A STUDY OF 2D ECHO CHANGES IN ASYMPTOMATIC TYPE 2 DIABETES

MELLITUS PATIENTS IN A TERITARY CARE HOSPITAL

BY

DR.G.RASHMI

DISSERTATION SUBMITTED TO
KALOJI NARAYANA RAO UNIVERSITY OF HEALTH SCIENCES
WARANGAL, TELANGANA

FOR AWARD OF MD DEGREE IN GENERAL MEDICINE

Under The GUidance Of
DR.SIVA SUBRAMANYAM, MD (gen.med.)

MNR MEDICAL COLLEGE AND HOSPITAL

FASALWADI, SANGAREDDY DIST., (TELANGANA)
2023-2024

DECLARATION BY THE CANDIDATE

I hereby declare that this dissertation/thesis entitled “A STUDY OF 2D ECHO CHANGES IN

ASMPTOMATIC TYPE 2 DIABETES MILLITUS PATIENTS IN A TERITARY CARE

HOSPITAL” is a bonafide research work done by DR.G.RASHMI.under the guidance of Dr.

SIVA SUBRAMANYAM Professor in the Deptartment of General medicine, MNR Medical

College and Hospital, Fasalwadi, Sangareddy.

Date:

Place: SANGAREDDY DR.G.RASHMI

ACKNOWLEDGMENT
I am grateful to the Professor and Head of the Department, Dr Narayana for permitting me to do

this thesis. I also express my deep sense of regard and gratitude to my guide, Dr. SIVA

SUBRAMANYAM for his valuable suggestions, guidance and encouragement throughout the

course of thesis.

I am thankful to assistant professors Dr. Shafee, Dr. Sanjay, Dr. Chaitanya for their kind help &

continuous support in doing this dissertation.

I thank my colleagues, juniors and friends in the department for their co-operation, support and

ever available assistance.

I am grateful to all my patients, who have submitted themselves to the study for their kind co-

operation.

DR.G.RASHMI

CERTIFICATE BY THE GUIDE

This is to certify that the dissertation “A STUDY OF 2D ECHO CHANGES IN

ASYMPTOMATIC TYPE 2 DIABETES MELLITUS PATIENTS IN A TERTIARY

CARE HOSPITAL” is a bonafied work of DR.G. RASHMI done in the Department of general

medicine, MNR Medical College And Hospital, Fasalwadi, Sangareddy under my supervision

and guidance in partial fulfilment of the regulation laid down by Kaloji Narayana Rao University

of Health Sciences for M.D., (GENERAL MEDICINE) degree examination to be held in April –

2024.

Sangareddy DR.SIVA SUBRAMANYAMM.D.Gen.Med

Date: Prof. in Department of General medicine

MNR MEDICAL COLLEGE AND HOSPITAL
WARANGAL

ENDORSEMENT BY THE H.O.D, PRINCIPAL

This is to certify that the dissertation entitled “A STUDY OF 2D ECHO CHANGES IN

ASYMPTOMATIC TYPE 2 DIABETES MILLITUS PATIENTS IN A TERITARY CARE

HOSPITAL” is a bonafied research work done by DR.G.RASHMI under the guidance of DR.

SIVA SUBRAMANYAM M.D, professor, Department of general medicine, MNR Medical

College and Hospital, Fasalwadi, Sangareddy.

DR. Dr., PROFESSOR & HOD

PRINCIPAL, DEPT OF GEN MEDICINE

MNR MEDICAL COLLEGE AND HOSPITAL

Date:

Place: SANGAREDDY
APPROVAL OF ETHICS COMMITTEE
 COPY RIGHT DECLARATION BY CANDIDATE

I hereby declare that Kaloji Narayana Rao University of Health Sciences, Warangal,

Telangana shall have the rights to preserve, use and disseminate this dissertation/thesis in print

or electronic format for academic/research purpose.

Date:

Place: SANGAREDDY DR.G.RASHMI

@ Kaloji Narayana Rao University of Health Sciences, Warangal, Telangana

 TABLE OF CONTENTS

S.NO. TOPIC PAGENO.

PART-I

1. INTRODUCTION 1

2. AIMSANDOBJECTIVESOFSTUDY 7

3 REVIEWOFLITERATURE 11

4. MATERIALANDMETHODS 42

5. RESULTSANDOBSERVATIONS 44

6. PREVIOUSSTUDIES 49

7. DISCUSSION 52

8. CONCLUSIONS&SUMMARY 55

9. BIBLIOGRAPHY 57

10. MASTERCHART 61

11. ANNEXURE (PROFORMA&ABBREVIATIONS) 65

 TABLES AND CHARTS

Table;1–IndianDiabeticRiskScore[IDRS]

Table;2 – Dipstick staging of proteinuria

Table;3-CorrelationofHbA1Cwithaveragebloodglucose
CHARTS

Chart;1–Sexdistributioninourstudygroup

Chart;2 -Treatment
 INTRODUCTION

Diabetes is one of the most important public health problems among non communicable

diseases.

Globally, prevalence of diabetes is steadily increasing and the total number of diabetic people

expected to be around 600 million people by 2030. In the year 2021, it is estimated that 537

million people had diabetes, which is projected to reach 643 million by 2030, and 783 million by

2045.

Diabetes causes 1.5 million deaths every year and additional 2.2 million deaths were attributed to

individuals having higher than optimal blood glucose, also prevalence of undiagnosed heart

failure is common among type 2 Diabetes mellitus patients. Thus, Type 2 DM patients are prone

for increased cardiovascular risk.

Cardiovascular disease accounts for up to 80% of the excess mortality in patients with type 2

diabetes.

The increased cardiovascular mortality risk in type 2 diabetic patients includes generalized

microvascular disease, coronary atherosclerosis, and autonomic neuropathy.

Apart from these, myocardial abnormalities (‘diabetic cardiomyopathy’) and heart failure also

plays an important role in the mortality risk.

In general, undiagnosed case of heart failure is common among type 2 diabetes patients
The cardiac changes in the diabetic patients are increased myocardial thickening (fibrosis) which

predominantly manifests in the form of diastolic dysfunction defined as the diabetic

cardiomyopathy. Diastolic dysfunction has been reported in many studies among these patients.

Type 2 diabetes mellitus patients are more prone for the increased cardiovascular risk.

Prevalence of left ventricular Diastolic Dysfunction in Type 2 DM who are asymptomatic,

normotensive patients with or without CAD is much higher.

By early detection of these changes by echocardiography, it will help in treating these patients

accordingly thereby reducing the cardiovascular mortality risk in these patients. So, in our study,

type 2 diabetes mellitus patients will be screened with echocardiography for early diagnosis of

myocardial changes and cardiac dysfunction.

 AIM OF THE STUDY

To determine the echocardiographic abnormalities in type 2 diabetes mellitus

patients with no cardiovascular complaints attending MNR hospital, Sangareddy.

 REVIEW OF LITERATURE

Diabetes mellitus refers to a group of common metabolic disorders that share the phenotype of

hyperglycemia.

Persons with diabetes are at increased risk for cardiovascular disease, which is the main cause of

morbidity and mortality in this population.

TYPES OF DIABETES: [9]

• Type 1 diabetes – Presents at younger age

- Genetic Susceptibility (HLA complex on Chr.6)

- Absolute insulin deficiency - A) Immune mediated

B) Idiopathic

• Type 2 diabetes - Insulin insensitivity of tissues with relative insulin deficiency

- Insulin secretory defect with insulin resistance

• Gestational diabetes

• Other types[9]

A) Mutations in genes of Beta cell function/ development

➢ Hepatocyte nuclear transcription factor (HNF)4α (MODY 1)

➢ Glucokinase (MODY 2)

➢ HNF-1 α (MODY 3)

➢ Insulin promoter factor-1 ((MODY 4)

➢ HNF-1 β (MODY 5)
 ➢ NeuroD1 (MODY 6)

➢ Pro-insulin or insulin

➢ Mitochondrial DNA

➢ Subunits of ATP-sensitive Potassium channel

➢ Other pancreatic islet proteins/regulators such as PAX4, BLK, KLF 11, SLC2A2, GATA 4,

GATA 6, RFX6, GLIS3

B) Genetic defects of Insulin action

➢ Leprechaunism

➢ Type A insulin resistance

➢ Lipodystrophy syndromes

➢ Rabson - Mendenhall syndrome

C) Exocrine Pancreas Disease

➢ Pancreatitis

➢ Cystic fibrosis

➢ Hemochromatosis
D) Endocrinopathies

➢ Cushing’s syndrome

➢ Acromegaly

➢ Glucagonoma

➢ Hyperthyroidism

➢ Pheochromocytoma

➢ Aldosteronism

E) Chemical/Drug induced

➢ Glucocorticoids

➢ Pentamidine, thiazides, anti-psychotics

➢ β agonists, calcineurin and mTOR inhibitors

F) Infections

➢ Congenital rubella

➢ CMV, Coxsackie virus

G) Uncommon forms of Immune-mediated disease

➢ Stiff person syndrome

➢ Anti- insulin receptor antibodies

H) Other genetic syndromes associated with DM

➢ Down’s syndrome

➢ Klinefelter syndrome

➢ Wolfram syndrome
EPIDEMIOLOGY :
Diabetes was found to be the seventh leading cause of death by WHO in 2016. Likewise the

worldwide prevalence of diabetes among people over 18 years of age has been raised from 4.7% (1980)

to 8.5% (2014)[10]. The prevalence has been raised rapidly in low-income and middle economic

countries. Diabetes mellitus is 9th leading cause of mortality globally in 2020. By 2030, 643 million people

would be affected worldwide. India has 100 million people ( 1 in 10 Indians) diagnosed with diabetes. In

2020, 7,00,000 Indians of diabetes died due to complications such as kidney disease, heart disease etc.

In India, diabetes is found to be high in southern part and in urban areas. Increasing urbanization,

Dietary changes, ageing population, reduced physical activity and unhealthy behaviour were found to

be the rapid, social and cultural changes causing increased occurrence of diabetes. Cardiovascular

disease remains a leading cause of morbidity and mortality. Diabetics have 2 to 4 times increased risk of

cardiovascular disease. Early diagnosis and appropriate treatment of diabetes will result in more

cardiovascular event free life years. Cardiovascular deaths account for 44% death in those with Type 1

DM and 52% of deaths in Type 2 DM.

