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Inicio Revista Española de Geriatría y Gerontología Tratamiento hipolipemiante en ancianos
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Vol. 36. Núm. 4.
Páginas 195-209 (enero 2001)
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Vol. 36. Núm. 4.
Páginas 195-209 (enero 2001)
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Tratamiento hipolipemiante en ancianos
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L.A. Álvarez-Sala*, M. Valderrama, F.J. Torres, P. Agudo, F.J. Rodríguez-Gorostiza, J. Millán
Unidad de Lípidos. Medicina Interna 3. Hospital General Universitario Gregorio Marañón
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Resumen

Los estudios de población adulta, que incluían cierto número de personas mayores, demostraron una inexistente o débil correlación en el binomio colesterol-enfermedad cardiovascular en la tercera edad. Aquellos que incluyeron un considerable volumen de personas en esas franjas de edad sí encontraban una importante relación; incluso al considerar el riesgo absoluto, no el relativo, éste era mayor en este grupo de población. Hay estudios que indican que la relación desaparece por encima de los 85 años de edad, y algunos dudan si se mantiene por encima de los 75 años.

Los grandes estudios prospectivos de intervención farmacológica indican que el tratamiento hipolipemiante en la tercera edad es tan eficaz como en los adultos más jóvenes. Sin embargo, y dado que el análisis de esta franja de edad se hizo retrospectivamente, y con un número pequeño de personas, hay en marcha varios estudios con distintas estatinas para establecer la eficacia y la oportunidad de tratar la hiperlipemia en la tercera edad. Los análisis costo-beneficio post-hoc disponibles con estatinas referidos a la tercera edad, indican que su uso estaría justificado.

Finalmente se revisan las opciones farmacológicas disponibles en la actualidad: estatinas, resinas y fibratos. La mayor potencia hipolipemiante de las primeras, y su tolerancia, hacen que sean de elección en el tratamiento de las hipercolesterolemias puras o asociadas con hipertrigliceridemias moderadas. En las hipertrigliceridemias puras o asociadas con una hipercolesterolemia leve, los fibratos son la primera elección. Se recuerda la importancia de ajustar las dosis de los fármacos en función de la función renal y/o hepática en esta edad, en la que es frecuente una insuficiencia real o funcional de los sistemas corporales de eliminación.

Palabras clave:
Hipercolesterolemia
Hiperlipidemia
Ancianos
Tercera edad
Estatinas
Summary

Studies of the adult population, that included some elderly subjects demonstrated a non-existing or weak correlation in the cholesterolcardiovascular disease relation in the elderly. Those including a considerable volume of persons in these age groups found a significant relationship; this was greater in the population group even when the absolute risk and not the relative one was considered. There are studies that indicate that this relationship disappears over the age of 85, and some doubt if it is maintained above age 75.

The large prospective studies on drug intervention indicate that hypolipemic drug treatment in the elderly is as efficient as in the younger adults. However, and given that the analysis of this age group was performed retrospectively, and with a small number of persons, there are several studies underway with different statins to establish the efficacy and usefulness of treating hyperlipemia in the elderly. The «post-hoc» cost-benefit analysis with statins in regards to the elderly age indicates that their use would be justified.

Finally, the pharmacological options presently available are reviewed: statins, resins and fibrates. The greater hypolipemic potency of the first ones and their tolerability make them the treatment of choice for the pure hypercholesterolemias or those associated with moderate hypertriglyceridemias. In the pure hypertriglyiceridemias or those associated with a mild hypercholesterolemia, the fibrates are the first choice treatment. The importance of adjusting the drug doses in function of the renal and/or hepatic function in this age, in which real or functional failure of the elimination body systems is frequent, is emphasized.

Key words:
Hypercholesterolemia
Hyperlipidemia
Elderly
Statins
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Bibliografía
[1.]
T.R. Dawber, F.E. Moore, G.V. Mann.
Coronary heart disease in the Framingham study.
Am J Public Health, 47 (1957), pp. 4-23
[2.]
The Pooling Project Research Group.
Relationship of blood pressure, serum cholesterol, smoking habit, relative weight and ECG abnormalities to incidence of major coronary events: final report of the pooling Project.
J Chronic Dis, 31 (1978), pp. 201-306
[3.]
L.A. Álvarez Sala, M. De Oya, P. Mata, J.A. Gómez Gerique.
