OBJECTIVE: To evaluate in adults with type 2 diabetes the extent to which the relation of left ventricular hypertrophy (LVH) to markers of systemic inflammation (fibrinogen and high-sensitivity C-reactive protein [hsCRP]) are affected by microangiopathy. RESEARCH DESIGN AND METHODS: We selected adults with type 2 diabetes using American Diabetes Association criteria from a population-based cohort, excluding those with medical history or electrocardiographic evidence of coronary heart disease or dialysis-dependent renal failure. LVH was assessed by echocardiogram. RESULTS: Of the 1299 eligible participants, 384 (29.6%) had LVH, which was associated with higher BMI, hsCRP, fibrinogen, and albuminuria in univariate analyses. After controlling for significant confounders, fibrinogen and albuminuria were higher in the presence of LVH (both P < 0.01), whereas hsCRP was not (P = 0.2), mostly because of the confounding effect of BMI. Adjustment for albuminuria abolished the relation of LVH to higher fibrinogen (P = 0.2). However, fibrinogen was significantly higher in participants with LVH among those without pathologic levels of albuminuria (<30 mg/g creatinuria), but not independent of BMI. Although hsCRP and fibrinogen were moderately correlated, fibrinogen, but not CRP, showed a significant relation with albuminuria. CONCLUSIONS: In adults with type 2 diabetes, echocardiographic LVH is associated with susceptibility to atherothrombosis and increased albuminuria, which is a marker of microangiopathy and endothelial dysfunction that appears in turn to be a relevant pathogenetic link between LVH and inflammation. However, in the absence of significant microalbuminuria, elevated BMI is a relevant pathogenetic factor in the relation of LVH to increased levels of markers of inflammation, potentially preceding development of significant albuminuria. In the presence of microangiopathy, we found that the atherothrombotic risk profile associated with LVH was independent of BMI and possibly reflected the association of LVH with a higher degree of endothelial dysfunction.
OBJECTIVE: To evaluate in adults with type 2 diabetes the extent to which the relation of left ventricular hypertrophy (LVH) to markers of systemic inflammation (fibrinogen and high-sensitivity C-reactive protein [hsCRP]) are affected by microangiopathy. RESEARCH DESIGN AND METHODS: We selected adults with type 2 diabetes using American Diabetes Association criteria from a population-based cohort, excluding those with medical history or electrocardiographic evidence of coronary heart disease or dialysis-dependent renal failure. LVH was assessed by echocardiogram. RESULTS: Of the 1299 eligible participants, 384 (29.6%) had LVH, which was associated with higher BMI, hsCRP, fibrinogen, and albuminuria in univariate analyses. After controlling for significant confounders, fibrinogen and albuminuria were higher in the presence of LVH (both P < 0.01), whereas hsCRP was not (P = 0.2), mostly because of the confounding effect of BMI. Adjustment for albuminuria abolished the relation of LVH to higher fibrinogen (P = 0.2). However, fibrinogen was significantly higher in participants with LVH among those without pathologic levels of albuminuria (<30 mg/g creatinuria), but not independent of BMI. Although hsCRP and fibrinogen were moderately correlated, fibrinogen, but not CRP, showed a significant relation with albuminuria. CONCLUSIONS: In adults with type 2 diabetes, echocardiographic LVH is associated with susceptibility to atherothrombosis and increased albuminuria, which is a marker of microangiopathy and endothelial dysfunction that appears in turn to be a relevant pathogenetic link between LVH and inflammation. However, in the absence of significant microalbuminuria, elevated BMI is a relevant pathogenetic factor in the relation of LVH to increased levels of markers of inflammation, potentially preceding development of significant albuminuria. In the presence of microangiopathy, we found that the atherothrombotic risk profile associated with LVH was independent of BMI and possibly reflected the association of LVH with a higher degree of endothelial dysfunction.
Authors: Jacob Christensen; Nino Emanuel Landler; Flemming Javier Olsen; Bo Feldt-Rasmussen; Ditte Hansen; Anne-Lise Kamper; Christina Christoffersen; Ellen Linnea Freese Ballegaard; Ida Maria Hjelm Sørensen; Sasha Saurbrey Bjergfelt; Eline Seidelin; Susanne Bro; Tor Biering-Sørensen Journal: Int J Cardiovasc Imaging Date: 2021-12-31 Impact factor: 2.357
Authors: Takuya Hasegawa; Bernadette Boden-Albala; Kazuo Eguchi; Zhezhen Jin; Ralph L Sacco; Shunichi Homma; Marco R Di Tullio Journal: Am J Hypertens Date: 2010-01-07 Impact factor: 2.689
Authors: Kazuo Eguchi; Bernadette Boden-Albala; Zhezhen Jin; Tatjana Rundek; Ralph L Sacco; Shunichi Homma; Marco R Di Tullio Journal: Am J Cardiol Date: 2008-04-11 Impact factor: 2.778
Authors: Matthew R Weir; Fawn Yeh; Angela Silverman; Richard B Devereux; James M Galloway; Jeffrey A Henderson; William J Howard; Marie Russell; Charlton Wilson; Robert Ratner; John Sorkin; Jason G Umans; Jerome L Fleg; Mario Stylianou; Elisa Lee; Barbara V Howard Journal: J Clin Hypertens (Greenwich) Date: 2009-10 Impact factor: 3.738
Authors: Vittorio Palmieri; Mary J Roman; Jonathan N Bella; Jennifer E Liu; Lyle G Best; Elisa T Lee; Barbara V Howard; Richard B Devereux Journal: J Am Soc Echocardiogr Date: 2007-07-12 Impact factor: 5.251