Xanthogranulomatous cholecystitis : sonographic and CT findings
A COMPARATIVE B-MODE SONOGRAPHIC MEASUREMENT OF …
Transcript of A COMPARATIVE B-MODE SONOGRAPHIC MEASUREMENT OF …
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A COMPARATIVE B-MODE SONOGRAPHIC MEASUREMENT OF
CAROTID ARTERY INTIMA MEDIA THICKNESS IN HYPERTENSIVE
AND NORMOTENSIVE ADULTS AT JOS.
BY
KOLADE-YUNUSA Hadijat Oluseyi (MBBS,)
DEPARTMENT OF RADIOLOGY
JOS UNIVERSITY TEACHING HOSPITAL, JOS
A DISSERTATION SUBMITTED TO THE NATIONAL
POSTGRADUATE MEDICAL COLLEGE OF NIGERIA IN PARTIAL
FULFILMENT OF THE REQUIREMENTS FOR THE AWARD OF
FELLOWSHIP IN THE FACULTY OF RADIOLOGY (FMCR)
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MAY 2014
SUMMARY
Background: The intima media thickness (IMT) has been established as an early
predictor of general arteriosclerosis in patients with hypertension. However, to date,
there is paucity of information on IMT of common carotid artery in healthy patients and
in patients with risk factors for cardiovascular diseases such as hypertension, diabetics
and obesity in study area. Therefore, the aim of this study was to compare the carotid
intima media thickness in patients with hypertension and normotensive adults attending
Jos University Teaching Hospital Jos, Nigeria.
Materials and Methods: This prospective study was conducted over a period of four
months (November 2012 to February 2013) on 200 hypertensive patients and 100
normotensive adults aged 18 – 70 years. The common carotid artery (CCA) was
scanned using an ALOKA SSD-3500 ultrasound scanner with Doppler facility and a
7.5MHz linear transducer. Three measurements of the CIMT were obtained at 1cm
proximal to the right and left carotid bulb and the mean value of the three
measurements was recorded.
Results: The age range of the 300 patients comprising of 104 males and 196 females
was 18 – 70 years with a mean age of 41.44 ±12. The overall mean CIMT was
0.89mm±0.13 and 0.61mm±0.10 for hypertensive and normotensive subjects
respectively. Mean CIMT was significantly higher in hypertensive compared to
normotensive subjects (p=0.000). CIMT correlated positively with age and blood
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pressure in hypertensives but had a negative correlation with BMI. However in
normotensives, CIMT correlated positively with age and BMI. Male hypertensives had
higher CIMT when compared to female. In hypertensive subjects, overall right and left
mean CIMT was 0.89 + 0.13 and 0.89 + 0.18, while in normotensives the overall right
and left mean CIMT value was 0.61 + 0.10 and 0.60 ± 0.10 respectively. There was no
significant difference between the two sides. Artherosclerotic plaques were seen in the
wall of the right CCA in six (3%) hypertensive patients, while none was seen in the
normotensive group.
Conclusion: This study has shown that there is a significant difference in the CIMT of
hypertensive compared to normotensive subject. Higher values of CIMT were seen in
hypertensive subject compared to normotensive. Age, sex, BMI and blood pressure
levels have significant effect on CIMT of hypertensive patients.
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INTRODUCTION
Hypertension is a chronic medical condition in which the systemic arterial blood
pressure is elevated; greater than or equal to 140/90mmHg. It is the most common
non-communicable cardiovascular problem worldwide afflicting humans. Approximately
15 to 37% of the world’s adult population is afflicted1 and in Nigeria its prevalence is
documented as 11.1%.2 In more than 95% of hypertensive patients there is no specific
underlying cause of hypertension and such patients are said to have essential/primary
hypertension or idiopathic/unknown aetiology whereas only a small percentage have an
identifiable cause (secondary hypertension).3
Hypertension causes thickening of the intima media of large vessels with subsequent
atheroma formation. Therefore hypertension is a risk factor for development of
atherosclerosis, a systemic condition primarily affecting elastic arteries (carotid, aorta,
and iliac arteries) as well as large and medium sized muscular arteries. Arterial wall
modifications represent an early involvement of the target organs in patients with
hypertension.4-7 Atherosclerotic plaques start developing in the carotid arteries and
aorta simultaneously, actually preceding plaque occurrence in the coronary arteries.8,9
Hypertension is one of the risk factors for stroke, myocardial infarction, heart failure,
peripheral vascular disease and arterial aneurysm and a leading cause of chronic kidney
disease. Assessment of subclinical and clinical target organ damage is a key element in
the management of patients with hypertension. Practical and applicable examination for
predicting the damage has been long-sought. One of such practical examination for
predicting organ damage is the B-mode ultrasonic measurements of intima media
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thickness (IMT) in the carotid arteries. Other practical examination includes fundoscopy
to check changes in the retinal and twenty-four-hour urinary excretion of protein and
albumin.
The B-mode ultrasonic measurements of intima media thickness of the carotid arteries
has been used extensively for evaluating the presence and progression of
arteriosclerosis in patients with hypertension. Ultrasound measurements of IMT and
plaque occurrence in the carotid arteries are important not only for the assessment of
structural alterations but also because the extent of atherosclerosis in these vessels
reflects the severity of arterial damage in other vascular territories.10,11
High resolution B-mode Ultrasonography is a non invasive, simple, safe, inexpensive,
precise and reproducible method of examining and evaluating the walls of common
carotid arteries for arterial wall thickening and atherosclerotic progression and
regression. It also provides a measure of CIMT and detects presence of stenosis and
plaques in patients with hypertension. This technique permits accurate quantification of
the CIMT, which is generally considered as an early marker of atherosclerosis
sonographically. Thickening of intima-media complex also reflects generalized
atherosclerosis12 and assessment of CIMT has been proposed as a noninvasive measure
of cardiovascular disease burden in adults.13 Extracranial carotid arteries provide
excellent and reproducible sites for IMT assessment because of their accessibility,
adequate size, and limited movement.14
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In this study B-mode ultrasound was used to compare the CIMT amongst hypertensive
subjects and normotensive healthy volunteers.
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JUSTIFICATION
The magnitude of the burden of hypertension requires not only an increase in public
awareness but, the prevention, detection, treatment, and control of this condition
should also receive high priority.15 High blood pressure is a chronic condition, and the
damage it causes to blood vessels and organs generally occurs over years. Increased
CIMT has been shown to be a predictor of coronary and cerebrovascular complication.16
Increased CIMT is directly associated with an increased risk of myocardial infarction.16
In resource-limited settings like ours where high cost of equipment and dearth of skilled
personnel restrict the use of more sophisticated equipment in monitoring the changes in
the heart and the vessels directly, measuring the CIMT in patients with hypertension
will not only allow early monitoring of patients but also, prevent cardiac and cerebral
complications like coronary heart disease and cerebrovascular accident. 17,18
Ultrasonography used in this study is a noninvasive relatively simple, safe, precise, and
reproducible method that has emerged as an imaging of choice in determining the
anatomic extent of arteriosclerosis in patients with hypertension. The measurement of
CIMT using ultrasound is being applied extensively for evaluating the presence and
progression of arteriosclerosis in patients with hypertension.
