Atrial fibrillation and coronary artery disease:An integrative review focusing on therapeutic implications of this relationship

The incidence of both atrial fibrillation(AF)and coronary artery disease(CAD)increases with advancing age.They share common risk factors and very often coexist.Evidence points to an intricate relationship between atrial tissue excitability and neuronal remodeling with ischemia at the microcirculatory level.In this review,we delineated this complex relationship,identified a common theme between the two,and discussed how the knowledge of this relationship translates into a positive and meaningful impact in patient management.Recent research indicates a high prevalence of CAD among AF patients undergoing coronary angiography.Further,the incidence of AF is much higher in those suffering from CAD compared to age-matched adults without CAD underlying this reciprocal relationship.CAD adversely affects AF by promoting progression via re-entry and increasing excitability of atrial tissue as a result of ischemia and electrical inhomogeneity.AF in turn accelerates atherosclerosis via endothelial dysfunctional and inflammation and together with enhanced thrombogenicity and hypercoagulability contribute to micro and macrothrombi throughout cardiovascular system.In a nutshell,the two form a vicious cycle wherein one disease promotes the other.Most AF recommendations focuses on rate/rhythm control and prevention of thromboembolism.Very few studies have discussed the importance of unmasking coexistent CAD and how the treatment of underlying ischemia will impact the burden of AF in these patients.Inflammation and endothelial dysfunction remain central to both disease processes and form a handsome therapeutic target in the management of the two diseases.The relationship between AF and CAD is complex and much more than mere coincidence.The two diseases share common risk factor and pathophysiology.Hence,it is impractical to treat them in isolation.Accordingly,we share the implications of managing underlying ischemia and inflammation to positively impact and improve quality of life among AF patients.

Role of fibrinogen,albumin and fibrinogen to albumin ratio in determining angiographic severity and outcomes in acute coronary syndrome

BACKGROUND Coronavirus disease 2019(COVID-19)pandemic unmasked the huge deficit in healthcare resources worldwide.It highlighted the need for efficient risk stratification in management of cardiovascular emergencies.AIM To study the applicability of the old,available and affordable nonconventional biomarkers:albumin and fibrinogen in their ability to predict angiographic severity and clinical outcomes in patients with acute coronary syndrome(ACS).METHODS In this prospective,observational study,166 consecutive patients with ACS were enrolled.Fibrinogen,albumin and their ratio were determined from serum.Patients with underlying chronic liver disease,active malignancy,autoimmune disease,active COVID-19 infection and undergoing thrombolysis were excluded.RESULTS Mean age of the population was 60.5±1.5 years,74.1%being males.ST elevation myocardial infarction(STEMI)was most common presentation of ACS seen in 57%patients.Fibrinogen albumin ratio(FAR)≥19.2,had a sensitivity of 76.9%and specificity of 78.9%[area under the receiver operating characteristic curves(AUROC)=0.8,P=0.001]to predict≤thrombolysis in myocardial infarction(TIMI)1 flow in culprit artery in STEMI patients.Even in non-STEMI patients,FAR≥18.85 predicted the same with 80%sensitivity and 63%specificity(AUROC=0.715,P=0.006).CONCLUSION Novel biomarkers,with their high cost,lack of availability and long turn over time are impractical for real-world use.Identifying≤TIMI 1 flow in the culprit artery has significant impact of management and outcome.Our study has shown that readily available biomarkers like fibrinogen and albumin can help identify these high-risk patients with good accuracy.This allows risk-stratification and individualization of treatment in ACS.

Blood cellular mutant LXR-α protein stability governs initiation of coronary heart disease

AIM: To investigate the role of [breast and ovarian cancer susceptibility 1(BRCA1)-associated RING domain 1(BARD1)]/BRCA1 E3-ubiquitin ligase complex in governing the stability of mutant liver X receptor-(LXR-α) protein in coronary heart disease(CHD) subjects.METHODS: The expression analysis of various genes was carried out by quantitative real time polymerase chain reaction and western blotting within blood mononuclear cells of human CHD subjects at various stages of coronary occlusion and their corresponding normal healthy counterparts.Immunoprecipitation experiments were performed to establish protein interactions between LXR-αand BARD1.Peripheral blood mononuclear cells were cultured and exposed to Vitamin D_3 and Cisplatin to validate the degradation of mutant LXR-αprotein in CHD subjects by BARD1/BRCA1 complex.RESULTS: The expression of mutant LXR-αprotein in CHD subjects was found to decrease gradually with the severity of coronary occlusion exhibiting a strong negative correlation,r =-0.975 at P < 0.001.Further,the expression of BARD1 and BRCA1 also increased with the disease severity,r = 0.895 and 0.873 respectively(P < 0.001).Immunoprecipitation studies established that BARD1/BRCA1 complex degrades mutant LXR-αvia ubiquitination.The absence of functional LXR-αprotein resulted in increased expression of inflammatory cytokines such as interleukin(IL)-6,IL-8 and interferon-and decreased expression of ABCA1(ATP-binding cassette A1)(r = 0.932,0.949,0.918 and-0.902 with respect to Gensini score;P < 0.001).Additionally,cell culture experiments proved that Vitamin D_3 could prevent the degradation of mutant LXR-αand restore its functional activity to some extent.CONCLUSION: Mutant LXR-αprotein in CHD subjects is degraded by BARD1/BRCA1 complex and Vitamin D_3 can rescue and restore its function.