A CLINICAL STUDY ON PREVALENCE OF COMPLICATIONS AMONG KNOWN HYPERTENSIVE PATIENTS ATTENDING THE

A Dissertation on

A CLINICAL STUDY ON PREVALENCE OF COMPLICATIONS AMONG KNOWN HYPERTENSIVE PATIENTS ATTENDING THE

HYPERTENSION OP AT A TERTIARY CARE HOSPITAL IN TAMILNADU

Submitted to

THE TAMILNADU Dr. M.G.R MEDICAL UNIVERSITY CHENNAI

in partial fulfillment of the regulations for the award of the degree of

M.D BRANCH – I GENERAL MEDICINE

GOVT.MOHAN KUMARAMANGALAM MEDICAL COLLEGE & HOSPITAL

SALEM – TAMILNADU

MAY 2021

DECLARATION BY THE CANDIDATE

I hereby declare that this dissertation titled “A CLINICAL STUDY ON PREVALENCE OF COMPLICATIONS AMONG KNOWN HYPERTENSIVE PATIENTS ATTENDING THE HYPERTENSION OP AT A TERTIARY CARE HOSPITAL IN TAMILNADU” is a bonafide and genuine work carried out by me from January 2019 and January 2020 under the guidance and supervision of Professor Dr. M. MANJULA M.D., Department of GENERAL MEDICINE, Government Mohan Kumaramangalam Medical College Hospital, Salem, Tamil Nadu,India.

This dissertation is submitted to The Tamilnadu Dr.M.G.R. Medical University towards the partial fulfilment of the requirement for the award of MD Degree in General Medicine(Branch I).

Date : Place :

Signature of the Candidate

Dr S. TAMILMATHY

CERTIFICATE FROM THE GUIDE

This is to certify that “A CLINICAL STUDY ON PREVALENCE OF COMPLICATIONS AMONG KNOWN HYPERTENSIVE PATIENTS ATTENDING THE HYPERTENSION OP AT A TERTIARY CARE HOSPITAL IN TAMILNADU”is a bonafide and genuine work carried out by DR.S. TAMILMATHY from January 2019 and January 2020 in a partial fulfillment of the university regulations of the Tamil Nadu DR.M.G.R Medical University ,Chennai, for M.D GENERAL MEIDICINE Branch I examination to be held in May 2021.

Date : Place :

Signature of the Guide Prof DR.M.MANJULA M.D, Department of General Medicine Government Mohan Kumaramangalam

Medical College Hospital, Salem

CERTIFICATE FROM THE HOD

This is to certify that “A CLINICAL STUDY ON PREVALENCE OF COMPLICATIONS AMONG KNOWN HYPERTENSIVE PATIENTS ATTENDING THE HYPERTENSION OP AT A TERTIARY CARE HOSPITAL IN TAMILNADU”is a bonafide and genuine work carried out by DR.S. TAMILMATHY from January 2019 and January 2020 in a partial fulfillment of the university regulations of the Tamil Nadu DR.M.G.R Medical University ,Chennai, for M.D GENERAL MEIDICINE Branch I examination to be held in May 2021.

Date :

Place : Signature of the HOD

Prof DR. S.SURESH KANNA M.D Department of General Medicine Government Mohan Kumaramangalam

Medical College Hospital, Salem

CERTIFICATE FROM THE DEAN

This is to certify that “A CLINICAL STUDY ON PREVALENCE OF COMPLICATIONS AMONG KNOWN HYPERTENSIVE PATIENTS ATTENDING THE HYPERTENSION OP AT A TERTIARY CARE HOSPITAL IN TAMILNADU” is a bonafide and genuine work carried out by DR.S. TAMILMATHY from January 2019 and January 2020 in a partial fulfillment of the university regulations of the Tamil Nadu DR.M.G.R Medical University ,Chennai, for M.D GENERAL MEIDICINE Branch I examination to be held in May 2021.

Date : Place :

Signature of the DEAN

Prof. DR. R.BALAJINATHAN M.D, THE DEAN

Government Mohan Kumaramangalam

Medical College Hospital, Salem

GOVERNMENT MOHAN KUMARAMANGALAM MEDICAL COLLEGE & HOSPITAL

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Dr. S.TAMILMATHY

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ACKNOWLEDGEMENT

I wish to express my sincere thanks to the respected Dean, Government

Mohan Kumaramangalam Medical College Hospital Prof.Dr.R.BALAJINATHAN M.D for having allowing me to avail the facilities needed for my dissertation study.

I express my heartfelt thanks and deep gratitude to my guide Prof. DR.M.MANJULA, M.D. for her generous help and guidance in the course of the study.

I also express my heartfelt thanks and deep gratitude to The Head of the Department of Medicine Prof. DR. S. SURESH KANNA, M.D. for his generous help and guidance in the course of the study.

My sincere thanks to Dr. D.VIJAYARAJU, M.D., Dr. J.A.

VASANTHAKUMAR M.D., Dr. V. RAJKUMAR M.D., and Dr.PALANIVELRAJAN M.D., for all the help and guidance.

I sincerely thank all my Asst. Professors, Senior Residents for their guidance and kind help.

My sincere thanks to all my friends and post-graduate colleagues for their whole hearted support and companionship during my studies

I thank all my PATIENTS, who formed the backbone of this study

without whom this study would not have been possible.

Lastly, I am ever grateful to the ALMIGHTY GOD for always

showering His blessings on me and my family.

ABBREVIATIONS:

SHTN – Systemic Hypertension BP – Blood Pressure

MAP – Mean Arterial Pressure SBP – Systolic Blood Pressure DBP – Diastolic Blood Pressure

DALY – Disability Adjusted Life Years JNC – Joint National Committee

ACC/AHA – American College of Cardiology / American Heart Association ABPM – Ambulatory Blood Pressure Monitoring

HBPM – Home Blood Pressure Monitoring OSA – Obstructive Sleep Apnoea

NSAIDS – Non Steroidal Anti-Inflammatory Drugs VEGF – Vascular Endothelial Growth Factors ABPI – Ankle Brachial Pressure Index

RAAS – Renin Angiotensin Aldosterone System ACEI – Angiotensin Converting Enzyme Inhibitors ARB – Angiotensin Receptor Blockers

BMI – Body Mass Index

LVH – Left Ventricular Hypertrophy ECG – ElectroCardioGram

GFR – Glomerular Filtration Rate

TABLE OF CONTENTS

Serial

no. Topic Page no.

