|
 
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| ORIGINAL ARTICLE |
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| Year : 2020 | Volume
: 17
| Issue : 1 | Page : 33-41 |
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Sonographic assessment of carotid arteries in adults with radiographic features of hypertensive cardiomegaly at Kano, North Western Nigeria
Mohammed Kabir Saleh, Mohammed Usman, Kabiru Isyaku, Mohammad Abba Suwaid, Anas Isma'il, Mansur Yahuza Adamu, Abdu Hamisu Dambatta, Idris Sule Kazaure
Department of Radiology, Bayero University/Aminu Kano Teaching Hospital, Kano, Nigeria
| Date of Submission | 02-Mar-2019 |
| Date of Acceptance | 04-Nov-2019 |
| Date of Web Publication | 30-May-2020 |
Correspondence Address:
Dr. Mohammed Kabir Saleh
Department of Radiology, Bayero University/Aminu Kano Teaching Hospital, Kano
Nigeria
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/njbcs.njbcs_4_19
Context: Hypertension is a chronic medical condition in which there is elevation of arterial blood pressure (s). Hypertensive cardiomegaly is a complication and effect of long standing systemic hypertension on the heart. Aims: This study is to relate a component of hypertensive heart disease with sonographic changes found in the carotid arteries of these patients, as they are directly linked to atherosclerotic effect of hypertension. Materials and Methods: In this prospective crosssectional study, four hundred (400) subjects with primary hypertension were recruited. The study group (200) is having cardiomegaly on PA chest radiograph. The carotid arteries of all participants were insonated on both gray scale and Doppler modes. Demographic characteristics, CIMT, and Doppler velocimetric indices (PSV, EDV, and RI) were generated and subjected to statistical analysis. Results: The mean age for the study group was 48.91 ± 10.0, consisting of 110 (53.9%) males and 90 (45.9%) females. Cardiothoracic ratio was seen to increase with age (P < 0.0001) and not associated with gender (P = 0.110). The mean carotid intimamedia thickness (CIMT) in the right and left was 1.3 ± 0.13 mm and 1.50 ± 0.18 mm, with the highest CIMT of 1.70 ± 0.25 mm seen at higher systolic readings (P = 0.002). Mean PSV of right common carotid artery (CCA) was 66.20 ± 21.81 cm/s and left CCA was 59.54 ± 22.75 cm/s, EDV of right CCA was 17.85 ± 5.97 cm/s and left CCA was 16.56 ± 6.44 cm/s, RI of right CCA was 0.72 ± 0.07 cm/s and left CCA was 0.72 ± 0.06 cm/s. Positive correlation was seen between age and CIMT (P = 0.001). 7.5% had echogenic smooth plaques. Conclusions: Carotid artery abnormalities continue to relate with severity of hypertension among patients with chest radiographic findings.
Keywords: Cardiomegaly, cardiothoracic ratio, carotid intima-media thickness, Doppler ultrasound, hypertension
How to cite this article:
Saleh MK, Usman M, Isyaku K, Suwaid MA, Isma'il A, Adamu MY, Dambatta AH, Kazaure IS. Sonographic assessment of carotid arteries in adults with radiographic features of hypertensive cardiomegaly at Kano, North Western Nigeria. Niger J Basic Clin Sci 2020;17:33-41 |
How to cite this URL:
Saleh MK, Usman M, Isyaku K, Suwaid MA, Isma'il A, Adamu MY, Dambatta AH, Kazaure IS. Sonographic assessment of carotid arteries in adults with radiographic features of hypertensive cardiomegaly at Kano, North Western Nigeria. Niger J Basic Clin Sci [serial online] 2020 [cited 2023 Jun 10];17:33-41. Available from: https://www.njbcs.net/text.asp?2020/17/1/33/285470 |
| Introduction | |  |
Hypertension is a chronic medical condition in which there is a elevation of arterial blood pressure and it is summarized by two measurements, called the systolic and diastolic readings, which currently stands at any measurement beyond 140/90 mmHg in adults.[1]
Hypertension is common in both developed and underdeveloped countries.[2] Nearly one billion people or approximately 26% of adult population of the world had hypertension as of the year 2000[2] and is more prevalent in men and in those with low socioeconomic status.[3]
Hypertension can be classified as either essential (primary) or non-esstential (secondary).[3] Essential hypertension means no specific medical cause can be found to explain the patient's condition and it constitutes 90–95% of cases,[3] whereas secondary hypertension indicates that the high blood pressure is as a result of another condition, such as kidney disease or even tumors (especially of the adrenal glands).
