Dissertation on
RED CELL DISTRIBUTION WIDTH AS A PREDICTOR OF SYSTEMIC HYPERTENSION
Submitted in partial fulfillment for the Degree of
M.D GENERAL MEDICINE BRANCH – I
THE TAMIL NADU DR.M.G.R MEDICAL UNIVERSITY CHENNAI
THE TAMIL NADU DR.M.G.R MEDICAL UNIVERSITY INSTITUTE OF INTERNAL MEDICINE
MADRAS MEDICAL COLLEGE CHENNAI – 600003
MAY 2018
CERTIFICATE
This is to certify that the dissertation titled “RED CELL DISTRIBUTION WIDTH AS A PREDICTOR OF SYSTEMIC HYPERTENSION” is the bonafide original work done by Dr SINJU SANKAR.P, post graduate student, Institute of Internal medicine, Madras medical college, Chennai-3, in partial fulfillment of the University Rules and Regulations for the award of MD Branch -1 General Medicine, under our guidance and supervision, during the academic year 2015-2018.
Prof. S.MAYILVAHANAN M.D., Director & Professor,
Institute of Internal Medicine, Madras Medical College &
RGGGH, Chennai – 600003.
Prof.S.USHALAKSHMI M.D., FMMC Professor of Medicine,
Institute of Internal Medicine, Madras Medical College &
RGGGH, Chennai – 600003
Prof.R.NARYANABABU. M.D., DCH.
DEAN,
Madras Medical College &
Rajiv Gandhi
Government General Hospital, Chennai 600003
DECLARATION
I, Dr. SINJU SANKAR.P, solemnly declare that dissertation titled
“RDW AS A PREDICTOR OF SYSTEMIC HYPERTENSION” is a bonafide work done by me at Madras Medical College and Rajiv Gandhi Government General Hospital, Chennai-3 during March 2017 to August
2017 under the guidance and supervision of my unit chief Prof. S.USHALAKSHMI.M.D.FMMC., Professor of Medicine, Madras
Medical College and Rajiv Gandhi Government General Hospital, Chennai.
This dissertation is submitted to Tamilnadu Dr. M.G.R Medical University, towards partial fulfillment of requirement for the award of M.D. DEGREE IN GENERAL MEDICINE BRANCH-I.
Place: Chennai -03
Date: Dr.SINJU SANKAR P
MD General Medicine,
INSTITUTE OF INTERNAL MEDICINE MADRAS MEDICAL COLLEGE
CHENNAI 600003
ACKNOWLEDGEMENT
I owe my thanks to Dean Prof.R.NARYANABABU.M.D.,DCH, Madras Medical College and Rajiv Gandhi Government General
Hospital, Chennai-3. for allowing me to avail thefacilities needed for my dissertation work.
I am grateful to beloved mentor Prof. S.MAYILVAHANAN M.D., Director and Professor, Institute of Internal Medicine, Madras Medical College and Rajiv Gandhi Government General Hospital, Chennai-03 for permitting me to do the study and for his encouragement.
With extreme gratitude, I express my indebtedness to my beloved Chief and teacher Prof. S.USHALAKSHMI.M.D.,FMMC., for his motivation, advice and valuable criticism, which enabled me to complete this work.
I am extremely thankful to my Assistant Professor Dr.APARNA SURESH, M.D., and Dr.M.SHARMILA M.D., for their guidance and encouragement.
I am also thankful to all my unit colleagues and other post graduates in our institute for helping me in this study and my sincere thanks to all the patients and their families who were co-operative during the course of this study.
CONTENTS
S NO TITLE PAGE NO
1 INTRODUCTION 1
2 AIMS AND OBJECTIVES 3
3 REVIEW OF LITERATURE 4
4 MATERIALS AND METHODS 42
5 OBSERVATION AND RESULTS 46
6 DISCUSSION 73
7 CONCLUSION 75
8 LIMITATIONS 76
9 BIBLIOGRAPHY 77
10 ANNEXURES
PROFORMA 88
ETHICAL COMMITTEE 91
PLAGIARISM REPORT 92
PLAGIARISM CERTIFICATE 94
INFORMATION SHEET 95
CONSENT FORM 96
MASTER CHART
ABBREVIATION CBC - Complete Blood Count MCV - Mean Corpuscular Volume RDW - Red Cell Distribution width
MCHC - Mean Corpuscular Hemoglobin Concentration
TC - Total Count
Hb - Hemoglobin
BP - Blood Pressure
HTN - Hypertension DM - Diabetes Mellitus
CHD - Coronary Heart Disease Pre-HTN - Prehypertension
CHF - Congestive heart failure ANS - Autonomic nervous system ARB - Angiotensin receptor blocker
ACEI - Angiotensin converting enzyme inhibitor RAAS - Renin angiotensinogen aldosterone system
INTRODUCTION
1
INTRODUCTION
1Hypertension is the leading cause of global burden of disease.
Hypertension increases the risk of CVD including CHD, CHF, ischemic and hemorrhagic cerebrovascular accident, renal failure and peripheral vascular disease.
2Red cell distribution width (RDW) is a parameter that measures variation in red blood cell size or red blood cell volume. RDW is increased according to the variation in red cell size (anisocytosis), i.e., when elevated RDW is reported on CBC, increased anisocytosis (increased variation in red cell size) is expected on peripheral blood smear review.
36Red cell distribution width (RDW), a red blood cell index, is used to evaluate different types of anaemia and also is an important predictor of morbidity and mortality in a variety of settings, especially in many cardiovascular diseases. Several studies have suggested increased RDW can be used as a marker of adverse clinical outcomes such as heart failure, hypertension and coronary artery disease
3Several lines of evidences found that inflammatory status is significantly related to ineffective erythropoiesis, and it has been suggested that inflammatory cytokines, such as interleukin (IL)-1 β, IL- 6, tumour necrosis factor (TNF)-α, 39desensitize bone marrow erythroid
2
progenitors to erythropoiesis, and inhibit red blood cell maturation and inturn promote anisocytosis. Increased RDW may be due to an underlying inflammatory state.
