A dissertation on
A STUDY ON METABOLIC SYNDROME IN PATIENTS WITH ISCHEMIC STROKE IN A TERTIARY CARE CENTRE
COIMBATORE
Dissertation submitted to
THE TAMIL NADU Dr M.G.R. MEDICAL UNIVERSITY CHENNAI, TAMIL NADU
with partial fulfillment of the regulations required for the award of degree of
M.D. GENERAL MEDICINE BRANCH- I
COIMBATORE MEDICAL COLLEGE, COIMBATORE
April 2020
CERTIFICATE
This is to certify that this dissertation titled “A STUDY ON METABOLIC SYNDROME IN PATIENTS WITH ISCHEMIC STROKE IN A TERTIARY CARE CENTRE COIMBATORE ” has been done by Dr. LATHA PRIYA.A under my guidance.
Further certified that this work is an original, embodying study of bonafide cases.
Department of Medicine,
Coimbatore Medical College Hospital, Coimbatore
Professor and Head of the Department, Dean,
Department of Medicine, Coimbatore Medical College Hospital, Coimbatore Medical College Hospital, Coimbatore
Coimbatore
CERTIFICATE - II
This is to certify that this dissertation titled “A STUDY ON METABOLIC SYNDROME IN PATIENTS WITH ISCHEMIC STROKE IN A TERTIARY CARE CENTRE COIMBATORE ” of the candidate Dr. LATHA PRIYA.A , with registration Number – 201711309 for the award of M.D. in the branch of General Medicine I personally verified the urkund.com website for the purpose of Plagiarism Check. I found that the uploaded thesis file contains from introduction to conclusion pages and result shows 9% ( NINE) percentage of plagiarism in the dissertation.
Guide & Supervisor Sign with Seal
DECLARATION
I Dr. LATHA PRIYA.A , declare that the Dissertation titled "A STUDY ON METABOLIC SYNDROME IN PATIENTS WITH ISCHEMIC STROKE IN A TERTIARY CARE CENTRE COIMBATORE" Submitted to the Dr.MGR Medical university Guindy, Chennai, is an original work done by me during the academic period from JUNE 2018- JUNE 2019 at the Department of Medicine, Coimbatore Medical College Hospital, Coimbatore, under the guidance and direct supervision of PROF. Dr.SIVAKUMAR.K in partial fulfilment of the rules & regulations of the Dr.MGR Medical University for MD Medicine post graduate degree.
All the details of the patients, the materials and methods used are true to the best of my knowledge.
I assure that this dissertation has not been submitted to or evaluated by any other Medical University.
Dr. LATHA PRIYA.A
ACKNOWLEDGEMENT
I wish to express my sincere thanks to our respected Dean Dr. B.ASOKAN, MCh for having allowed me to conduct this study in our
hospital. I express my heartfelt thanks and deep gratitude to the Head of department of Medicine Prof Dr K. SWAMINATHAN , MD for his generous help and guidance in the course of the study.
I’m thankful to my guide PROF.DR.K. SIVAKUMAR ,M.D for his valuable help and encouragement for doing my study.
I sincerely thank all Professors, Asst Professor Dr.RAMESH M.D, Dr.YUVRAJ MURUGANANDHAM M.D, 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 back bone of this study without whom this study would have not been possible.
Last but not the least I thank my parents and relatives for having extended unconditional support throughout my life.
ABBREVIATIONS
CAD - Coronary artery disease HDL - High density lipoprotein LDL - Low density lipoprotein VLDL - Very low density lipoprotein CVD - cerebrovascular disease CRP – Creactive protein
PPAR - Peroxisome proliferator activated receptor ACA - Anterior cerebral artery
MCA - Middle cerebral artery PCA - Posterior cerebral artery
ACOM - Anterior communicating artery PCOM - Posterior communicating artery ICA - Internal carotid artery
PICA - Posterior inferior cerebellar artery TIA - Transient ischemic attack
TABLE OF CONTENTS
S.NO CONTENT PAGE NO
1 INTRODUCTION 1
2 AIM OF THE STUDY 2
3 REVIEW OF LITERATURE 3
4 MATERIALS AND METHODS 40
5 OBSERVATION AND RESULTS 42
6 SUMMARY 74
7 CONCLUSION 77
8 BIBLIOGRAPHY
9 ANNEXURES
1) PROFORMA 2) CONSENT FORM 3) MASTER CHART
LIST OF FIGURES
S.NO FIGURES PAGE NO
1 COMPONENTS OF METABOLIC SYNDROME 9
2 MOLECULAR MECHANISM IN INSULIN
RESISTANCE
13
3 INFLAMMATORY MEDIATORS IN INSULIN
RESISTANCE
15
4 TYPES OF STROKE 20
5 CLASSIFICATION OF STROKE 21
6 BRANCHES OF ANTERIOR CEREBRAL ARTERY 26
7 SEGMENTS OF ANTERIOR CEREBRAL ARTERY 27
8 BRANCHES OF MIDDLE CEREBRAL ARTERY 27
9 SEGMENTS OF MIDDLE CEREBRAL ARTERY 28
10 BRANCHES OF POSTERIOR CEREBRAL ARTERY 28
11 SEGMENTS OF POSTERIOR CEREBRAL ARTERY 29
12 CIRCLE OF WILLIS 30
13 BRANCHES OF CIRCLE OF WILLIS 31
14 ROLE OF FAST 36
15 SOURCES OF EMBOLI 37
16 COMMON SITES OF ATHEROSCLEROSIS 39
LIST OF TABLES
S.NO TABLE PAGE NO
1 Age wise distribution of ischemic stroke patients 42
2 Sex wise of ischemic stroke patients 43
3 Type of artery involved 44
4 Percentage distribution of smokers 45
5 Percentage distribution of duration of smoking 46
6 Percentage distribution of known diabetics 47
7 Percentage distribution of duration of diabetes 48 8 Percentage of known hypertensives in stroke patients 49 9 Percentage of fasting blood sugar in stroke patients 50
10 Distribution of triglycerides 51
11 Distribution of alcoholics 52
12 Distribution of blood pressure 53
13 High density lipoprotein in relation to relation to sex 54
14 Waist circumference in relation to sex 56
15 Percentage prevalence of metabolic syndrome 58 16 Percentage of stroke patients fulfilled all 5 criteria 59 17 Glasgow coma scale at the time of admission 60 18 Admission time to hospital after stroke onset 61
19 Metabolic syndrome versus sex 62
20 Fasting blood sugar in relation to sex 63
21 Relationship between triglycerides in relation to sex 64 22 Distribution of blood pressure in relation to sex 65 23 Relationship between HDL in relation to sex 66 24 Relationship between waist circumference and sex 67 25 Type of infarct and arterial territory in metabolic syndrome 68 26 Age in relation to stroke pattern and arterial territory 69 27 Distribution of known diabetics in relation to metabolic
syndrome
70
28 Distribution of smoking in relation to metabolic syndrome 71 29 Metabolic syndrome in relation to GCS at the time of
admission
72
LIST OF CHARTS
S.NO CHARTS PAGE NO
1 Age distribution 42
2 Sex distribution 43
3 Type of infarct – artery involved 44
4 Smokers 45
5 Duration of smoking 46
6 Known diabetics 47
7 Duration of diabetes 48
8 Known Hypertensives 49
9 Fasting blood sugar 50
10 Triglycerides 51
11 Alcoholic 52
12 Blood pressure 53
13 High density lipoprotein 54
14 Sex distribution of HDL 55
15 Waist circumference 56
16 Waist circumference ratio 57
17 Metabolic syndrome 58
18 ATP3 CRITERIA- all 5 criteria fulfilled 59
19 GCS on admission 60
20 Admission time to hospital 61
21 Metabolic syndrome versus sex 62
22 Fasting blood sugar versus sex 63
23 Triglycerides versus sex 64
24 Blood pressure versus sex 65
25 HDL Versus sex 66
26 Waist circumference versus sex 67
27 Metabolic syndrome versus artery involved 68
28 Age versus artery involved 69
29 Metabolic syndrome versus known diabetes 70
30 Smokers versus metabolic syndrome 71
31 GCS at admission versus metabolic syndrome 72
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INTRODUCTION
Stroke is the most common disease involving the central nervous system and one of the leading cause of death and disability in the world.
