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| Lifetime risk of developing coronary heart disease | ||
Sir--The Framingham Heart Study investigators 1 show that the lifetime risk of coronary heart disease at age 40 years is one in two for men and one in three for women. This finding implies a high burden in health and costs for developed and developing countries. For the most efficient and economic results, who should be screened first? Besides factors such as hypertension, smoking, diabetes, and hyperlipidaemia, we propose that all persons older than 30 years with the following clinical factors should be screened: overweight (body mass index [BMI] over 27 kg/m2), a resting heart rate (pulse) over 85 per min, or a pulse×mass index over 1·0 (pulse×BMI divided by 1730 or 72×24).
Overweight is a first range risk factor, and every unit in excess of BMI implies an excess in mortality due to cardiovascular disease of about 8-10%.2 Moreover, caloric restriction has consistently increased the lifespan in all species studied .3 So, we compared caloric intake with life expectancy in the 20 most developed countries and found that, indeed, an ingestion of 280 kcal less every day corresponds to 25 months longer lifespan. We also compared the relation between pulse or resting heart rate and BMI in the pulse×mass index. Surprisingly, we found that if there is a relation of three to one between pulse and BMI (eg, 72 to 24) and this relation was maintained proportional as BMI increases, then the enlarged mortality becomes predictable--eg, for a BMI of 33 and a theoretically corresponding pulse of 99 (1/3), the pulse×mass index (33×99÷1730) is 1·9 or almost two-fold, corresponding with the known doubling of mortality with this BMI. The same tendency is found for every increase of BMI and pulse.
This finding probably indicates the relation between hyperinsulinaemia, stimulation of sympathetic nervous system, and oxidative metabolism that is seen in obese patients and which improves when they exercise regularly or lose weight. The other surprise was that when we compared prospectively, in a preliminary group of 20 patients, pulse×mass index with the calculations of cardiovascular disease risk factors according to the Framingham Heart Study, the correlation was highly significant (r=0·94; p<0·05), especially in patients over 40 years, despite the pulse×mass index being more sensitive for younger patients.4
We correlated pulse with BMI, because resting heart rate indicates oxidative metabolic rate and activity of the sympathetic nervous system, such as under stress or hyperinsulinaemia. A pulse rate of over 85 is a known risk factor for cardiovascular disease, and pulse reducing drugs, such as ß-blockers, reduce mortality. In all mammals, the slower the pulse, the longer the lifespan, and vice versa.5
Cardiovascular drugs that reduce mortality (such as ß-blockers or diuretics) can also reduce the pulse×mass index. Potent vasodilators that increase pulse rate and retain water, do not reduce mortality.
*Enrique Sanchez-Delgado, Heinz Liechti
Laboratorios Solka SA, km16 1/2 Carretera
Masaya, PO Box A-02, Managua, Nicaragua (e-mail: solka@ibw.com.ni)
1 Lloyd-Jones DM, Larson MG, Beiser A, Levy D. Lifetime risk of developing coronary heart disease. Lancet 1999; 353: 89-92.
2 Stevens J, et al. The effects of age on the association between body-mass index and mortality. N Engl J Med 1998; 338: 1-7.
3 Finkel E. Piecing together the puzzle of ageing. Lancet 1997; 350: 1150.
4 Sánchez-Delgado E. Presented at the II National Congress of Clinical Specialties, Managua, Nicaragua, 24-27 June 1998, and XIV Central American Congress of Internal Medicine, San Salvador, El Salvador, 18-21 Nov, 1998.
5 Levine HJ. Rest heart rate and life expectancy. JACC
1997; 30: 1104-06.
(UNPUBLISHED), COMPLEMENTARY LETTER TO THE EDITOR:
February 1, 1999
Dear Dr. Richard Horton,
we are very pleased in greeting you again from Nicaragua. In our CORRESPONDENCE (Letter to the Editor) from January 19, 1999, we commented about the -The Framingham Heart Study 1 (Lancet Jan. 09, 99) and we informed you about our results and our proposal for the use of the pulse×mass index as a sensible indicator of the cardiovascular risk, which highly correlates with the calculations of the CVS risk factorsaccording to the Framingham Heart Study.
Due to the space limitations of our letter, we could not refere to the many lines of evidence supporting the usefullness of the pulse×mass index, but as you can note in our letter, there are at least seven lines of evidence. We would like to mention other lines of evidence. For instance, you could have an athlete with "only" muscles and a Body Mass Index of 27, but at the same time a Rest Heart Rate (Pulse) of 55/min. As you can easily calculate his pulse×mass index (27×55÷1730) is 0.86 or lower than the normal 1.0. This corresponds better to his physical fittness, than BMI alone. Moreover, we analyzed the results of Gunnar Erikssen et.al. about Changes in physical fittness and changes in mortality (Lancet 1998;352:759-62).
In his Table 3, he shows a total mortality of 1.16 for an increase of 10.1 bpm (or 1 S.D.)in the Resting Heart Rate (that means 72+10.1=82.1 bpm). To an increase of 2.7 kg/m2 (or 1 S.D.) of the Body Mass Index (that is 24+2.7=26.7 BMI), correspondes a total mortality of 1.12. That means, together RHR+BMI, gave an empirical, real, total mortality of 28 % (1.28) above the average. If we did not know the empirical results, but we decide to calculate the pulse×mass index of 82.1×26.7÷1730, we will find a result of 1.27 which as you can see is almost identical to the empirical data of 1.28.
We also analyzed the results of the UKPDS Study (Lancet Sept. 12, 1998), which found that Metformin reduces the mortality while Sulphonylurea and/or Insuline reduce the microvascular events, but not the mortality.
If we apply the pulse×mass index as a pharmacological principle, we can reason that Metformin improves the Glucose metabolism without promoting hyperinsulinism, weigth gain or sympathic (pulse) stimulation. At the other hand, Sulphonylurea and/or Insuline improve the Glucose metabolism but at expense of hyperinsulinism, weigth gain and sympathic (pulse) stimulation. That could explain the results of less complications but not less mortality, since the pulse×mass index is not positively affected. It would be very interesting to examine if Acarbose, which inhibits carbohydrate absorption, wihtout affecting insuline or sympathic, could give, at least to some extents, similar results like with Metformin.
We would be very appreciative to hear your comments.
With best regards, yours sincerely
Enrique Sánchez-Delgado
Heinz Liechti