In almost all contemporary societies, blood pressure rises with age and the risk of becoming hypertensive later in life is considerable.[4] However, a complex interaction between genes and enviromental conditions is being examined in the pathogenesis of essential hypertension. Genetic variants with both low [5] and high (though rare)[6] effects on blood pressure have been identified though still poorly understood. Environmental factors are centered toward lifestyle which include exercise, weight gain or loss, and alcohol intake.[7]
Secondary hypertension results from identifiable causes, most common of which is renal diseases.[8] Others include endocrine disorders like Cushing's syndrome, hyperthyroidism, acromegaly, Conn's syndrome, hyperparathyroidism, and pheochromocytoma.[8],[9]
Hypertension is rarely accompanied by any symptoms though it might present with headaches, lightheadedness, vertigo, tinnitus, altered vision, or fainting episodes.[10] On physical examination, ophthalmoscopy can be used to detect hypertensive retinopathy.[11] Some additional signs and symptoms may suggest secondary origin of diseases, which include truncal obesity, moon-face, a buffalo hump, and purple stretch marks suggesting Cushing's syndrome.[8]
Current best practice is to follow up a single raised clinic reading with ambulatory measurements, or less ideally with home blood pressure monitoring over the course of 7 days.[12]
Investigative tools relevant in the management of hypertensive patients include frontal chest radiograph, echocardiography, serum electrolytes, lipid profile, and electrocardiography.[8]
The clinical outcomes that results from prolonged persistent elevation of blood pressure are referred to as complications [13] and are multi-organ or multisystemic. These include diffuse atherosclerosis and its manifestation which include abnormalities of blood flow due to atherosclerotic coronary artery disease, microvascular disease, as well as cardiac dysrhythmias, and sudden cardiac death.[14],[15],[16],[17],[18],[19] Other effects include diastolic dysfunction and congestive heart failure.[19],[20]
Vascular abnormalities results from microvascular complication to intimal thickening, hyperplasia of the media wall, and hyaline degeneration in the subsequent, sclerotic stage.[21]
The World Health Organization has identified that hypertension, or high blood pressure, is the leading cause of cardiovascular mortality and that more than 50% of the hypertensive populations worldwide are unaware of their condition.[22] About 37% of the adult population in Nigeria is said to be hypertensive, and the prevalence of hypertension is increasing with a consequent rise in the burden of its complications.[23]
Despite these tremendous number of individuals affected and the consequent financial burden and implications, there is still paucity of such studies in this part of the world. Although other individuals have tried to look at sonographic assessment of the effect of hypertension on the carotid intima-media thickness (CIMT),[24],[25] a new dimension will be added to this study, which is cardiomegaly as a result of hypertension, as seen on frontal chest radiograph.
The evaluation of this condition (hypertension) uses simple investigative modality (chest radiograph), which shows outline of the heart (on antero-posterior and lateral views).[26] While carotid wall thickness is an early marker of atherosclerosis and subclinical organ damage, this constitutes a very good opportunity to evaluate hypertension-induced vascular end-organ damage. Sonographic assessment of the carotid arteries is safe and easy, as it is free of ionizing radiation, cheap, available, and easily reproducible. It has high sensitivity and specificity in detecting cervical carotid artery (as high as 94% and 96%, respectively). As such, cardiovascular complications of hypertension can be sought for and impending risks can be predicted, especially to the central nervous system. Thus, it is important to screen hypertensive patients by carotid Doppler ultrasound to assess the risk of atherosclerosis and carotid blood vessels remodeling.[27]
Therefore, this study aims to evaluate the abnormalities likely to occur in the carotid arteries of hypertensive patients who have started showing signs of cardiac complication in the form of cardiomegaly.
| Materials and Methods | | |
This was a prospective cross-sectional study carried out at the Department of Radiology, Aminu Kano Teaching Hospital (AKTH) Kano, North-western Nigeria over a period of 1 year. The study population was adults, males and females between 22 and 65 years. Patients with essential hypertension being referred from cardiovascular clinic to the Radiology department for chest radiographic examination as part of their routine workup were recruited.
Before commencement of the study, ethical approval was sought and obtained from the ethics and research committee of the AKTH, Kano. Informed written consent was also obtained from the study patients after explaining the procedure to them, after which basic information and sociodemographic data were collected and documented. These include age, gender, weight, height, and blood pressure.
The patients included in this are adult patients with primary hypertension, those patients aged between 22 and 65 years, and those who willingly consented to participate in the study. Patients aged less than 22 years and more than 65 years, normotensive individuals/patients, those individuals/patients having other risk factors for atherosclerosis other than hypertension, like diabetes, hyperlipidemia, those patients with other causes of cardiomegaly, and those patients who declined consent for participation were excluded from the study.