38Considering the above situation, we hypothesis that high blood pressure does damage to endothelia cells promoting the secretion of inflammatory cytokines which supresses the erythropoiesis and inhibit red cell maturation and anisocytosis. Therefore, as a sensitive index of inflammatory status in this process, RDW could be a potential predictor of hypertension in pre-hypertensive and normal individual.
37Based on these factors current study is aimed to use RDW as predictor of hypertension in normal individuals and pre-hypertensive individuals.
AIMS AND OBJECTIVES
3
AIMS AND OBJECTIVES
To study the red cell distribution as a predictor of systemic hypertension in medicine department in Rajiv Gandhi Government hospital, Chennai
40To study the importance of determining red cell distribution width in predicting the onset of hypertension in pre-hypertensive individuals
REVIEW OF LITERATURE
4
REVIEW OF LITERATURE RED CELL DISTRIBUTION WIDTH
3Red cell distribution width is a parameter of red blood cell which measures the variation in red cell size or volume.
35If RDW is elevated in complete blood count, it means that there is increased variation in size of red blood cell in peripheral blood smear.RDW can be reported either as coefficient of variation (CV) that is RDW CV or it can be expressed as standard deviation (SD) that is RDW- SD.
RDW-CV(%)
It is calculated from standard deviation and MCV The formula is :
RDW-CV (%) =1 SD of RBC volume /MCV * 100
Since RDW -CV is derived from MCV it is affected by the average RBC size
RDW-SD(fl)
34This is the measurement of width of RBC in distribution histogram.
It is measured by calculating the width in femtolitre, at 20% height of RCC size in distribution histogram.
5
Elevated RDW gives clue about the presence of two different red cell populations.
REFERENCE RANGE
32RDW-CV 11.6-14.6%1 RDW -SD 39-46F1
6
7
Increased RDW provide a clue for the diagnosis of nutritional deficiency anaemia such as iron, folate, or vitamin B12 deficiency anaemia
RDW becomes elevated before other red blood cell parameters.
RDW IN ANAEMIAS
30Normal RDW and low MCV is present in the following conditions:
Heterozygous thalassemia
Haemoglobin E trait
Anaemia of chronic disease
Increased RDW and low MCV is present in the following conditions
Sickle cell-βthalassemia
Iron deficiency
29Normal RDW and increased MCV is present in the following conditions:
Chronic liver disease
Aplastic anaemia
Antivirals, alcohol , chemotherapy
Increased RDW and normal MCV is associated with the following conditions:
Early iron, vitamin B12, or folate deficiency
Dimorphic anaemia (for example, iron and folate deficiency)
8
Sickle cell disease
Chronic liver disease
31Elevated RDW and increased MCV is present in the following conditions:
Immune haemolyticanaemia
Cytotoxic chemotherapy
Folate or vitamin B12 deficiency
Chronic liver disease
Normal RDW and normal MCV is present in the following conditions:
Anaemia of chronic disease
Acute blood loss or hemolysis
Anaemia of renal disease
9
10
5COLLECTION OF SAMPLES
Sample : venous blood, collected by venipuncture
Tube : purple EDTA tube which contains EDTA potassium salt which serves as anticoagulant
11
HYPERTENSION
6Hypertension is among the most leading causes of global burden of disease. Approximately 7.6 million deaths (13–15% of the total) and 92 million disability-adjusted life years worldwide were attributable to high blood pressure in 20012. Hypertension increases by two times the risk of cardiovascular diseases, including coronary heart disease (CHD), congestive heart failure (CHF), ischemic and hemorrhagic stroke, renal failure, and peripheral arterial disease2.
27Although antihypertensive therapy reduces the risks of cardiovascular and renal disease, large segments of the hypertensive population are either untreated or inadequately treated2.
12
EPIDEMIOLOGY
29Blood pressure is prevalent in both developing and industrialised country.Tracking of blood pressure is very important to know the prevalence of hypertension even from young age. Hypertension is more common in men in early adulthood whereas the incidence is more in women in age more than 60 years.
28Family history, dietary intake and lifestyle influence the onset of hypertension. Hypertension is more common in obese individuals and is also associated with high sodium intake. Urine sodium to potassium ratio is more determinant of hypertension than potassium alone.
7Alcohol consumption, psychological stress, sedentary lifestyle contributes to hypertension. The degree of acculturation is influencing hypertension prevalence. High blood pressure in age less than 55yrs
13
occur in patients with a positive family history.
GENETIC CONSIDERATION
8Recent studies consider that genes coding for renin angiotensin aldosterone system contributes for hypertension. Genetic associations of diabetes, obesity and insulin resistance also contributes for hypertension.
Other genes include ANP( atrial natriuretic peptide) gene, AT1 receptor gene also contributes to hypertension.
PATHOGENESIS
26Hypertension is mainly determined by cardiac output and peripheral resistance. Cardiac output is determined by stroke volume and heart rate. So factors influencing these factors contribute to the pathogenesis of hypertension.
14
27 Stroke volume is determined by contractility of myocardium and this is dependent on ventricular mass. Peripheral resistance is dependent on the vascular diameter and it is also affected by autonomic nervous system.
INTRAVASCULAR VOLUME
8Sodium being a predominant extracellular action ,is the primary determinant of the extracellular fluid volume. When intake of NaCl increases the capacity of the kidney to excrete the same, vascular volume expands initially and cardiac output also increases. 27But since certain vascular beds retain the capacity to auto-regulate the blood flow they help in maintaining the blood flow by increasing the peripheral resistance and blood pressure is raised.
