Procedimiento y aplicación de los cuestionarios

Linear regression analysis showed a strong correlation between left ventricular mass index and waist circumference, r= 0.45, p<0.00001. Left ventricular mass index also showed a strong correlation with visceral fat, r= 0.44, p<0.00001. A moderately strong correlation was seen between LVMI and waist-hip ratio, r= 0.30, p= 0.0009. Left ventricular mass index correlated better with WC and VF, than with W/H ratio, (Figures 3,4 and 5).

Figure 3: Relationship between WC and LVMI

Legend: LVMI= Left ventricular mass index, WC= waist circumference, r= 0.45

p<0.00001

Figure 4: Relationship between VF and LVMI

Legend: LVMI= Left ventricular mass index, VF= Visceral fat r= 0.44

p< 0.00001

Figure 5: Relationship between W/H ratio and LVMI

Legend: LVMI= Left ventricular mass index, W/H= waist-hip ratio

r= 0.30 p= 0.0009

CHAPTER FIVE DISCUSSION

The obesity epidemic is attracting more attention around the world and it continues to be a source of concern. The index study has demonstrated the relationship between measures of central obesity and left ventricular mass. It also showed the co-existence of LV diastolic dysfunction.

Subjects and controls were age matched. Age is known to affect diastolic function over the age of 60 years.⁸⁰ This age group is not capturedin this study,the oldest participant recruited being 59 years old.

It was observed that 13(21.7%) of the controls had pre-obesity, while 3(5%) were obese even though they did not have central obesity. This reflects the draw back of the use of BMI as an index of adiposity as persons with a heavy muscle mass would appear to be overweight or obese. This fact has been raised by other investigators.¹⁰⁷ Among the subjects, 24(40%) had pre-obesity and 35(58.3%) were obese. This shows that becoming obese suggests central obesity. However adipose tissue effects on cardiac structure and function cannot be adequately elucidated as the BMI does not make a distinction between fat and fat free mass. This underscores the need for body fat and particularly, visceral fat measurements.⁸⁰ The subjects in this study were recruited based on their waist circumference. It was shown in this study that, waist-hip ratio correlated positively with left ventricular mass, and the correlation was even stronger with visceral fat and waist

circumference which are more direct measures of central obesity than the waist-hip ratio.

Visceral fat correlated better with LV mass than the waist-hip ratio.

A study done by Yusuf et al¹³⁰ in which 27,000 participants from 52 countries were studied, showed that with regard to cardiovascular risk, obesity needs to be redefined in terms of central obesity rather than BMI. Yusuf et al¹³⁰ found that waist-hip ratio significantly increased the estimate of myocardial infarction attributable to obesity by three fold. These observations highlight the concept that regional fat distribution, rather than increased BMI should be considered in the assessment of cardiac risk attributable to excess body weight.¹³⁰ A study done by Seidel et al⁵ in assessing obesity,showed that mortality and morbidity vary with the distribution of body fat, the highest risk linked to excess visceral fat. This has propelled the need for body composition measurements in assessing those at risk.

LVH by voltage criteria (Araoye) was not significantly different in subjects compared to controls. LVH was seen in 1(1.67%) subject and 3(5%) controls. Using the Sokolo-Lyon criteria, the controls had taller voltages. None of the subjects (0%), and 4(6.7%) controls had ECG evidence of LVH. A study done by Pontiroli et al¹²⁵ showed that obese persons had lower chest lead voltages than the controls.This study is consistent with earlier work done in demonstrating taller voltages in the chest leads among controls.¹²⁵ The dampening effect of adipose tissue is known to be associated with this.

QTc is an index of physiological variability of ventricular repolarization. An increase of QTc is a possible risk factor for ventricular arrhythmias and sudden death.¹⁴² In addition, prolonged QTc is an index of sympathetic over activity and previous studies have shown that increased sympathetic activity is present in obesity and hypertension particularly when the two conditions co-exist.¹⁴ Prolonged QTc and LVH are common in both obesity and arterial hypertension , and are risk factors for cardiovascular disease and sudden death.¹³² This study did not show a difference in QTc in subjects compared to controls. This is probably due to the fact that in this study, hypertensives were excluded.