Stroke risk increases among people with sedentary lifestyle, smokers, dyslipidemia, obesity, raised blood pressure and insulin resistance in recent years.
Metabolic syndrome is a cluster of diseases like obesity, systemic hypertension, diabetes mellitus and hyperlipidemia.
It is found that metabolic syndrome is associated with high risk and early risk for stroke development especially ischemic stroke.
Diabetes is a major risk factor for stroke and prevalence of diabetes is increasing alarmingly in India leading to increased prevalence of stroke
Thus, identification and treating risk factors associated with stroke may reduce the chances the stroke events in future
Women with components of metabolic syndrome poses a double risk for ischemic events
Thus it is proposed to establish the relationship with metabolic syndrome defined by modified national cholesterol education program adult treatment panel criteria.
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AIM OF THE STUDY
1) To study the prevalence of metabolic syndrome in 100 ischemic stroke patients
2) To study the role of various metabolic syndrome components and its strength of association in causation of ischemic stroke
3) To study the association between the metabolic syndrome and ischemic stroke
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REVIEW OF LITERATURE
METABOLIC SYNDROME:
A prediabetic collection of symptom and more important risk factor of stroke compared to type 2 diabetes mellitus. “Diabetes Capital” of the world was INDIA already and projected to have highest number of individuals at the end of year 2020 suffering from atherothrombotic cardiovascular disease. This concept highlights co-occurrence of risk factors of type 2 diabetes and CAD. Epidemiological studies have confirmed that metabolic syndrome was common in ethnic groups like Caucasians, Mexican- Americans, Asian Indians, Chinese, Polynesians, afro Americans and Micronesians.
History
The term "metabolic syndrome" was introduced in 1950s, but came in existence at late 1970s to compare the risk factors with diabetes . Haller coined the term "metabolic syndrome" in 1977 for relationship between obesity, hyperlipidemia, diabetes, and hyperuricemia on atherosclerosis..
Gerald M. Reaven, in 1988 proposed insulin resistance as the underlying factor and proposed constellation of abnormalities called Syndrome X. Reaven had not included obesity as part of the condition.
Numerous synonyms were Insulin resistance syndrome, Syndrome X, Reaven's syndrome. Deadly combination includes central obesity,
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hypertension, dyslipidemia (high triglyceride and low HDL), and glucose intolerance is now a well-recognised entity. The clinical manifestations of metabolic syndrome vary in different populations such as Caucasians mainly dyslipidemia, African population mainly hypertension, Native Americans mainly hyperglycemia and South Asians show both hyperglycemia and accelerated ischemic heart disease.………..
Criteria of ATP III identified 6 components
Abdominal obesity
Atherogenic dyslipidemia
Increased blood pressure
Insulin resistance and glucose intolerance.
Pro- inflammatory state Pro- thrombotic state
ABDOMINAL OBESITY –
Very strongly linked with the metabolic syndrome clinically presented as increased waist circumference. Deficiency of leptins or resistance leads to tissue deposition of fat. This results in visceral or central deposition of fat leading to insulin resistance. Genetic factors and sex are also the main determinants with males central and females by peripheral fat distribution are more common.
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Numerous theories included are
1) “COMMON SOIL” THEORY: it describes that visceral adiposity and metabolic disorders were not causally linked, but the end-result of common genetical and environmental factors.
2) Visceral adipocytes were metabolically more active and excess adipose tissue lipolysis leading to increased plasma concentrations of free fatty acids (FFA).
3) Because of anatomical proximity to liver, metabolic products of visceral adipocytes (mainly FFA) drain via the portal venous system directly to the liver.
Excess FFA is strongly evidenced as the leading cause of insulin resistance leading to intracellular accumulation of triglycerides and fatty acid metabolites (fatty acid CoA’s, diacyl glycerol and ceramides) in the insulin responsive tissues that interferes with upstream insulin signaling events in skeletal muscle & liver. So, insulin resistance in metabolic syndrome was post-receptor in origin.
ATHEROGENIC DYSLIPIDEMIA includes - raised triglyceride level
- Decreased HDL cholesterol concentration - Normal concentrations of LDL cholesterol
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Other lipoprotein abnormalities were elevated remnant lipoproteins, elevated apolipoprotein B, small LDL particles and small HDL particles were also have atherogenic properties.
Hepatic FFA increased delivery leads to elevated triglyceride synthesis and elevated hepatic VLDL apoB-100 secretion which in turn raises the activity of cholesterol ester transfer protein (CETP) leading to increased transfer of triglyceride from VLDL to LDL and HDL for exchange with cholesterol. Those triglyceride-enriched lipoproteins were good substrates for the enzyme hepatic lipase and triglycerides leading to.………...
(i) raised HDL cholesterol clearance from blood and (ii) with formation of highly atherogenic, small, dense, LDL particles . South Asian populations showed low muscle mass and high body fat at non-obese body mass index with tendency to central fat deposition since childhood.
Elevated blood pressure - Hypertension is included as one of the metabolic risk factors. Leptins increases blood pressure by activating the sympathetic system. Hyperinsulinemia causes secondary renal sodium retention also contributes to the hypertension. blunting of the biologic effect of a potent endothelium-derived vasodilator, nitric oxide, and, increased production of vasoconstrictors such as angiotensin II leads to endothelial dysfunction.