15
AUTONOMIC NERVOUS SYSTEM
The autonomic nervous system plays an important role in maintaining hypertension. The main mediators are adrenaline, noradrenaline and dopamine.
9The receptors are alpha1, alpha 2 , beta 1 and beta 2 receptors. The mediators act on different receptors and act via positive and negative feed back mechanisms to regulate blood pressure.
24Many reflexes alter blood pressure on minute basis.Arterial baroreflex is mediated stretch receptors in the carotid sinuses and the aortic arch. The blood pressure increases as rate of firing of these baroreceptors increases and as a result, sympathetic outflow decreases and results in reduced arterial blood pressure and heart rate. This is the major mechanism which results in rapid buffering of sudden fluctuations of arterial blood pressure that may occur during change of posture and change in behaviour or physiologic stress, and also changes in volume of blood.
23As the activity ofbaroreceptors is continued its threshold is set at higher pressures. Patients with abnormal autonomic nervous function and defective baroreflex function have labile arterial blood pressures with difficult-to-control episodic spikes of blood pressure associated with tachycardia.
16
RENIN ANGIOTENSIN ALDOSTERONE
10The renin-angiotensin-aldosterone system helps in regulating blood pressure mainly via the angiotensin II which is a vasoconstrictor and aldosterone which retains sodium. Renin is synthesized from its precursor which is inactive precursor prorenin. Renin is synthesized in the circulation from renal afferent renal arteriole.
25The three primary stimuli for renin secretion:
Reduced NaCl transport in the thick ascending limb of the loop (distal )that is present near the afferent arteriole (macula densa).
Reduced pressure or stretch in the renal afferent arteriole (baroreceptor mechanism)
Autonomic nervous system stimulation of renin-secreting cells via β1 adrenoreceptors.
17
18
PATHOLOGICAL CONSEQUENCES OF HYPERTENSION
19
20
BRAIN
22Hypertension is the leading cause of stroke in the world.
Hypertension increases the risk of stroke. Hypertension also increases the risk of dementia and cognitive impairment . Blood flow to brain is auto regulated between mean arterial pressure between 50-150mm hg. Patient with malignant hypertension is due to failure of these auto regulatory mechanisms . 11This results in vasodilatation and hyper perfusion leading to hypertensive encephalopathy . The symptoms are headache, altered sensorium, projectile vomiting. If hypertensive encephalopathy is not treated patient may go for seizures, coma and death within hours. So patient must be treated efficiently.
Treatment of hypertension decreases the risk of both ischemic and hemorrhagic stroke.
21
22
KIDNEY
12Kidney is the organ which can be both a target organ for end organ damage due to hypertension and also a cause for hypertension.
Mechanisms of kidney failure induced hypertension are decreased excretion of sodium chloride , and increased secretion of RAAS and increased sympathetic activity leading to secondary hypertension . Hypertension can cause ESRD. 21Atherosclerotic leisions affect afferent arterioles and lead to glomerular damage and ensues in kidney failure.
23
24
HEART
20Hypertension is the most important risk factor for developing cardiac problems. Hypertension leads to structural and functional problems and changes of cardiac tissue. This can be in the form of left ventricular hypertrophy, arrhythmias, coronary vascular atherosclerosis.
13Left ventricular hypertrophy can in-turn lead to other complications like stroke, congestive heart failure and sudden cardiac arrest so preventing and controlling hypertension can lead to prevention of complications associated with hypertension. Hypertension should be therefore diagnosed at an early stage and properly treated so that all these complications can be prevented.
19Hypertension can be in the form of systolic or diastolic dysfunction. Diastolic dysfunction is the earliest consequence of hypertensive heart disease. If the patient is having elevated diastolic blood pressure they are more prone for developing hypertensive cardiac disease. The diastolic dysfunction can be accurately assessed by cardiac catheterisation.
25
Cardiac disease can be in the form of hypertrophy and dilatation
26
Hypertrophy of ventricular musculature
27
PERIPHERAL ARTERIES
14Peripheral arteries are one of the major site of developing atherosclerosis and hypertension.
Patient with peripheral arterial disease is at increased risk for developing cardiac disease in future.
28
JNC8 GUIDELINES
29
Comparison of Current Recommendations with JNC7 Guidelines
30
BLOOD PRESSURE CLASSIFICATION
SECONDARY CAUSES OF SYSTOLIC AND DIASTOLIC HYPERTENSION
31
RARE MENDELIAN FORMS OF HYPERTENSIO
32
MANAGEMENT OF HYPERTENSION
15Hypertension can be managed either pharmacologically or along with exercise and diet. If individuals prone for hypertension are closely monitored they can be given life style modifications and the onset of hypertension can be delayed to a certain extent. So screening the general population for the onset of hypertension is very important. So the preventive measures of hypertension should begin with simple measurement of hypertension.
1) LIFESTYLE MODIFICATIONS 2) PHARMACOLOGICAL THERAPY
Beta blockers
Aldosterone antagonist
ACE inhibitors
Calcium channel blockers
Diuretics
Direct vasodilators
Alpha antagonist LIFESTYLE MODIFICATIONS
16Lifestyle modifications can effectively prevent hypertension. This includes weight reduction, salt restricted diet, DASH type diet plan,The above table shows the various life style modifications. DASH diet is the diet aimed to improve or prevent hypertension.
33
This includes incorporating fresh fruits and vegetables in the diet and reduction of saturated fatty acid content in food.
Physical activity plays an important role in controlling hypertension.Patient should be advised to engage in healthy lifestyle by promoting walking, jogging, and other cardio exercises.
Alcohol consumption should be reduced as it is a very important risk factor for hypertension. Alcohol along with smoking increases the risk of hypertension and other cardiovascular diseases.