Even through Computed tomography (CT) and Magnetic Resonance Imaging (MRI)
have increasing role in the evaluation of patients with cardiovascular disease such as
hypertension; their use is limited by cost and limited availability in our local setting.
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There is also paucity of research concerning the effect and the use of CIMT as an
independent predictor of the likelihood of not only cerebrovascular diseases but also
general arteriosclerosis in hypertensive patients in this environment. Therefore, the
outcome of this study will be useful in the management and follow up of hypertension
and its complications in our environment.
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AIMS AND OBJECTIVES OF THE STUDY
Broad:
1. To compare CIMT in hypertensive and normotensive adults in Jos.
Specific:
1. To correlate CIMT with age, sex and, body mass index in both hypertensive patients
and normotensive adults in Jos.
2. To establish the relationship between CIMT and blood pressure of hypertensive
adult patients.
HYPOTHESIS
There is a significant difference in the CIMT of hypertensive and normotensive adults.
SUBHYPOTHESIS
1. Age, sex and blood pressure levels have a significant effect on CIMT.
2. Body mass index does not have a significant effect on CIMT.
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ANATOMY
Embryology
The primitive aorta consists of a portion lying ventral to the foregut (ventral aorta), a
portion lying in the first pharyngeal arch, and a dorsal portion lying dorsal to the gut
(dorsal aorta). The common carotid artery develops from the third arch which arises
directly from the ventral aorta and also forms the first part of the internal carotid artery
(ICA). The remainder of the ICA is formed by the cranial portion of the dorsal aorta.
The external carotid artery arises as a bud from the third aortic arch.19,20
Gross Anatomy and Histology
The principal arteries of supply to the head and neck are the two CCA21,22. They differ
in length and mode of origin.21,22 (Figure1). The left CCA arises from the aortic arch in
front and to the right of the origin of the left subclavian artery and lies anterior to it up
to the sternoclavicular joint. The right CCA begins behind the right sternoclavicular joint
at the bifurcation of the brachiocephalic artery into right CCA and right subclavian
artery. In the neck both CCA have essentially similar courses and relationships. Each
CCA passes upwards and slightly laterally. They bifurcate at the level of the upper
border of the thyroid cartilage slightly below the angle of the mandible, at the level of
C3 vertebra, into the internal and external carotid arteries.21,23 At its point of division,
each CCA shows a dilatation, termed the carotid bulb.21 The CCA is contained in the
carotid sheath, which is continuous with the deep cervical fascia.
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Figure 1: A Schematic diagram showing the origin of the common carotid arteries.
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This sheath also encloses the internal jugular vein and vagus nerve, the vein lying
lateral to the artery, and the nerve between the artery and vein on a plane posterior to
both. The CCA usually has no side branches,21,23 while ICA has only cranial but no
extracranial branches. The ICA gives supply to the brain alongside the vertebral artery
(VA). The external carotid artery (ECA) has facial, cervical and skull branches.21
The arterial wall is composed of three layers: intima, media and adventitia.24 The intima
is the innermost layer consisting of a single thickness of endothelial cells. The media is
the thickest layer of the vessel wall, consisting of smooth muscle cells. The adventitia is
the outermost layer, consisting of connective tissue sheath. Internal elastic lamina
separates the intima from the media; while external elastic lamina separates the media
from the adventitia. Of the three layers, intima-media represents the actual arterial wall
and can be easily measured by high-resolution Ultrasonography.25
Anatomic Variations
The left CCA varies in its origin more than the right. In the majority of abnormal cases
the left common carotid artery arises from the brachiocephalic trunk and if the
brachiocephalic trunk is absent, the two carotids arise usually by a single trunk.22,26 The
right CCA may arise above the level of the upper border of the sternoclavicular joint and
this variation occurs in about 12% of cases. In other cases, the right CCA may arise as
a separate branch from the arch of the aorta or in conjunction with the left CCA.
In the majority of abnormal cases, the bifurcation of CCA occurs higher than usual with
the artery dividing opposite or even above the hyoid bone; more rarely it occurs below
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or opposite the middle of the larynx or the lower border of the cricoids cartilage. Rarely,
the CCA ascends in the neck without any subdivision into either external or internal
carotid and in a few cases the CCA has itself been found absent .22, 26
SONOGRAPHIC ANATOMY
B-Mode ultrasound is a well suited imaging modality to visualize the CCA, which is CCA
is generally imaged as far proximal as possible and followed distally to the level of
birfurcation.27 Although the origin of the right CCA is often located as it arises from the
innominate artery, the left CCA originates from the arch and its origin is not accessible
to ultrasound imaging.28 The carotid bulb is identified as a mild widening of CCA at the
bifurcation.28 The artery walls are usually best observed in the CCA where the vessel
course is parallel to the skin surface and is located at a right angle to the ultrasound
beam. Loss of wall interfaces are seen when the near and far walls of the vessel are
curvilinear and not at right angles to the ultrasound beam. This makes it difficult to
measure the CIMT and this phenomenon is observed in the carotid bulb and the
proximal portion of ICA when the walls are not parallel leading to suboptimal
visualization. This problem can be overcome by placing the ultrasound transducer at
right angle to the vessels. Proximal to bifurcation of the CCA into internal and external
carotid arteries, it dilates to form the carotid bulb. The origin of bulb can be recognized
in most, though not all subjects. The carotid artery bulb is defined as the site where the
artery begins to dilate slightly and vessel walls curve out being no longer parallel to
each other.
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B-mode ultrasound displays the vascular wall as a regular pattern that correlates with
anatomical layers.29 The wall boundaries appear as two parallel echogenic lines
separated by hypoechoic space in longitudinal views of carotid arteries. The CIMT is
formed by the two parallel echogenic lines and intervening hypoechoic band, which
consist of the leading edges of two anatomical boundaries: the lumen-intima and
media-adventitia interface29 (Figure 2). Variations in IMT between different locations,
such as the inflow side of branches, the inner curvature at bends and opposite the flow
divider at bifurcations may reflect differences in local hemodynamic forces. However, an
IMT greater than 0.9-1mm is almost certainly indicative of atherosclerosis and increased
risk of cardiovascular disease.30
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Figure 2: Longitudinal sonogram showing the measurement of common carotid intima
media thickness (arrows). Common carotid artery (CCA), external carotid artery (ECA),
and internal carotid artery (ICA)
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LITERATURE REVIEW
Hypertension is a chronic medical condition of important public health challenges
worldwide. It is a major contributor to global disease burden and one of the leading
preventive causes of premature deaths. In USA it is estimated that at least 65 million
adults had hypertension in 1999 to 2000, with total hypertension prevalence rate of
31.3%.31 There is a consistent gradient of hypertension prevalence rising from 16% in
West Africa (Nigeria and Cameroon), to 26% in the Caribbean and 33% in the United
state.32 Hypertension is widespread in the sub-Saharan Africa with a high prevalence in
the urban areas.33 In Nigeria crude prevalence is estimated as 11.1%.2
It has been suggested that hypertension is one of the factors that can cause vascular
endothelial damage. This theory is based on the ‘Response to injury’ model of
atherosclerosis.34 According to the model, hemodynamic factors particularly
hypertension and chemical factors in the blood induce dysfunction of the endothelium.