Arteriosclerosis.
Tratado de Medicina Interna, pp. 431-446
[4.]
WHO cooperative trial on primary prevention of ischemic heart disease with clofibrate to lower serum cholesterol.
Final mortality follow-up: report of the Committee of Principal Investigators.
Lancet, 2 (1984), pp. 600-604
[5.]
Lipid Research Clinics Program.
The Lipid Research Clinic Coronary Primary Prevention Trial results. I. Reduction in incidence of coronary heart disease.
JAMA, 251 (1984), pp. 351-364
[6.]
M.H. Frick, O. Elo, K. Haapa, O.P. Heinonen, P. Heinsalmi, P. Helo, et al.
Helsinki Heart Study: Primary Prevention Trial with gemfibrozil in middleaged men with dyslipemia. Safety of treatment, changes in risk factors and incidence of coronary heart disease.
N Engl J Med, 317 (1987), pp. 1237-1245
[7.]
P. Leren.
The Oslo diet-heart study. Eleven years report.
Circulation, 42 (1970), pp. 935-942
[8.]
Coronary Drug Project Research Group.
Clofibrate and niacin in coronary heart disease.
JAMA, 231 (1975), pp. 360-381
[9.]
Group of Physicians of the Newcastle upon Tyne Region.
Trial of clofibrate in the treatment of ischaemic heart disease.
BMJ, 4 (1971), pp. 767-775
[10.]
L.A. Carlson, G. Rosenhamer.
Reduction of mortality in the Stockholm Ischaemic Heart Disease Secondary Prevention Study by combined treatment with clofibrate and nicotinic acid.
Acta Med Scand, 223 (1988), pp. 405-418
[11.]
P.L. Canner, K.G. Berge, N.K. Wenger, J. Stamler, L. Friedman, R.J. Prineas, et al.
for the Coronary Drug Project Research Group. Fifteen year mortality in Coronary Drug Project patients: long term benefit with niacin.
J Am Coll Cardiol, 8 (1986), pp. 1245-1255
[12.]
M.F. Muldoon, S.B. Manuck, K.A. Matthews.
Lowering cholesterol concentrations and mortality: a quantitative review of primary prevention trials.
Br Med J, 303 (1990), pp. 276-282
[13.]
J.E. Rossouw, B. Lewis, B.M. Rifkind.
The value of lowering cholesterol after myocardial infarction.
N Engl J Med, 323 (1990), pp. 1112-1119
[14.]
M.F. Oliver.
Might treatment of hypercholesterolemia increase non-cardiac mortality?.
Lancet, 337 (1991), pp. 1529-1531
[15.]
Report of the National Cholesterol Education Program Expert Panel on detection, prevention and treatment of high cholesterol in adults..
Arch Intern Med, 148 (1988), pp. 36-69
[16.]
Scandinavian Simvastatin Survival Study Group.
Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S).
Lancet, 344 (1994), pp. 1383-1389
[17.]
J. Pekkanen, S. Linn, G. Heiss, C.M. Suchindran, A. Leon, B.M. Rifkind.
Tenyear mortality from cardiovascular disease in relation to cholesterol level among men with and without preexisting cardiovascular disease.
N Engl J Med, 322 (1990), pp. 1700-1707
[18.]
The Long-Term Intervention with Pravastatin in Ischaemic Disease (LIPID) Study Group..
Prevention of cardiovascular events and death with pravastatin in patients with coronary heart disease and a broad range of initial cholesterol levels.
N Engl J Med, 339 (1998), pp. 1349-1357
[19.]
J. Shepherd, S.M. Cobbe, I. Ford, C.G. Isles, A.R. Lorimer, P.W. Macfarlane, et al.
for the West of Scotland Coronary Prevention Study Group. Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia.
N Engl J Med, 333 (1995), pp. 1301-1307
[20.]
Compliance and adverse event withdrawal: their impact on the West of Scotland Coronary Prevention Study..
Eur Heart J, 18 (1997), pp. 1718-1724
[21.]
F.M. Sacks, M.A. Pfeffer, L.A. Moye, J.L. Rouleau, J.D. Rutherford, T.G. Cole, et al.
for the Cholesterol and Recurrent Events Trial Investigators. The effect of pravastatin on coronary events after myocardial infarction in patients with average cholesterol levels.
