Utilidad pronóstica de las cifras ambulatorias de presión arterial en pacientes de edad avanzada con insuficiencia cardíaca. Resultados del estudio DICUMAP / Prognostic value of ambulatory blood pressure values in elderly patients with heart failure. Results of the DICUMAP study

Introducción La monitorización ambulatoria de la presión arterial (MAPA) ha demostrado la utilidad en la evaluación pronóstica de los pacientes hipertensos con insuficiencia cardíaca (IC) con o sin otras enfermedades cardiovasculares. El objetivo de este estudio consistió en determinar si la MAPA puede identificar a pacientes con IC con un peor pronóstico. Métodos y resultados Estudio multicéntrico prospectivo en el que se incluyeron pacientes ambulatorios y clínicamente estables con IC. Todos los pacientes se sometieron a una MAPA. Se incluyó un total de 154 pacientes de 17 centros. La edad media fue de 76,8 años (±8,3) y el 55,2% eran mujeres. En total, el 23,7% presentaba IC con fracción de eyección reducida (IC-FEr), el 68,2% se encontraba en la clase funcional II de la NYHA y el 19,5%, en la clase funcional III de la NYHA. Al cabo de un año de seguimiento se produjeron 13 (8,4%) muertes, 10 de ellas atribuidas a la IC. En 19 de los 29 pacientes que precisaron hospitalización, esta se debió a la IC. La presencia de un patrón no dipper de PA se asoció a un mayor riesgo de reingreso o muerte al año de seguimiento (25% frente al 5%; p=0,024). Según un análisis de regresión de Cox, una clase funcional más avanzada de la NYHA (razón de riesgos instantáneos, 3,51; IC del 95%, 1,70-7,26; p=0,001; comparación entre las clases III y II de la NYHA) y una mayor reducción nocturna proporcional de la PA diastólica (razón de riesgos instantáneos, 0,961; IC del 95%, 0,926-0,997; p=0,032 por cada reducción del 1% de la PA diastólica) se asociaron a muerte o reingreso al cabo de un año de manera independiente. Conclusiones En los pacientes de edad avanzada con IC crónica, un patrón no dipper de PA determinado mediante MAPA se asoció a un mayor riesgo de hospitalización y muerte por IC (AU)

Introduction Ambulatory blood pressure monitoring (ABPM) has demonstrated value in the prognostic assessment of hypertensive patients with heart failure (HF) with or without other cardiovascular diseases. The objective of this study was to evaluate whether ABPM can identify subjects with HF with a worse prognosis. Methods and results Prospective multicenter study that included clinically stable outpatients with HF. All patients underwent ABPM. A total of 154 patients from 17 centers were included. Their mean age was 76.8 years (±8.3) and 55.2% were female. In total, 23.7% had HF with a reduced ejection fraction (HFrEF), 68.2% were in NYHA functional class II, and 19.5% were in NYHA functional class III. At one year of follow up, there were 13 (8.4%) deaths, of which 10 were attributed to HF. Twenty-nine patients required hospitalization, of which 19 were due to HF. The presence of a non-dipper BP pattern was associated with an increased risk for readmission or death at one year of follow-up (25% vs. 5%; p=.024). According to a Cox regression analysis, more advanced NYHA functional class (hazard ratio 3.51; 95%CI 1.70-7.26; p=.001; for NYHA class III vs. II) and a higher proportional nocturnal reduction in diastolic BP (hazard ratio 0.961; 95%CI 0.926-0.997; p=.032 per 1% diastolic BP reduction) were independently associated with death or readmission at one year. Conclusion In older patients with chronic HF, a non-dipper BP pattern measured by ABPM was associated with a higher risk of hospitalization and death due to HF (AU)

Prognostic value of ambulatory blood pressure values in elderly patients with heart failure. Results of the DICUMAP study.

INTRODUCTION: Ambulatory blood pressure monitoring (ABPM) has demonstrated value in the prognostic assessment of hypertensive patients with heart failure (HF) with or without other cardiovascular diseases. The objective of this study was to evaluate whether ABPM can identify subjects with HF with a worse prognosis. METHODS AND RESULTS: Prospective multicenter study that included clinically stable outpatients with HF. All patients underwent ABPM. A total of 154 patients from 17 centers were included. Their mean age was 76.8 years (± 8.3) and 55.2% were female. In total, 23.7% had HF with a reduced ejection fraction (HFrEF), 68.2% were in NYHA functional class II, and 19.5% were in NYHA functional class III. At one year of follow up, there were 13 (8.4%) deaths, of which 10 were attributed to HF. Twenty-nine patients required hospitalization, of which 19 were due to HF. The presence of a non-dipper BP pattern was associated with an increased risk for readmission or death at one year of follow-up (25% vs. 5%; p=.024). According to a Cox regression analysis, more advanced NYHA functional class (hazard ratio 3.51; 95% CI 1.70-7.26; p=.001; for NYHA class III vs. II) and a higher proportional nocturnal reduction in diastolic BP (hazard ratio 0.961; 95%CI 0.926-0.997; p=.032 per 1% diastolic BP reduction) were independently associated with death or readmission at one year. CONCLUSION: In older patients with chronic HF, a non-dipper BP pattern measured by ABPM was associated with a higher risk of hospitalization and death due to HF.

"Real World" Eligibility for Sacubitril/Valsartan in Unselected Heart Failure Patients: Data from the Swedish Heart Failure Registry.

