1. DEFINICIÓN.
“No existe una línea divisoria que separa la hipertensión de la
normotensión, cuanto más baja, menor es la
morbimortalidad”.
Sir George Pickering.
El riesgo cardiovascular comienza a partir de
115/75 mmHg (JNC-VII).
2. Prevalencia de HTA en Americanos de ≥ 35 años por
edad y genero
PAS ≥ 140 mm Hg o PAD ≥ 90 mm Hg o medicación antihipertensiva
NHANES III (1988-1994)
Hombres
90
Mujeres
80
70
Pacientescon HTA (%)
60
50
40
30
20
10
0
35-44 45-54 55-64 65-74 75+
Adapted from Wolz M, et al. Am J Hypertens. 2000;13:103-104.
J Clin Hipertens 2005 Le Jacq Communications, Inc.
3. Prevalencia de HTA en Europa
HTA (≥ 160 mm Hg) en personas de edad 35-64 años
(Países Europeos seleccionados)
25 Hombres
Mujeres
20
Pacientes con HTA (%)
15
10
5
0
Denmark Finland (North France Germany (Urban Sweden United Kingdom
(Glostrup) Karelia) (Strasbourg) Augsburg) (Gothenburg) (Glasgow)
Adapted from British Heart Foundation.
European Cardiovascular Disease Statistics, 2000 Edn. 2000.
4. En Latinoamérica ~ 9 de cada 10 hipertensos
no alcanza las metas
País Prevalencia Conocido Tratados Controlados Mortalidad
% s % % CV %
%
Argentina 28.1 54 42 18 23.5
Brasil 26.8 50.8 40.5 10.2 27.5
Chile 33.7 59,8 36.3 11.8 28.4
Colombia 23 41 46 15 28
Ecuador 28.7 41 23 6.7 28
México 30,5 56.4 23 19.2 -
Paraguay 34 36 27 7 28
Peru 24 39 14.7 14 -
Uruguay 33 68 48 11 29.5
Venezuela 33 55 30 12 20.6
Journal of Hypertension 2009, Vol 27 No 00
5. El Problema en Venezuela (1/2)
≥ 20 años
< 20 años
Habitantes:
28384132
≥ 20 años: 17.240.140
Normotensos Hipertensos
Venezuela:
5.689.246 de
Hipertensos
http://www.ine.gov.ve/poblacion/distribucion.asp
6. El Problema en Venezuela (2/2)
Norm otensos Hipertensos
Venezuela:
5.689.246 de
Hipertensos
Controlados No controlados
Venezuela:
Controlados: 682709
No controlados: 5006537
http://www.ine.gov.ve/poblacion/distribucion.asp
7. EL PROBLEMA DE LA HTA NO ES SOLO LAS
CIFRAS DE PA.
HAY QUE VERLA COMO:
•Un signo clínico.
Enfermedad
•Una enfermedad. Vascular
•Un factor de riesgo. Hipertensiva
8. Síndrome de HTA Primaria
HTA
Membranopatía TG
Sindrome
Resistencia a
Obesidad central HTA
Insulina
Anormalidad
Miocardica HDLc
Intolerancia
a la glucosa
DM
9. SINDROME DE HIPERTENSION ARTERIAL
Factores genéticos
Aumento de PS
Hiperlipemia
Resistencia a Insulina Irreversible
Obesidad
HVI
Endurecimiento arterial Reversible
Cambios neuroendocrinos
Anormalidades de la funcion renal
Anormalidad de factores
de la coagulación
Nuetel J. Am J. Hypertens. 1999; 12 (suppl 1): S 164
Nuetel J. Am J. Hypertens. 1999; 12 (suppl 1): S 215
10. Límites de presión arterial (mmHg) para definir
hipertensión
ESH/ESC Guidelines. J Hypertens 2007;25:1105-87
11. REPERCUSIÓN DE LA HTA.
Framingham Heart Study – Riesgo de eventos cardiovasculares por status hipertensivo en pacientes con edad 35-64 años;
