Diabetes mellitus is a syndrome of chronic hyperglycemia due to relative insulin deficiency, resistance, or both. Globally, an estimated 422 million adults are living with diabetes mellitus, according to the latest 2016 data from the World Health Organization (WHO). Diabetes prevalence is increasing rapidly; previous 2013 estimates from the International Diabetes Federation put the number at 381 million people having diabetes. The number is projected to almost double by 2030. Type 2 diabetes makes up about 85-90% of all cases. Increases in the overall diabetes prevalence rates largely reflect an increase in risk factors for type 2, notably greater longevity and being overweight or obese. Diabetes is usually irreversible and, although patients can have a reasonably normal lifestyle, its late complications result in reduced life expectancy and major health costs. These include macrovascular disease, leading to an increased prevalence of coronary artery disease, peripheral vascular disease and stroke, and microvascular damage causing diabetic retinopathy and nephropathy. Cardiovascular Morbidity and Mortality: Cardiovascular disease is increased in individuals with type 1 or type 2 DM. The Framingham Heart Study revealed a marked increase in PAD, CHF, CAD, MI, and sudden death (risk increase from one to five-fold) in DM. The prognosis for individuals with diabetes who have coronary artery disease or MI is worse than for non-diabetics. CHD is more likely to involve multiple vessels in individuals with DM. After controlling for all known cardiovascular risk factors, type 2 DM increases the cardiovascular death rate twofold in men and fourfold in women. The American Heart Association has designated DM as a “CHD risk equivalent,” and type 2 DM patients without a prior MI have a similar risk for coronary artery–related events as non- diabetic individual who have had a prior MI. The absence of chest pain (“silent ischemia”) is common in individuals with diabetes, and a thorough cardiac evaluation should be considered prior to major surgical procedures. The increase in cardiovascular morbidity and mortality rates in diabetes appears to relate to the synergism of hyperglycemia with other cardiovascular risk factors. In the UKPDS, the number of cardiovascular events in patients with type 2 diabetes are not differ between the standard and intensively treated groups during the trial but were reduced at follow-up 17 years later (legacy effect) or (metabolic memory). Effects Of Diabetes on The Myocardium Both systolic and diastolic abnormalities have been demonstrated in patients with Diabetes without symptomatic evidence of cardiovascular disease. These abnormalities correlate with glycemic control, duration of diabetes and evidence of retinopathy/neuropathy. The observation that myocardial dysfunction is present in the absence of coronary artery disease, valvular disease, and the sequelae of associated cardiovascular risk factors. “Diabetic cardiomyopathy” This term was first used in 1972 by Rubler et al, describing myocardial dysfunction in patients with diabetes in the absence of coronary artery disease, hypertrophy, or valvular heart disease.

The Clinical materials were of Type-2 Diabetes Mellitus individuals selected from General Medicine outpatient and inpatient department in the This was a prospective study done among all the patients with Type-2 Diabetes Mellitus individuals selected from General Medicine out- patient and in-patient department in the Government Dharmapuri Medical College & Hospital, Dharmapuri, Tamil Nadu, India in the September 2024 – March 2025,Informed consent was taken from the subjects. Ethical committee approval was obtained for this study. About 100 patients were subjected to initial assessment it included through clinical examination, routine blood investigation consisting of complete blood count, biochemistry investigation, ECG, estimation of HbA1c and echocardiography were done from which 50 patients were included in the study. Patients with following criteria are excluded from the study Patients with abnormal resting ECG suggestive of ischemic heart disease or bundle branch block etc. Presence of comorbid disease known to influence Left ventricular dysfunction: - Thyroid disease, Alcoholism and Hypertension. Evidence of heart disease and clinical heart disease patient, Peripheral vascular disease, Cigarette smoking and Dyslipidemia Only patients who were in sinus rhythm, free from signs and symptoms congestive cardiac failure, Hypertension, Anemia, Ischemic heart disease were included for this study. They were divided into two groups according to the Glycemic status one group consisted of HbA1C levels < 7, and the other group consisted of HbA1C levels > 7. The number patients included in to each group were 25. All of them were subjected to echocardiography done at the Department of Cardiology, GGH, Guntur. Echocardiography was performed in the post absorptive phase. ESOATE equipment which has the capabilities of performing two-dimensional, M-mode, Pulsed wave and continuous wave Doppler and color flow imaging was used to obtain echo cardiogram images. Phased array transducers 2.5 - 3.5 MHz frequencies were used to obtain 2-D / M-mode echocardiography. Images were obtained with subjects in 30-degree lateral decubitus position. All measurements were performed in the freeze images from all the patients, good quality images suitable for the measurements and interpretations were obtained and recorded. For assessment of LV function the following parameters were calculated from the M- mode echocardiogram obtained at the level of mitral valve chordae. Left Ventricular VOLUME Left Ventricular MASS Left Ventricular GEOMETRY –ratio of LV mass to volume i.e. relative wall thickness (RWT) Left Ventricular FUNCTION: Diastolic Properties 1. Calculation of Early left ventricular inflow velocities (E), 2. Peak atrial contraction in Systole (a) 3. Calculation of E/a ratio and 4. Deceleration time (DT) 5. Isovolumic relaxation time (IVRT) 6. Left atrial size LV ejection fraction was calculated using the following formula, EF = (LVEDV - LVESV) / LVEDV × 100

