To improve the manuscript, consider the following suggestions

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  Address Heterogeneity : Conduct further analyses to explore and explain the sources of heterogeneity.

  
  
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  Strengthen Quality Assessment : Apply more stringent criteria for study quality in future analyses.

  
  
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  Include RCTs : If available, include RCTs in future updates to strengthen causal inferences.

  
  
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  Control for Confounders : Ensure that potential confounders are adequately controlled for the analysis.

  
  
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  Consider Treatment Effects : Incorporate data on psoriasis treatments and their potential impact on AF risk.

  
  
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  Include Asymptomatic AF : Expand the scope to include asymptomatic AF cases to provide a more complete picture of the risk.

  
  
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  Discuss Generalizability : Discuss the potential limitations in generalizing the findings to different populations.

  
  
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  Explore Mechanisms : Conduct or review studies that delve into the biological mechanisms underlying the association between psoriasis and AF.

By addressing these limitations and considering these suggestions, the manuscript could provide an even more robust and comprehensive understanding of the relationship between psoriasis and atrial fibrillation.

Psoriasis is a pervasive chronic dermatological affliction that impacts an estimated 3% of the adult population. The precise etiology of psoriasis is not fully elucidated; however, it is posited to arise from a combination of genetic susceptibility and exposure to various environmental stimuli. The confluence of these genetic and environmental elements incites an aberrant immune response characterized by the activation of T cells that target peptides derived from keratinocytes. The severity of chronic plaque psoriasis is typically gauged by the extent of the affected total body surface area (TBSA). A plethora of research has delineated a correlation between the TBSA compromised by psoriasis and an elevated risk of developing cardio-metabolic disorders, irrespective of conventional risk factors. In light of these scientific findings, the American College of Cardiology (ACC) has recently promulgated lipid management guidelines that classify psoriasis as a chronic inflammatory condition. This classification acknowledges its potential to augment the risk of atherosclerosis, thereby advocating for proactive discussions on the initiation of early lipid-lowering therapeutic interventions. The initial documentation of a correlation between psoriasis and vascular disorders was articulated in a seminal study by McDonald and colleagues in 1978. Since then, an ever-growing body of evidence has emerged, underscoring the significance of psoriasis as an independent risk factor for cardiovascular disease. In the intervening decade and a half, a multitude of expansive studies have reported findings that draw a connection between psoriasis and a range of cardiovascular conditions, encompassing hypertension, hyperlipidemia, arterial stiffness, subclinical coronary artery disease, and myocardial infarction. A pivotal study aimed to ascertain whether psoriasis confers an independent risk for coronary artery disease (CAD), a condition typically associated with diabetes, which is widely recognized as a significant risk factor for atherosclerosis and its attendant cardiovascular complications. In this comparative investigation, patients with psoriasis were enrolled alongside age and sex-matched control groups comprising individuals with type 2 diabetes mellitus. The study utilized coronary artery calcium (CAC) scores as a metric, with thresholds of >100 and >400 to delineate the presence and severity of CAD. The results indicated that the CAC scores of patients with psoriasis were not significantly different from those of the diabetic controls, suggesting a comparable level of CAD risk. However, when compared to a control group of healthy individuals, who were at least five times larger in number, the differences in CAC scores became more pronounced. This finding implies that psoriasis may stand as an independent and equivalent risk factor for CAD, akin to diabetes mellitus. Furthermore, a recent study employing coronary computer tomography angiography (CCTA) revealed that patients with psoriasis exhibited a higher burden of noncalcified plaques and possessed high-risk plaque characteristics similar to those seen in patients with hyperlipidemia. Notably, these patients with psoriasis were younger and had fewer traditional risk factors for CAD, underscoring the potential for psoriasis to exert a direct influence on cardiovascular health. In a follow-up analysis using repeated CCTA, a significant reduction in total plaque burden and noncalcified plaque was observed among patients with psoriasis whose disease severity had improved over the course of one year. This suggests that the management and amelioration of psoriasis may have a beneficial impact on reducing the cardiovascular risks associated with the condition. These findings collectively highlight the importance of recognizing psoriasis as a systemic inflammatory disease with potential implications for cardiovascular health, and they underscore the need for vigilant monitoring and proactive management of cardiovascular risk factors in individuals with psoriasis. Psoriasis, recognized as a chronic inflammatory disorder, has been identified by the American College of Cardiology (ACC) lipid guidelines as a condition that can modify the risk profile for hyperlipidemia and coronary artery disease (CAD). This acknowledgment underscores the importance of considering psoriasis when assessing cardiovascular risk, particularly in the context of lipid management. For patients with psoriasis who do not fulfill the traditional criteria for statin therapy, the ACC guidelines recommend a personalized approach to management. This involves a collaborative discussion between healthcare providers and patients to determine the most appropriate course of action regarding statin therapy, considering the individual’s overall cardiovascular risk profile, including the potential impact of psoriasis. A noteworthy study by Wu et al., leveraging the extensive Nurses’ Health Study II database, sought to elucidate the relationship between hypercholesterolemia and the incidence of psoriasis and psoriatic arthritis. Over a period of 1,320,765 person-years of follow-up, involving 95,540 women, the study identified 646 new cases of psoriasis and 165 cases of psoriatic arthritis. The findings revealed that hypercholesterolemia was associated with a 25% increased risk of developing psoriasis and a 58% increased risk of psoriatic arthritis, after adjusting for multiple variables. Furthermore, the study observed that the duration of hypercholesterolemia was a significant factor, with women experiencing hypercholesterolemia for more than seven years exhibiting an elevated risk of developing psoriasis. This association suggests a meaningful link between psoriasis, hypercholesterolemia, and potentially psoriatic arthritis. However, the study could not definitively establish causality, as the evidence connecting hyperlipidemia as a causative factor in the development of psoriasis remains limited. These findings contribute to the growing body of research that implicates systemic inflammation and metabolic dysregulation in the pathogenesis of psoriasis and its associated comorbidities. They also highlight the need for further investigation into the bi-directional relationship between psoriasis, hyperlipidemia, and cardiovascular risk, and the development of targeted therapies and preventive strategies to mitigate these risks.