N Engl J Med, 335 (1996), pp. 1001-1009
[22.]
J.R. Downs, M. Clearfield, S. Weis, E. Whitney, D.R. Shapiro, P.A. Beere, et al.
for the AFCAPS/TexCAPS Research Group. Primary prevention of acute coronary events with lovastatin in men and women with average cholesterol levels. Results of AFCAPS/TexCAPS.
JAMA, 279 (1998), pp. 1615-1622
[23.]
E.J. Graves.
Detailed diagnoses and procedures, National Hospital Discharge Survey, 1989.
Vital Health Stat, 13 (1991), pp. 1-236
[24.]
V. Fuster, Z.A. Fayad, J.J. Badimon.
Acute coronary syndromes: biology.
Lancet, 353 (1999), pp. SII5-9
[25.]
W.B. Kannel, T. Gordon.
Cardiovascular risk factors in the aged: the Framingham Study.
Proceedings of the Second Conference on the Epidemiology of Aging. Bethesda (Maryland): National Institutes of Health, pp. 65-89
[26.]
M. Moser.
The management of cardiovascular disease in the elderly.
J Am Geriatr Soc, 30 (1982), pp. S20-S29
[27.]
A.M. Garber, H.C. Sox, B. Littenberg.
Screening asymptomatic adults for cardiac risk factors: the serum cholesterol level.
Ann Intern Med, 110 (1989), pp. 622-639
[28.]
R. Benfante, D. Reed.
Is elevated serum cholesterol level a risk factor for coronary heart disease in the elderly?.
JAMA, 263 (1990), pp. 393-396
[29.]
E. Barrett-Connor, L. Suárez, K. Khaw, M.H. Criqui, D.L. Wingard.
Ischemic heart disease risk factors after age 50.
J Chronic Dis, 37 (1984), pp. 903-908
[30.]
D.J. Gordon, B.M. Rifkind.
Treating high blood cholesterol in the older patient.
Am J Cardiol, 63 (1989), pp. 48H-52H
[31.]
R.A. Kronmal, K.C. Cain, Z. Ye, G.S. Omenn.
Total serum cholesterol levels and mortality risk as a function of age: a report based on the Framingham data.
Arch Intern Med, 153 (1993), pp. 1065-1073
[32.]
S.M. Rubin, S. Sidney, D.M. Black, W.S. Browner, S.B. Hulley, S.R. Cummings.
High blood cholesterol in elderly men and the excess risk for coronary heart disease.
Ann Intern Med, 113 (1990), pp. 916-920
[33.]
A.W. Weverling Rijnsburger, G.J. Blauw, A.M. Lagaay, D.L. Knook, A.E. Meinders, R.G. Westendorp.
Total cholesterol and risk of mortality in the oldest old.
Lancet, 350 (1997), pp. 1119-1123
[34.]
H.M. Krumholz, T.H. Seeman, S.S. Merill, C. Mendes de Leon, V. Vaccarino, D.I. Silverman, et al.
Lack of association between cholesterol and coronary heart disease mortality and morbility and all-cause mortality in persons older than 70 years.
JAMA, 272 (1994), pp. 1335-1340
[35.]
P. Zimetbaum, W.H. Frishman, W.L. Ooi, M.P. Derman, M. Aronson, L.I. Gidez, et al.
Plasma lipids and lipoproteins and the incidence of cardiovascular disease in the very elderly. The Bronx Aging Study.
Arterioscler Thromb, 12 (1992), pp. 416-423
[36.]
S.B. Hulley, T.B. Newman.
Cholesterol in the elderly. Is it important?.
JAMA, 272 (1994), pp. 1372-1374
[37.]
W.S. Aronow, A.H. Herzig, F. Etienne, P. D'Alba, J. Ronquillo.
41-month follow-up of risk factors correlated with new coronary events in 708 elderly patients.
J Am Geriatr Soc, 37 (1989), pp. 501-506
[38.]
M.C. Corti, J.M. Guralnik, M.E. Salive, T. Harris, L. Ferrucci, R.J. Glynn, et al.
Clarifying the direct relation between total cholesterol levels and death from coronary heart disease in older persons.
Ann Intern Med, 126 (1997), pp. 753-760
[39.]
