Nitrate therapy is likely to be as effective in treating acute heart failure as a combination of diuretic and opiate therapy. High dose nitrate with low dose diuretic is likely to improve outcome compared with low-dose nitrate and high dose diuretic. Level of Evidence
Full Answer
Should morphine be used in the treatment of acute heart failure?
Jun 17, 2017 · Serelaxin failed to meet the primary endpoints in a large phase 3 study. Now we may add morphine treatment on this failure list. Treatment with furosemide and nitroglycerin remains on the list but also here the underlying scientific evidence is poor.
What are the best drugs to treat heart failure?
Jan 04, 2016 · The cornerstone of AHF treatment is diuretics and vasodilators, such as nitrates. Due to a lack of randomised controlled trials, the use of nitrates for management of AHF is not universally adopted. While organic nitrates are among the oldest treatments for chronic stable angina, they are underutilised in AHF.
Should opiates be used in patients with decompensated heart failure?
Jun 01, 2013 · When given by repeat IV bolus (every 3–5 min), both high-dose NTG (2 mg) 28 and ISDN (4 mg) 29, 30 have been associated with improved outcomes (i.e., reduced need for mechanical ventilation, intensive care unit admission and hospital length of stay) without induction of harm.
Why do heart failure patients need multiple medicines?
The treatment focuses on reducing afterload with vasodilators such as nitrates (sublingual, intravenous, or topical), hydralazine (intravenous), and ACE inhibitors.
Does morphine help with heart problems?
Is morphine used for the heart?
Can you take morphine with congestive heart failure?
What is the best treatment for AHF?
The cornerstone of AHF treatment is diuretics and vasodilators, such as nitrates. Due to a lack of randomised controlled trials, the use of nitrates for management of AHF is not universally adopted. While organic nitrates are among the oldest treatments for chronic stable angina, they are underutilised in AHF. Organic nitrates are available as sublingual tablets, capsules, sprays, patches, ointments or intravenous (IV) solutions, all of which are potent vasodilators. Because of the challenges in AHF research, a data imbalance between acute and chronic HF treatment exists as more studies have been performed in the latter. Thus, the current level of evidence for the use of nitrates in AHF is only rated as 1C, i.e., ‘expert opinion’.[5,6] The purpose of this article is to review the clinical efficacy and safety data of nitrates in AHF.
What is the purpose of the article on nitrates in AHF?
The purpose of this article is to review the clinical efficacy and safety of nitrates in acute heart failure (AHF) by examining various trials on nitrates in AHF. Management of AHF can be challenging due to the lack of objective clinical evidence guiding optimal management. There have been many articles suggesting that, despite a benefit, nitrates are underused in clinical practice. Nitrates, when appropriately dosed, have a favourable effect on symptoms, blood pressure, intubation rates, mortality and other parameters.
What is the most commonly used IV NO source for AHF?
Overall, the two most commonly used IV NO sources used clinically in the setting of AHF is the organic nitrate donor nitroglycerin, and the inorganic nitrate source sodium nitroprusside (SNP). Nitroglycerin potently dilates large arteries (including coronary arteries) but has less effect on smaller arterioles, while SNP is a predominant arteriolar dilator. That makes SNP is effective in recompensating patients with AHF.[13] Other important clinical differences between organic and inorganic nitrates are summarised in Table 1.[14]
How long does it take for nitrite to develop haemodynamic tolerance?
It is well documented that patients receiving IV organic nitrate develop haemodynamic tolerance in as little as 4 hours. Nitrite (NaNO2) does not suffer this limitation and thus may have a future therapeutic role. Physiologically, in healthy subjects, NaNO2 selectively dilates pulmonary capacitance vessels and results in a modest reduction in systemic arterial pressure. However, clinical outcomes in AHF with NaNO2 are less clearly defined.
How to overcome nitrate tolerance?
Strategies suggested to overcome nitrate tolerance are to increase the dosage, or adding hydralazine concurrently (75 mg four times per day). [39] The favourable interaction between hydralazine and nitrates has been demonstrated in the Veterans Heart Failure Trial (V-HeFT) and in the African-American Heart Failure Trial (A-HeFT). This study showed beneficial effects on LV function and exercise capacity; most importantly it has been shown to improve survival in large studies in patients with severe heart failure. Although prevention of tolerance is only one of the possible mechanisms to explain the benefit of this combination.[40,41] Other strategies to overcome nitrates tolerance is allowing nitrate-free interval. This strategy is more applicable in managing chronic heart failure.[42]
What is AHF in medical terms?
Acute heart failure (AHF) presents symptoms primarily the result of pulmonary congestion due to elevated left ventricular (LV) filling pressures with or without reduced ejection fraction (EF). Common precipitating pathology includes coronary artery disease (CAD), hypertension and valvular heart diseases, in addition to other non-cardiac conditions, such as diabetes, anaemia and kidney dysfunction.[1,2] Additionally, AHF poses major medical and socioeconomic burdens. It represents the most common discharge diagnosis in patients over 65 years of age in the US, and an AHF patient that requires hospitalisation has a 90-day mortality approaching 10 %.[3,4]
What is nitrates used for?
Nitrates as a Treatment of Acute Heart Failure
What is AHF management?
Acute heart failure (AHF) is a life-threatening medical condition, where urgent diagnostic and treatment methods are of key importance. However, there are few evidence-based treatment methods. Interestingly, despite relatively similar ways of management of AHF throughout the globe, mid-term outcome in East Asia, including South Korea is more favorable than in Europe. Yet, most of the treatment methods are symptomatic. The cornerstone of AHF management is identifying precipitating factors and specific phenotype. Multidisciplinary approach is important in AHF, which can be caused or aggravated by both cardiac and non-cardiac causes. The main pathophysiological mechanism in AHF is congestion, both systemic and inside the organs (lung, kidney, or liver). Cardiac output is often preserved in AHF except in a few cases of advanced heart failure. This paper provides guidance on AHF management in a time-based approach. Treatment strategies, criteria for triage, admission to hospital and discharge are described.
