Impact of glucose intolerance and insulin resistance on cardiac structure and function: sex-related differences in the Framingham Heart Study

Framingham Heart Study, Burlington, Mass, USA.
Circulation (Impact Factor: 14.43). 01/2003; 107(3):448-54.
Source: PubMed


Although insulin resistance has been implicated in the pathogenesis of left ventricular (LV) hypertrophy, previous studies have yielded inconsistent results and are limited by referral bias.
We examined the relations between echocardiographic LV measurements and glucose tolerance status in 2623 Framingham Study subjects (1514 women, mean age 53 years) free of myocardial infarction and heart failure. We also evaluated the relations of insulin resistance (homeostasis model, HOMA-IR) and LV and left atrial (LA) measures within the normal and abnormal glucose tolerance categories (the latter included impaired glucose tolerance, impaired fasting glucose, and newly diagnosed diabetes). LV mass (adjusted for age, height, heart rate, and systolic blood pressure) increased across categories of worsening glucose tolerance; the trend was more striking in women (P<0.001) compared with men (P=0.054). In subjects with normal (n=2022) and abnormal glucose tolerance (n=327), covariate-adjusted LV mass and LV wall thickness increased across HOMA-IR quartiles in women (P<0.001) but not men. In contrast, covariate-adjusted LA size increased with worsening glucose tolerance and across HOMA-IR quartiles in the normal and abnormal glucose tolerance groups in both sexes. Adjustment for body mass index considerably attenuated the relations of LV/LA measures and HOMA-IR, rendering them statistically nonsignificant in the normal glucose tolerance group.
In our large community-based sample, LV mass and wall thickness increased with worsening glucose intolerance, an effect that was more striking in women compared with men. Insulin resistance was associated with increased LV mass in women alone, but this relation was largely accounted for by obesity.