Psoriasis is a prevalent chronic immunological skin disorder, distinguished by the presence of erythematous plaques covered with silvery scales, predominantly affecting the extensor aspects of the body. In the United States of America (USA), an estimated 7.5 million adults are affected by psoriasis, which is roughly equivalent to 3% of the total population. It is important to note that the prevalence of psoriasis can vary significantly by region, ranging from as low as 0.09% to as high as 11.4%. Beyond its impact on the skin, psoriasis has been linked to a heightened risk of several comorbidities, including but not limited to metabolic syndrome, hypertension, diabetes mellitus, and dyslipidemia. The pathophysiology of psoriasis is characterized by a proinflammatory state, marked by elevated levels of Th1, Th17, tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6). This chronic inflammatory milieu has been suggested to increase the susceptibility of psoriasis patients to cardiovascular diseases. Recent studies have consistently demonstrated a connection between psoriasis and an increased risk of coronary artery disease (CAD), myocardial infarction, and subclinical atherosclerosis. The association between psoriasis and atrial fibrillation (AF), which is recognized as the most prevalent arrhythmia encountered in clinical practice, has also been increasingly recognized. The pathophysiology of AF is now understood to have an inflammatory component, which may intersect with the inflammatory processes inherent to psoriasis. Given that AF is associated with a significant increase in mortality risk, the importance of early detection and intervention cannot be overstated. Timely identification and management of AF are crucial for improving patient outcomes and reducing the associated morbidity and mortality. The recognition of psoriasis as a potential risk factor for AF underscores the need for a holistic approach to patient care, where dermatological conditions are not viewed in isolation but as part of a broader spectrum of health risks that may impact overall cardiovascular health.

