Prevención primaria cardiovascular diabetes, rol de la Aspirina
1. REUNION DE PAPER SECCIÓN ENDOCRINOLOGIA Julián Vega Adauy Residente Medicina Interna UdeC
2.
3.
4.
5. Sir John Vane PREMIO NOBEL MEDICINA 1982 ASPIRINA INHIBE LA SÍNTESIS DE PROSTAGLANDINAS Samuelsson Bergström
6. Food and Drug Administration E.E.U.U (FDA) En enero 2004 rechazó la Aspirina para prevención primaria de cardiopatía coronaria
7.
8. I, González-Maqueda. Rev Esp Cardiol Supl. 2007 LA ENFERMEDAD CORONARIA DEL DIABÉTICO. DIAGNÓSTICO, PRONÓSTICO Y TRATAMIENTO
9.
10.
11.
12. R. Baechler y cols. Rev. méd. Chile 2002 FRCV ASOCIADOS A DIABETES MELLITUS
13. EL CUARTETO DE LA MUERTE IR DM2 HTA OBSD DZP Disfunción endotelial, complicaciones macro-micro
14. MANIFESTATIONS OF ATHEROTHROMBOSIS ARE COMMONLY FOUND IN MORE THAN ONE ARTERIAL BED IN AN INDIVIDUAL PATIENT *1 1. Coccheri S. Eur Heart J 1998; 19(suppl): P1268. *Data from CAPRIE study (n=19,185) Coronary disease Cerebrovascular disease Peripheral arterial disease 24.7% 3.8% 11.8% 29.9% 3.3% 7.4% 19.2%
17. Resultados UKPDS Stratton IM, et al. BMJ . 2000 P <.0001 P = .035 P = .021 P = .0001 Reducción de riesgo con 1% de declinación annual de A1C 0% 15% 30% 45% MICRO VASCULAR 37% PAD 43% AVE IAM 14% 12% ICC Cx Catarata 16% 19%
57. 10-year CHD risk levels at which the number of cardiovascular disease events prevented is closely balanced to the number of serious bleeding events.CHD = coronary heart disease. Ann Intern Med 2009;150:396-404
84. REUNION DE PAPER SECCIÓN ENDOCRINOLOGIA Julián Vega Adauy Residente Medicina Interna UdeC
85.
Notes de l'éditeur
• Atherothrombosis is a vascular disease which can affect the coronary, cerebral and peripheral circulation. • It is a progressive, generalized disorder with many clinical manifestations – either acute or chronic and often multiple in any single patient. • Simple stenosis in an atherosclerotic artery may give rise to angina, a transient ischemic attack or intermittent claudication. • Atherothrombosis in the coronary arteries is the major cause of acute coronary syndrome, defined as unstable angina and non-Q-wave myocardial infarction. • Atherothrombosis of the cerebral arteries can result in TIA or ischemic stroke. • In the peripheral arteries, athero thrombosis can contribute to the progression of peripheral arterial disease, producing intermittent claudication (leg pain on walking that is relieved by rest) as well as ischemic necrosis and, potentially, loss of the limb. References 1. Drouet L. Cereobrovasc Dis 2002; 13 (suppl 1): 1–6
References: 1. Lichtman JH et al. Circulation 2002; 105: 1082–7. 2. CAPRIE Steering Committee. Lancet 1996; 348: 1329–39. 3. Coccheri S. Eur Heart J 1998; 19(suppl): P1268. A person suffering from any one manifestation of atherothrombosis is at risk of future disabling or life-threatening events caused by the same underlying disease process. 1 The CAPRIE trial enrolled 19,185 patients with either established peripheral arterial disease (PAD), 2,3 a recent myocardial infarction or recent ischemic stroke in approximately equal distribution. However, based on the baseline characteristics of these patients, many of them already had a prior history of ischemic events. Thus, at study entry ~26% of the patients had ischemic vascular disease in at least two vascular beds, demonstrating the generalized nature of atherothrombosis. 3 For example, 11.8% of patients had both coronary disease and PAD, 7.4% had both coronary and cerebrovascular disease, 3.8% had a combination of cerebrovascular disease and PAD, and 3.3% had disease of all three arterial beds. 3 Over time this overlap will most probably increase (in the CAPRIE trial more than 2,000 patients experienced a major ischemic event over the mean 1.9 year follow-up, and many others developed other ischemic events such as transient ischemic attack and angina). 3
In the UKPDS, each 1% decrease in annual mean A1C level reduced the risk of microvascular complications by 37%, peripheral vascular disease (PVD) by 43%, myocardial infarction (MI) by 14%, stroke by 12%, heart failure by 16%, and cataract extraction by 19%. These data indicate that over time there is a quantifiable relationship between the risk of complications of diabetes and glycemia. Reference Stratton IM, Adler, AI, Neil HA, et al. Association of glycemia with macrovascular and microvascular complications of type 2 diabetes (UKPDS 35): prospective observational study. BMJ. 2000; 321:405-412.
Skyler JS. Endocrinol Metab Clin 1996
The chart on the right side of Figure 8 reflects the effect of A1C levels on event rates and covers a large range from 5.5% to 11%. It demonstrates that the risk of MI doubles from one extreme to another, showing that A1C is related to CHD. However, if we calculate the size of the effect, each 1% change in A1C is equivalent to about a 15% rise in risk of MI. Therefore, even if you bring someone's A1C level down from 10% to 6%, it is unlikely you will fully eliminate the 2- to 4-fold excess of cardiovascular disease in people with diabetes. On the other hand, a 15% change per 1% A1C is not trivial. A 2% change in A1C would reduce risk 30%, an effect similar to that seen in statin trials.[41] Therefore, it makes sense to use both approaches -- glucose and lipid control -- in at-risk people. Another reason to further examine the chart on the right side of Figure 8 is to understand why the slope is relatively gentle, reflecting modest impact of A1C on event risk. A possible explanation is that there is already increased risk of cardiovascular disease prior to the onset of type 2 diabetes. The increased triglycerides, decreased HDL, increased systolic blood pressure, and increased glucose and insulin levels that these patients have are all components seen in the various definitions of the metabolic syndrome, thus combining their effects to increase macrovascular risk beyond that which relates to A1C alone.
The hazard ratio was 0.67 (95 percent confidence interval, 0.46 to 0.97; P<0.04) for the comparison with nondiabetic subjects who had prior coronary heart disease and 1.43 (95 percent confidence interval, 1.00 to 2.03; P<0.05) for the comparison with nondiabetic subjects who did not have prior coronary heart disease.
CHD coronary heart disease; CVD cardiovascular disease; KQ key question. KQ 1: Does aspirin chemoprevention in patients without known cardiovascular disease reduce the risk for myocardial infarction, stroke, and death? KQ 2: Does aspirin chemoprevention increase major gastrointestinal bleeding, hemorrhagic strokes, or both? KQ 3: What is the balance of benefits and harms for aspirin therapy in patients with different levels of cardiovascular risk?
Summary of Primary Prevention Trials
Meta-analysis of total coronary heart disease events.P
Estimated MIs prevented and estimated harms of using aspirin for 10 years in a hypothetical cohort of 1000 men.Estimates are based on age and 10-year CHD risk. CHD = coronary heart disease; GI = gastrointestinal; MI = myocardial infarction.
10-year CHD risk levels at which the number of cardiovascular disease events prevented is closely balanced to the number of serious bleeding events.CHD = coronary heart disease.