What is AHF in medical terms?
AHF is a rapid onset or acute worsening of symptoms and/or signs of HF, associated with elevated plasma levels of natriuretic peptides (NPs). 1)It requires immediate medical management and, usually, urgent hospital admission. It can be a first occurrence of AHF (de novo) or, more frequently, acute decompensation of chronic heart failure (ADHF). De novo AHF is mainly caused by primary cardiac dysfunction (mainly ACS), while ADHF may be precipitated by infection, uncontrolled hypertension, rhythm disturbances or non-compliance with the prescribed drugs/diet. 1),2)AHF is a multifaceted syndrome with various clinical phenotypes, such as acute pulmonary edema (APE), hypertensive HF, cardiogenic shock (CS) and others. 7)It may present with impaired or preserved left ventricular ejection fraction, or disturbance of right ventricle function. Although considered as a primarily cardiac syndrome, AHF may lead to systemic disorders and affect all vital organs due to insufficient blood circulation4)caused by high level of venous back-pressure and/or low cardiac output.
How much is the mortality rate for morphine?
In the cohort of all patients 30-day mortality was higher among patients receiving morphine (26.7% vs 8% in the no morphine group.)
How many patients were in the morphine treatment arm?
Only a small number of patients (6%) were initially included in the treatment (morphine) arm, though after propensity score matching, an equal number (275) of patients were enrolled in both the treatment and non-treatment groups.
Which group of patients was more likely to receive intravenous medications, IV nitrates, vaso
Similarly, patients in the “morphine” group were more likely to receive intravenous medications, IV nitrates, vasopressors, and ventilator support. As such, it appears that opiates were more frequently used in the setting of acute severe presentations.
Does morphine increase mortality?
Additional studies have also shown an association between the use of morphine in acute heart failure and an increase in mortality. Peacock et al reported data from the ADHERE registry and demonstrated that the use of morphine in patients with acute heart failure is an independent predictor of increased in-hospital mortality 7. Similarly, a 2011 study from Israel found that the use of morphine in acute heart failure was independently associated with in-hospital death in a multivariate analysis (OR 2 with 95% CI 1.1 – 3.5.) 8 This study by Miro and colleagues provides similar data, though it is somewhat unique in examining Emergency Department patients and interventions specifically.
Does morphine cause heart failure?
Patients in the “morphine” group had higher rates of ischemic heart disease, cerebrovascular disease, peripheral artery disease, dementia, a worse functional status, and higher NYHA class of heart failure than those in the “without morphine” group, meaning that this was a patient population with higher comorbid disease. This has the potential to bias the results of mortality toward the morphine cohort.
Is opium safe for heart failure?
The European Society of Cardiology guidelines on the treatment of heart failure recommend against the routine use of opiates 3, while the American Heart Association recommends opiate use in heart failure be limited to the palliative care of patients with end-stage HF and severe respiratory distress 4.
Is ST elevation myocardial infarction included in this study?
Patients found to have ST-elevation myocardial infarction who subsequently developed a cute heart failure were not included in this study. Although this represented only 3% of AHF cases encountered, and is not likely to affect overall outcomes of this study, its exclusion does limit the applicability of results to this subgroup of patients.
How many people were hospitalized with morphine in 2004?
Results: There were 147 362 hospitalisations in ADHERE at December 2004, 20 782 of whom (14.1%) received morphine and 126 580 (85.9%) did not. There were no clinically relevant differences between the groups in the initial age, heart rate, blood pressure, blood urea nitrogen, creatinine, haemoglobin, ejection fraction or atrial fibrillation. A higher prevalence of rest dyspnoea, congestion on chest radiography, rales and raised troponin occurred in the morphine group. Patients on morphine received more inotropes and vasodilators, were more likely to require mechanical ventilation (15.4% vs 2.8%), had a longer median hospitalisation (5.6 vs 4.2 days), more ICU admissions (38.7% vs 14.4%), and had greater mortality (13.0% vs 2.4%) (all p<0.001). Even after risk adjustment and exclusion of ventilated patients, morphine was an independent predictor of mortality (OR 4.84 (95% CI 4.52 to 5.18), p<0.001).
Is morphine a long term therapy?
Objective: Morphine is a long-standing therapy in acute decompensated heart failure (ADHF), despite few supporting data. A study was undertaken to compare the outcomes of patients who did and did not receive morphine for ADHF.
Is morphine safe for pulmonary oedema?
Historically, morphine was considered “the most important agent used in the treatment of a cute pulmonary oedema”, 1 2 and it is still a well accepted treatment for patients with acute decompensated heart failure (ADHF). 3 Despite the fact that there is surprisingly little evidence supporting its routine use, the recently published European Society of Cardiology guidelines for the diagnosis and treatment of acute heart failure 3 state that “morphine is indicated in the early stage of the treatment of patients admitted with a severe acute heart failure, especially if associated with restlessness and dyspnoea”. Conversely, no major American cardiology or emergency medicine society has endorsed or published any recommendations on the treatment of ADHF regarding morphine.
Does morphine cause increased adverse events?
Conclusions: Morphine is associated with increased adverse events in ADHF which includes a greater frequency of mechanical ventilation, prolonged hospitalisation, more ICU admissions and higher mortality.