Apart from sodium, all serum electrolytes were in the normal range. Electrolyte derangements associated with prolonged QTc such as hypokalemia, hypocalcemia were absent. Persons taking any medication were excluded from the study.

This study showed that persons with central obesity had a significantly larger left atrium than controls. A study done by Morricone et al⁴³ in which visceral fat was measured using computed tomography showed that left atrial enlargement correlated with central obesity. LA enlargement typically occurs in the setting of increased left ventricular mass¹⁵ with abnormal LV relaxation. A lower E:A-wave ratio seen in the subjects may induce a higher atrial contraction and a progressive enlargement of the left atrium. As a consequence, left atrial enlargement may mediate the excess risk of atrial fibrillation associated with obesity.¹⁴

The centrally obese subjects had a greater mean IVS and LVPW thickness than the controls. This is similar to what was shown in the study by Morricone et al and other studies.15,43,106 Interventricular septal and LV posterior wall thickness were shown to have a strong correlation with visceral adipose tissue.^43,106

LVDd was not different in subjects compared with controls. In a study among South African blacks, in which waist circumference was correlated with LV geometry, there was no statistical difference in LVDd when subjects were compared with controls.¹⁰⁶

This study has demonstrated that central obesity is associated with increased left ventricular mass, and alterations in left ventricular geometry, predominantly of the concentric type. LV mass and relative wall thickness were greater in the subjects compared to controls. LV mass correlated strongly with measures of central obesity. The results of a multiethnic study of 5004 persons aged 45 to 84 years revealed that obesity is associated with concentric left ventricular hypertrophy.¹³³ Waist circumference and fat mass were found to correlate positively with LV mass. Another study by Woodiwiss et al¹⁰⁶ in South Africans of African ancestry demonstrated that obesity promotes left ventricular concentric rather than eccentric remodeling and hypertrophy independent of blood pressure. Waist circumference was related to relative wall thickness, concentric hypertrophy and concentric remodeling.¹⁰⁶ Several other studies have demonstrated LV concentric hypertrophy and remodeling in obesity. 14,134,135,136,137 Some studies have

138,139,140,

confounders, and the subjects were severely obese.^14,106 Genetic mechanisms could be evoked to partially explain the LV geometric patterns. Genetic studies have indicated that obesity has a strong impact on cardiac gene expression, a specific cardiac transcriptome which could be considered as precursor signs for future cardiac disease.¹⁴¹ LVH and dysfunction are features of ACC/AHA stage B classification of heart failure. Subclinical LVH may occur several years before the onset of heart failure and sudden death.⁸⁴ LVH is also a risk factor for arrhythmias.¹²⁹

Persons with central obesity had a lower mean mitral valve E:A-wave ratio and a longer deceleration time, when compared to controls. Grade 1 diastolic dysfunction was demonstrated among the subjects. This is consistent with studies done by other investigators which demonstrated that persons with central obesity have a lower ratio between early and atrial diastolic filling wave velocities and a prolonged deceleration time.^14,43 Isovolumic relaxation time is also known to be prolonged in central obesity.⁴³ This is more prevalent in severe obesity. In this study, isovolumic relaxation time was found to be similar in subjects and in controls. This may be due to the fact that subjects with severe obesity were relatively few. The diastolic dysfunction shown in the subjects may also mediate the increase in atrial diameter noted in these individuals.¹⁴ The controls had predominantly normal diastolic function.

Systolic function was preserved in subjects with central obesity. There was no statistical difference in the left ventricular fractional shortening and ejection fraction when subjects

were compared to controls. This is consistent with other studies done in which the influence of obesity on LV structure and function were evaluated which demonstrated normal systolic function.^142,143.

