Electrophysiologic effects of milrinone in patients with congestive heart failure

Goldstein, Richard A.; Geraci, Stephen A.; Gray, Elayne L.; Rinkenberger, Robert L.; Dougherty, Anne H.; Naccarelli, Gerald V.

doi:10.1016/0002-9149(86)90847-7

Cited by 52 publications

(4 citation statements)

References 18 publications

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“…n = 9; * P \ 0.05, significantly different from control that PDE-III inhibitors have been observed to be proarrhythmic in clinical trials. However, while milrinone had no effect on the ECG variables or refractory period in humans with CHF [31], it decreased QT c and ventricular refractoriness as well as increased the incidence of VF and mortality in acute myocardial infarction [32]. On the other hand, amrinone was reported to increase the action potential duration and facilitated AV conduction but was not arrhythmogenic in post-coronary occluded dogs [33].…”

Section: Qt C Interval In Regulating Arrhythmogenicitymentioning

confidence: 97%

Antiplatelet Agents Sarpogrelate and Cilostazol Affect Experimentally-induced Ventricular Arrhythmias and Mortality

et al. 2008

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Antiplatelet agents, sarpogrelate (SAR), a 5-hydroxy tryptamine 2A receptor antagonist and cilostazol (CIL), a phosphodiesterase-III inhibitor, were observed to be beneficial in attenuating cardiac remodeling and improving cardiac function in congestive heart failure due to myocardial infarction in rats; however, CIL increased ventricular tachycardia and mortality. In order to study the effects of these antiplatelet agents on arrhythmias, Sprague-Dawley rats were pretreated with either SAR or CIL (5 mg/kg/day) for 2 weeks and were then either injected cumulative doses of epinephrine (Epi) or subjected to coronary occlusion. Saline-treated animals served as controls. Electrocardiographic analysis revealed that SAR pretreatment decreased the incidence and severity of ventricular arrhythmias (time of onset of arrhythmias as well as the occurrence of premature ventricular contractions, salvos, tachycardia, and fibrillations), whereas CIL treatment augmented the incidence of cardiac arrhythmias due to both Epi and coronary occlusion. None of the drugs affected the corrected QT interval significantly. Furthermore, the levels of cyclic adenosine monophosphate (cAMP) in left ventricle were markedly higher in CIL-pretreated rats when compared to SAR-pretreated or control rats. It is suggested that an excessive level of cAMP may contribute to increase incidence of ventricular arrhythmias and mortality in animals pretreated with CIL, unlike the SAR-pretreated rats.

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Section: Qt C Interval In Regulating Arrhythmogenicitymentioning

confidence: 97%

Antiplatelet Agents Sarpogrelate and Cilostazol Affect Experimentally-induced Ventricular Arrhythmias and Mortality

et al. 2008

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“…Given the variability in baseline VPC frequency, other more stringent criteria have been used to assess treatment effects [26]. However, the trends associated with the administration of OPC-8212 would appear to be in contrast to the controversial arrythmogenic potential of other inotropic agents [5][6][7][8]. Furthermore, despite the fact that other agents have more prominent hemodynamic actions in patients with congestive heart failure, this improvement has not been uniformly associated with a reduction in ventricular arrhythmias and the incidence of sudden cardiac death [9].…”

Section: Discussionmentioning

confidence: 99%

“…1Department of Medicine, University of Minnesota, Minneapolis; and 2Valley Hospital, Ridgewood, New Jersey limited by potential side effects, including the provocation of ventricular arrhythmias [6][7][8][9]. OPC-8212 is a quinolone derivative that has potent inotropic activity in vitro and beneficial hemodynamic effects in preliminary studies in patients with congestive heart failure [10][11][12].…”

mentioning

confidence: 99%

OPC-8212 in the treatment of congestive heart failure: Results of a pilot study

Kubo

Rector

Strobeck

et al. 1988

Cardiovasc Drug Ther

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To characterize the effects of OPC-8212, a quinolone inotropic agent, in patients with heart failure, we utilized invasive hemodynamics, exercise testing, 24-hour ambulatory electrocardiograms, and two patient self-assessment questionnaires, before and after 1 month of treatment with OPC-8212, in 17 patients with moderate to severe congestive heart failure. There were no significant changes from baseline in heart rate (83 +/- 8 beats/min), mean arterial pressure (70 +/- 15 mmHg), pulmonary wedge pressure (18 +/- 7 mmHg), or cardiac index (2.3 +/- 0.4 L/min/m2) following treatment with OPC-8212. Both exercise duration (5.3 +/- 1.6 min) and peak oxygen consumption (12.0 +/- 2.9 mL/kg/min) were unchanged by OPC-8212. Two independent patient self-assessment scores, the Sickness Impact Profile and the Minnesota Living with Heart Failure Questionnaire, showed improvements from 6.8 to 5.4 and 49 to 38, respectively (both p less than .05), suggesting that the patients reported an improvement in daily functioning. The median ventricular premature contraction count and frequency were reduced from 1,118 beats to 243 beats (p less than 0.05) and 11/1,000 beats to 2.4/1,000 beats (0.05 less than p less than 0.10), respectively. Two patients developed agranulocytosis during longer-term treatment following this 1-month study. These data demonstrate that OPC-8212 did not have significant effects on hemodynamics or exercise tolerance. However, the improvement in patient self-assessment scores and the trend for improvement in ventricular arrhythmia profiles suggest that OPC-8212 may have some benefit for patients with congestive heart failure, but additional placebo-controlled, double-blind studies are necessary.

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“…Third, the higher myocardial oxygen consumption due to the inotropic effect of these PDE3 inhibitors can increase the frequency of arrhythmias [33,45]. One should be aware of these adverse effects of PDE3 inhibitors if they are to be used as inotropic drugs, particularly in heart failure patients [13,33,34,[46][47][48].…”

Section: Undesirable Effects Of Phosphodiesterase 3 Inhibitors In Thementioning

confidence: 99%

Effects of cilostazol in the heart

Kanlop

Chattipakorn

2011

Journal of Cardiovascular Medicine

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Cilostazol is a selective phosphodiesterase 3 (PDE3) inhibitor approved by the Food and Drug Administration for treatment of intermittent claudication. It has also been used in bradyarrhythmic patients to increase heart rates. Recently, cilostazol has been shown to prevent ventricular fibrillation in patients with Brugada syndrome. Cilostazol is hypothesized to suppress transient outward potassium (Ito) current and increase inward calcium current, thus, maintaining the dome (phase 2) of action potential, decreasing transmural dispersion of repolarization and preventing ventricular fibrillation. Although many PDE3 inhibitors have been shown to increase cardiac arrhythmia in heart failure, cilostazol has presented effects that are different from other PDE3 inhibitors, especially adenosine uptake inhibition. Owing to this effect, cilostazol could be an effective cardioprotective drug, with its beneficial effects in preventing arrhythmia. In this review, the cardiac electrophysiological effects of cilostazol are presented and its possible cardioprotective effects, particularly in preventing ventricular fibrillation, are discussed, with emphasis on the need to further verify its clinical benefits.

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Electrophysiologic effects of milrinone in patients with congestive heart failure

Cited by 52 publications

References 18 publications

Antiplatelet Agents Sarpogrelate and Cilostazol Affect Experimentally-induced Ventricular Arrhythmias and Mortality

Antiplatelet Agents Sarpogrelate and Cilostazol Affect Experimentally-induced Ventricular Arrhythmias and Mortality

OPC-8212 in the treatment of congestive heart failure: Results of a pilot study

Effects of cilostazol in the heart

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