This injury may be followed by aggregation of blood platelets, oxidized lipids, and
smooth muscle cells in the intima resulting in plaque formation. A plaque is defined as a
focal structure that encroaches into the arterial lumen of at least 0.5 mm or 50% of the
surrounding IMT value or demonstrates a thickness greater than 1.5 mm as measured
from the media-adventitia interface to the intima-lumen interface.29 These plaques may
narrow the arterial lumen, thus interfering with blood flow. Plaques can rupture or
crack open, causing the sudden formation of a thrombus which may cause a myocardial
infarction if it completely blocks the blood flow in the heart (coronary), or stroke if it
completely blocks the internal carotid artery or its branches.35
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Atherosclerosis affects the inner lining of an artery, assuming serious health epidemic
in developed countries and rising prevalence in developing nations.36 The risk of
development of atherosclerosis increases with age, male gender, family history,
cigarette smoking, hypercholesterolemia, stress, obesity, hypertension and diabetes.37,38
Several studies have shown a significant relationship between IMT and the above
mentioned cardiovascular risk factors.39,40 The pathogenesis of atherosclerosis remains
unknown, but most theories invoke some damage to the endothelium or underlying
media.37
Hypertension may play some role in the pathogenesis of atherosclerosis causing
endothelial damage which results in dysfunction of the arterial endothelium with
decreased local availability of nitric oxide and thus impaired vasodilator capacity.36 This
has been considered an important early event in atherogenesis. Extracranial carotid
artery (ECA) atherosclerosis has been associated with hypertension-related stroke. In a
community based study in Taiwan comprising of 270 normotensive and 263
hypertensive patients. (146 with hypertension and 117 with borderline hypertension),
hypertensive patients tend to develop carotid stenosis and increased IMT when
compared with normotensives.41
Increased CIMT is considered to represent an early atherosclerotic change of the
artery.42 Furthermore, it can predicts stroke and acute myocardial infarction.16,43
Hypertension is a major risk factor for development of stroke and CVD in developing
and developed world. Hypertension is also a leading risk factor for coronary heart
disease and represents 2.5% and 10.9% of all cardiovascular disease burdens in
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developing and developed world respectively.44 Stroke is the third leading cause of
death in Afro-Americans, and is an important cause of mortality and morbidity
worldwide. Mortality rates are higher in Blacks than in Whites in the United States at
ages below 70 years.45 Higher prevalence of hypertension, diabetes, obesity (in
women), elevated lipoprotein(s) level, smoking (in men), and low socioeconomic status
have been linked to the higher stroke incidence and mortality in Afro-Americans as
compared with Whites.45 Studies based on hospital populations from several countries
in Africa suggest that there is increasing morbidity and mortality from stroke and the
situation in Nigeria is unlikely to be different.46 O’Leary et al,16 having examined over
5800 patients ( 65 years of age) with high resolution Ultrasonography, found that
increased CIMT is directly associated with an increased risk of myocardial infarction and
stroke in older adults without a history of cardiovascular disease. Plaque and intima-
media thickening may reflect different biological aspects of atherogenesis with
distinctive relations to clinical vascular disease. Johnsen and Mathiesen47 found that
plaque measured in the carotid bulb or internal carotid artery is strongly related to
hyperlipidemia and smoking and is a stronger predictor for Myocardial Infarction,
whereas CIMT is strongly related to hypertension and ischemic stroke.
There are various methods of imaging the CIMT including radiographic methods after
arteries have developed advanced calcified atherosclerotic plaque, IMT can be partially
estimated by the distance between the outer edges of calcification and the outer edges
of an angiographic dye column within the artery lumen.30 Angiography also has a role
in assessing the lumen size however vessel thickness cannot be assessed by it as
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angiography provides only a “luminogram“.30 Angiography is also a complex technique
which is invasive due to the process of catheterization, use of X-ray radiation, and
angiographic contrast agents.30 Radiographic IMT may also be approximated using
advanced Computed Tomography (CT) scanners due to their ability to use software to
reconstruct the images. Nevertheless, one of the concerns with all CT scanners is the
amount of absorption dose of X-ray delivered to the patient, and also cumulative doses
of X-ray if used to track the disease status over time.30 Magnetic Resonance (MR)
coronary angiography has developed rapidly over the past years, however, there are
still several technical hurdles to be crossed. Even though MR coronary angiography
techniques continues to improve, but at this time its applicability for assessing
cardiovascular risk still remains limited.36
With ultrasound, IMT can be measured from either outside the body in larger arteries
which are relatively superficial (e.g. carotids, brachial, radial and/or femoral arteries),
and/or internally by intravascular ultrasonography using special catheters to visualize
blood vessel walls from within.30 The relative availability of ultrasound, absence of
ionizing radiation, its non-invasiveness and lower cost when compared with most other
methods, makes it an ideal imaging method. Furthermore, it does not have any known
short or long term adverse effect on the patients’ health status even with repeated
measurements.30 Ultrasound is increasingly being used as the primary method for
assessing the severity of disease in carotid artery, since it represents a noninvasive and
inexpensive method which is easy to perform with adequate reproducibility, and is
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capable of delineating the of intra-luminal anatomy and assessment of the extent of the
atherosclerotic process.
Hypertension causes structural changes in the vessels, including thickening of the wall
of the vessel which has been demonstrated in vivo and in vitro.48 Gariepy48
demonstrated a strong correlation between ultrasonic and histological IMT
measurements. It was noted that increase in the arterial wall thickness observed in the
common carotid and femoral artery of hypertensive patients were not due to age of the
patients as compared to the normotensive subjects.48 The study also found a strong
correlation between CIMT and age in normotensive subjects but not in hypertensive
patients. A group of 74 hypertensive patients aged 18-45 years and 20 normotensive
subjects followed up for 5 years in a study by Puato M et al 49 developed an increase in
the mean IMT (m-IMT) and mean of maximum IMT (M-MAX IMT).This was observed to
a greater degree in white-coat hypertensive subjects and sustained hypertensive
subjects compared with normotensive control subjects. Age was also noted to be
relevant for the increment in M-MAX IMT, whereas body mass index played some role in
the increment of m-IMT. In a study carried out by Pauletto et al 50 to determine factors
which underlie the increased carotid intima media thickness in borderline hypertensives
as compared to normotensive subject, blood pressure levels were found to be a main
determinant of m-IMT while the interaction of blood pressure with other risk factors
such as age and plasma lipids is more relevant for advanced intima-media thickening
such as M-MAX IMT.
