الفهرس 
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Abstract
Atherosclerosis and arterial stiffening may coexist and the
correlation of these parameters in patients with premature coronary artery
disease (CAD) has not been well elucidated. Tissue Doppler imaging of
the ascending aorta may be used in the assessment of elastic properties of
the great arteries.
Our study aims to investigate the correlation between aortic
stiffness and premature CAD using parameters derived from twodimensional
and tissue Doppler imaging (TDI) echocardiography of the
ascending aorta.
Thirty consecutive subjects males younger than 45 years and
females younger than 55 years old who were hospitalized with diagnosis
of acute coronary syndrome and had undergone coronary angiography.
The control group included thirty age–sex matched individuals without a
diagnosis of CAD. Aortic stiffness index (SI), aortic distensibility (D),
and pressure-strain elastic modulus (Ep ) were calculated from the aortic
diameters measured by two-dimensional M-mode echocardiography and
blood pressure obtained by sphygmomanometry. Aortic systolic velocity
(SAo), and early (EAo) and late (AAo) diastolic velocities were
determined by pulse-wave TDI from the anterior wall of ascending aorta
3 cm above the aortic cusps in parasternal long-axis view.
Aortic Stiffness index was higher [median 46.25 vs. median11.85;
p <0.001] and distensibility was lower (median 129 x 10-5 cm2 /dyn vs.
median 660× 10-5 cm2 /dyn; p = <0.001) in patients with CAD compared
to the control group. Pressure strain elastic modulus was significantly
higher in CAD group when compared with control group (median
1543.50 kpa Vs 304.50 Kpa).
EAo was significantly lower in the CAD group (8.05 ± 1.99cm/s
vs. 13.94 ± 1.03cm/s, p < 0.001). The difference in EAo remained
significant when CAD patients with a left ventricular ejection fraction
>50% was compared to the control group. SAo and AAo velocities of
ascending aorta were similar in control and CAD groups.
Limitations
There are some caveats in our study. Using a cross-sectional
design, we can only observe an association between vascular parameters
and CAD, but cannot establish a causal relationship. And, our data may
not indicate the clinical use of aortic TDI parameters in clinical practice
for risk stratification purposes in patients without CAD. Decreased LV
function may have an impact on aortic stiffness parameters. Whereas, a
previous trial has shown correlation of LVEF with SAo velocity (which
was not significantly different between the two groups in our study) (266).
Nevertheless, the impact of stroke volume changes on aortic TDI
velocities needs further investigation. We successfully measured aortic
TDI parameters in all of the study participants, however low image
quality may impair these measurements. Although we have adjusted for
all of the major confounders in the analysis, the presence of unknown
confounders cannot be ignored.