LIFESTYLE MODIFICATIONS TO MANAGE HYPERTENSION
34
PHARMACOLOGICAL THERAPY
17Once hypertension is diagnosed it should be adequately controlled using various drugs specifically to control hypertension. Drugs helps not only in controlling hypertension but also in preventing the cardiovascular and other complications of hypertension.
The various drugs mentioned above known as antihypertensive medicines are the ones with different mechanism of action which act at different levels to control hypertension.
These can be action at the level of blood vessel, kidney, and cardiovascular system or specific ion channel blocker.
35
36
37
38
39
40
EXAMPLES OF ORAL DRUGS USED IN TREATMENT OF HYPERTENSION
41
MATERIALS AND METHODS
42
MATERIALS AND METHODS
This study was conducted at the Institute of Internal Medicine, Rajiv Gandhi Government General Hospital (RGGGH), Madras Medical College, Chennai 600003.
ETHICAL COMMITTEE APPROVAL Obtained
STUDY DURATION
This study was conducted over a period of six months.
STUDY POPULATION
Patients having hypertension and undergoing treatment in medical ward and hypertensive op
SAMPLE SIZE 100
TYPE OF STUDY
Observational study INCLUSION CRITERIA
1) Age > 25 and <60 years
2) Pre-hypertensive and hypertensive patients
43
EXCLUSION CRITERIA 1) Patients with anaemia 2) Patients with dyslipidemia 3) Patients with CKD, CAD, CVA 4) Patients with diabetes mellitus 5) Sepsis
6) Terminally ill patients
44
DATA COLLECTION AND METHODS
Patients selected for observational study as per inclusion / exclusion criteria are subjected to detailed history taking, clinical examination and relevant investigations.
Routine blood investigations- complete blood count [TC/RBS /Hb/RDW /platelet]
Patients aged between 25 and 60 years, diagnosed with essential hypertension of one year or more were enrolled in the study. Patients with haematological disorder, chronic liver disease, chronic kidney disease, any systemic disease including rheumatologic disorders that could affect blood count, chronic hepatobiliary disease, peripheral artery disease, stroke, inflammatory bowel disease or diseases of terminal ileum malignant disorder and diabetes mellitus type 2 were excluded from the study.
The characteristics of the patients including age, gender, duration of hypertension and other medical conditions were recorded on a standardized data collection form. Blood samples were drawn and the complete blood count was determined by Beckman Coulter’s AutomatedHaematology Analyzer .
RDW was recorded and compared in cases (hypertensives), pre- hypertensives, and normotensives. The normal RDW range was taken between Standard Deviation (SD) - 36-46 fl (femtolitre)
45
Pre-hypertensives were selected based on systolic blood pressure between 120-139 mm Hg and diastolic blood pressure between 80-89 mm Hg.
Normotensives are those with blood pressure less than 120/80 mm Hg.
All the data obtained were entered in the proforma (enclosed).
Data were analyzed using SPSS package and by chi-square tests,
OBSERVATION AND RESULTS
46
. OBSERVATIONS AND RESULTS
0%
10%
20%
30%
40%
50%
60%
70%
80%
90%
100%
20-30 YEARS
31-40YEARS 41-50 YEARS
ABOVE 50 YEARS 0%
19%
38%
78%
0%
56%
41%
10%
100%
25% 21% 13%
Percentage
Comparison of age group
NORMAL
PREHYPERTENSIVE HYPERTENSIVE
AGE_GROUP
Total 20-30
YEARS
31- 40YEARS
41-50 YEARS
ABOVE 50 YEARS
GROUP
HYPERTENSIVE
Count 0 3 16 31 50
% within
AGE_GROUP 0.0% 18.8% 38.1% 77.5% 50.0%
PREHYPERTENSIVE
Count 0 9 17 4 30
% within
AGE_GROUP 0.0% 56.2% 40.5% 10.0% 30.0%
NORMAL
Count 2 4 9 5 20
% within
AGE_GROUP 100.0% 25.0% 21.4% 12.5% 20.0%
Total
Count 2 16 42 40 100
% within
AGE_GROUP 100.0% 100.0% 100.0% 100.0% 100.0%
47
CROSS TAB
SEX Total
FEMALE MALE
GROUP
HYPERTENSIVE
Count 22 28 50
% within
SEX 50.0% 50.0% 50.0%
PREHYPERTENSIVE
Count 14 16 30
% within
SEX 31.8% 28.6% 30.0%
NORMAL
Count 8 12 20
% within
SEX 18.2% 21.4% 20.0%
Total
Count 44 56 100
% within
SEX 100.0% 100.0% 100.0%
0%
20%
40%
60%
80%
100%
FEMALE MALE
50% 50%
32% 29%
18% 21%
Percentage
Comparison of age group
NORMAL
PREHYPERTENSIVE HYPERTENSIVE
48
GROUP
50%
30%
20%
Group
HYPERTENSIVE PREHYPERTENSIV E
GROUP Frequency Percent
Valid Percent
Cumulative Percent
Valid
HYPERTENSIVE 50 50.0 50.0 50.0
PREHYPERTENSIVE 30 30.0 30.0 80.0
NORMAL 20 20.0 20.0 100.0
Total 100 100.0 100.0
49
Descriptives
N Mean Std.