Psoriatic arthritis (PsA) is a debilitating chronic inflammatory condition that affects the joints in conjunction with psoriasis, often resulting in significant joint deformities, persistent pain, and reduced physical function. The systemic nature of inflammation in both PsA and psoriasis can lead to a variety of extra-articular manifestations, including an increased risk for cardiovascular comorbidities. PsA tends to have an earlier age of onset compared to many other rheumatological conditions, which means that the associated cardiovascular risks can emerge decades before the typical onset of cardiovascular disease (CVD) in the general population. This early onset is particularly concerning because it is linked to an accelerated process of subclinical atherosclerosis, which can culminate in increased morbidity and mortality rates. It is estimated that 20% to 50% of individuals with inflammatory rheumatological disorders, such as PsA, exhibit cardiovascular abnormalities. In fact, cardiovascular disease stands as one of the primary causes of death in patients with inflammatory rheumatologic conditions. In PsA, there is evidence of endothelial dysfunction, which is an early and critical event in the development of atherosclerosis. Additionally, myocardial oxidative stress and structural changes in the atrial and ventricular chambers of the heart, known as remodeling, are observed. These factors contribute to the heightened risk of cardiovascular events in PsA patients. Despite the clear association between CVD and increased morbidity and mortality in rheumatologic diseases, there remains a relative scarcity of data from large-scale, population-based studies. This gap in knowledge underscores the need for further research to better understand the mechanisms linking PsA with cardiovascular risks and to develop effective strategies for risk reduction. Cardiovascular risk stratification and management are essential components of comprehensive care for patients with PsA. It is recommended that lifestyle interventions targeting modifiable cardiovascular risk factors be initiated early in the disease course. A multidisciplinary approach to care, which includes pharmacological treatments as well as lifestyle modifications, is advocated to optimize outcomes and improve the prognosis for patients with PsA. This holistic strategy aims to address both the rheumatological and cardiovascular aspects of the disease, thereby reducing the overall burden of comorbidities and enhancing the quality of life for individuals living with PsA.

In recent years, a growing body of literature has implicated psoriasis as a significant risk factor for a variety of cardiovascular diseases, including but not limited to stroke, heart failure, myocardial infarction, coronary artery disease, and overall cardiovascular mortality. The interest in psoriasis has intensified, particularly due to its classification as an autoimmune inflammatory condition and its recognized status as an independent risk factor for atrial fibrillation (AF), the most common sustained arrhythmia. Despite the observed association between psoriasis and AF, the underlying mechanisms that link these two conditions remain elusive. However, several epidemiological studies have reported that patients with psoriasis exhibit higher P-wave duration (PWD) and atrial electromechanical delay (AEMD) compared to healthy individuals. Both PWD and AEMD are known to be associated with an increased risk of developing AF. The chronic systemic inflammation characteristic of psoriasis is thought to increase the ratio of lymphocytes and levels of C-reactive protein (CRP), which may induce AF by altering atrial structure. While the exact mechanisms behind the epidemiological link between psoriasis and AF risk are not fully understood, several biological and pathophysiological hypotheses have been proposed. Psoriasis is known to exacerbate systemic inflammation, which may contribute to AF. Inflammatory mediators such as interleukin (IL)-2, IL-6, IL-12, and tumor necrosis factor (TNF)-α are associated with increased arterial stiffness, a known risk factor for AF. A mouse model has suggested that elevated levels of TNF-α and IL-17, commonly found in psoriasis patients, could play a role in the initiation of subsequent AF. P wave dispersion (PWD) is an electrocardiographic marker that reflects the inhomogeneous distribution of the sinus impulse and is considered a non-invasive clinical biomarker for AF. Prolonged P wave dispersion is linked to a higher risk of developing AF. Atrial electromechanical delay (AEMD) is an echocardiographic parameter that correlates with the onset of AF under certain clinical conditions. Studies have indicated that psoriasis patients more frequently exhibit prolonged P wave dispersion and AEMD, which may be due to the electrophysiological and structural changes in the atrium induced by increased inflammation. Given the evidence from biological and epidemiological studies suggesting an increased risk of AF in psoriasis patients, it is imperative for physicians to closely monitor these patients and assess their risk for AF. Further research is needed to confirm this association and to elucidate the exact roles of genetic factors, inflammatory pathways, and other risk factors in the development of AF in psoriasis patients. This knowledge will be crucial for the development of targeted preventive and therapeutic strategies to mitigate the cardiovascular risks in this patient population.