Arachidonic acid pathway products such as Endothelin-1, cyclooxygenase and lipooxygenase is the most important mechanism involved .
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INSULIN RESISTANCE –
A physiological change in action of insulin manifested as resistance to disposal of insulin-mediated glucose. A fundamental defect which links the individual components of metabolic syndrome, although strength of association with insulin resistance to those components were variable in different populations and even within the populations. Glucose intolerance frequently manifest in long standing insulin resistance is an independent risk factor for CVD ITSELF.
Measurement of the insulin resistance-
By research, Intravenous glucose tolerance test (IVGTT) was the standard method for measuring insulin resistance ,but was impractical in clinical settings.
Previous studies had shown that fasting insulin of > 12.2 mU/L to be highly specific for insulin resistance. TGL /HDL-C concentration ratio is also an equally powerful predictor of insulin resistance.
Abnormalities associated with insulin Resistance and raised glucose.
1. Impaired fasting blood glucose & Impaired glucose tolerance
2. Abnormal uric acid metabolism- raised Plasma uric acid levels &
reduced renal clearance of uric acid.
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3. Dyslipidemia – raised triglycerides & post prandial lipemia; mreduced HDL-C & LDL
4. Hemodynamic – raised activity of sympathetic system , Blood Pressure
& Renal retention of sodium.
5. Haemostatic- raised Plasma activator inhibitor-1 & serum fibrinogen.
6. Endothelial dysfunction - elevated Mononuclear cell adhesion and Plasma concentration of asymmetric dimethyl - arginine and decreased Endothelial- dependent vasodilatation.
7. Reproductive – Poly cystic ovary syndrome
A PROINFLAMMATORY STATE - clinically recognized by raised C- reactive protein (CRP) commonly present in all persons with metabolic syndrome and is related to obesity, because of excess adipose tissue releases inflammatory cytokines leading to elevated CRP levels.
A PROTHROMBOTIC STATE - recognized by raised plasma plasminogen activator inhibitor (PAI)-1 and fibrinogen, and also associated with metabolic syndrome. So prothrombotic and proinflammatory state are interconnected metabolically.
Pathogenesis of the Metabolic Syndrome
a) Abnormal Body Fat Distribution and obesity: Obesity contributes to dyslipidemia, hyperglycemia and hypertension and thus contributing to
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metabolic syndrome risk factor. Adipose tissue excess releases several products like nonesterified fatty acids (NEFA), PAI-1,adiponectin and they overloads muscle and liver with lipids and therefore enhances insulin resistance. Elevated CRP levels and less adiponectin levels accompanying obesity signify a pro inflammatory state. Raised PAI-1 also linked to a prothrombotic state.
b) Insulin resistance
Figure 1- components of metabolic syndrome
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c) Other Contributing Factors – Advancing age - metabolic syndrome prevalence increases with age, affecting about 10 percent people in their 20s and 40 percent people in their 60s.
Race -greater risk for metabolic syndrome seen in Asians and Hispanics than other races.
3) Elevated C - Reactive protein- Elevated levels of CRP are linked to obesity and metabolic syndrome suggests that there is a strong relationship between inflammation and derangement of metabolic parameters. Studies reveal that elevated CRP increased progressively from 1.9 for those with one risk factor to 6.8 when all the ATP III criteria were present.
4) Plasminogen activator inhibitor-1 (PAI-1) is a protein from endothelial cells released into the circulation which inhibits tissue-type plasminogen activator (t-PA) leading to reduced plasmin (fibrinolysin) and thereby increases levels of circulating fibrinogen. Both PAI-1 and fibrinogen correlates with insulin level and its precursors.
5) Microalbuminuria- in both diabetic and hypertensive individuals it is an early indicator regarding metabolic syndrome, and the WHO recommendation of more than 20µg linked with the definition of microalbuminuria
6) Uric acid one of the powerful risk marker of CVD.
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7) Serum gamma - glutamyl transpeptidase, fibrinogen, factor - VIII, cytokines like IL-6 & 10, TNF-α, adhesion molecules like ICAM 1 &
VCAM.………
8) Serum homocysteine levels.
Molecular Mechanisms of Metabolic Syndrome and Possible Therapeutic Targets
Intra and intercellular signaling pathways in Metabolic syndrome has shown the involvement of various factors which are linked as potential therapeutic targets for treatment and its prevention.
Inflammation: Cytokines and Transcriptional Factors
The activation of pro inflammatory state usually associated with insulin resistance which are induced by obesity. Adipose tissue-derived factors secretion dysregulation in obese individuals play a major role in chronic inflammatory condition that are associated with obesity. Factors like adipokines such as leptins, adiponectins, resistins, retinol-binding protein 4 and visfatin and classical chemokines and cytokines like tumor necrosis factor- α. these factors are derived from adipocytes, and from macrophages, which
shows there is a overlapping features between metabolic response and immune responses. Innate immunity activation through the Toll-like receptors which are caused by raised levels of nutritional fatty acids leading to inflammation. Partial protection in toll like receptor 4 deficient animals
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against high fat diet-induced resistance of insulin contributes to reduced liver and fat inflammatory gene expression.
Inflammatory pathways are intervened by obesity leading to insulin resistance by serine kinases activation which are involved in transcription factors action such as kinase-β and Jun kinase-1, a Jun kinase isoform.
activation of these factors by several stimuli such as specific membrane receptors like proinflammatory cytokines, Toll-like receptors, and advanced glycation end productsreceptors or nonreceptor pathway which are triggered by oxidative stress. The transcription factor NF-kappa causes insulin resistance caused by increased hepatic activity of kinase activity in liver steatosis which is obesity associated contributed to increased gene expression of the cytokines like interleukin-6, tumor necrosis factor-α, and interleukin-1.insulin resistance in addition frequently results from insulin receptor substrate-1 phosphorylation, a process that are catalyzed by Jun kinase-1.A similar phosphorylating mechanism in case of b kinase has been reported along with other transcriptional factors like NF beta kinase.
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Figure 2- Molecular Mechanism in Insulin Resistance Mitochondrial Activity
Mitochondrial activity defect can lead to resistance of insulin as described recently in the elderly and in children of type 2 diabetes patients mitochondrial function impairment are linked to reduced function to cardiac and metabolic diseases.
Activation of Peroxisome Proliferator-Activated Receptor γ Receptors as a Therapeutic Target in Insulin Resistance
The molecular mechanisms which include convergent pathways that are involved in metabolic syndrome appears to be the most likely therapeutic target. The nuclear receptor peroxisome proliferator-activated receptor in this
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context is an important transcriptional regulator an the activity of which are modulated by specific agonists binding like thiazolidinediones.
