2005, Number 4
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Rev Med Inst Mex Seguro Soc 2005; 43 (4)
Causality in Cardiology: Concepts in Evolution
Méndez GF
Language: Spanish
References: 20
Page: 357-363
PDF size: 91.00 Kb.
ABSTRACT
This paper describes several concepts about causality from Empedocles, Aristoteles and Galeno, to Koch and Hill and the evolution of these concepts related to cardiovascular diseases. Also defines cause and risk, and the philosophical theories about scientific knowledge: inductive versus refutation analysis. On these basis, the study of cardiovascular disease’s causality, especially coronary heart disease, allows us the identification of several risk factors involved in its development. However, even with the presently coronary heart disease risk charts (from Framingham and European studies) the higher probability for the development of a cardiovascular ischemic event is around 40 %, establishing an important degree of uncertainty. With the improvement in molecular biology techniques, genetics have attempted to analyse several genetic polymorphisms in search of the origin of coronary heart disease. Unfortunately, less than 10 % of these polymorphisms have had a positive correlation with coronary heart disease being of minor risk that those obtained for having the diagnosis of type 2 diabetes mellitus or hypercholesterolemia. On these basis, the requirement of new population research projects in which clinical and genetic risk factors are to be studied for the appropriate understanding of the causality process of cardiovascular diseases must be a worldwide priority.
REFERENCES
Rothman KJ. Causes. Am J Epidemiol 1976;104:587-592.
2. Susser M. What is a cause and how do we know one? A grammar for pragmatic epidemiology. Am J Epidemiol 1991;133:635-648.
3. Sutter MC. Assigning causation in disease: beyond Koch’s postulates. Perspect Biol Med 1996;39:581-592.
4. Kupper LL, Hogan MD. Interaction in epidemiologic studies. Am J Epidemiol 1978;108:447-453.
5. Maclure M. Popperian refutation in epidemiology. Am J Epidemiol 1985;121:343-350.
6. Wall S. Epidemiology for prevention. Int J Epidemiol 1995;24:655-664.
7. Viniegra L. Explicación y causalidad en el campo de la salud. Higiene 2003;5:19-33.
8. Evans AS. Causation and disease: a chronological journey. The Thomas Parran Lecture. Am J Epidemiol 1978; 108:249-258.
9. Weiss NS. Inferring causal relationships: elaboration of the criterion of “dose-response”. Am J Epidemiol 1981;113:487-490.
Hill AB. The environment and disease: Association or causation? Proc R Soc Med 1965;58:295-300.
Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, Izzo JL jr, et al. Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension 2003;42:1206-1252.
Sturm AC. Cardiovascular genetics: Are we there yet? J Med Genet 2004;41:321-323.
Kannel WB. Bishop lecture. Contribution of the Framingham Study to preventive cardiology. J Am Coll Cardiol 1990;15:206-211.
Lloyd-Jones DM, Wilson PW, Larson MG, Beiser A, Leip EP, D’Agostino RB, et al. Framingham risk score and prediction of lifetime risk for coronary heart disease. Am J Cardiol 2004;94:20-24.
De Backer G, Ambrosioni E, Borch-Johnsen K, Brotons C, Cifkova R, Dallongeville J, et al. European guidelines on cardiovascular disease prevention in clinical practice. Third Joint Task Force of European and other Societies on Cardiovascular Disease Prevention in Clinical Practice (constituted by representatives of eight societies and by invited experts). Atherosclerosis 2004;173:381-391.
McCarthy JJ, Parker A, Salem R, Moliterno DJ, Wang Q, Plow EF, et al. Large scale association analysis for identification of genes underlying premature coronary heart disease: cumulative perspective from analysis of 111 candidate genes. J Med Genet 2004; 41:321-323.
Hamsten A, Eriksson P. Thrombospondins and premature coronary artery disease. Time beyond genotype-phenotype association studies. Arterioscler Thromb Vasc Biol 2003;23:6-7.
Tsikouris JP, Suarez JA, Meyerrose GE. Plasminogen activator inhibitor-1: physiologic role, regulation, and the influence of common pharmacologic agents. J Clin Pharmacol 2002; 42:1187-1199.
Hanefeld M, Schmechel H, Schwanebeck U, Lindner J, The DIS Group. Predictors of coronary heart disease and death in NIDDM: The diabetes intervention study experience. Diabetologia 1997;40:S123-S124.
Oseguera-Moguel J. Enfermedades cardiovasculares: presente y futuro basados en la biología molecular. Rev Invest Clin 2003;55:155-160.