36-años de seguimiento
E. Art. Coronaria A. C. V. E. Art. Periférica I. C. C.
Incidencia Bianual por 1000 ajustada
50
45,4
40
Normotensos
Hipertensos
por edad
30
22,7 21,3
20
13,9
12,4
9,5 9,9
10 6,2 7,3 6,3
5
3,3 2,4 3,5 2,1
2
0
Hombre Mujere Hombre Mujere Hombre Mujere Hombre Mujere
s s s s s s s s
RR 2.0 2.2 3.8 2.6 2.0 3.7 4.0 3.0
Exc. Riesgo 22.7 11.8 9.1 3.8 4.9 5.3 10.4 4.2
12. Efecto de la Presión Arterial sobre
la mortalidad por Cardiopatía Isquémica
81
48
Tasa de mortalidad
por 10.000 personas - año 37 44
35
31
38
26
24 24 25
25
25
21 17
PAS
PAD 14
(mm Hg.)
13
(mm Hg.) 10
12
13
12 >160
9
>100 9 140–159
90–99 9
80–89 120–139
75–79
70–74 <120
<70
Neaton JD. Arch Intern Med 1992;152:56
MRFIT: Múltiple Risk Factor Intervention trial.
13. Hipertensión Arterial Sistémica e Incidencia de
eventos cardiovasculares
10
Normal
Alta
8
Incidencia acumulada de
eventos CV %
6
4
Normal
2 Optima
0
0 2 4 6 8 10 12 14
Optima
N. Eng J Med 2001:3045, 1291
14. Hipertensión Arterial Sistémica E Incidencia De
Evento Cerebrovascular
45
PA normal
40
35 Limítrofe
Frecuencia x 10 000
30 Elevada
25
20
15
10
5
0
Mujeres Hombres
Framingham
15. Hipertensión Arterial Sistémica e Incidencia de
Cardiopatía Isquémica
PA normal
250
Limítrofe
Elevada
200
Frecuencia x 10 000
150
100
50
0
Mujeres Hombres
Framingham
16. Control de PA y RR de Mortalidad
Hombre
2.0 Mujeres
1.5
RR de Muerte
1.0
0.5
0
Normotensos Hipertensos Tratados, Hipertensos Tratados
no controlados y Controlados
Hypertension 1999; 13: (5 suplemento) 128-32
17. Propención del paciente HTA a tener factores de
riesgo adicionales
Hombres Mujeres
None
None 17%
4+ RFs 4+ RFs
19%
8% 12%
3 RFs
1 RF
22% 3 RFs
1 RF 27%
20%
26%
2 RFs
2 RFs
25%
24%
Kannel WB. Am J Hypertens. 2000;13:3S-10S.
19. Dislipidemia es más común en Pacientes con HTA*
PA Normal
40 PA alta
37 36
Pacientes con CT ≥ 6.5 mmol/L
Tto Antihipertensivos 35
35
30 28
(≥ 250 mg/dL) (%)
25
20 18 19
15
10
5
0
Hombres Mujeres
*HTA definida como PA ≥ 150/ ≥ 95 mm Hg
MacMahon M, et al. Arteriosclerosis. 1985;5:391-396.
20. Hipertension y Dislipidemia Mayores
Factores de Riesgo para EAC
Estudio de Framingham
Edad
350 140
70
Probabilidas de EAC/1000
300 120
Probabilidad de EAC/1000
250 60
100
200 80
150 50 60
100 40
40
50 20
0 0
<204 205- 235- 265- >295
100 120 140 160 180 200 234 264 294
PAS (mm Hg) Hombres CT (mg/dL) Hombres
Kannel W. In: Hypertension: Pathophysiology and Treatment. New York: McGraw-Hill, Inc.; 1977:888-909
Castelli WP.Am J Med. 1984;76:4-12.
21. Efecto aditivo del colesterol y la PAS sobre el riesgo de
muerte por EAC
34
N = 316,099
21 23
Muertes/10,000
pacientes-año
17 18
12 17
13
11
12 8 14
10
9 8
8
6 6 5
245+ 6 6 6 142+
221-244
4 3 132-141
203-220 3 125-131
118-124 Quintiles
182-202
Quintiles Colesterol PAS(mm Hg)
< 182 < 118
(mg/dL)*
Neaton JD, Wentworth D. Arch Intern Med. 1992;152:56-64.
22. Prevalencia HTA y Dislipidemia en Hombres como
función de Tolerancia a la Glucosa
Dislipidemia
Hipertension
60
50
Pacientes (%)
40
30
20
10
0
Tolerancia glucosada normal Glucosa alterada en ayunas DM tipo 2
Isomaa B, et al. Diabetes Care. 2001;24:683-689.