S. Behar, E. Graff, H. Reicher-Reiss, V. Boyko, M. Benderly, A. Shotan, et al.
Low total cholesterol is associated with high total mortality in patients with coronary heart disease. The Bezafibrate Infarction Prevention (BIP) Study Group.
Eur Heart J, 18 (1997), pp. 52-59
[40.]
R.W. Sherwin, D.N. Wentworth, J.A. Cutler, S.B. Hulley, L.H. Kuller, J. Stamler.
Serum cholesterol levels and cancer mortality in 361,662 men screened for the Multiple Risk Factor Intervention Trial.
JAMA, 257 (1987), pp. 943-948
[41.]
A. Keys, C. Aravanis, H. Blackburn, R. Buzina, A.S. Dontas, F. Fidanza, et al.
Serum cholesterol and cancer mortality in the Seven Countries Study.
Am J Epidemiol, 121 (1985), pp. 870-883
[42.]
D.R. Jacobs, M.F. Muldoon, L. Rastam.
Invited commentary: low blood cholesterol, nonillness mortality, and other nonatherosclerotic disease mortality: a search for causes and confounders.
Am J Epidemiol, 141 (1995), pp. 518-522
[43.]
C. Iribarren, D.M. Reed, R. Chen, K. Yano, J.H. Dwyer.
Low serum cholesterol and mortality. Which is the cause and which is the effect?.
Circulation, 92 (1995), pp. 2396-2403
[44.]
J.A. Garrido.
Manejo de la dislipemia en ancianos y mujeres.
Enfermedades cardiovasculares. Nutrición, genética y epidemiología, pp. 71-84
[45.]
MRC/BHF Heart Protection Study of cholesterol-lowering therapy and of antioxidant vitamin supplementation in a wide range of patients at increased risk of coronary heart disease death:.
early safety and efficacy experience.
Eur Heart J, 20 (1999), pp. 725-741
[46.]
S.J. Lewis, L.A. Moye, F.M. Sacks, D.E. Johnstone, G. Timmis, J. Mitchell, et al.
Effect of pravastatin on cardiovascular events in older patients with myocardial infarction and cholesterol levels in the average range. Results of the Cholesterol and Recurrent Events (CARE) trial.
Ann Intern Med, 129 (1998), pp. 681-689
[47.]
S.J. Lewis, F. Sacks, E. Braunwald.
Cholesterol lowering in older patients.
Ann Intern Med, 131 (1999), pp. 155-156
[48.]
H.B. Rubins, S.J. Robins, D. Collins, C.L. Fye, J.W. Anderson, M.B. Elam, et al.
for the Veterans Affairs High-Density Lipoprotein Cholesterol IntervenÁlvarez-tion Trial Study Group. Gemfibrozil for the secondary prevention of coronary heart disease in men with low levels of high density lipoprotein cholesterol.
N Engl J Med, 341 (1999), pp. 410-418
[49.]
D.A. Ganz, K.M. Kuntz, G.A. Jacobson, J. Avorn.
Cost-effectiveness of 3-hydroxi-3-methylglutharyl coenzyme A reductase inhibitor therapy in older patients with myocardial infarction.
Ann Intern Med, 132 (2000), pp. 780-787
[50.]
J.D. Graham, P.S. Corso, J.M. Morris, M. Segui-Gómez, M.C. Weinstein.
Evaluating the cost-effectiveness of clinical and public health measures.
Annu Rev Public Health, 19 (1998), pp. 125-152
[51.]
S.A. Grover, L. Coupal, S. Paquet, H. Zowall.
Cost-effectiveness of 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors in the secondary prevention of cardiovascular disease: forecasting the incremental benefits of preventing coronary and cerebrovascular events.
Arch Intern Med, 159 (1999), pp. 593-600
[52.]
M. Johannesson, B. Jonnson, J. Kjekshus, A.G. Olsson, T.R. Pedersen, H. Wedel.
Cost-effectiveness of simvastatin treatment to lower cholesterol levels in patients with coronary heart disease. Scandinavian Simvastatin Survival Study (4S).
N Engl J Med, 336 (1996), pp. 332-336
[53.]
C.M. Helgason, P.A. Wolf.
American Heart Association Prevention Conference IV: prevention and rehabilitation of stroke.
Circulation, 96 (2001), pp. 701-707
[54.]
P.A. Wolf, J. Kannel.
Current status of risk factors for stroke.
