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Amrinone
Amrinone
Amrinone
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Amrinone
Clinical data
Trade namesInocor
Other namesinamrinone (USAN US)
AHFS/Drugs.comInternational Drug Names
Routes of
administration		Intravenous
ATC code
Legal status
Legal status
  • In general: ℞ (Prescription only)
Pharmacokinetic data
Bioavailabilityn/a
Protein binding10 to 49%
MetabolismHepatic
Elimination half-life5 to 8 hours
ExcretionRenal (63%) and fecal (18%)
Identifiers
  • 5-amino-3,4'-bipyridin-6(1H)-one
CAS Number
PubChem CID
IUPHAR/BPS
DrugBank
ChemSpider
UNII
KEGG
ChEBI
ChEMBL
CompTox Dashboard (EPA)
ECHA InfoCard100.056.700 Edit this at Wikidata
Chemical and physical data
FormulaC10H9N3O
Molar mass187.202 g·mol−1
3D model (JSmol)
  • O=C2C(/N)=C\C(\c1ccncc1)=C/N2
  • InChI=1S/C10H9N3O/c11-9-5-8(6-13-10(9)14)7-1-3-12-4-2-7/h1-6H,11H2,(H,13,14) checkY
  • Key:RNLQIBCLLYYYFJ-UHFFFAOYSA-N checkY
  (verify)

Amrinone, also known as inamrinone, and sold as Inocor, is a pyridine phosphodiesterase 3 inhibitor.[1] It is a drug that may improve the prognosis in patients with congestive heart failure.[2] Amrinone has been shown to increase the contractions initiated in the heart by high-gain calcium induced calcium release (CICR).[3] The positive inotropic effect of amrinone is mediated by the selective enhancement of high-gain CICR, which contributes to the contraction of myocytes by phosphorylation through cAMP dependent protein kinase A (PKA) and Ca2+ calmodulin kinase pathways.[3]

Actions

[edit]

Increases cardiac contractility, vasodilator. Acts by inhibiting the breakdown of both cAMP and cGMP by the phosphodiesterase (PDE3) enzyme. There is a long-standing controversy regarding whether the drug actually increases cardiac contractility in diseased myocardium (and therefore whether it is of any clinical use). The issue has been reviewed extensively by Dr Peter Wilmshurst, one of the first cardiologists and researchers to question the drug's efficacy.[4]

PDE-III inhibition and cardiac function

[edit]

PDE III is present in cardiac muscle, vascular smooth muscle and platelets. PDE III degrades the phosphodiester bond in cAMP to break it down.[5][6] When PDE III is inhibited, cAMP cannot be inactivated. An increase in cAMP with the administration of amrinone in vascular smooth muscle produces vasodilation by facilitating calcium uptake by the sarcoplasmic reticulum (a special type of smooth ER) and decreasing the calcium available for contraction.[5][7] In myocytes, the increase of cAMP concentration increases in turn the activity of PKA; this kinase improves the Ca2+ inward current through the L-type Ca2+ channels, which leads to calcium-induced calcium release from the sarcoplasmic reticulum, giving rise to a calcium spark that triggers the contraction; this results in an inotropic effect. Furthermore, PKA phosphorylates and deactivates the phospholambans that inhibit SERCA, which is an enzymatic pump that, to terminate the contraction, removes the Ca2+ from the cytoplasm, stores it back in the sarcoplasmic reticulum and promotes the subsequent arterial relaxation as well, producing a lusitropic effect. Both inotropic and lusitropic effects justify the use of amrinone to treat heart failure. Amrinone decreases the pulmonary capillary wedge pressure while increasing cardiac output, as it functions as an arterial vasodilator and increases venous capacitance while decreasing venous return.[5] There is a net decrease in myocardial wall tension, and O2 consumption when using amrinone. Amrinone also has beneficial effects during diastole in the left ventricle, including relaxation, compliance and filling in patients with congestive heart failure.[5]

Indications

[edit]

Short-term management of severe CHF (not used long term because of increased mortality, probably due to heart failure).