A total of 200 hypertensive patients with chest radiographic findings of hypertensive heart disease, with an equal number of control subjects (those patients that are hypertensive but with normal cardiac size on chest X-ray) were studied.
This was derived using the Fisher's statistical and I.T research formula for sample size determination as follows:
n = Z 2P(1- P)/d2 (1)
Where
n = Minimum sample size
Z = Standard deviation (constant of 1.96 corresponding to 95% confidence interval).
P = Proportion in target population with hypertensive cardiomegaly was 21% in a similar study.[27]
Therefore, n = 1.962 × 0.21× [1- 0.21]/0.052
= 254.8
≈ 255.
Based on the records of hypertensive patients seen in the department for chest radiograph, this was adjusted as follows:
Adjusted sample size for populations study less than 10,000 was
Where
n= Minimum sample size for infinite population (>10,000)
= sample size for finite population
= size of population
Substituting these values in the formula:
= 301/[1+(301/480)]
= 301/[1 + 0.627]
= 185.00.
This is rounded up to 200.
Therefore, 200 patients were selected from hypertensive patients with cardiomegaly (i.e., CTR > 50%) and 200 hypertensive patients without cardiomegaly were selected as controls for the study.
Technique of chest radiograph
The PA chest radiographs were obtained with a 35 × 43 cm using a Philips static General Electric (GE) MS-185 basic X-ray machine (Waukesha, WI, USA). The patient stands erect, chin raised, hands on hips with palms out and shoulder forward. The central ray was centered at the T5 region. Top of the image receptor was set above the shoulders in an average patient. Direction of ray was perpendicular to the image receptor at a source to image distance of 180–300 cm (72–120''). Collimation was set at the upper border to vertebra prominence. Exposure was done at the end of 2nd deep inspiration. The acquired chest radiograph was then assessed for evidence of cardiomegaly.[26]
Technique of carotid Doppler ultrasound
Ultrasound examination of the CCA intima-media thickness (IMT) was done using the 7.5-MHz linear transducer of E-saote Europe 2014 ultrasound machine ï equipped with electronic calipers The patient lying supine to the right of the examiner and a pillow support under the neck to achieve the desired neck extension position and the head turned 45° away from the side was examined after the application of adequate amount of coupling gel. To ensure adequate compliance with inclusion and exclusion criteria, a brief history was taken and clinical examination of the neck was also done. Right and left common carotid arteries were located by multiple longitudinal and transverse scans. At the beginning of the examination, the vessels were assessed in B-Mode, adjusting the optimizing factors such as frequency, depth, gain, time gain compensation, and focal zone for optimal view.
The study protocol involved scanning of the far wall of the right and left carotid arteries which spans from the superior aspect of the clavicle to the angle of the mandible while the internal jugular vein was used as a window.[25] The reference point of measurement of IMT was 1 cm before the carotid bulb, which is seen as a fusiform dilatation of the carotid arteries at about C2/C3 level.[25] Two parallel echogenic lines (double line pattern), which correspond to the lumen–intima and the media–adventitia interfaces [Figure 1], were seen to represent the IMT. Three (3) readings were obtained and their mean used as the final reading in order to reduce the intraobserver variation. Sampling volume size of 2–3 mm and Doppler angle of less than 60° were used. Plaques appearance and morphology were assessed when identified; these include plaque ulceration, calcification, and composition. | Figure 1: Intima-media layer, IMT of the carotid artery as seen on longitudinal sonogram. Normal thickness is 0.74-0.8 m
Click here to view |
Duplex mode was activated to produce color flow and a triplex or pulsed wave to provide a wave-form tracing [Figure 2]. | Figure 2: Common carotid artery spectrum showing low resistance character
Click here to view |
Images of the IMT (in millimeter-mm) and Doppler velocimetric indices were printed using Sony UP 895MD videographic printer.
Data analysis
The data obtained was analyzed using Statistical Package for Social Sciences (IBM SPSS Statistics version 20). Results were expressed as mean/standard deviation and or median with interquartile ranges for non-normally distributed variables. Level of significance was set at P < 0.05. Chi-square test was used to determine relationship between categorical variables such as gender, cardiothoracic ratio (CTR), and BMI, while students t-test was used for inferential statistics among quantitative variables such as blood pressure and Doppler velocimetric indices. ANOVA and regression analysis were conducted to determine differences of Doppler parameter (RI, PSV, and EDV) on right and left sides and between groups.
| Results | | |
A total of 400 hypertensive patients were successfully recruited for this study, with 200 being hypertensive and having features of hypertensive cardiomegaly (CTR > 50%) on frontal chest radiograph, and the remaining 200 being only hypertensive with a normal frontal chest radiograph (CTR < 50%), serving as controls.