The role of PPAR gamma in glucose homeostasis which are indicated by genetic studies in humans, the Pro12Ala polymorphism in the PPAR gamma gene was associated with glucose homeostasis enhancement, whereas dominant-negative mutations leading to severe resistance of insulin. In animals like mice lacking PPAR gamma were prone to develop resistance of insulin ,and a mutation that increases PPAR gamma activity which protects from insulin resistance that is obesity related.
PPAR gamma agonists enhance the action of insulin, by 2 major mechanisms, and lipid metabolism activation and inflammatory mediators reduction are involved. PPAR gamma agonists regarding metabolic action improves sensitivity of insulin by induction of gene expression that are involved in differentiation of adipocytes, lipids and glucose uptake, and storage of fatty acids. PPAR gamma agonists in addition exerts other indirect effects by regulation of several target genes like adiponectin, an insulin- sensitizing factor, or the resistin, insulin resistance inducer, which are increased or decreased by PPAR gamma activation respectively.
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Figure 3- inflammatory mediators in insulin resistance
Major anti-inflammatory actions in several systems are exerted by PPAR activation. In the setting of the MetS, because of ligands of PPAR it has been shown to reduce the inflammatory mediators production as well as tumor necrosis factor-α and tumor necrosis factor-α induced signaling in case of obesity. Anti-inflammatory actions of PPAR ligands most importantly appear to be mediated and linked by trans NF-kappa signaling repression with subsequent inflammatory gene expression reduction. LXR, additionally a different member of the nuclear receptor superfamily, has known to be target of PPAR gene. Ligands of LXR had been shown with improvement of glucose metabolism in animals and an effect which contributes to improvement on insulin sensitivity which is mediated by PPAR gamma gene.
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Clinical Criteria for Diagnosis of Metabolic Syndrome
a) EGIR criteria:………..
European Group for the Study of Insulin Resistance (EGIR) (1999) requires insulin resistance defined “ around 25% of the fasting insulin values without diabetes plus two or more criteria mentioned below”
WAIST CIRCUMFERENCE 94 CMS in males
80 cms in females
ELEVATED TRIGLYCERIDES 2.0 mmol/L
DECREASED HDL <1.0 mmol/L
ELEVATED BLOOD PRESSURE 140/90 mm Hg
ELEVATED FASTING GLUCOSE 6.1 – 7.0 mmol/L 2) NCEP ATP III CRITERIA:
RISK FACTOR DEFINING LEVEL
FASTING GLUCOSE >110 mg/dL
TRIGLYCERIDES >150 mg/dL
HDL cholesterol Men < 40 mg/dL
Women < 50 mg/Dl
BLOOD PRESSURE >130/85 mm Hg
Waist circumference Males > 40 inches Females > 35 inches
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REVISED NCEP ATP 3 CRITERIA 0CT 2005
RISK FACTOR DEFINING LEVEL
FASTING GLUCOSE >100 mg/Dl or treatment for raised glucose
TRIGLYCERIDES >150 mg/dL or treatment for raised TGL
HDL Males <40 mg/dl
Females < 50 mg/dl for low HDL WAIST CIRCUMFERENCE Males > 40 inches
Females > 35 inches
BLOOD PRESSURE >130/85 mmhg
c) World Health Organization………/……
In 1998, a World Health Organization (WHO) consultation group framed a working definition of the metabolic syndrome. A potential disadvantage was special testing of glucose status inspite of routine clinical assessment.
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Advantages:
i) each syndrome component linked to raised cardiovascular risk.
ii) B efore detection of glycaemic disorders, These features of metabolic syndrome can be present for up to 10 years.
Insulin resistance, identified by one of the following:
• Type 2 diabetes
• Impaired fasting glucose
• Impaired glucose tolerance
Plus any 2 of the following: ………
Antihypertensive medication and/or high blood pressure (140 mm Hg systolic or 90 mm Hg diastolic).
Plasma triglycerides 150 mg/dL
HDL cholesterol <35 mg/dL in men or <39 mg/dL in women
BMI >30 kg/m2 & /or waist: hip ratio >0.9 in men, >0.85 in women.
Urinary albumin excretion rate 20 microgm/min or albumin:creatinine ratio 30 mg/g
E) AHA/NHLBI………
They updated the NCEP ATP III definition & recommended that the metabolic syndrome be identified as the presence of three or more of these components.
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Elevated waist circumference:
Men — equal to or greater than 40 inches (102 cm) and Women — equal to or greater than 35 inches (88 cm)
Elevated triglycerides: Equal to or greater than 150 mg/dL
Reduced HDL (“good”) cholesterol:
Men — Less than 40 mg/dL; Women — Less than 50 mg/dL
Elevated blood pressure: > 130/85 mm Hg or use of medication for hypertension.
Elevated fasting glucose: > 100 mg/dL (5.6 mmol/L) or use of medication for hyperglycemia
F) International Diabetic Federation (IDF)
It defines metabolic syndrome as the presence of central obesity (Waist circumference > 94 cm males ;> 80cm females) + any 2 of the following 4 factors:
Raised triglyceride level (>150 mg/dl),
Reduced HDL cholesterol (< 40males; <50 females),
Raised blood pressure (>130/85 mmHg) and
Raised fasting plasma glucose (>100mg/dl).
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STROKE
World Health Organization has defined stroke as “neurological deficit of cerebrovascular cause that persists beyond 24 hours or is interrupted by death within 24 hours”
Figure 4- Classification of stroke
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Types of stroke
Figure 5- Types of stroke include: A) ischemic stroke due to build-up of atherosclerotic plaques, B) embolic stroke from blood clots that stick to plaques and break off, C) hemorrhagic stroke from bleeding into the subarachnoid space, and D) intracerebral hemorrhage from tiny vessel ruptures due to hypertension.
i) Ischemic stroke – was due to thrombosis, embolism, or systemic hypoperfusion (Watershed or Border Zone stroke), or venous thrombosis.
Ischemic stroke accounts for about 80%...
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ii) Hemorrhagic stroke – was due to intracerebral hemorrhage, subarachnoid hemorrhage, subdural hemorrhage, or epidural hemorrhage. The risk of hemorrhagic stroke quintuples in cocaine and amphetamine abuse.
Thrombotic stroke
In thrombotic stroke, around the atherosclerotic plaques a thrombus forming process develops in the affected artery that leads to gradual narrowing of the lumen of the artery and to the distal tissue , the blood flow is impeded.
Since there is gradual blockage of artery , the onset of symptomatic thrombotic strokes was slower. A occluding or non occluding thrombus itself leads to an embolic stroke if the thrombus breaks off-at which point it is then called an
"embolus.
Thrombotic stroke can be divided into two types depending on the type of involved vessel:
a) Large vessel disease - involves the common and internal carotids, vertebral artery, and the Circle of Willis. Common Causes include:
o Atherosclerosis o Dissection
o Takayasu & Giant cell arteritis
o Moyamoya syndrome &Fibromuscular dysplasia
b) Small vessel disease - involves the intracerebral arteries, branches of the Circle of Willis, middle cerebral artery, stem, and arteries arising from the distal vertebral and basilar artery.
