In this study, we investigated the potential association between WPP and CCF in patients with STEMI who underwent p-PCI. Our findings revealed a significant correlation between WPP and poor CCF. Moreover, through multivariate logistic regression analysis, we identified WPP as an independent predictor of poor collateral flow in this patient population. Moreover, DM, pre-infarction angina, Killip class III/IV, and multivessel disease were also found to be independent predictors of CCF.
When a coronary artery becomes occluded or severely stenosed in patients with STEMI, a remodeling process is triggered, leading to the enlargement of pre-existing, non-functional arterioles. This process initiates the development of CCF in response to the redistribution of blood flow and increased shear stress [21, 22]. The formation of CCF occurs in two distinct stages known as angiogenesis and arteriogenesis [23]. Various factors, including hypoxia, hypoperfusion, shear stress, cytokines, time of occlusion, DM, and severity of CAD, play critical roles in stimulating these stages [24]. In our study, we observed that DM and multivessel disease are predictive for poor CCF in patients with STEMI. Despite some findings suggesting that DM increases coronary collateral formation, our study indicates that the collaterals formed in diabetic patients are inadequate compared to those without diabetes, and even coronary collaterals are negatively affected by DM. Additionally, the insufficiency of antegrade coronary flow in multivessel disease may impede the effective development of CCF, which serves as a protective mechanism against cardiac ischemia.
HT, a well-known risk factor of CAD, can contribute to reduced myocardial flow reserve. Interestingly, an inverse relationship between CCF and SBP and PP was shown for the first time by Koersalman et al.[25] In their study including 237 patients, patients with high preintervention SBP had fewer collaterals, and also the group with good collaterals had lower SBP and PP [25]. It is well known that SBP and DBP which increase concomitantly due to age related changes in arterial stiffness, begin to diverge after approximately 50–55 years of age, resulting an increase in SBP and a decrease in DBP [26]. Factors such as elastin thinning, degradation and replacement by collagen in the arterial wall are thought to contribute to this process [26]. These changes present as wide pulse pressure in cardiac examination. Although the pathophysiologic pathways are not fully understood, current researches suggest that WPP related to extensive cardiovascular disease [9, 10]. However, the literature exploring the relationship between WPP and CCF is currently limited. Therefore, our study aimed to investigate the potential association between WPP and CCF in patients with STEMI. Our study showed that WPP is a negative predictor of CCF, unlike SBP, DBP, MAP and even PP. In our study, the observed association between WPP and poor collateral development may be attributed to several underlying mechanisms. The inverse association currently found between WPP and good CCF may be described by functional and structural remodeling, termed microvascular rarefaction of coronary arterioles, in response to increased PP [27, 28]. This process comprises obliteration of pre-existing blood vessels, particularly arteriolar vessels 100–150 mm in diameter. Moreover, Boudier et al.[29] suggested that the resulting decrease in micro vascularity would increase both peripheral vascular resistance and pulse pressure. In addition, increased PP reflects greater arterial stiffness, impaired endothelial function, and altered vasomotor tone, which may hinder the development and recruitment of collateral vessels. These findings support the notion that arterial stiffness may act as a barrier to collateral growth, thereby reducing the capacity for collateral-dependent perfusion during myocardial infarction. Although this complex and bidirectional relationship between PP and CCF remains unclear, WPP appears to be a predictor of poor CCF.
Previous studies have emphasized the importance of coronary collateral development in limiting the extent of myocardial damage and improving clinical outcomes following STEMI.[30–32] Aslanjari et al.[2] have demonstrated that patients without collaterals are at a higher risk of developing cardiogenic shock. In addition, they observed a significant protective effect against cardiogenic shock, even with the presence of smallest degree of collateral flow to the ischemia related artery. Our study, which reveals that Killip class III/IV heart failure is a predictor of poor CCF, supports previous research and underscores the impact of CCF on the development of acute heart failure. However, contrary to previous findings, cardiogenic shock rates were similar between the two groups in our study. The lower proportion of patients with cardiogenic shock (Killip class IV) in our study compared to the study of Aslanjari et al.[2], as well as differences in the classification of CCF, may have influenced the results. Further studies are warranted to explore this topic further.
The development of such collaterals is time dependent process. A previous study found that history of pre-infarct angina can provide stimuli resulted in collateral development [33]. Similar to these findings, pre-infarction angina was also significantly more common in the good CCF group in this study. Furthermore, the presence of pre-infarction angina was identified as an independent predictor of good CCF. This finding is intriguing as pre-infarction angina may signify ongoing ischemia and a state of chronic vascular dysfunction. Such a milieu might influence the development of collaterals, leading to compensatory mechanisms in response to acute ischemic events.
Overall, our study emphasizes the clinical importance of WPP as a potential indicator of poor CCF in patients with STEMI undergoing p-PCI. This parameter, easily obtainable from BP measurement, may help identify individuals at higher risk of impaired collateralization and, therefore, enable interventional cardiologists to tailor treatment strategies for improved outcomes. Nonetheless, our study contributes valuable insights into understanding the complex interplay between hemodynamic factors and coronary collateral formation. However, additional research is necessary to corroborate our findings and elucidate the precise mechanisms linking WPP to coronary collateralization.
Limitations
Our study had several limitations. Firstly, the measurement of BP at hospital admission may be influenced by preprocedural stress responses and concurrent drug therapy, which may not align with current guideline [16]. Secondly our study protocol only encompassed angiographically visualized coronary collaterals with a diameter exceeding 100 µm. Lastly, in our study, the WPP was not categorized into subgroups such as high systolic-low diastolic BP (isolated systolic hypertension), low systolic-low diastolic BP and high systolic-high diastolic BP. Consequently, the association of these subgroups with collateralization could not be evaluated.