The study population's age ranged from 22–65 years and a cumulative mean of 48.91 ± 10.0. More than 50% of the participants were >50 years of age. However, the mean age for the study group was 52.93 ± 8.07 and 44.88 ± 10.22 for the control [Table 1]. This shows that the controls are of lower age group compared to the study group, and is statistically significant (P< 0.0001).
Amazingly, there is no statistical significance when gender of the two groups were compared (P-value > 0.05). There were 204 males and 196 females, giving 51% and 49%, respectively [Figure 3]. For the study and control groups, there were 110 males (53.9%) and 90 females (45.9%), and 94 males (46.1%) and 106 females (54.1%), respectively. | Figure 3: Pie char t showing gender distribution of the study participants (this figure is not cited in the text)
Click here to view |
The body mass index (BMI) of the groups were obtained and compared. The study group shows higher BMI compared to the control. This ranges from normal to overweight to obesity. The mean BMI was 27.23 ± 6.08 seen in patients with hypertensive cardiomegaly (CTR of > 50%), while the control group shows a BMI that is lower (25.32 ± 4.34). However, this difference is statistically significant (P-value < 0.0001).
One hundred and ten (110, 53.9%) males in the study group have CTR > 50% and 90 (45.9%) were females (P = 0.110, >0.005). It was observed that CTR in percentage is related to the patients' age. The CTR is seen to increase with age. The mean age of participants with CTR above 50% was 52.93 ± 8.07, which constituted the majority (132, 66.0%), while that of participants with CTR below 50% was 44.88 ± 10.22. This was found to be statistically significant as older subjects more likely to have abnormal CTR (>50%) compared to younger ones (P< 0.0001).
The mean IMT readings obtained in the study group was 13.0 ± 0.13 mm and 15.0 ± 1.80 mm on the respective sides for the right CCA and left CCA, and 10.0 ± 0.2 mm and 0.90 ± 0.2 mm in the control on the right and left sides, respectively.
Velocimetric indices in the study population obtained were 66.20 ± 21.81 cm/s and 59.54 ± 22.75 cm/s for the mean peak systolic velocity (PSV) on the right and left CCA, respectively, while 58.14 ± 35.98 cm/s and 51.13 ± 31.55 cm/s are the mean in the control group. Mean end-diastolic velocity (EDV) obtained is 17.85 ± 5.97 cm/s and 16.56 ± 6.44 cm/s. Mean EDV in the control is 15.15 ± 8.28 cm/s and 13.60 ± 7.12 cm/s. The mean resistive index (RI) on the right and left CCA in the study group is 0.72 ± 0.07 and 0.72 ± 0.06, while in the control patients 0.73 ± 0.06 and 0.72 ± 0.08. All these readings obtained were statistically significant (P< 0.001), except for the reading obtained in the left EDV between the study and the control (P = 0.096).
Thirty participants (7.5%) were found to be having plaques. All of the plaques were echogenic, smooth, and regular. The percentage diameter reduction of RCCA among these participants ranged between 10% and 42%. Twelve of them (40%) had percentage diameter reduction less than 20%, 14 (46.7%) had percentage diameter reduction between 20% and 40%, while 4 (13.3) had percentage diameter reduction >40% (up to 42%).
Sociodemographic characteristics of the participants
This study involved 400 known hypertensive patients, with age range 22–65 years and mean of 48.91 ± 10.0. One in two of the participants were >50 years of age.
There was nearly equal representation of the two genders, with slight preponderance of males (51%).
Relationship between age and CTR
[Figure 4] shows the relationship between age and CTR. Below 30 years, none of the participants had CTR > 50%. Above 30 years, there was a gradual increase in the proportion of participants with CTR > 50% such that between 41 and 50 years, nearly equal number of participants had CTR below and above 50%. At >50 years, majority of the participants (66.0%) had CTR > 50%. The mean age of participants with CTR above 50% was 52.93 ± 8.07, while that of participants with CTR below 50% was 44.88 ± 10.22. Further analysis showed that there was statistically significant relationship between age and CTR, with older subjects more likely to have large CTR compared to younger ones (P< 0.0001).
More males (53.9%) had CTR > 50% compared to females (45.9%). However, this relationship was not statistically significant (P = 0.110) [Table 2].
The mean BMI of participants with CTR > 50% (27.23 ± 6.08) was found to be higher than that of subjects with CTR < 50% (25.32 ± 4.34). Further analysis showed that participants with high BMI had higher risk of having CTR > 50% compared to those with low BMI (P < 0.001)” The relationship is statistically significant [Table 3].