In the present study, most of the participants belonged to >50 years age group. Out of the 50 participants in the study, 26 (52%) were male and 24(48%) were female. Equal distribution of the two groups was done with 25 participants in each group i.e. Group 1(HBA1C7).Some of the important parameters between the two groups found that 50.36 and 51.24 were the mean age of group 1 and group 2 respectively. The mean duration of suffering from diabetes is 4.20 and 4.92 in group 1 and group 2 respectively. Mean HBA1C levels are 6.39 and 8.01 in group 1 and group 2 respectively (p value=0.0001) and it was statistically significant. The mean FBS is 129.02 and 182.2 in group 1 and group 2 respectively. The mean PPBS was 211.02 in group 1 and 249.02 in group 2 and it was not statistically significant. The mean BMI of group 1 was 26.87 and 26.85 was mean BMI of group 2.With regards to duration of diabetes mellitus, In group 1, majority of the study participants (24) were suffering from diabetes for the last 7 months. The remaining 1 participant is suffering from diabetes from 8 12months.In group 2, majority of the study participants 19 were suffering from diabetes for the last 7 months. The remaining 6 participant is suffering from diabetes from 8-12months.Distribution according to complication found that 52% of the study populations were not presenting any complication associated with diabetes. 26% of the study population presented with albuminuria, 16% with autonomic neuropathy, and 6%with Retinopathy. In group 1, 68% of the study populations were not presenting any complication associated with diabetes. 20% of the study population presented with albuminuria, 12% with autonomic neuropathy. In group 2, 36% of the study population were not presenting any complication associated with diabetes. 32% of the study population presented with albuminuria, 20% with autonomic neuropathy, and 12% with retinopathy. Table1: Distribution of study groups based on imaging findings GROUP 1 GROUP 2 Variable N Mean SD N Mean SD P value Ventricular Septal wall thickness 25 0.84 0.08 25 0.846 0.12 0.83 LV Posterior Wall Thickness 25 0.81 0.12 25 0.79 0.086 0.49 LV end diastolic dimension in cm 25 4.2 0.39 25 4.31 0.43 0.34 LV end systolic dimension 25 2.8 0.28 25 2.77 0.30 0.22 Fractional shortening 25 30.8 5.3 25 29.85 5.98 0.55 EF% 25 57.36 2.70 25 57.84 2.3 0.50 Aortic root dimensions 25 2.78 0.47 25 2.82 0.45 0.75 Left atrial dimension 25 2.91 0.30 25 2.85 0.33 0.50 Ewave 25 60.48 5.67 25 60.64 4.57 0.91 AWave 25 63.41 3.79 25 63.25 4.64 0.89 E/Aratio 25 0.95 0.11 25 0.96 0.09 0.72 IVRT(ms) 25 94.48 10.02 25 92.80 11.33 0.58 Deceleration time 25 244.02 6.31 25 246.02 5.70 0.24 Table 1 showing the distribution of the study groups based on the important parameters in imaging. There was no statistical significant difference observed in imaging between the groups. Table2: Distribution of the study population based on LV diastolic dysfunction Group1 Group2 LVDD Frequency Percentage Frequency Percentage Normal 11 44 4 16 Grade 1 11 44 13 52 Grade 2 3 12 8 32 Total 25 100 25 100 Group 1 Group 2 P value LVDD Frequency Percentage Frequency Percentage 0.03 Normal 11 44 4 16 With LVDD 14 56 21 84 Total 25 100 25 100 Table showing distribution of study population based on LV Diastolic dysfunction. 14 participants out of 25 in group1 were observed to have LV diastolic dysfunction. Out of which 11(44%) were having grade1 LVDD and 3(12%) were having grade2 LVDD. 11 (44%) participants whose HbA1c was <7, were not diagnosed to have a LVDD. 21 participants out of 25 in group 2 were observed to have LV diastolic dysfunction. Out of which 13(52%) were having grade 1 LVDD and 8 (32%) were having grade 2 LVDD. 4 (16%) participants whose HbA1c was >7, were not diagnosed to have a LVDD. The result was found to be statistically significant with p value <0.05.

