Introduction: The presence of cerebral microbleeds (CMBs) has been described using MRI in patients with cardiovascular risk factors or prior stroke and could predict future cognitive dysfunction or cardiovascular mortality. CMBs are highly frequent (> 50%) in patients with infective endocarditis (IE). However, the association of CMBs and clinical factors in patients' valvular disease without IE remains unclear. Hypothesis: Valvular heart disease without IE confers a risk factor for microbleeds. Methods: We retrospectively examined data from the consecutive 96 patients ( 72 ± 9 years, 49 men) with severe valvular disease who underwent T2*-weighted brain MRI before cardiac surgery. The patients with neurological abnormalities or IE were excluded. Conventional echocardiography was performed to evaluate the left ventricular volume and valvular abnormalities. CMBs were coded by researchers blind to clinical details, who independently assessed the presence and location of CMBs using a standardized form. The study population consisted of 59 patients with severe aortic stenosis (AS) (group A) and 40 patients with severe aortic or mitral regurgitation (group B). Results: CMBs were found in 26 patients (27%), 14 (15%) had multiple CMBs. CMBs were most frequently seen in the lobar locations (69%), followed by deep or infratentorial locations (62%). No significant relationship was found between CMBs in dyslipidemia, diabetes mellitus, smoking status, anticoagulant, and antiplatelet therapy in both groups. In group A, the HAS-BLED score was higher in patients with CMBs, and the presence of CMBs was associated with hypertension (P<0.05); however, no significant differences were observed in the left ventricular mass index (LVMI), LV end-diastolic volume (LVEDV), any aortic valve severity parameters. In group B, there were significant differences in LVMI and LVEDV between patients with CMBs and those without (154 ± 40 g/m 2 vs 125 ± 32 g/m 2 , P < 0.01 ; 150 ± 39 ml vs 111 ± 38 ml, P<0.01). Conclusion: CMBs were frequently observed in severe valvular heart disease without IE. The presence of CMBs was independent of antiplatelet or anticoagulant therapy. In aortic or mitral regurgitation patients, LV remodeling may contribute to the development of CMBs.