RISK FACTORS:

TYPE 1 DM:
• Family H/O

• Environmental factors

 Exposure to some viral infections

TYPE 2 DM:
• Family H/O of diabetes

• Unhealthy diet

• Physical inactivity

• Overweight (BMI ≥ 25 kg/m2 )

• High blood pressure

 • Increasing age

• Ethnicity/ Race

• H/o of gestational diabetes or delivery of big baby

• Poor nutrition during pregnancy

• PCOD

• Acanthosis nigricans

• Metabolic syndrome

• H/o CVD

• Triglyceride level > 250 mg/dl, HDL cholesterol < 35 mg/ dl

• Impaired glucose tolerance (IGT) [12

PATHOGENESIS

There are eight distinct patho-physiologic abnormalities which is associated with type

2 diabetes mellitus (T2DM). The insulin resistance is characterized by decreased peripheral glucose

uptake and also increased glucose production and there by hyperglycemia and high circulating insulin

levels. The insulin resistance further causes increased lipolysis, leading to increased free fatty acid levels

and intermediary lipid metabolites in blood contributes to a further increase in glucose production

endogenously, a reduction in peripheral glucose utilization and impaired beta-cell function in long run.

As the beta-cell function of pancreas is well decreased at this stage, it won’t able to maintain normal

plasma glucose levels by compensatory insulin secretion and again progressively worsens over time.

Concomitantly, pancreatic alpha-cells produces glucagon inappropriately, particularly in the post-

prandial period. It has been said that both impaired insulin and increased glucagon secretion in T2DM

are due to the gastrointestinal incretin hormones deficiency primarily as inadequate release or

response to food intake. Hypothalamic insulin resistance (central nervous system) also decrease the
ability of insulin to suppress glucose production, and renal tubular glucose reabsorption capacity may be

increased despite hyperglycemia in T2DM. These pathophysiologic abnormalities should be taken into

account for the treatment of patients with T2DM [13] . Ultimately the main pathophysiology in T2DM

are mainly due to insulin resistance, hyperinsulinemia and glucose toxicity [14] . Impaired glucose

homeostasis, altered metabolic status, impaired energy production and accumulations of advanced

glycation end products and oxidative stress and endothelial dysfunction form the some of the

postulating mechanisms in the pathogenesis of diabetic cardiomyopathy [15].

SCREENING FOR DM
American diabetes association provided guidelines to screen a asymptomatic adults for testing

prediabetes and diabetes. Testing for pre-diabetes and diabetes should be done in all individuals who

are over-weighted (BMI ≥ 25 kg/ m2 ) and having additional risk factors. In the absence of those risk

factors, screening should be done in all individuals of age > 45 years. Even if they are negative for pre-

diabetes and diabetes screening should be done at-least every three years of interval.

GLYCOSYLATED HEMOGLOBIN
The term glycation means adding of sugar residue to an - NH2 group of a protein

molecule. Glycation will also occur in hemoglobin, membrane protein and lens protein. In HbA1c,

glycation occurs in each beta chain on N- terminal valine residue. HbA1c provides a retrospective index

of blood glucose level over a period of 6 – 8 weeks. It is a reliable indicator of diabetic control over past

90 days, treatment effectiveness and the risk of development of short and long –term complications.

HbA1c values & interpretations:

• Risk of Hypoglycaemia: < 4.5%

• Non-diabetic range: 4.5 - 5.8%

 • Pre-diabetic range: 5.8 - 6.5%

• Diabetic range: > 6.5%

CONDITIONS WHICH GIVES TO FALSE ELEVATION / REDUCTION OF HbA1c:

• Hereditary persistence of fatal Hb

• Hemoglobinopathies (Thalassemia)

• Uraemia

GUIDELINES FOR ONGING, COMPREHENSIVE MEDICAL CARE FOR DIABETIC

PATIENTS:
➢ Glycaemic control targets should be optimized and individualized by frequent blood glucose testing –

every 2 weeks in uncontrolled patients until target glycaemic value is attained and every 3 months

in controlled patients (HbA1c < 7%)

➢ Self-monitoring of blood glucose with individualized frequency is advised.

➢ HbA1c should be done every 3 months in uncontrolled diabetic patients and every 6 months to 1
year (ie., 2- 4 times/ year)

➢ Fundus examination should be done in the first visit itself and every 1- 2 years during follow-up.

➢ Screening for diabetic kidney disease using urine micro-albumin and serum creatinine annually.

➢ Foot examination for neuropathy should be done daily by the patient themselves, at-least 1- 2 times/
year by physician.

➢ Blood pressure measurement should be done every quarterly.

➢ ECG should be done annually.

➢ Treadmill test have to done five years after diagnosing diabetes mellitus, later at-least once in two
years.

➢ Lipid profile should be done annually, if abnormal then it is done every 6 months.

➢ Prophylactic anti-platelet therapy should be considered based on the individuals.

➢ Patient education regarding diabetes management should be given annually.

➢ Medical nutrition education and therapy must be done annually.

TREATMENT GOALS FOR ADULT DM PATIENTS:

Goals should be individualized for every patient. Goals may be differing for certain patient

population depending on geographic distribution, genetic inheritance and dietary habits. The

recommendations by American Diabetic Association[16] are :

COMPLICATIONS :
There are many complications in patients with T2DM depending on various factors such as

dietary habits, associated lifestyle, smoking, alcoholism, other metabolic diseases. Apart from these,

complications depend on duration of T2DM, hyperglycemia and hyperinsulinemia. The complications

may be classified into acute and chronic complications.

Acute complications are mainly

• Hypoglycaemia

• Hyperglycaemia- hyperosmolar non ketonic coma, diabetic ketoacidosis.

CHRONIC COMPLICATIONS

Chronic complications mainly due to vascular (micro-vascular & macrovascular) and

metabolic changes because of long duration of hyper-glycemia and due to secondary factors, such as

hypertension, hyper - lipidemic and sedentary life style habits. These causes the functional alterations

progress to early structural changes in many organs. When the early changes once set in, progression to

irreversible damage and end stage depends on various factors apart from hyperglycemia.

MICROVASCULAR:
EYE:

• Macular oedema

• Retinopathy (Proliferative / non – proliferative)

• Glaucoma

• Cataract

NEPHROPATHY (Declining Renal function) :

• Diabetic kidney disease

NEUROPATHY :

• Diabetic peripheral neuropathy

• Autonomic neuropathy

MACROVASCULAR
Cardiac complications:

1. Coronary artery disease

2. Small vessel disease

3. Diabetic cardiomyopathy

4. Heart failure

5. Cardiac autonomic neuropathy.

OTHERS:
Gastrointestinal:

• Gastroparesis,

• Nocturnal diarrhea

Genitourinary:

• Cystopathy,

• Female sexual dysfunction

Infections – Possess high risk for Gram negative organism, M. tuberculosis, S. aureus, Candida spp

Dermatologic complications

• Xerosis, Pruritus

• Pigmented periorbital papules,

• Bullous disease,
 • Necrobiosis lipoidica diabeticorum,

• Acanthosis nigricans, Lipoatrophy

Cheiroarthropathy

Hearing loss, Periodontal disease etc.

DIABETIC HEART DISEASE

Cardiac disease that develops as a direct consequence of diabetes mellitus in patients with type
1 and type 2 diabetes is known as Diabetic Heart Disease. It consists of

1) Coronary artery disease

2) Cardiac autonomic neuropathy

3) Diabetic cardiomyopathy

These diseases are characterized by molecular, structural and functional changes in the
myocardium.

Coronary artery disease is the most recognized cardiac complication of diabetes.

Autonomic neuropathy and Diabetic cardiomyopathy although common, are often undiagnosed

complications with devastating consequences and increased mortality.

CARDIAC AUTONOMIC NEUROPATHY :

It is associated with impairment of autonomic control of the cardiovascular system and is a

major cause of silent cardiovascular events in patients without overt cardiac disease. It is

estimated to affect atleast 65% of those diabetics with increasing diabetic duration and age.

The sole risk factor for the development of CAN in type 1 diabetes is Dysglycemia, whereas the
risk factors for the development of CAN in type 2 diabetes include Dysglycemia , hypertension,

obesity, metabolic syndrome, smoking, increasing age, microvascular complications .

Clinical Features : The autonomic nervous system involvement in CAN occurs in an

ascending length-dependent manner. Therefore, the vagus nerve, which is the longest

parasympathetic nerve, is involved early resulting in parasympathetic denervation and

sympathetic predominance.

Patients at this early stage will be asymptomatic (sub-clinical stage) and the diagnosis can

only be made based on heart rate variability (HRV), baroreflex sensitivity tests or

increased left ventricular torsion on cardiac imaging.Towards the end stage of

disease, sympathetic denervation results in unresponsiveness of heart rate and blood

pressure to sleep, exercise, stress, or chemical stimulation such as adenosine. At this stage,

patients become symptomatic with light-headedness, weakness, palpitations, fainting and

syncope on standing. Other features that can be associated with CAN include reduced

exercise tolerance, silent myocardial ischaemia, intraoperative complications (hypotension,

bradycardia, and the need for vasopressor support), and foot complications including foot

ulcers due to associated sudomotor dysfunction, Charcot neuroarthropathy and lower limb

amputations. Poor response of heart rate and blood pressure during exercise in turn fail to

increase cardiac output accordingly, leading to poor exercise tolerance.

The signs associated with CAN include tachycardia, orthostatic hypotension, reverse

dipping, and non-dipping on ambulatory blood pressure. Monitoring Orthostatic

hypotension indicates an advanced stage of CAN and suggests a poor prognosis with

higher mortality in diabetic patients with CAN. Orthostatic hypotension is mainly

attributable to the damage to the efferent sympathetic vasomotor fibres, particularly in the

splanchnic vasculature. Other contributing factors are reduced cardiac output,

postprandial blood pooling, insulin-induced hypotension and volume depletion due to

diuretics. Patients can sometimes present with postural orthostatic tachycardia

syndrome, which is characterised by the presence of orthostatic symptoms occurring on

standing, an increase in heart rate of ≥ 30 beats/minute when moving from a recumbent to

a standing position that lasts more than 30 seconds and the absence of orthostatic

hypotension (more than 20 mmHg drop in systolic blood pressure).

