Cardiovascular diseases (CVD) are the leading cause of death worldwide, accounting for 31.8 % of global mortality and 26.6 % of deaths among Indians in 2017 [1], [2]. Coronary artery disease (CAD) is caused by plaque formation in the blood vessels of coronary arteries, which affects 1.72 % of the global population and causes nine million deaths annually [3], [4]. Atherosclerosis, a chronic inflammatory condition, is the primary pathological step leading to CAD and develops through the accumulation of inflammatory cells, lipids, and monocyte subset-derived macrophages [5], [6]. Many studies have shown that activated platelets are involved in the development and progression of atherosclerosis and play an essential role in the inflammation of coronary arteries [7], [8], [9]. Recent studies have revealed that several cytokines/chemokines are released from activated platelets, promoting the interaction of platelets with endothelial cells and leukocytes, inducing inflammatory responses, and contributing to the development of atherothrombosis and CAD [9], [10].

Triggering receptor expressed on myeloid cells like transcript 1 (TLT-1) widely distributed on the surface of thrombin-activated platelets and in the alpha granules of resting platelets [11], [12]. Upon platelet activation, a shortened portion (17 kDa) of TLT-1 is released into the circulation as soluble TLT-1 (sTLT-1) [12]. It has been observed that individuals with inflammatory disorders have higher levels of sTLT-1 in the blood. This may enhance platelet aggregation by promoting actin polymerisation and adhesion to the endothelium [13]. Increased plasma soluble TLT-1 levels were observed in sepsis and acute respiratory distress syndrome patients [14], [15]. A recent study reported that elevated levels of sTLT-1 are associated with CAD and enhanced inflammation in the arterial lumen during atherosclerosis [16]. Numerous studies have suggested that interactions between platelets and immune cells induce persistent inflammation in CAD [17], [18]. However, the role of sTLT-1 interaction with circulatory immune cells and inflammatory cytokines/chemokines needs to be elucidated. Therefore, the present study aimed to investigate the association of circulatory sTLT-1 with immune cells, platelet-immune cell aggregation markers, and cytokines/chemokines in the severity of CAD.