23. Riesgo Cardiovascular Global:
La amenaza
Dislipidemia Dislipidemia
Hipertensión Hipertension
CT 5.4 mmol/L X5.3 CT 6.1 mmol/L
PAS 165 mm Hg PAS 195 mm Hg
X2.6 (210 mg/dL) (235 mg/dL)
X1.9 X3.0
X1.3 X8.7 X1.7
X4.5
X3.5 X5.2 X2.9
X2.3
Intolerancia a Glucosa Fumar
X1.8 X1.7
La comparación del riesgo se hace respecto a Hombre de 40 años, no fumador, con
CT4.7 mmol/L (185 mg/dL), PAS 120 mm Hg, y sin intolerancia a la glucosa, sin
HVI en ECG con probabilidad de desarrollar EAC 15/1000 (1.5%) en 8 años
Kannel W. In: Hypertension: Pathophysiology and Treatment. New York: McGraw-Hill, Inc.; 1977:888-909.
24. CÁLCULO DEL RIESGO CV TOTAL
• En aquellas personas con enfermedad coronaria
o su equivalente o con ≤ 1 factor de riesgo, no
es necesario calcular el riesgo a 10 años.
• El nivel de riesgo para personas sin EAC o
equivalente de EAC y con ≥ 2 factores de riesgo
se calcula utilizando el algoritmo de
Framingham.
Expert Panel on Detection, Evaluation, and Treatment of High Blood
Cholesterol in Adults (ATP III). JAMA 2001; 285:2486 – 97.
25. CÁLCULO DEL RIESGO CV TOTAL
DETERMINAR LA CATEGORÍA DE RIESGO TOTAL
Categoría de riesgo Riesgo a 10 años
EAC o equivalente de riesgo de > 20 %
EAC
+ de 2 Factores de riesgo 10 – 20 %
0 – 1 factor de riesgo < 10 %
Expert Panel on Detection, Evaluation, and Treatment of High Blood
Cholesterol in Adults (ATP III). JAMA 2001; 285:2486 – 97.
26. RIESGO ESTIMADO PARA 10 AÑOS
SCORE DE FRAMINGHAM SEGÚN EDAD
Hombres
MUJERES HOMBRES Colesterol 20-39 40-49 50-59 60-69 70 – 79
Total años años años años años
Edad Puntos Edad Puntos <160 0 0 0 0 0
20-34 -7 20-34 -9 160-199 4 3 2 1 0
35-39 -3 35-39 -4 200-239 7 5 3 1 0
40-44 0 40-44 0 240-279 9 6 4 2 1
45-49 3 280 + 11 8 5 3 1
45-49 3
Mujeres
50-54 6 50-54 6 Colesterol 20-39 50-59 60-69 70 – 79
40-49 años
Total años años años años
55-59 8 55-59 8
<160 0 0 0 0 0
60-64 10 60-64 10
160-199 4 3 2 1 1
65-69 12 65-69 11
200-239 8 6 4 2 1
70-74 14 70-74 12 240-279 11 8 5 3 2
75-79 16
75-79 13 280 + 13 10 7 4 2
20-39 40-49 50-59 60-69 70 – 79 HOMBRES MUJERES HOMBRES Y MUJERES
años años años años años
No Tratad No Tratad
No PAS PAS HDL Puntos
0 0 0 0 0 tratado o tratado o
fumador
< 120 0 0 < 120 0 0 60 + -1
Fumador 8 5 3 1 1
120-129 0 1 120-129 1 3
20-39 40-49 50-59 60-69 70 – 79 50 – 59 0
años años años años años 130-139 1 2 130-139 2 4
40 – 49 1
No
0 0 0 0 0 140-159 1 2 140-159 3 5
fumador
< 40 2
Fumador 9 7 4 2 1 160 + 2 3 160 + 4 6
www.nhlbi.nh.gov
27. SCORE TOTAL DE FRAMINGHAM EN 10 AÑOS
HOMBRES MUJERES
PUNTO TOTAL RIESGO EN 10 AÑOS PUNTO TOTAL RIESGO EN 10 AÑOS
<9 <1%
<0 <1%
9 - 12 1%
0-4 1%
13 -14 2%
5-6 2%
15 3%
7 3%
16 4%
8 4%
17 5%
9 5%
10 6% 18 6%
11 8% 19 8%
12 10% 20 11%
13 12% 21 14%
14 16% 22 17%
15 20% 23 22%
16 25% 24 27%
17 ó + >30% 25 ó + >30%
www.nhlbi.nh.gov
28. Gías Europeas: Estimación del Riesgo Coronario en
Pacientes de Prevención Primaria
No Fumador Fumador
Colesterol Total mg/dL 150 200 250 300 mg/dL 150 200 250 300
mmol/L 4 5 6 7 8 mmol/L 4 5 6 7 8
Nivel de riesgo a 10años en hombres 180 180
160 Edad 160
Muy alto > 40%
140 70 140
Alto 20% to 40%
120 120
Moderado 10% to 20%
Leve 5% to 10%
180 180
bajo < 5% Edad
160 160
PAS (mm Hg) 60
140 140
120 120
180 180
160 Edad 160
140 50 140
120 120
180 180
160 Edad 160
140 40 140
120 120
Wood D, et al. Atherosclerosis. 1998;140:199-270.
