lxxix
lxxx Table 14 Frequency of Echo LVH in participants using LVM /H2 Vs LVM / BSA
LVMI Obese
(n=150)
Frequency( %)
Non Obese (n= 80)
Frequency( %)
Total
LVM/ H2 106(70.7) 5(6.2) 111
LVM/BSA 68 (45.4) 5(6.2) 73
LVMI = Left ventricular mass index
LVM/H2 = Left ventricular mass index to height2
LVM/BSA = Left ventricular mass indexed to body surface area.
lxxxi
CHAPTER SIX DISCUSSION
In Africa, there are few studies on obesity and even fewer studies on the use of echocardiography for evaluation of left ventricular hypertrophy in obese subjects. Considering the rising global epidemic of obesity,1,2,3 it is likely that adverse health consequences of excess adiposity will escalate in the future. Left ventricular hypertrophy is one of the cardiac complications of obesity and echocardiographically determined LVH is a powerful independent predictor of cardiovascular morbidity and mortality.34,35 The prognosis of LVH is also related to the underlying geometric pattern. Echo permits early detection of structural cardiac abnormalities long before the development of overt clinical disease. This would enable institution of measures to reverse these changes and prevent life threatening complications and consequences.
The present study has demonstrated that obesity is associated with increased left ventricular wall thickness (IVSD and PWTd), increased left ventricular internal diameter (LVIDd), increased left ventricular mass and hypertrophy (LVM, LVH). From the study the mean IVSd and PWTd were similar in the non obese control group (9.56mm and 9.41mm respectively) as demonstrated in other studies 168 but in the obese group the IVSd in thicker than the PWTd (12.46 and 11.07mm respectively) suggesting that obesity targets the inter ventricular septum more than the posterior wall. This is further supported
lxxxii
by the fact that in table 8 correlations between the measures of obesity and IVS were stronger than those with posterior wall. The mechanism of cardiac hypertrophy in obesity involves haemodynamic and metabolic factors. Obesity produces an increase in total blood volume and cardiac output caused by the increased metabolic demand induced by excess body weight.97 This leads to ventricular chamber dilatation, increase in wall stress, myocardial mass and left ventricular hypertrophy.102
The values of the echocardiographic determinants of left ventricular hypertrophy and LVM were higher in male subjects than female subjects in both obese and control groups (tables 6 and 7). This agrees with findings in other studies80,81 that male sex is associated with higher left ventricular mass than females. 80 However recent reports indicate that the prognostic implications of left ventricular hypertrophy are more pronounced in females than males. 169 In other wise healthy subjects followed up for four years in whom LVH was defined as LVM adjusted in height of >143g/m in men and > 102g/m in women, the relative risk of cardiovascular death for each increment of 50g/m in LV mass was 1.73 in men and 2.12 in women, and a relative risk of all cause death of 1.49 in men and 2.01 in women.35
The relative impacts of the measures of obesity namely BMI, WC and WHR on echocardiographic determinants of left ventricular hypertrophy were assessed in this study (tables 8 - 12). The body mass index was strongly
lxxxiii
correlated with all the echo parameters namely IVSd, LVIDd, PWTd, LVM and LVMI when the subjects were pooled together. When the subjects were separated according to degrees of body mass index, strong correlations with LVMI was noticed with class II and class II obesity (table 10). Progressive increases in BMI was also associated with progressive increases in LVMI (table 9, figure 1). This was more prominent in females probably because the females were more in number in the obese group and also because females have a higher percentage of body fat than men at a similar BMI.37
The finding agrees with the findings of the Framingham heart study 31 where body mass index was found to be strongly correlated with left ventricular mass, left ventricular wall thickness and left ventricular internal dimension after adjusting for blood pressure and age. The Framingham heart study showed that body mass index was associated with the prevalence of echocardiographic left ventricular hypertrophy, particularly in subjects with BMI exceeding 30kg/m2.
Similar result were found by dela maza et. al.128 who found positive correlations between LVM and BMI, triceptal skinfold thickness and blood pressure while Hammond et. al.124 found BMI and height to be strong independent predictors of LVM.