Reverse dipping (reversal of normal physiological drop in blood pressure at night) and

non-dipping are commonly found in diabetic patients with CAN, due to sympathetic

predominance during the night, leading to the development of nocturnal hypertension and

left ventricular hypertrophy. Patients with CAN are susceptible to silent myocardial

ischemia and/or infarction. There is a prolongation of subjective anginal threshold, and

there is a delayed and diminished appreciation of ischemic pain, associated with early ECG

changes prior to the onset of ischemic symptoms. Asymptomatic ischemia can induce

lethal arrhythmias, which is especially important in patients with CAN who have

prolonged QT interval.

Long term progression is associated with lack of bp response to sleep or exercise indicating

damage to sympathetic nervous system.

CARDIOMYOPATHY
Disorders characterized by morphologically and functionally abnormal myocardium in absence

of any other disease that is sufficient by itself to cause the observed phenotype.

• Primary cardiomyopathies - Predominantly confined to the heart muscle

• Secondary cardiomyopathies - Myocardial involvement is one of a component of any systemic or

multiorgan disorder.
3 types of cardiomyopathy :

1) Dilated cardiomyopathy

2) hypertrophic cardiomyopathy

3) Restrictive cardiomyopathy

ETIOLOGY:
The causes of cardiomyopathies are varied in adults, dilated cardiomyopathy the most common cause is

CAD (Ischemic cardiomyopathy) and hypertension, although valvular disease, viral myocarditis and

genetic predisposition may also be responsible. neuromuscular diseases and idiopathic myocarditis are

the most common cause of dilated cardiomyopathy, and present during the first year of life in children.

Neuromuscular diseases that may lead to dilated cardiomyopathy in children include Becker muscular

dystrophy, Duchenne muscular dystrophy & Barth syndrome (an X-linked genetic disorder consisting of

dilated cardiomyopathy, neutropenia and skeletal myopathy.

The common causes are

INFLAMMATORY MYOCARDITIS
• Infectious

➢ Viral myocarditis-more commonly coxsackie, adenovirus, hepatitis - C

➢ Bacterial- diphtheria, lyme’s disease

➢ Systemic fungal infections

• Non- infectious

➢ Granulomatous inflammatory diseases - sarcoidosis, giant cell myocarditis

➢ Eosinophilic myocarditis

➢ Collagen vascular disease

➢ Peripartum cardiomyopathy

TOXIC
➢ Alcohol, catecholamines

➢ Chemotherapeutic agents- anthracyclines

➢ Interferon

➢ Heavy metal poisoning like pb, Hg

➢ occupational exposure

METABOLIC CAUSES
➢ Endocrinopathies- diabetes, pheochromocytoma, hyperthyroidism and hypothyroidism

➢ Nutritional deficiencies- thiamine, carnitine, selenium

➢ Electrolyte deficiencies-calcium, Magnesium, PO4

➢ Hemochromatosis

➢ Obesity

INHERITED METABOLIC PATHWAY DEFECTS

FAMILIAL
➢ Becker muscular dystrophy

➢ Duchenne muscular dystrophy

➢ Myocardial myopathies

➢ Skeletal and cardiac myopathy

➢ Arrhythmogenic right ventricular dysplasia

OVERLAP WITH NONDILATED CARDIOMYOPATHY

➢ Hemochromatosis

➢ Amyloidosis

IDIOPATHIC MISCELLANEOUS
➢ Arrhythmogenic right ventricular dysplasia

➢ LBBB
➢ Tachycardia related cardiomyopathy

DIABETIC CARDIOMYOPATHY
Diabetic cardiomyopathy is defined by the existence of abnormal myocardial structure and

performance in the absence of other cardiac risk factors such as CAD, HTN and significant

vascular diseases in individuals with diabetes mellitus. { aha }. It is characterized by left ventricle

(LV) concentric hypertrophy and perivascular and interstitial fibrosis which leads to diastolic dysfunction.

There are 4 stages of diabetic cardiomyopathy and there is overlap with the HF classifications of both

New York Heart Association Class and the American Heart Association Stage /American College of

Cardiology.

DIABETIC CARDIOMYOPATHY STAGES [18]

STAGE 1: Diastolic Heart Failure with normal Ejection Fraction > 55%

NYHA CLASS 1: The individual is asymptomatic and there is no limitation of physical activity.

ACC/AHA HF stage A: At risk of Heart Failure, but there is no structural heart disease or symptoms.

STAGE 2: Symptomatic Heart Failure with systolic and diastolic dysfunction

NYHA CLASS 2: Slight limitation during ordinary physical activity with palpitation, fatigue, dyspnea or
angina.

ACC/AHA HF STAGE B: Asymptomatic structural heart disease.

STAGE 3: Symptomatic Heart Failure due to hypertension, microvascular disease or viral disease.

NYHA CLASS 3: There is marked limitation of ordinary physical activity. Symptoms occur during minimal
physical activity.

ACC/AHA HF STAGE C: Symptomatic Heart Failure with structural heart disease.

STAGE 4: Symptomatic Heart Failure, with contribution from multiple confounder including coronary
artery disease.
NYHA CLASS 4: Symptoms of heart failure at rest. Unable to carry out any physical activity without
discomfort.

ACC/AHA HF STAGE D: Refractory Heart Failure requiring specialist interventions.

Risk factors for diabetic cardiomyopathy : hyperglycemia, systemic insulin resistance and impaired

cardiac insulin metabolic signaling are major clinical abnormalities in diabetes mellitus and all

are involved in pathogenesis of diabetic cardiomyopathy.

PATHOGENESIS OF DIABETIC CARDIOMYOPATHY

CHANGES IN STRUCTURE & SIGNALING PATHWAYS
1. LEFT VENTRICULAR HYPERTROPHY:

The Framingham study found that significant increase in LV wall thickness was seen

only in women with diabetes. But, in a Study conducted in Native Americans, suggested that

both woman and men with diabetes had higher LV wall thickness and mass. Among the diabetic

patients Increased LV mass was seen only in patients with diabetes but not those with impaired

glucose tolerance or impaired fasting glucose. In diabetics, the changes in myocardial geometry

are due to consequence of long-term diabetes changes such as obesity / hyperglycemia not due

to early defect. LV hypertrophy development predicts the increased risk of stroke and heart

failure with reduced ejection fraction and mortality. There is a significant interaction between

central obesity and diabetes on the risk for LVH. Apart from this, concentric LVH is produced by

obesity, independent of hypertension. Cytokines produced by expanded adipose tissue of

obesity plays a role in the development of LVH. In obese humans, leptin induces cardiac

hypertrophy.

Likewise, an adipokine (resistin), released from macrophages, induce cardiomyocyte

hypertrophy in vitro via MAPK and IRS-1 signaling pathways. A significant correlation was seen

between circulating levels of interleukin 6 and the risk of obesity-associated heart failure.

Hyperinsulinemia and Insulin resistance also been correlated with increased LV mass and

partially account for the association of cardiac hypertrophy and obesity and there is an

association with increased risk of heart failure [19]

2. MYOCARDIAL LIPOTOXICITY: Diabetes, insulin resistance, obesity and impaired glucose

tolerance are found to be associated with increased intra-myocardial lipid, independent of

circulating triglycerides [20] . The increase in cardiac triglyceride accumulation is associated

 only with diastolic dysfunction not systolic dysfunction [20, 21] . In wellcontrolled diabetics,

myocardial triglycerides appear to be normal [22].

3. INCREASED OXIDATIVE STRESS:

An increase in oxidative stress play an important role in producing diabetic cardiomyopathy, but

the actual mechanisms involved in reactive oxygen species (ROS) production among diabetic

patients’ heart is not well understood.

Mechanism for Free Fatty Acid (FFA) - induced cardiac dysfunction in diabetes. Increased FFA uptake in

cardiac myocyte precipitates cardiomyocyte dysfunction by multiple mechanisms in vivo including

increased mitochondrial and cytosolic reactive oxygen species (ROS) generation and ER stress.

FFAmediated ROS generation leads to uncoupling of mitochondria, which reduces mitochondrial ATP

production. ER- Endoplasmic Reticulum; Cyt C- Cytochrome C; FAOX- Fatty Acid oxidation.

4.CELL DEATH: In diabetics, there is an increased apoptosis of cardiac myocytes, but mechanism is

not well understood. Renin-angiotensin system (RAS) activation correlated with increased oxidative

stress, necrosis and apoptosis in cardiomyocytes and endothelial cells in the hearts of diabetic patients

and end stage heart failure. It is found that inhibition of RAS has reduced first hospitalization rate from

heart failure and echocardiographic findings of LV diastolic function improved in Type 2 diabetes
patients.

5.INTERSTITIAL FIBROSIS DM cardiomyopathy is characterized by perivascular and interstitial fibrosis.

It has been found that in diabetic patient’s heart biopsies, there is an increase in collagen deposition

between myofibers and around intramural vessels.

6. DIASTOLIC DYSFUNCTION (DD) : Diastolic dysfunction develops first before systolic dysfunction.

Altered calcium homeostasis and increased cardiac lipid accumulation was found to be associated with

DD in T2DM patients.

7. SYSTOLIC DYSFUNCTION (SD) : Systolic dysfunction is measured in the form of reduced ejection
fraction which occurs due to the alterations in the cardiac contractility. It occurs mainly due to

microvascular injury to the myocardium which impairs the cardiac perfusion.

8. IMPAIRED CONTRACTILE RESERVE: The diabetic autonomic dysfunction causes the impaired

contractile reserve of the cardiac myocytes and it is also due to microvascular injury in coronary

vasculature.