29. Riesgo Adicional en el paciente ipertenso
ESH/ESC Guidelines. J Hypertens 2007;25:1105-87
30. Individuos de alto o muy alto riesgo
ESH/ESC Guidelines. J Hypertens 2007;25:1105-87
31. Objetivos del Tratamiento
Metas
Situación Clínica Meta de PA en mmHg
DM < 130/80
Enfermedad renal, EAP,CIC <130/80
Enfermedad renal ( Proteinuria > 1 < 125/75
gr/día)
Ancianos, ACV, HVI, IC, <140/90
Embarazo,,Grupos etnicos
Niños y adolescentes < P95 ajustado para edad, altura y género
32. Hypertension Optimal Treatment (HOT): El
Control de PA Reduce Eventos CV*
Subgrupo de diabetes
p=0.005
30
PA Diastólica
(todos)
24.4
25
IM, ACV, mortalidad CV/
Meta Obtenido
1000 pac-año
20 18.8 ≤90 85.2 mm Hg
≤85 83.2 mm Hg
≤80 81.1 mm Hg
15
11.9
10
5
0 ≤90 mm Hg ≤85 mm Hg ≤80 mm Hg
(n=501) (n=501) (n=499)
*Evaluación del tipo PROBE (Prospective, Randomized, Open with Blinded End-point). Tratamiento con felodipina,
incrementos de dosis y terapia concomitante (IECA o b-bloqueador ± diuretico) para obtener la meta. Adicionalmente,
la mitad fueron aleatorizados a aspirina. Presión arterial media 105 mm Hg, en cada grupo.
IM=infarto miocárdico. ACV=Accidente cerebrovascular. PA=presión arterial. CV=cardiovascular.
Hansson L et al. Lancet. 1998;351:1755-1762.
The prevalence of hypertension increases steadily with age in both genders according to NHANES III estimates for 1988-1994. In this survey, hypertension was defined as an SBP of 140 mm Hg, a DBP of 90 mm Hg, or taking antihypertensive medication. Up to age 34 years of age, hypertension generally affects 10% of the population. By 65 years of age, however, more than 50% of individuals on average are hypertensive. Wolz M, Cutler J, Roccella EJ, et al. Statement from the National High Blood Pressure Education Program: Prevalence of hypertension. Am J Hypertens. 2000;13:103-104.
The most reliable data on the incidence of high BP across Europe come from the MONICA project, which defined hypertension as systolic pressures of 160 mm Hg. Between 2% (Toulouse, France) and 21% (North Karelia, Finland) of European men aged 35-64 years have hypertension. For European women aged 35-64 years, between 2% (Catalonia, Spain, and Ghent, Belgium) and 17% (East Germany) have hypertension. British Heart Foundation. European Cardiovascular Disease Statistics, 2000 Edn. 2000.
