10. EELL CCOONNTTIINNUUOO CCAARRDDIIOOVVAASSCCUULLAARR
Arteriosclerosis
Remodelado vascular
Hipertensión
Diabetes
Dislipidemia
Obesidad Central
LVH
Grosor IM
Infarto lacunar
Microalbuminuria
IM, Angina
ACV
Insuficiencia Cardiaca Congestiva
Insuficiencia Renal
Enfermedad Arterial Periferica Eventos
recurrentes
no mortales
ICC
IRC
Diálisis
Demencia
Genes
Estilo de vida Muerte
Adaptado de Dzau et al. Circulation 2006;114:2850-2870.
11. EELL CCOONNTTIINNUUOO UURRBBAANNOO
Estilos de Vida Nacimiento
Consumo de Lácteos
1..
Ver televisión
Internet
Sedentarismo
Comida
Chatarra
Azúcar blanca
Grasas Trans
Jarabe de Maíz
alto en Fructosa
Harina blanca
Grasas Saturadas
Pesticidas
Herbicidas
Desechos
industriales
Stress laboral
Polución y
Degradación
ambiental
Drogas
Sodio excesivo
Meneses D. El corazón en tus manos 2010
44. ¿ Que buscamos en un medicamento
antihpertensivo ?
1.Reducción sostenida de presión arterial
2.Disminuir la Morbimortalidad
a. Por Cardiopatía Isquémica
b. Por Ictus e Ictus grave
c. Enfermedad Renal Terminal
d. Por Insuficiencia cardiaca
3. Fácil de tolerar
4. Bajo costo
45.
46. ¿ Que buscamos en un medicamento
antihpertensivo ?
1.Reducción sostenida de presión arterial
2.Disminuir la Morbimortalidad
a. Por Cardiopatía Isquémica
b. Por Ictus e Ictus grave
c. Enfermedad Renal Terminal
d. Por Insuficiencia cardiaca
3. Fácil de tolerar
4. Bajo costo
51. ¿ Que buscamos en un medicamento
antihpertensivo ?
1.Reducción sostenida de presión arterial
2.Disminuir la Morbimortalidad
a. Por Cardiopatía Isquémica
b. Por Ictus e Ictus grave
c. Enfermedad Renal Terminal
d. Por Insuficiencia cardiaca
3. Fácil de tolerar
4. Bajo costo
62. ¿ Que buscamos en un medicamento
antihpertensivo ?
1.Reducción sostenida de presión arterial
2.Disminuir la Morbimortalidad
a. Por Cardiopatía Isquémica
b. Por Ictus e Ictus grave
c. Enfermedad Renal Terminal
d. Por Insuficiencia cardiaca
3. Fácil de tolerar
4. Bajo costo
70. ¿ Que buscamos en un medicamento
antihpertensivo ?
1.Reducción sostenida de presión arterial
2.Disminuir la Morbimortalidad
a. Por Cardiopatía Isquémica
b. Por Ictus e Ictus grave
c. Enfermedad Renal Terminal
d. Por Insuficiencia cardiaca
3. Fácil de tolerar
4. Bajo costo
75. ¿ Que buscamos en un medicamento
antihpertensivo ?
1.Reducción sostenida de presión arterial
2.Disminuir la Morbimortalidad
a. Por Cardiopatía Isquémica
b. Por Ictus e Ictus grave
c. Enfermedad Renal Terminal
d. Por Insuficiencia cardiaca
3. Fácil de tolerar
4. Bajo costo
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Hours to Days
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Global Remodeling
Days to Months
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79.
80. ¿ Que buscamos en un medicamento
antihpertensivo ?