9. CHANGES IN MYOCARDIAL METABOLISM

10. ALTERED SUBSTRATE UTILIZATION

11. MITOCHONDRIAL DYSFUNCTION

PATHOPHYSIOLOGIC MECHANISMS OF DIABETIC CARDIOMYOPATHY

CLINICAL FEATURES

Early symptoms involve

• Exertional intolerance with dyspnoea varying severity

• Fatigueness

• Pedal oedema due to right ventricle dysfunction

• Ascites Later severe symptoms of heart failure ensue such as (due to reduced ejection fraction)

• Shortness of breath

• Orthopnoea

• Paroxysmal nocturnal dyspnoea

 • Palpitation

• Sudden cardiac death[20]

PHYSICAL EXAMINATION

• Cyanosis may be present in acute presentation

• Pedal oedema

• Raised jugular venous pressure(JVP).

• Apical impulse shifted to down and outward (may not be in restrictive type).

• S3, S4 may be heard.

• Loud P2, with wide split

• Murmurs may be heard due to valvular involvement (Mitral valve involvement is more common
due to annular dilatation) .

DILATED CARIOMYOPATHY :

In dilated cardiomyopathy the common first symptoms are

• Exertional intolerance.

• Left sided congestive features occur earlier than the right sided.

• Valvular regurgitation occurs due to annular dilation. Mitral regurgitation will appear earlier

during decompensation; tricuspid regurgitation occurs with right ventricular dysfunction.

• Atrial size may be increased; atrium may also be primarily involved.

• Left ventricular wall thickness may be normal or decreased

• Left ventricular diastolic dimension which is normally < 55mm, here it is increased usually > 60mm.
 • Left ventricular ejection fraction (LVEF) which is normally > 55%, here it is decreased. When the

symptoms are very severe LVEF will be usually < 30%.

• Arrhythmias may also occur in these patients that may be ventricular tachyarrhythmia or

conduction block, sometimes atrial fibrillation.

INVESTIGATIONS:
Usually in asymptomatic individuals’ cardiomyopathy is diagnosed incidentally during routine

medical screening or family evaluation of already diagnosed patients [21]. Hence diagnosis of

cardiomyopathy starts from the detailed history of symptoms and diseases, family history, personal

history of habits, drug or treatment history.

Assessment of performance abilities is done in routine and desired activities.

▪ Assessment of volume status of the patient is done along with orthostatic blood

pressure and BMI

▪ Chest radiograph

▪ Electrocardiograph

▪ 2D and Doppler echocardiogram

▪ MRI of myocardium for evidence of inflammation and fibrosis

▪ Haematology tests for

• Haematocrit/ haemoglobin

• WBC with differential count and eosinophilic count

• Erythrocyte sedimentation rate

▪ Biochemical tests:

• Serum electrolytes with calcium and magnesium

• Blood urea nitrogen and serum creatinine

• Total liver function tests including albumin and total protein

 • Thyroid function tests- thyroid stimulating hormone

• Lipid profile

• Cardiac biomarkers- troponin levels

• Creatine kinase isoforms

• Serum iron and transferrin saturation

Screening for Infections

• Viral – Influenza, ECHO virus, Coxsackie

• HIV

• Lyme’s disease

▪ Serology for active rheumatological disease

▪ Screening for breathing disorders

ELECTROCARDIGRAPHY IN CARDIOMYOPATHY : The findings in ECG of these patients vary

widely. Most of the findings are

▪ Sinus bradycardia

▪ Atrial enlargement

▪ ST depression

▪ Pathologic Q waves

▪ Prolonged corrected QTc interval

▪ Left ventricular hypertrophy

▪ Ventricular tachyarrhythmia

▪ Atrial fibrillation[22,23] .

ECHOCARDIOGRAPHY : Echocardiography is one of the non-invasive examinations of the heart

using reflected ultrasound waves. It delineates and evaluates the structures of the heart and as well as

the direction of blood flow within it by placing a transducer over the body. Echocardiography is one of
the widely recognized appropriate imaging modality in evaluating heart disease. The assessment

includes chamber quantification, valvular heart disease, pulmonary hypertension, left ventricular

systolic and diastolic function, pericardial disease, congenital heart disease and intracardiac masses.

There are different types of Echocardiography. They are

▪ 2D-Transthoracic Echocardiography

▪ Stress Echocardiography

▪ Doppler Echocardiography

▪ Transoesophageal Echocardiography

▪ Real time 3D Echocardiography

2D-TRANSTHORACIC ECHOCARDIOGRAPHY (TTE):

Single dimensional echocardiography records the motion of the heart at high frame rate 1000-

2000 frames per second in M (motion based) mode. But two-dimensional echocardiography records at

the rate of 30-2000 frames per second for the cross-sectional display of the cardiac structures.

CHAMBER QUANTITATION:

VENTRICULAR MEASUREMENT: Left ventricular linear dimensions are one of the parameters which

help in the management of patients with valvular heart disease especially in volume overload status and

symptoms. LV internal dimensions at end diastole (LVIDd) and end systole (LVIDs) are measured at

perpendicular to the long axis of the left ventricle at the level of cords or mitral leaflet at the tissue

blood interface.

Normal LV internal dimensions at end diastole (LVIDd) is less than or equal to 5.3cm for male

and 5.9cm for female.

American Society of Echocardiography recommended the following formula for the estimation of

Left Ventricular Mass (LVM).

LV mass =0.8*[1.04*{(LVIDd+PWTd+IVSd)^3 - (LVIDd)^3}]+ 0.6gm

Where, LV = Left ventricle

LVIDd = LV internal diameter at end diastole

PWTd = Posterior Wall Thickness of LV at end diastole

IVSd = Inter Ventricular Septal wall thickness at end diastole

The normal reference range varies between men and women.

For men, 88-224 gm. For women, 67-162 gm.

Normal left ventricular wall thickness and Inter Ventricular Septal wall thickness at end diastole is < 0.9

cm and more than 1.0 cm is considered to be hypertrophied left ventricle.

Right ventricular wall thickness > 5mm indicates right ventricular hypertrophy. Right ventricular mid

cavity diameter at end diastole should be less than that of the left ventricle or else RV dilatation is said

to be present.

RV functional volume measurement is challenging and it is measured by fractional area change of RV at

end systole and end diastole. If < 35% it is said to be abnormal. Factors affecting right ventricular size are

mainly the afterload and pressure changes and also diseases like myocardial infarction and right

ventricular dysplasia.

LEFT ATRIUM:

The enlargement of left atrium is one of the predictors of cardiovascular outcomes. Left atrium

is measured when it is at its largest dimension i.e. at ventricular end systole. Left atrium volumes are

usually calculated by using area length. The normal LA volume is 22+/- 6ml/m^2 when it is indexed for

BSA.

EJECTION FRACTION:

Left ventricular ejection fraction (LVEF) guides us for making therapeutic decision. It helps to

identify the patients for drug therapy initiation (E.g. ACE inhibitors and Beta blockers in patients with

LVEF < 40%) and for internal cardiac defibrillators implantation.

LVEF is calculated from end systolic volume and end diastolic volume.
 EF = (EDV- ESV) / EDV

EDV- End Diastolic Volume

ESV – End Systolic Volume

Normal reference Range:

EF: > 55%

EDV: < 104 ml for female

< 155 ml for male

DIASTOLIC FUNCTION:
Doppler Echocardiography is used to measure or assess the diastolic function. About half of the

newly diagnosed heart failure patients have normal or near normal left ventricular systolic function but

these patients are frequently having abnormal diastolic function. Mitral inflow velocities, pulmonary

vein velocities and myocardial tissue velocities of left ventricle are also used to assess the left ventricular

diastolic dysfunction. There are four major mitral inflow velocity parameters. They are

▪ Peak early filling (E) inflow velocity

▪ Late diastolic filling (A) inflow velocity

▪ E/A ratio ▪ Deceleration time (DT) of early filling inflow velocity (E’)

▪ Deceleration time (DT) of late filling inflow velocity (A’)

The mitral Peak early filling (E) inflow velocity mainly reflects the left atrial- left ventricle pressure

gradient in early diastole. It is affected by preload and alterations in LV relaxation. Mitral late diastolic

filling (A) inflow velocity mainly reflects the left atrial- left ventricle pressure gradient in late diastole and

it is affected by Left ventricular compliance and LA contraction.

Diastolic Dysfunction grading:

Left ventricular Diastolic dysfunction( LVDD) represents the first stage of diabetic
cardiomyopathy preceding changes in systolic function , reinforcing the importance of early examination

of ventricular function in individuals with diabetes. ( ref : parimal sarkar )

The diastolic abnormalities are present in diabetic patients without overt diabetic complications of the

cardiovascular system. It is the earliest and specific functional abnormality in diabetic cardiomyopathy

and can affect patients who are free of macrovascular complications, even in newly diagnosed DM

patients or in those with a disease duration of less than 1 year. It refers to a condition in which

abnormalities in mechanical function are present during diastole. The causes of diastolic dysfunction

may be subdivided into a decrease in passive myocardial diastolic compliance, and an impairment in

active left ventricular relaxation. Abnormalities in diastolic function may occur in the presence or

absence of a clinical syndrome of heart failure and with normal or abnormal systolic function.

Grade 1: Normal where E velocity is dominant i.e. E/A is > 1, E/e’ >1

Grade 2: impaired LV relaxation where A velocity is dominant i.e. E/A is < 1, E/e’ is <1

Grade 3: Pseudo normal where normal E velocity is dominance i.e. E/A is >1, E/e’ < 1

Grade 4: Restrictive filling where increased E velocity i.e. E/A is >2, E/e’< 1.

OBJECTIVES:

 To assess the cardiac status of type 2 DM patients by echocardiography, who are

otherwise asymptomatic clinically of any cardiovascular symptoms

  To compare the echocardiographic changes in Type 2 DM patients with the socio-

demographic factors (age and sex), duration of DM, glycemic control

MATERIAL AND METHODS

STUDY SETTING: Study was conducted in the Department of General Medicine, MNR

medical college and hospital, Fasalwadi, Sangareddy, Telangana.