Neurol Clin, 1 (1983), pp. 317-343
[55.]
J.D. Neaton, H. Blackburn, D. Jacobs, L. Kuller, D.J. Lee, R. Sherwin, et al.
Serum cholesterol level and mortality findings for men screened in the Multiple Risk Factor Intervention Trial. Multiple Risk Factor Intervention Trial Research Group.
Arch Intern Med, 152 (1992), pp. 1490-1500
[56.]
E. Lindenstrom, G. Boysen, J. Nyboe.
Influence of total cholesterol, high density lipoprotein cholesterol, and triglycerides on risk of cerebrovascular disease: the Copenhagen City Heart Study.
Br Med J, 309 (1994), pp. 11-15
[57.]
Prospective Studies Collaboration.
Cholesterol, diastolic blood pressure, and stroke: 13.000 strokes in 450.000 people in 45 prospective cohorts.
Lancet, 1 (1995), pp. 647-653
[58.]
J.F. Plehn, B.R. Davis, F.M. Sacks, J.M. Rouleau, M.A. Pfeffer, V. Bernstein, et al.
Reduction of stroke incidence after myocardial infarction with Pravastatin. The Cholesterol and Recurrent Events (CARE) Study.The Care Investigators.
Circulation, 99 (1999), pp. 216-223
[59.]
G.J. Blauw, A.M. Lagaay, A.H. Smelt, R.G. Westendorp.
Stroke, statins, and cholesterol. A meta-analysis of randomized, placebo-controlled, double-blind trials with HMG-CoA reductase inhibitors.
Stroke, 28 (1997), pp. 946-950
[60.]
P.R. Hebert, J.M. Gaziano, C.H. Hennekens.
An overview of trials of cholesterol lowering and risk of stroke.
Arch Intern Med, 155 (1995), pp. 50-55
[61.]
J. Marta-Moreno, C. Echeandia, A. Oliveros-Cid, A. Figuerola, S. Mola.
Estatinas (inhibidores de la HMG-CoA reductasa), colesterol e ictus.
Rev Neuro, 27 (1998), pp. 827-830
[62.]
R.P. Byington, B.R. Davis, J.F. Plehn, H.D. White, J. Baker, S.M. Cobbe, et al.
Reduction of Stroke Events With Pravastatin: The Prospective Pravastatin Pooling (PPP) Project.
Circulation, 103 (2001), pp. 387-392
[63.]
J.R. Crouse, R.P. Byington, C.D. Furberg.
HMG-CoA reductase inhibitor therapy and and stroke risk reduction: an analysis of clinical trial data.
Atherosclerosis, 138 (1998), pp. 24
[64.]
A.G. Dyker, C.J. Weir, K.R. Lees.
Influence of cholesterol on survival after stroke: retrospective study.
Br Med J, 314 (1997), pp. 1584-1588
[65.]
H. Tanaka, Y. Ueda, M. Hayashi.
Risk factors for cerebral hemorrhage and cerebral infarction in a Japanese rural community.
Stroke, 13 (1982), pp. 62-73
[66.]
R.S. Rosenson, C.C. Tangney.
Antiatherothrombotic properties of statins. Implications for cardiovascular event reduction.
JAMA, 279 (1998), pp. 1643-1650
[67.]
M. Moser.
Physiological differences in the elderly. Are they clinically important?.
Eur Heart J, 9 (1988), pp. 55-61
[68.]
Sociedad Española de Arteriosclerosis, Sociedad Española de Medicina Interna, Liga Española para la Lucha contra la Hipertensión Arterial..
Recomendaciones para la prevención primaria de la enfermedad cardiovascular.
Clin Invest Arteriosclerosis, 6 (1994), pp. 62-102
[69.]
M.V. Huff, J.R. Burnett.
3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors and hepatic apolipoprotein B secretion.
Curr Opin Lipidol, 8 (1997), pp. 138-145
[70.]
N.A. Le, W. Innis-Whitehouse, X. Li, R. Bakker-Arkema, D. Black, W.V. Brown.
Lipid and apolipoprotein levels and distribution in patients with hypertriglyceridemia: effect of triglyceride reductions with atorvastatin.
Metabolism, 49 (2000), pp. 167-177
[71.]
M.H. Davidson, E.A. Stein, D.B. Hunninghake, L. Ose, C.A. Dujovne, W. Insull, et al.
