CARDIOVASCULAR JOURNAL OF AFRICA • Volume 35, No 3, September – October 2024 138 AFRICA marker of subclinical atherosclerosis. These results suggest that CHA2DS2-VASc score may be associated not only with clinical atherosclerosis but also with subclinical atherosclerosis. Shang et al. reported that CHA2DS2-VASc scores ≥ 2 in males and ≥ 3 in females were associated with carotid plaques. They also showed that male patients with a CHA2DS2-VASc score ≥ 2 had a 2.3-fold increased risk of developing carotid plaques.4 On the other hand, in our study, patients with CHA2DS2-VASc score ≥ 2 had a 7.4-fold increased risk of developing AVS than those with a CHA2DS2-VASc score < 2. Previous studies have shown the relationship between AVS and CV risk factors and morbidity and mortality.14,15 On the other hand, Rosa et al. reported that AVS was not associated with a higher risk of death and cardiac death.16 However, a meta-analysis by Pradelli et al. showed that increased absolute event rate in subjects with AVS reduced when the other known CV risks were taken into account. Therefore we believe that the negative association between AVS and cardiac death might be due to the higher baseline CV risks of the patient subgroups included in the study by Rosa et al.17 On the contrary, there are studies showing the association of AVS and CVmortality and morbidity in high-risk populations.18,19 Our results showing the association between AVS and CHA2DS2VASc score may contribute more information to this argument. Nevertheless, the results of our study do not allow us to support the correlation between CV prognosis and CHA2DS2-VASc score in AVS. Further studies should be designed to ascertain this issue. Our study determined that LVEF was lower in patients with AVS than in those without AVS. In our multivariate analysis, LVEF was also found to be an independent predictor of AVS. This may be explained by increased atherosclerotic burden leading to a decrease in LVEF in patients with AVS. Also, clinical studies show that low wall shear stress plays a significant role in the initiation of atherosclerosis within the coronary arterial wall and the progression of calcium deposition on the leaflets. In the same way, the non-coronary cusp was found to be affected initially, probably due to the low shear stress on the endothelium in diastole, given the absence of diastolic coronary flow in this cusp.6 Likewise, as LVEF decreased, shear stress through the aortic valve might decrease. Reduced shear stress might lead to repetitive injury and inflammation, progressive thickening and calcification of the aortic valve leaflets. LVEDD, PWT, IVST,LADandascendingaortameasurements by TTE were statistically higher in patients with AVS compared to patients without AVS in our study. This can be explained by the higher prevalence of HT in AVS, as was also observed in our study. We also detected LVDD more often in the AVS (+) than in the AVS (–) group. Both AVS and LVDD have been reported to be related to many CV risk factors, especially HT and DM and this may explain the relationship we found between them.20,21 DM, FBG level, as well as OAD and insulin therapies were statistically higher in the AVS (+) group in our study. Although hyperlipidaemia is a risk factor for AVS, TC and LDL-C levels were lower in the AVS (+) group. It might be because of the high prevalence of patients with hyperlipidaemia in the AVS (+) group using statins. Inflammation plays a critical role in both the pathophysiology of AVS and atherosclerosis.9 We also determined that WBC and neutrophil counts were higher in patients with AVS than in those without AVS. Additionally, we detected a correlation between AVS grade and CHA2DS2-VASc score. Our study is the first to report the relationship between AVS and CHA2DS2-VASc score and show a progressive rise in CHA2DS2-VASc score along with the grade of AVS. It seems logical to control risk factors for AVS as one would for CAD. There are several limitations in our study. First, it was a single-centre, cross-sectional and observational study having the limits inherent in its design. Second, data of the study population were obtained from the electronic medical report of our hospital, which had a selective bias. Third, unfortunately, we could not find a universally accepted AVS definition in the literature. A prospective cohort study to more accurately determine the prognostic value of the CHA2DS2-VASc score is necessary. Conclusion CHA2DS2-VASc score was higher in patients with AVS compared to those without AVS. Furthermore, the CHA2DS2-VASc score increased as the AVS grade increased. The pathophysiology of AVS is thought to have an inflammatory component besides a degenerative process, which is related to CV diseases. TTE, commonly used clinically, can easily detect AVS. A diagnosis of AVS might change the treatment goals of patients to decrease CV risk in the population. References 1. January CT, Wann LS, Alpert JS, Calkins H, Cigarroa JE, et al. 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol 2014; 64(21): e1–76. 2. Funabashi N, Uehara M, Takaoka H, Kobayashi Y. The CHA2DS2VASc score predicts 320-slice CT-based coronary artery plaques and >50% stenosis in subjects with chronic and paroxysmal atrial fibrillation. Int J Cardiol 2014; 172(1): e234–237. 3. Kim KH, Kim W, Hwang SH, Kang WY, Cho SC, et al. The CHA2DS2VASc score can be used to stratify the prognosis of acute myocardial infarction patients irrespective of presence of atrial fibrillation. J Cardiol 2015; 65(2): 121–127. 4. Shang L, Zhao Y, Shao M, Sun H, Feng M, et al. The association of CHA2DS2-VASc score and carotid plaque in patients with non-valvular atrial fibrillation. PLoS One 2019; 14(2): e0210945. 5. Bonow RO, Carabello BA, Kanu C, de Leon AC, Jr., Faxon DP, et al. ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/ American Heart Association Task Force on Practice Guidelines (writing committee to revise the 1998 guidelines for the management of patients with valvular heart disease): developed in collaboration with the Society of Cardiovascular Anesthesiologists: endorsed by the Society for Cardiovascular Angiography and Interventions and the Society of Thoracic Surgeons. Circulation 2006; 114(5):e84–231. 6. Branch KR, O’Brien KD, Otto CM. Aortic valve sclerosis as a marker of active atherosclerosis. Curr Cardiol Rep 2002; 4(2): 111–11 7. 7. Prasad Y, Bhalodkar NC. Aortic sclerosis – a marker of coronary atherosclerosis. Clin Cardiol 2004; 27(12): 671–673. 8. Di Minno MND, Di Minno A, Ambrosino P, Songia P, Pepi M, et al. Cardiovascular morbidity and mortality in patients with aortic valve sclerosis: A systematic review and meta-analysis. Int J Cardiol 2018;
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