Observaciones similares fueron hechas en el estudio Framingham sobre la relación entre la hipertensión y la incidencia de eventos vasculares cerebrales. La diferencia del poder patogénico de la hipertensión entre los dos géneros no es tan manifiesta como en el caso de la cardiopatía isquémica, lo que indica que para la génesis de esta última están involucrados otros factores aparte de la elevación de las cifras de presión. Vuelve a apreciarse que cifras limítrofes elevan dos veces y medio el riesgo de EVC en comparación con los sujetos que tienen cifras normales, en ambos géneros y la PA elevada aumenta 8 y 9 veces el riesgo de EVC en mujeres y hombres respectivamente.
Las observaciones del estudio Framingham demostraron que la incidencia de síndromes coronarios aumenta cuando se comparan sujetos con PA deseable con hipertensos. Nótese que cifras limítrofes de hipertensión casi doblan el riesgo de enfermedad coronaria en hombres y en mujeres y que las cifras elevadas de PA más que triplican este riesgo en los dos géneros. También puede apreciarse que el riesgo de la hipertensión es mucho más manifiesto en los hombres que en las mujeres, aunque este riesgo mayor ya lo tienen con respecto a las mujeres los hombres con PA normal.
Epidemiologic research has shown that hypertension usually occurs in conjunction with other CV risk factors. Data from the Framingham Study clearly illustrate the co-existence of risk factors in the hypertensive population. In the Framingham population, < 20% of hypertension cases occurred in isolation. Nearly one third of all patients (30% in men and 32% in women) had 3 or more risk factors for CV in addition to hypertension. Kannel WB. Risk stratification in hypertension: new insights from the Framingham Study. Am J Hypertens. 2000;13:3S-10S.
While the presence of a single CV risk factor can dramatically increase the patient’s risk of CHD, risk factors often do not exist in isolation. Using data from a random sample of Australian men and women, MacMahon and colleagues examined the prevalence of hypercholesterolemia (defined as TC 6.5 mmol/L [ 250 mg/dL]) in patients with hypertension (BP 150/ 95 mm Hg) or who were taking antihypertensive medication. The incidence of hypercholesterolemia in men and women with hypertension or who were taking antihypertensive medications was significantly higher than that in men and women who did not have elevated BP. In addition, the prevalence of elevated TC:HDL-C ratios was higher among hypertensive men and women than in patients with normal BP. MacMahon M, Macdonald GJ, Blacket RG. Plasma lipoprotein levels in treated and untreated hypertensive men and women: the National Heart Foundation of Australia risk factor prevalence study. Arteriosclerosis. 1985;5:391-396.
Large epidemiologic studies illustrate the risk associated with hypertension and elevated TC levels. The Framingham Heart Study is a large epidemiologic study initiated in 1949 that examined the impact of cardiovascular (CV) risk factors on CHD in 5209 randomly selected American men and women. At entry, the large majority of patients were free of cardiovascular disease (CVD). A clear, curvilinear relationship was observed between SBP and subsequent development of CVD. A strong relationship between TC levels and the rate of CHD was apparent by the sixth year of follow-up in the Framingham Study. The incidence of CHD in male subjects aged 30-49 years with TC levels of > 7.6 mmol/L (> 295 mg/dL) was approximately 6 times that of subjects with TC levels of between 5.3 and 6.0 mmol/L (205-234 mg/dL). Today’s guidelines for hypertension and lipid management are based largely on data from large epidemiologic trials like the Framingham study. These data have unequivocally shown the benefit of managing these risk factors. Kannel W. Importance of hypertension as a major risk factor in cardiovascular disease. Hypertension: Pathophysiology and Treatment . New York: McGraw-Hill, Inc.; 1977:888-909. Castelli WP. Epidemiology of coronary heart disease: the Framingham Study. Am J Med. 1984;76:4-12.
Using data from the Multiple Risk Factor Intervention Trial (MRFIT), Neaton and colleagues examined the additive effect of TC levels and SBP on CHD death rates. Note the generally strong, graded relationship between increasing cholesterol levels and CHD death across SBP levels and the generally strong relationship between small increases in SBP and CHD death across TC levels. When risk factors were analyzed together, patients in both the highest TC and the highest SBP quintiles had an approximately 11-fold greater risk of CHD death than patients who were in both the lowest TC and the lowest SBP quintiles. Neaton JD, Wentworth D. Serum cholesterol, blood pressure, cigarette smoking, and death from coronary heart disease. Overall findings and differences by age for 316,099 white men. Multiple Risk Factor Intervention Trial Research Group. Arch Intern Med. 1992;152:56-64.