1. INTRODUCTION 1

2. AIMS AND OBJECTIVES 3

3. REVIEW OF LITERATURE 4

4. MATERIALS AND METHODS 31

5. RESULTS 35

6. DISCUSSION 71

7. CONCLUSION 74

8. LIMITATIONS OF STUDY 75

9. ANNEXURES

• REFERENCES

• ETHICAL COMMITTEE APPROVAL FORM

• CONSENT FORM

• PROFORMA FOR DATA COLLECTION

• ABBREVIATIONS

• MASTER CHART

• KEY TO MASTER CHART

LIST OF FIGURES:

S.No Figures Page no

1. Relationship between blood pressure and renal sodium handling 15 2. End organ damages in systemic hypertension 17 3. Current differential treatment recommendations for end organ damages 20 4. Pathogenesis and clinical presentation of hypertensive heart disease 22 5. Renin angiotensin aldosterone system 25 6. renal function based on eGFR & albuminuria. 26 7. Keith Wagner- grading of hypertensive retinopathy 27 8. Scheie- grading of hypertensive retinopathy 28

9. Hypertensive vasculopathy 29

LIST OF TABLES :

S.No. Tables Page

no.

1. JNC 7 Classification of hypertension 2003 8 2. ACC / AHA Classification of hypertension 2017 8

3. Causes of secondary hypertension 11

4. Causes of resistant hypertension 13

5. Median value and IQR of different variables 36 6. Gender distribution among study population. 37 7. Distribution of salt restricted diet among study population. 38 8. Distribution of smoking habits among study population 39 9. Distribution of alcohol intake among study population 40 10. Distribution of family history of hypertension among

study population 41

11. Distribution of lifestyle pattern among study population 42 12. Distribution of BMI among study population 43 13. Distribution of drug regimen among study population 45 14. Distribution of complications at the time of diagnosis

among study population 47

15. Distribution of various end organ damages among study

population 49

16. Distribution of cerebral end organ damage among study

population 51

17. Distribution of echocardiographic findings among study

population 52

18. Distribution of retinal changes among study population 54

19. Distribution of renal functions among study population 56

20. Correlation between high SBP and complications 60

21. Correlation between smoking and complications at

diagnosis 61

22. Correlation between alcohol intake and complications at

diagnosis 61

23. Correlation between Lifestyle pattern and complications

at diagnosis 62

24. Correlation between Gender and complications at

diagnosis 63

25. Correlation between family history and complications at

diagnosis 64

26. Correlation between Lifestyle habits and time taken to

develop complications 65

ABSTRACT

BACKGROUND: Hypertension is one of the leading causes of premature mortality and morbidity in india as well as world. Uncontrolled hypertension results in various complications (Coronary artery heart disease, Stroke, Cardiac failure, Chronic kidney disease and its further complications, Peripheral vascular disease, Retinopathy).These complications and its sequelae makes it essential to know the current trending prevalence of complications. There is also a need for increased public health education to increase the awareness of uncontrolled hypertension and its complications.

AIMS AND OBJECTIVES:

• To Assess the prevalence of various complications of hypertension.

• To assess the time duration from the point of diagnosis of hypertension to the development of complications.

• To assess the risk factors for early development of complications.

• To assess the knowledge about the hypertension and its sequelae, adherence to drug intake, among the subjects.

METHODOLOGY: All hypertensive patients who have met the inclusion and

exclusion criteria, after obtaining proper consent with approval from the

institutional ethical committee, sample of 2000 was selected and proceeded.

Patients were interviewed for demographic data such as age and sex, history of other comorbid conditions along with presenting complaints were noted .Further these patients were subjected to physical examination for clinical signs. These findings were recorded on a predesigned and pretested proforma including patient history, cardiac evaluation, renal function tests, urine albumin, ABPI and fundus examination.

RESULTS:

In our study population of 2000, we found male preponderance (58.2%)

probably due to life style habits such as smoking and alcohol. Prevalence of

complications, out of 2000 participants 422(21.2%) had cardiac

complications 435(21.8%) had CNS complications, 13(0.7%) had

Peripheral Vascular Diseases,604(30.2%) had renal complications and

35(1.8%) had eye complications. 1% of individuals had more than one

complication we also found statistically significant correlations among

High systolic BP at diagnosis, smoking, alcohol, sedentary life style habits,

family history, drug compliance and multiple drug therapy. These factors

significantly influences the end organ damages.

1

INTRODUCTION

High blood pressure was awarded the place of third position for the most attributable burden of disease in south Asian countries [1]. Systemic Hypertension (HTN) exerts a substantial public health burden on most of the healthcare systems in India [2,3]. HTN is directly responsible for 57% of all cerebrovascular accident deaths and 24% of all coronary artery heart disease (CAHD) deaths in India [4]. The WHO rates HTN as one of the most important causative factors for premature deaths worldwide [5].

In the Global and Regional Burden of Disease and Risk Factors study (2001), which was the systematic analysis for attributable deaths and attributable disease burden, HTN was ranked second only to child underweight for age in south Asian countries [6].

About 20.6% of Indian hypertensive men and 20.9% of Indian hypertensive women were contributing to the global burden of HTN ,according to the analysis of world wide data lancet 2005 [7].

Uncontrolled hypertension will end up in various end organ damages subsequently leading to organ dysfunction and failure like concentric LVH progressing to systolic and diastolic dysfunction ending up in cardiac failure.

Not only the cardiovascular system, but also the brain, kidneys, retina,

peripheral vascular system are also affected. But only about one fourth of the

2

treated patients in india was having their BP under control, according to a

multicenter study from India on awareness, treatment, and adequacy of control

of HTN[8].

3

AIMS AND OBJECTIVES

1. To assess the prevalence of various complications of hypertension.

2. To assess the time duration from the point of diagnosis of hypertension to the development of complications.

3. To assess the risk factors for early development of complications.

4. To assess the knowledge and awareness about the hypertension and its

control by correlating with the compliance of drug intake and end organ

damage.

4

REVIEW OF LITERATURE

3.1 . HISTORY OF RESEARCH FROM BLOOD PRESSURE TO HYPERTENSION;

Time line of hypertension starts as far back as 2600BC, from the ancient historical records reporting the name as HARD PULSE DISEASE, which was used to be treated by acupuncture, venesection and sucking out the blood by leeches.

