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Investigation of mindin levels in hypertensive patients with left ventricular hypertrophy and QRS fragmentation on electrocardiography.
Acta Cardiologica 2017 December 22
PURPOSE: Mindin was associated with diabetic nephropathy, podocyte injury, colitis, allergic asthma, liver ischaemia and reperpusion injury and ischaemic brain injury. On the other hand, it was reported as a protective factor against obesity, cardiac hypertrophy, fibrosis and remodelling. Fragmented QRS complexes (fQRS) are markers of altered ventricular depolarisation owing to a prior myocardial scar and fibrosis. In this study, we aimed to investigate mindin levels in hypertensive patients with left ventricular hypertrophy and fQRS on electrocardiography.
METHODS: This observational case-control study enrolled 70 (36 female) hypertensive patients with fQRS and 38 (23 female) hypertensive control patients. All patients were evaluated by transthoracic echocardiography. Mindin levels were measured by the enzyme-linked immunosorbent assay (ELISA). Clinical, echocardiographic and laboratory data were compared between patient and control groups.
RESULTS: There was no significant difference between patient and control groups in terms of clinical, echocardiographic and routine laboratory parameters. The mindin levels were significantly higher in the patient group than controls (11.3 (7.21-19.31) vs 4.15 (2.86-6.34); p < .001). Multiple logistic regression analyses defined increased mindin levels as an independent predictor for the presence of fQRS (Odds ratio: 1.733; p = .034). Mindin levels >6.74 predicted the presence of fQRS with a sensitifity of 84.3% and specificity of 79.9% on receiver operating characteristic (ROC) curve analysis (The area under the curve:0.889; Confidence Interval: 0.827-0.951; p < .001).
CONCLUSION: Mindin expressin is upregulated in hypertensive patients with fQRS complexes. In contrary to previous studies, increased mindin levels may be associated with myocardial fibrosis.
METHODS: This observational case-control study enrolled 70 (36 female) hypertensive patients with fQRS and 38 (23 female) hypertensive control patients. All patients were evaluated by transthoracic echocardiography. Mindin levels were measured by the enzyme-linked immunosorbent assay (ELISA). Clinical, echocardiographic and laboratory data were compared between patient and control groups.
RESULTS: There was no significant difference between patient and control groups in terms of clinical, echocardiographic and routine laboratory parameters. The mindin levels were significantly higher in the patient group than controls (11.3 (7.21-19.31) vs 4.15 (2.86-6.34); p < .001). Multiple logistic regression analyses defined increased mindin levels as an independent predictor for the presence of fQRS (Odds ratio: 1.733; p = .034). Mindin levels >6.74 predicted the presence of fQRS with a sensitifity of 84.3% and specificity of 79.9% on receiver operating characteristic (ROC) curve analysis (The area under the curve:0.889; Confidence Interval: 0.827-0.951; p < .001).
CONCLUSION: Mindin expressin is upregulated in hypertensive patients with fQRS complexes. In contrary to previous studies, increased mindin levels may be associated with myocardial fibrosis.
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