STUDY POPULATION:

Inpatients and outpatients diagnosed with Type 2 Diabetes mellitus patients attending

Department of General Medicine, MNR medical college and hospital, Fasalwadi, Sangareddy,

Telangana, meeting the inclusion criteria.

STUDY DESIGN: A hospital based observational cross sectional study was conducted.

DURATION OF THE STUDY: 18 months

TIME FRAME: November 2022 to May 2024.

ELIGIBILITY CRITERIA:

Inclusion criteria

1. All adult patients both known Type 2 diabetic patents and newly diagnosed T2DM

patients with no cardiac symptoms attending MNR medical college and Hospital,

Sangareddy.

2. Patients who gave the consent .

Exclusion criteria

1. Known coronary artery disease patients

2. Known valvular Heart disease patients

3. Hypertension

4. Chronic alcoholics

5. Smokers

6. Chronic obstructive pulmonary disease patients

7. Patients who didn’t give the consent

SAMPLE SIZE: 130 Inpatients and outpatients diagnosed with Type 2 Diabetes mellitus

patients without cardiac symptoms attending Department of General Medicine, MNR medical

college and hospital, Fasalwadi, Sangareddy, Telangana, meeting the eligibility criteria were

taken as study sample.

Sample size was calculated using the below formula

n= (Zα + Z1-β )2 p q

d2

Zα= relative deviate for α (at 95% confidence interval) i.e 1.96

Z1-β= relative deviate for β (at 95% confidence interval) i.e 0.84

p = 5.42% (based on the previous study)

q = 1-p = 94.58%

d = absolute precision (precision taken as 5.6%)

n= 128.15, rounded to 130

Calculated sample size = 130

SAMPLING TECHNIQUE: Simple random technique was used to select the study sample.

DATA COLLECTION TOOLS:

Data was collected by interviews using a structured questionnaire. Questionnaire consisted of

details regarding

 Patient history
  Symptoms if any

 Duration and details of the disease

 Treatment that they were undergoing

Procedure and analysis of study:

The study was undertaken after obtaining Ethical clearance from the Institutional Research

Ethics Committee.

Study group consists of 130 inpatients and outpatients diagnosed with Type 2 Diabetes mellitus

with no cardiac symptoms attending Department of General Medicine, MNR medical college

and hospital meeting the eligibility criteria were taken as study sample.

Informed consent was taken from all the study participants.

Patients were interviewed by structured questionnaire for the symptoms, history duration and

details of the disease and treatment that they are undergoing.

All patients satisfying the inclusion criteria were included in this study, documented and

subjected to 2D echocardiography at MNR Medical college and Hospital.

All the eligible candidates are screened with complete physical examination, blood pressure

measurement to rule out hypertension and necessary investigations to exclude anemia, renal

disease and liver disease which could affect the outcomes of this study.

STATISTICAL ANALYSIS:
Data was collected, compiled and entered in Microsoft Excel. The data was refined, coded to

analyze the objectives of the research. Data was analyzed using SPSS version 20.0. Results were

explained in the form of baseline identification and with various outcomes of the research. The

results were summarized and displayed with appropriate usage of graphical presentation in the

form of pie charts and bar graphs. Descriptive statistics was done for all data: Mean and standard

deviation (SD) for quantitative variables (continuous data) and frequency counts for qualitative

variables (categorical data). Comparison of proportions was done using chi-square test and

means were compared among multiple groups using ANOVA test. Correlations were seen using

Pearson’s correlation test. Statistical significance level was set at 5% i.e. p value of 0.05.

RESULTS
 A total of 130 subjects were included in the final analysis.

TABLE 1: DISTRIBUTION OF AGE (YEARS) IN STUDY POPULATION

AGE GROUP NO.OF PATIENTS PERCENTAGE

<40 11 9.0%

41-50 42 32.0%

51-65 67 51.5%

>65 10 7.5%

TOTAL 130 100%

GRAPH 1: DISTRIBUTION OF AGE (YEARS) IN STUDY POPULATION

AGE GROUP

70
60
50
40
30
20
10
0
<40 41-50 51-65 >65

In the study population majority of the patients were in the age group 51 - 65 years (51.5%)

followed by 41-50 years (32%), more than 65years (7.5%) and less than 40 years (9%).

TABLE 2: DISTRIBUTION OF SEX IN THE STUDY POPULATION

 SEX NO.OF PATIENTS PERCENTAGE

Male 70 54.0%

Female 60 46.0%

TOTAL 130 100%

GRAPH 2: DISTRIBUTION OF SEX IN THE STUDY POPULATION

SEX

46%
Male
Female
54%

In this study, majority of the patients were male with 54% and female were 46%.

TABLE 3: DURATION OF DIABETES MELLITUS IN THE STUDY POPULATION

 DURATION OF
DIABETES MELLITUS NO.OF PATIENTS PERCENTAGE
(YEARS)

<5 44 34.0%

6-10 51 39.5%

11-15 21 15.5%

>15 14 11.0%

TOTAL 130 100%

In our study, about 51 patients had diabetes mellitus for duration of 6-10 years (39.5%).

GRAPH 3: DURATION OF DIABETES MELLITUS IN THE STUDY POPULATION

DURATION OF DIABETES MELLITUS

60

50

40

30

20

10

0
<5 6─10 11─15 >15
.

TABLE 4: DESCRIPTIVE ANALYSIS OF HbA1c IN THE STUDY POPULATION

 HbA1c NO. OF PATIENTS PERCENTAGE

<7.0 45 35.0%

7-8.5 63 48.2%

>8.5 21 16.8%

TOTAL 130 100%

GRAPH 4: DESCRIPTIVE ANALYSIS OF HbA1c IN THE STUDY POPULATION

HbA1c

70
60
50
40
30
20
10
0
<7.0 7-8.5 >8.5

In our study population, most of the patients having the HbA1c fall in the group with

range of 7 - 8.5 (48.2%).

TABLE 5: DISTRIBUTION OF LEFT VENTRICUALR HYPERTROPHY BASED ON IV SEPTAL WALL

THICKNESS

SEPTALWALLTHICKNESS NO. OF PATIENTS PERCENTAGE

Normal (<1cm) 96 74.5%

Left ventricle hypertrophy (>1cm) 34 25.5%

TOTAL 130 100%

GRAPH 5: DISTRIBUTION OF LEFT VENTRICUALR HYPERTROPHY BASED

ON IV SEPTAL WALL THICKNESS

SEPTAL WALL THICKNESS

26%

Normal (<1cm)
Left ventricle hypertrophy
(>1cm)

74%

In our study, 34 patients had left ventricular hypertrophy (25.5%) with increased septal

wall thickness (>1 cm).

TABLE 6: DISTRIBUTION OF LEFT VENTRICUALR HYPERTROPHY BASED ON

LV POSTERIOR WALL THICKNESS IN DIASTOLE (LVPWd)

 LVPWd FREQUENCY PERCENTAGE

Normal (<1cm) 101 78.0%

Left ventricle hypertrophy (>1cm) 29 22.0%

TOTAL 130 100%

GRAPH 6: DISTRIBUTION OF LEFT VENTRICUALR HYPERTROPHY BASED ON LV

POSTERIOR WALL THICKNESS IN DIASTOLE (LVPWd)

LVPWd

22%

Normal (<1cm)
Left ventricle hypertrophy
(>1cm)

78%

In our study, 29 patients had left ventricular hypertrophy (22%) with increased left

ventricular posterior wall thickness (>1cm).

TABLE 7: DISTRIBUTION OF LEFT ATRIAL ENLARGEMENT IN THE STUDY POPULATION

 LEFT ATRIUM NO. OF PATIENTS PERCENTAGE

Normal 112 86.4%

Left atrial enlargement 18 13.6%

TOTAL 130 100%

GRAPH 7: DISTRIBUTION OF LEFT ATRIAL ENLARGEMENT IN THE STUDY

POPULATION

LEFT ATRIUM

14%

Normal
Left atrial enlargement

86%

In the study group, 18 of patients had enlarged left atrium (13.6%).

TABLE 8: DESCRIPTIVE ANALYSIS OF DIASTOLIC DYSFUNCTION IN THE STUDY POPULATION

 DIASTOLIC NO. OF PATIENTS PERCENTAGE
DYSFUNCTION

Grade 1 27 21.2%

Grade 2 7 5.8%

Grade 3 3 2.0%

Normal 93 71.0%

TOTAL 130 100%

GRAPH 8: DESCRIPTIVE ANALYSIS OF DIASTOLIC DYSFUNCTION IN THE STUDY POPULATION

DIASTOLIC DYSFUNCTION
21%

5% Grade 1

Grade 2
2%
Grade 3

Normal

72%

In our study, 29% of population found to have diastolic dysfunction of which 21.2% of

patients with grade 1, 5.8% of patients had grade 2 and 2% of patients had grade 3

diastolic dysfunction.

TABLE 9: DESCRIPTIVE ANALYSIS OF EJECTION FRACTION IN THE STUDY POPULATION

 EJECTION FRACTION NO.OF.PATIENTS PERCENTAGE

Normal (>55%) 108 83%

Reduced EF (< 55%) 22 17%

TOTAL 130 100%

GRAPH 9: DESCRIPTIVE ANALYSIS OF EJECTION FRACTION IN THE STUDY POPULATION

EJECTION FRACTION
17%

Normal (>55%)
Reduced EF (< 55%)

83%

In this study, 17% of population had reduced ejection fraction (<55%) in the

echocardiography.

TABLE 10: DESCRIPTIVE ANALYSIS OF AORTIC VALVE IN THE STUDY POPULATION

 AORTIC VALVE FREQUENCY PERCENTAGE

Aortic regurgitation (AR) 2 1.4%

Aortic stenosis (AS) 6 4.6%

Normal (N) 122 94.0%

TOTAL 130 100%

GRAPH 10: DESCRIPTIVE ANALYSIS OF AORTIC VALVE IN THE STUDY POPULATION

AORTIC VALVE

2% 5%

Aortic regurgitation(AR)
Aortic stenosis(AS)
Normal(N)

94%

In our study, 6% of population had aortic valvular involvement. Aortic stenosis was seen

in 4.6% and Aortic regurgitation (AR) was seen in 1.4%.