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o Lipohyalinosis (lipid hyaline build-up due to hypertension and aging) and fibrinoid degeneration (stroke involving these vessels are known as lacunar infarcts)
o Microatheromas from the larger arteries Embolic stroke
Refers to the arterial access blockage of a part of the brain by an embolus—a traveling particle or debris in the arterial blood stream originating from elsewhere either be a blood clot or a ruptured plaque or fat (e.g., from bone marrow from a broken bone), air, an infected particle and also cancerous cells. Because the embolic blockage is sudden onset, symptoms usually are maximal at the start. And also, the symptoms may be transient as the emboli lyses and then moves to a different location or dissipates.
Common causes include
• Atrial fibrillation and Sustained atrial flutter
• Rheumatic mitral or aortic valve disease
• Bioprosthetic and mechanical heart valves\
• Atrial or ventricular thrombus or Left atrial myxoma
• Sick sinus syndrome
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• Recent myocardial infarction (within one month) & Coronary artery bypass graft (CABG) surgery
• Symptomatic congestive heart failure with ejection fraction <30 percent and Dilated cardiomyopathy
• Libman-Sacks, Infective & Marantic endocarditis Antiphospholipid syndrome
• Complex atheroma in the ascending aorta or proximal arch of aorta Systemic hypoperfusion (Watershed stroke)
Systemic hypoperfusion is the reduction of blood flow to all parts of the body including brain especially "watershed" areas --- border zone regions supplied by the major cerebral arteries. It is most commonly due to
1) cardiac pump failure from cardiac arrest or arrhythmias, or from reduced cardiac output as a result of myocardial infarction, pulmonary embolism, pericardial effusion, or bleeding.
2) Hypoxemia.
Hemorrhagic stroke
A hemorrhagic stroke, or cerebral hemorrhage occurs when a blood vessel in the brain ruptures or bleeds. This interrupts the brain's blood 8 supply and if the bleeding continues, it can cause increased intracranial pressure. In addition, blood irritates brain tissue, disrupting the delicate
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chemical balance. In this respect, hemorrhagic strokes are more dangerous than their more common counterpart, ischemic strokes.
ISCHEMIC/EMBOLIC STROKE A. ANATOMY
1. Carotid Artery distribution- carotid arteries perfuse the major part the cerebrum. Common Carotid Artery on either side divides into the Internal Carotid Artery and the External Carotid Artery and then the Internal Carotid Artery then divides into Anterior Cerebral Artery (ACA) and the Middle Cerebral Artery (MCA).
a. ACA-supplies the medial surface of the frontal lobe, parietal lobe and occipital lobe
b. MCA-the largest branch of the internal carotid artery
2. Vertebrobasilar Artery distribution-perfuses the base of cerebrum and majority of cerebellum. then, the two Vertebral Arteries joins to form the Basilar Artery. Then Branching from the Basilar Artery are the 2 Posterior Cerebral Arteries (PCA).
The posterior communicating artery is a branch of the internal carotid
artery before just it divides into its terminal branches - the anterior and middle cerebral artery. The anterior cerebral artery supplies the antero lateral portion of the circle of Willis,but does not contributed by middle cerebral artery.
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The right and left posterior cerebral arteries then arises from the basilar artery, which is formed by the union of left and right vertebral arteries.
The vertebral arteries arises from the subclavian arteries and anterior communicating artery connecting the two anterior cerebral arteries.
All the arteries that are involved give off cortical and central branches and they supply the interior of the circle of Willis and the Interpeduncular fossa.
Figure 6- branches of anterior cerebral artery
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Figure 7- segments of anterior cerebral artery
Figure 8- branches of middle cerebral artery
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Figure 9- segments of middle cerebral artery
Figure 10- segments of posterior cerebral artery
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Figure 11-branches of posterior cerebral artery
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Figure 12- circle of willis
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Figure 13- branches of circle of willis
CIRCLE OF WILLIS CLINICAL SIGNIFICANCE
The circle of Willis has the great clinical significance because of its unique structure, function, and location. As it is the connection between the anterior and posterior cerebral circulations, the circle of willis supplies the brain and protects against ischemia. But however it is one of the most common site for intracranial aneurysms. Around 85% of intracranial aneurysms occurs at the anterior circulation, either at the junction of ICA-PCom , the MCA or within ACOM. posterior circulation aneurysms are commonly located at basilar artery bifurcation or the PICA-VA junction. Aneurysms mostly likely cause symptomatic mass effect like headache or oculomotor nerve palsy. Intracranial
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aneurysms also contribute for intra-aneurysmal thrombi formation subsequently that embolize in a downstream vessel leading to distal ischemia.
A subclavian steal phenomenon therefore occurs when there was a significant stenosis or subclavian artery occlusion proximal to the vertebral artery origin. In those circumstances , blood is carried from the contralateral vertebral artery to the basilar artery and retrogradely through the ipsilateral vertebral to the subclavian artery, distal to the blockage forming a collateral flow to the arm affected. Subclavian steal syndrome demonstrates the symptoms of ischemia in posterior circulation such as vertigo or ataxia that are precipitated during exercise involving the upper extremity supplied by the subclavian artery that is stenotic.
B. CLASSIFICATION OF ISCHEMIC EVENTS 1. Transient Ischemic Attacks (TIAs)
A transient episode of temporary reduction in perfusion to a focal area of the brain leading to short-lived functional disturbance. The patient then experiences a temporary focal neurological deficit such as slurring of speech, aphasia, amaurosis fugax (monocular blindness), weakness or paralysis of a limb. The rapid onset of symptoms which is usually less than 5 minutes and duration is usually 2-15 minutes but may last up to 24 hours.
There is no neurological deficit after the attack & can last as single episode in a lifetime to more than 20 episodes in one day. Usually signifies the only warning sign of an impending stroke.
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2. Reversible Ischemic Neurological Deficit (RIND)
Focal brain ischemia in which the deficit improves over a maximum of 72 hours and deficits may not completely resolve .
3. Cerebral Infarction
Permanent neurological disorder, the patient presents with fixed neurological deficits usually presents in three forms:
1. Stable - the neurological deficit was permanent and will not improves or deteriorates.
2. Improving - return of previously lost neurological function over several days to weeks.
3. Progressive- the neurological status continues to deteriorate following the initial onset of focal deficits, may see a stabilization period, followed by further progression.
C. PATHOPHYSIOLOGY
1. plaque formation due to atherosclerosis results in narrowing or occlusion of arteries and thus predispose to formation of thrombus.