From 629 to 626BC,The Ashurbanipal Library at Nineveh is having details of iatrogenic bleeding by venesection and leeches.[9]

From 1913 to 1925,the terms HYPERTONIE ESSENTIAL by frank and HYPERTENSIVE VASCULAR DISEASE by janeway were coined.[10]

In 1905,Nikolai Sergeyevich Korotkoff had given the description of stethoscopic sounds enhanced the knowledge in measuring blood pressure.[10]

In 1900s, first chemical substance used in management of hypertension was SODIUM THIOCYANATE, by treupel and edinger and hines at mayo clinic. It was withdrawn due to its potential serious adverse effects.[10]

In 1923, first SYMPATHECTOMY was performed by surgeon fritz and

advised by Kraus.[9]

5

In 1948, chemical sympathectomy was introduced like tetraethyl ammonium chloride.[10]

In 1949,HYDRALAZINE was first studied by Reubi. This drug is still in use especially in the toxaemia of pregnancy.[10]

The greatest break through came up in 1957 by Freis, Wilson and Parish when they introduced the CHLORTHIAZIDE.

In 1960s, BETABLOCKERS were introduced.

In 1980s, ACE inhibitors and calcium channel blockers were extensively studied and currently they became the first line drugs in management.[10]

And many more new drugs and chemicals are in the horizon to find the best one which will be effectively lowering the BP with negligible side effects to prevent the end organ damages.

3.2 EPIDEMIOLOGY

Various Studies from different parts of India have reported increasing trend in prevalence of hypertension as well as low awareness and control of blood pressure.

To determine the true prevalence of hypertension in the country, two

recent studies have been conducted with uniform tools and nationwide

sampling such as Fourth National Family Health Survey evaluated

hypertension in a large population based sample (n = 799,228) reporting

hypertension in 13.8% men vs. 8.8% women (overall 11.3%) aged 15–49 and

6

15–54 respectively and (age > 18 years, n = 1,320,555) Fourth District Level Household Survey reporting overall prevalence of hypertension was 25.3%

with greater prevalence in men (27.4%) than women (20.0%). This report corresponds to 207 million indians (men 112 million, women 95 million) are hypertensive .

Based on the reports of Global Burden of Diseases study, hypertension

has led to 1.63 million deaths in India in 2016 as compared to 0.78 million in

1990 (+108%). The disease burden (DALYs) attributable to hypertension

increased from 21 million in 1990 to 39 million in 2016 (+89%). [11]

7

3.3. DEFINITION OF HYPERTENSION:

Hypertension is diagnosed when SBP is persistently above 140mmHg and DBP is above 90mmHg in at least 2 measurements taken in the clinic or by a healthcare provider on at least 2 visits, which are at least 1-4 weeks apart, except in the case of hypertensive urgencies and hypertensive emergencies, where hypertension is diagnosed during the first visit itself.

3.4 CLASSIFICATION AND STAGES OF HYPERTENSION:

Patients with hypertension are classified as

• Grade 1 Hypertension: systolic 140-159 mmHg and/or diastolic 90-99 mmHg

• Grade 2 Hypertension : systolic 160-179 mmHg and/or diastolic 100- 109 mmHg

• Grade 3 Hypertension : systolic 180 or above and/or diastolic 110 or above

• Isolated systolic hypertension: systolic >140 but diastolic <80

• Hypertensive urgency: Severe asymptomatic hypertension with Systolic >180 Diastolic >120

• Hypertensive emergency: Severe hypertension accompanied by cardiac

(e.g. acute left ventricular failure), neurological (e.g. hypertensive

encephalopathy), or renal dysfunction.

8

TABLE 1: JNC 7 CLASSIFICATION OF HYPERTENSION [2003]

SBP DBP

NORMAL <120 <80

PRE HYPERTENSION 120-139 80-89

STAGE 1 HTN 140-159 90-99

STAGE 2 HTN ≥160 ≥100

TABLE 2: ACC/AHA CLASSIFICATION OF HYPERTENSION [2017]

SBP DBP

Normal <120 <80

Elevated 120-129 <80

Stage 1 HTN 130-139 80-89

Stage 2 HTN ≥140 ≥90

9

3.5.BLOOD PRESSURE MEASUREMENT:

Blood pressure can be measured as following:

(1) office BP measurement by manual sphygmomanometer or automated oscillometric device

(2) ABPM – ambulatory BP monitoring (3) home BP monitoring.

ABPM is the gold standard as the elevations in 24-hour BP on ABPM are strongly associated with stroke and CV events because ABPM provides average awake and asleep blood pressure values, range of blood pressure, and nocturnal blood pressure Values. These measurements will be useful in identifying the underlying causes of hypertension like in OSA[obstructive sleep apnea] in which ABPM will show the “non-dipping” pattern, which means normal decline of atleast 10% of BP during sleep will not occur.

ABPM can also assess the response to medication and able to quantify the BP

control. Finally whenever available, ABPM should be used to confirm the

initial diagnosis as well as a valuable tool for monitoring during treatment,

especially in difficult-to-treat or resistant hypertension. But ABPM is not

practically possible in developing countries like us and cost can be a barrier in

widespread usage in india. In such scenarios , home blood pressure

measurement is an excellent alternative. Elevated home blood pressure

readings are also associated with CV events, though there is less evidence

than with ABPM.[13,14].

10

3.6.CAUSES OF ERRORS DURING BP MEASUREMENT:

• overdistended bladder

• small size cuff

• inadequate rest prior to measurement

false high SBP

& DBP

• large cuff size false low SBP &

DBP

• deflating cuff very quickly

• postural variation

• white coat effect varying

measurements

11

3.7.CAUSES OF HYPERTENSION:

About 80% of the hypertensive patients are having primary or essential or idiopathic hypertension. Remaining 20% will be having a specific secondary cause most common being the renal and renovascular causes. And other causes include hyperaldosteronism, pheochromocytoma, cushing syndrome, hypothyroidism, hyperthyroidism, obstructive sleep apnea syndrome, etc,.

TABLE 3: CAUSES OF SECONDARY HYPERTENSION

12

3.8.RESISTANT HYPERTENSION:

3.8.1. DIAGNOSIS OF RESISTANT HYPERTENSION:

Resistant hypertension is diagnosed when the target blood pressure level is not achieved such that < 140/90 mm Hg for patients without co morbid illness and < 140/85 mm Hg for patients with diabetes and chronic kidney disease, in spite of the treatment with at least three antihypertensive agents of different classes in correct combination and at the highest tolerated doses , among which one drug should be the diuretic. Resistant hypertension also includes the use of at least four drugs for the effective control of BP.