Effects in congestive heart failure

[edit]

Congestive heart failure (CHF) is characterized by a reduction in ventricular performance and abnormalities in peripheral circulation and organs.[6] A reduced release of endothelium derived relaxing factor (EDRF) causes a decrease in the stimulation of guanylate cyclase, and cyclic GMP (cGMP) levels fall in vascular smooth muscle. This impairs relaxation in the vasculature and is a part of the vicious cycle of CHF.[6] Patients with CHF have a down-regulation of their β-1 adrenergic receptors which alters their ability to activate intracellular adenylate cyclase, which catalyzes cAMP formation.[5] cAMP is the second messenger that controls the level of calcium available to allow the heart to contract. An IV administration of amrinone has been shown to increase cardiac output (CO) and stroke volume (SV), while concurrently reducing the filling pressure of the left ventricle and decreasing the resistance in the peripheral vasculature.[2][8][9] This does not lead to an increase in heart rate or blood pressure.[2][8][9] The improvement in performance of the ventricles is likely to result from a direct stimulation of the depressed myocardium as well as a decrease in peripheral vascular resistance.[10]

Contraindications

[edit]

Patients with aortic stenosis, hypertrophic cardiomyopathy, or history of hypersensitivity to the drug.

Precautions

[edit]

May increase myocardial ischemia. Blood pressure, pulse, and ECG should be constantly monitored. Amrinone should only be diluted with normal saline or 1/2 normal saline; no dextrose solutions should be used. Furosemide, a loop diuretic, should not be administered into an IV line delivering amrinone.

Side effects

[edit]

Thrombocytopenia is the most prominent and dose-related side effect, but it is transient and asymptomatic. Nausea, diarrhea, hepatotoxicity, arrhythmias and fever are other adverse effects.

Amrinone discovery and progression

[edit]

Early studies in patients with heart failure showed that amrinone produced short-term hemodynamic improvement, but had limited long-term clinical benefit.[7] Some serious side effects of long term administration included sustained ventricular tachycardia resulting in circulatory collapse, worsening myocardial ischemia, acute myocardial infarction, and worsening congestive heart failure.[7][11] Amrinone has good absorption from the gastrointestinal tract [12] and has led to gastrointestinal upset when taken orally. The oral form of the drug is no longer in use.[11] Currently, only acute intravenous administration takes place.[11] The effects of amrinone vary widely with species and experimental condition; therefore, its inotropic effects are variable.[3] A loss in sensitivity to phosphodiesterase 3 inhibitors, including amrinone, has been observed in end stage heart failure in humans; other treatment options may be more useful for improvement in these stages.[3]

Naming

[edit]

Amrinone is the INN, while inamrinone is the United States Adopted Name, which was adopted in 2000 in an attempt to avoid confusion with amiodarone.[13]

Synthesis

[edit]
Amrinone synthesis:[14][15][16][17]

See also: Milrinone and Pelrinone.

References

[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Amrinone

View on Grokipedia
from Grokipedia
Amrinone, also known as inamrinone (renamed in 2000 to avoid confusion with ), is a pyridine-based ( that functions as a positive inotropic agent and vasodilator. Approved by the FDA in 1984, it was primarily administered intravenously for the short-term management of decompensated congestive (CHF) in patients unresponsive to conventional therapies such as , diuretics, or vasodilators. By selectively inhibiting PDE3 in cardiac and vascular , amrinone elevates intracellular (cAMP) levels, which promotes calcium influx into myocardial cells to enhance contractility while also reducing systemic through , thereby increasing without significantly elevating myocardial oxygen demand. Its pharmacokinetic profile includes a of approximately 1.2 L/kg, protein binding of 10-49%, a of 5-8 hours, hepatic , and primarily renal . Typical dosing began with a of 0.75 mg/kg over 2-3 minutes, followed by a maintenance of 5-10 μg/kg/min, with a maximum daily dose of 10 mg/kg; it must be diluted in saline rather than dextrose-containing solutions to avoid incompatibility. Developed in the late by Alousi and colleagues as a nonglycosidic, noncatecholamine cardiotonic agent, amrinone represented a pioneering shift toward PDE3 inhibitors and served as the forerunner to subsequent drugs like , demonstrating rapid onset of action and a favorable initial in preclinical studies. Marketed under the brand name Inocor for intravenous use, it gained approval for acute CHF treatment, but the oral formulation was not approved due to multicenter trials showing lack of sustained efficacy, increased mortality from arrhythmias and calcium overload in chronic settings, and adverse effects including (affecting up to 46% with prolonged exposure), ventricular arrhythmias (up to 9%), , , and rare ; the IV formulation was discontinued from the U.S. market in 2000. Contraindicated in to the drug or its , with use requiring caution in severe obstructive valvular ; its use required close monitoring of , electrocardiograms, platelet counts, and renal/hepatic function to mitigate risks. Despite these limitations, amrinone's introduction influenced the evolution of pharmacotherapy toward more cardioprotective strategies, such as inhibitors and beta-blockers.

