Vasodilators in the management of acute heart failure

Elkayam, Uri; Janmohamed, Munir; Habib, Munira; Hatamizadeh, Parta

doi:10.1097/01.ccm.0000297161.41559.93

Cited by 61 publications

(38 citation statements)

References 64 publications

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“…The clinical response to NTG is known to be highly variable between patients; this may be explained by vascular resistance to NTG in patients with heart failure. 6,18 Katz et al 19 reported a two-fold increase in femoral artery blood velocity after intra-arterial infusion of NTG in normal subjects. However, this response was markedly attenuated in patients with heart failure and could be overcome only by increasing the dose, suggesting vascular resistance to NTG in patients with heart failure.…”

Section: Discussionmentioning

confidence: 99%

Low‐dose nitroglycerin improves microcirculation in hospitalized patients with acute heart failure

Uil

Lagrand

Spronk

et al. 2009

European J of Heart Fail

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AimsImpaired tissue perfusion is often observed in patients with acute heart failure. We tested whether low-dose nitroglycerin (NTG) improves microcirculatory perfusion in patients admitted for acute heart failure. Methods and resultsIn 20 acute heart failure patients, NTG was given as intravenous infusion at a fixed dose of 33 mg/min. Using Sidestream Dark Field (SDF) imaging, sublingual microvascular perfusion was evaluated before (T0, average of two baseline measurements) and 15 min after initiation of NTG (T1). In a subgroup of seven patients, SDF measurements were repeated after NTG had been stopped for 20 min. Capillaries were defined as microvessels with a diameter of ,20 mm. Perfused capillary density (PCD) was determined as the parameter of tissue perfusion. Values are expressed as median and interquartile range (P25; P75). The median age of the subjects was 60 (52; 73) years, and 65% were male. Patients were stable before starting NTG. Nitroglycerin decreased central venous pressure [17 (13; 19) mmHg at T0 vs. 16 (13; 17) mmHg at T1, P ¼ 0.03] and pulmonary capillary wedge pressure [23 (18; 31) mmHg at T0 vs. 19 (16; 25) mmHg at T1, P ¼ 0.03]. It increased PCD [10.7 (9.9; 12.5) mm mm 22 at T0 vs. 12.4 (11.4; 13.6) mm mm 22 at T1, P ¼ 0.01]. After cessation of NTG, PCD returned to baseline values (P ¼ 0.04). ConclusionLow-dose NTG significantly reduces cardiac filling pressures and improves microvascular perfusion in patients admitted for acute heart failure.--

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Section: Discussionmentioning

confidence: 99%

Low‐dose nitroglycerin improves microcirculation in hospitalized patients with acute heart failure

Uil

Lagrand

Spronk

et al. 2009

European J of Heart Fail

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“…There have been reports that vasodilators may decrease BNP (89); however, there is also the potential of increasing plasma renin level (89). The effect of NTG on coronary blood flow has not been investigated in ADHF but is known to increase coronary flow in other scenarios.…”

Section: Vasodilatormentioning

confidence: 99%

Cardiorenal Syndrome in Acute Decompensated Heart Failure

Sarraf

Masoumi²,

Schrier³

2009

Clinical Journal of the American Society of Nephrology

150

114

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Renal dysfunction is highly prevalent in patients with heart failure. Furthermore, worsening renal function in patients with acute decompensated heart failure (ADHF), the so-called cardiorenal syndrome, impacts short and long-term morbidity and mortality. In recent years, more evidence has surfaced from clinical trials and heart failure registries that a complex cross-talk between the kidney and heart in patients with ADHF exists. Meanwhile, management of patients presenting with ADHF and concomitant renal dysfunction continues to be challenging. Therefore, understanding the interaction of the heart and kidneys is pivotal in tailoring therapy of these patients. We have extensively reviewed the pathophysiology of ADHF, the role of neurohoromones as well as other biomarkers and predictors of mortality in these patients based on the current evidence. Moreover, we have discussed the current and future pharmacologic and non-pharmacologic therapies for treatment of this deadly disease. The strength of the evidence is limited, however, due to a paucity of randomized controlled trials in this patient population. What is evident from current national statistics; however, are the poor results in treating the congestion of ADHF. In this regard, the role of secondary hyperaldosteronism is discussed in the diuretic section as well as diuretic resistance in ADHF. In conclusion, since renal function is the single most important prognostic factor in the outcome of patients with ADHF, a better understanding of the pathophysiology of the cardiorenal syndrome is needed to target therapy and ultimately improve the mortality of patients with ADHF.

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“…Nitrates may ameliorate the abnormal cardiovascular hemodynamics in ADHF by promoting vasodilation and consequently reducing ventricular filling pressure, systemic vascular resistance, pulmonary vascular resistance, and pulmonary capillary wedge pressure 3, 15. Additional benefits may be related to a reduction in subendocardial ischemia and mitral regurgitation 6. However, tachyphylaxis may develop and a constant dose of nitrates may fail to have a persistent effect, depending on the duration of use.…”

Section: Discussionmentioning

confidence: 99%

Impact of Nitrate Use on Survival in Acute Heart Failure: A Propensity‐Matched Analysis

Parker

Austin

et al. 2016

JAHA

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BackgroundThere is limited evidence that the use of nitrates in acute decompensated heart failure early after presentation to a hospital can improve clinical outcomes. We aimed to determine whether early nitrate exposure is associated with improved survival in a large retrospective cohort study.Methods and ResultsWe examined 11 078 acute decompensated heart failure patients who presented to emergency departments in Ontario, Canada, between 2004 and 2007, in the Enhanced Feedback For Effective Cardiac Treatment and the Emergency Heart failure Mortality Risk Grade studies. In propensity‐matched analyses, we examined the effect of nitrate administration in the acute emergency department setting for its impact on death at 7, 30, and 365 days. In propensity‐matched analyses, we found no difference in survival between those who received nitrates in the emergency department and the non‐nitrate comparator group. Hazard ratios for mortality were 0.76 (95% CI; 0.51, 1.12) over 7 days, 0.97 (95% CI; 0.77, 1.21) over 30 days, and 0.91 (95% CI; 0.82, 1.02) over 1 year of follow‐up. There was no significant difference in survival or hospital length of stay between nitrate and non‐nitrate controls in extended follow‐up. There was also no significant effect of nitrates in subgroups stratified by presence of chest pain, troponin elevation, chronic nitrate use, and known coronary artery disease.ConclusionsIn acute decompensated heart failure, use of nitrates acutely in the emergency department setting was not associated with improvement in short‐term or near‐term survival. Our study does not support generalized use of nitrates when the primary goal of therapy is to reduce mortality.

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Vasodilators in the management of acute heart failure

Cited by 61 publications

References 64 publications

Low‐dose nitroglycerin improves microcirculation in hospitalized patients with acute heart failure

Low‐dose nitroglycerin improves microcirculation in hospitalized patients with acute heart failure

Cardiorenal Syndrome in Acute Decompensated Heart Failure

Impact of Nitrate Use on Survival in Acute Heart Failure: A Propensity‐Matched Analysis

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