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Several factors such as age, body mass index, and blood pressure have been shown to
influence the CIMT. There is a strong positive correlation of CIMT with age in both
hypertensive and normotensive subjects as CIMT is seen to increase with age.51,52 In a
case control study by Sharma51 using high resolution ultrasound to evaluate the IMT in
203 hypertensive patients (cases) and 101 normotensive individuals (controls) aged 35-
65 years, the mean CIMT was significantly higher in hypertensive patients compared to
the control group, p<0.001. In the cases, IMT on the right side was 0.968 mm and that
of left side was 0.969 mm while in control group IMT of right side was 0.551 mm and
that of left side was 0.555 mm. A significant difference in both CIMT was also found
between the smoker and non-smoker hypertensive patients (p<0.02). Adaikkappan M52
compared the CIMT of 260 primary hypertensive patients aged 35-55 years with 70
normotensives over a period of 3years. He reported a significant difference in IMT of
hypertensive and normotensive with P < 0.01. In that study the average CIMT for
normotensives was 0.74 mm and 0.72 mm for the right and left side respectively
whereas for hypertensives, it was 1.01mm and 1.09mm respectively. The mean systolic
(154mm Hg) and mean diastolic (101.38mm Hg) BP values were also significantly
higher when compared with normotensives (114/79mm Hg) and BP values correlated
positively with CIMT. The mean systolic velocities (79.4cm/s and 79cm/s) of right and
left CCA respectively were also elevated in hypertensives when compared with
normotensives (58cm/s and 56cm/s). CCA size was also larger in hypertensives (7.9cm
and 7.8cm), when compared with normotensives (6.8cm and 6.9cm) on the right and
left side respectively. Honzikova et al 53 investigated the influence of age, body mass
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index and blood pressure on CIMT of 27 hypertensive patients aged (47.2+/-8.7 years)
and 23 normotensive subjects aged (44.1+/-8.1 years) with 24hrs recording of blood
pressure performed. There was a significant difference in the CIMT (0.60+/-0.08mm vs.
0.51+/-0.07 mm; p<0.001) between hypertensive and normotensive subjects and the
CIMT correlated positively with age (p<0.001) and body mass index (p<0.01) in
normotensives. However, increased carotid IMT in hypertensive patients was not
additively influenced by either age or body mass index rather influence of blood
pressure predominates. Therefore, blood pressure rather than age and body mass index
has a greater influence in increasing CIMT in hypertensives compared to normotensive
subjects in whom age and body mass index have an additive role on CIMT as reported
in this study. In a study by Umeh et al 54 in Ibadan where ultrasound was used to
evaluate the IMT of CCA in adults with primary hypertension in Nigeria, there was a
significant difference in CIMT in hypertensive when compared with normotensives.
CIMT values showed positive correlation with age and varies with subject’s age and sex.
The mean CIMT for the right values were 0.756mm ± 0.130 and 0.751mm ± 0.129 for
the hypertensive group and 0.638mm ± 0.088 and 0.670mm ± 0.107 for the control
group on the left and right sides respectively. Male hypertensives were also noted to
have higher CIMT values. Okeahialam in Jos55 also demonstrated a significant
difference in the CIMT of hypertensive and normotensive subjects in a study where
CIMT was used as a measure of cardiovascular disease burden in Nigeria Africans with
hypertension and diabetics. The mean CIMT for the right and left CCA were 0.93±0.21
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and 0.93±0.15 for hypertensive and 0.91±0.17 and 0.91±0.13 for normotensive
subjects.
Plavnik et al 56 evaluated the CCA and common femoral arteries of 63 normotensives
aged 20-74 years and 52 hypertensive patients aged 23-72 years and correlated IMT
values with the blood pressure, cardiac structures and several clinical and biological
parameters. The IMT in the carotid and femoral arteries were higher in hypertensive
than in normotensive subjects (0.67 ± 0.13 and 0.62 ± 0.16 vs 0.54 ± 0.09 and 0.52 ±
0.11 mm, respectively, P<0.0001). In normotensive patients, there was significant
correlation between IMT and age, body mass index and 24hrs systolic blood pressure
for both the carotid and common femoral arteries. In hypertensives, the CIMT
correlated positively with age and 24hrs systolic blood pressure and these parameters
were the most important determinants of CIMT in hypertensive while femoral IMT
correlated only with 24-hrs diastolic blood pressure. Body mass index was found to
have no impact on arterial wall thickening for both carotid and femoral arteries of
hypertensive patients. In addition neither the systolic nor diastolic blood pressure values
obtained at presentation correlated with CIMT in the normotensive or in the
hypertensive group. Most studies have suggested that age is the strongest determinant
of carotid wall thickening, and systolic blood pressure has been considered as the
secondary determinant in hypertensive and normotensive subjects.9,48,57 The impact of
blood pressure levels in hypertensive has been considered as an accelerated form of
aging and hypertensive patients develop an aging process in their arterial wall earlier in
life.56
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Patients with hypertension demonstrate increases in CIMT and the number of plaques
as well as a decrease in the ratio of internal diameter to external diameter in carotid
arteries compared with normotensive subjects.58 Recent studies have shown that the
increase in CIMT paralleled the increase in left ventricular wall thickness and left
ventricular mass in hypertensive patients.58 These findings suggest an association
between cardiac and vascular hypertrophy in patients with hypertension.
CIMT assessed by ultrasonography is regarded as an early predictor of general
arteriosclerosis in patients with essential hypertension and can be used to predict end
organ damage in patient with essential hypertension. Takiuchi et al 59 performed
carotid ultrasonography, echocardiography, urinalysis, and fundoscopy in 184 patients
(64 12 years old, 96 males and 88 females) with various stages of essential
hypertension. All carotid ultrasonographic parameters were significantly associated with
albuminuria, retinal arteriosclerosis, and left ventricular mass index. Among all carotid
parameters, maximum CIMT showed the highest correlation coefficient of the severity
of target organ damage and maximum CIMT was an independent factor for predicting
target organ damage in hypertension. Lemne60 compared IMT and plaque occurrence in
the carotid arteries of men with borderline hypertension and normotensive control
subjects. His findings showed a slight increase in overall CIMT and more plaque in the
borderline hypertensive subjects than normal patients which was more evident in the
right carotid arteries. Päivänsalo et al 61 evaluated carotid artherosclerosis in middle
aged hypertensive and control subject, and found that male sex, age, smoking and
cholesterol were the most significant risk factor for plaque and intima media thickness
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and there was a significant difference in CIMT between hypertensives and
normotensives.
Several methods can be employed in the measurement of IMT on ultrasound.62 All
employ multiple measurements at either limited number of sites or single
measurements at multiple sites. The large Atherosclerosis Risk in Community (ARIC)
study63 used the technique of multiple carotid sites measurement of IMT obtained from
the far wall of the right, left CCA, ICA and carotid bulb. Salonen64 et al also measured
the IMT as a focal area of maximal thickness at any position along the entire length of
the right and left CCA. Both methods are accurate on reproducibility validation
assessments but inter-observer variation is always greater than intra-observer variation.
These methods are also complex and time consuming unlike the method employed by
Sidhu et al62 in which measurement of the IMT was obtained 1cm proximal to the
carotid bulb. Studies have shown that ICA does not accurately reflect the overall
process of atherosclerosis because of the propensity of disease to form at flow divider.62
However, the technique of measurement of IMT 1cm proximal to the CCA is more
representative of the overall atherosclerosis and can be used to access atherosclerosis
risk disease.62
An accurate measurement of IMT is possible when measured 1cm proximal to the
carotid bulb because at this level the CCA lies parallel to the skin surface and it is at
right angles to the ultrasound beam. Where the carotid bulb widens and proximal ICA
arises, the arterial wall is unlikely to be parallel to the ultrasound beam and
measurements are likely to be inaccurate. Studies using multiple measurements from
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different sites are cumbersome and are unable to consistently visualize the near wall of
the CCA, ICA and far wall of ICA.62 However, when measured 1cm proximal to the
carotid bulb, visualization of the far wall of CCA is nearly always possible which further
makes this method more accurate62
The technique of measurement of the IMT used in this study (1cm proximal to the
carotid bulb) was chosen because this method is simple, reliable, and reproducible.
