure NHE1 activity. While the treatment with ω3 FAs did not affect the SBP, lipid analysis of plasma revealed a significant decrease in omega-6/omega-3 ratio, correlated with a significant reduction in left ventricular mass index in SHR. The NHE1 activity was significantly higher in SHR compared with W. While in W the NHE1 activity was similar in both groups, a significant decrease in NHE1 activity was detected in SHRs supplemented with ω3 FAs, reaching values comparable with W. Altogether, these findings revealed that diet supplementation with ω3 FAs since early age prevents the development of cardiac hypertrophy in SHR, perhaps by decreasing NHE1 activity, without altering hemodynamic overload.