Inadequate control of BP has to be confirmed by ABPM or HBPM mainly to ensure the adherence to drug therapy.[15]

3.8.2. PSEUDO RESISTANT HYPERTENSION:

It is defined as persistently uncontrolled HTN at clinic, for reasons other than true resistance to drug therapy. Causes of pseudo resistant HTN includes

• Poor adherence to drugs

• White coat effect

• Faulty office BP measurement techniques

• Severe arterial calcification

• Clinician inertia – inadequate dosing or irrational drug combinations

for BP control. [15]

13

3.8.3.CAUSES OF RESISTANT HYPERTENSION:

TABLE 4: CAUSES OF RESISTANT HYPERTENSION

1. HYPERVOLEMIA

2. SYMPATHETIC OVERACTIVITY

3. DRUG INDUCED

4. UNDIAGNOSED SECONDARY HYPERTENSION

HYPERVOLEMIA can be due to excessive sodium intake , inadequate dosing of diuretics, renal failure, cardiac failure, drugs which can cause sodium retention like mineralocorticoid receptor agonists, estrogens, NSAIDS,drugs causing fluid retention such as arteriolar vasodilators like hydralazine, minoxidil. SYMPATHETIC OVERACTIVITY due to chronic stress, chronic pain, fear phobia, hyperventilation, paroxysm of panic causing systemic vasoconstriction. DRUGS include

• NSAIDs by its inhibition of renal prostaglandin production,decrease renal blood flow, retain sodium.

• glucocorticoids,

• licorice suppressing the metabolism of cortisol by beta hydroxysteroid dehydrogenase and stimulating mineralocorticoid receptor.

• erythropoetin stimulating agents increase vascular production of

vasoconstrictors like thromboxane.

14

• calcineurin inhibitors like cyclosporine/tacrolimus can enhance sympathetic nervous system activity and renal vasoconstriction leading to sodium and water retention.

• antidepressants like monoamine oxidase inhibitors .

• sympathomimetics like nasal decongestants

• oral contraceptives with estrogen

• anti-VEGF as VEGF stimulate nitric oxide production and causes vasodilatation

• cocaine and amphetamines.

UNDIAGNOSED SECONDARY HYPERTENSION , which includes

• renal and reno vascular causes like renal failure and renal artery stenosis

• endocrine causes like hyperaldosteronism, both hyper and hypo thyroidism, congenital adrenal hyperplasia, pheochromocytoma.

• Sleep disturbances like obstructive sleep apnea.[15,16]

15

3.9.MECHANISM OF HYPERTENSION:

Pathophysiology behind hypertension arises from the two major pillars such as IMPAIRED PRESSURE NATRIURESIS and STIFFENING OF ARTERIES leading to increased sodium and water retention and increased peripheral vascular resistance respectively.

FIGURE 1.Relationship between blood pressure and renal sodium handling.

16

Pressure natriuresis is a protective mechanism against hypertension, when blood pressure raises ,there occurs the increase in renal arteriolar pressure causing increased blood flow in renal vasarecta which stimulates the local paracrine production of nitric oxide and ATP. These paracrine agents act at multiple sites to inhibit tubular sodium reabsorption. In hypertensives pressure natriuresis occurs at high BP.

3.10.END ORGAN DAMAGES IN HYPERTENSION:

Throughout the world, Systemic Hypertension is the leading risk

factor for morbidity and mortality because of the end organ damages

attributable to its hemodynamic changes. The presence and severity of typical

end organ damage and secondary diseases can be detected early in

hypertension patients to prognosticate their health scenario and thereby aiding

them in further evaluation and management. The classic end organ damage

includes vascular and hemorrhagic stroke, retinopathy, coronary artery heart

disease/myocardial infarction and heart failure, proteinuria and renal failure

and atherosclerotic change such as development of stenoses and aneurysms in

particular to the vascular tree.

17

.

Figure 2: end organ damages in arterial hypertension.

3.10.1. DIAGNOSIS OF EARLY HYPERTENSIVE END ORGAN DAMAGE:

• Electrocardiographic evidence of Left ventricular hypertrophy by using sokolo lyon or cornell voltage criteria.

• Left ventricular mass of ≥ 125 g/m2 in men and ≥ 110 g/m2 in women

• Intima-media thickness [IMT] > 0.9 mm or arterio -sclerotic plaque

observed by ultrasound examination.

18

• Ankle-Brachial pressure Index [ABPI] < 0.9

• Raised Serum creatinine levels

Men 1.3–1.5 mg/dL (115–133 μmol/L) Women 1.2–1.4 mg/dL (107–124 μmol/L)

• Urinary albumin excretion in the range of microalbuminuria 30–

300 mg/24 hours.

• Measuring albumin-creatinine ratio in men ≥ 22mg/g creatinine and inwomen ≥ 31 mg/g creatinine

• Calculated glomerular filtration rate of <60 mL/ min/1.73 m2 or

creatinine clearance <60 mL/min. Hypertensive end organ damages

can be diagnosed at early reversible stages so that to prevent the

irreversible organ failure contributing to the increase in mortality

and morbidity.[17,18].

19

3.10.2.ANTIHYPERTENSIVE AGENTS OF CHOICE HYPERTENSIVE END ORGAN DAMAGE:

In case of subclinical end organ damage like only left ventricular hypertrophy, albuminuria and mild renal dysfunction, ACE inhibitors or ARBs are the choice. In case of irreversible end organ damages like prior myocardial infarction, betablockers and RAAS inhibitors can be used. For angina pectoris [chronic stable angina in coronary artery heart disease], beta blockers and calcium channel blockers can be used. For heart failure, diuretics, beta blockers, RAAS inhibitors, MR antagonists can be used.

For chronic renal sufficiency with proteinuria, loop diuretics and

RAAS inhibitors can be used with monitoring. For peripheral arterial

occlusive disease, calcium channel blockers can be used.[17,18].

20

Figure 3: current differential treatment recommendations for the end organ

damages[17].

21

3 .11: CORONARY ARTERY DISEASE AND HYPERTENSION :

Hypertension and coronary artery heart disease is the strongest and the

most common association . In hypertension, there occurs increase of

transmural pressure in arterial vessels, with an increase in mechanical stress

and endothelial permeability favours the lipid deposition along the arterial

wall progressing to the atherosclerotic plaque. Also ,it is observed that

decline in coronary reserve is caused by hypertension associated

microvascular as well as macrovascular resistance leading to endothelial

dysfunction and structural remodelling.[19] Because of the pressure

overload in systemic hypertension, there occurs medial hypertrophy and

perivascular collagen deposition favouring the remodelling process.[19,20].

