The aim of the present study was to measure regional ventricular function at rest and during stress in order to assess if patients with Type II diabetes have subclinical myocardial dysfunction and if it is related to risk factors. Seventy subjects (35 patients with Type II diabetes with no symptoms, signs or history of heart disease, and 35 age- and sex-matched healthy controls) had echocardiography at rest and during dobutamine stress. Myocardial velocities were measured off-line from digital loops of colour tissue Doppler. Subendocardial function was assessed from the mean longitudinal velocities of four basal segments (apical views) and radial function from the velocities of the basal posterior wall (parasternal view). Systolic functional reserve was calculated as the increase in velocity from baseline. Longitudinal peak systolic velocity was lower in patients with diabetes, at rest (5.6 +/- 1.4 compared with 6.5 +/- 1.1 cm/s) and at peak stress (10.9 +/- 2.8 compared with 14.3 +/- 2.1 cm/s) (both P <0.01). Functional reserve was impaired in patients with diabetes (+5.4 +/- 2.0 compared with +7.7 +/- 1.7 cm/s; P <0.01). Radial systolic velocity was higher in patients with diabetes (5.4 +/- 1.3 compared with 4.7 +/- 1.4 cm/s; P <0.05). Resting longitudinal systolic function correlated inversely with low-density lipoprotein-cholesterol ( r =-0.53), glycated haemoglobin ( r =-0.48), age ( r =-0.41) and diastolic blood pressure ( r =-0.38) (all P < 0.05). Peak stress systolic velocity correlated inversely with glycated haemoglobin ( r =-0.46) and age ( r =-0.44) (both P < 0.01). In conclusion, patients with Type II diabetes and no clinical heart disease have impaired subendocardial function of the left ventricle at rest and peak stress, which is related to glycated haemoglobin and serum low-density lipoprotein-cholesterol.

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Longitudinal function of the left ventricle is governed by the subendocardial myocardial fibres, whereas radial function is due mainly to contraction of circumferential fibres, localised in the subepicardial layer of the myocardium.1 In patients with diabetes or hypertension the subendocardial fibres are more likely to be affected by microvascular ischaemia. This can be caused by structural changes in the coronary vasculature that reduce myocardial perfusion such as arterial wall thickening, decreased capillary density, and periarteriolar fibrosis, and by haemodynamic changes such as increased wall stress, and the microcirculatory effects of endothelial dysfunction.2 Since tissue Doppler echocardiography can now assess longitudinal and radial myocardial velocities separately, we tested the further hypothesis that subendocardial dysfunction is related to conduit arterial stiffness. METHODS Study groupWe studied 83 subjects (mean (SD) age 54 (12) years, 59 men), including 27 normal individuals and 56 patients with varying degrees of left ventricular (LV) dysfunction caused by diabetes (35), hypertension (17), and ischaemic dilated cardiomyopathy (4). We excluded patients not in sinus rhythm, or with ventricular aneurysm or severe regional wall motion abnormalities, mitral or aortic stenosis, or more than mild valvar regurgitation. Twenty nine patients were taking an angiotensin converting enzyme (ACE) inhibitor, 23 a diuretic, 8 a β blocker, 27 a statin, and 7 a calcium antagonist. The protocol was approved by the local research ethics committee, and each subject gave informed consent. Arterial stiffnessSubjects were studied after resting supine for 15 minutes in a temperature controlled environment. The stiffness parameter β was calculated according to the formula:where Ps and Pd are systolic and diastolic blood pressure in the brachial artery measured by an automated sphygmomanometer (Omron 705CP, Tokyo, Japan), and Ds and Dd are the maximal and minimal diameters of the right common carotid artery measured by ultrasonic high resolution wall tracking (Aloka SSD-5500, Tokyo, Japan; 7.5 MHz linear array probe).3 Adjustable gates were positioned at the junctions of the intima and media, and diameter was calculated and displayed in real time as the difference between the displacement waveforms of the anterior and posterior walls. Measurements were taken as a mean of five beats; β was log transformed for analyses, because its distribution was skew. EchocardiographyImmediately after assessment of arterial stiffness, subjects were studied by conventional and tissue Doppler echocardiography (Vingmed System 5, GE Vingmed, Horten, Norway), using a 1.5-2.5 MHz transducer. Digital echocardiographic data were acquired and transferred to a Macintosh computer. Conventional echocardiographyM mode tracings from the parasternal long axis view were used to measure septal thickness, LV diameter, and posterior wall thickness, and LV mass index was calculated (method of Devereux with the application of the Penn convention). Cross sect...

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