الفهرس 
Arterial StiffnessOnly 14 pages are availabe for public view
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Abstract
Large arteries were once considered as inert conduits, but are now recognized to play an important physiological role in buffering the oscillatory changes in blood pressure resulting from intermittent ventricular ejection. This action reduces pulse pressure, smoothies peripheral blood flow and improves the efficiency of the cardiovascular system as a whole.
The normal human aorta is not a stiff tube, but is characterized by elastic properties with a buffering windkessel function. Aortic stiffening may cause an increase in aortic pulse pressure, left ventricular load, and ultimately left ventricular hypertrophy. This, together with the decreased diastolic trans myocardial pressure gradient, interacts with coronary flow and flow reserve
Increased central arterial stiffening is a hallmark of the aging process and the consequence of many disease states such as diabetes, atherosclerosis, and chronic renal compromise. Accordingly, there is a marked increase in the incidence and prevalence of clinical surrogate markers of vascular stiffness, such as pulse pressure and isolated systolic hypertension, with age and these associated conditions
Thus stiffening of large arteries leads to a number of adverse haemodynamic consequences, including a widening of pulse pressure and, ultimately, the development of isolated systolic hypertension.
Aortic stiffness is a hallmark of aging, and classic cardiovascular risk factors play a role in accelerating this process. Current changes in medicine, which focus on preventive care, have led to a growing interest in noninvasive evaluation of aortic stiffness. Aortic stiffness has emerged as a good tool for further risk stratification because it has been linked to increased risk of atherosclerotic heart disease, myocardial infarction, heart failure, and stroke. This has led to the invention and validation of multiple methods to measure aortic stiffness
Hypertension is a major risk factor for coronary, cerebrovascular, and renal diseases and is the greatest cause of stroke, the mechanisms of which are generally attributed to the reduction in the caliber or number of small arteries or arterioles with a resulting increase in total peripheral resistance and mean blood pressure (MBP).
Arterial stiffness has long been viewed as a consequence of long-standing hypertension. However, recent studies have suggested that arterial stiffness may contribute to the pathogenesis of hypertension.
Currently, carotid to femoral pulse-wave velocity (PWV) is the favored technique for assessing aortic stiffness, but it has its limitations. It is highly dependent upon the accuracy of the path length of pulse travel, and differences in path lengths vary the PWV by as much as 30%.
Evaluation of the aorta is a routine part of the standard echocardiographic examination. Transthoracic echocardiography permits adequate assessment of several aortic segments, particularly the aortic root and proximal ascending aorta. Studies have shown a good correlation between aortic distensibility calculated using echo-cardiography and non-invasive brachial artery pressure measurements and aortic distensibility calculated invasively, using contrast aortography and direct aortic pressure recordings.
Aim of the Study
Is to compare aortic morphology and stiffness between hypertensive patients and normotensive subjects and to assess the independent determinants of aortic root stiffness and distensibility in Hypertension.
Subjects and Methods
The study was carried on 60 patients above 40 years of age.
They were classified into two groups:
Group-(A) included 40 Hypertensive individuals (with diagnosis based on 3 outpatient measures of BP ≥140/90 mmHg or patients who are on regular antihypertensive medications). Group-(B) included 20 Normotensive controls.
All Subjects had been subjected to full history taking, General examination with measuring height, weight then body Mass Index (BMI), Blood pressure measurements. Full Transthoracic Echocardiographic examination including calculation of elastic parameters of the aorta.
The diameter of the ascending aorta was measured from the parasternal long axis view by 2D guided M-mode tracing at 3 cm above the aortic valve
Results
There was no significant difference between patients and controls regarding age and gender distribution.
No significant difference between two groups regarding incidence of Diabetes Mellitus or smoking.
Mean value of BMI was higher in hypertensive group (group A) Mean±SD 30.548±4.390, in comparison to normotensive group (group B) mean±SD 28.374±3.542, but the difference was statistically non-significant.
Systolic Blood Pressure (SBP) ranges between 120 and 145 mmHg and the mean value is 132.375±7.844 while Diastolic Blood Pressure (DBP) ranges between 80 and 100mmHg, and the mean value is 91.625±6.242 in hypertensive patients.
LV mass and mass index were significantly higher among hypertensive patients.
Both groups had normal left ventricular systolic function with normal ejection fraction values.
Diastolic dysfunction was more common in hypertensive patients.
Group A subject show statistical significant higher value regarding Aortic Stiffness index (p value <0.001) and statistical significant lower value regarding Aortic Strain (p value <0.001), Aortic distensibility (p value <0.001) & Aortic systolic diameter (p value 0.047) in comparison in to group B.
The correlations between different parameters (in group A hypertensive patients) with aortic stiffness parameters are listed below:
o Positive correlation between age and aortic stiffness index which is statistically significant (r = 0.424, P-value= 0.006).
o Positive correlation between BMI and aortic stiffness index which is statistically significant (r = 0.364, P-value= 0.021).
o Positive correlation between systolic blood pressure and aortic stiffness index which is statistically significant (r = 0.496, P-value= 0.001).
o Positive correlation between left ventricular mass and aortic stiffness index which is statistically significant (r = 0.454, P-value= 0.003).
o Negative correlation between left ventricular mass index and aortic distensibility index which is statistically significant (r = -0.323, P-value= 0.042).
o Positive correlation between E/E’ and aortic stiffness index which is statistically significant (r = 0.434, P-value= 0.005).
E/E‘ were found significantly (P<0.0001) related to aortic stiffness and considered as the main predictor for increasing aortic stiffness while BMI approached statistical significance (P= 0.067).