Lipid-altering efficacy and safety of simvastatin 80 mg/day: worldwide long-term experience in patients with hypercholesterolemia.
Nutr Metab Cardiovasc Dis, 10 (2000), pp. 253-262
[72.]
G. O'Driscoll, D. Green, R.R. Taylor.
Simvastatin, an HMG coenzyme A reductase inhibitor, improves endothelial function within 1 month.
Circulation, 95 (1997), pp. 1126-1131
[73.]
J. Dupuis, J.C. Tardif, P. Cernacek, P. Theroux.
Cholesterol reduction rapidly improves endothelial function after acute coronary syndromes. The RECIFE (reduction of cholesterol in ischemia and function of the endothelium) trial.
Circulation, 99 (1999), pp. 3227-3233
[74.]
O. Hernández-Perera, D. Pérez-Sala, J. Navarro-Antolín, R. Sánchez-Pascuala, G. Hernández, C. Díaz, et al.
Effects of 3-hydroxy-3-methylglutaryl-CoA reductase inhibitors, atorvastatin and simvastatin, on the expression of endothelin-1 and endothelial nitric oxide synthase in vascular endothelial cells.
J Clin Invest, 101 (1998), pp. 2711-2719
[75.]
W.H. Kaesemeyer, R.B. Caldwell, J. Huang, R.W. Caldwell.
Pravastatin sodium activates endothelial nitric oxide synthase independent of its cholesterol-lowering actions.
J Am Coll Cardiol, 33 (1999), pp. 234-241
[76.]
R. De Caterina, P. Libby, H.B. Peng, V.J. Thannickal, T.B. Rajavashisth, M.A. Gimbrone.
Nitric oxide decreases cytokine-induced endothelial activation. Nitric oxide selectively reduces endothelial expression of adhesion molecules and proinflammatory cytokines.
J Clin Invest, 96 (1995), pp. 60-68
[77.]
C. Bustos, M.A. Hernández-Presa, M. Ortego, J. Tuñón, L. Ortega, F. Pérez, et al.
HMG-CoA reductase inhibition by atorvastatin reduces neointimal inflammation in a rabbit model of atherosclerosis.
J Am Coll Cardiol, 32 (1998), pp. 2057-2064
[78.]
S. Colli, S. Eligni, M. Lalli, M. Camera, R. Paoletti, E. Tremoli.
Vastatins inhibit tissue factor in cultured human macrophages: a novel mechanism of protection against atherothrombosis.
Arterioscler Thromb Vasc Biol, 17 (1997), pp. 265-272
[79.]
A. Hackman, Y. Abe, W. Insull Jr, H. Pownall, L. Smith, K. Dunn, et al.
Levels of soluble cell adhesion molecules in patients with dyslipidemia.
Circulation, 93 (1996), pp. 1334-1338
[80.]
S. Niwa, T. Totsuka, S. Hayashi.
Inhibitory effect of fluvastatin, an HMGCoA reductase inhibitor, on the expression of adhesion molecules on human monocyte cell line.
Int J Immunopharmacol, 18 (1996), pp. 669-675
[81.]
D. Kaczmarek, T. Hohlfeld, G. Wambach, K. Schror.
The actions of lovastatin on platelet function and platelet eicosanoid receptors in type II hypercholesterolaemia. A double-blind, placebo-controlled, prospective study.
Eur J Clin Pharmacol, 45 (1993), pp. 451-457
[82.]
A. Szczeklik, J. Musial, A. Undas, P. Gajewski, P. Góra, J. Swadzba, et al.
Inhibition of thrombin generation by simvastatin and lack of additive effect of aspirin in patients with marked hypercholesterolemia.
J Am Coll Cardiol, 33 (1999), pp. 1286-1293
[83.]
G. Dangas, J.J. Badimon, D.A. Smith, A.H. Unger, D. Levine, J.H. Shao, et al.
Pravastatin therapy in hyperlipidemia: effects on thrombus formation and the systemic hemostatic profile.
J Am Coll Cardiol, 33 (1999), pp. 1294-1304
[84.]
P.M. Ridker, N. Rifai, M.A. Pfeffer, F. Sacks, E. Braunwald.
For the Cholesterol and Recurrent Events (CARE) Investigators. Long-term effects of pravastatin on plasma concentrations of C-reactive protein.