Another measure of obesity namely the waist circumference (WC) was assessed in this study. WC is a measure of abdominal obesity. Abdominal obesity using WC is defined as WC > 88cm in females and > 102cm in males.
lxxxiv
Strong correlations between WC and echo parameters were demonstrated in this study and all were statistically significant (P<0.001, table 8).
When the subjects were separated according to degrees of waist circumference, strong correlations with echo parameters was seen in females but not in males at WC >88cm in females and >102cm in males. This has demonstrated that the preferential deposition of fat centrally is associated with increased cardiovascular risk especially in females25. It is worthy to note that abdominal obesity is not only a risk factor for cardiovascular disease world wide but also for all cause mortality in men and women.170 In the Trandolapril Cardiac Evaluation (TRACE) register, the mortality rate was increased by 23%
in patients with abdominal obesity as compared with patients who were not abdominally obese. Excluding diabetes and hypertension from the multivariate analysis did not change the findings. This implies that the impact of obesity on all-cause mortality is mediated by mechanisms other than diabetes and hypertension.170,171
The waist hip ratio (WHR), another measure of abdominal obesity was weakly correlated with echo parameters in this study. When the subjects were separated according to degrees of waist hip ratio there was no correlation between abdominal obesity as measured by waist hip ratio and echo parameters (table 12). The waist circumference (WC) is therefore the preferred measure of
lxxxv
abdominal obesity for assessment of the impact of obesity on echocardiographic determinants of left ventricular hypertrophy.
The findings in this study support those of sukmoko et. al. 129 who found significant correlation between BMI, waist circumference and left ventricular mass. This is however slightly different from those of Avignon et. al.127 who found correlations between BMI, WHR and left ventricular mass. One feature common in all the above studies however is the BMI which showed strong correlation with LVM and even stronger correlations with LVM/H2 in males and females (r = 0.708, p < 0.001 and r = 0.799, p < 0.001) respectively. (table 8).
Pathologic hypertrophy as against physiologic hypertrophy is an independent risk factor for cardiovascular events such as stroke, heart failure, arrythmias and sudden death34-36. Alterations in cardiac structure may be present, even without any clinical signs of heart disease. It is apparent from this study that a variety of adaptations and alterations in cardiac structure occur as excessive adipose tissue accumulates even in the absence of systemic hypertension or underlying organic heart disease.
To meet increased metabolic needs in obesity, circulating blood volume, plasma volume and cardiac out put all increase. The increase in blood volume in turn increases venous return to the right and the left ventricles, eventually producing dilation of these cardiac cavities, increasing wall tension. This leads
lxxxvi
to LVH, which is usually accompanied by a decrease in diastolic chamber compliance, eventually resulting in an increase in left ventricular filling pressure and progressive ventricular enlargement103. As long as LVH adapts to LV chamber enlargement, systolic function is preserved. When LVH fails to keep pace with progressive left chamber dilation, wall tension increases even more and systolic dysfunction ensues. This could then lead to heart failure and increased risk of arrythmias and sudden death.36
Weight reduction regresses left ventricular hypertrophy 157-159 and this occurs regardless of whether the subjects have normal or high blood pressure.
There is strong evidence that weight loss in over weight or obese individuals reduces risk factors for diabetes and cardiovascular diseases. 58 Thus weight loss measures should be instituted early enough to prevent these complications of obesity.
The LV geometric pattern found in majority of the obese subjects in this study is eccentric ventricular hypertrophy (EVH) with a frequency of 46%. This agrees with studies by other authors that EVH is the most common geometric pattern associated with obesity. However this study also identified a significant proportion of concentric hypertrophy (24.7%) in the obese subjects who were apparently normotensive by casual blood pressure measurement. Within the pathophysiological concept established, especially in studies by Alpert et. al. 107 and Alexander 108, eccentric ventricular hypertrophy is associated with obesity.