Medical uses

Indications

Amrinone, also known as inamrinone, was primarily indicated for the short-term intravenous management of severe congestive (CHF) in patients who had not responded adequately to standard therapies such as , diuretics, or vasodilators. This included cases of decompensated characterized by low , where it served as a rescue therapy to improve in acute settings. Its use was restricted to situations requiring immediate intervention, leveraging its positive inotropic and vasodilatory effects to support cardiac function. Although approved for these uses, amrinone injection was withdrawn from the U.S. market in and is no longer available for prescription as of 2025, though it remains available in select international markets. Historically, off-label applications included adjunctive therapy in acute complicated by , where low-dose infusions demonstrated improvements in and in small studies. Additionally, amrinone was employed to manage low states following open-heart surgery, often in combination with other agents like to stabilize in postoperative . The recommended dosage regimen began with an initial of 0.75 mg/kg administered intravenously over 2 to 3 minutes, followed by a continuous of 5 to 10 mcg/kg/min. Subsequent adjustments were made based on the patient's hemodynamic response, with the total daily dose not exceeding 10 mg/kg under normal circumstances. Due to the risk of serious adverse effects and lack of evidence for sustained benefits, amrinone was not approved for long-term therapy and was recommended for use only up to 48 hours in controlled clinical settings with ECG monitoring and access to equipment. It was not recommended for use in the acute phase following due to a lack of supporting data from large-scale studies.

Effects in congestive heart failure

Amrinone produced significant hemodynamic improvements in patients with congestive heart failure (CHF), primarily through its positive inotropic and vasodilatory actions. Intravenous administration typically increased by 20% to 40%, by approximately 30% to 35%, and measures of contractility such as dP/dt by 20% to 30%, while decreasing systemic by 20% to 30% and left ventricular end-diastolic pressure without substantially altering or . These changes reduced and preload, thereby enhancing ventricular unloading and improving overall cardiac performance in the short term. In acute decompensated CHF, amrinone provided rapid symptom relief, including reduced dyspnea and fatigue, often within hours of initiation. Short-term trials demonstrated improved exercise tolerance, with increases in maximal oxygen uptake and duration of exercise by 20% to 50% in responsive patients. These benefits stemmed from the drug's ability to transiently reverse pump failure by elevating intracellular cyclic AMP via phosphodiesterase-3 inhibition, as detailed in its . Key clinical studies from the late and , involving patients with severe chronic CHF, consistently showed these acute hemodynamic and symptomatic improvements but no evidence of long-term survival advantages. For instance, a trial in 10 patients reported sustained enhancements in and lasting up to 4 hours post-infusion. Similarly, a 1984 open-label study of 17 refractory cases confirmed a 26% to 40% rise in with corresponding reductions in pulmonary capillary wedge pressure, alongside clinical stabilization during short-term use. These findings from early investigations, which preceded larger trials of related agents, underscore amrinone's role in bridging acute exacerbations. Amrinone was most effective in patients with New York Heart Association (NYHA) class III or IV CHF characterized by systolic dysfunction and low , particularly those refractory to and diuretics. Selection favored individuals with elevated filling pressures and reduced ejection fractions below 30%, where the drug's balanced inotropic and vasodilatory profile could optimize without excessive .