22

Figure 4:pathogenesis and clinical presentation of hypertensive heart

disease.

23

3.12.HYPERTENSIVE CEREBROVASCULAR DAMAGE:

Hypertensive cerebrovascular damage can be microvascular and macrovascular complications. Macrovascular complications such as ischemic or hemorrhagic stroke caused by atherosclerotic [thrombotic/embolic]

vascular occlusion or fibrinoid degeneration of the vascular architecture.

Early hypertensive microvascular complications include lacunar stroke, small microhemorrhages, focal or diffuse white matter edema, later on may lead to vascular dementia.[21]

Arterial hypertension attributes to the leading risk factor as well as the causative factor for stroke. The role of hypertension in acute cerebro vascular accident is very essential to understand the need and significance of treatment of hypertension. Hemorrhagic stroke due to hypertension results from spontaneous rupture of small penetrating deep arterial system in brain matter.

The commonest sites of intracerebral haemorrhage in brain are putamen, basal ganglia, thalamus, cerebellum and pons in the order of decreasing frequency.

Small vessels in these areas are prone to vascular injury such as

lipohyalinosis as well as fibrinoid degeneration leading to charcot bouchard

aneurysms in hypertensive patient. Haemorrhage in other than the above areas

of brain suggests the possibilities of some other causes of bleeds like

neoplasms, bleeding or coagulation disorders, trauma, vascular malformation

and cerebral amyloid angiopathy.[21,22]

24

3.13. HYPERTENSIVE NEPHROPATHY:

Most often it takes about 15 to 20 years for a patient of hypertensive nephropathy to be called a patient of chronic renal failure. This transformation from nephropathy to chronic kidney disease will happen unnoticed and without clinical symptoms. Detecting renal end organ damage in the stage of nephropathy will help us to prevent further worsening and development of irreversible renal failure. By means of easily measured parameters such as albuminuria, serum creatinine, blood urea nitrogen and calculated eGFR – glomerular filtration rate.[21]

The recommended target blood pressure for hypertensive nephropathy

with or without proteinuria is <130/80 mm Hg. RAAS inhibitors such as

angiotensin converting enzyme inhibitors, angiotensin receptor blockers,

direct renin inhibitors such as aliskiren have proven nephroprotective effects

and may help in preventing the progression to chronic renal failure.[23]

25

Figure 5: Renin angiotensin aldosterone system.

26

RENAL function according to calculated egfr and albuminuria:

Figure 6: Renal function based on eGFR& albuminuria.

27

3.13. HYPERTENSIVE RETINOPATHY:

There are three independent distinct manifestations of sysatemic arterial hypertension on retina, optic nerve as well as the choroidal circulation which include

1. Hypertensive retinopathy 2. Hypertensive optic neuropathy 3. Hypertensive choroidopathy. [24]

Figure 7: Grading of hypertensive retinopathy. – keithwagner

28

Figure8: Scheie grading of hypertensive retinopathy.

Out of the three manifestations, retinopathy is the one which is recognised as the cardiovascular risk stratification. The WHO gives the criteria for malignant hypertension as severe systemic arterial hypertension with bilateral retinal haemorrhages and exudates.[25]. But controversy exists that presence of only papilloedema without retinopathy in the presence of elevated systemic blood pressure, might be just a variant of malignant hypertension only after excluding the other causes of pailloedema like CNS space occupying lesions and benign intracranial hypertension.[26] Several theories have been proposed for the pathogenesis of papilloedema due to systemic arterial hypertension include: (i) ischaemia, (ii) raise dintracranial pressure, and (iii) as a part of hypertensive retinopathy/

encephalopathy.[25,26] Other ocular manifestations caused by raised

systemic arterial hypertension such as retinal vein occlusion, retinal artery

microaneurysms, non arteritic anterior schemic neuropathy, cranial nerve

palsies affecting ocular movements and may even present as symptomatic

diplopia and ophthalmoplegia.[25]

29

3.14. HYPERTENSIVE VASCULOPATHY:

Hypertensive vasculopathy is defined as the endothelial dysfunction with small and large arterial wall remodelling. This remodelling and endothelial dysfunction reduces the dilation capacity of the high resistance vessels .Measurement of the ankle-brachial pressure Index with the pulse wave velocity and augmentation index even more accurately specify the cardiovascular mortality risk and prevent hypertensive patients from being misclassified as low risk.

Figure 9: Hypertensive Vasculopathy.

30

Ankle Brachial pressure Index:

The ankle brachial pressure index is a ratio of measured systolic blood pressure at the ankle as numerator and measured systolic pressure in the arm as denominator. The ABPI measurement is easy to perform and offers quick interpretation so that this index will be helpful in diagnosing and evaluating peripheral arterial vascular disease. Nowadays ABPI is included as a cardiovascular risk factor. The value of ABPI<0.9 has been proven to increase the risk of future myocardial infarction. Thus the value of measured ABPI is independent of other known risk factors stratified for cardiovascular disease.

ABPI provides additional risk stratification in individuals with Framingham risk between 10-20% in 10 years. In this intermediate risk group reduced ABPI will move the patient to high risk group requiring secondary prevention strategy where as normal ABPI will lower the risk requiring primary prevention strategy. It also indicates that peripheral vessels are having atherosclerosis in spite of the patients being asymptomatic. In patients with reduced ABPI will be having reduced functional capacity of limbs.

Functional capacity of limbs can be manifested as decreased speed of walking

and/or reduced walking distance observed during a six minute walk test.

31

MATERIALS AND METHODS:

SOURCE OF DATA:

All hypertensive patients attending the hypertension clinic in Government Mohan Kumaramangalam Medical College and Hospitals, Salem during time period of 1 year from January2019 to January 2020.

METHOD OF COLLECTION OF DATA:

All hypertensive patients who have met the inclusion and exclusion criteria, after obtaining proper consent with approval from the institutional ethical committee, sample of 2000 was selected and proceeded.

STUDY DESIGN:

• An observational, prospective study

• Sample size: 2000 patients.

• Patients were interviewed for demographic data such as age and sex, history of other comorbid conditions along with presenting complaints were noted .Further these patients were subjected to a physical

examination for clinical signs. These findings were recorded on a

predesigned and pretested proforma.