TABLE 11: DESCRIPTIVE ANALYSIS OF MITRAL VALVE IN THE STUDY POPULATION

 Mitral Valve Frequency Percentages

Mitral regurgitation (MR) 2 1.5%

Normal (N) 128 98.5%

TOTAL 130 100%

GRAPH 11: DESCRIPTIVE ANALYSIS OF MITRAL VALVE IN THE STUDY POPULATION

Mitral Valve

2%

Mitral regurgitation (MR)

Normal (N)

98%

In our study, 1.5% of population had mitral valve regurgitation.

TABLE 12: DESCRIPTIVE ANALYSIS OF LEFT VENTRICLE DILATATION IN THE STUDY

POPULATION

LVID FREQUENCY PERCENTAGES

Normal 125 96.2%

Dilated left ventricle 5 3.8%

TOTAL 130 100%

GRAPH 12: DESCRIPTIVE ANALYSIS OF LEFT VENTRICLE DILATATION IN THE STUDY

POPULATION

LVID

4%

Normal
Dilated left ventricle

96%

In this study group, 3.8% had enlarged left ventricle.

TABLE 13: ECHOCARDIOGRAPHIC CHANGES IN THE STUDY GROUP

 ECHO CHANGES NO. OF PATIENTS PERCENTAGE

Diastolic dysfunction (Grade 1, 2 & 3) 37 28.46%

Reduced Ejection Fraction 22 16.9%

Increased Inter-Ventricular Septal Thickness 34 26.15%

Increased LV Posterior Wall Thickness 29 22.3%

Left Atrial Enlargement 18 13.8%

Valvular Involvement 10 7.69%

Dilated Left Ventricle 5 3.8%

In our study, about 37 patients were found to have diastolic dysfunction and about 34 patients

showed left ventricular hypertrophy in the form of increased inter-ventricular septal thickness

(>1cm) and 29 patients showed left ventricular hypertrophy in the form of increased LV

posterior wall thickness (>1cm).

GRAPH 13: BAR DIAGRAM SHOWING ECHOCARDIOGRAPHIC CHANGES IN THE STUDY

GROUP

ECHO CHANGES

Dilated Left Ventricle

Valvular Involvement

Left Atrial Enlargement

Increased LV Posterior Wall Thickness

Increased Inter-Ventricular Septal Thickness

Reduced Ejection Fraction

Diastolic dysfunction (Grade 1, 2 & 3)

0 5 10 15 20 25 30 35 40

TABLE 14: COMPARISON OF ECHO CARDIOGRAPHIC CHANGES IN TYPE 2 DIABETES

PATIENTS ACROSS AGE GROUP

Age Groups
Chi
Parameters <40 41-50 51-65 >65 P value
square
(N=11) (N=42) (N=67) (N=10)
Left Atrial Enlargement
LA 1 (9.09%) 1 (2.38%) 7 (10.44%) 9 (90.0%) 50.234 <0.001**
Diastolic Dysfunction
3(27.27%
Grade1 8 (19.04%) 15 (22.38%) 1 (10.0%)
)
Grade2 0 (0%) 2 (4.76%) 4 (5.97%) 1 (10.0%) 14.768 0.435
Grade3 0 (0%) 2 (4.76%) 1 (1.49%) 0 (0%)
Reduced Ejection Fraction
1 (9.09%) 4 (9.52%) 15 (22.38%) 2 (20.0%) 5.091 0.248
EF (%)
Left Ventricle Hypertrophy
1 (9.09%) 4 (9.52%)
IVSd 20 (29.85%) 9 (90.0%) 20.675 0.010**

LVPWd 1 (9.09%)
2 (4.76%) 18 (26.86%) 8 (80.0%) 28.932 0.023*
LV mass
Left
Ventricle 3 (27.2%) 6 (14.28%) 11 (16.4%) 4 (40.0%) 13.143 0.063
hypertrophy
LVID
Dilated
Left 0 (0.0%) 2 (4.76%) 2 (2.98%) 1 (10.0%) 4.788 0.764
Ventricle
Valvular Involvement
Aortic
Stenosis 0 (0%) 0 (0%) 5 (7.46%) 1 (10.0%)
Aortic
Regurgitation 0 (0%) 0 (0%) 1 (1.49%) 1 (10.0%)
11.987 0.456
Mitral
1 (10.0%)
Regurgitation 0 (0%) 0 (0%) 1 (1.49%)
*Significant; ** Highly significant

TABLE 15: COMPARISON OF ECHOCARDIOGRAPHIC CHANGES IN TYPE 2 DIABETES

PATIENTS ACROSS DURATION OF DM
 Duration of DM
Chi P
Parameters <5 6-10 11-15 >15
square value
(N=44) (N=51) (N=21) (N=14)
Left Atrial Enlargement

LA 2 (4.54%) 5 (9.8%) 4 (19.05%) 7 (50%) 17.987 0.001**

Diastolic Dysfunction

Grade1 8(18.18%) 6 (28.57%) 1 (7.14%)

12(23.53%)
3.566 1.758
Grade2 0 (0%) 1 (1.96%) 4 (19.05%) 2 (14.28%)
Grade3 0 (0%) 1 (1.96%) 1 (4.76%) 2 (14.28%)
Reduced Ejection Fraction
3 9 5 5
EF (%) 7.187 0.345
(6.82%) (17.65%) (23.8%) (35.7%)
Left Ventricle Hypertrophy
5 8
IVSd 10 (47.62%) 11(78.57%) 25.213 0.016*
(11.36%) (15.68%)
4 7
LVPWd 8 (38.09%) 10 (71.43%) 24.902 0.011*
(9.09%) (13.72%)
LV mass
Left Ventricle
5 11
Hypertrophy 5 (23.81%) 3 (21.43%) 12.197 0.210
(11.36%) (21.57%)

LVID
Dilated Left 0
3 (5.9%) 1 (4.8%) 1 (7.14%) 6.054 0.672
Ventricle (0%)
Valvular Involvement
Aortic
0 (0%) 1 (1.96%) 3 (14.28%) 2 (14.28%)
Stenosis
8.123 0.156
Aortic
Regurgitati on 0 (0%) 2 (3.92%) 0 (0%) 0 (0%)

Mitral
Regurgitati 0 (1.3%) 0 (3.03%) 2 (12%) 2.987 0.987
0 (1.54%)
on
*Significant; ** Highly significant

TABLE 16: COMPARISON OF ECHOCARDIOGRAPHIC CHANGES IN TYPE 2

DIABETES PATIENTS ACROSS HbA1c VALUES

 HbA1c
Chi
Parameters P value
<7.0 (N=45) 7-8.5 (N=63) >8.5 (N=21) square

Left Atrial Enlargement

LA 4 (8.89%) 6 (9.52%) 8 (38.09%) 15.218 0.002**
Diastolic Dysfunction
Grade 1 12 (26.67%) 12 (19.05%) 3 (14.28%)
Grade 2 2 (4.44%) 5 (7.94%) 0 (0%) 1.234 0.345
Grade 3 1 (2.22%) 2 (3.17%) 0 (0%)
Reduced Ejection Fraction
EF (%) 2 (4.44%) 13 (20.63%) 7 (33.33%) 0.540 0.842
Left Ventricle Hypertrophy
IVSd 10 (22.22%) 11 (17.46%) 14 (66.67%) 20.168 0.001**
LVPWd 7 (15.56%) 10 (15.87%) 12 (57.14%) 19.451 0.001**
LV mass
Left
Ventricle 8 (17.78%) 13 (20.63%) 3 (14.28%) 6.032 0.712
hypertrophy
LVID
Dilated Left
1 (2.22%) 3 (4.76%) 1(4.76%) 1.912 0.530
Ventricle
Valvular Involvement
Aortic
2 (4.44%) 3 (4.76%) 1(4.76%)
Stenosis
Aortic 1(4.76%)
0 (0%) 1 (1.58%) 2.569 0.219
Regurgitation
Mitral 1(4.76%)
0 (0%) 1 (1.58%)
Regurgitation
** Highly significant

TABLE 17: COMPARISON OF ECHOCARDIOGRAPHIC CHANGES IN TYPE 2 DIABETES

PATIENTS BETWEEN GENDER

 Gender
Parameters Chi square P value
Male (N=70) Female (N=60)
Left Atrial Enlargement
LA 6 (8.57%) 12 (20%) 4.127 0.050*
Diastolic Dysfunction
Grade1 15 (21.42%) 12 (20%)
Grade2 5 (7.14%) 2 (3.33%) 3.921 0.567
Grade3 2 (2.85%) 1 (1.67%)
Reduced Ejection Fraction
EF (%) 8 (11.42%) 14 (16.66%) 6.145 0.032*
Left Ventricle Hypertrophy
IVSd 18 (25.71%) 16 (26.67%) 1.110 0.894
LVPWd 16 (22.86%) 13 (21.67%) 1.023 0.562
LV mass
Left Ventricle
12 (17.14%) 12 (20%) 0.901 0.814
hypertrophy
LVID
Dilated Left
2 (2.85%) 3 (5%) 0.735 0.169
Ventricle
Valvular Involvement
Aortic Stenosis 1 (1.42%) 5 (8.33%)
Aortic
2 (2.85%) 0 (0%)
Regurgitation 1.034 1.345
Mitral
1 (1.42%) 1 (1.67%)
Regurgitation

*Significant
 DISCUSSION

A hospital based observational cross sectional study was conducted on 130 inpatients and

outpatients diagnosed with Type 2 Diabetes mellitus patients attending Department of General

Medicine, MNR medical college and hospital, Fasalwadi, Sangareddy, Telangana, meeting the

inclusion criteria. Study duration was 18 months from November 2022 to May 2024.

In the study population, majority of the patients were in the age group 51-65 years (51.5%)

followed by 41-50 years (32%), more than 65years (7.5%) and less than 40 years (9%). In a

study by Calvin Ke et al., (2024), mean age was 58.3 years. In another study by Parimal

Sarkar et al., (2022), 6% patients were 30–40 years old, 34% patients were 41–50 years old and

60% patients were 51–60 years old. The mean age (mean ± SD) of patients was 52.8± 6.28 years.

