Introduction: changes ultimately lead to structural changes (ventricular

Introduction: –

Diabetes mellitus is a chronic metabolic disease characterized by elevated plasma glucose levels as a consequence of insulin deficiency, impaired action of insulin secondary to insulin resistance, or a combination of both abnormalities. If left untreated, it can cause many long term complications include cardiovascular disease (CVD), stroke, chronic kidney disease (CKD), foot ulcer & damage to the eyes. (1)

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Dr Basma Edan Candidate of Iraqi Board of Internal Medicine-Karbala Center

Dr Karim Al-Naffi Professor of internal Medicine Karbala Medical College

CVD is a major contributor to morbidity and mortality among patients with DM. Diabetes alone is an independent risk factor for CVD and is considered a CVD equivalent. Concomitant risk factors in patients with diabetes, such as hypertension, obesity, and dyslipidemia, also contribute to the development of CVD and should be identified early through screening)1).

One of the most common cardiovascular problems that had been found to be associated with DM is left ventricular hypertrophy(LVH)

LVH is a disproportional growth of individual muscle cells in the heart, leading to increased heart weight and heart failure.  Diabetic patients are at high risk of developing LVH, and heart failure is the leading cause of death in diabetes (2). 

LVH also may be a consequence of the effect of a chronically increased left ventricular afterload, such as in systemic hypertension or aortic stenosis, or a result of an intrinsic abnormality of myocytes.  LVH had many detrimental effects, it may lead to diastolic dysfunction, may reduce coronary flow reserve and may facilitate ventricular arrhythmias (3).


Hyperglycemia, hyperinsulinemia with insulin resistant & hyperlipidemia which occur in DM, lead to series of changes that include oxidative stress & increased reactive oxygen species (ROS) generation, AGEs formation, mitochondrial dysfunction, inflammation with activation of NF-kB pathway & inflammatory mediators, in addition to other mechanisms like RAAS over activation, endothelial dysfunction, substrate shift toward increased free fatty acid (FFA) oxidation. All these changes ultimately lead to structural changes (ventricular hypertrophy & fibrosis) & functional changes (systolic, diastolic dysfunction) (4).

There are multiple risk factors that associated with development of LVH in DM which include hypertension, obesity, dyslipidemia & diabetic nephropathy.

LVH can be detected by electrocardiography (ECG), echocardiography or cardiac magnetic resonance imaging (MRI).

ECG is the cheapest and most readily available of the three tests for LVH. while its specificity is acceptably high, its clinical utility is limited by its very low sensitivity, Common ECG criteria for the diagnosis of LVH include: – Cornell voltage criteria, Sokolow-Lyon voltage criteria, Romhilt-Estes point score system (5-6).

Echocardiography if available, should be the test of choice to assess for LVH. It is much more sensitive than ECG and can also detect other abnormalities such as left ventricular dysfunction and valvular disease. This test uses transthoracic or trans esophageal ultrasonography to measure the left ventricular end-diastolic diameter, posterior wall thickness, and inter ventricular septum thickness. From these measurements and the patient’s height and weight, the left ventricular mass index can be calculated (7).

Cardiac MRI is the gold standard test for LVH, as it is even more accurate and reproducible than echocardiography. It can precisely estimate a patient’s LVM and assess for other structural cardiac abnormalities. MRI use, however, is severely restricted in clinical practice due to its high cost and limited availability (8).

Aim of the study: –

Because the Cardiovascular system(CVS) complications account for the highest mortality in DM & LVH is an ominous prognostic sign for cardiac event, the aim of this study is to see if there is any relationship between LVH &DM characteristics.

Patients& Method: –

 In our cross section observational analytic study, 101 patients were recruited from inpatient ward & outpatient internal medicine clinic in Imam Al- Hussein medical city during period from May 2016 to May 2017.

Inclusion criteria include

 1) patients on oral or injectable anti diabetic therapy among already diagnosed DM.

 2) patients not on anti-diabetic therapy but fulfilling the American diabetes association definition of DM.                  

3) gestational DM.

Exclusion criteria include: – 

1) Hypertension    2) Ischemic heart disease   3) Heart failure 4) Stroke 5) Hypertrophic cardiomyopathy 6) Valvular & congenital heart disease   7) Renal failure 8) Athletes.


Parameters studied: –  Patient particulars such as age, gender, height, weight ,  BSA  ,BMI ,and blood pressure were measured, and routine and relevant investigations like CBC, ECG,  HbA1c, serum urea and creatinine,  liver function test(LFT),  lipid profile, general urine exam(GUE) for albumin and echocardiography .  Blood pressure (BP) was measured with mercury sphygmomanometers and cuffs of appropriate size. Hypertension was defined as a BP recording 140/90 mm Hg or higher& the mean of three seated BP measurements, separated by a minimum interval of five minutes, was obtained.

ECG : A resting 12-lead ECG was recorded for each subject at10 mm/mV and 25 mm/s with the subject lying supine. There have been multiple ECG criteria proposed for diagnosing LVH ( Sokolow, cornell, & Romhilt estes criteria)

Echocardiography:  M-mode and pulsed Doppler echocardiography were performed according to the recommendations of the American Society of Echocardiography  using a commercially available ultrasound system (3.5 MHz transducer; VIVD-9 General Electric) in the supine and left lateral decubitus position,  Left ventricular  dimensions were measured from 2D-guided, M-mode echocardiograms of the left ventricle (LV)at the level of mitral leaflet tips or the papillary muscle using the parasternal view. The thicknesses of the left ventricular posterior wall and the ventricular septum were measured. These values were used to calculate the LVM , LV end-diastolic and end-systolic dimensions were measured at the level of tips of the mitral leaflets as the largest and the smallest LV dimensions, respectively.

The  following equation provides a reasonable determination of LVM in grams:

LVM = 0.8 (1.04 (LVID+PWT+IVST3? LVID3)) + 0.6g .

The upper limit of LVM was 162 g in females and 224 g in males.the upper limit of the LVMI was 95 g/m2 in female and 115 g/m2 in males(9). LV EF was calculated using the two-dimensional directed M-mode method and the modified Simpson’s rule when possible. Systolic dysfunction was defined by evidence of regional wall motion abnormalities and/or an EF of 0.05) ,as shown by table 1.


Table 1 Relationship between LVM & type of DM , duration, type of treatment :-



 There is no significant association had been found between LVM & HbA1c ,as shown by table 2.


Table 2 Relationship between LVM & HbA1c :-


Albuminuria were insignificantly associated with LVM (P> 0.05), as shown in table 3.

Table 3 Relationship between LVM & albuminuria:-


There was no significant relationship between LVM & lipid abnormalities, but there was significant association between LVM & age BMI, BSA , P >0.05 as shown in table 4 .

Table 4 Relationship between LVM & age, BMI , BSA:-


 Same results was found for LVMI. Diastolic function assessment revealed that 38 patients (37.6%) had DD , while the remaining 63 (62.4%) had not.

DD was significantly associated with older age, where the frequency of patients with DD increased with the advancing age and the higher proportion (93.3%) was reported in those aged > 60 years, (P 60 years, (P