Effects of a twenty-four-hour milrinone infusion in patients with severe heart failure and cardiogenic shock as a function of the hemodynamic initial condition

Klocke, R. K.; Mager, G.; Kux, A.; Höpp, H. W.; Hilger, H. H.

doi:10.1016/0002-8703(91)90833-4

Cited by 65 publications

(14 citation statements)

References 22 publications

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“…The first one is related to stimulation of cAMP synthesis by adenylyl cyclase, a membrane-bound enzyme converting ATP to cAMP, and the second mechanism is related to slowing down of cAMP degradation by inhibition of myocardial phosphodiesterases (PDEs), enzymes eliminating cAMP by its conversion to 5′AMP. The end result in both cases appears to be an increase in intracellular cAMP concentration which produces a number of stimulatory myocardial effects including increases in contractile function.Although short-term PDE inhibitor infusions were proven to be beneficial in maintaining cardiac systolic function [1][2][3][4], chronic oral treatment with PDE inhibitors has been shown to increase the morbidity and mortality in …”

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confidence: 99%

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Myocardial Phosphodiesterases and Regulation of Cardiac Contractility in Health and Cardiac Disease

Osadchii

2007

Cardiovasc Drugs Ther

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Phosphodiesterase (PDE) inhibitors are potent cardiotonic agents used for parenteral inotropic support in heart failure. Contractile effects of these agents are mediated through cAMP-protein kinase A-induced stimulation of I (Ca2+) which ultimately results in increased Ca(2+)-induced sarcoplasmic reticulum Ca(2+) release. A number of additional effects such as increases in sarcoplasmic reticulum Ca(2+) stores, stimulation of reverse mode Na(+)-Ca(2+) exchange, direct or cAMP-mediated effects on sarcoplasmic reticulum ryanodine receptor, stimulation of the voltage-sensitive sarcoplasmic reticulum Ca(2+) release mechanism, as well as A(1) adenosine receptor blockade could contribute to positive inotropic responses to PDE inhibitors. Moreover, some PDE inhibitors exhibit Ca(2+) sensitizer properties as they could increase the affinity of troponin C Ca(2+)-binding sites as well as reduce Ca(2+) threshold for thin myofilament sliding and facilitate cross-bridge cycling. Inotropic responses to PDE inhibitors are significantly reduced in cardiac disease, an effect largely attributed to downregulation of cAMP-mediated signalling due to sustained sympathetic activation. Four PDE isoenzymes (PDE1, PDE2, PDE3 and PDE4) are present in myocardial tissue of various mammalian species, of which PDE3 and PDE4 are particularly involved in regulation of cardiac myocyte contraction. PDE cAMP-hydrolysing activity is preserved in compensated cardiac hypertrophy but significantly reduced in animal models of heart failure. However, clinical studies have not revealed any changes in distribution profile as well as kinetic and regulatory properties of myocardial PDEs in failing human hearts. A reduction of PDE inhibitors-induced contractile responses in heart failure has therefore been ascribed to reduced cAMP synthesis due to uncoupling of adenylyl cyclase from beta-adrenoreceptor. In cardiac myocytes, PDEs are targeted to distinct subcellular compartments by scaffolding proteins such as myomegalin, mAKAP and beta-arrestins. Over subcellular microdomains, cAMP hydrolysis by PDE3 and PDE4 allows to control the activity of local pools of protein kinase A and therefore the extent of protein kinase A-mediated phosphorylation of cellular proteins.

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mentioning

confidence: 99%

“…Although short-term PDE inhibitor infusions were proven to be beneficial in maintaining cardiac systolic function [1][2][3][4], chronic oral treatment with PDE inhibitors has been shown to increase the morbidity and mortality in…”

mentioning

confidence: 99%

Myocardial Phosphodiesterases and Regulation of Cardiac Contractility in Health and Cardiac Disease

Osadchii

2007

Cardiovasc Drugs Ther

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“…Dopamine is preferable when moderate hypotension and hypoperfusion are present as vasoconstriction in the peripheral vessels is often needed to maintain vital organ tissue perfusion 20 . Phosphodiesterase inhibitors, Amrinone and Milrinone can increase contractility without adrenergic stimulation leading to improved cardiac output and pulmonary pressure 23 , with less effect on myocardial work 20 . These agents should be reserved for those in whom catecholamine have failed to improve cardiac performance or those in whom arrhythmia or ischemia limits the catecholamine dose because of their longer half-life especially in patients with renal impairment.…”

Section: Treatment General Supportive Measuresmentioning

confidence: 99%

Pulmonary Hypertension in A Patient with Systemic Sclerosis

S.T¹,

Ezennaka²

2017

IOSR JDMS

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INTRODUCTION:Cardiogenic shock (CS) is defined as a state of critical end organ hypoperfusion due to reduced cardiac output.The most frequent cause is acute myocardial infarction (AMI) with subsequent ventricular dysfunction in about 80% of cases. In spite of the advances made in the treatment of AMI, cardiogenic shock remains a leading cause of death with mortality rates approaching 40-50%. AIM: The purpose of this review is to highlight the current concepts in the management of cardiogenic shock. MATERIALS AND METHODS: A systematic review of published literature using PubMed and Med Line was done using search items like "cardiogenic and shock". Secondary references obtained from this publication were identified by manual search and reviewed as relevant. RESULTS: Cardiogenic shock is characterized by inadequate tissue perfusion in the setting of adequate intravascular volume. The treatment involves general supportive measures which include; adequate oxygenation and ventilation, correction of electrolytes and acid-base abnormalities, pain reliefand restoration of sinus rhythm. Revascularizationand mechanical supports are also necessary. CONCLUSION:The diagnosis and management of cardiogenic shock are difficult and require extensive knowledge and clinical experience. In spite of the significant advances made, the management still remains a challenge.

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“…Their chronic use did not show benefits and even caused, in some groups of patient, higher mortality when compared with control individuals [33][34][35] . Enoximone has similar effects, acting like phosphodiesterase inhibitors, improving myocardial contractility and causing dilation of vascular smooth muscles 36 .…”

Section: Arq Bras Cardiol Volume 72 (Nº 4) 1999mentioning

confidence: 99%

“…ACE inhibitors, even though available for intravenous use, have a prolonged action period, which makes their withdrawal difficult if deleterious effects occur after their introduction. Digitalis may worsen the hemodynamic condition of the patient, because it causes peripheral vasoconstriction and may increase oxygen consumption 33 . Digitalis has been reserved for control of atrial tachyarrhythmias.…”

Section: Arq Bras Cardiol Volume 72 (Nº 4) 1999mentioning

confidence: 99%

Cardiogenic shock

Knobel¹

1999

Arq. Bras. Cardiol.

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Effects of a twenty-four-hour milrinone infusion in patients with severe heart failure and cardiogenic shock as a function of the hemodynamic initial condition

Cited by 65 publications

References 22 publications

Myocardial Phosphodiesterases and Regulation of Cardiac Contractility in Health and Cardiac Disease

Myocardial Phosphodiesterases and Regulation of Cardiac Contractility in Health and Cardiac Disease

Pulmonary Hypertension in A Patient with Systemic Sclerosis

Cardiogenic shock

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