Jump to navigation Jump to search
Clinical data
  • US: C (Risk not ruled out)
Routes of
ATC code
Legal status
Legal status
Pharmacokinetic data
Protein binding10 to 49%
Elimination half-life5 to 8 hours
ExcretionRenal (63%) and fecal (18%)
CAS Number
PubChem CID
E number{{#property:P628}}
ECHA InfoCard{{#property:P2566}}Lua error in Module:EditAtWikidata at line 36: attempt to index field 'wikibase' (a nil value).
Chemical and physical data
Molar mass187.198 g/mol

WikiDoc Resources for Amrinone


Most recent articles on Amrinone

Most cited articles on Amrinone

Review articles on Amrinone

Articles on Amrinone in N Eng J Med, Lancet, BMJ


Powerpoint slides on Amrinone

Images of Amrinone

Photos of Amrinone

Podcasts & MP3s on Amrinone

Videos on Amrinone

Evidence Based Medicine

Cochrane Collaboration on Amrinone

Bandolier on Amrinone

TRIP on Amrinone

Clinical Trials

Ongoing Trials on Amrinone at Clinical

Trial results on Amrinone

Clinical Trials on Amrinone at Google

Guidelines / Policies / Govt

US National Guidelines Clearinghouse on Amrinone

NICE Guidance on Amrinone


FDA on Amrinone

CDC on Amrinone


Books on Amrinone


Amrinone in the news

Be alerted to news on Amrinone

News trends on Amrinone


Blogs on Amrinone


Definitions of Amrinone

Patient Resources / Community

Patient resources on Amrinone

Discussion groups on Amrinone

Patient Handouts on Amrinone

Directions to Hospitals Treating Amrinone

Risk calculators and risk factors for Amrinone

Healthcare Provider Resources

Symptoms of Amrinone

Causes & Risk Factors for Amrinone

Diagnostic studies for Amrinone

Treatment of Amrinone

Continuing Medical Education (CME)

CME Programs on Amrinone


Amrinone en Espanol

Amrinone en Francais


Amrinone in the Marketplace

Patents on Amrinone

Experimental / Informatics

List of terms related to Amrinone

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]


Amrinone (INN) or inamrinone (USAN, changed in 2000 to prevent confusion with amiodarone[1]), trade name Inocor, is a pyridine phosphodiesterase 3 inhibitor.[2] It is a drug that may improve the prognosis in patients with congestive heart failure.[3] Amrinone has been shown to increase the contractions initiated in the heart by high gain calcium induced calcium release (CICR).[4] 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.[4]


It is used in the treatment of congestive heart failure.

It has been studied for use before coronary artery bypass surgery.[5]


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.[6]

PDE- III inhibition and cardiac function

PDE III is present in cardiac muscle, vascular smooth muscle and platelets. PDE III degrades the phosphodiester bond in cAMP to break it down.[7][8] 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.[7][9] Since amrinone inhibits PDE III, it also inhibits the L type Ca2+ current in myocytes as well as facilitating an increase in Ca2+ uptake by the sarcoplasmic reticulum (SR).[4] This may contribute to its positive inotropic effect on cardiac myocytes.[4] Amrinone decreases the pulmonary capillary wedge pressure while increasing cardiac output because it functions as an arterial vasodilator and increases venous capacitance while decreasing venous return.[7] 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.[7]


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

How Inamrinone is used to correct Congestive Heart Failure

Congestive heart failure (CHF) is characterized by a reduction in ventricular performance and abnormalities in peripheral circulation and organs.[8] 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.[8] 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.[7] 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.[3][10][11] This does not lead to an increase in heart rate or blood pressure.[3][10][11] This 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.[12]


Patients with Aortic Stenosis, Hypertrophic Cardiomyopathy, or history of hypersensitivity to the drug.


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

Side effects

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


IV bolus and infusion as described earlier.

Pediatric dosage

Safety in children has not been established.