2. Aggregation of platelets
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3. a. Vessel wall injury→sub endothelium injury→ activation of platelets b. Release of ADP from activated platelets leads to aggregation of platelets.
c. platelet-plug consolidation by RBCs, coagulation factors, and fibrin network formation.
d. Thromboxane A2 (TX A2) produced by platelets and endothelium promotes aggregation of platelets and vasoconstriction.
3. Coagulation Cascade
a. is a series of enzyme complexes present on the platelet surface and endothelium leading to production of thrombin.
b. Fibrinogen to Fibrin is then converted by thrombin.
Risk Factors for Stroke
• Hypertension Diabetes mellitus
• cardiac disease importantly atrial fibrillation
• Cigarette smoking
• Transient ischemic attacks
Raised Serum Cholesterol and Lipids
• Physical inactivity
• Obesity
• Excessive alcohol intake / abuse of drugs
35
Symptoms of stroke occurs alone or in combination lasting a few minutes or several hours. When someone around you are noticed with one or more of those warning signs, should seek immediate medical attention. Poor public knowledge of warning signs and risk factors of stroke limits the effective intervention and prevention of stroke.
Sudden weakness or numbness involving face, arm or leg on one side of the body
Difficulty in speech or language understanding
Reduced or blurring of vision in one or both eyes
Severe, sudden headache
Unexplainable dizziness
If we notice the signs of a stroke, we should think "FAST" and should do the following:
Face. Ask the person to smile. Does one side of the face droop?
Arms. Ask the person to raise both arms. Does one arm drift downward?
Or is one arm unable to raise up?
Speech. Ask the person to repeat a simple phrase. Is his or her speech slurred or strange?
Time. Should Note the time when symptoms first started.
36
Figure 14- role of FAST Metabolic Syndrome and Cerebral Atherosclerosis
The risk increases for incident events of cerebral ischemia which are observed in patients of metabolic syndrome and they derive in a great part to enhance the development and progression of atherosclerotic lesions thus affecting large arteries supplying brain. insulin resistance in this setting represents a crucial factor in underlying association of Metabolic syndrome with atherosclerosis and because of this leading to cause multiple pro-athero thrombotic effects in both on the fibrinolytic system and in the vascular endothelium.31
37
FIGURE 15- sources of emboli
38
Metabolic Syndrome and Carotid Atherosclerosis
The increased prevalence of thickness of carotid intima-media and atherosclerotic plaques involving carotid artery had been shown to be higher in individuals with the Metabolic Syndrome. They are also at increased risk for carotid atherosclerosis progression and metabolic risk factors which synergize to produce atherosclerosis of carotid artery . Resistance of insulin had deleterious linked to carotid artery atherosclerosis, leading from dysfunction of endothelium to formation of plaque. Thus, interventions linked resistance of insulin reduces atherosclerosis of carotid arteries development in patients with Metabolic syndrome and patients with type 2 diabetes mellitus.
39
Figure 16- common sites of atherosclerosis
40
MATERIALS AND METHODS
The study was a cross sectional study conducted in 100 patients with ischemic stroke consisting of 65 males and 35 females admitted in general wards at the tertiary care center Coimbatore medical college hospital during the period of one year from june 2018 to june 2019.
Inclusion criteria
1. Both male and female patients of acute ischemic stroke of age group 30 to 70 years
2. Patients with no evidence of intracranial or sub arachnoid hemorrhage Exclusion criteria
1. Patients with hemorrhagic stroke.
100 cases of ischemic stroke patients with CT /MRI proven in patients with first episode of stroke were enrolled in the study
Metabolic syndrome was defined according to revised NCEP ATP 3 CRITERIA
The clinical diagnosis was made by
Eliciting detailed history from patient or their relatives
Mode of onset
41
Time of onset
Associated symptoms like head ache, vomiting ,convulsion
History of smoking and alcohol
History of hypertension, diabetes, TIA
Carotid artery and peripheral pulsations
Level of consciousness on admission
Central nervous system examination
Clinical diagnosis confirmed by CT brain
42
OBSERVATION AND RESULTS
TABLE 1- AGE WISE DISTRIBUTION OF ISCHEMIC STROKE PATIENTS
AGE IN YEARS NO OF PATIENTS PERCENTAGE
31-40 9 9%
41-50 32 32%
51-60 41 41%
61-70 18 18%
The most common age group affected by ischemic stroke patients studied was 51-60 years (41%) followed by 41-50 years (32%).
CHART 1- AGE DISTRIBUTION
31-40 41-50 51-60 61-70
43
TABLE 2 – SEX WISE DISTRIBUTION OF ISCHEMIC STROKE PATIENTS
SEX NO OF PATIENTS PERCENTAGE
MALE 65 65%
FEMALE 35 35%
Out of 100 ischemic stroke patients studied, 65 % were males and 35%
were females.
65%
35%
CHART 2- SEX DISTRIBUTION
MALE FEMALE
44
TABLE 3- TYPE OF INFARCT – ARTERY INVOLVED TYPE OF INFARCT NO OF PATIENTS PERCENTAGE
MCA 76 76%
PCA 21 21%
ACA 3 3%
MCA- Middle cerebral artery PCA- Posterior cerebral artery ACA- Anterior cerebral artery
Most common arterial territory involved in our study was MIDDLE CEREBRAL ARTERY (76%) followed by posterior cerebral artery (21%) followed by anterior cerebral artery ( 3%)
76%
21%
3%
CHART 3- TYPE OF INFARCT - ARTERY INVOLVED
MCA PCA ACA
45
TABLE 4 –PERCENTAGE DISTRIBUTION OF SMOKERS
SMOKER NO OF PATIENTS PERCENTAGE
YES 56 56%
NO 44 44%
None of the females in our study had the habit of smoking. Out of 100 ischemic stroke patients studied , 56 % were smokers and 44% were non smokers. Out of 65 male patients studied , 56 % were smokers.
56
44
YES NO
CHART 4 - SMOKERS
46
TABLE 5- PERCENTAGE DISTRIBUTION OF DURATION OF SMOKING
DURATION OF SMOKING NO OF PATIENTS PERCENTAGE
< 10 YRS 5 9%
> 10 YRS 51 91%
Out of 56 smokers with ischemic stroke, 91% ( 51) patients had duration of smoking more than 10 years and 9% ( 5) patients had duration of smoking less than 10 years.
< 10 YRS > 10 YRS
5
51
CHART 5- DURATION OF SMOKING
47
TABLE 6 –PERCENTAGE DISTRIBUTION OF KNOWN DIABETES MELLITUS
KNOWN DM NO OF PATIENTS PERCENTAGE
YES 65 65%
NO 35 35%
OUT of 100 ischemic stroke patients studied, 65 % of patients were known diabetics and 35 % were not a known diabetics.