In a recent study by Vasudha V. Sardesai et al., (2022), the mean age of diabetic patients

without cardiovascular symptoms was 56.3 ± 8.60 years and maximum number of cases (52.3%)

was in the age group between 51 and 60 years of age. As per Mukhtarahmed Bendigeri et al.,

(2019), mean age of the patients with type 2 diabetes mellitus was 53.698 ± 11.3096 years.

According to a previous study by Dr. Uddhav Khaire et al., (2018), majority of the patients

were in the age group 51-60 years (41.0%) followed by 41-50 years (30%), 61-70 years (20.0%)

and 30- 40 years (9%). As per a study by Aniruddha Londhe et al., (2016), 14% type 2 DM

patients were in the age group of 30–39 years, 24% patients were in the age group of 40–49

years, 28% patients were in the age group of 50–59 years, 24% patients were in the age group of

60–69 years, and 10% were in the age group of ≥70 years. In a study by I. V. Ramchandra Rao

et al., (2015), 28% type 2 DM patients were in the age group of 31-40 years, 20% patients were

in the age group of 51–60 years, 16% patients were in the age group of 61–70 years, 4% patients

were in the age group of 41–50 years, and 2% were in the age group of ≥71 years.
14% type 2 DM patients were in the age group of 30–39 years, 24% patients were in the age

group of 40–49 years, 28% patients were in the age group of 50–59 years, 28% patients were in

the age group of 60–69 years, and 10% were in the age group of ≥70 years

In this study, majority of the patients were male with 54% and female were 46%. In a study by

Calvin Ke et al., (2024), 47.2% were women 52.8% were men. In another study by Parimal

Sarkar et al., (2022), 40% patients were female and 60% patients were male. In a recent study

by Vasudha V. Sardesai et al., (2022), males were 58.5%, whereas females were 41.5%.

According to Mukhtarahmed Bendigeri et al., (2019), 54.7% were male diabetics and 45.3%

were female diabetics. Contrary to the present study, in a previous study by Dr. Uddhav Khaire

et al., (2018), majority of the patients were female with 64% and male was 36%. Also in a study

by Aniruddha Londhe et al., (2016), majority of the patients were female with 60% and male

were 40%. In a study by I. V. Ramchandra Rao et al., (2015), majority of the patients were male

with 66% and female was 34%.

In our study, about 51 patients had diabetes mellitus for duration of 6-10 years (39.5%). 34% had

diabetes mellitus for duration of <5 years. 15.5% had diabetes mellitus for duration of 11-15

years. 11% had diabetes mellitus for duration of >15years. In a study by Parimal Sarkar et al.,

(2022), 18% patients were in <10 years duration of diabetes, 82% patients were in >10 years

duration of diabetes. The mean duration of diabetes in years (mean ± SD) of patients was

16.5800 ± 6.2671 years. In a recent study by Vasudha V. Sardesai et al., (2022), Patients with

duration of diabetes more than 5 years were 39.2%. Sex and duration of diabetes showed no

significant relation with 2D Echo findings. (p = 0.724 and P = 0.067, respectively), but there was

significant correlation between abnormal 2D Echo findings and age (p = 0.01). 2D Echo

abnormalities increase with increasing age. In a study by Karan Jain et al., (2018), most of the
patients (56%) had diabetes for <1year while 32% and 12% patients had diabetes for 1-3 years

and >3 years respectively. The mean duration of diabetes was 16.48 ± 13.37 months. According

to a previous study by Dr. Uddhav Khaire et al., (2018), most of the patients (55%) had

diabetes for 6-10 years while 23%, 18% and 4% patients had diabetes for 3-5 years, >10 years

and 0-2 years respectively. In a study by Aniruddha Londhe et al., (2016), most of the patients

(42%) had diabetes for 0-5 years while 40%, 14% and 4% patients had diabetes for 6-10 years,

11-15 years and >15 years respectively. In a previous study by I. V. Ramchandra Rao et al., (2015),

most of the patients (46%) had diabetes for upto 5 years while 22%, 18% and 14% patients had

diabetes for 5-10 years, denovo and >10 years respectively.

In our study population, most of the patients fall in the group having the HbA1c with a range of

7-8.5 % (48.2%). 35% of the patients having the HbA1c fall in the group with range of <7.0%.

16.8% of the patients having the HbA1c fall in the group with range of >8.5%. In a study by

Parimal Sarkar et al., (2022), 36% patients had HBA1c level 6.5–8.0%, 44% patients had HBA1c

level 8.1–10.0% and 20% patients had HBA1c level >10.0%. The mean HBA1c (mean ± SD) of

patients was 8.7572 ± 1.5427%. According to Mukhtarahmed Bendigeri et al., (2019), mean

HBA1C level was 9.943 ± 2.27%. There was statistical significant difference in HBA1C values

between diabetic and non diabetic groups (p<0.001). In a study by Karan Jain et al., (2018), the

mean Hba1c (%) was 8.01±1.23 in type 2 diabetic patients. According to a previous study by Dr.

Uddhav Khaire et al., (2018), majority (45%) patients had HBA1c level >8.0%, 39% patients had

HBA1c level 7.1–8.0% and 16% patients had HBA1c level 6.5-7.0%. In a study by Aniruddha

Londhe et al., (2016), majority (42%) of the type 2 DM cases had HBA1c level of 7.1–8.0%,

followed by 36% had HBA1c level of 8.1–10.0%, followed by 14% had HBA1c level of >10.0%,
followed by 8% had HBA1c level of 6.4-7%.

In our study, 34 patients had left ventricular hypertrophy (25.5%) with increased septal wall

thickness. 29 patients had left ventricular hypertrophy (22%) with increased left ventricular

posterior wall thickness. In a recent study by Parimal Sarkar et al., (2022), 8% patients had

LVSD and 12% patients had concentric left ventricular hypertrophy (LVH). According to a

previous study by Mukhtarahmed Bendigeri et al., (2019), there was significant association

pertaining to the presence of LVH between diabetic and non-diabetic groups (p=0.012). Among

the diabetic group, 11.3% had LVH while 88.7% had no evidence of LVH. Among the controls,

none of the subjects had any evidence of LVH. In a study by I. V. Ramchandra Rao et al.,

(2015), 12% had LVH, 24% had ischemia, 62% had LVH and ischemia, 12% were normal.

Karan Jain et al., (2018) study results showed that mean LV hypertrophy (%) was 13.1±2.33 in

patients without LVDD and 18.8±1.36 in patients with LVDD. This difference was statistically

significant. Mean LV mass (g) was 149.02 ± 6.74 in patients without LVDD and 158.20 ± 4.01

in patients with LVDD. This difference was statistically significant. According to a previous

study by I. V. Ramchandra Rao et al., (2015), 22% had LVD.

In the study group, 18 of patients had enlarged left atrium (13.6%).

In our study, 29% of population found to have diastolic dysfunction of which 21.2% of patients

had grade 1, 5.8% of patients had grade 2 and 2% of patients had grade 3 diastolic dysfunction.

In a study by Parimal Sarkar et al., (2022), 64% (64) patients had LVDD, of which 93.8% (60)

patients had LVDD grade 1 and 6.3% (4) patients had LVDD grade 2. In a study by Karan Jain

et al., (2018), 30% patients were detected with Left Ventricular Diastolic Dysfunction (LVDD).
In a previous study by Dr. Uddhav Khaire et al., (2018), Diastolic Dysfunction was seen in 45%

of type 2 DM. Out of which, 11% of patients had grade 1, 24% of patients had grade 2 and 10%

of patients had grade 3 diastolic dysfunction.

In this study, 17% of population had reduced ejection fraction in the echocardiography. In a study

by Parimal Sarkar et al., (2022), the mean EF (mean ± SD) of patients was 62.5160 ±

7.4088%. Results of a previous study by Mukhtarahmed Bendigeri et al., (2019) showed a

significant difference between the groups with a p-value of 0.019. Mean ejection fraction was

better in the control group 60.00 ±0.000 compared to the diabetic group 57.64±7.179 with a

mean difference of 2.358. Karan Jain et al., (2018) study results showed that mean LV ejection

fraction (%) was 65.17 ± 3.24 in patients without LVDD and 64.07 ± 2.74 in patients with

LVDD. This difference was statistically significant.

In our study, 1.4 % of population had aortic valvular involvement. The most common lesion is

Aortic stenosis (4.6%). In our study, 1.5% of population had mitral valve regurgitation. In this

study group, 3.8% had enlarged left ventricle. In our study, about 28.46% patients were found to

have diastolic dysfunction and about 26.15% patients showed left ventricular hypertrophy in the

form of increased inter-ventricular septal thickness and 22.3% patients showed left ventricular

hypertrophy in the form of increased LV posterior wall thickness. In this study, when

Echocardiographic changes in type 2 diabetes patients were compared across the age group, left

atrial enlargement; left ventricular hypertrophy in the form of inter-ventricular septal thickness

and left ventricular posterior wall thickness were found to be statistically significantly different

among the different age groups, majority of the cases found in the age group of >65years.

In a recent study by Parimal Sarkar et al., (2022), in LVDD, 3.1% patients were 30–40 years
old, 21.9% patients were 41–50 years old and 75.0% patients were 51–60 years old. Association

of age with LVDD was statistically significant (p = 0.0002).

In the present study, when Echocardiographic changes in type 2 diabetes patients were compared

across different groups of patients based on duration of diabetes, left atrial enlargement; left

ventricular hypertrophy in the form of inter-ventricular septal thickness and left ventricular

posterior wall thickness were found to be statistically significantly different among different

groups of patients based on duration of diabetes, majority of the cases were with diabetes for

>15years. In a recent similar study by Parimal Sarkar et al., (2022), where in the LVDD Group,

3.1% patients were in <10 years duration of diabetes, 96.9% patients were in >10 years duration

of diabetes. The association between duration of diabetes and LVDD was statistically significant

(P < 0.0001).

