The aim of the present study was to determine the effects of a 4-week exercise training intervention on blood glucose, insulin sensitivity, BMI (body mass index) and cardiorespiratory fitness in patients with Type 2 diabetes, and to identify and establish criteria for patients who are more likely to improve their blood glucose from short-term exercise training. A randomized, controlled trial of exercise training, comprising two supervised and one non-supervised sessions of individualized cardiorespiratory and resistance exercise per week, was performed in 132 healthy patients with Type 2 diabetes (exercise training group, n =68), with the aim of accumulating a minimum of 150 min of moderate-intensity exercise for 4 weeks. BMI, waist circumference, blood pressure, blood lipid profile, blood glucose, insulin, insulin sensitivity [calculated by HOMA IR (homoeostasis model assessment of insulin resistance) and QUICKI (quantitative insulin check index)], β-cell function (calculated by HOMA β-Cell ), HbA 1c (glycated haemoglobin) and V ̇ O 2max (maximal oxygen consumption) were measured at baseline and at 4 weeks. The exercise training group had significant improvements in V ̇ O 2max , BMI and triacylglycerols (triglycerides). There were no significant changes in blood glucose, HOMA IR , QUICKI or HOMA β-Cell . Decreases in blood glucose were significantly predicted by baseline blood glucose and HbA 1c , with these variables accounting for 15.9% of the change in blood glucose ( P <0.001). ROC (receiver operator characteristic) curve analysis revealed that patients with a blood glucose >8.85 mmol/l (sensitivity=73%, specificity=78%) and HbA 1c >7.15% (sensitivity=79%, specificity=60%) were more likely to achieve a clinically significant decrease in blood glucose. In conclusion, in apparently healthy patients with Type 2 diabetes, a 4-week exercise intervention improved cardiorespiratory fitness, BMI and triacylglycerols. Elevated blood glucose and HbA 1c predicted improvements in blood glucose.

To date, the main cardiovascular application of TDI (tissue Doppler imaging) has been in myocardial evaluation. In the present study, we investigated the feasibility and reproducibility of assessing arterial elasticity using the DC (distensibility coefficient) measured by TDI, the correlation of this with the DC obtained by other methods and the DC in patients with various degrees of cardiovascular risk. We studied 450 subjects (256 men; age, 51±10 years) with and without risk factors of cardiovascular disease. Arterial displacement was measured from TDI, and B-mode and M-mode images of the common carotid artery in the longitudinal plane, and the DC with each method was compared. Linear regression showed a good correlation between all three methods. The results for TDI and B-mode were comparable [(21±10) compared with (21±10)×10 −3 /kPa respectively; P =not significant], but there were significant differences between TDI and M-mode [(21±10) compared with (31±13)×10 −3 /kPa respectively; P <0.0001] and between B-mode and M-mode [(21±10) compared with (31±13)×10 −3 /kPa respectively; P <0.0001]. Similarly, Bland–Altman analysis showed the least variability in the DC between TDI and B-mode, and there were no significant differences between the average measurements. The TDI DC also had the lowest paired difference for inter-observer variability [(−0.1±1.1)×10 −3 /kPa; P =not significant]. In conclusion, the results of the present study suggest that TDI of the carotid arteries is feasible, comparable with B-mode measurements, more robust than M-mode and less variable than the other methods.

Inactivity is associated with endothelial dysfunction and the development of cardiovascular disease. Exercise training has a favourable effect in the management of hypertension, heart failure and ischaemic heart disease. These beneficial effects are probably mediated through improvements of vascular function and, in this issue of Clinical Science , Hägg and co-authors propose a coronary artery effect. The use of a Doppler technique for non-invasive assessment of coronary flow reserve in a small animal model is an exciting aspect of this study. If feasible in the hands of other investigators, the availability of sequential coronary flow measurements in animal models may help improve our understanding of the mechanisms of disorders of the coronary circulation.

Subclinical left ventricular (LV) dysfunction may be identified by reduced longitudinal contraction. We sought to define the effects of subclinical LV dysfunction on radial contractility in 53 patients with diabetes mellitus with no LV hypertrophy, normal ejection fraction and no ischaemia as assessed by dobutamine echocardiography, in comparison with age-matched controls. Radial peak myocardial systolic velocity (S m ) and early diastolic velocity (E m ), strain and strain rate were measured in the mid-posterior and mid-anteroseptal walls in parasternal views and each variable was averaged for individual patients (radial contractility). These variables were also measured in the mid-posterior and mid-anteroseptal walls in the apical long-axis view and each variable was averaged for individual patients (longitudinal contractility). Mean radial S m , strain and strain rate were significantly increased in diabetic patients (2.9±0.6 cm/s, 28±5% and 1.8±0.4 s -1 respectively) compared with controls (2.4±0.7 cm/s, 23±4% and 1.6±0.3 s -1 respectively; all P <0.001), but there was no difference in E m (3.3±1.2 compared with 3.1±1.1 cm/s, P =not significant). In contrast, longitudinal S m , E m , strain and strain rate were significantly lower in diabetic patients (3.6±1.1 cm/s, 4.3±1.6 cm/s, 21±4% and 1.6±0.3 s -1 respectively) than in controls (4.3±1.0 cm/s, 5.7±2.3 cm/s, 26±4% and 1.9±0.3 s -1 respectively; all P ⩽ 0.001). Thus radial contractility appears to compensate for reduced longitudinal contractility in subclinical LV dysfunction occurring in the absence of ischaemia or LV hypertrophy.