1.Reducción sostenida de presión arterial
2.Disminuir la Morbimortalidad
a. Por Cardiopatía Isquémica
b. Por Ictus e Ictus grave
c. Enfermedad Renal Terminal
d. Por Insuficiencia cardiaca
3. Fácil de tolerar
4. Bajo costo
In the 2006 update of Heart Disease and Stroke Statistics, published by the American Heart Association, cardiovascular disease (CVD) was listed as the number 1 killer of men and women in the United States. Since 1900, CVD has been the number 1 killer in the United States every year except 1918. Nearly 2500 Americans die of CVD each day, an average of 1 death every 35 seconds. CVD claims more lives each year than the next 4 leading causes of death combined, which are cancer, chronic lower respiratory diseases, accidents, and diabetes mellitus.
The cost of CVD and stroke in the United States for 2006 is estimated at $403.1 billion. This figure includes health expenditures and lost productivity resulting from morbidity and mortality.
In 2002, 2.4 million deaths were reported in the United States. This is a 42% decrease in the overall age-adjusted death rate compared with 1950. This graph shows that the decline is due to the decrease in mortality for some of the leading causes of death including heart disease, stroke, and unintentional injuries.
In a Framingham cohort study, the lifetime risk of developing hypertension (blood pressure [BP] ≥140/90 mm Hg) was 90% both for participants who reached the age of 55 years free of hypertension (data not shown) and for participants who reached the age of 65 years free of hypertension.
The high lifetime risk for hypertension was similar for men and women and did not differ for participants aged 55 years versus 65 years.
More than half of the 55-year-old participants and about two thirds of the 65-year-old participants developed hypertension within 10 years of follow-up, indicating the importance of adopting lifestyle changes for maintaining optimal BP and preventing the development of hypertension.
References
Vasan RS, Beiser A, Seshadri S, et al. Residual lifetime risk for developing hypertension in middle-aged women and men. The Framingham Heart Study. JAMA. 2002;287:1003-1010.
A study of more than 57,000 HTN patients aged 35 years or older in a large managed-care organization, found that 56% of these individuals also had other risk factors for CVD that included diabetes, hyperlipidemia, and obesity, ie, a body mass index (BMI) of 30 kg/m2 or greater.
In addition to HTN, 39% of the patients had 1 other risk factor (ie, diabetes, hyperlipidemia, or obesity), 14% had 2 other risk factors, and 3% had all 3 of these risk factors.
Other findings of this study indicated that these additional risk factors (especially diabetes) substantially increased the risk of CVD events.
According to ATP III, the metabolic syndrome consists of a constellation of risk factors that place patients at risk for both the development of type 2 diabetes and atherosclerotic disease. The hallmarks of the syndrome are:
Abdominal obesity
Atherogenic dyslipidemia – characterized by elevated triglycerides, small LDL particles, and low HDL
Elevated blood pressure
Insulin resistance with or without glucose intolerance
A prothrombotic state
A proinflammatory state
Lipid and nonlipid risk factors of metabolic origin not only increase the risk of type 2 diabetes, but enhances the risk for coronary heart disease at any given LDL cholesterol level.
Reference:Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. JAMA. 2001;285:2486-2497.
BP Reductions as Small as 2 mmHg Reduce the Risk of CV Events by
Up to 10%
Data from a meta-analysis of 61 prospective, observational studies have also provided powerful evidence that throughout middle and old age, BP is strongly and directly related to vascular mortality.7 Perhaps most striking are the practical implications of these data: even a small, 2 mmHg fall in mean systolic BP would be associated with large absolute reductions in premature deaths and disabling strokes.7 As shown here, a 2 mmHg lower mean systolic BP could lead to a 7% lower risk of ischemic heart disease (IHD) death and a 10% lower risk of stroke death.
7Prospective Studies Collaboration. Age-specific relevance of usual blood pressure to vascular mortality: a meta-analysis of individual data for one million adults in 61 prospective studies. Lancet. 2002;360:1903-1913.
Throughout middle and old age, usual blood pressure (BP) is strongly and directly related to cardiovascular disease (CVD) mortality, without any evidence of a threshold down to at least 115/75 mm Hg.
In this meta-analysis, information was obtained regarding usual BP and causes of death for 1 million adults without known CVD at the time of enrollment in 61 prospective observational BP studies.
