Clinical importance of the renin-angiotensin system in chronic heart failure: double blind comparison of captopril and prazosin.

Bayliss, J; Norell, Michael S.; Canepa‐Anson, R; Reid, C.; Poole-Wilson, P. A.; Sutton, George C.

doi:10.1136/bmj.290.6485.1861

Cited by 99 publications

(37 citation statements)

References 27 publications

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“…α-adrenolityki nie są zalecane w celu obniżania ciśnienia tętniczego z powodu wątpliwości dotyczą-cych braku bezpieczeństwa w HFrEF (aktywacja neurohormonalna, retencja płynów, pogorszenie HF) III A [458,464,465] diltiazem i werapamil nie są zalecane w celu obniżenia ciśnienia tętniczego ze względu na swój ujemny wpływ inotropowy i ryzyko pogorszenia HF…”

Section: Niedobór żElaza I Niedokrwistośćunclassified

2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure

Ponikowski

Voors

Anker³

et al. 2016

Kardiol Pol

460

446

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Section: Niedobór żElaza I Niedokrwistośćunclassified

2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure

Ponikowski

Voors

Anker³

et al. 2016

Kardiol Pol

460

446

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“…The decrease in plasma arginine-vasopressin and in minimal urine osmolality that was observed in patients with lower renin ( figure 4) [17][18][19][20][21][22][23] Because cross-tolerance from one vasodilator to another does not always occur, mechanisms other than neurohormonal overstimulation must also be involved in the production of tachyphylaxis to vasodilators.…”

Section: Resultsmentioning

confidence: 99%

Differential long-term intrarenal and neurohormonal effects of captopril and prazosin in patients with chronic congestive heart failure: importance of initial plasma renin activity.

Mettauer¹,

Rouleau

Bichet³

et al. 1986

Circulation

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Fifty patients with congestive heart failure received, by infusion, 15 ml/kg body weight water load, and systemic hemodynamic, renal function, and neurohumoral parameters values were measured before, 2 days, and 1 month after randomly allocating patients to prazosin or captopril therapy. Both prazosin and captopril caused similar and persistent hemodynamic changes, but important differences existed between their renal and neurohumoral effects. After 1 month of continuous therapy, captopril increased creatinine clearance from 71 to 84 ml/min/1.732 (p < .05), increased the water load excreted in 5 hr from 50% to 71% (p < .005), and increased 5 hr sodium excreted from 6.8 to 14.7 meq (p < .005). Captopril also caused a decrease in plasma norepinephrine from 568 to 448 pg/ml (p < .005), in plasma epinephrine from 94 to 73 pg/ml (p < .05), and in plasma aldosterone from 57 to 28 ng/dl (p< .005), without changing plasma vasopressin. These beneficial effects were greater after 1 month of therapy than after 2 days. The only beneficial effect of prazosin was to increase water excretion from 49% to 59% (p < .05). The long-term response to captopril was similar in patients with higher (> 2.5 ng/ml/hr) and lower renin levels. However, in patients with lower renin levels, prazosin decreased pulmonary capillary wedge pressure (24.8 to 21.8 mm Hg, p < .05), decreased plasma arginine vasopressin (1.16 to 0.75 pg/ml, p < .05), increased water excretion (62% to 85%, p < .005), and decreased plasma epinephrine (81 to 46 pg/ml, p < .05), while in patients with higher renin levels none of these beneficial effects were noted. We conclude (1) that captopril produces long-term beneficial renal and neurohumoral effects that prazosin does not despite similar hemodynamic changes with the two drugs, (2) that these effects are at least partially dependent on the initial neurohumoral and hemodynamic status of the patient, and (3) that through hemodynamic improvement vasodilators may chronically interrupt vasopressin overstimulation.

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“…Moxonidine increased mortality in patients in the MOXCON trial in HFrEF [11] and there are concerns of the risk in HFrEF patients of neurohormonal activation, fluid retention and worsening HF with alphaadrenoceptor antagonists. [12][13][14] Lastly in the setting of acute heart failure (AHF) i.v. nitrates (or sodium nitroprusside, starting with 0.3 μg/kg/min and increasing up to 5 μg/kg/min) are recommended to lower blood pressure.…”

Section: The Steps To Good Bp Control In Heart Failurementioning

confidence: 99%

The Management of Co-Morbidities in Patients with Heart Failure – Hypertension

Coats¹,

Rosano

Lopatin

2017

ICFJ

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The 2016 ESC/HFA HF guidelines carry an important section on the treatments of co- morbidities in HF. Foremost of these in terms of frequency and its relevance to the aetiology of HF, especially HFpEF is hypertension. In this artcile we will review what the recent guidelines say about the management of hypertension in the setting of HF, both HFrEF and HFpEF and expand on some of the practical advice.

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Clinical importance of the renin-angiotensin system in chronic heart failure: double blind comparison of captopril and prazosin.

Abstract: Nineteen patients with chronic heart failure participated in a double blind crossover trial of captopril and prazosin -two drugs with differing neuroendocrine effects-to determine whether neuroendocrine changes could ex-

Cited by 99 publications

References 27 publications

2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure

2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure

Differential long-term intrarenal and neurohormonal effects of captopril and prazosin in patients with chronic congestive heart failure: importance of initial plasma renin activity.

The Management of Co-Morbidities in Patients with Heart Failure – Hypertension

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