The detection of preclinical heart disease is a new direction in diabetes care. This comment describes the study by Vinereanu and co-workers in this issue of Clinical Science in which tissue Doppler echocardiography has been employed to demonstrate subtle systolic and diastolic dysfunction in Type II diabetic patients who had normal global systolic function and were free of coronary artery disease. The aetiology of early ventricular dysfunction in diabetes relates to complex intramyocardial and extramyocardial mechanisms. The initiating event may be due to insulin resistance, and involves abnormal myocardial substrate utilization and uncoupling of mitochondrial oxidative phosphorylation. Dysglycaemia plays an important role via the effects of oxidative stress, protein kinase C activation and advanced glycosylation end-products on inflammatory signalling, collagen metabolism and fibrosis. Extramyocardial mechanisms involve peripheral endothelial dysfunction, arterial stiffening and autonomic neuropathy. The clinical significance of the ventricular abnormalities described is unknown. Confirmation of their prognostic importance for cardiac disease in diabetes would justify routine screening for presymptomatic ventricular dysfunction, as well as clinical trials of novel agents for correcting causal mechanisms. These considerations could also have implications for patients with obesity and the metabolic syndrome.

Abnormal left ventricular (LV) filling is common, but not universal, in hypertensive LV hypertrophy (LVH). We sought to elucidate the relative contributions of myocardial structural changes, loading and hypertrophy to LV dysfunction in 113 patients: 85 with hypertensive LVH and 28 controls without LVH and with normal filling. Patients with normal dobutamine stress echocardiography and no history of coronary artery disease were selected, in order to exclude a contribution from ischaemia or scar. Abnormal LV filling was identified in 65 LVH patients, based on Doppler measurement of transmitral filling and annular velocities. All patients underwent grey-scale and colour tissue Doppler imaging from three apical views, which were stored and analysed off line. Integrated backscatter (IB) and strain rate imaging were used to detect changes in structure and function; average cyclic variation of IB, strain rate and peak systolic strain were calculated by averaging each segment. Calibrated IB intensity, corrected for pericardial IB intensity, was measured in the septum and posterior wall from the parasternal long-axis view. Patients with LVH differed significantly from controls with respect to all backscatter and strain parameters, irrespective of the presence or absence of abnormal LV filling. LVH patients with and without abnormal LV filling differed with regard to age, LV mass and incidence of diabetes mellitus, but also showed significant differences in cyclic variation ( P <0.01), calibrated IB in the posterior wall ( P <0.05) and strain rate ( P <0.01), although blood pressure, heart rate and LV systolic function were similar. Multivariate logistic regression analysis demonstrated that age, LV mass index and calibrated IB in the posterior wall were independent determinants of abnormal LV filling in patients with LVH. Thus s tructural and functional abnormalities can be detected in hypertensive patients with LVH with and without abnormal LV filling. In addition to age and LVH, structural (not functional) abnormalities are likely to contribute to abnormal LV filling, and may be an early sign of LV damage. IB is useful for the detection of myocardial abnormalities in patients with hypertensive LVH.

Echocardiographic analysis of regional left ventricular function is based upon the assessment of radial motion. Long-axis motion is an important contributor to overall function, but has been difficult to evaluate clinically until the recent development of tissue Doppler techniques. We sought to compare the standard visual assessment of radial motion with quantitative tissue Doppler measurement of peak systolic velocity, timing and strain rate (SRI) in 104 patients with known or suspected coronary artery disease undergoing dobutamine stress echocardiography (DbE). A standard DbE protocol was used with colour tissue Doppler images acquired in digital ciné-loop format. Peak systolic velocity (PSV), time to peak velocity (TPV) and SRI were assessed off-line by an independent operator. Wall motion was assessed by an experienced reader. Mean PSV, TPV and SRI values were compared with wall motion and the presence of coronary artery disease by angiography. A further analysis included assessing the extent of jeopardized myocardium by comparing average values of PSV, TPV and SRI against the previously validated angiographic score. Segments identified as having normal and abnormal radial wall motion showed significant differences in mean PSV (7.9±3.8 and 5.9±3.3 cm/s respectively; P < 0.001), TPV (84±40 and 95±48 ms respectively; P = 0.005) and SRI (-1.45±0.5 and -1.1±0.9 s -1 respectively; P < 0.001). The presence of a stenosed subtending coronary artery was also associated with significant differences from normally perfused segments for mean PSV (8.1±3.4 compared with 5.7±3.7 cm/s; P < 0.001), TPV (78±50 compared with 92±45 ms; P < 0.001) and SRI (-1.35±0.5 compared with -1.20±0.4 s -1 ; P = 0.05). PSV, TPV and SRI also varied significantly according to the extent of jeopardized myocardium within a vascular territory. These results suggest that peak systolic velocity, timing of contraction and SRI reflect the underlying physiological characteristics of the regional myocardium during DbE, and may potentially allow objective analysis of wall motion.