Pharmacology

Mechanism of action

Amrinone exerts its primary pharmacological effects through selective inhibition of phosphodiesterase III (PDE3), an enzyme predominantly expressed in cardiac myocytes and vascular cells, which prevents the hydrolysis of (cAMP) and thereby elevates intracellular cAMP concentrations. This inhibition is specific to PDE3, distinguishing amrinone from non-selective inhibitors, and occurs without direct stimulation of beta-adrenergic receptors. The increased cAMP levels activate (PKA), which phosphorylates key targets in the pathway, including L-type calcium channels (Cav1.2), phospholamban, and . of L-type calcium channels enhances calcium influx during the action potential, while phospholamban relieves its inhibition on the Ca²⁺-ATPase (), promoting faster calcium reuptake and relaxation; additionally, decreases myofilament sensitivity to calcium, promoting faster relaxation (). These actions collectively amplify intracellular calcium transients, leading to stronger myocardial contractions and positive inotropic effects. In vascular smooth muscle, the elevated cAMP similarly activates PKA, which reduces intracellular calcium levels by promoting sequestration and efflux, resulting in smooth muscle relaxation and that decreases systemic . Amrinone also indirectly increases (cGMP) levels through cross-talk between cAMP and cGMP signaling pathways, further contributing to without directly inhibiting phosphodiesterases that target cGMP. At higher doses, amrinone exhibits a biphasic dose-response curve, where excessive calcium influx can lead to cellular calcium overload, potentially reversing the inotropic effect and inducing arrhythmias.

Amrinone is administered exclusively by intravenous injection or infusion, as the oral formulation has been discontinued. The drug exhibits rapid , typically within 2 to 5 minutes after intravenous administration. Following intravenous administration, amrinone distributes widely with a of approximately 1.0 to 1.2 L/kg and is bound to plasma proteins by 10% to 49%. It crosses the but has limited penetration of the blood-brain barrier. Metabolism occurs primarily in the liver through and pathways, independent of enzymes, yielding pharmacologically inactive metabolites such as N-acetyl-amrinone, N-glycolyl-amrinone, and conjugates. No active metabolites are formed. Elimination is predominantly renal, with 70% to 80% of the dose recovered in as unchanged and conjugates over 96 hours. The elimination is approximately 3.6 hours in healthy individuals but is prolonged to about 5.8 hours in patients with congestive owing to decreased clearance. In adult patients with renal impairment (CrCl <10 mL/min), administer 50-75% of the dose; no adjustment is necessary for CrCl ≥10 mL/min. No routine dose adjustment is required for hepatic impairment, though close monitoring is recommended in cases of . Amrinone may potentiate when coadministered with other vasodilators. It is chemically incompatible with , resulting in precipitate formation if mixed in the same intravenous line; separate administration with line flushing is advised.

Safety and tolerability

Contraindications

Amrinone is contraindicated in patients with known hypersensitivity to the drug or related compounds such as , as well as to excipients like or bisulfites, due to the risk of severe allergic reactions including or . The drug is absolutely contraindicated in obstructive cardiomyopathies, such as or idiopathic hypertrophic subaortic (IHSS), where its positive inotropic effects can increase the across the outflow tract, potentially worsening obstruction and hemodynamic instability. Amrinone should not be used in patients with severe aortic or pulmonic valvular disease, as it may aggravate valvular or regurgitation, leading to further compromise of . Historically, long-term use of amrinone was contraindicated following clinical trials that demonstrated lack of sustained efficacy in congestive and increased risks of harm, including accelerated ventricular dysfunction and high mortality rates up to 63% at , leading to its abandonment for chronic therapy.

Precautions

Due to its vasodilatory effects, amrinone requires careful monitoring to prevent hemodynamic instability during administration. Patients receiving amrinone should undergo continuous electrocardiographic (ECG) monitoring for arrhythmias, frequent assessments to detect , and evaluation of fluid status to maintain adequate cardiac filling pressures, particularly in those on concomitant diuretics. Additionally, frequent platelet counts are recommended, as occurs in up to one-third of patients and may necessitate close observation if counts fall below 150,000/mm³. Amrinone must be diluted only in normal (0.9%) or half-normal (0.45%) saline to concentrations of 1–3 mg/mL for infusion, as dextrose-containing solutions lead to chemical degradation over 24 hours; it should not be mixed with furosemide or alkaline solutions in intravenous lines due to immediate precipitate formation. In special populations, dose reduction is advised for patients with renal or hepatic impairment to account for potential decreased clearance and increased risk of toxicity. Elderly patients exhibit heightened sensitivity to hypotension, warranting conservative dosing and vigilant monitoring. Amrinone is classified as pregnancy category C, with use recommended only if the potential benefit justifies the risk, given the absence of adequate controlled studies in pregnant women. For perioperative use, amrinone carries a risk of , and infusions should be tapered gradually to mitigate rebound effects upon discontinuation. In cases of overdose, is supportive, involving discontinuation of the and administration of vasopressors to address severe , as no specific exists.

