Coronary slow flow phenomenon (CSFP) is characterized by the delayed contrast filling of terminal vessels of a coronary artery in the presence of normal or nearly normal epicardial coronary arteries (with stenosis <40%) during coronary angiography (CAG) [1,2]. Since the CSFP was first described by Tambe, it has garnered significant attention within the field of cardiology [3]. The incidence of CSFP in patients undergoing CAG for suspected coronary artery disease has been reported between 1% and 7% in previous studies [4,5]. Although the precise pathogenesis of CSFP remains elusive, studies have shown that systemic or local inflammation, oxidative stress, endothelial dysfunction, microvascular vasomotor dysfunction, diffuse atherosclerosis, and/or a combination of all listed factors are associated with CSFP [[6], [7], [8]].

Given that inflammation plays a crucial role in cardiovascular disorders and metabolic disorders, several recent studies have focused on the compound immune-inflammatory scores that incorporate biomarkers of inflammation and hematological parameters [9,10]. The commonly investigated compound risk scores, including neutrophil-lymphocyte ratio (NLR), platelet-lymphocyte ratio (PLR), and systemic immune-inflammation index (SII), are derived from the peripheral blood biomarkers such as platelets, neutrophils, monocytes, and lymphocytes and demonstrated an association with the presence of high-risk atherosclerotic cardiovascular disease, as well as poorer outcomes with the cardiovascular disorders [[11], [12], [13]]. Furthermore, the higher levels of NLR was recently demonstrated to be associated with the CSFP [14].

In 2020, a new compound immune-inflammatory risk score was created and validated by Fuca et al., known as the pan-immune-inflammation value (PIV) [15]. This parameter encompasses all peripheral blood cell populations, including neutrophils, monocytes, lymphocytes, and platelets, serving as a reflector of uncontrolled inflammatory pressure. PIV has been proposed as a stronger and more reliable predictor of clinical outcomes than classical immune-inflammatory markers in cancer [16,17] and ST-elevation myocardial infarction (STEMI) patients [18], but the relationship with CSFP is unclear. Therefore, considering the pathogenesis of CSFP, we evaluated the relationship between PIV values and CSFP in patients with angiographically normal coronary arteries.