A low HDL-C is associated with increased cardiovascular risk.¹⁶ The National Cholesterol Education Program Adult Treatment panel III (NCEP ATP III) has listed HDL-C <40mg/dl as an index of increased cardiovascular risk.¹⁶ HDL-C was significantly lower in subjects compared to controls, p=0.03. It was shown that 8(66.7%) of the subjects, and 3(25%) of controls had a low HDL-C. A more sensitive and specific index is the ratio of total cholesterol: HDL-C^120,123 which was significantly higher in the subjects than the controls, p= 0.009. These findings are indicative of cardiovascular risk.

Obesity, especially central obesity is associated with a low HDL-C and hypertriglyceridemia.¹⁵¹ In this study, there was no statistical difference in the triglyceride values of subjects compared to controls. Triglyceride levels in blacks are generally lower than in whites, with or without coronary heart disease.¹⁴⁴ However, high triglyceride levels are associated with hypertension and insulin resistance¹⁴⁴ which is a feature of type 2 diabetes mellitus. Hypertensives and diabetics were excluded from this study.

Serum sodium was significantly lower in subjects compared to controls. This is a common finding in the setting of hypercholesterolemia.¹⁵² Among the subjects 6(50%) of

pseudohyponatremia.¹⁵² Cholesterol is insoluble and would artifactually lower sodium levels by increasing the solid fraction of plasma. All other electrolytes were similar in subjects and controls and were within normal limits.

Creatinine clearance was not different statistically when subjects were compared with controls. Overweight and obesity are believed to be associated with renal damage, however this is commonly associated with hypertension.¹²² Hypertensives were excluded from this study. The small sample size may also play a role.

No difference was noted statistically in the liver function tests comparing the subjects with the controls, except in total bilirubin, which showed a marginal difference, being higher in subjects compared to controls. Total bilirubin comprises the direct (water soluble) and the indirect (lipid soluble) fractions. There was no statistical significance noted with the direct bilirubin. There is however a paucity of data on adipose tissue effects on biliubin.

There was no statistical difference in the transaminases as well as alkaline phosphate values of the subjects and controls. A study done in 1216 workers from an electronics manufacturing factory in Taiwan showed that central obesity was associated with elevated alanine amino transferase.¹⁴⁵ Chlorinated hydrocarbons are a common feature of electronics factories and are associated with hepatic toxicity and malignancy. None of the

subjects or controls worked in an electronics factory. Deranged liver enzymes are commoner in morbidly obese persons who were relatively few and were not among those randomly selected.

CONCLUSION

This study has demonstrated the strong correlation between measures of central obesity and left ventricular mass. Central obesity was shown to be associated predominantly with concentric left ventricular hypertrophy and remodeling. It also showed the presence of diastolic dysfunction, preserved systolic function and dyslipidemia in persons with central obesity. Waist circumference and visceral fat as measures of central obesity correlated better with left ventricular mass than waist-hip ratio.

RECOMMENDATIONS

Echocardiography and fasting lipid profile should be a part of the routine work up in persons with central obesity.

Waist circumference and visceral fat measurements should be preferred as measures of central obesity

Longitudinal studies to prognosticate LVH and diastolic dysfunction with dyslipidemia in central obesity would be beneficial.

There is no doubt that only a strong and effective public health message as well as counseling by Health Care givers will minimize the potentially explosive effect of being overweight and obese on the prevalence of heart failure which remains a disease characterized by a grim prognosis, high mortality and enormous cost to health services.

The gymnasium should be brought into the work place, so people can work and also keep healthy. Exercise should be isotonic. Our lifestyle and environment have to be made less prone to breeding obese individuals.

There is a need for broad based programs which facilitate healthy eating habits such as diets low in fats/ cholesterol and high in fiber rather than fast food, as well as activity levels for all age groups.

LIMITATIONS OF THE STUDY

The bench mark for visceral fat measurements is imaging (Computed Tomography, Magnetic Resonance Imaging). This could not be done due to the exorbitant cost of these procedures.

Tissue Doppler imaging for the further evaluation of left ventricular function could also not be done. This would have provided an additional window on left ventricular diastolic function in a manner complimentary to mitral inflow patterns, making it possible to distinguish between normal and pseudonormal patterns.

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