32

INCLUSION CRITERIA:

1. Age> 30 years 2. Either sex

3. Willing to involve in the study 4. Patients in euglycemic status.

Exclusion criteria:

1. Age ≤ 30 years

2. Not willing to involve in the study 3. Secondary hypertension

4. Patients with pre-exixting systemic disease prior to the diagnosis of hypertension.

5. Patients who are all known case of diabetes mellitus.

33

PARAMETERS included in the study Patient details:

1.Age 2.Sex 3.BMI

4 Life style habits including smoking, alcohol, salt restriction in diet 5.When the patient was diagnosed to have hypertension?

6.When the target BP was attained?

7.What was the BP at the time of diagnosis of hypertension?

8.Is there any complications at the time of diagnosis?

9.History of drug therapy

10. Adherence to drug regimen

34

Investigations:

1.Laboratory investigations including blood urea and creatinine, urine complete, random blood sugar

2.ECG

3.ECHOCARDIOGRAM 4.USG KUB

5.FUNDUS EXAMINATION

6.ABPI

35

RESULTS AND STATISTICS:

Descriptive Statistics N = 2000 participants 1. Age distribution

Median age of participants – 57 years (Interquartile range IQR = 13 years)

36

2.Median Systolic BP at diagnosis – 170 mm Hg (Interquartile range IQR = 20 mm Hg)

3.Median time taken to attain target BP – 7 months (Interquartile range IQR = 3 months)

4.Median time taken for complications to develop – 3 years (IQR – 2 years) Table 5: median value and IQR of different variables:

VARIABLES MEDIAN VALUE INTERQUARTILE RANGE Median age of

participants 57 years 13years

Median SBP @

diagnosis 170mmHg 20mmHg

Median time taken to

attain target BP 7 months 3months

Median time taken for complications to

develop

3 years 2 years

37

5.GENDER distribution:

Total participants = 2000[100%]

Male = 1164 [58.20%]

Female = 836 [41.80%]

Table 6: Gender distribution among study population:

Gender Frequency Percentage

Male 1164 58.20%

Female 836 41.80%

38

6.DISTRIBUTION OF SALT RESTRICTED DIET AMONG THE PARTICIPANTS

Total participants = 2000

Following salt restriction in diet = 809[40.45%]

Not following salt restriction = 1191[59.55%]

Table 7: Distribution of salt restricted diet among study population:

salt restriction Frequency percentage

Following 809 40.45%

Not following 1191 59.55%

40.45% yes

59.55% no

0% 0%

39

7.SMOKERS AMONG THE PARTICIPANTS:

Total participants = 2000 Smokers – 782 (39.1%)

Non smokers – 1218 [60.09%]

Table 8: Distribution of smoking habits among study population:

Smoking habits frequency Percentage

Smokers 782 39.1%

Non smokers 1218 60.09%

smokers 39%

non smokers 61%

0% 0%

40

8. ALCOHOLICS AMONG THE PARTICIPANTS

Total participants = 2000 Alcoholic – 742 (37.1%) Non alcoholic – 1258 [62.9%]

Table 9: Distribution of alcohol intake among study population:

Life style frequency percentage

Alcoholic 742 37.1%

Non alcoholic 1258 62.9%

alcoholic 37%

non alcoholic 63%

0% 0%

41

9. FAMILY HISTORY OF HYPERTENSION:

798(39.9%) had family history of hypertension.

56(2.8%) had family history of young hypertension and complications.

Table 10: Distribution of family history of hypertension among study population:

Family history of Frequency Percentage

Hypertension 798 39.9%

Young hypertension &

complications 56 2.8%

0.00%

20.00%

40.00%

60.00%

80.00%

100.00%

120.00%

family h/o HTN family h/o young HTN

& complications

42

10. lifestyle habits

Lifestyle – Sedentary 1165 (58.3%)

Table 11: Distribution of life style pattern among study population:

Lifestyle frequency Percentage

Sedentary 1165 58.3%

Active 835 49%

active 41.7%

sedentary 58%

0% 0%

43

11. Distribution of BMI among participants:

Underweight -2 [.1%]

Normal - 129 [6.5%]

Overweight - 835 [42.3%]

Obese - 1005 [50.9%]

Table 12: Distribution of BMI among study population:

BMI frequency Percentage

Underweight 2 0.1%

Normal 129 6.5%

Overweight 835 42.3%

Obese 1005 50.9%

44

45

12.Distribution of drug regimen among the participants:

Drug regimen

Single drug – 398 (20.1%) Double drug – 688 (34.7%) Triple drug – 874 (44.1%) More than 3 drugs – 23 (1.2%)

Table 13: Distribution of drug regimen among study population:

Drug regimen frequency Percentage

Single drug 398 20.1%

Double drug 688 34.7%

Triple drug 874 44.1%

More than 3 drugs 23 1.2%

46

13.Complications at the time of diagnosis.

Overall Complications at the time of diagnosis in 994 individuals (47.2%)

Out of 2000 participants, 47.2% presented with complications at the time of

diagnosis. This group of patients are missed in early screening process.

47

Table 14: Distribution of complications at the time of diagnosis among study population:

Parameter Frequency Percentage

Complications at the

time of diagnosis 994 47.2%

n=2000

994[47.2%]

48

14. END ORGAN DAMAGE:

Out of 2000 participants, 1509 patients are having end organ damage.[75.45%]

Parameter frequency Percentage

End organ damage 1509 75.45%

n=2000

1509

49

15. Proportion of end organ damage, out of 2000 participants 422(21.2%) had cardiac complications,

435(21.8%) had CNS complications, 13(0.7%) had Peripheral Vascular Diseases, 604(30.2%) had renal complications and 35(1.8%) had eye complications.

1% of individuals had more than one complication.

Table 15: Distribution of various end organ damages among study population:

variables frequency Percentage

Cardiac 422 21.2%

CNS 435 21.8%

PVD 13 0.7%

Renal 604 30.2%

eye 35 1.8%

50

16. Distribution of cerebral end organ damage:

Out of 2000, 507 has cerebral end organ damage, out of 507, 435 has only CNS damage, rest 72 are having multiple end organ damages.

262(13.1%) had ischemic stroke, 222(11.1%) had hemorrhagic stroke,

23(1.2%) had other events like TIA, Encephalopathy, and PRES.

24.3%

30.2%

21.8%

21.2%

1.8% 0.7%

no EOD renal CNS cardiac eye PVD

51

Table 16: Distribution of cerebral end organ damage among study population:

variables frequency Percentage

Ischemic stroke 262 13.1%

Hemorrhagic stroke 222 11.1%

Others like TIA,

encephalopathy, PRES 23 1.2%

52%

44%

4%

n=507

ischemic stroke hemorrhagic stroke others like TIA,PRES

52

17. Echo findings among the participants:

In Echocardiogram,

715(35.8%) had Concentric LVH only,

195(9.8%) had LVH and Diastolic dysfunction, 359(18%) had systolic dysfunction.

