Relation of Left Ventricular Hypertrophy to Inflammation and Albuminuria in Adults With Type 2 Diabetes
The Strong Heart Study
- Vittorio Palmieri, MD1,
- Russell P. Tracy, PHD2,
- Mary J. Roman, MD1,
- Jennifer E. Liu, MD1,
- Lyle G. Best, MD3,
- Jonathan N. Bella, MD1,
- David C. Robbins, MD4,
- Barbara V. Howard, PHD4 and
- Richard B. Devereux, MD1
- 1Weill Medical College of Cornell University, New York, New York
- 2University of Vermont, Burlington, Vermont
- 3Missouri Breaks Industries Research, Timber Lake, South Dakota
- 4MedStar Research Institute, Washington, D.C
- Address correspondence to Vittorio Palmieri, MD, Federico II University Hospital, via Pansini 5 (edificio 1), Naples 80131, Italy. E-mail: vpalmieri{at}med.cornell.edu
- Address requests for reprints to Richard B. Devereux, MD, Weill Medical College of Cornell University, 525 East 68th St., Box 222 (Cardiology), Rm. K-415, New York, NY 10021. E-mail: rbdevere{at}med.cornell.edu
Abstract
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 1,299 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.
- CRP, C-reactive protein
- dBP, diastolic blood pressure
- ECG, electrocardiogram
- hsCRP, high-sensitivity C-reactive protein
- LV, left ventricular
- LVH, left ventricular hypertrophy
- sBP, systolic blood pressure
Footnotes
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A table elsewhere in this issue shows conventional and Système International (SI) units and conversion factors for many substances.
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- Accepted July 9, 2003.
- Received February 28, 2003.
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