The mean IMT was higher in the study groups compared to the control. For right CCA, the IMT for the study and control groups was 0.13 and 0.10, respectively, (P< 0.001), while for left CCA, it was 0.15 and 0.09, respectively (P< 0.001) [Table 4]. | Table 4: Variation in IMT between study (CTR >50%) and control (CTR <50%) groups
Click here to view |
Further analysis showed that CTR can be used to predict IMT (see below).
[Figure 5] shows the curve fit for variation between left CCA and CTR. The regression equation derived from the above operation can be used to predict IMT of left CCA when CTR is known. The equation is: | Figure 5: Curve fit for variation between left common carotid artery and CTR
Click here to view |
IMT = (Slope × CTR) + Constant
Lt (IMT) = (0.004 × CTR) + (-0.076)
The equation is statistically significant for this estimation (P = 0.001).
[Figure 6] shows the curve fit for variation between right CCA and CTR. The regression equation derived from the above operation can be used to predict IMT of right CCA when CTR is known. The equation is: | Figure 6: Curve fit for variation between right common carotid artery and CTR
Click here to view |
Rt (IMT) = (0.001 × CTR) +0.036
The equation is statistically significant for this estimation (P = 0.045).
[Table 5] shows the effect of systolic BP on IMT of right and left common carotid arteries. There was a linear relationship between systolic BP and IMT. The relationship was more significant in the left CCA where a maximum thickness (0.17 mm) was found in participants with systolic BP between 140 and 159 mmHg. Statistical analysis showed that there was proportional relationship between systolic BP and IMT in right (P = 0.002) and left (P< 0.0001) common carotid arteries.
The mean PSV and EDV in the right and left carotid arteries were higher among the study participants compared to control group. [Table 6] The right PSV in the study group was 66.20 compared to 58.14 in the control group (P< 0.001). The mean left PSV in the study group was 59.54 compared to 51.13 in the control group (P< 0.001). The mean right EDV in the study group was 17.85 compared to 15.15 in the control group (P< 0.001), while the mean left EDV in the study group was 16.56 compared to 13.60 in the control group (P = 0.096). The mean right RI in the study group was 0.72 compared to 0.73 in the control group (P< 0.036), while the mean left RI was the same in the study and control groups (P< 0.001). | Table 6: Velocimetric indices of study group (CTR >50%) compared to control (CTR <50%)
Click here to view |
Thirty participants (7.5%) were found to be having plaques. All of the plaques were echogenic, smooth, and regular. The percentage diameter reduction of RCCA among these participants ranged between 10% and 42%. Twelve of them (40%) had percentage diameter reduction less than 20%, 14 (46.7%) had percentage diameter reduction between 20% to 40%, while 4 (13.3%) had percentage diameter reduction >40% (up to 42%) [Figure 7]. | Figure 7: Percentage diameter reduction of RCCA among participants with plaque
Click here to view |
| Discussion | | |
This study tends to find/point out the possible abnormalities in the common carotid arteries of hypertensive patients who already have shown features of cardiac size enlargement. Thus, a positive correlation between various complications of hypertension can be achieved. A total number of 400 hypertensive individuals were involved in this study, with 200 having hypertensive cardiomegaly (50%) and the other 200 (50%) having normal cardiac contour on frontal radiograph serving as controls.
The age ranges for the study population obtained were between 22 and 65 years with mean age of 48.91 ± 10.0. The lowest and highest age range frequencies are 21–30 and >50 years constituting 6.0% (24) and 52.5% (210), respectively. [Figure 4]. This indicated raising blood pressure with advancing age, which is in conformity with the previous studies of Carretero and Oparil.[3] and Vasan et al.[4] This is further supported in this study that age has a linear relationship with blood pressure. Majority of the participants, 132 out of 200 (66.0%) with hypertensive cardiomegaly were above 50 years of age. The mean age (in years) of these participants with CTR above 50% was 52.93 ± 8.07. [Figure 5]. Thus, there is a significant statistical relationship between advanced age and cardiac size (P< 0.0001).
In this study, there was no statistical difference in gender with 204 (51%) males and 196 (49%) females. This is in contrast with Carretero and Oparil,[3] who pointed out that hypertension is more prevalent in men although as women approached menopause, this difference is abolished. This disparity could be attributed to the ages of the study population, whose mean age was 52.93 ± 8.07, i.e., the women were either menopausal or approaching it. No significant statistical relationship was also obtained in this study between gender and hypertensive cardiomegaly, despite the fact that more males (53.9%) had CTR > 50% (X 2 = 2.561, P = 0.110) [Table 2].