PURPOSE: PARADIGM-HF demonstrated the superiority of sacubitril/valsartan over enalapril in patients with heart failure and reduced ejection fraction (HF-REF). How widely applicable sacubitril/valsartan treatment is in unselected patients with HF-REF is not known. We examined eligibility of patients with HF-REF for treatment with sacubitril/valsartan, according to the criteria used in PARADIGM-HF, in the Swedish Heart Failure Registry (SwedeHF). METHODS: Patients were considered potentially eligible if they were not hospitalized, had symptoms (NYHA class II-IV) and a reduced LVEF (≤ 40%), and were prescribed an angiotensin-converting enzyme inhibitor (ACEI) or angiotensin receptor blocker (ARB) at a dose equivalent to enalapril ≥ 10 mg daily. In these patients, we evaluated further eligibility according to the main additional PARADIGM-HF inclusion criteria. RESULTS: Of 12,866 outpatients in NYHA functional class II-IV with an LVEF ≤ 40%, 9577 were prescribed at least 10 mg of enalapril (or equivalent) daily. Complete additional data were available for 3099 of these patients (32.4%) and of them 75.5% were potentially eligible for treatment with sacubitril/valsartan. The most common reason for ineligibility was a low natriuretic peptide level (n = 462, 14.9%). Only a small proportion of patients were ineligible due to low eGFR or serum potassium level. Because only 78% of patients were taking ≥ 10 mg enalapril or equivalent daily, only 58.9% of all patients (75.5% of 78%) were eligible for sacubitril/valsartan. CONCLUSIONS: Between 34 and 76% of symptomatic patients with HF-REF in a 'real world' population are eligible for treatment with sacubitril/valsartan, depending on background ACEI/ARB dose. The most common reason for ineligibility is a low natriuretic peptide level.

Aspirin inhibits the acute venodilator response to furosemide in patients with chronic heart failure.

OBJECTIVES: We sought to determine the effect of aspirin on the venodilator effect of furosemide in patients with chronic heart failure (CHF) BACKGROUND: Furosemide has an acute venodilator effect preceding its diuretic action, which is blocked by nonsteroidal anti-inflammatory, drugs. The ability of therapeutic doses of aspirin to block this effect of furosemide in patients with CHF has not been studied. For comparison, the venodilator response to nitroglycerin (NTG) was also studied. METHODS: Eleven patients with CHF were randomized to receive placebo, aspirin at 75 mg/day or aspirin at 300 mg/day for 14 days in a double-blind, crossover study. The effect of these pretreatments on the change in forearm venous capacitance (FVC) after 20 mg of intravenous furosemide was measured over 20 min by using venous occlusion plethysmography. In a second study, the effect of 400 microg of sublingual NTG on FVC was documented in 11 similar patients (nine participated in the first study). RESULTS: Mean arterial pressure, heart rate and forearm blood flow did not change in response to furosemide. After placebo pretreatment, furosemide caused an increase in FVC of 2.2% (95% confidence interval [CI] -0.9% to 5.2%; mean response over 20 min). By comparison, FVC fell by -1.1% (95% CI -4.2% to 1.9%) after pretreatment with aspirin at 75 mg/day, and by -3.7% (95% CI -6.8% to -0.7%) after aspirin at 300 mg/day (p = 0.020). In the second study, NTG increased FVC by 2.1% (95% CI -1.6% to 5.8%) (p = 0.95 vs. furosemide). CONCLUSIONS: In patients with CHF, venodilation occurs within minutes of the administration of intravenous dose of furosemide. Our observation that aspirin inhibits this effect further questions the use of aspirin in patients with CHF.

Attenuation of endothelin-1 induced vasoconstriction by 17beta estradiol is not sustained during long-term therapy in postmenopausal women with coronary heart disease.

OBJECTIVES: The goal of this study was to determine the long-term effects of estrogen replacement therapy on the response to endothelin-1 (ET-1) in postmenopausal women with coronary heart disease. BACKGROUND: It is thought that the vasoconstrictor ET-1 is involved in the development and progression of atherosclerosis. Estrogen replacement may slow the development of atherosclerosis in postmenopausal women. METHODS: Nineteen of 20 postmenopausal women randomized to either three months of 2 mg oral estradiol or placebo completed the double-blind placebo-controlled protocol. Change in forearm blood flow (FBF) in response to a 60 min brachial arterial infusion of ET-1 (5 pmol/min) was measured before randomization, after one month of randomized therapy and after three months of therapy using venous occlusion plethysmography. RESULTS: Estrogen treatment had no effect on baseline FBF. Systolic and diastolic blood pressure and heart rate did not change in response to estrogen therapy or ET-1. Before randomization, in response to ET-1, FBF was reduced by -21.9% (mean response over 60 min) in the placebo group and -19.0% in the estradiol group (p = 0.67). After one month of therapy, the response was attenuated in the estrogen group, -10.0%, compared with the placebo group, -23.6 (difference in means 13.6%, 95% confidence interval [0.7%, 26.6%], p = 0.041). After three months of therapy, there was no difference in response between the placebo group, -27.0%, and estrogen group, -30.2% (p = 0.65). CONCLUSIONS: In postmenopausal women with coronary heart disease, estrogen therapy inhibits the vasoconstrictor response to ET-1 after one month of therapy. This effect is lost after three months of therapy, suggesting that tachyphylaxis to one potentially beneficial action of estradiol develops during chronic treatment.