Amrinone discovery and progression

Early studies in patients with heart failure showed that amrinone produced short-term hemodynamic improvement, but had limited long-term clinical benefit.[9] 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.[9][13] Amrinone has good absorption from the gastrointestinal tract [14] and may lead to some gastrointestinal upset when taken orally. The oral form of the drug is no longer in use.[13] Currently, only acute intravenous administration takes place.[13] The effects of amrinone vary widely with species and experimental condition; therefore inotropic effects are variable.[4] A loss in sensitivity to PDE III inhibitors has been observed in end stage heart failure in humans and thus other treatment options may be necessary to improvement in these stages.[4]


  1. "Amrinone Becomes Inamrinone". USP Quality Review. United States Pharmacopeia. 73. March 2000.
  2. Hamada Y, Kawachi K, Yamamoto T; et al. (August 1999). "Effects of single administration of a phosphodiesterase III inhibitor during cardiopulmonary bypass: comparison of milrinone and amrinone". Japanese circulation journal. 63 (8): 605–9. doi:10.1253/jcj.63.605. PMID 10478810.
  3. 3.0 3.1 3.2 Klein N.A., Siskind S.J., Frishman W.H., Sonnelblick E.H., LeJemtel T.H. (1981). "Hemodynamic Comparison of Intravenous Amrinone and Dobutamine in Patients With Chronic Congestive Heart Failure". American Journal of Cardiology. 48: 170–175. doi:10.1016/0002-9149(81)90587-7.
  4. 4.0 4.1 4.2 4.3 4.4 4.5 Xiong W., Ferrier G.R., Howlett S.E. (2004). "Diminished Inotropic Response to Amrinone in Ventricular Myocytes from Myopathic Hamsters Is Linked to Depression of High-Gain Ca2+-Induced Ca2+ Release". The Journal of Pharmacology and Experimental Therapeutics. 310: 761–773. doi:10.1124/jpet.103.064873.
  5. Kikura M, Sato S (January 2002). "The efficacy of preemptive Milrinone or Amrinone therapy in patients undergoing coronary artery bypass grafting". Anesth. Analg. 94 (1): 22–30, table of contents. doi:10.1097/00000539-200201000-00005. PMID 11772795.
  6. Wilmshurst P. "The HealthWatch Award 2003: Dr Peter Wilmshurst - "Obstacles to honesty in medical research"".
  7. 7.0 7.1 7.2 7.3 7.4 Levy J.H., Ramsay J., Bailey J.M. (1990). "Levy J.H., Ramsay J., Bailey J.M.". Journal of Cardiothoracic Anesthesia (4): 7–11.
  8. 8.0 8.1 8.2 LeJemtel T.H., Scortichini D., Levitt B., Sonnenblick E.H. (1989). "Effects of Phosphodiesterase Inhibition on Skeletal Muscle Vasculature". American Journal of Cardiology. 3: 27–30.
  9. 9.0 9.1 9.2 Packer M., Medina N., Yushak M. (1984). "Hemodynamic and clinical limitations of long- term inotropic therapy with amrinone in patients with severe chronic heart failure". Circulation. 70: 1038–1047. doi:10.1161/01.cir.70.6.1038.
  10. 10.0 10.1 Carabello B.A. (1980). "Effects of Amrinone on Myocardial Energy Metabolism and Hemodynamics in Patients with Severe Congestive Heart Failure Due to Coronary Artery Disease". Circulation. 62: 28–34.
  11. 11.0 11.1 Konstam M.A., Cohen S.R., Weiland D.S., Martin T.T., Das D., Isner J.M., Salem D.N. (1986). "Relative Contribution of Inotropic and Vasodilator Effects of Amrinone- induced Hemodynamic improvement in congestive heart failure". American Journal of Cardiology. 57: 242–248. doi:10.1016/0002-9149(86)90899-4.
  12. LeJemtel T.H., Keung E., Ribner H.S., Davis R., Wexler J., Blaufox D.M., Sonnenblick E.H. (1980). "Sustained Beneficial Effects of Oral Amrinone on Cardiac and Renal Function in Patients With Severe Congestive Heart Failure". American Journal of Cardiology (45): 123–129.
  13. 13.0 13.1 13.2 Rettig G., Sen S., Frohlig G., Schieffer H., Bette L. (1986). "Withdrawal of long-term amrinone therapy in patients with congestive heart failure: a placebo controlled trial". European Heart Journal. 7: 628–631.
  14. Alousi A.A., Farah A.E., Lesher G.Y., Opalka C.J. (1979). "Cardiotonic Activity of Amrinone- Win 40680 [5-Amino-3, 4- bipyridin- 6(1H)-one]". Circultaion (45): 666–677.