lxxxvii
Nevertheless, many authors agree that in obese subjects with systemic hypertension, there is a double stimulus to develop hypertrophy that could be concentric or mixed. 135, 172 A 24 hour ambulatory blood pressure monitoring should therefore be recommended in the obese to detect cases of masked hypertension and nocturnal hypertension. Masked hypertension occurs in individuals in whom office readings underestimate out-of-office blood pressure readings and occurs in ten percent of patients. It clearly increases cardiovascular risk. 173 Nocturnal hypertension occurs in individuals whose blood pressures fail to dip at night during sleep. Nocturnal hypertension increases the aggregate haemodynamic load on the cardiovascular system and is a much stronger predictor of cardiovascular outcome than office measurements. 174
Left ventricular geometric patterns have prognostic implications with the worst prognosis associated with concentric hypertrophy105 followed by eccentric hypertrophy and concentric remodeling. Higher frequency of concentric remodeling (22.5%) was identified in the controls than the obese (12.6%). This is probably due to the increased blood volume and ventricular dilatation associated with the pathophysiology of obesity.
The results of the present study also showed that echo LVH occurred in 70.7% of the obese subjects when the LVM/H2 criterion was used for indexation and 45.4% of the obese when LVH/BSA criterion was used. This reveals a significant difference in the echo LVH diagnosis using the LVM/H2 criterion
lxxxviii
and therefore presents a more sensitive index for diagnosis. Under diagnosis of echo LVH is potentially dangerous as the obese patient may not be motivated to lose weight as appropriate to curb an entity of high cardiovascular risk.
Considering the high frequency of echo LVH depicted by the present study in the obese, obese subjects should have echocardiography done as part of their workup to enable identification of patients with higher cardiovascular risk and implementation of weight loss measures to control the ventricular remodeling process. There is also need for longitudinal studies to know the prognosis in obese subjects with LVH and abnormal geometric pattern.
lxxxix
CONCLUSION
The present study has demonstrated strong correlations between BMI, WC and echocardiographic determinants of left ventricular hypertrophy such as IVSd, LVIDd, PWTd, LVM/H2, LVM/BSA. BMI and WC had stronger correlations with echocardiographic parameters than WHR.
BMI and WC should therefore be the preferred measures for the assessment of the impact of obesity in relation to left ventricular hypertrophy.
This study has also demonstrated a higher frequency of eccentric LVH in the obese population than other geometric patterns followed by concentric hypertrophy.
Echo LVH occurred in 70.7% of obese subjects and 6.2% of controls using LVM/H2 criterion.
LVM/H2 identified more cases of echo LVH (70.7%) in the obese than LVM/BSA (45.4%).
LVM/H2 therefore should be the preferred index for identification of echo LVH in obese populations.
xc
RECOMMENDATIONS
In view of the double cardiovascular risk imposed by obesity and left ventricular hypertrophy, it is recommended that:
1. Health education programmes should be organized by medical practitioners, nutritionists and government in public institutions and in the community warning individuals on the predisposing factors to obesity such as high calorie foods, excessive eating and sedentary life style and their consequences.
2. Medical practitioners should be alert to capture cases of obesity and manage them properly using diet and exercise as preliminary steps in primary, secondary and tertiary health institutions. Weight loss can regress left ventricular hypertrophy.
3. A 24 hour ambulatory blood pressure monitoring should be part of routine evaluation of all obese patients to detect nocturnal hypertension and masked hypertension in those who are apparently normotensive by casual blood pressure measurement. Masked hypertension is said to be present in ten percent of patients and correlates with higher cardiovascular risk.
4. Echocardiography should be part of routine investigation for obesity.
xci
5. LVM/H2 should be the recommended index for defection of echo LVH in obese population.
6. There is also need for longitudinal studies to prognosticate LVH and abnormal geometric patterns in obese subjects.
xcii
LIMITATIONS OF THE STUDY
The relationship between other measures of obesity such as percentage body fat estimation triceptal and subscapular skin folds thickness to echocardiographic determinants of left ventricular hypertrophy could not be assessed in this study.