Obesity is a risk factor for hypertension and, if present, tends to worsen its prognosis. In this study, the mean BMI of the study group was 27.23 ± 6.08, which denotes overweight when compared to controls that are only hypertensives. There was a significant statistical relationship between higher BMI and increased CTR which denotes cardiomegaly (P< 0.001). This is in conformity with the study of Milutinović et al.[29] who found increased frequency of cardiac enlargement in obese hypertensives. It is believed that obesity adds to blood pressure burden. Mark [30] in their study of the progression of hypertensive heart disease also mentioned obesity as a major contributor to left ventricular hypertrophy among hypertensives. This could explain why this study group had cardiomegaly.
Increased cardiovascular and total mortality risk is associated with increased CIMT.[31] This study showed a significant statistical relationship between high blood pressure and right and left CIMT (P = 0.002 and P < 0.001). The highest mean IMT reading of 1.70 ± 0.25 mm was obtained on the left CCA at a systolic blood pressure range of 140–159 mmHg while the reading on the right was 1.50 ± 0.18 mm at 160–179 mmHg. These findings agree with Su et al.[32] who concluded that hypertension strongly influence carotid atherosclerosis, reinforcing the hypothesis that hypertension has a major role in the pathogenesis of atherosclerosis.
As noted above, higher CIMT were obtained at a higher systolic blood pressure, with a significant statistical relationship (P = 0.002 and P < 0.001). This is in concert with Arnett et al.[33] study, where they found that the CIMT is dependent on systolic blood pressure and not related to the diastolic blood pressure, just like in this study. A linear relation was also observed between systolic blood pressure (mmHg) and IMT. This relationship was seen to be more significant on the left where the highest mean IMT reading of 1.70 ± 0.25 mm was found (P< 0.001).
Positive significant statistical relationship was obtained between age and thickening of CIMT. This is in line with the studies of Su et al.[32] and Vicenzini et al.[34]
The mean CIMT on the right and left sides was 1.3 ± 0.13 mm and 1.50 ± 018 mm, respectively, among the study group. While it was 1.00 ± 0.20 mm and 0.90 ± 0.20 mm on the right and left carotid arteries, respectively, among the controls, who are also hypertensives. These readings obtained are way higher both in the study group and the control than those of normal individuals in this environment. Dambatta et al.[35] got 0.75 ± 0.10 mm and 0.71 ± 0.09 mm as means CIMT for males and females.
The readings obtained are higher even in studies among hypertensive individuals. Umeh et al.[24] also had higher readings of CIMT among hypertensive patients compared to normal individuals. Their readings were 0.756 ± 0.130 mm and 0.751 ± 0,129 mm on the left and right sides. However, their readings are still lower than those obtained in this study.
There is disparity in the CIMT readings on the right and left sides (1.3 ± 0.13 mm and 1.50 ± 018 mm) in this study. This shows higher IMT reading on the left CCA, as was obtained by Dambatta et al.[35] even among normal. The result obtained is also in line with results obtained by Vicenzini et al.;[34] they also observed a small but significant side difference with higher IMT values on the left side (right, 0.95 ± 0.19 mm; left, 0.97 ± 0.21 mm; P <.0001).
Using statistical analysis, there is a significant relationship between abnormal/higher CTR (>50%) and thicker IMT (P< 0.001). Thus, group 1 shows higher IMT and CTR. And using regression equation, the IMT of both carotid arteries can be predicted from obtained CTR.
IMT = (Slope × CTR) + Constant
Lt (IMT) = (0.004 × CTR) + (-0.076)
Rt (IMT) = (0.001 × CTR) +0.036
These equations are statistically significant having a P value of 0.001 and 0.045 on the left and right sides, respectively (P< 0.005). This is quite interesting, because using simple and cheap radiological investigation like the plain PA chest radiograph in hypertensive individuals, a sensitive and important parameter like the CIMT can be predicted. This also serves as a pointer to the atherosclerotic burden in that individual. This is in conformity with Rayner et al.[31] findings that chest radiograph is a valuable tool in the evaluation of hypertensives.
In this study, there is significant (P< 0.001) disparity in all the Doppler velocimeteric indices obtained between the study groups. The PSV of the study group on the right is 66.20 ± 21.81 cm/s, while on the left is 59.54 ± 22.75 cm/s. The control PSV on the right and left sides is 58.14 ± 35.98 cm/s and 51.13 ± 31.55 cm/s, respectively. The same applies for the EDV [Table 5]. The reading in the control group is somewhat lower than the study group. And when the study and control values are compared to values from normal individuals, the resultant comparison shows that the readings from the study group and control (all being hypertensive) are lower than that of normal individuals. This is in conformity with the study done by Agunloye and Mayowa [23] where they found a lower PSV and EDV in the common carotid of hypertensive individuals when compared to normal controls. The above pattern for EDV is likely due to the greater burden of atherosclerosis disease on vascular walls of hypertensive patients during the natural course of hypertension with resultant progressive decline in cardiac output during the diastolic phase of the cardiac cycle.