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Available from: Helen Parise, Jan 21, 2014
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    • "The Latin-American Diabetes Association (ALAD) Clinical Guides [12] [13] as well as the Clinical Guide from Chilean Health Ministry suggested the diagnosis of IFG when the fasting plasma glucose is between 100 and 125 mg/dL [14]. Beyond the differences existing in order to establish the normal limit for fasting plasma glucose, the evidences coincide that glucose levels in the stage of prediabetic keep a direct relation with the risk of developing diabetes in the future, and this also constitutes an independent risk factor for cardiovascular diseases (CVD) [15] [16]. Both conditions, T2DM and CVD, are related with other factors such as dyslipidemia , arterial hypertension (HTA), abdominal obesity, sedentary, oxidative stress, metabolic syndrome (MS), and family data [17] [18]. "
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    ABSTRACT: Aim: To study the evolution of impaired fasting glucose (IFG), considering glucose and HbA1c levels and risk factors associated, in a period of 6 years. Methods: We studied 94 subjects with impaired fasting glucose (IFG) that were diagnosed in 2005 and followed up to 2012. Glucose and HbA1c levels were determined. A descriptive analysis of contingence charts was performed in order to study the evolution in the development of type-2 diabetes mellitus (T2DM). Results: Twenty-eight of ninety-four subjects became T2DM; 51/94 remained with IFG; and 20/94 presented normal fasting glucose. From the 28 diabetic subjects, 9 had already developed diabetes and were under treatment with oral hypoglycemic agents; 5 were diagnosed with plasma glucose < 126 mg/dL, but with HbA1c over 6.5%. In those who developed diabetes, 15/28 had a family history of T2DM in first relative degree. Also, diabetic subjects had a BMI significantly higher than nodiabetics (t test: P < 0.01). The individuals that in 2005 had the highest BMI are those who currently have diabetes. Conclusion: The IFG constitutes a condition of high risk of developing T2DM in a few years, especially over 110 mg/dL and in obesity patients.
    Journal of Diabetes Research 08/2014; 2014(9541):710370. DOI:10.1155/2014/710370 · 2.16 Impact Factor
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    • "Cardiac imaging in db/db mice showed diastolic insufficiency and increased systolic function. These alterations are similar to findings from patients with insulin resistance and early-stage diabetes that show diastolic dysfunction, but no signs of systolic impairment or structural changes [44,45]. The smaller weight of the db/db hearts is in part explained bý the shorter LV parasternal length. "
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    ABSTRACT: Background The aim of this study was to probe cardiac complications, including heart-rate control, in a mouse model of type-2 diabetes. Heart-rate development in diabetic patients is not straight forward: In general, patients with diabetes have faster heart rates compared to non-diabetic individuals, yet diabetic patients are frequently found among patients treated for slow heart rates. Hence, we hypothesized that sinoatrial node (SAN) dysfunction could contribute to our understanding the mechanism behind this conundrum and the consequences thereof.Methods Cardiac hemodynamic and electrophysiological characteristics were investigated in diabetic db/db and control db/+mice.ResultsWe found improved contractile function and impaired filling dynamics of the heart in db/db mice, relative to db/+controls. Electrophysiologically, we observed comparable heart rates in the two mouse groups, but SAN recovery time was prolonged in diabetic mice. Adrenoreceptor stimulation increased heart rate in all mice and elicited cardiac arrhythmias in db/db mice only. The arrhythmias emanated from the SAN and were characterized by large RR fluctuations. Moreover, nerve density was reduced in the SAN region.Conclusions Enhanced systolic function and reduced diastolic function indicates early ventricular remodeling in obese and diabetic mice. They have SAN dysfunction, and adrenoreceptor stimulation triggers cardiac arrhythmia originating in the SAN. Thus, dysfunction of the intrinsic cardiac pacemaker and remodeling of the autonomic nervous system may conspire to increase cardiac mortality in diabetic patients.
    Cardiovascular Diabetology 08/2014; 13(1):122. DOI:10.1186/s12933-014-0122-y · 4.02 Impact Factor
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    • "Abnormal glucose homeostasis was found correlated with impaired LV diastolic function [16], and this relationship has been shown to be independent of blood pressure, LV geometry, total plasma lipids and obesity [17]. In a large community-based sample, LV mass and wall thickness increased across categories of worsening glucose tolerance [18]. Moreover, cardiometabolic profile and inflammation markers have been shown to be more severely altered in men and women with both IFG and IGT compared with those with IFG alone. "
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    ABSTRACT: Background Insulin resistance (IR) is currently considered a crucial cardiovascular (CV) risk factor, which seems to play a dominant role in the evolution toward cardiac and vascular impairment. Early IR-induced cardiac dysfunction can be assessed by Doppler-derived myocardial systolic strain rate (SR) index, measured at baseline and after dobutamine stress echocardiography (DSE). Methods Thirty IR patients (HOMA-IR = 7 ± 5.2, age 52.6 ± 2.1 years), and 20 healthy, age and sex matched controls were studied. IR had been diagnosed in all patients in the 3 months preceding the study. Dobutamine echocardiography was performed in all subjects to exclude ischemic heart disease, and left ventricular contractile reserve (LVCR) was then assessed. LVCR was evaluated as an increase in the peak of an average longitudinal SR, measured in the basal and mid segments of 2 and 4 chamber ventricular walls. Results No significant differences between the 2 groups were revealed by baseline echocardiography. In contrast, after DSE a significant decrease of Delta SR was found in the IR group in comparison to the controls (0.54 ± 0.31 s−1vs 1.14 ± 0.45 s−1; p < 0.0001). Conclusions Our results show that IR, even if isolated and arising within a short time period, not only represents the initial phase of future diabetes, but may adversely affect heart function, as evidenced by the depressed LVCR. Our data strengthen the need for attention to be paid to IR state and for an early therapeutic approach.
    Cardiovascular Diabetology 04/2013; 12(1):66. DOI:10.1186/1475-2840-12-66 · 4.02 Impact Factor
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