There is minimal inter and intra observer error.62 This method allows rapid identification
of the target area and ensures that an identical area is assessed on follow-up. This
method of measurement of IMT is more representative of the overall atherosclerosis
and can be used to access atherosclerosis risk.62
.
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MATERIALS AND METHODS
Study design
This hospital based cross sectional study was carried out over a period of three months
from November 2012 to February 2013 at Jos University Teaching Hospital Jos, Nigeria.
Patients were recruited based on the inclusion criteria until the targeted sample size
was attained.
Study area
This study was carried out in the Department of Radiology, Jos University Teaching
Hospital (JUTH). The Hospital is a 600-bed tertiary Health institution situated at the Jos-
East local government of Jos metropolis. It serves Plateau State and majority of the
States in the North Central geopolitical zone of Nigeria. Jos is the capital of Plateau
state. The state has over 30 different ethnic groups and estimated land mass of about
30,913 square kilometers with a population of 3,178,712 people.65 The main occupation
is farming while most of the urban populations are civil servants. The adult literacy rate
was estimated as 59.1% and 36.5% for males and females respectively.65
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STUDY SAMPLE SIZE
The minimum sample size for the study was 200 subjects calculated using the following
formula66
N = Z 2 p q
d2
Where:
N= Minimum sample size
Z= the standard normal deviation corresponding to 95% levels of significance
(1.96)
P= Prevalence rate of hypertension is 11.1%2
q= 1 - p
d= Degree of accuracy desired, set at 5%.
Calculation
N = 1.96 2 x 0.11 x 0.89
0.05 2
N = 0. 3795
0.052
N= 151.8
30
To take care of invalid samples, 10% of the minimum sample size of 151.8 was
added to the minimum sample size, thus:
10% of 151.8= 15.2
Hence, 151.8 +15.2 =167.0
Hence, the common carotid arteries of 300 subjects comprising of 200
hypertensive subjects and 100 normotensive subjects attending Jos University Teaching
Hospital were scanned.
31
Study population
This study was conducted on hypertensive patients and normotensive volunteers aged
18 to 70 years who met the inclusion criteria. The subjects were recruited using random
sampling.
Inclusion criteria:
1. Adult patients attending Cardiology clinic with confirmed primary hypertension with
blood pressure ≥ 140/90, aged 18-70 years.
2. Normotensive adults aged 18-70 years attending the general outpatient department.
Exclusion criteria:
1. Subjects below 18 years of age and above 70 years.
2. Patients with other associated cardiovascular risk factors such as diabetes, smoking
and hypercholesterolemia.
3. Hypertensives on medication with blood pressure level < 140/90mmg.
4. Patients with diagnosed secondary hypertension. This information was obtained
from the patient’s hospital record file.
5. Unwillingness to participate.
32
6. Pregnant women because of physiological changes and accompanying dilation of
CCA.67
7. Subjects in whom imaging circumstances were very poor, with limited boundary
visualization of CCA or where there is anatomical constraint either a high carotid
artery bifurcation or a short neck.
33
Ethical consideration
A well structured questionnaire was self administered (Appendix I) after an informed
written consent was obtained from the subjects before enlistment into the study
(Appendix II). Approval to carry out the study was obtained from the ethical committee
of the Jos University Teaching Hospital (Appendix III). The subjects were informed of
the safety of ultrasound scan and were guaranteed freedom to withdraw from the study
at any stage without consequences. The data collected from the participants were
recorded serially and kept with utmost confidentiality.
34
METHODOLOGY
To ensure adequate compliance with inclusion and exclusion criteria, brief history was
taken and general physical examination of the subjects was done. All patients had their
fasting blood sugar level and fasting total cholesterol level checked in the chemical
pathology laboratory and those with normal fasting blood sugar level between 2.5-
5.5mmol and normal total cholesterol level between 3.5-6.5mmol were included in
study. The blood pressure of the patients were measured by the same senior
physician/Senior registrar in the cardiology clinic at presentation in a sitting position on
the left arms using standard mercury sphygmomanometer (Accosson, cuff 12cm X
15cm) Hypertension was defined as blood pressure levels higher than or equal to
140/90 mmHg in at least two consecutive measurements.68 Hypertension was classified
using W.H.O classification as Grade 1 hypertension (systolic blood pressure (SBP) 140-
159mmHg, diastolic blood pressure (DBP) 90-99mmHg); Grade 2 hypertension (SBP
160-179mmHg, DBP 100-109mmHg) and Grade 3 hypertension (SBP≥180mmHg,
DBP≥110mmHg).68 All normotensive subjects had their blood pressure checked at the
General outpatient clinic and those with normal blood pressure ≤120/80mmHg were
recruited for the study. The height (in meters) and weight (in kilograms) of each
subject was taken using meter rule and Beam weighing scale respectively. The body
mass index (BMI) was calculated as ratio of measured weight to square of the
measured height (Kg/m2). BMI was classified using WHO classification as underweight
(BMI<18.5); Normal (BMI 18.5-24.9); Overweight (BMI 25.0-29.9); Obese (BMI ≥30).69
35
The examination of the CIMT was performed using the 7.5 MHz linear transducer
ALOKA SSD-3500 ultrasound scanner equipped with Doppler facility. Patients were
requested to remove jewellery around the neck. The B mode ultrasound of the CIMT
were done with the subject lying supine to the right of the examiner with pillow support
under the neck to achieve the desired neck extension and head turned 450 away from
the side being scanned. Adequate amount of coupling gel was applied to the scan area
to eliminate air gap between probe and skin surface. Right and left CCA were located by
multiple longitudinal and transverse scans.
Three repeated measurements of CIMT were obtained in the longitudinal plane at the
point of maximal thickness on the far wall of both CCA 1cm proximal to the carotid
bulb, where it is clear of plaques. The position of the carotid bulb is defined as the point
where the far wall deviated away from the parallel plane of the distal CCA (Figure 3).
The IMT is the distance between the inner echogenic line representing the intima -blood
interface and the outer echogenic line representing the adventitia-media junction
(Figure 2). Measurements were repeated thrice on each side, unfreezing on each
occasion and relocating the position of maximal IMT. The mean of the three
measurements on each side was recorded. The overall mean was arrived at by
averaging the mean of the right and left CIMT of hypertensive and normotensive
subjects.
36
Figure 3: Sonogram showing longitudinal image of the CCA. Note the carotid bulb
(white arrow) as the point where the far wall deviates away from the parallel plane of
the distal CCA.
37
STATISTICAL ANALYSIS
The data obtained from the subjects was recorded in the questionnaire (Appendix 1)
and was analyzed using Statistical Package for Social Sciences (SPSS) for windows
version 19.0 (SPSS inc. Chicago, Illinois, USA). Mean ±standard deviation was used to
summarize the variables. Comparison of mean and proportion was considered
statistically significant if P value was equal to or less than 0.05. The results were
presented in form of tables and figures.