The analysis involved a correction for potential regression dilution bias by relating mortality during each decade of age at death to the estimated usual BP at the start of that decade.
Throughout the BP range >115/75 mm Hg to 175/105 mm Hg, usual BP was found to be more strongly related to CVD than previously estimated.
At ages 40 to 69 years, each increase of 20 mm Hg usual systolic BP (or, equivalently, 10 mm Hg usual diastolic BP) was associated with more than double the rate of stroke death and double the rate of death from coronary heart disease (CHD) and other vascular causes.
The age-specific associations were similar for men and women.
Other risk factors (including cholesterol, diabetes, smoking, and weight) were not found to have any significant effect on the risk.
Extrapolating from these data, a 10-mm Hg lower usual systolic BP or a 5-mm Hg lower usual diastolic BP throughout middle age would be associated with about a 40% lower risk of stroke death and about a 30% lower risk of death from CHD.
Recommended Lifestyle Modifications and Their Individual Effects on Blood Pressure
The adoption of a healthy lifestyle is critical to preventing high blood pressure and to the management of persons who already have hypertension. This slide depicts the lifestyle modifications that are recommended by the JNC-7 Committee to prevent or to manage hypertension and their effects on systolic blood pressure. Whether there is an additive effect on blood pressure reduction when 2 or more lifestyle modifications are combined has not been extensively investigated.
References:
Chobanian AV, Bakris GL, Black HR, et al, for the National High Blood Pressure Education Program Coordinating Committee. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA. 2003;289:2560-2572.
Blumenthal JA, Sherwood A, Gullette ECD, et al. Exercise and weight loss reduce blood pressure in men and women with mild hypertension: effects on cardiovascular, metabolic, and hemodynamic functioning. Arch Intern Med. 2000;160:1947-1958.
En el estudio Control-Project se analizaron las opiniones de los médicos participantes respecto a las posibles causas del inadecuado control de sus pacientes. Como muestra la diapositiva, la causa principal aducida fue el incumplimiento de las medidas no farmacológicas (cambios de estilo de vida) por parte del paciente, seguido del bajo cumplimiento del tratamiento farmacológico.
Bibliografía
1. Marquez-Contreras E, Coca A, de la Figuera M, Divisón JA, Llisterri JL, Sobrino J, et al., en nombre de los investigadores del estudio Control-Project. Perfil de riesgo cardiovascular de los pacientes hipertensos no controlados en Atencion Primaria: estudio Control-Project. Med Clin (Barc) 2007; (en prensa).
KEY MESSAGE: In many of the large hypertension trials, including
HOT, LIFE, ALLHAT, CONVINCE, and ASCOT, multidrug therapy
involving 2 or more drugs was required for patients to achieve their
BP targets. [1-5]
References
Hansson L, Zanchetti A, Carruthers SG, et al. Effects of intensive blood-pressure lowering
and low-dose aspirin in patients with hypertension: principal results of the Hypertension
Optimal Treatment (HOT) randomised trial. HOT Study Group. Lancet. 1998;351:1755-62.
2: Dahlöf B, Devereux RB, Kjeldsen SE, et al. Cardiovascular morbidity and mortality in the
Losartan Intervention For Endpoint reduction in hypertension study (LIFE): a randomised trial
against atenolol. Lancet. 2002;359:995-1003.
Cushman WC, Ford CE, Cutler JA, et al. Success and predictors of blood pressure control
in diverse North American settings: the antihypertensive and lipid-lowering treatment to prevent
heart attack trial (ALLHAT). J Clin Hypertens (Greenwich). 2002;4:393-404.
4. Black HR, Elliott WJ, Grandits G, et al. Principal results of the Controlled Onset Verapamil
Investigation of Cardiovascular End Points (CONVINCE) trial. JAMA. 2003;289:2073-82.