Large arteries were once considered as inert conduits, but are now recognized to play an important physiological role in buffering the oscillatory changes in blood pressure resulting from intermittent ventricular ejection. This action reduces pulse pressure, smoothies peripheral blood flow and improves the efficiency of the cardiovascular system as a whole.
The normal human aorta is not a stiff tube, but is characterized by elastic properties with a buffering windkessel function. Aortic stiffening may cause an increase in aortic pulse pressure, left ventricular load, and ultimately left ventricular hypertrophy. This, together with the decreased diastolic trans myocardial pressure gradient, interacts with coronary flow and flow reserve
Increased central arterial stiffening is a hallmark of the aging process and the consequence of many disease states such as diabetes, atherosclerosis, and chronic renal compromise. Accordingly, there is a marked increase in the incidence and prevalence of clinical surrogate markers of vascular stiffness, such as pulse pressure and isolated systolic hypertension, with age and these associated conditions
Thus stiffening of large arteries leads to a number of adverse haemodynamic consequences, including a widening of pulse pressure and, ultimately, the development of isolated systolic hypertension.
Aortic stiffness is a hallmark of aging, and classic cardiovascular risk factors play a role in accelerating this process. Current changes in medicine, which focus on preventive care, have led to a growing interest in noninvasive evaluation of aortic stiffness. Aortic stiffness has emerged as a good tool for further risk stratification because it has been linked to increased risk of atherosclerotic heart disease, myocardial infarction, heart failure, and stroke. This has led to the invention and validation of multiple methods to measure aortic stiffness
Hypertension is a major risk factor for coronary, cerebrovascular, and renal diseases and is the greatest cause of stroke, the mechanisms of which are generally attributed to the reduction in the caliber or number of small arteries or arterioles with a resulting increase in total peripheral resistance and mean blood pressure (MBP).
Arterial stiffness has long been viewed as a consequence of long-standing hypertension. However, recent studies have suggested that arterial stiffness may contribute to the pathogenesis of hypertension.
Currently, carotid to femoral pulse-wave velocity (PWV) is the favored technique for assessing aortic stiffness, but it has its limitations. It is highly dependent upon the accuracy of the path length of pulse travel, and differences in path lengths vary the PWV by as much as 30%.
Evaluation of the aorta is a routine part of the standard echocardiographic examination. Transthoracic echocardiography permits adequate assessment of several aortic segments, particularly the aortic root and proximal ascending aorta. Studies have shown a good correlation between aortic distensibility calculated using echo-cardiography and non-invasive brachial artery pressure measurements and aortic distensibility calculated invasively, using contrast aortography and direct aortic pressure recordings.
Aim of the Study
Is to compare aortic morphology and stiffness between hypertensive patients and normotensive subjects and to assess the independent determinants of aortic root stiffness and distensibility in Hypertension.
Subjects and Methods
The study was carried on 60 patients above 40 years of age.
They were classified into two groups:
Group-(A) included 40 Hypertensive individuals (with diagnosis based on 3 outpatient measures of BP ≥140/90 mmHg or patients who are on regular antihypertensive medications). Group-(B) included 20 Normotensive controls.
All Subjects had been subjected to full history taking, General examination with measuring height, weight then body Mass Index (BMI), Blood pressure measurements. Full Transthoracic Echocardiographic examination including calculation of elastic parameters of the aorta.
The diameter of the ascending aorta was measured from the parasternal long axis view by 2D guided M-mode tracing at 3 cm above the aortic valve
Results
There was no significant difference between patients and controls regarding age and gender distribution.
No significant difference between two groups regarding incidence of Diabetes Mellitus or smoking.
Mean value of BMI was higher in hypertensive group (group A) Mean±SD 30.548±4.390, in comparison to normotensive group (group B) mean±SD 28.374±3.542, but the difference was statistically non-significant.
Systolic Blood Pressure (SBP) ranges between 120 and 145 mmHg and the mean value is 132.375±7.844 while Diastolic Blood Pressure (DBP) ranges between 80 and 100mmHg, and the mean value is 91.625±6.242 in hypertensive patients.
LV mass and mass index were significantly higher among hypertensive patients.
Both groups had normal left ventricular systolic function with normal ejection fraction values.
Diastolic dysfunction was more common in hypertensive patients.
Group A subject show statistical significant higher value regarding Aortic Stiffness index (p value <0.001) and statistical significant lower value regarding Aortic Strain (p value <0.001), Aortic distensibility (p value <0.001) & Aortic systolic diameter (p value 0.047) in comparison in to group B.
The correlations between different parameters (in group A hypertensive patients) with aortic stiffness parameters are listed below:
o Positive correlation between age and aortic stiffness index which is statistically significant (r = 0.424, P-value= 0.006).
o Positive correlation between BMI and aortic stiffness index which is statistically significant (r = 0.364, P-value= 0.021).
o Positive correlation between systolic blood pressure and aortic stiffness index which is statistically significant (r = 0.496, P-value= 0.001).
o Positive correlation between left ventricular mass and aortic stiffness index which is statistically significant (r = 0.454, P-value= 0.003).
o Negative correlation between left ventricular mass index and aortic distensibility index which is statistically significant (r = -0.323, P-value= 0.042).
o Positive correlation between E/E’ and aortic stiffness index which is statistically significant (r = 0.434, P-value= 0.005).
E/E‘ were found significantly (P<0.0001) related to aortic stiffness and considered as the main predictor for increasing aortic stiffness while BMI approached statistical significance (P= 0.067).