Circulation, 100 (1999), pp. 230-235
[85.]
T.E. Strandberg, H. Vanhanen, M.J. Tikkanen.
Effect of statins on C-reactive protein in patients with coronary artery disease.
[86.]
P.M. Ridker, M. Cushman, M.J. Stampfer, R.P. Tracy, C.H. Hennekens.
Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men.
N Engl J Med, 336 (1997), pp. 973-979
[87.]
G.L. Vega, S.M. Grundy.
Lovastatin therapy in nephrotic hyperlipemia: effects on lipoprotein metabolism.
Kidney Int, 33 (1988), pp. 1160-1168
[88.]
J. Garrido, G. Pía, J. González-Moraleja, P. Sesma.
Indicaciones del tratamiento hipolipemiante en el anciano: experiencia de una unidad de lípidos y revisión de la literatura.
Ann Med Intern, 15 (1998), pp. 305-310
[89.]
D.S. Wang, D.H. Solomon, H. Mogun, J. Avorn.
HMG-CoA reductase inhibitors and the risk of hip fractures in elderly patients.
JAMA, 283 (2000), pp. 3216
[90.]
D.R. Illingworth, J.A. Tobert.
A review of clinical trials comparing HMGCoA reductase inhibitors.
Clin Ther, 16 (1994), pp. 366-385
[91.]
L.R. Pierce, D.K. Wysowski, T.P. Gross.
Myopathy and rhabdomyolysis associated with lovastatin-gemfibrozil combination therapy.
JAMA, 264 (1990), pp. 71-75
[92.]
K. Schoonjans, B. Staels, J. Auwerx.
Role of the peroxisome proliferatoractivated receptor (PPAR) in mediating the effects of fibrates and fatty acids on gene expression.
J Lipid Res, 37 (1996), pp. 907-925
[93.]
H.U. Kloer, C. Luley, C.S. Wang.
Fenofibrate treatment in type II hyperlipoproteinemia: effects on lipoprotein lipids, apolipoproteins, LCAT, cholesterol ester transfer and post-heparin lipases.
Atherosclerosis, 59 (1987), pp. 213-221
[94.]
B. Vessby, H. Lithell, H. Ledermann.
Elevated lipoprotein-lipase activity in skeletal muscle tissue during treatment of hypertriglyceridemic patients with bezafibrate.
Atherosclerosis, 44 (1982), pp. 113-118
[95.]
N. Vu Dac, K. Schoonjans, V. Kosykh, J. Dallongeville, J.C. Fruchart, B. Staels, et al.
Fibrates increase human apolipoprotein A-II expression through activation of the peroxisome proliferator-activated receptor.
J Clin Invest, 96 (1995), pp. 741-750
[96.]
B. Staels, J. Dallongeville, J. Auwerx, K. Schoonjans, E. Leitersdorf, J.C. Fruchart.
Mechanism of action of fibrates on lipid and lipoprotein metabolism.
Circulation, 98 (1998), pp. 2088-2093
[97.]
M.J. Tikkanen.
Fibric acid derivatives.
Curr Opin Lipidol, 3 (1992), pp. 29-33
[98.]
Y. Tsai, J. Yuan, D.B. Hunninghake.
Effect of gemfibrozil on composition of lipoproteins and distribution of LDL sub-species.
Atherosclerosis, 95 (1992), pp. 35-42
[99.]
R. Alonso, L.A. Alvarez Sala, M. De Oya.
Hiperlipidemia. Tratamiento actual.
Tratado de terapéutica cardiológica, pp. 17-37
[100.]
D.R. Illingworth.
An overview of lipid-lowering drugs.
Drugs, 36 (1998), pp. 63-71
[101.]
W.R. Hazzard.
Dyslipoproteinemia in the elderly: to treat or not to treat?.
Am J Med, 107 (1999),
[102.]
Sociedad Española de Arteriosclerosis, Sociedad Española de Cardiología..
Evidencias clínico-experimentales y recomendaciones para el tratamiento de la hiperlipemia en los pacientes con cardiopatía isquémica. Documento Consenso de la Sociedad Española de Arteriosclerosis y la Sociedad Española de Cardiología.
Clin Invest Arteriosclerosis, 6 (1994), pp. 103-111
Copyright © 2001. Sociedad Española de Geriatría y Gerontología
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