38
RESULTS
A total of 300 subjects comprising of 200 hypertensives and 100 normotensives
participated in the study. The mean ages of subjects were 50.62 + 10.46 years and
47.04 + 11.39 years for hypertensives and normotensives respectively. The difference
in age was statistically significant (p=0.000).
Among the hypertensives 33.5% were male and 66.5% were females while in the
normal subjects 37% were male and 63% were female. The difference in the gender
ratio was not statistically significant (p=0.438). The predominant age group in
hypertensives is age group 51-60 years accounting for 57(28.5%) while in
normotensives the predominant age group is age group 31-40years accounting for
39(39.0%) of patients investigated (Table 1, Fig 4).
39
Table 1: Age distribution among Hypertensive and Normotensive
subjects in Jos.
Age group Hypertensive Normotensive
(Years) Frequency Percent (%) Frequency Percent (%)
21 – 30 3 1.5 1 1.0
31 – 40 49 24.5 39 39.0
41 – 50 46 23.0 21 21.0
51 – 60 57 28.5 22 22.0
61 – 70 45 22.5 17 17.0
Total 200 100.0 100 100.0
40
Figure 4: Bar chart showing age distribution among normotensive and
hypertensive subjects.
1
39
21 22
17
3
49
46
57
45
0
10
20
30
40
50
60
21-30 31-40 41-50 51-60 61-70
pe
rce
nta
ge(%
)
Age group (years)
Nomotensive Hypertensive
41
The overall mean CIMT for the hypertensive group in this study was 0.89 + 0.13 and
0.62 + 0.10 for the normotensive group. The difference in CIMT is statistically
significant (p=0.000). In hypertensive subjects, overall right and left mean CIMT was
0.89 + 0.13 and 0.89 + 0.18 respectively, while in normotensives the overall right and
left mean CIMT value was 0.61 + 0.10 and 0.62 + 0.10 respectively. There was no
statistically significant between the two sides in both hypertensives (p= 0.386) and
normotensives (p=0.018).
The mean CIMT for male and female hypertensives were 0.92±0.16 and 0.87±0.12
respectively (p=0.11) and 0.62±0.09 and 0.61±0.09, (p= 0.70) amongst normotensive
males and females respectively. Male CIMT values were higher than female CIMT value
in both groups. However, gender difference in CIMT was not statistically significant in
both hypertensives (P=0.11) and normotensives (P=0.70) (Table2).
42
Table 2: Mean CIMT of both hypertensive and normotensive subjects
by gender.
Sex Hypertensives Normotensives
Freq RCIMT LCIMT Mean Freq RCIMT LCIMT Mean
(mm) (mm) CIMT(mm) mm mm CIMT(mm)
Male 67 0.92 0.91 0.92 37 0.61 0.63 0.62
Female 133 0.86 0.87 0.87 63 0.61 0.61 0.61
Total 200 100
P =0.11 P = 0.70
43
In hypertensives, the mean CIMT for age group 21-30 and 61- 70 was 0.70mm and
0.95mm respectively and in normotensives mean CIMT for age group 21- 30 and 61-70
was 0.52mm and 0.83mm respectively (Table 3). The CIMT progressively increased
with age in both hypertensives and normotensives. This increase was statistically
significant (p=0.000) in both hypertensives and normotensives. (Table 3 and fig 5). The
CIMT is higher in all age groups among hypertensives compared with corresponding
normotensives. Age has a strong correlation with CIMT in both hypertensive and
normotensive subjects (Pearson correlation =0.35 and 0.88 in hypertensives and
normotensives respectively).
44
Table 3: Mean CIMT value with age group in hypertensives and
normotensives.
Age group Hypertensives Normotensives
(Years) RCIMT LCIMT Mean CIMT RCIMT LCIMT Mean CIMT
mm mm mm mm mm mm
21 – 30 0.67 0.73 0.70 0.51 0.52 0.52
31 – 40 0.81 0.84 0.83 0.60 0.61 0.61
41 – 50 0.83 0.87 0.85 0.65 0.66 0.66
51 – 60 0.96 0.93 0.95 0.76 0.77 0.77
61 – 70 0.98 0.92 0.95 0.82 0.83 0.83
P =0.000
45
Figure 5: Graph showing relationship between age and CIMT in
hypertensives and normotensives.
0.520.61
0.66
0.770.83
0.7
0.83 0.85
0.95 0.95
0
0.1
0.2
0.3
0.4
0.5
0.6
0.7
0.8
0.9
1
21-30 Years 31-40 Years 41-50 Years 51-60 Years 61-70 Years
Me
an C
IMT
(mm
)
Age group
NORMOTENSIVES HYPERTENSIVES
46
The mean BMI for the hypertensive group was 29.09±5.68 and 26.58± 6.17 for the
normotensive group. The difference in BMI of subjects in both groups was statistically
significant (p=0.001). The CIMT values in hypertensive subjects were significantly
higher than in normotensive subject in each BMI grouping (p=0.000), (Table 4 and fig
6). However, BMI has a negative correlation with CIMT in hypertensives (Pearson
correlation = -0.23) and positive correlation in normotensives (Pearson correlation=
0.22). These correlations were however not statistically significant (p=0.020) in
hypertensive and (p=0.024) normotensives.
47
Table 4: BMI with mean CIMT in both hypertensives and
normotensives
BMI Hypertensives Normotensives
Freq RCIMT LCIMT Mean Freq RCIMT LCIMT Mean
(mm) (mm) CIMT(mm) (mm) (mm) CIMT(mm)
< 18.5 1 0.87 0.90 0.89 2 0.50 0.53 0.52
18.5 – 24.9 52 0.92 0.91 0.92 35 0.58 0.61 0.60
25.0 – 29.9 69 0.91 0.91 0.91 43 0.61 0.61 0.61
≥ 30 78 0.82 0.85 0.84 20 0.68 0.66 0.67
200 100
P=0.000
48
Figure 6: Graph showing relationship between BMI and CIMT in
hypertensives and normotensives.
0.520.6 0.61
0.67
0.89 0.92 0.910.84
0
0.1
0.2
0.3
0.4
0.5
0.6
0.7
0.8
0.9
1
<18.5 18.5-24.9 25.0 -29.0 ≥30
Me
an C
IMT
(mm
)
BMI
NORMOTENSIVE HYPERTENSIVE
49
The mean systolic and diastolic blood pressure was 157.0mmHg±15.5 and
97.6mmHg±11.2 respectively for hypertensive subjects. There is a difference in the
mean CIMT value for each systolic and diastolic blood pressure groupings. The CIMT
values for hypertensives with SBP of 140- 159, 160-179 and > 180mmHg were 0.87,
0.91 and 0.99mm respectively while CIMT values for DBP 90-99, 100-109 and
>110mmHg was 0.88, 0.90 and 0.97mm respectively. The mean CIMT increased
progressively with increasing systolic and diastolic blood pressures. However this
findings was not statistically significant (p=0.07 for SBP and p=0.17 for DBP) (Table 5
and fig 7; Table 6 and fig 8). Both systolic and diastolic blood pressure had a strong
positive correlation with CIMT (Pearson correlation for SBP is 0.22 and DBP is 0.21). In
hypertensives, age and systolic blood pressure are the most important determinants of
CIMT.