731(36%) had normal study

Table 17: Distribution of Echocardiographic findings among study population :

variables frequency Percentage

Concentric LVH alone 715 35.8%

LVH with diastolic

dysfuction 195 9.8%

Systolic dysfunction 359 18%

Normal study 731 36%

53 0

100 200 300 400 500 600 700 800

normal conc LVH

alone LVH with diastolic dysfunction

systolic dysfunction

echo findings n=2000

echo findings n=2000

54

18. FUNDUS EXAMINATION FINDINGS AMONG THE PARTICIPANTS:

On fundus examination,

705(35.3%) showed Grade 1 retinal changes, 385(19.3%) showed Grade 2 retinal changes, 69(3.5%) showed Grade 3 retinal changes.

52 (2.6%) showed grade 4 retinopathy changes 789(29.4%) had normal fundus

Table 18: Distribution of retinal changes among study population:

Retinal changes frequency Percentage

Grade 1 705 35.3%

Grade 2 385 19.3%

Grade 3 69 3.5%

Grade 4 52 2.6%

normal 789 29.4%

55 0

100 200 300 400 500 600 700 800 900

normal grade1 grade2 grade3 grade4

fundus findings n=2000

fundus findings n=2000

56

19. RENAL FUNCTIONS AMONG THE PARTICIPANTS: N=2000 Calculated GFR based on sex, body weight, serum creatinine.

Normal – 310(15.5) – G1

Mildly decreased – 931(46.6) – G2

Mild to moderately decreased – 196(9.8) – G3A Moderate to severely decreased – 204(10.2) – G3B Severely decreased – 269(13.5) – G4

ESRD – 90(4.5) – G5

Table 19: Distribution of renal functions among study population:

Renal function frequency Percentage

G1 310 15.5%

G2 931 46.6%

G3A 196 9.8%

G3B 204 10.2%

G4 269 13.5%

G5 [ESRD] 90 4.5%

57

Totally 125(6.3%) individuals were on dialysis

0 100 200 300 400 500 600 700 800 900 1000

G1 G2 G3A G3B G4 G5

GFR among participants N= 2000

58

Inferential statistics:

1. Correlation between the systolic blood pressure at the time of diagnosis and time taken to develop complications.

Systolic blood pressure at diagnosis is taken along X axis and time taken for the complications to develop along the Y axis .both the variables are compared and analysed.

Correlation – Between SBP/MAP at diagnosis with time taken for the complications to develop.

There is no correlation between SBP at diagnosis and the time taken for

complications to develop. (Spearman’s rho ρ = -0.095)

59

2. Correlation between the mean arterial blood pressure and time taken for the complications to develop.

There is no correlation between MAP at diagnosis and the time taken for

complications to develop. (Spearman’s rho ρ = -0.078)

60

3. Correlation between the time taken to attain target BP and time taken for complications to develop.

There is no correlation between time taken to attain target BP and the time taken for complications to develop. (Spearman’s rho ρ = -0.025)

4. Correlation between the high systolic BP & complications:

Table 20: Correlation between high SBP and complications:

SBP > 180 Total

Complication at diagnosis of HTN

Yes No

Yes 553 386 939

No 161 900 1051

Out of 714 individuals with Systolic BP > 180 mm Hg, 553 individuals (77.5%) had complications at the time of diagnosis. (p <0.001)

( test)

61

5. Correlation between complications at diagnosis & smoking:

Table 21: Correlation between smoking and complications at diagnosis:

Smoking Total

Complication at diagnosis of HTN

Yes No

Yes 424 515 939

No 358 693 1051

Complications at the time of diagnosis & Smoking (p <0.001) significant

6. Correlation between complications at diagnosis and alcohol intake:

Table 22: Correlation between alcohol intake and complications at diagnosis:

Alcohol

Total

no yes

ANY

COMPLICATIONS

@ time diagnosis

No

Count 709 339 1048

%within

Alcohol 56.8% 45.7% 52.7%

Yes

Count 539 402 941

%within

Alcohol 43.2% 54.3% 47.3%

Total

Count 1248 741 1989

%within

Alcohol 100.0% 100.0% 100.0%

Complications at the time of diagnosis & Alcohol (p <0.001) significant

62

7. Correlation between complications at diagnosis and lifestyle pattern:

Table 23 : Correlation between lifestyle pattern and complications at diagnosis:

Lifestyle

Total Active Sedent

ary

ANY

COMPLICATIONS

@ time diagnosis

No

Count 574 481 1055

%within

Lifestyle 69.0% 41.3% 52.8%

Yes

Count 258 684 942

%within

Lifestyle 31.0% 58.7% 47.2%

Total

Count 832 1165 1997

%within Lifestyle

100.0

%

100.0

%

100.0

%

Complications at the time of diagnosis & type of lifestyle (p <0.001)

significant

63

8. Correlation between complications at diagnosis and gender:

Table 24: Correlation between gender and complications at diagnosis:

Gender

Total Male Female

ANY

COMPLICATIONS

@ time diagnosis

No

Count 593 462 1055

%within

Gender 51.0% 55.3% 52.8%

Yes

Count 570 374 944

%within

Gender 49.0% 44.7% 47.2%

Total

Count 1163 836 1999

%within

Gender 100.0% 100.0% 100.0%

Complications at the time of diagnosis & Gender (p = 0.059) not significant

(Not associated). Gender has no role with complications

64

9. Correlation between family history and complications at diagnosis:

Table 25: Correlation between family history and complications at diagnosis:

Family H/O essential HPN *ANY COMPLICATIONS @ time diagnosis Crosstabulation

COMPLICATIONS ANY

@ time diagnosis Total

No Yes

Family H/O essential

HPN

No

Count 663 536 1199

%within Family H/O essential

HPN 55.3% 44.7% 100.0%

Yes

Count 390 407 797

%within Family H/O essential

HPN 48.9% 51.1% 100.0%

Total

Count 1053 943 1996

%within Family H/O essential

HPN 52.8% 47.2% 100.0%

Family history and complications at time of diagnosis (p = 0.005)

significant

65

10. Correlation between Time to develop complications and life style habits such as smoking, alcohol and salt restriction:

Table 26: Correlation between life style habits and time taken to develop complications:

smokers Early development of

complications P VALUE =0.025 alcoholics Early complications 0.016

No salt restriction Early complications 0.284( not significant)

• Smoking and time to develop complications (Mann Whitney test) P = 0.025 (Significant)

• Alcohol and time to develop complications (Mann Whitney test) P=0.016 (Significant)

• SRD and time to develop complications (Mann Whitney test)

P =0.284 Not significant

66

11. Correlation between BMI and time taken to develop complications:

• BMI class and the time to develop complications (Kruskalwallis H test)

n=574

(p = 0.316) Not significant

67

12. Correlation between drug regimen and time taken for the complications to develop:

• Type of drug therapy and time to develop of complications (Kruskal Wallis test: p <0.001). After post hoc analysis, the group taking more than 3 drugs was found to be having a significantly different median time taken for the development of complications.