The RI in both the study and control was within the normal range for normal individuals [Table 5]. This is in conformity with many previous studies by Agunloye and Mayowa [23] Thus, RI provides a poor correlation of disease severity. This can be explained by the fact that the CCA supplies 2 different resistance beds as pointed out by Frauchiger et al.[36]
Less than 8% of the study population had plaques in their CCA. All the plaques were found in the study group and located within the carotid bulb. This conformed to studies by Takiuchi et al.[25] and Rosfors et al.[37] However, in slight contrast to Takiuchi et al., the patients in this study has 100% ventricular enlargement. Also in conformity with Prisant et al.,[38] the plaques are seen in individuals with IMT readings above 10.0 mm.
The plaques seen were echogenic, smooth, and regular with about 40% diameter reduction. Thus, they are hemodynamically insignificant. This was also the finding of Rosfors et al.[37] that these type of plaques are commoner in hypertension and are smaller in size.
| Conclusion | | |
The prevalence of carotid artery abnormalities in the form of thickening of the carotid intima-media wall as a marker of the degree of atherosclerosis was high among individuals with radiographic features of hypertensive cardiomegaly in Kano, compared to the controls. These changes/complications are seen to have a positive and strong correlation with age, cardiothoracic ratio, obesity, and systolic blood pressure, while poorly correlate with gender.
This study confirms the presence of vascular risk in the presence of abnormal/thickened carotid intima-media wall and that chest radiography still remains relevant in the initial screening and long-term follow-up of patients with hypertension.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | |
| 2. | Kearney PM, Whelton M, Reynolds K, Muntner P, Whelton PK, He J. Global burden of hypertension: Analysis of worldwide data. Lancet 2005;365:217-23.  |
| 3. | Carretero OA, Oparil S. Essential hypertension. Part 1: Definition and etiology. Circulation 2000;101:329-35. |
| 4. | Vasan RS, Beiser A, Seshadri S, Larson MG, Kannel WB, D'Agostino RB, et al. Lifetime risk for developing hypertension in middle-aged women and men: The Framingham study. J Am Med Assoc 2002;287:1003-10. |
| 5. | Ehret GB, Munroe PB, Rice KM, Johnson AD, Chasman DI, Smith AD, et al. Genetic variants in novel pathways influences blood pressure and cardiovascular disease risk. Nature 2011;478:103-9. |
| 6. | Lifton RP, Gharavi AG, Geller DS. Molecular mechanisms of human hypertension. Cell 2001;104:545-56. |
| 7. | Whelton PK, He J, Appel LJ, Cutler JA, Havas S, Kotchen TA, et al. “Primary prevention of hypertension: Clinical and public health advisory from The National High Blood Pressure Education Program”. J Am Med Assoc 2002;288:1882-8. |
| 8. | O'Brien E, Beevers DG, Lip, Gregory YH. ABC of Hypertension. London: British Medical Journal Books. Blackwell Publishing Ltd; 2007. ISBN 1-4051-3061-X. |
| 9. | Wilson JD, Foster DW, Kronenberg HM. Endocrine hypertension. In: Dluhy RG, Williams GH. editors. Williams Textbook of Endocrinology. 9 th ed. Philadelphia; Montreal: W.B. Sanders; 1998. p. 729-49. |
| 10. | Fisher ND, Williams GH. “Hypertensive vascular disease”. In: Kasper DL, Braunwald E, Fauci AS, editors. Harrison's Principles of Internal Medicine. 16 th ed. New York, NY: McGraw-Hill; 2005. p. 1463-81. |
| 11. | Wong T, Mitchell P. The eye in hypertension. Lancet 2007;369:425-35. |
| 12. | National Clinical Guideline Centre. 7 Diagnosis of Hypertension, 7.5 Link from evidence to recommendations. Hypertension (NICE CG 127). National Institute for Health and Clinical Excellence. 2011. p. 102. |
| 13. | White WB Defining the problem of treating the patient with hypertension and arthritis pain. Am J Med 2009;122(5 Suppl):S3-9. |
| 14. | Insull W. The pathology of atherosclerosis: Plaque development and plaque responses to medical treatment. American J Med 2009;122 (1 Suppl):S3-14. |