In this study, we found high Trans mitral A/E ratio as evidence of reduced diastolic function, left ventricular chamber compliance, and changes in the left atrial pressure. In the presence of mild diastolic dysfunction, early filling is often reduced, leading to an exaggerated atrial contribution to left ventricular filling and a high A/E ratio.In more advanced heart failure, this pattern is often lost due to high left atrial and left ventricular pressure and the A/E ratio pseudo- normalizes or increases, complicating interpretation.Hameedullah et al in their study population of 60 patients with type 2 DM found that there was strong correlation between HbA1c level and diastolic indices (‘P’ < 0.05). Diastolic dysfunction was more frequent in poorly controlled diabetic patients, and its severity is correlated with glycemic control.Prior studies have shown that the prevalence of diastolic dysfunction in asymptomatic newly diagnosed Type 2 diabetics as 42%. Mean of HbA1C (%) was found higher in group with as compared to group without LVDD. S Kumar et al suggesting that glycemic control may be an important determinant of diastolic function.Dikshit NM et al in a prospective study to assess normotensive diabetic patients by echocardiographic and Doppler parameters found a total of 50 diabetics out of which 33 (66%) patients had diastolic dysfunction.In a study done by Attali et al it was observed that LV diastolic dysfunction was present in patients who were free of cardio vascular disease, had diabetes of less than 5 years. Hyperglycemia influences heart metabolism, the production of advanced glycosylation end products, oxidative stress, and protein kinase C activation that leads to Left ventricular diastolic dysfunction which is earlier manifestation of diabetic cardiomyopathy. The relation between glycemic control and diastolic indexes in study supports the hypothesis that hyperglycemia by itself can lead to Subclinical Cardiomyopathy.Results indicate that diabetic patients with worse glycemic control are at an increased risk of early diastolic dysfunction. Therefore, in our study, patients with type 2 diabetes had increased isovolumic relaxation time, and an increased A/E ratio compared with normal volunteers.These results are consistent with prior studies in asymptomatic normotensive type 1 and 2 diabetic patients zabalgoitia M (2001), Shivalkar (2005). Also, diastolic dysfunction was closely related to the duration of diabetes.There was one study done by Ann m. Grandi et al, showed a close relationship between glycemic control and left ventricular diastolic dysfunction in 36 type 1 diabetic patients which improved with glycemic control.Hiramastn et al found that a short-term glycemic control resulted in a decrease in diastolic dysfunction which was found in 48 out of 246 patients who were randomly selected and treated with insulin for 6 months. Doppler Echo was done twice, at 1 and 6 months after the initiation of insulin treatment and results were comparable.The diagnostic role played by BNP in early detection of asymptomatic diastolic dysfunction in type-2 diabetes is still controversial.Dencker et al demonstrated that BNP was significantly higher in patients with abnormal diastolic dysfunction (26.0 ± 3.4 vs. 5.3 ± 3.4, p < 0.001) in a cohort of 33 patients with poorly regulated type 2 diabetes.A 17-year follow-up of 1441 patients from the DCCT trial more unambiguously demonstrated the benefit of intensive glycemic control in T1DM. They indicate finally that indicate that intensive glycemic control reduced the long-term risk of CVD in patients with T1DM.Intensive therapy in the UKPDS significantly improved the rate of micro vascular disease in T2 DM patients.Dungan et al study glycemic liability index, indicating increased glycemic variability, was associated with higher mortality, independent of hypoglycaemia.Clinical implication concerns the possibility to better control glycemic profile in order to reduce heart disease progression or even to reverse it, especially in patients with short duration of diabetes without history of cardiovascular event. In fact, in the early stages of diabetes, structural modifications seem to be partially reversible.The occurrence of HF in diabetic patients is responsible for increased mortality in this population. The evidence of increase incidence of HF in diabetes is strongly supported by the results of numerous clinical trials, metabolic disturbances; interstitial fibrosis, cardiomyocyte loss, small vessel disease, and cardiac autonomic neuropathy are incriminated.It is crucial to actively screen for patients at risk and institute appropriate therapy as soon as possible. The multifactorial nature of cardiac dysfunction in diabetic patients indicates that various strategies might be effective for preventing or delaying the development of HF and its complications. Presently, tight glycemic control and use of ACE inhibitors seem to be basic therapeutic strategies.Dueto the diabetogenic potential, it seems reasonable to avoid concomitant therapy with thiazide diuretics and β-blockers.

In patients with type 2 diabetes without clinical evidence of heart disease and HbA1c >7, there was a diastolic dysfunction with higher trans mitral A/E ratio, more prolonged isovolumic relaxation time in comparison with patients with type 2 diabetes without clinical evidence of heart disease and hemoglobin A1C<7 subjects. Furthermore, HbA1c correlated with diastolic Doppler indices.

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