Deviation
Std. Error 95% Confidence Interval for Mean
Minimum Maximum Lower
Bound
Upper Bound WBC
HYPERTENSIVE 50 6504.0000 1346.94818 190.48724 6121.2016 6886.7984 4400.00 9900.00 PREHYPERTENSIVE 30 6256.6667 1314.03126 239.90819 5765.9993 6747.3340 4400.00 8900.00 NORMAL 20 6215.0000 1353.85415 302.73099 5581.3768 6848.6232 4500.00 8900.00 Total 100 6372.0000 1331.67169 133.16717 6107.7674 6636.2326 4400.00 9900.00 HBgdl
HYPERTENSIVE 50 12.9200 1.12122 .15856 12.6014 13.2386 11.00 15.50 PREHYPERTENSIVE 30 13.1367 1.09654 .20020 12.7272 13.5461 11.50 15.00 NORMAL 20 13.9900 1.35798 .30365 13.3544 14.6256 11.50 15.60 Total 100 13.1990 1.22280 .12228 12.9564 13.4416 11.00 15.60 RDWflSD
HYPERTENSIVE 50 47.9000 3.47293 .49115 46.9130 48.8870 39.20 55.20 PREHYPERTENSIVE 28 45.5464 2.23664 .42269 44.6791 46.4137 40.20 48.80 NORMAL 20 40.0550 1.40018 .31309 39.3997 40.7103 38.50 44.50 Total 98 45.6265 4.11531 .41571 44.8015 46.4516 38.50 55.20 RBSmg
HYPERTENSIVE 50 127.4000 11.22861 1.58796 124.2089 130.5911 110.00 150.00 PREHYPERTENSIVE 30 128.9333 8.84710 1.61525 125.6298 132.2369 120.00 150.00 NORMAL 20 128.0000 9.51453 2.12751 123.5471 132.4529 110.00 150.00 Total 100 127.9800 10.15633 1.01563 125.9648 129.9952 110.00 150.00
50 6050
6100 6150 6200 6250 6300 6350 6400 6450 6500 6550
HYPERTENSIVE PREHYPERTENSIVE NORMAL 6504
6257
6215
Comparison of WBC in groups
12.20 12.40 12.60 12.80 13.00 13.20 13.40 13.60 13.80 14.00
HYPERTENSIVE PREHYPERTENSIVE NORMAL 12.92
13.14
13.99
Comparison of HB in groups
51
Correlations
WBC HBgdl RDWflSD RBSmg GROUP
GROUP
Correlation Coefficient
-.086 .284** 0.676** .078 1.000 Sig. (2-
tailed)
.397 .004 .000 .439 .
N 100 100 100 100 100
**. Correlation is significant at the 0.01 level (2-tailed).
36.00 38.00 40.00 42.00 44.00 46.00 48.00
HYPERTENSIVE PREHYPERTENSIVE NORMAL 47.90
45.55
40.06
Comparison of RDW in groups
52
GROUP * RDW_GROUP Crosstabulation
RDW_GROUP
Total
NORMAL (36-48)
ABNORMAL (>48)
GROUP
HYPERTENSIVE
Count 11 39 50
% within
RDW_GROUP 24.4% 70.9% 50.0%
PRE
HYPERTENSIVE
Count 14 16 30
% within
RDW_GROUP 31.1% 29.1% 30.0%
NORMAL
Count 20 0 20
% within
RDW_GROUP 44.4% 0.0% 20.0%
Total
Count 45 55 87
% within
RDW_GROUP 100.0% 100.0% 100.0
% Pearson Chi-Square=35.165** P<0.001
0%
10%
20%
30%
40%
50%
60%
70%
80%
90%
100%
NORMAL(36-48) ABNORMAL(>48) 24%
31% 71%
29%
44%
0%
NORMAL
PREHYPERTENSIVE HYPERTENSIVE
53
Descriptives
N Mean
Std.
Deviation
Std.
Error
95% Confidence Interval for Mean
Minimum Maximum Lower
Bound
Upper Bound
RDWflSD
HYPERTENSIVE 50 47.9000 3.47293 .49115 46.9130 48.8870 39.20 55.20 PREHYPERTENSIVE 28 45.5464 2.23664 .42269 44.6791 46.4137 40.20 48.80 NORMAL 20 40.0550 1.40018 .31309 39.3997 40.7103 38.50 44.50 Total 98 45.6265 4.11531 .41571 44.8015 46.4516 38.50 55.20
54
GROUP * RDW_GROUP Crosstabulation
RDW_GROUP
Total NORMAL(36-48) ABNORMAL(>48)
GROUP
HYPERTENSIVE Count 11 39 50
% within RDW_GROUP 24.4% 70.9% 50.0%
PREHYPERTENSIVE Count 14 16 30
% within RDW_GROUP 31.1% 29.1% 30.0%
NORMAL Count 20 0 20
% within RDW_GROUP 44.4% 0.0% 20.0%
Total
Count 45 55 87
% within RDW_GROUP 100.0% 100.0% 100.0%
55
MALE - GROUP * RDW_GROUP Crosstabulation
RDW_GROUP Total
NORMAL(36-48) ABNORMAL(>48)
GROUP
HYPERTENSIVE
Count 7 21 28
% within RDW_GROUP 30.4% 63.6% 50.0%
PREHYPERTENSIVE
Count 4 12 16
% within RDW_GROUP 17.4% 36.4% 28.6%
NORMAL
Count 12 0 12
% within RDW_GROUP 52.2% 0.0% 21.4%
Total
Count 23 33 56
% within RDW_GROUP 100.0% 100.0% 100.0%
56
Pearson Chi-Square=21.913** P<0.001
0%
10%
20%
30%
40%
50%
60%
70%
80%
90%
100%
NORMAL(36-48) ABNORMAL(>48) 30%
64%
17%
36%
52%
0%
NORMAL
PREHYPERTENSIVE HYPERTENSIVE
57
FEMALE –GROUP * RDW_GROUP Crosstabulation RDW_GROUP
Total NORMAL
(36-48)
ABNORMA L(>48)
GROUP
Hypertensive
Count 4 18 22
% within
RDW_GROUP 18.2% 81.8% 50.0%
Prehypertensive
Count 10 4 14
% within
RDW_GROUP 45.5% 18.2% 31.8%
Normal
Count 8 0 8
% within
RDW_GROUP 36.4% 0.0% 18.2%
Total