Previous study by Mukhtarahmed Bendigeri et al., (2019), observed that left ventricular

diastolic dysfunction in 2D echo between the two groups. There was significant association

pertaining to the presence of LVDD between the two groups with a p-value <0.001. Among the

diabetic population, 66% had evidence of LVDD while 34% had no evidence of LVDD. Among

the controls, none of the subjects had any evidence of LVDD.

In our study, when Echocardiographic changes in type 2 diabetes patients were compared across

different groups of patients based on HbA1c levels, left atrial enlargement; left ventricular

hypertrophy in the form of inter-ventricular septal thickness and left ventricular posterior wall

thickness were found to be statistically significantly different among the groups with majority of

the cases being in the group with HbA1c levels of >8.5%. In a recent similar study by Parimal

Sarkar et al., (2022), where in LVDD, 9.4% patients were HBA1c level 6.5–8.0, 59.4% patients
were HBA1c level 8.1–10.0 and 31.3% patients were HBA1c level >10.0. Association of HBA1c

with LVDD was statistically significant (P < 0.0001).

In the current study, when Echocardiographic changes in type 2 diabetes patients were compared

across gender, left atrial enlargement; reduced ejection fraction were found to be statistically

significantly different among males and females with majority of the cases were being females.

In a recent study by Parimal Sarkar et al., (2022), in LVDD, 34.4% patients were female and

65.6% patients were male. The association of sex with LVDD was not statistically significant (p

= 0.1257).
 SUMMARY

A hospital based observational cross sectional study was conducted on 130 inpatients and

outpatients diagnosed with Type 2 Diabetes mellitus patients attending Department of General

Medicine, MNR medical college and hospital, Fasalwadi, Sangareddy, Telangana, meeting the

inclusion criteria. Study duration was 18 months from November 2022 to May 2024.

Salient findings:

 Majority of the patients were in the age group 51-65 years (51.5%). In this study,

majority of the patients were male with 54%.

 39.5% patients had diabetes mellitus for 6-10 years. 34% had diabetes for <5 years.

15.5% had for 11-15 years. 11% had for >15years.

 Most of the patients (48.2%) had HbA1c in the range of 7-8.5%. 35% of the patients had

HbA1c in the range of <7.0%. 16.8% of the patients of the patients had HbA1c in the

range of >8.5%.

 25.5% patients had left ventricular hypertrophy with increased septal wall thickness >1

cm. 22% patients had left ventricular hypertrophy with increased left ventricular posterior

wall thickness >1 cm. 13.6% of patients had enlarged left atrium.

 29% of population found to have diastolic dysfunction of which 21.2% of patients with

grade 1, 5.8% of patients had grade 2 and 2% of patients had grade 3 diastolic

dysfunction.

 17% of population had reduced ejection fraction to <55% in the echocardiography.

 6% of population had aortic valvular involvement. Aortic stenosis was seen in 4.6% and

Aortic regurgitation (AR) was seen in 1.4%.

 1.5% of population had mitral valve regurgitation. 3.8% had enlarged left ventricle.

 When Echocardiographic changes in type 2 diabetes patients were compared across the

age groups, left atrial enlargement; left ventricular hypertrophy in the form of inter-

ventricular septal thickness and left ventricular posterior wall thickness were found to be

statistically significantly different among the different age groups, majority of the cases

found in the age group of >65years.

 When Echocardiographic changes in type 2 diabetes patients were compared across

different groups of patients based on duration of diabetes, left atrial enlargement; left

ventricular hypertrophy in the form of inter-ventricular septal thickness and left

ventricular posterior wall thickness were found to be statistically significantly different

among different groups of patients based on duration of diabetes, majority of the cases

were with diabetes for >15years.

 When Echocardiographic changes in type 2 diabetes patients were compared across

different groups of patients based on HbA1c levels, left atrial enlargement; left ventricular

hypertrophy in the form of inter-ventricular septal thickness and left ventricular posterior

wall thickness were found to be statistically significantly different among the groups with

majority of the cases being in the group with HbA1c levels of >8.5%.

 When Echocardiographic changes in type 2 diabetes patients were compared across

gender, left atrial enlargement and reduced ejection fraction were found to be statistically
significantly different among males and females with majority of the cases were being

females.
 CONCLUSION

Major echocardiographic changes found in type 2 DM were diastolic dysfunction (Grade 1, 2

& 3) of which majorly grade 1, increased inter-ventricular septal thickness, increased LV

posterior wall thickness, reduced ejection fraction. Left atrial enlargement, left ventricular

hypertrophy in the form of inter-ventricular septal thickness (>1cm) and left ventricular

posterior wall thickness (>1cm) were found to be statistically significantly higher in the age

group of >65years, cases with duration of diabetes for >15years, and in the group with HbA1c

levels of >8.5% when compared to their counter groups. Left atrial enlargement and reduced

ejection fraction (<55%) were found to be statistically significantly higher in females than

males.
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 STUDY PROFORMA

• Name of the patient:

• Age :
• Sex :
• Occupation:
• Address:
• Phone number:
• department :
• Date of admission
• Date of discharge :
• H/O Increased frequency of mictuirition
• H/O Thirst
• H/O Urinary difficulties
• H/O Blurring of vision
• H/O Diminution of colour vision
• H/O Sudden loss of vision
• H/O Floaters
• H/O Previous eye surgeries (photo coagulation)
• H/O Pedal edema
• H/O Oliguria
• H/O Puffiness of face
• H/O Abdominal distension
PAST HISTORY: Year of diagnosis of DM /HTN /any other chronic illness
TREATMENT HISTORY:
PERSONAL HISTORY:
• H/O Alcohol intake
• Duration
• Quantity
• H/O Smoking:
• Duration :
• Quantity
• H/O Weight loss
FAMILY HISTORY:
• Diabetes:
• Hypertension
GENERAL PHYSICAL EXAMINATION:
• Height: cms
• Weight: Kgs
• B.M.I:
• Pallor:
• Icterus:
• Clubbing:
• Cyanosis:
• Lymphadenopathy:
VITAL PARAMETERS:
• Pulse:
• B.P:
• Respiratory rate:
• Temperature:
SYSTEMIC EXAMINATION:
• CENTRAL NERVOUS SYSTEM:
• Fundoscopic examination:
• Positive Findings
• CARDIOVASCULAR SYSTEM:
• Positive Findings
• RESPIRATORY SYSTEM:
• Positive Findings
PROVISIONAL DIAGNOSIS
INVESTIGATIONS
• CBP
• CUE
• RFT
• RBS
• FBS, PLBS for diagnosing diabetics
• HBA1C
• LFT
• Serum electrolytes
• Thyroid Profile
• Lipid profile
• Electrocardiography
• Echocardiograph
RESEA
RCH
PATIEN
T
INFOR
MATIO
N
LEAFL
ET
(Patient Information Leaflet)

 Study A STUDY OF 2D ECHO CHANGES IN

Title:
ASYMPTOMATIC TYPE 2 DIABETES MELLITUS PATIENTS IN
A TERTIARY CARE HOSPITAL

 Principal investigator’s name: DR.G.RASHMI

 Principal investigator’s title: P.G.(Department of General Medicine)

 Place: MNR Medical College and Hospital, Sangareddy

You can go through the information leaflet and take decision whether to be part of
the study or not. Your decision will not have any effect on your medical care now or in
the future. You can opt out of the study anytime. If you do opt out, it will not affect
the quality of treatment you get now or in the future.

1. About the Study

• The study will be done by taking detailed history, clinical examination, and
investigations in patients with acute onset of stroke. The aim is to know evaluation
of retinopathy and nephropathy in relation to hBa1c levels.
2. Who should take part in the study?
• Patients with type2 diabetes mellitus and with and without chronic kidney disease
 and with visual defects, retinopathy
3. Do I need to take any medicines or undergo any investigations?
• There is no need to take any medications for this study. This study needs blood
investigations for knowing FBS, PLBS, Hba1c levels.
4. Are there any disadvantages/Risks of taking part in the study?
• The study has absolutely no disadvantages and no risks.
5. What are the advantages of taking part in the study?
• The study is about your health status. It may help in early detection of abnormality
if any. Moreover, you will be contributing to the betterment of the health system
in the society.
6. If I don’t take part, will it affect my treatment?
• Absolutely not. You will be getting the treatment as per the hospital policies.
7. How long is the study?
• It is limited to the time of your hospital stay.
8. What if I want to opt out of the study?
• You can opt out of the study anytime. If you opt out of the study, it will not affect
either the course or quality of treatment you get now or in the future.
9. Where can I get further information?
• If you have any further questions about the study or if you need any further
information now or at any time in the future, please contact:

Name: DR.G.RASHMI

Address: P.G. Department of General Medicine,

MNR Medical College and Hospital,

Sangareddy
 INFORMED CONSENT FORM

Title: "ASTUDY OF 2DECHO CHANGES IN ASYMPTOMATIC TYPE 2

DIABETES MELLITUS PATIENTS IN A TERTIARY CARE HOSPITAL"

 Principal investigator: DR.G.RASHMI

 Guide: DR SIVA SUBRAMANYAM

 Name: Age/Sex: Date:

 Address:

 Informant/Guardian:
 I have been given full information about the study in the language I understand.
 I understand its nature, purpose and duration. I have had a chance to ask questions about
the study and all of my questions have been answered to my satisfaction.
 I understood that I’m free to withdraw from the study at any given time. I have been
given a copy of consent form to keep. By signing this I have not given up my legal
rights.
 I understood that I’m entirely free to decide whether or not to take part in this study and
I’m also free to discontinue my involvement with the study at any time. I understand
that there is no penalty for not participating in this study or for withdrawing from the
study.
 I fully understand that there is absolutely no risk for me by participating in this study.
The participation or non participation in this study will not influence the course of my
treatmentor management in the hospital now or in the future

Name of the Investigator: Name of the Participant:

Signature: Signature/ thumb impression:

 Name and Signature of witness:

సమ్మ తి పత్రము

A STUDY OF 2D ECHO CHANGES IN

ASYMPTOMATIC TYPE 2 DIABETES MELLITUS PATIENTS IN A TERTIARY CARE HOSPITAL