5. Dahlöf B, Sever PS, Poulter NR, et al. Prevention of cardiovascular events with an
antihypertensive regimen of amlodipine adding perindopril as required versus atenolol adding
bendroflumethiazide as required, in the Anglo-Scandinavian Cardiac Outcomes Trial-Blood
Pressure Lowering Arm (ASCOT-BPLA): a multicentre randomised controlled trial. Lancet.
2005;366:895-906.
The reason for this escape phenomenon is that there are alternative pathways to synthesise AII that are independent of the ACE pathway.
The introduction of selective angiotensin II receptor blockers permits us not only to block the effects which result from the activation of the AT1-receptor, but also to increase the stimulation of the AT2-receptor which seems to attenuate the growth of vascular walls.
Obesity is associated with a chronic state of low-grade inflammation. Models of inflammation in obesity include a major role for macrophages in molecular changes in adipose tissue.
Metabolic and endocrine function alterations in adipose tissue increase the release of free fatty acids, hormones, and proinflammatory molecules. Increasing adiposity produces physical changes and modification of adipocyte paracrine function. Adipocytes begin secreting TNF, an inflammatory cytokine.
TNF stimulates preadipocytes to produce monocyte chemoattractant protein-1 (MCP-1). Endothelial cells also respond to cytokines by secreting MCP-1; either endothelial cells or adipocytes could attract macrophages to adipose tissue.
Obesity induces secretion of leptin (and/or decreases production of adiponectin) by adipocytes, which may promote macrophage accumulation. Oxidative damage in the endothelium due to an increasingly lipolytic environment may also increase macrophage recruitment.
The presence and activity of macrophages in adipose tissue in the obese state perpetuates a vicious cycle of increased macrophage recruitment and inflammatory cytokine production, and impaired adipocyte function.
VEGF = vascular endothelial growth factorJNK = c-Jun amino-terminal kinase
Monotherapy Achieved High Goal Rates
Using an olmesartan medoxomil-based treatment regiment resulted in a dose-dependent increase in blood pressure goal rate attainment.
Total Cohort: Data taken from 179 evaluable patients with a mean baseline BP of 161/97 mm Hg.
<130/85 mm Hg: Olmesartan medoxomil 20 mg/d resulted in 20% of patients achieving the blood pressure goal of < 130/85 mm Hg, which was increased to 35% with the titration of olmesartan medoxomil to 40 mg/d. Titration to olmesartan medoxomil 40 mg/d resulted in a 15% increase in blood pressure goal rate attainment. The addition of HCTZ 12.5 mg/d to olmesartan medoxomil 40 mg/d resulted in 56% of patients achieving the blood pressure goal of < 130/85 mm Hg. The addition of HCTZ 12.5 mg/d to olmesartan medoxomil 40 mg/d resulted in a 21% increase in blood pressure goal rate attainment. Titration of HCTZ 12.5 mg/d to HCTZ 25 mg/d plus olmesartan medoxomil 40 mg/d resulted in 69% of patients achieving the blood pressure of < 130/85 mm Hg. Titration to HCTZ 25 mg/d resulted in a 13% increase in blood pressure goal rate attainment.
<140/90 mm Hg: Olmesartan medoxomil 20 mg/d resulted in 35% of patients achieving the blood pressure goal of < 140/90 mm Hg, which was increased to 59% with the titration of olmesartan medoxomil to 40 mg/d. Titration to olmesartan medoxomil 40 mg/d resulted in a 24% increase in blood pressure goal rate attainment. The addition of HCTZ 12.5 mg/d to olmesartan medoxomil 40 mg/d resulted in 74% of patients achieving the blood pressure goal of < 140/90 mm Hg. The addition of HCTZ 12.5 mg/d to olmesartan medoxomil 40 mg/d resulted in a 15% increase in blood pressure goal rate attainment. Titration of HCTZ 12.5 mg/d to HCTZ 25 mg/d plus olmesartan medoxomil 40 mg/d resulted in 83% of patients achieving the blood pressure of < 140/90 mm Hg. Titration to HCTZ 25 mg/d resulted in a 9% increase in blood pressure goal rate attainment.