YES NO
65
35
CHART 6- KNOWN DIABETICS
48
TABLE 7- PERCENTAGE DISTRIBUTION OF DURATION OF DIABETES
DURATION OF DIABETES NO OF PATIENTS PERCENTAGE
< 5 YRS 18 28%
> 5YRS 47 72%
Out of 56 % of ischemic stroke patients with known history of diabetes studied , 72% had history of diabetes for more than 5 years duration and 28%
had history of diabetes less than 5 years duration.
28%
72%
CHART 7 - DURATION OF DIABETES
< 5 YRS > 5YRS
49
TABLE 8- PERCENTAGE OF KNOWN HYPERTENSIVES IN STROKE PATIENTS
KNOWN HT NO OF PATIENTS PERCENTAGE
YES 49 49%
NO 51 51%
Out of 100 ischemic stroke patients studied, 49% were known hypertensives and 51% were not a known hypertensives.
49%
51%
CHART 8 -KNOWN HYPERTENSIVES
YES NO
50
TABLE 9 – PERCENTAGE OF FASTING BLOOD SUGAR IN STROKE PATIENTS
FASTING BLOOD SUGAR NO OF PATIENTS PERCENTAGE
> 100 74 74%
< 100 26 26%
Out of 100 ischemic stroke patients studied , 74 % patients had FBS more than equal to 100 mg/dl, whereas 26 % patients had FBS less than 100mg/dl.
74%
26%
CHART 9 -FASTING BLOOD SUGAR
> 100 < 100
51
TABLE 10- DISTRIBUTION OF TRIGLYCERIDES
TRIGLYCERIDES NO OF PATIENTS PERCENTAGE
> 150 78 78%
< 150 22 22%
Out of 100 patients studied, 78% had triglycerides more than or equal to 150 mg/dl whereas 22% had less than 150 mg/dl.
78
22
> 150 < 150
CHART 10
TRIGLYCERIDES
52
TABLE 11- DISTRIBUTION OF ALCOHOLICS IN STROKE PATIENTS
ALCOHOLIC NO OF PATIENTS PERCENTAGE
YES 47 47%
NO 53 53%
Out of 100 patients, 47% of ischemic stroke patients were alcoholics and 53
% were non alcoholics.
YES NO
47
53
CHART 11- ALCOHOLIC
53
TABLE 12- BLOOD PRESSURE DISTRIBUTION IN STROKE PATIENTS
BLOOD PRESSURE NO OF PATIENTS PERCENTAGE
> 130/85 64 64%
< 130/85 36 36%
Out of 100 patients studied, 64% of ischemic stroke patients had blood pressure more than or equal to 130/85mm hg whereas 36 % of patients had blood pressure less than 130/85 mm hg
> 130/85 < 130/85 64
36
CHART 12- BLOOD PRESSURE
54
TABLE 13 – HIGH DENSITY LIPOPROTEIN IN RELATION TO SEX
HDL MALES FEMALES
NORMAL 17 7
LOW 48 28
24%
76%
CHART 13- HIGH DENSITY LIPOPROTEIN
NORMAL LOW
55
Out of 65 male patients studied, 48 patients had high density lipoprotein less than 40 mg/dl.
Out of 35 female patients studied, 28 patients had high density lipoprotein less than 50 mg/dl.
So, out of 100 patients , 76% had low HDL levels and 24% had normal HDL levels
48
28 17
7
MALE FEMALE
SEX
CHART 14- SEX WISE DISTRIBUTION OF HDL
LOW NORMAL
56
TABLE 14- WAIST CIRCUMFERENCE IN RELATION TO SEX
WAIST CIRCUMFERENCE
MALES (>40 INCHES)
FEMALES (>35 INCHES)
NORMAL 25 10
HIGH 40 25
40
25 25
10
MALE FEMALE
SEX
CHART 15- WAIST CIRCUMFERENCE
HIGH NORMAL
57
Out of 65 male patients studied, 40 patients had waist circumference more than 40 inches.
Out of 35 female patients studied, 25 patients had waist circumference more than 35 inches.
So, out of 100 ischemic stroke patients studied, 65% patients had high waist circumference and 35 % had normal range.
35%
65%
CHART 16-WAIST CIRCUMFERENCE
NORMAL HIGH
58
TABLE 15- PERCENTAGE PREVALENCE OF METABOLIC SYNDROME IN STROKE PATIENTS
METABOLIC SYNDROME NO OF PATIENTS PERCENTAGE
PRESENT 80 80%
ABSENT 20 20%
Out of 100 ischemic stroke patients studied, 80% patients had metabolic syndrome and 20% were non-metabolic.
80%
20%
CHART 17- METABOLIC SYNDROME
PRESENT ABSENT
59
TABLE 16- PERCENTAGE OF STROKE PATIENTS WHO FULLFILLED ALL 5 CRITERIA OF METABOLIC SYNDROME
FULFILLED ALL 5 CRITERIA OF METABOLIC SYNDROME
NO OF PATIENTS PERCENTAGE
YES 45 45%
NO 55 55%
Out of 80 patients with metabolic syndrome, 45 % patients fulfilled all the 5 criteria of metabolic syndrome.
45
55
YES NO
CHART 18- ATP 3 CRITERIA- ALL 5
CRITERIA FULFILLED
60
TABLE 17- GLASGOW COMA SCALE OF STROKE PATIENTS AT THE TIME OF ADMISSION
GCS ON ADMISSION NO OF PATIENTS PERCENTAGE
MILD >13 27 27%
MODERATE 9-12 47 47%
SEVERE <8 26 26%
At the time of admission to our hospital, 47% patients presented with ischemic stroke had moderate GCS( 9-12 ) followed by 27% patients had mild GCS (>13) followed by 26 % patients had severe GCS ( <8)
27%
47%
26%
CHART 19- GCS ON ADMISSION
MILD MODERATE SEVERE
61
TABLE 18- ADMISSION TIME TO HOSPITAL AFTER ONSET OF STROKE SYMPTOMS
ADMISSION TIME TO HOSPITAL
NO OF PATIENTS
PERCENTAG E
< 6 HRS 27 27%
6-24 HR 54 54%
> 24 HR 19 19%
Out of 100 patients studied , 54% patients were admitted in hospital in 6 to 24 hrs of initiation of stroke followed by 27 % patients were admitted within 6 hrs duration followed by 19 % patients were admitted after 24 hrs of onset of
stroke.
27%
54%
19%
CHART 20- ADMISSION TIME TO HOSPITAL
< 6 HRS 6-24 HR > 24 HR
62
TABLE 19- METABOLIC SYNDROME VS SEX
out of 65 male patients, 51 male patients had metabolic syndrome , 14 patients were non metabolic and out of 35 female patients , 29 female patients had metabolic syndrome and 6 patients were non metabolic.
