The key objective of the present longitudinal study is to assess the risk factors associated with the AHF classification in accordance with the symptoms and signs of AHF patients. Based on the research findings, the following conclusions have been made. Firstly, there is a significant relationship between the key symptoms and indicators of AHF and elevated d-dimer levels.
D-Dimer can be defined as a byproduct of cross-linked fibrin's plasmin-mediated breakdown, and it serves as an important marker for thrombogenesis. It can also indicate a hypercoagulable condition that develops following the rupture of plaque [6] The production of fibrin in the endogenous fibrinolytic system and the following progression of breakdown determine the plasma concentrations of D-dimer [6]. Moreover, a number of studies have identified a relationship between heart failure and hemostatic problems [7, 8]. Furthermore, multiple studies have shown that increased D-dimer levels in HF patients who are hospitalized are linked to poor outcomes [9,10,11].
The vascular system of AHF patients is especially susceptible to thromboembolic events and this is due to coagulation abnormalities in such individuals. Research has shown that there may be a relationship between plasmin-mediated fibrin degradation (another sensitive indicator of ongoing thrombosis), and d-dimer levels (a key marker of a thrombotic burden that indicates the turnover of fibrin secondary to plaque rupture at vascular sites), and an inflammatory vascular state. [12] In AHF patients, this may be an indication of a systemic prothrombotic condition that is characterized by localized vessel wall-related fibrin production and breakdown. Moreover, this is associated with unstable atherosclerotic plaque activity. [13] The predictive impact of d-dimer impacts the mortality of AHF patients. The mechanism underlying this may be influenced by the different pathogenic pathways of thrombotic events that are involved in processes of atherosclerosis, inflammatory conditions and infectious disease.[14] Moreover, a number of studies have shown a strong correlation between d-dimer levels and increased mortality in patients with heart disease. [14-17]. Research thus indicates that higher D-dimer levels could independently predict all-cause mortality in HF patients during a 1-year follow-up [18].
In terms of HF, it has already been established that acute HF and outpatients have higher levels of d-dimer in their bodies [19,20]. Nonetheless, very few studies have examined this risk in AHF patients based on their clinical symptoms and signs. D-dimer has always been considered a key indicator of a temporary hypercoagulable state, although recent research has indicated that this condition can be persistent, particularly in those who have been hospitalised due to heart failure (HF) patients. [21] Moreover, HF patients often experience immobility and hemodynamic changes that have pro-thrombotic causes, although such changes are reversible and treatable. Additionally, endothelial damage, persistent hemodynamic irregularities, and chronic systemic inflammatory condition in HF patients may be able to control the long-term risk factors of thrombosis. There also appears to be a relationship between elevated D-dimer levels and HF prognosis, and this reflects cardiac functional status and the severity of the disease severity. Ultimately, this is caused by haemodynamic changes and impaired blood flow in HF patients. Moreover, the inflammatory reactions that occur in HF patients could be due to increased D-dimer levels, which induce the synthesis and release of inflammatory cytokines [22]. Thus, in turn, this increases the disease burden in such individuals.
Despite the fact that the ordinary logistic regression also highlighted a significant relationship between the "cold and dry" and lower patient age (OR 0.95, 95% CI (-0.084;0.011); P=0.011), it was surmised that this risk factor had no significance in patients with AHF. This is because the average age of patients in group I was 68.5±21.82 years, group II was 68.64±1.45 years, group III was 64.11±2.15 years, and group IV was 61.41±2.36 years. Patients with AHF, particularly those who are elderly, are more likely to experience complications, readmission, and mortality [23]. Additionally, the age disparities between the four groups are not significant, which suggests that there could be potential confounders that were not able to be controlled.
Limitations
It is important to note that there are several limitations associated with this research, the first of which is that the sample size is quite small, Additionally, it is possible that the observed differences in clinical outcomes are influenced by confounders that could not be controlled. Moreover, the d-dimer levels of patients in this population may be impacted by multiple comorbidities (i.e., malignancies and deep vein thromboembolism). [24] This clinical observational trial was also carried out in China with Chinese participants, and this largely impacts the generalisability of the findings. What’s more, the research participants were assessed for AHF through a clinical examination performed in the acute setting, and thus their symptoms could be non-specific. Therefore, future researchers should consider examining the topic using more accurate assessment methods and larger sample sizes in order to fully understand the risk factors impacting AHF patients.