| 15. | Liapis CD, Avgerinos ED, Kadoglou NP, Kakisis JD. What a vascular surgeon should know and do about atherosclerotic risk factors. J Vasc Surg2009;49:1348-54. |
| 16. | Riccioni G. The effect of antihypertensive drugs on carotid intima-media thickness: An up-to-date review . Curr Med Chem2009;16:988-96. |
| 17. | Safar ME, Jankowski P. Central blood pressure and hypertension: Role in cardiovascular risk assessment. Clin Sci 2009;116:273-82. |
| 18. | Werner CM, Böhm M. The therapeutic role of RAS blockade in chronic heart failure . Ther Adv Cardiovasc Dis 2008;2:167-77. |
| 19. | Steinmetz M, Nickenig G “[Cardiac sequelae of hypertension]”. Internist (in German) 2009;50:397-409. |
| 20. | Hennersdorf MG, Strauer BE “[The heart in hypertension]”. Internist (in German) 2007;48:236-45. |
| 21. | |
| 22. | Chockalingam A. Impact of World hypertension day. Can J Cardiol 2007;23:517-9. |
| 23. | Agunloye AM, Mayowa OO. Exploring carotid sonographic parameters associated with stroke risk among hypertensive stroke patients compared to hypertensive controls. JUM 2014;33:975-83 |
| 24. | Umeh EO, Agunloye AM, Adekanmi AJ, Adeyinka AO. Ultrasound evaluation of intima-media thickness of carotid arteries in adults with primary hypertension at Ibadan, Nigeria. West Afr J Med 2013;32:62-7. |
| 25. | Takiuchi S, Kamide K, Miwa Y, Tomiyama M, Yoshii M, Matayoshi T, et al. Diagnostic value of carotid intima–media thickness and plaque score for predicting target organ damage in patients with essential hypertension. J Hum Hypertens 2004;18:17-23. |
| 26. | Ryan S, McNicholas M, Eustace S. Radiology of the heart. In. Anatomy for Diagnostic Imaging. 2 nd ed. Edinburgh: Saunders Elsevier Publishers; 2004. p. 125-31. |
| 27. | Messerli FH, Ketelhut R. Left ventricular hypertrophy – An independent risk factor. J Cardiovasc Pharmacol 1991;17:S59-67. |
| 28. | Ibrahim T. Research Methodology and Dissertation Writing for Health and Allied Health Professionals. Cress Global Link Ltd. Abuja; 2010. p. 70. |
| 29. | Milutinović S, Apostolović S, Tasić I. Left atrial size in patients with arterial hypertension. Srp Arh Celok Lek 2006;134:100-5. |
| 30. | Mark HD. The progression of hypertensive heart disease. Circulation 2011;123:327-34. |
| 31. | Rayner BL, Goodman H, Opie LH. The chest radiograph. A useful investigation in the evaluation of hypertensive patients. Am J Hypertens 2004;17:507-10. |
| 32. | Su TC, Jeng JS, Chien KL, Sung FC, Hsu HC, Lee YT. Hypertension status is the major determinant of carotid atherosclerosis. A community-based study in Taiwan. Stroke 2001;32:2265-71. |
| 33. | Arnett DK, Tyroler HA, Burke G, Hutchinson R, Howard G, Heiss G. Hypertension and subclinical carotid artery atherosclerosis in blacks and whites. The atherosclerosis risk in communities study. Arch Intern Med 1996;156:1983-9. |
| 34. | Vicenzini E, Ricciard MC, Puccinelli F, Altieri M, Vanacore N, Piero VP, et al. Common carotid artery intima-media thickness determinants in a population study. J Ultrasound Med 2007;26:427-32. |
| 35. | Dambatta AH, Tabari AM, Isyaku K, Idris SK, Suwaid MA, Saleh MK, et al. B-mode ultrasonographic measurement of common carotid artery intima-media thickness among healthy adults in Kano, Nigeria. West Afr J Ultrasound 2008;9:12-7. |
| 36. | Frauchiger B, Schmid HP, Roedel C, Moosmann P, Staub D. Comparison of carotid arterial resistive indices with intima-media thickness as sonographic markers of atherosclerosis. Stroke 2001;32:836-41. |
| 37. | Rosfors S, Hallerstam S, Jensen-Urstad K, Zetterling M, Carlström C. Relationship between intima-media thickness in the common carotid artery and atherosclerosis in the carotid bifurcation. Stroke 1998;29:1378-82. |
| 38. | Prisant M, Zemel PC, Nichols FT, Zemel MB, Sowers RJ, Carr AA, et al. Carotid plaque associations among hypertensive patients. Arch Intern Med 1993;153:501-6. |
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7]
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6]
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