Using data from 4483 subjects aged 35-70 years who were participating in a large study of type 2 diabetes, Isomaa and colleagues compared the prevalence of CV risk factors in patients with type 2 diabetes (n = 1697), impaired fasting glucose/impaired glucose tolerance (n = 798), or insulin resistance with normal glucose tolerance (n = 1998). The risk factors evaluated included hypertension, dyslipidemia, obesity, and microalbuminuria. This slide shows the prevalence of dyslipidemia and hypertension among male patients in each of these patient groups. Compared with patients with normal glucose tolerance, the prevalence of dyslipidemia and hypertension increased with increasing glucose intolerance and was approximately 2-fold greater among patients with type 2 diabetes. Isomaa B, Almgren P, Tuomi T, et al. Cardiovascular morbidity and mortality associated with the metabolic syndrome. Diabetes Care. 2001;24:683-689.
The interaction of multiple risk factors may lead to multiplicative, rather than merely additive, increases in CV risk. These Venn diagrams depict the increases in risk associated with the presence of multiple CV risk factors in 2 hypothetical 40-year-old male patients, compared with the CVD risk of a 40-year-old male nonsmoker with TC 4.7 mmol/L (185 mg/dL) and SBP 120 mm Hg, who is not glucose intolerant, and who does not have LVH. The Venn diagram on the left illustrates the interaction of risk factors in a patient with moderately elevated TC (5.4 mmol/L [210 mg/dL]), hypertension (SBP 165 mm Hg), and glucose intolerance. While each risk factor alone results in a 1.3- to 1.9-fold increase in CVD risk, the interaction of all 3 risk factors results in a 4.5-fold increase in CVD risk. The Venn diagram on the right shows the interaction of risk factors in a patient with elevated TC (6.1 mmol/L [235 mg/dL]) and severe hypertension (SBP 195 mm Hg) and who smokes. Each individual risk factor results in a 1.7- to 3.0-fold increase in CVD risk. However, the presence of all 3 risk factors results in an 8.7-fold increase in risk. Kannel W. Importance of hypertension as a major risk factor in cardiovascular disease. Hypertension: Pathophysiology and Treatment . New York: McGraw-Hill, Inc.; 1977:888-909.
The recommendations of the Second Joint Task Force of European and other societies on coronary prevention also recognize the multifactorial nature of CVD risk. The first step toward determining treatment goals and modalities for both hypertension and lipid management is to estimate coronary risk. Factoring SBP, TC, smoking status, and age, this chart is used to estimate absolute 10-year risk of CHD in men in whom symptomatic CHD or other atherosclerotic disease has not developed. A similar, though not identical, chart is used to estimate coronary risk in women. Wood D, De Backer G, Faergeman O, et al. Prevention of coronary heart disease in clinical practice: recommendations of the Second Joint Task Force of European and other Societies on Coronary Prevention. Atherosclerosis. 1998;140:199-270.
In the Hypertension Optimal Treatment (HOT) study, (n=18,790) hypertensive patients (DBP 100-115 mm Hg) from 26 countries were randomly assigned to 1 of 3 DBP target groups: ≤90 mm Hg, ≤85 mm Hg, and ≤80 mm Hg. The long-acting dihydropyridine CCB felodipine was given as baseline therapy, with the addition of other agents as needed to reach goal. The mean age of the study group was 61.5 years. After a mean of 3.8 years of follow-up, DBP was reduced to 85.2 mm Hg in the group assigned to the ≤90 mm Hg goal, to 83.2 mm Hg in the group assigned to ≤85 mm Hg, and to 81.1 mm Hg in the group assigned to ≤80 mm Hg. Results in the subgroup of 1501 diabetic patients are shown here. The rate of major CV events (fatal/nonfatal MI, fatal/nonfatal stroke, and all other CV deaths) was reduced by approximately 50% in the group assigned a DBP goal ≤80 mm Hg compared with those assigned a goal of ≤90 mm Hg ( p =0.005). The difference between groups remained significant ( p =0.045) when silent MI was included in the analysis (data not shown). The rate of stroke was reduced by 30% and the rate of all MI by 50% in the ≤80 mm Hg group compared with the ≤90 mm Hg group, although these reductions did not achieve statistical significance (data not shown). Hansson L et al. Lancet . 1998;351:1755-1762.