The chronic inflammatory state induced by psoriasis is increasingly recognized as a potential contributor to the initiation and perpetuation of atrial fibrillation (AF). Histopathological examinations of atrial tissue from patients with AF have consistently reported the presence of inflammatory cell infiltration and cardiomyocyte necrosis. This observation is corroborated by epidemiological studies that have demonstrated elevated levels of acute inflammatory markers, such as C-reactive protein (CRP), IL-1, IL-6, and tumor necrosis factor (TNF)-α, in patients with AF compared to those in sinus rhythm. Moreover, higher levels of these inflammatory markers have been linked to a decreased likelihood of successful cardioversion, suggesting a negative impact on treatment outcomes. Pro-inflammatory cytokines, particularly TNF-α, have been implicated in directly affecting the atrial myocardium, leading to structural and electrical remodeling through multiple mechanisms. TNF-α activates the transforming growth factor-beta (TGF-β) signaling pathway, which is known to promote fibrosis. TNF-α increases the secretion of matrix metalloproteinases-2 and -9 (MMP-2 and MMP-9) from myofibroblasts, which have been shown to mediate atrial structural remodeling in animal models. Platelet-derived growth factor-A synthesized and secreted by infiltrating mast cells, stimulates cell proliferation and collagen expression in cardiac fibroblasts, contributing to atrial fibrosis and structural remodeling. Both TNF-α and platelet-derived growth factor-A (PDGF-A) have been shown to signal electrical remodeling. TNF-α can interfere with calcium influx in pulmonary vein cardiomyocytes, potentially inducing arrhythmias. PDGF-A has been shown to reduce the duration of action potentials and calcium transients, which can also be pro-arrhythmic. The interplay between structural and electrical remodeling, driven by inflammatory processes, is likely a key factor in the development of AF. It is important to consider that other comorbidities, such as depression, may also play a role in the development of AF among patients with psoriasis. A study by Egeberg et al. found that patients with psoriasis who also had depression were at a higher risk of developing incident AF compared to those without depression. This highlights the complexity of the relationship between psoriasis, inflammation, and AF, and underscores the need for a comprehensive approach to patient care that considers both dermatological and psychiatric comorbidities. In light of these findings, it is essential for healthcare providers to be vigilant in monitoring psoriasis patients for signs of AF and to consider the potential role of inflammation in the development of cardiovascular complications. Further research is necessary to fully elucidate the mechanisms by which psoriasis-related inflammation contributes to AF and to develop targeted therapies that may mitigate this risk.

A comprehensive understanding of the progression and long-term effects of cardiovascular complications is crucial for formulating evidence-based strategies for monitoring and managing these conditions over time. In the context of psoriasis and its association with cardiovascular diseases, such as atrial fibrillation (AF), the need for a clear understanding of this natural history is particularly pertinent. However, several challenges exist in the current body of research that support cardiovascular benefits or risks in psoriasis patients. The evidence supporting cardiovascular benefits is constrained, partly due to a scarcity of treatment data specific to psoriasis patients. The overall study heterogeneity may be influenced by factors such as publication bias and the lack of randomization in study designs. The presence of confounding factors like smoking, coronary artery disease (CAD), and obesity, which are independently associated with both AF and psoriasis, can complicate the interpretation of study significance. These factors are also linked to increased levels of proinflammatory markers, such as tumor necrosis factor-alpha (TNF-α), which play a role in the pathogenesis of AF. The absence of randomized studies introduces potential bias, as observational studies can only establish correlation rather than causality. The exclusion of asymptomatic AF from studies might result in an underestimation of the true risk of AF in the psoriasis population. Despite these limitations, studies such as the one by Hritvik Jain and colleagues, which leverage substantial database registries, provide valuable early and intermediate-term data. The commendable work of these authors contributes significantly to the field by offering insights that can inform clinical practice.

Ethics approval and consent to participate

This is a review of a recently published article in Current Problems in Cardiology, no ethics approval and consent to participate was required.

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Not applicable.

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Not applicable, please contact author for data requests.

Funding

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CRediT authorship contribution statement

Hong Zeng: Conceptualization, Data curation, Formal analysis, Investigation, Methodology, Project administration, Resources, Supervision, Validation, Visualization, Writing – original draft, Writing – review & editing. Qi Shu: Conceptualization, Data curation, Formal analysis, Investigation, Methodology, Project administration, Resources, Validation, Visualization, Writing – original draft, Writing – review & editing. Jing Fang: Conceptualization, Data curation, Formal analysis, Investigation, Methodology, Project administration, Resources, Validation, Visualization, Writing – original draft, Writing – review & editing. Hailin Du: Conceptualization, Data curation, Formal analysis, Investigation, Methodology, Project administration, Resources, Validation, Visualization, Writing – original draft, Writing – review & editing. Ying Xue: Conceptualization, Data curation, Formal analysis, Investigation, Methodology, Project administration, Resources, Validation, Visualization, Writing – original draft, Writing – review & editing.