Factors in Cardiac Structure and Function in T2DM
Factors in Cardiac Structure and Function in T2DM
Background We hypothesized that clinical factors other than glycemic control may influence abnormal cardiac function in patients with type 2 diabetes mellitus (T2DM). We aimed to investigate the independent factors for abnormal cardiac function among clinical factors in T2DM.
Methods We studied 148 asymptomatic patients with T2DM without overt heart disease. Echocardiographic findings were compared between diabetic patients and 68 age-matched healthy subjects. Early (E) and late (A) diastolic mitral flow velocity and early diastolic mitral annular velocity (e') were measured for assessing left ventricular (LV) diastolic function. We evaluated insulin resistance, non-esterified fatty acid, high-sensitive CRP, estimated glomerular filtration rate, waist/hip ratio, abdominal visceral adipose tissue (VAT), subcutaneous adipose tissue (SAT) and other clinical characteristics in addition to glycemic control. VAT and SAT were quantified by computed tomography.
Results In T2DM, E/A and e' were significantly lower, and E/e', left atrial volume and LV mass were significantly greater than in control subjects. In multivariate liner regression analysis, VAT was an independent determinant of left atrial volume (β =0.203, p=0.011), E/A (β =−0.208, p=0.002), e' (β =−0.354, p<0.001) and E/e' (β=0.220, p=0.003). Age was also an independent determinant, whereas fasting plasma glucose and hemoglobin A1c levels were not. In addition to systolic blood pressure, waist-hip ratio (β=0.173, p=0.024) and VAT/SAT ratio (β=0.162, p=0.049) were independent determinants of LV mass.
Conclusion Excessive visceral fat accompanied by adipocyte dysfunction may play a greater role than glycemic control in the development of diastolic dysfunction and LV hypertrophy in T2DM.
Diabetes mellitus may cause myocardial injury even in the absence of coronary artery disease, hypertension or valvular disease. This cardiac dysfunction increases the risk of heart failure and subsequent mortality independently of underlying coronary artery disease and other cardiovascular risk factors. Although the mechanisms of myocardial injury in diabetes mellitus are complex, several studies have identified diastolic dysfunction and left ventricular (LV) hypertrophy as major characteristics of abnormal cardiac function and structure in diabetes mellitus using echocardiography, even in the absence of hypertension, Using animal models, many previous investigations have documented possible mechanisms underlying myocardial injury in diabetic mellitus. However, the pathophysiology of diabetic myocardial injury has been still unclear in the clinical setting. Not only glycemic control, but many other factors including hyperinsulinemia, increased fatty acids, inflammation, renal function and myocardial steatosis have been postulated to contribute to the development of abnormal function and structure in diabetic mellitus. Nevertheless, the independent influence of these factors on cardiac functional pmeters beyond glycemic control has not been adequately evaluated in humans. In addition, few studies have included a control group, and comparison with age-matched controls is essential to evaluate LV diastolic dysfunction and hypertrophy because even healthy subjects > 60 years old may have significant diastolic dysfunction.
Recently, visceral fat accumulation has gained attention as playing an important role in the development and pathophysiology of type 2 diabetes mellitus (T2DM). Excessive visceral fat is closely associated with adipocyte dysfunction accompanied by increased inflammatory cytokine secretion and reduced anti-inflammatory adiponectin secretion, which can lead to cardiac and endothelial dysfunction. Thus, we hypothesized that visceral fat accumulation may be associated with abnormal cardiac function and structure in T2DM.
The aims of our study were the following: (1) to clarify if diastolic dysfunction and LV hypertrophy are characteristics of abnormal cardiac function and structure in T2DM in comparison with age-matched healthy controls; and (2) to investigate the independent factors for diastolic dysfunction and LV hypertrophy among clinical factors including glycemic control, blood pressure, insulin resistance, fatty acid and visceral fat.
Abstract and Introduction
Abstract
Background We hypothesized that clinical factors other than glycemic control may influence abnormal cardiac function in patients with type 2 diabetes mellitus (T2DM). We aimed to investigate the independent factors for abnormal cardiac function among clinical factors in T2DM.
Methods We studied 148 asymptomatic patients with T2DM without overt heart disease. Echocardiographic findings were compared between diabetic patients and 68 age-matched healthy subjects. Early (E) and late (A) diastolic mitral flow velocity and early diastolic mitral annular velocity (e') were measured for assessing left ventricular (LV) diastolic function. We evaluated insulin resistance, non-esterified fatty acid, high-sensitive CRP, estimated glomerular filtration rate, waist/hip ratio, abdominal visceral adipose tissue (VAT), subcutaneous adipose tissue (SAT) and other clinical characteristics in addition to glycemic control. VAT and SAT were quantified by computed tomography.
Results In T2DM, E/A and e' were significantly lower, and E/e', left atrial volume and LV mass were significantly greater than in control subjects. In multivariate liner regression analysis, VAT was an independent determinant of left atrial volume (β =0.203, p=0.011), E/A (β =−0.208, p=0.002), e' (β =−0.354, p<0.001) and E/e' (β=0.220, p=0.003). Age was also an independent determinant, whereas fasting plasma glucose and hemoglobin A1c levels were not. In addition to systolic blood pressure, waist-hip ratio (β=0.173, p=0.024) and VAT/SAT ratio (β=0.162, p=0.049) were independent determinants of LV mass.
Conclusion Excessive visceral fat accompanied by adipocyte dysfunction may play a greater role than glycemic control in the development of diastolic dysfunction and LV hypertrophy in T2DM.
Introduction
Diabetes mellitus may cause myocardial injury even in the absence of coronary artery disease, hypertension or valvular disease. This cardiac dysfunction increases the risk of heart failure and subsequent mortality independently of underlying coronary artery disease and other cardiovascular risk factors. Although the mechanisms of myocardial injury in diabetes mellitus are complex, several studies have identified diastolic dysfunction and left ventricular (LV) hypertrophy as major characteristics of abnormal cardiac function and structure in diabetes mellitus using echocardiography, even in the absence of hypertension, Using animal models, many previous investigations have documented possible mechanisms underlying myocardial injury in diabetic mellitus. However, the pathophysiology of diabetic myocardial injury has been still unclear in the clinical setting. Not only glycemic control, but many other factors including hyperinsulinemia, increased fatty acids, inflammation, renal function and myocardial steatosis have been postulated to contribute to the development of abnormal function and structure in diabetic mellitus. Nevertheless, the independent influence of these factors on cardiac functional pmeters beyond glycemic control has not been adequately evaluated in humans. In addition, few studies have included a control group, and comparison with age-matched controls is essential to evaluate LV diastolic dysfunction and hypertrophy because even healthy subjects > 60 years old may have significant diastolic dysfunction.
Recently, visceral fat accumulation has gained attention as playing an important role in the development and pathophysiology of type 2 diabetes mellitus (T2DM). Excessive visceral fat is closely associated with adipocyte dysfunction accompanied by increased inflammatory cytokine secretion and reduced anti-inflammatory adiponectin secretion, which can lead to cardiac and endothelial dysfunction. Thus, we hypothesized that visceral fat accumulation may be associated with abnormal cardiac function and structure in T2DM.
The aims of our study were the following: (1) to clarify if diastolic dysfunction and LV hypertrophy are characteristics of abnormal cardiac function and structure in T2DM in comparison with age-matched healthy controls; and (2) to investigate the independent factors for diastolic dysfunction and LV hypertrophy among clinical factors including glycemic control, blood pressure, insulin resistance, fatty acid and visceral fat.