Count 22 22 44
% within
RDW_GROUP 100.0% 100.0% 100.0%
Pearson Chi-Square=19.481** P<0.001
0%
10%
20%
30%
40%
50%
60%
70%
80%
90%
100%
NORMAL(36-48) ABNORMAL(>48) 18%
82%
46%
18%
36%
0%
NORMAL
PREHYPERTENSIVE HYPERTENSIVE
58
smokers GROUP * RDW_GROUP Crosstabulation
RDW_GROUP
Total NORMAL
(36-48)
ABNORMAL (>48)
GROUP
HYPERTENSIVE
Count 5 13 18
% within
RDW_GROUP 38.5% 56.5% 50.0%
PREHYPERTENSIVE
Count 3 10 13
% within
RDW_GROUP 23.1% 43.5% 36.1%
NORMAL
Count 5 0 5
% within
RDW_GROUP 38.5% 0.0% 13.9%
Total
Count 13 23 36
% within
RDW_GROUP 100.0% 100.0% 100.0%
Pearson Chi-Square=10.345** P=0.006
0%
10%
20%
30%
40%
50%
60%
70%
80%
90%
100%
NORMAL(36-48) ABNORMAL(>48) 39%
57%
23%
39% 44%
0%
NORMAL
PREHYPERTENSIVE HYPERTENSIVE
59
Alcoholic GROUP * RDW_GROUP Crosstabulation
RDW_GROUP
Total NORMAL
(36-48)
ABNORMAL (>48)
GROUP
HYPERTENSIVE
Count 5 17 22
% within
RDW_GROUP 33.3% 68.0% 55.0%
PREHYPERTENSIVE
Count 3 8 11
% within
RDW_GROUP 20.0% 32.0% 27.5%
NORMAL
Count 7 0 7
% within
RDW_GROUP 46.7% 0.0% 17.5%
Total
Count 15 25 40
% within
RDW_GROUP 100.0% 100.0% 100.0%
Pearson Chi-Square=14.206** P=0.001
0%
20%
40%
60%
80%
100%
HYPERTENSIVE PREHYPERTENSIVE NORMAL
33% 20%
47%
68% 32%
0%
ABNORMAL(>48) NORMAL(36-48)
60
AGE_GROUP * RDW_GROUP hypertensive Crosstabulation
RDW_GROUP Total
NORMAL(36- 48)
ABNORMAL(>48)
AGE_GR OUP
31- 40YEA
RS
Count 1 2 3
% within
RDW_GROUP 9.1% 5.1% 6.0%
41-50 YEARS
Count 7 9 16
% within
RDW_GROUP 63.6% 23.1% 32.0%
ABOVE 50 YEARS
Count 3 28 31
% within
RDW_GROUP 27.3% 71.8% 62.0%
Total
Count 11 39 50
% within
RDW_GROUP 100.0% 100.0% 100.0%
Pearson Chi-Square=7.379* P=0.025
0%
10%
20%
30%
40%
50%
60%
70%
80%
90%
100%
NORMAL(36-48) ABNORMAL(>48)
9% 5%
64%
23%
27%
72% ABOVE 50 YEARS
41-50 YEARS 31-40YEARS
61
AGE_GROUP * RDW_GROUP Crosstabulation
RDW_GROUP Total NORMAL
(36-48)
ABNORMAL (>48)
AGE_GROUP
31- 40YEARS
Count 1 1 2
% within
RDW_GROUP 14.3% 4.8% 7.1%
41-50 YEARS
Count 4 3 7
% within
RDW_GROUP 57.1% 14.3% 25.0%
ABOVE 50 YEARS
Count 2 17 19
% within
RDW_GROUP 28.6% 81.0% 67.9%
Total
Count%
within RDW_GROUP
7 21 28
100.0% 100.0% 100.0%
Pearson Chi-Square=6.647* P=0.036
0%
10%
20%
30%
40%
50%
60%
70%
80%
90%
100%
NORMAL(36-48) ABNORMAL(>48)
14% 5%
57%
14%
29%
81% ABOVE 50 YEARS
41-50 YEARS 31-40YEARS
62
AGE_GROUP * RDW_GROUP Crosstabulation RDW_GROUP
Total NORMAL
(36-48)
ABNORMAL (>48)
AGE_GROUP
31- 40YEARS
Count 3 2 5
% within
RDW_GROUP 30.0% 50.0% 35.7%
41-50 YEARS
Count 7 0 7
% within
RDW_GROUP 70.0% 0.0% 50.0%
ABOVE 50 YEARS
Count 0 2 2
% within
RDW_GROUP 0.0% 50.0% 14.3%
Total
Count 10 4 14
% within
RDW_GROUP 100.0% 100.0% 100.0%
Pearson Chi-Square=8.120* p=0.017
0%
10%
20%
30%
40%
50%
60%
70%
80%
90%
100%
NORMAL(36-48) ABNORMAL(>48) 30%
50%
70%
0%
0%
50%
ABOVE 50 YEARS 41-50 YEARS 31-40YEARS
63
AGE_GROUP * RDW_GROUP Crosstabulation{ RDW AND HYPERTENSION} FEMALES
RDW_GROUP
Total NORMAL
(36-48)
ABNORMAL (>48)
AGE_GROUP
31-40YEARS
Count 0 1 1
% within
RDW_GROUP 0.0% 5.6% 4.5%
41-50 YEARS
Count 3 6 9
% within
RDW_GROUP 75.0% 33.3% 40.9%
ABOVE 50 YEARS
Count 1 11 12
% within
RDW_GROUP 25.0% 61.1% 54.5%
Total
Count
% within RDW_GROUP
4 18 22
100.0% 100.0% 100.0%
Pearson Chi-Square=2.394 p=0.302
64
PREHYPERTENSIVE MALES
RDW_GROUP
Total NORMAL
(36-48)
ABNORMAL (>48)
AGE_GROUP
31- 40YEARS
Count 2 2 4
% within
RDW_GROUP 50.0% 16.7% 25.0%
41-50 YEARS
Count 2 8 10
% within
RDW_GROUP 50.0% 66.7% 62.5%
ABOVE 50 YEARS
Count 0 2 2
% within
RDW_GROUP 0.0% 16.7% 12.5%
Total
Count 4 12 16
% within
RDW_GROUP 100.0% 100.0% 100.0%
Pearson Chi-Square=2.133 P=0.344
65
AGE_GROUP * RDW_ pre hypertensive GROUP Crosstabulation
RDW_GROUP Total NORMAL
(36-48)
ABNORMAL (>48)
AGE_GROUP
31- 40YEARS
Count 5 4 9
% within
RDW_GROUP 35.7% 25.0% 30.0%
41-50 YEARS
Count 9 8 17
% within
RDW_GROUP 64.3% 50.0% 56.7%
ABOVE 50 YEARS
Count 0 4 4
% within
RDW_GROUP 0.0% 25.0% 13.3%
Total
Count 14 16 30
% within
RDW_GROUP 100.0% 100.0% 100.0%