12.Linear regression model for time taken to develop complications.

Y= b0 + b1x1+ b2x2+ … +bnxn

Salt restriction and Family history of essential hypertension

significantly influence the time taken to develop the complications.

68

Model Unstandardized

Coefficients Standardi Coefficien zed

ts

t Sig.

B Std .

Error Beta

1 )Constant( 4.865 .744 6.540 .000

Salt restriction

diet .-383 .173 .-090 -2.211 .027

Smoking -.285 .197 -.066 -1.450 .148

Alcohol -.199 .202 -.045 -.984 .326

Lifestyle -.224 .179 -.053 -1.256 .210

antihypertensive

medications -.256 .165 -.068 -1.549 .122

drug

compliance .151 .220 .029 .685 .494

family history essential hypertensive

1.078 - .193 .-254 -5.585 .000

BMI class .027 .165 .007 .162 .871

69

13. Relation between Retinopathy and Complications:

There is a weak positive correlation between Complications at diagnosis and

the fundus examination findings. (Spearman’s rho ρ = 0.142)

70

14.Relationship of Dialysis with drug compliance / BP at diagnosis:

There is a weak negative correlation between Drug compliance and the GFR (Spearman’s rho ρ = -0.315) and between Drug compliance and Dialysis (Spearman’s rho ρ = -0.123). There is a weak negative correlation between Drug compliance and the SBP at diagnosis (Spearman’s rho ρ = -0.254).

15. Correlation between drug compliance and time taken to develop complications:

• Compliance and time taken to develop complications (Mann Whitney test) (P =0.157) Not significant

16. Correlation between the drug compliance and time taken to achieve target BP:

Compliance and time taken to achieve target BP (Mann Whitney test)

(p <0.001) Significant

71

DISCUSSION

Correlation between SBP at diagnosis and the time taken for complications to develop (Spearman’s rho ρ = -0.095) is not statistically significant.

Correlation between MAP at diagnosis and the time taken for complications to develop (Spearman’s rho ρ = -0.078) is not statistically significant. There is no correlation between time taken to attain target BP and the time taken for complications to develop. (Spearman’s rho ρ = -0.025). Correlation between high systolic BP & complications at the time of diagnosis is statistically significant. Out of 714 individuals with Systolic BP > 180 mm Hg, 553 individuals (77.5%) had complications at the time of diagnosis. (p <0.001) ( X ² test) Correlation between complications at the time of diagnosis &

Smoking habit (p <0.001) is statistically significant. Correlation between complications at the time of diagnosis & Alcohol (p <0.001) is statistically significant Correlation between complications at the time of diagnosis & type of lifestyle (p <0.001) is statistically significant.

Correlation between complications at the time of diagnosis & Gender (p = 0.059) is not significant (Not associated) - Gender has no role with complications.

Correlation between family history and complications at time of diagnosis (p

= 0.005) is statistically significant.

Correlation between smoking and time to develop complications (Mann

Whitney test)P = 0.025 is statistically significant. Correlation between alcohol

72

and time to develop complications (Mann Whitney test)P=0.016 is statistically significant.

Correlation between SRD and time to develop complications (Mann Whitney test) P =0.284 is statistically not significant. Correlation between BMI and time taken to develop complications (Kruskal Wallis H test)n=574(p = 0.316) is statistically significant Correlation between type of drug therapy and time to develop of complications (Kruskal Wallis test: p <0.001) is statistically significant. After post hoc analysis, the group taking more than 3 drugs was found to be having a significantly different median time taken for the development of complications.

Salt restriction and Family history of essential hypertension significantly influence the time taken to develop the complications.

There is a weak positive correlation between Complications at diagnosis and the fundus examination findings. (Spearman’s rho ρ = 0.142)

There is a weak negative correlation between Drug compliance and the GFR (Spearman’s rho ρ = -0.315) and between Drug compliance and Dialysis (Spearman’s rho ρ = -0.123).

There is a weak negative correlation between Drug compliance and the SBP

at diagnosis (Spearman’s rho ρ = -0.254). Correlation between compliance

and time taken to develop complications (Mann Whitney test) (P =0.157)is

statistically not significant Correlation between the drug compliance and time

taken to achieve target BP: (Mann Whitney test)(p <0.001) is statistically

73

significant. Thus, in this study we found statistically significant correlations between

1. High systolic BP at diagnosis and complications at the time of diagnosis (p<0.001)

2. Smoking and complications at the time of diagnosis (p<0.001) 3. Alcohol and complications at the time of diagnosis (p<0.001)

4. Sedentary lifestyle habits and complications at the time of diagnosis (p<0.001)

5. Family history and complications at the time of diagnosis (p<0.001) 6. Smoking and early development of complications (p=0.025)

7. Alcohol and early development of complications (p=0.016)

8. Multiple drug therapy and early development of complications (p<0.001)

9. Salt restriction in diet and family history of essential hypertension significantly influence the early development of complications

10. Drug compliance and delay in time to achieve target BP (p<0.001)

74

CONCLUSION:

In our study population of 2000, we found male preponderance (58.2%) probably due to life style habits such as smoking and alcohol.

Prevalence of complications, out of 2000 participants 422(21.2%) had cardiac complications,

435(21.8%) had CNS complications, 13(0.7%) had Peripheral Vascular Diseases, 604(30.2%) had renal complications and 35(1.8%) had eye complications.

1% of individuals had more than one complication.

In this study, various risk factors influencing the hypertension complications

were discussed. Concluding from all the data , early diagnosis and adequate

control of BP would prevent most of the complications.

75

LIMITATIONS:

1. This study was carried out in single centre, large multicentric trials should be conducted for better understanding.

2. Certain parameters like drug compliance were based on patients

history alone. Better objective evaluation is essential .