This was due to the unavailability of the equipments required for measurement.
xciii
REFERENCES
1. Eckel RH, York DA, Rossner S, et al. American Heart Association prevention conference VII. Obesity a worldwide epidemic related to heart disease and stroke: an executive summary. Circulation 2004; 110: 2968 – 2975.
2. World Health Organization Technical report series 894: Obesity:
preventing and managing the global epidemic Geneva: World Health Organization 2000.
3. Engeland A, Bjorge T, Sogaard AJ, et al. Body mass index in adolescence in relation to total mortality: a 32 year follow up of 227,000 Norwegian boys and girls. Am J Epidemiol 2003; 157: 517 – 523
4. Flegal KM, Carroll MD, Ogden CL, et al. prevalence and trends in obesity among US adults, 1999 – 2000. JAMA 2002; 288: 1723 – 1727.
5. Flegal KM, Carroll MD, Kuczmarski RJ, et al. Overweight and obesity in the United States: prevalence and trends; 1960 – 1994. Int J Obes Relat.
Metab Disord. 1998; 22: 39 – 47.
6. Himes OH, Bonchard C. Do the new metropolitan life insurance weight – height tables correctly assess body frame and body fat relationship? Am J Public Health. 1985; 75: 1076 – 1079.
7. Clinical Guidelines on the identification, Evaluation and Treatment of overweight and obesity in Adults: The Evidence report; National Institutes of Health. Obes Res. 1998; Suppl 2: 51S – 209S.
xciv
8. Ogden CL, flegal KM, Carol MD, et al. Prevalence and trends in overweight among US children and adolescents, 1999 – 2000. JAMA 2002; 288: 1728 – 1732.
9. Kuczmarski RJ, Flegal KM, Campbell SM, et al. Increasing prevalence of overweight assmong US adults: The National Health and Nutrition Examinations Surveys, 1960 to 1991. JAMA 1994; 272: 205 – 211.
10. Mokdad AH, Serdula MK, Dietz WH, et al. The spread of obesity epidemic in the United States, 1991 – 1998. JAMA 1999; 272: 205 – 211.
11. Eckel RH. Obesity and Heart disease: a statement for health care professionals from the Nutrition committee, American Heart Association.
Circulation 1997; 96:3248 – 3250.
12. Eckel RH, Krauss RM. American Heart Association call to action:
Obesity as a major risk factor for coronary heart disease. AHA Nutrition Committee. Circulation 1998; 97:2099 – 2100.
13. Klein S, Burke LE, Bray GA, et al. American Heart Association council on Nutrition, Physical Activity, and metabolism. Clinical implications of obesity with specific focus on cardiovascular disease: a statement for professionals from the American. Heart Association Council on Nutrition, Physical Activity, and metabolism: endorsed by the American College of Cardiology foundation. Circulation 2004; 110: 2952 – 2967.
14. Berghorfer A, Pischon T, Reinhold T et al. Obesity prevalence from a European Perspective. BMC Public Health. 2008; 8 : 200 -201.
xcv
15. Gao Y, Griffiths S, Chan EY. Community based interventions to reduce over weight and obesity in China: a systematic review of Chinese and English literature. J Public Health (oxf) 2008; 30:436-448.
16. Wilks R, McFarland - Anderson N, Bennet F, et al. Obesity in peoples of African diaspora. Ciba found Symp. 1996; 201: 37- 48.
17. Uwaifo GI, Arioglu E. Obesity. eMedicine Specialties. Endocrinology and Metabolic disorders 2006; 10: 1- 11.
18. Olupitan RC, Adedevoh BK. Therapeutic effects of the low calorie diet in obesity. W. African Med J. 1967; 16:141 – 144.
19. Adeyemo A, Luke A, Cooper R, et al. A genome wide scan for body mass index among Nigerian Families. Obes Res 2003; 11 (2): 266 – 273.
20. Garow JS. Obesity: Oxford Text book of medicine 3rd Edition. Oxford New York. Oxford University press 1996. 3: 1301 – 1314
21. Quetelete AD. Physique De L' Homme, quoted by pengelly CDR. Body mass index and abdominal girth in the diagnosis of obesity. Proc. R. Col.