50
Table 5: Systolic blood pressure (SBP) with mean CIMT value in
Hypertensives.
SBP Frequency RCIMT LCMIT Mean CIMT
(mmHg) (mm) (mm) (mm)
140 – 159 136 0.86 0.88 0.87
160 – 179 56 0.93 0.89 0.91
≥180 8 1.00 0.99 0.99
200
P=0.07
51
Fiqure 7: Graph showing relationship between Systolic blood pressure
and CIMT in hypertensives.
0.87
0.91
0.99
0.8
0.82
0.84
0.86
0.88
0.9
0.92
0.94
0.96
0.98
1
140-159 160-179 ≥180
Me
an C
IMT
(mm
)
Systolic blood pressure(mmHg)
52
Table 6: Diastolic blood pressure (DBP) with mean CIMT value in
Hypertensives.
DBP Frequency RCIMT LCIMT Mean CIMT
(mmHg) (mm) (mm) (mm)
90 - 99 145 0.88 0.88 0.88
100 – 109 41 0.90 0.90 0.90
≥110 14 0.97 0.97 0.97
200
P =0.17
53
Fiqure 8: A graph showing relationship between diastolic blood
pressure and CIMT in hypertensives.
0.88
0.9
0.97
0.82
0.84
0.86
0.88
0.9
0.92
0.94
0.96
0.98
90-99 100-109 ≥110
Me
an C
IMT
(mm
)
Diastolic blood pressure(mmHg)
54
Carotid Plaques were seen in the CCA wall of six hypertensive patients (3%) in this
study, while none was seen in the CCA of normotensive subjects. These plaques were
more evident in the right CCA (Figures 9). These patients are scheduled to have
ultrasound monitoring to assess future progression of the plaques.
55
Figure 9: B-mode sonogram showing a calcific focus (black arrow) in the wall of the
right common carotid artery.
56
DISCUSSION
Hypertension, a non communicable disease is a common illness or disease in Sub-
Saharan Africa as it is in most parts of the world. Therefore, adequate monitoring of
cardiovascular risks cannot be overemphasized. This study has revealed the importance
of noninvasive sonographic investigation in the monitoring of hypertensive patients.
Other studies had investigated CIMT in normal subject documenting baseline values of
normal CIMT in their environment/geographic location. However, this study compared
the IMT in hypertensive and normal cohort group and also correlated CIMT with age,
sex, BMI and blood pressure levels.
The mean ages of subjects were 50.62 + 10.46 years and 47.04 + 11.39 years for
hypertensives and normotensives respectively. The difference in age was statistically
significant (p=0.000). The mean age in hypertensives was higher than in normotensives
and this may be due to the fact that advanced age is a risk factor for developing
hypertension. Hypertension in the young is commonly due to a specific disease like
renal and endocrine disease, known as secondary hypertension. In this study patients
with secondary hypertension were excluded. There was also a female preponderance
amongst hypertensive and normotensive subjects in this study.
The overall CIMT value was higher in hypertensive subjects than normotensives
subjects (0.89mm Vs 0.61mm) and this difference was statistically significant. This is
consistent with previous studies done.53,56,60 None of the reviewed previous studies
researched had a contrary finding. These differences in the overall CIMT in the two
cohort groups is presumably due to higher blood pressure levels in the hypertensive
57
group. In hypertensive elevated blood pressure level can cause injury/damage to the
endothelium of blood vessels with subsequent thickening of intima media complex via
medial hypertrophy,55,61 a process specifically related to the disease. This thickening of
the arterial wall is probably an adaptative mechanism to compensate for the persistent
increase in blood pressure levels.56 and the thickening of the vessel wall have been
demonstrated in vivo and vitro.48 This effect is not seen in normotensive subjects whose
blood pressure levels are essentially normal, and thus normal CIMT is present in this
group.52,53,55 Therefore increase in blood pressure has a significant effect on the intima
media thickness.
In this study the overall mean CIMT of 0.89mm±0.13 in hypertensive subjects were
higher compared to values from previous studies, Honzikova53 and Plavnik56 recorded
0.60 mm and 0.67mm respectively and Lemne60 in Sweden had an overall value of
0.73mm. On the contrary, the overall mean CIMT in normotensive subjects in this study
was lower than 0.69mm obtained in study by Lemne et al 60 but higher than 0.51mm
and 0.54mm recorded by Honzikova53 and Plavnik56 respectively. The differences in
CIMT observed in various studies in both hypertensives and normotensives could be
due to sampling methods, sampling size, and racial differences. The sample size in this
study was comparably larger than in other studies.53,56,60 Differences in life styles, diet
and social habits, for instance high alcohol intake as well as chronic intake of potato
chips in the study environment (Jos) is known to induce a proinflammatory state which
is a risk factor for atherosclerosis55 and may be responsible for the differences in the
CIMT observed in this study and other studies.
58
In this study, the method used at arriving at CIMT value involved taking three
measurements 1cm proximal to right and left carotid bulb and the mean value of the
three measurements were recorded for each side; this was different from the method
employed in some other studies.56,60 This method is simple, reliable, and reproducible.
There is minimal inter and intra observer error.62 Using this method allows rapid
identification of the target area and ensures that an identical area is assessed on follow-
up.62 Certain infections such has viral hepatitis and human immunodeficiency virus
infection have been shown to be associated with increased CIMT probably due to
presence of proinflammatory cells which are risk factor in artherogenesis.55.61
Bilaterally, there was a noticeably higher right and left CIMT value in hypertensives
compared to normotensives (0.89mm±0.13 and 0.89mm±0.18 Vs 0.61±0.10mm and
0.62mm±10) in this study. Many other studies shows similar trend, Sharma51 recorded
0.968mm and 0.969mm vs 0.551 and 0.555mm; Adaikkappan52 recorded 1.01mm and
1.09mm vs 0.74mm and 072mm; Umeh54 recorded 0.751mm±0.129 and
0.756mm±0.130 vs 0.670mm± 0.107 and 0.638mm±0.088; Okehialam55 recorded
93mm±0.21 and 0.93mm±0.15 vs 0.91mm±0.17 and 0.91mm±0.13; Planvnik56
recorded 0.67mm±0.13 and 0.62±0.09 vs 0.54mm±0.09 and 0.52mm±0.11 for
hypertensives and normotensives respectively.