In the Hypertension Optimal Treatment (HOT) study, (n=18,790) hypertensive patients (DBP 100-115 mm Hg) from 26 countries were randomly assigned to 1 of 3 DBP target groups: ≤90 mm Hg, ≤85 mm Hg, and ≤80 mm Hg. The long-acting dihydropyridine CCB felodipine was given as baseline therapy, with the addition of other agents as needed to reach goal. The mean age of the study group was 61.5 years. After a mean of 3.8 years of follow-up, DBP was reduced to 85.2 mm Hg in the group assigned to the ≤90 mm Hg goal, to 83.2 mm Hg in the group assigned to ≤85 mm Hg, and to 81.1 mm Hg in the group assigned to ≤80 mm Hg. Results in the subgroup of 1501 diabetic patients are shown here. The rate of major CV events (fatal/nonfatal MI, fatal/nonfatal stroke, and all other CV deaths) was reduced by approximately 50% in the group assigned a DBP goal ≤80 mm Hg compared with those assigned a goal of ≤90 mm Hg ( p =0.005). The difference between groups remained significant ( p =0.045) when silent MI was included in the analysis (data not shown). The rate of stroke was reduced by 30% and the rate of all MI by 50% in the ≤80 mm Hg group compared with the ≤90 mm Hg group, although these reductions did not achieve statistical significance (data not shown). Hansson L et al. Lancet . 1998;351:1755-1762.
In the Hypertension Optimal Treatment (HOT) study, (n=18,790) hypertensive patients (DBP 100-115 mm Hg) from 26 countries were randomly assigned to 1 of 3 DBP target groups: ≤90 mm Hg, ≤85 mm Hg, and ≤80 mm Hg. The long-acting dihydropyridine CCB felodipine was given as baseline therapy, with the addition of other agents as needed to reach goal. The mean age of the study group was 61.5 years. After a mean of 3.8 years of follow-up, DBP was reduced to 85.2 mm Hg in the group assigned to the ≤90 mm Hg goal, to 83.2 mm Hg in the group assigned to ≤85 mm Hg, and to 81.1 mm Hg in the group assigned to ≤80 mm Hg. Results in the subgroup of 1501 diabetic patients are shown here. The rate of major CV events (fatal/nonfatal MI, fatal/nonfatal stroke, and all other CV deaths) was reduced by approximately 50% in the group assigned a DBP goal ≤80 mm Hg compared with those assigned a goal of ≤90 mm Hg ( p =0.005). The difference between groups remained significant ( p =0.045) when silent MI was included in the analysis (data not shown). The rate of stroke was reduced by 30% and the rate of all MI by 50% in the ≤80 mm Hg group compared with the ≤90 mm Hg group, although these reductions did not achieve statistical significance (data not shown). Hansson L et al. Lancet . 1998;351:1755-1762.
In the Hypertension Optimal Treatment (HOT) study, (n=18,790) hypertensive patients (DBP 100-115 mm Hg) from 26 countries were randomly assigned to 1 of 3 DBP target groups: ≤90 mm Hg, ≤85 mm Hg, and ≤80 mm Hg. The long-acting dihydropyridine CCB felodipine was given as baseline therapy, with the addition of other agents as needed to reach goal. The mean age of the study group was 61.5 years. After a mean of 3.8 years of follow-up, DBP was reduced to 85.2 mm Hg in the group assigned to the ≤90 mm Hg goal, to 83.2 mm Hg in the group assigned to ≤85 mm Hg, and to 81.1 mm Hg in the group assigned to ≤80 mm Hg. Results in the subgroup of 1501 diabetic patients are shown here. The rate of major CV events (fatal/nonfatal MI, fatal/nonfatal stroke, and all other CV deaths) was reduced by approximately 50% in the group assigned a DBP goal ≤80 mm Hg compared with those assigned a goal of ≤90 mm Hg ( p =0.005). The difference between groups remained significant ( p =0.045) when silent MI was included in the analysis (data not shown). The rate of stroke was reduced by 30% and the rate of all MI by 50% in the ≤80 mm Hg group compared with the ≤90 mm Hg group, although these reductions did not achieve statistical significance (data not shown). Hansson L et al. Lancet . 1998;351:1755-1762.