Physicians, Edinburgh 1994; 24: 174 – 180.
22. Kraemer H, Berkowitz RI, Hammer LD. Methodological difficulties in the studies of obesity. 1. Measurement Issues. Ann Behave Med. 1990;
12: 112 – 118.
23. Must A, Dallal CE, Dietz WH. Reference data for obesity 85th and 95th percentiles of body mass index (wt/h2) and tricepts skinfold thickness.
Am J Clin Nutr 1991; 53: 839 – 846.
xcvi
24. Manson JE, Willet WC, Stampter MJ, et al. Body weight and mortality among women. N Eng J Med. 1995; 333: 677 – 685.
25. Yusuf S, Hawken S, Ounpuu S, et al. INTER HEART study investigators.
Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTER HEART Study): case – control study. Lancet 2004; 364: 937 – 952.
26. Amodu PH, Mba IO, Lawson L. Prevalence of obesity and dyslipidaemia in hypertensives seen in Abuja, Nigeria. Scard J. Clin Lab Invest. Suppl.
2005; 240: 14 – 17.
27. Fadupin GT, Joseph EU, Keshinro OO. Prevalence of obesity among type 2 diabetics in Nigeria: a case study of patients in Ibadan, Oyo State, Nigeria. Afri. J. Med Sci. 2004; 33 (4): 381 – 384.
28. Kannel WB, Gardon T, Offut D. Left ventricular hypertrophy by electrocardiogram: prevalence, incidence and mortality in the Framingham study. Ann Intern Med 1969; 71:89 – 105.
29. Savage DD, Abbott RD, Podgett S, et al. Epidemiological features of left ventricular hypertrophy in normotensive and hypertensive subjects. In:
Ter Keurs HEDJ, Schipperheyn JJ, eds. Left ventricular hypertrophy. The Hague: Martins Nighoff, 1983: 2 – 15.
30. Levy D, Murabito JM, Anderson KM et al. Echocardiographic left ventricular hypertrophy: clinical characteristics. The Framingham study.
Clin Exp Hypertens 1992;14:85 – 97.
xcvii
31. Lauer MS, Anderson KM, Kannel WB, et al. The impact of obesity on left ventricular mass and geometry. The Framingham Heart Study. JAMA 1991; 266 (2): 231 – 236.
32. Lauer MS, Anderson KM, Levy D. Separate and joint influences of obesity and mild hypertension on left ventricular mass and geometry: the Framingham Heart Study. J Am Coll Cardiol. 1992; 19 (1): 130 – 134.
33. Alpert MA. Obesity cardiomyopathy; pathophysiology and evalution of the clinical syndrome. Am J Med Sci 2001; 321: 225 – 236.
34. Levy D, Garrison RJ, Savage DD, et al. Left ventricular mass and incidence of coronary heart disease in an elderly cohort: The Framingham Heart study. Ann Intern Med 1989; 110: 101 – 107.
35. Levy D, Garrison RJ, Savage DD, et al. prognostic implications of echocardiographically determined left ventricular mass in the Framingham Heart study. N Eng J Med 1990; 322: 1561 – 1566.
36. Haider AW, Lanson MG, Benjamin EJ, et al. Increased left ventricular mass and hypertrophy are associated with increased risk for sudden death.
J Am Coll. Cardiol 1998; 32: 1454 – 1459.
37. Flier OS, Maratos-Flier E. Obesity: In (Eds) Harrison’s Principles of Internal Medicine 16th Edition, New York, The McGraw Hill companies 2005: 422 – 429.
38. Lissner L, Hertman BL. Dietary fat and obesity: Evidence from epidemiology. Eur J Clin Nutrition 1995; 49: 79 – 90.
xcviii
39. Williamson DF, Madans J, Anda RF, et al Recreational physical activity and ten years weight change in a U.S.A national cohort. Int. Obes 1993;
17: 279 – 296.
40. Krauss RM, Winston M, Fletcher BJ, et al. Obesity: Impact on cardiovascular disease. Circulation 1998; 98: 001 – 010.