Pearson Chi-Square=4.055 P=0.132
66
NORMOTENSIVE MALES
RDW_GROU P
Total NORMAL
(36-48)
AGE_GROUP
20-30 YEARS
Count 2 2
% within
RDW_GROUP 16.7% 16.7%
31-40YEARS
Count 2 2
% within
RDW_GROUP 16.7% 16.7%
41-50 YEARS
Count 4 4
% within
RDW_GROUP 33.3% 33.3%
ABOVE 50 YEARS
Count 4 4
% within
RDW_GROUP 33.3% 33.3%
Total
Count 12 12
% within
RDW_GROUP 100.0% 100.0%
67
NORMOTENSIVE FEMALES
RDW_
GROUP
Total
NORMAL (36-48)
AGE_
GROUP
31-40YEARS
Count 2 2
% within
RDW_GROUP 25.0% 25.0%
41-50 YEARS
Count 5 5
% within
RDW_GROUP 62.5% 62.5%
ABOVE 50 YEARS
Count 1 1
% within
RDW_GROUP 12.5% 12.5%
Total
Count 8 8
% within
RDW_GROUP 100.0% 100.0%
68
AGE_GROUP * RDW_GROUP Crosstabulation
RDW_GROU P
Total
NORMAL (36-48)
AGE_GROU P
20-30 YEARS
Count 2 2
% within
RDW_GROUP 16.7% 16.7%
31-40YEARS
Count 2 2
% within
RDW_GROUP 16.7% 16.7%
41-50 YEARS
Count 4 4
% within
RDW_GROUP 33.3% 33.3%
ABOVE 50 YEARS
Count 4 4
% within
RDW_GROUP 33.3% 33.3%
Total
Count 12 12
% within
RDW_GROUP 100.0% 100.0%
69
RESULTS AGE DISTRIBUTION
The number of people who are hypertensive are more in the age group >50yrs by about 77.5%
In the age group between 40-50 yrs the number of pre- hypertensives are more by 40.5%
In the age group between 30-40 yrs also, number of pre- hypertensives are more
SEX DISTRIBUTION
The distribution of hypertension is more in both males and females in the age group more than 50 yrs
Pre-hypertensives are equal in both males and females in the age
group 30-50 years
RDW AND HYPERTENSION
RDW is more in the hypertensive group i.e.70.9% of the individuals enrolled for the study had increased RDW
RDW is in borderline elevation in pre-hypertensive group .i.e.
29.9% has borderline elevation of RDW.
RDW is normal in normotensive group
70
RDW AND HYPERTENSION IN MALES
RDW is more in hypertensive males
63.6% of hypertensive males enrolled for the study had increased RDW when compared to the remaining hypertensive individuals
Pearson Chi-Square=21.913** P<0.001 RDW AND PRE-HYPERTENSION
RDW is more in pre-hypertensive individuals with hypertension
That is 36.4% of pre-hypertensive males had increased RDW as compared to others
Pearson Chi-Square=21.913** P<0.001
RDW AND HYPERTENSION IN FEMALES
RDW was increased in females with hypertension 81.8% of
females with hypertension who were enrolled in to study had increased RDW
Pearson Chi-Square=19.481** P<0.001
RDW AND PRE-HYPERTENSION IN FEMALES
RDW was normal in majority of the pre-hypertensive individuals who were enrolled in to the study 18.2% of the pre-hypertensive females had increased RDW
Even though the RDW was more in hypertensive males and females, the RDW in pre-hypertensive females was mostly normal
71
But the overall significance was greater when the study was considered as a whole
Thus RDW was found to be significantly higher in hypertensive and pre- hypertensive individuals
RDW AND HYPERTENSIVES WHO ARE ALCOHOLICS
68% of the alcoholics who are hypertensives who were enrolled in to the study was found to have increased RDW
Pearson Chi-Square=14.206** P=0.001
RDW AND PRE-HYPERTENSIVES WHO ARE ALCOHOLICS
32%ofalcoholics who were pre-hypertensives who were enrolled in to thestudy was found to have increased RDW
Pearson Chi-Square=14.206** P=0.001
RDW AND HYPERTENSIVES WHO ARE SMOKERS
56.5%who are smokers and hypertensives had increased RDW who were enrolled into the study.
Pearson Chi-Square=10.345** P=0.006
72
RDWAND PRE-HYPERTENSIVESWHOARE SMOKERS
43.5% of pre-hypertensive individuals who are smokers had increased RDW who were enrolled in to the study
Pearson Chi-Square=10.345** P=0.006
DISCUSSION
73
DISCUSSION
In this study, 50 hypertensive individuals, 30 pre-hypertensive individuals and 20 controls were analysed in RGGGH hypertensive and medical out patient department foraperiodof6 months.
These cases and controls were analysed and they were examined in detail and were selected based on inclusion and exclusion criteria.
