Rational use of diuretics in acute decompensated heart failure

Goebel, Jason; Bakel, Adrian B. Van

doi:10.1007/s11897-008-0024-y

Cited by 14 publications

(9 citation statements)

References 57 publications

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“…This is of clinical relevance given the potential risk of hypokalemia with loop diuretics (and the associated proarrhythmic effects). 24 Our results indicate that the effects of Ucn2 cotreatment to enhance renal function and diuretic/ natriuretic responsiveness (without additional potassium depletion) during furosemide administration in CHF would be beneficial, perhaps most especially in otherwise diuretic-resistant patients with volume overload.…”

Section: Discussionmentioning

confidence: 73%

“…The latter action may be especially germane in this setting because aggressive diuretic therapy carries a danger of arrhythmias subsequent to severe electrolyte and volume depletion. 24 Although Ucn2 is a potent vasodilator, acting directly on vascular tone 2,36 (indicated here by significant reductions in CTPR) and indirectly by reducing circulating levels of the vasoconstrictor angiotensin II 23 (as assessed by decreases in PRA) and by inhibiting endothelin-1-induced arterial constriction, 35 the combination of Ucn2 and furosemide did not result in an additional decrease in MAP above that achieved by furosemide alone. This is likely to be attributed to the sizable improvement in CO induced by Ucn2.…”

Section: Discussionmentioning

confidence: 75%

“…From a therapeutic perspective, the combination of Ucn2 and diuretic therapy (producing further declines in peripheral resistance without supplementary reductions in blood pressure) could be appealing in this respect because excessive diuresis bears the potential risk of hypotension and worsening renal function. 24 Intriguingly, hematocrit dropped after Ucn2 treatment, despite an active diuresis and associated negative fluid balance in these animals, conceivably pointing to an acute shift of fluid from the extravascular to vascular compartments. It is also possible that the peptide has an effect on red blood cell production, given the report of Ucn2 gene expression in bone marrow, 37 although this is unlikely to have produced the precipitous hematocrit declines (and posttreatment increases) observed in this study because bone marrow effects are usually seen over days/weeks and months.…”

Section: Discussionmentioning

confidence: 88%

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Urocortin 2 Inhibits Furosemide-Induced Activation of Renin and Enhances Renal Function and Diuretic Responsiveness in Experimental Heart Failure

Rademaker

Charles

Nicholls

et al. 2009

Circ: Heart Failure

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Background— Urocortin 2 (Ucn2), a novel peptide with therapeutic potential in heart failure, and diuretics have opposing effects on renal function and the renin-angiotensin-aldosterone system. Because any prospective new treatment is likely to be used in conjunction with standard diuretic therapy, it is necessary to investigate the combined effects of these agents. Methods and Results— Ucn2 and furosemide were administered for 3 hours, both singly and combined, in 7 sheep with pacing-induced heart failure. Compared with time-matched controls, separate Ucn2 and furosemide administration significantly increased urine output (furosemide>Ucn2), urine sodium (furosemide>Ucn2), potassium (furosemide>Ucn2), and creatinine excretion (Ucn2>furosemide) and creatinine clearance (Ucn2>furosemide). Compared with furosemide treatment alone, Ucn2+furosemide produced a further diuresis ( P <0.05), natriuresis ( P <0.05), and a sustained increase in creatinine excretion ( P <0.05) and clearance ( P <0.05), without additional potassium elimination. All active treatments reduced mean arterial pressure (Ucn2+furosemide=furosemide>Ucn2), left atrial pressure (Ucn2+furosemide>Ucn2>furosemide), and peripheral resistance (Ucn2+furosemide=Ucn2>furosemide), whereas only Ucn2, singly and in combination with furosemide, increased cardiac output and dP/dt(max). In contrast to the increase in plasma renin activity elicited by furosemide alone, Ucn2 and Ucn2+furosemide markedly reduced plasma renin activity. All active treatments decreased plasma aldosterone (Ucn2+furosemide=Ucn2>furosemide), whereas only Ucn2 and Ucn2+furosemide reduced vasopressin and natriuretic peptide concentrations. Conclusion— Ucn2 cotreatment with furosemide enhanced hemodynamic and renal function and diuretic responsiveness (without additional potassium depletion) in experimental heart failure. Furthermore, Ucn2 reversed furosemide-induced increases in plasma renin activity and induced greater decreases in plasma aldosterone and vasopressin. These data indicate that adjunct Ucn2 therapy with diuretics in heart failure is beneficial.

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Section: Discussionmentioning

confidence: 73%

Section: Discussionmentioning

confidence: 75%

Section: Discussionmentioning

confidence: 88%

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Urocortin 2 Inhibits Furosemide-Induced Activation of Renin and Enhances Renal Function and Diuretic Responsiveness in Experimental Heart Failure

Rademaker

Charles

Nicholls

et al. 2009

Circ: Heart Failure

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“…By blocking distal tubule sodium reabsorption, thiazide-type diuretics (TD) can antagonize the renal adaptation to chronic LD therapy and potentially improve diuretic resistance due to rebound sodium retention (12,15). Several of the other mechanisms of action of different diuretic classes are summarized in Table 1 (16).…”

Section: Overcoming Diuretic Resistance In Edematous Statesmentioning

confidence: 99%

Combination of Loop Diuretics With Thiazide-Type Diuretics in Heart Failure

Jentzer

DeWald

Hernandez

2010

Journal of the American College of Cardiology

344

232

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Volume overload is an important clinical target in heart failure management, typically addressed using loop diuretics. An important and challenging subset of heart failure patients exhibit fluid overload despite significant doses of loop diuretics. One approach to overcome loop diuretic resistance is the addition of a thiazide-type diuretic to produce diuretic synergy via "sequential nephron blockade," first described more than 40 years ago. Although potentially able to induce diuresis in patients otherwise resistant to high doses of loop diuretics, this strategy has not been subjected to large-scale clinical trials to establish safety and clinical efficacy. We summarize the existing literature evaluating the combination of loop and thiazide diuretics in patients with heart failure in order to describe the possible benefits and hazards associated with this therapy. Combination diuretic therapy using any of several thiazide-type diuretics can more than double daily urine sodium excretion to induce weight loss and edema resolution, at the risk of inducing severe hypokalemia in addition to hyponatremia, hypotension, and worsening renal function. We provide considerations about prudent use of this therapy and review potential misconceptions about this long-used diuretic approach. Finally, we seek to highlight the need for pragmatic clinical trials for this commonly used therapy.

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“…Unfortunately, the prognostic profile is worse in ADHF patients in whom beta-blocker therapy initiation is delayed, or where treatment is reduced or discontinued [5][6][7]. The current mainstays of initial therapy in this setting include loop diuretics, intravenous (IV) vasodilators and parenteral inotropes, but these are not without problems [8][9][10], and, given the persistently high morbidity and mortality rates, an exploration of new treatment regimes remains crucial.…”

Section: Introductionmentioning

confidence: 99%