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Abstract Background COVID-19 infection is the most serious global public health crisis of the century. With no approved treatments against it, investigational treatments are being used despite limited safety data. Besides being at higher risk of complications of COVID-19 infection, patients with underlying cardiovascular disease are more likely to develop cardiac-related side effects of treatment. We present a case of sinus arrest with junctional escape related to lopinavir–ritonavir. Case summary A 67-year-old man, with underlying stable ischaemic heart disease, acquired COVID-19 infection. He had a prolonged duration of fever and cough. He subsequently developed acute respiratory distress and required intensive care unit (ICU) care. Given his severe infection, he was started on lopinavir–ritonavir. Hydroxychloroquine was not used as he had a prolonged QTc interval. During observation in the ICU, the patient developed recurrent episodes of sinus arrest with junctional escape. Initial concerns were of myocarditis, but he had no ST-segment changes on ECG, with mild elevations of highly sensitive troponin I and a normal transthoracic echocardiogram. A multidisciplinary team discussion involving the intensivist, infectious disease physicians, and cardiologist; the decision was made to stop treatment with lopinavir–ritonavir. Within 48 h, the bradyarrhythmia resolved. The patient did not require transvenous and permanent pacemaker insertion. Conclusion Current efficacy and safety evidence of lopinavir–ritonavir as a treatment in COVID-19 patients is limited. Although uncommonly reported, those with underlying cardiovascular disease are at increased risk of bradyarrhythmia-related adverse effects of lopinavir–ritonavir. When initiating investigational therapies, especially in patients with cardiovascular conditions, adequate counselling and close monitoring are required.

Background: The growing cardiovascular disease (CVD) epidemic calls for further research to identify novel biomarkers for earlier detection and as potential therapeutic targets. Biomarkers Regulated on Activation, Normal T Cell Expressed and Secreted (RANTES), extracellular matrix metalloproteinase inducer (EMMPRIN), and matrix metalloproteinases (MMP-2, and MMP-9) are linked to proatherogenic and proinflammatory pathways of CVD development, the majority of which are coronary artery disease (CAD) and stroke. We evaluated potential factors affecting these four biomarkers and established their association with CVD. Methods: This is a cross-sectional analysis using a nested case-control design involving 580 participants aged 21–75 years from the prospective multi-ethnic cohort study. A total of 290 CVD cases and 290 age-and sex-matched controls were identified. All participants underwent interviews, health screenings, and provided blood samples, including biomarkers RANTES, EMMPRIN, and MMPs. CVD was defined based on previous medical history. Results: The average age of the participants was 55.7(SD = 10.3) years of age, and 34.6% were female. Arrhythmia history and low-density lipoprotein (LDL) levels were significant factors of logEMMPRIN (β = −0.124 [−0.245, −0.003] and β = 0.111 [0.0, 0.191], respectively). Only female sex (β = 0.189 [0.078, 0.300]) for logRANTES and age (β = 0.033 [0.010, 0.055]) for logMMP-2 and logMMP-9 were significant. The Indian ethnicity (β = 0.192 [0.048, 0.335]) and highly sensitive C-reactive protein (hs-CRP) levels (β = 0.063 [0.011, 0.116]) were statistically significant for logMMP-9. No association was detected between biomarkers and CVD. Conclusions: In this multi-ethnic study cohort, RANTES was associated with sex, EMMPRIN was associated with a history of arrhythmia and LDL levels, MMP-2 with age, and MMP-9 with ethnicity and hs-CRP levels. The biomarker serum levels were not associated with CVD.