They were assigned to 3 groups. Patients with hypertension were assigned as cases and those with blood pressure between 120/80 to 139/89 and with a family history of hypertension were assigned in pre- hypertensive group. And a set of 20 normal individuals were included as controls.
They were advised to do complete blood count, RBS, Hb, and were asked about history of smoking and hypertension.
The results were analysed and comparative study was done. The results obtained were analysed using various statistical tests like chi- square, ANOVA and p value were obtained.
In a study conducted by Tanindi A, Topal FE,TopalF,Celik B aimed to search to know if RDW values are different in the healthy population and the patients with pre-hypertension and hypertension who are otherwise healthy, based on the widely accepted theory of RDW as a prognostic marker for inflammation.
74
In this study, One-hundred and twenty-eight patients with hypertension, 74 patients with pre-hypertension and 36 healthy controls were enrolled in the study. And these cases and controls were analysed for complete blood count, random blood sugar and were analysed after adjusting for age, hb, cbc and RDW, SD whose normal value is between 36-46 femtolitre (FL),was analysed and it was found out in this study that RDW was found to be higher in hypertensive and pre-hypertensive individuals compared to normal controls.
CONCLUSION
75
CONCLUSION
After this study we have come to the conclusion that in patients with hypertension and those who are prone for hypertension .i.e. pre- hypertensives had significantly elevated RDW compared to normal controls. Thus this study can be used for giving primordial prevention in those patients who are in the pre-hypertensive stage and life-style modifications can be advised.
RDW being a simple parameter which is easily available in a simple routine CBC can thus be used as a novel predictor of hypertension.
It is a cost effective measure for predicting hypertension.
LIMITATIONS
76
LIMITATIONS
One of the limitations is sample size which is less and this study should be tested in large number of patients.
Extended follow up of patients was not possible
BIBLIOGRAPHY
77
BIBLIOGRAPHY
1. Lancet (Lo Borne Y, Smith JG, Melander O, Hedblad B, Engström G (2011) Red cell distribution width and risk for first hospitalization due to heart failure: a population-based cohort study. Eur J Heart Fail 13: 1355–
1361. doi: 10.1093/eurjhf/hfr127 PMID: 21940730
2. AdamssonEryd S, Borne Y, Melander O, Persson M, Smith JG, Hedblad B, et al. (2013) Red blood cell distribution width is associated with incidence of atrial fibrillation. J Intern Med.
3. Engström G, Smith JG, Persson M, Nilsson PM, Melander O, Hedblad B (2014) Red cell distribution width, haemoglobin A1c and incidence of diabetes mellitus. J Intern Med.
4. Park TS, Zambidis ET (2009) A role for the renin-angiotensin system in hematopoiesis. Haematologica 94: 745–747. doi: 10.3324/
haematol.2009.006965 PMID: 19483149
5. Park HK, Kim MC, Kim SM, Jo DJ (2013) Assessment of two missense polymorphisms (rs4762 and rs699) of the angiotensinogen gene and stroke.
ExpTher Med 5: 343–349. PMID: 23251296
6. Remkova A, Remko M (2010) The role of renin-angiotensin system in prothrombotic state in essential hypertension. Physiol Res 59: 13–23. PMID:
78
19249905
7. Zia E, Melander O, Björkbacka H, Hedblad B, Engström G (2012) Total and differential leucocyte counts in relation to incidence of stroke subtypes and mortality: a prospective cohort study. J Intern Med 272: 298–304. doi:
10.1111/j.1365-2796.2012.02526.x PMID: 22303818
8. Söderholm M, Zia E, Hedblad B, Engström G (2014) Leukocyte count and incidence of subarachnoid haemorrhage: a prospective cohort study.
BMC Neurol 14: 71. doi: 10.1186/1471-2377-14-71 PMID: 24708536
9. Wen Y (2010) High red blood cell distribution width is closely associated with risk of carotid artery ath- erosclerosis in patients with hypertension.
ExpClinCardiol 15: 37–40. PMID: 20959889
10. Rosvall M, Janzon L, Berglund G, Engström G, Hedblad B (2005) Incidence of stroke is related to carot- id IMT even in the absence of plaque.
Atherosclerosis 179: 325–331. PMID: 15777549
11. Rosvall M, Janzon L, Berglund G, Engström G, Hedblad B (2005) Incidence of stroke is related to carot- id IMT even in the absence of plaque.
Atherosclerosis 179: 325–331. PMID: 15777549
79
12. Automated blood cell counts: state of the art. Buttarello M, Plebani M. Am J Clin Pathol. 2008;130:104–116
13. Red cell distribution width and high sensitivity C-reactive protein as risk markers in hypertension. TK J, Mathew R, V J, T V. Int J Med Sci Public Health. 2012;1:138–142.
14. Red cell distribution width and inflammation in patients with non-dipper hypertension. Özcan F, Turak O, Durak A, İşleyen A, Uçar F, Giniş Z, Uçar F, Başar FN, Aydoğdu S. Blood Press. 2013; 22:80–85
15. Red cell distribution width in patients with prehypertension and hypertension. Tanindi A, Topal FE, Topal F, Celik B. Blood Press. 2012;21:177–181
16. Usefulness of a complete blood count-derived risk score to predict incident mortality in patients with suspected cardiovascular disease. Anderson JL, Ronnow BS, Horne BD, Carlquist JF, May HT, Bair TL, Jensen KR, Muhlestein JB; Intermountain Heart Collaborative (IHC) Study Group. Am J Cardiol. 2007;99:169–174
17. Relation between red blood cell distribution width and cardiovascular event rate in people with coronary disease; for the Cholesterol and Recurrent Events (CARE) Trial Investigators. Tonelli M, Sacks F, Arnold M, Moye L, Davis B, Pfeffer M. Circulation. 2008; 117:163–168