Adverse effects

Amrinone is generally well-tolerated in short-term intravenous use for acute , with most adverse effects occurring at low incidences below 5% and being transient in nature, as reported in clinical trials involving 462 patients. Common side effects include gastrointestinal disturbances, hematologic changes, and cardiovascular events, which typically resolve upon discontinuation of the drug.

Hematologic Effects

The most notable hematologic adverse effect is thrombocytopenia, occurring in approximately 2.4% of patients, which is reversible and reaches its nadir around 2-3 days after initiation of therapy.

Gastrointestinal Effects

Gastrointestinal side effects are mild and infrequent, including nausea in 1.7% of patients, vomiting in 0.9%, and diarrhea in about 1.6%. These symptoms are usually self-limiting and do not require intervention beyond supportive care.

Cardiovascular Effects

Cardiovascular adverse events include ventricular arrhythmias in 3% of patients, in 1.3%, and , which may arise from the drug's vasodilatory properties. These effects are more common during and often resolve with dose adjustment or cessation.

Other Effects

manifests as elevated liver enzymes in 1-2% of cases, particularly with prolonged administration, while fever occurs in 0.9% of patients. and reactions, presenting as a flu-like with arthralgias and , have been observed infrequently. Intravenous can cause local irritation, pain, and tissue at the injection site. Prolonged use of amrinone has been associated with increased risks, including accelerated left ventricular dysfunction, exacerbated myocardial ischemia, and life-threatening arrhythmias, leading to higher rates of adverse events (up to 83%) and treatment withdrawal in 34% of patients in long-term studies. Platelet monitoring is recommended during therapy to detect early.

Chemistry

Structure and properties

Amrinone has the molecular formula C₁₀H₉N₃O and a molecular weight of 187.2 g/mol. Its is 5-amino-3,4'-bipyridin-6(1H)-one, featuring a bipyridine core with an amino group at position 5 and a keto function at position 6. The compound exists as a pale yellow crystalline powder. Amrinone base is poorly soluble in but forms a lactate salt for intravenous use, which enhances to approximately 25 mg/mL at 4.1. Predicted pKa values are 11.01 for the strongest acidic site and 4.87 for the strongest basic site. The original (USAN) was "amrinone," but in 2000, the USAN Council and USP Nomenclature Committee changed it to "inamrinone" to avoid confusion with ; the (INN) remains "amrinone" worldwide. Amrinone is light-sensitive and requires storage at (15–30°C), protected from light and freezing to maintain stability.

Synthesis

The original synthesis of amrinone, or 5-amino-3,4'-bipyridin-6(1H)-one, was detailed in a assigned to Sterling-Winthrop Research Institute. One primary route begins with the condensation of α-(4-pyridinyl)-β-(dialkylamino)acrolein, such as the dimethylamino derivative, and malonamide in refluxing using as base, yielding 3-carboxamide-5-(4-pyridinyl)-2(1H)-pyridinone after cyclization. This intermediate undergoes a by heating with aqueous at 60–100°C, followed by acidification with , to afford amrinone. An alternative pathway in the same patent starts with the condensation of the acrolein derivative and α-cyanoacetamide under similar conditions to form 3-cyano-5-(4-pyridinyl)-2(1H)-pyridinone. Partial hydrolysis of the nitrile group with concentrated sulfuric acid produces the 3-carboxamide intermediate, which is then converted to amrinone via the Hofmann rearrangement as described. A third route involves nitration of 5-(4-pyridinyl)-2(1H)-pyridinone-3-carboxylic acid using a mixture of concentrated sulfuric and nitric acids at 70–90°C to give the 3-nitro derivative, followed by reduction through catalytic hydrogenation with palladium on carbon to yield amrinone. Another reported synthesis utilizes 5-(4-pyridinyl)-2(1H)-pyridone as the starting material, followed by at the 3-position in a of nitric and acetic acids, and subsequent reduction of the nitro group to the amino functionality, providing an efficient access to amrinone. For pharmaceutical use, amrinone is typically converted to its lactate salt to enhance , as the exhibits low aqueous (approximately 0.7–0.9 mg/mL at neutral pH). This salt is formed by reacting amrinone with in , and the product is purified by recrystallization from solvents such as dimethylformamide- mixtures. The primary patents for these processes date to the 1970s, with no significant updates to the synthesis routes reported after 2000.

