Conduit arterial stiffness is associated with impaired left ventricular subendocardial function

Abstract

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...

The role of ventricular–arterial coupling in cardiac disease and heart failure: assessment, clinical implications and therapeutic interventions. A consensus document of the European Society of Cardiology Working Group on Aorta & Peripheral Vascular Diseases, European Association of Cardiovascular Imaging, and Heart Failure Association

“…A stiff and narrow aorta leads to high Zc and low aortic distensibility, whereas a distensible, wide aorta to a low Zc and increased aortic distensibility. The local stiffness parameter beta can also be calculated according to the formula Beta = ln (Ps/Pd)/(Ds − Dd/Dd), where Ps and Pd are systolic and diastolic BP in the brachial artery measured by an automated sphygmomanometer, and Ds and Dd are the maximal and minimal diameters of the right common carotid artery measured by ultrasonic high resolution wall tracking or of the aorta by echocardiography …”

Echocardiographic Characterization of Postnatal Development in Mice with Reduced Arterial Elasticity

“…Reduced arterial compliance, or increased arterial stiffness, is correlated with LV hypertrophy and decreased systolic and/or diastolic function in humans [4, 3, 5]. Reduced arterial size is also correlated with changes in LV function in humans, particularly in extreme cases such as aortic stenoses [34–36].…”

“…Arterial compliance is an inverse measure of arterial stiffness. Decreased compliance of the large arteries in humans is correlated with impaired left ventricular (LV) subendocardial function [3], concentric LV hypertrophy [4], impaired LV diastolic function [5], and is an important predictor of cardiovascular mortality [6]. However, there has been limited investigation into the temporal relationship between decreased arterial compliance and cardiac function in animal models.…”

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“…LV filling is impaired (abnormalities of active relaxation and passive stiffness of the myocardium) in combination with abnormal ventriculo‐arterial coupling 12 , 13 . However, with emerging technologies that question the accuracy of normal systolic function, the pathophysiology of HFNEF remains controversial 14 .…”