The mean CIMT value in the left CCA was higher than the right CCA (0.62mm±10 Vs
0.61mm±10) in normotensive group of patients studied. Although, this findings was not
statistically significant (P=0.18). This result was consistent with the study by Sharma51
but contrary to findings in other studies.52,54 There was no difference in the measured
59
CIMT value between the left and right CCA in hypertensive group (0.89±0.13 Vs
0.89±0.13) and this finding is similar to those in a study in Jos by Okeahialam.55
However some other studies showed a difference in values between the measured left
and right CIMT with the left CIMT value higher than right.51,52,54 while another study60
showed right CIMT value to be higher than the left. In this study, equal value of CIMT
observed on both CCA for hypertensive and the higher value of CIMT recorded in the
left CCA in normotensive, are contrary to the findings of Lemme60 who recorded higher
CIMT value in the right CCA for both hypertensive and normotensive subjects. The
reason for such differences between IMT of right and left common carotid artery sides
are unknown. However, the left common carotid is a direct branch of the aorta while
right common carotid results from division of brachiocephalic trunk. Therefore it is
possible that dissimilarities have existed in the arterial growth between both arteries
and/or that flow mediated mechanical forces applied to carotid wall differ between the
two sides.67
The mean CIMT value of male and female hypertensives were higher than the mean
CIMT value of male and female normotensive (male and female hypertensives CIMT
values were 0.92mm vs 0.87mm, while in normotensive males and females CIMT value
were 0.62mm vs 0.61mm. In both groups males have a higher CIMT value than
females. This relationship was not statistically significant (Hypertensive P=0.11 and
Normotensive P=0.70). This finding was consistent with other studies38,54,61 and may
be explained by the sex variation in the development of artherosclerosis. Males have a
higher chance of developing artherosclerosis more often than women37,38, although the
60
reasons are not known but may be due to the fact that males are more prone to
psychological and environmental stress than females.38,55
There was progressive increase in CIMT from age 18 years to 70 years in hypertensive
and normotensive groups of patients. The CIMT values in hypertensive subjects were
higher than CIMT value of normotensive subjects in each age group. Most of the
studies reviewed also consistently showed with increased CIMT with age.51,53,54,56,61
This study also showed that age has a strong correlation with CIMT values recorded in
both hypertensive and normotensive subjects investigated (Pearson correlation 0.35
and 0.88 in hypertensives and normotensives respectively). The increase in mean CIMT
with age in normotensive subjects could probably be due to specific effect of aging on
the arterial wall or probably be due to exposure to risk factor not measured or captured
in this study. In hypertensives, higher CIMT value with age could probably be due to
the combined effect of increase blood pressure levels and aging process on the intima
media. Also the impact of blood pressure levels on the intima media has been
considered as an accelerated form of aging and hypertensive patients develop aging
process in their arterial walls earlier in life than normotensives.
There was also progressive increase in mean CIMT with BMI in normotensive subjects.
This was statistically significant. Mean CIMT correlated positively with BMI in
normotensive but negatively in hypertensive subjects. Similar finding was
demonstrated in the studies by Honzikova and Planvik.53,56 BMI has been shown to
influence the CIMT but the role of BMI in arterial wall thickening is poorly understood
and its influence is probably independent of age.49
61
Most studies have suggested that age is the strongest determinant of carotid wall
thickness and systolic blood pressure has been considered as a secondary determinant
in hypertensive subject.9,48,57
In this study, CIMT correlated positively with systolic and diastolic blood pressure of
hypertensive patient. (Pearson correlation for SBP is 0.22 and DBP 0.21). This was
consistent with several other studies52,53,56 despite differences in the methodology
employed in measurement of blood pressure. While blood pressure was taken at
presentation in this study; other studies used 24hrs systolic and diastolic blood pressure
measurement method.53,56 Also, CIMT was noticed to increase with increasing blood
pressure levels.
A plaque is defined as a focal structure arising from the intima media layer of the
arterial wall and encroaching into the arterial lumen.29 Plaques are sometimes found in
the wall of the vessel of hypertensive patients. Carotid Plaques were seen in the
vascular wall of six hypertensive patients (3%) in this study, while none was noted in
the CCA of normotensive subjects. These plaques were more evident in right CCA. This
finding is similar to what was recorded by Lemne60 et al study where they also recorded
higher number of plaques in hypertensives which were also evident in the right carotid
arteries. Umeh54 et al in Ibadan also recorded a higher number of plaques among
hypertensive subjects.
62
CONCLUSION
This study has shown that there is a significant difference in the CIMT of hypertensive
compared to normotensive subject. Higher values of CIMT were seen in hypertensive
subject compared to normotensive from age groups 18-70 years. Age, sex, BMI and
blood pressure levels have significant effect on CIMT of hypertensive patient. CIMT
increases with increasing blood pressure levels and advancing age in hypertensive
subjects. It also revealed that CIMT increases with age and with increasing BMI in
normotensives. Male hypertensives had higher CIMT than the female counterpart. B-
mode ultrasound is a reliable, readily available, cheap and noninvasive imaging modality
that is useful in the management of hypertension.
Limitations
The limitations encountered during this study included that some sizes and contours of
the neck posed difficulty in examination, presence of calcium deposits in the wall of the
carotid artery made it difficult to evaluate the thickness of the intima media and the end
segment of the carotid artery in some patients was not clearly depicted by ultrasound.
However these subjects were excluded from the study.
Recommendation
It is recommended that all hypertensive patients should have routine carotid USS for
CIMT measurement. Noninvasive B-mode ultrasound should be used as basic predictive
63
investigation for CIMT and government health promotional activities should include
routine check of CIMT in hypertensive patients.
64
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APPENDIX I
RESEARCH QUESTIONAIRES
1. Serial No.: ________________________________________
2. Age: ____________________________________________
Address: _______________________________________
3. SEX a) MALE b) FEMALE
4. HEIGHT (m) 5. WEIGHT (kg) 6. BMI
7. BLOOD PRESSURE a) SYSTOLIC b) DIASTOLIC
CAROTID INTIMA THICKNESS MEASUREMENT
8. RIGHT COMMON CAROTID ARTERY a) mm b)
9. LEFT COMMON CAROTID ARTERY a) mm b)
PRESENCE OF PLAQUES
10. RIGHT COMMON CAROTID ARTERY a) YES b) NO
11. LEFT COMMON CAROTID ARTERY a) YES b) NO
12. BOTH a) YES b) NO
75
APPENDIX II
CONSENT FORM
My name is Dr Kolade-Yunusa H.O, a senior resident doctor in the department of
Radiology, Jos University Teaching Hospital, I am undertaking a study on the “B – Mode
sonographic measurement of carotid artery intima media thickness in hypertensive and
normotensive patients in Jos University Teaching Hospital, North-Central Nigeria” and
would like you to participate in the programme.
This study will help in the management of hypertenension in Jos and the environs.
The study will involve asking you to wear comfortable loose fitting clothing and to
remove all jewelleries around the area to be examined. You will also be asked few
questions before doing ultrasound on you. Your blood pressure, height and weight will
also be taken and recorded. Please be informed that all answers you provided and the
ultrasound findings will be treated with utmost confidentiality. You will be assigned a
number so that your name will not be used for any information.
During the examination, you will be asked to lie down on the examination couch in
supine position with the shoulder placed on a pillow and the neck extended and head
turned slightly 450 away from the side being scanned. Ultrasound gel will be applied on
the skin of your neck and a transducer move to and fro on it.
Your participation in the study is voluntary and as such you are free to decline consent
or willingness to participate in the study.The examination will be performed free of
charge . You will not suffer any consequences if you decide not to participate in the
study or decide to opt out.
Kindly sign this form below
I _______________ have understood the study as directly explained to me and I am
willing to participate.
Interviewers’ ______________________ Sign & Date ______________
Participant’s sign/thumbprint _______________ Sign & Date_______________
Witness __________________________ Sign & Date _______________
76
APPENDIX III