51
29 14
6
MALE FEMALE
SEX
CHART 21- METABOLIC SYNDROME VS SEX
PRESENT ABSENT
METABOLIC SYNDROME
SEX
MALE FEMALE
PRESENT 51 29
ABSENT 14 6
CHI SQUARE TEST P VALUE - 0.001
SIGNIFICANT
63
TABLE 20- FASTING BLOOD SUGAR IN RELATION TO SEX
FASTING BLOOD SUGAR
SEX
MALE FEMALE
> 100 45 29
< 100 20 6
CHI SQUARE TEST P VALUE - 0.138 NON SIGNIFICANT
45 male patients had FBS >100 mg/dl and 29 female patients had FBS < 100 mg/dl.
45
29 20
6
MALE FEMALE
SEX
CHART 22- FASTING BLOOD SUGAR VS SEX
> 100 < 100
64
TABLE 21- RELATIONSHIP BETWEEN TRIGLYCERIDES IN RELATION TO TRIGLYCERIDES
TRIGLYCERIDES
SEX
MALE FEMALE
> 150 49 29
< 150 16 6
CHI SQUARE TEST P VALUE - 0.390 NON SIGNIFICANT
49 male patients had triglycerides > 150 mg/dl and 29 female patients had triglycerides <150 mg/dl.
MALE FEMALE
SEX 49
29 16
6
CHART 23- TGL VS SEX
> 150 < 150
65
TABLE 22- DISTRIBUTION OF BLOOD PRESSURE IN RELATION TO SEX
BLOOD PRESSURE
SEX
MALE FEMALE
> 130/85 40 24
< 130/85 25 11
CHI SQUARE TEST P VALUE - 0.484 NON SIGNIFICANT
40 male patients had blood pressure more than 130/85 mm Hg and 24 female patients had blood pressure more than 130/85 mm Hg. P value non significant
MALE FEMALE
SEX 40
25 24
11
CHART 24- BLOOD PRESSURE VS SEX
> 130/85 < 130/85
66
.TABLE 23- RELATIONSHIP BETWEEN HDL IN RELATION TO SEX
DL
SEX
MALE FEMALE
LOW 48 28
NORMAL 17 7
CHI SQUARE TEST P VALUE - 0.492 NON SIGNIFICANT
48 male patients with ischemic stroke had HDL less than 40 mg/dl whereas 28 female patients with ischemic stroke had HDL less than 50 mg/dl. P value non significant.
48
28 17
7
MALE FEMALE
SEX
CHART 25- HDL VS SEX
LOW NORMAL
67
TABLE 24- RELATIOSHIP BETWEEN WAIST CIRCUMFERENCE AND SEX
WAIST CIRCUMFERENCE
SEX
MALE FEMALE
HIGH 40 25
NORMAL 25 10
CHI SQUARE TEST P VALUE - 0.323 NON SIGNIFICANT
40 male stroke patients had waist circumference more than 40 inches and 25 female stroke patients had waist circumference more than 35 inches. P value non significant.
40
25 25
10
MALE FEMALE
SEX
CHART 26- WAIST CIRCUMFERENCE VS SEX
HIGH NORMAL
68
TABLE 25- TYPE OF INFARCT AND ARTERIAL TERRITORY IN RELATION TO METABOLIC SYNDROME
TYPE OF INFARCT
METABOLIC SYNDROME
PRESENT ABSENT
MCA 60 16
PCA 19 2
ACA 1 2
KRUSKAL WALLIS TEST P VALUE - 0.062 NON SIGNIFICANT
Middle cerebral artery (60 patients) is the most commonly involved artery in stroke patients with metabolic syndrome followed by posterior cerebral artery (19 patients) followed by anterior cerebral artery (1 patient). P value non significant.
60
19 16
1 2 2
PRESENT ABSENT
METABOLIC SYNDROME
CHART 27- METABOLIC SYNDROME VS ARTERY INVOLVED
MCA PCA ACA
69
TABLE 26- AGE IN RELATION TO STROKE PATTERN AND ARTERIAL TERRITORY INVOLVED
AGE IN YRS
TYPE OF INFARCT
MCA PCA ACA
31-40 4 2 3
41-50 20 12 0
51-60 35 6 0
61-70 17 1 0
KRUSKAL WALLIS TEST P VALUE - 0.001
SIGNIFICANT
Middle cerebral artery was most commonly affected artery and involved in age group of 51-60 years followed by age group of 41-50 years .The next commonly affected artery is posterior cerebral artery in 41 -50 years age group . ( P value is significant)
4 2 3
20
12
0 35
6
0 17
1 0
MCA PCA ACA
TYPE OF INFARCT
CHART 28- AGE VS ARTERY INVOLVED
31-40 41-50 51-60 61-70
70
TABLE 27- DISTRIBUTION OF KNOWN DIABETICS IN RELATION TO METABOLIC SYNDROME
KNOWN DM
METABOLIC SYNDROME
PRESENT ABSENT
YES 54 11
NO 26 9
CHI SQUARE TEST P VALUE - 0.295 NON SIGNIFICANT
54 ischemic stroke patients who were known diabetics, had metabolic syndrome and 11 ischemic stroke patients who were known diabetics were non metabolic. ( p value non significant)
54
11 26
9
PRESENT ABSENT
METABOLIC SYNDROME
CHART 29- METABOLIC SYNDROME VS KNOWN DM
YES NO
71
TABLE 28- DISTRIBUTION OF SMOKING IN RELATION TO METABOLIC SYNDROME
SMOKER
METABOLIC SYNDROME
PRESENT ABSENT
YES 45 11
NO 35 9
CHI SQUARE TEST P VALUE - 0.920 NON SIGNIFICANT
45 male smokers with ischemic stroke had metabolic syndrome and 11 male smokers with ischemic stroke were non metabolic.( P value non significant)
45
11 35
9
PRESENT ABSENT
METABOLIC SYNDROME
CHART 30- SMOKER VS METABOLIC SYNDROME
YES NO
72
TABLE 29 - METABOLIC SYNDROME IN RELATION TO GCS AT THE TIME OF ADMISSION
GCS
METABOLIC SYNDROME
PRESENT ABSENT
MILD 10 17
MODERATE 45 2
SEVERE 25 1
KRUSKAL WALLIS TEST P VALUE - 0.001
SIGNIFICANT GCS- GLASGOW COMA SCALE
MILD - >13
MODERATE- 9-12 SEVERE- <8
10
17 45
2 25
1
PRESENT ABSENT
METABOLIC SYNDROME
CHART 31- GCS AT ADMISSION VS METABOLIC SYNDROME
MILD MODERATE SEVERE
73
Out of 80 ischemic stroke patients with metabolic syndrome studied ,45%
had moderate GCS , 25 % had severe GCS and 10% had mild GCS at the time of admission (P value significant) whereas in non metabolic stroke patients 17 % had mild GCS , 2% had moderate GCS and 1% had severe GCS.
SO, most of the stroke patients with metabolic syndrome had moderate to severe GCS at time of admission compared to non metabolic stroke patients.