41. Yang W, Kelly T, He J. Genetic epidemiology of obesity. Epidemiol Rev 2007; 29: 49 – 61.
42. Garrow JS (Ed) Health Implications of obesity in obesity related disease.
London, Churchill Livingstone 1988; 1 – 19.
43. Durnin J, Wormenslay J. Body fat assessment from total body density and its estimation from skin fold thickness. Bristish J Nutr. 1974; 32: 77 – 97.
44. Gibson RS (Ed). Laboratory Assessment of body composition in principles of nutritional assessment. New York Oxford University press.
1990; 263 – 284.
45. Obesity: Wikipedia, the free encyclopedia. 11 – 15 – 2006, 1 – 7 (http://
enwikipedia. org/wiki/obesity)
46. Garrow JS (Ed). Measurement of energy stores in obesity and related disease. London, Churchill Living stone; 1988: 25 – 54.
47. Strychar I. Diet in management of weight loss. CMAJ 2006; 174 (1): 56 – 63.
xcix
48. Bravata DM, Sanders L, Huang J, et al. Efficacy and safety of low carbohydrate diets: a systematic review. JAMA 2003; 289 (14): 1837 - 1850
49. Shick SM, Wing RR, Klem ML, et al. Persons successful at long term weight loss and maintenance continue to consume a low energy, low – fat diet. J Am Diet Assoc 1998; 98 (4): 408 – 413.
50. Tate DF, Jeffery RW, Sherwood NE, et al. Long term weight losses associated with prescription of higher physical activity goals. Are higher levels of physical activity protective against weight regain? Am. J. Clin.
Nutr. 2007; 85 (4): 954 – 959.
51. Science Based Solutions to Obesity: What are the roles of Academic, Government, Industry, and Health Care? Proceedings of a symposium, Boston. Massachusetts USA Am. J. Clin Nutr. 2005; 82 (1 Suppl): 2675 – 2735.
52. Anderson TW, Konz EC, Friedrich RC, et al. Long term weight loss maintainance: a meta – analysis of US studies. Am.J. Clin. Nutr. 2001; 74 (5): 579 – 584.
53. Willamson DF, Pamu KE, Thun M, et al. Prospective study of intentional weight loss and mortality in never – smoking overweight US women aged 40 – 64 years. Am. J. Epidemiol 1995; 141 (12): 1128 – 1141.
54. Gwinup G. Weight loss without dietary restriction: efficacy of different forms of aerobic exercise. Am .J. Sports Med 1987; 15 (3): 275 – 279.
c
55. Fumento M. The fat of the land: Our Health Crisis and how overweight Americans can help themselves. Penguin (Non classics) 1997: 126.
56. Shaw K, Gennat H, O' Rourke P, et al. Exercise for overweight or obesity. Cochrane data base of systematic reviews (on line) 2006; 4:
CD003817.
57. Rucker D, Padnal R, Li SK, et al. long term pharmacotherapy for obesity and overweight: up dated meta – analysis BMJ 2007; 335 (7631): 1194 – 1199.
58. National Institute for Health and Clinical Excellence. Clinical Guideline 43; obesity: the prevention, identification, assessment and management of weight and obesity in adults and children. London 2006.
59. Encinosa WE, Bernard DM, Chenc C, et al. Health care utilization and outcome after bariatric surgery. Medical care 2006; 44 (8): 706 – 712 60. Sjostrom L, Narbro K, Sjostrom CD, et al. Effects of bariatric surgery on
mortality in Swedish obese subjects N Engl. J. Med. 2007; 357 (8): 741 – 752.
61. Adams TD, Gress RE, Smith SC, et al. Long term morality after gastric bypass surgery. N. Engl .J. Med. 2007; 357 (8): 753 – 761.
62. Sjostrom L. Surgical treatment of obesity; an over view and results of SOS study In: Bray GA, Bouchand C. (eds) Hand book of obesity:
clinical applications 2nd edn Basel: Marcel Decker, 2004: 359 – 389.