Olfactory dysfunction may predict myocardial injury in COVID-19 patients.

As a hypothesis, in the coronavirus disease 2019 (COVID-19) pandemic, growing evidence suggests a possible correlation between increased cytokine levels, olfactory dysfunction and myocardial injury. Puntmann et al. studied the cardiovascular magnetic resonance imaging of patients who survived COVID-19 and showed that 78% of the patients had cardiac involvement, and even if the disease had healed, 60% continued to have myocardial inflammation [1]. Haehner et al. showed that 64.7% of COVID-19 patients had ‘sudden smell loss’ [2]. In their autopsy study, Solomon et al. reported that there was no damage to olfactory bulbs or tracts of COVID-19 patients [3] whereas Torabi et al. reported significant increase in local tumour necrosis factor alpha (TNF-α) levels of the olfactory epithelium in COVID-19 patients [4]. Based on this, it has been observed that covid-19 disease has more frequent occurrence of sudden olfactory dysfunction than other flu diseases, cardiac involvement and thrombogenic events are more frequent, and it is a ‘cytokine storm’ since the first symptom phase. In addition we showed a direct relationship between the severity of heart failure and that of olfactory dysfunction. An important hypothesis explaining this clinical relationship is that TNF-α and interleukin-1 (IL-1) levels increase in heart failure patients and in those with olfactory dysfunction [5]. Considering this literature and two important recent studies, the similarity between the frequency of cardiac involvement (78%) and that of sudden smell loss (64.7%) in COVID-19 patients suggests that olfactory dysfunction in COVID-19 patients can be a predictor of myocardial injury. When olfactory dysfunction is detected in COVID-19 patients, providing optimal primary and secondary cardiovascular prevention can positively contribute to the disease course.

Declaration of Competing Interest

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.