History and development

Discovery

Amrinone was discovered in 1976 by a team of researchers at Inc. (later Sterling-Winthrop) as part of a systematic screening effort to identify novel positive inotropic agents for the treatment of . The compound, chemically known as 5-amino-3,4'-bipyridin-6(1H)-one, emerged from this program as a structurally unique, non-glycoside, non-catecholamine agent with promising cardiotonic properties, distinct from traditional glycosides or sympathomimetic drugs. It was initially synthesized and patented in 1977 under U.S. Patent 4,004,012 by inventors George Y. Lesher and Charles J. Opalka Jr., assigned to Inc., highlighting its potential as a new class of . Preclinical investigations, led by key researchers including Alexander A. Alousi and Allen E. Farah at the Sterling-Winthrop Research Institute, demonstrated amrinone's potent inotropic effects in various animal models. In isolated papillary muscle preparations, amrinone (3–100 μg/ml) produced dose-dependent increases in developed tension and the rate of tension development (dF/dt) without prolonging the contractile cycle or time to peak tension. In vivo studies in anesthetized dogs showed that intravenous bolus doses of 1–10 mg/kg elevated cardiac contractile force and maximum left ventricular dP/dt by up to 100–200%, while oral doses of 2–10 mg/kg yielded rapid onset and sustained effects lasting several hours. Complementary experiments in unanesthetized dogs confirmed these findings, with infusions (10–100 μg/kg/min) maintaining hemodynamic improvements without . Additionally, amrinone exhibited vasodilatory activity in anesthetized canine models of drug-induced , reducing systemic vascular resistance and enhancing through combined inotropic and peripheral effects. Toxicity profiles from these early studies indicated a favorable margin at therapeutic doses. In mice, the intravenous LD50 was 150 mg/kg, and observations in dogs and other species showed no significant adverse effects on electrocardiograms, , or renal function at doses producing marked inotropy, underscoring amrinone's low . The initial preclinical data were published in 1979 by Alousi, Farah, Lesher, and Opalka in Circulation Research, establishing amrinone as a for further development. Subsequent mechanistic studies in the late , building on broader research into (PDE) inhibitors from the early , revealed amrinone's selectivity for PDE3, marking it as the first compound in this class to demonstrate cardiac-specific inhibition of cyclic AMP degradation.

Clinical progression and naming

Amrinone's clinical development began with early Phase I and II trials in the late and early , which demonstrated short-term hemodynamic improvements, including increased and reduced pulmonary capillary wedge pressure, in patients with severe congestive (CHF). These trials involved small cohorts and focused on intravenous administration, showing positive inotropic and vasodilatory effects without significant short-term adverse outcomes in stable patients. Building on these findings, the U.S. (FDA) approved amrinone lactate injection (branded as Inocor) on July 31, 1984, for short-term intravenous management of CHF in patients unresponsive to other therapies, marking it as the first approved for this indication. Efforts to develop an oral formulation for chronic use followed, but multicenter randomized, double-blind, placebo-controlled withdrawal studies in the mid-1980s revealed no sustained improvements in exercise tolerance, cardiac performance, or symptoms after discontinuation, indicating limited long-term despite initial hemodynamic gains. As a result, the oral form was never approved for marketing, and use remained restricted to short-term . Amrinone received designation for CHF treatment, granting seven years of exclusive approval status upon its launch to encourage development for this rare severe condition. By the late , concerns over lack of survival benefits and potential risks, including observed in trials, further limited its role to acute settings. Regulatory and market evolution continued into the 2000s, with the Adopted Names (USAN) Council and renaming the drug inamrinone effective July 1, 2000, to prevent dispensing errors due to phonetic similarity with ; the (INN) amrinone was retained globally. The branded product Inocor was discontinued by its manufacturer in March 2000 and is no longer commercially available in the . As of 2025, inamrinone/amrinone remains off-market and is rarely used, with availability limited to potential compounding by pharmacies in exceptional cases, though its prescription is not standard due to superior alternatives like , which offers a better safety profile for short-term inotropic support. The 2022 (AHA)/ (ACC)/Heart Failure Society of America (HFSA) guidelines do not recommend inamrinone for routine goal-directed medical therapy in , reserving intravenous inotropes like or for select refractory cases in advanced stages to palliate symptoms or bridge to advanced therapies, without endorsing amrinone specifically. No new indications or reformulations have emerged, reflecting its diminished role amid advances in pharmacotherapy.

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