Inhaled prostacyclin for treatment of pulmonary hypertension after cardiac surgery or heart transplantation: A pharmacodynamic study

Haraldsson, Åsa; Kieler-Jensen, Niels; Se, Ricksten

doi:10.1016/s1053-0770(96)80047-4

Cited by 102 publications

(55 citation statements)

References 18 publications

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“…The ability of prostaglandins to rapidly dilate pulmonary vessels and decrease PVR has led to their use in reversibility testing in heart transplant candidates with severe PH. Prostaglandins safely lower PVR in most patients without causing significant side effects [35]. One case report and several small series described longer (ie, weeks) intravenous infusion of prostaglandins to "bridge" patients to heart transplant [36,37].…”

Section: Prostaglandinsmentioning

confidence: 99%

“…One case report and several small series described longer (ie, weeks) intravenous infusion of prostaglandins to "bridge" patients to heart transplant [36,37]. In patients with high PVR after cardiac surgery, inhaled prostacyclin decreased PVR by 29% and improved right ventricular performance [35]. During mitral valve surgery, inhaled iloprost was superior to intravenous nitroglycerin in preventing acute right ventricular failure during weaning from cardiopulmonary bypass [38].…”

Section: Prostaglandinsmentioning

confidence: 99%

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Pulmonary Vasodilation in Acute and Chronic Heart Failure: Empiricism and Evidence

Guglin

2011

Curr Heart Fail Rep

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Pulmonary hypertension in heart failure is associated with exercise intolerance and adverse outcomes. With the availability of multiple drugs that cause pulmonary vasodilation and decrease pulmonary arterial pressure, pulmonary hypertension becomes an attractive therapeutic target. Out of several classes of medications, oral phosphodiesterase inhibitors emerge as the most promising in terms of symptomatic improvement, hemodynamic benefits, reverse cardiac remodeling, and functional capacity. Future trials will show whether the use of these drugs translates to decreased morbidity and mortality in heart failure.

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Section: Prostaglandinsmentioning

confidence: 99%

Section: Prostaglandinsmentioning

confidence: 99%

Pulmonary Vasodilation in Acute and Chronic Heart Failure: Empiricism and Evidence

Guglin

2011

Curr Heart Fail Rep

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“…Inhalational vasodilatory agents, such as prostacyclin or its analogues and nitric oxide (NO), have a direct, selective effect on the pulmonary vasculature [23,35,36,37]. NO diffuses into the pulmonary vascular smooth muscle cells, causing vasodilation, and its effects are localised as it rapidly binds to plasma proteins and haemoglobin.…”

Section: Inhaled Therapiesmentioning

confidence: 99%

Acute right ventricular failure—from pathophysiology to new treatments

Mebazaa¹,

Kárpáti²,

Renaud³

et al. 2009

Applied Physiology in Intensive Care Medicine

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The right ventricle (RV) provides sustained low-pressure perfusion of the pulmonary vasculature, but is sensitive to changes in loading conditions and intrinsic contractility. Factors that affect right ventricular preload, afterload or left ventricular function can adversely influence the functioning of the RV, causing ischaemia and right ventricular failure (RVF). As RVF progresses, a pronounced tricuspid regurgitation further decreases cardiac output and worsens organ congestion. This can degenerate into an irreversible vicious cycle.The effective diagnosis of RVF is optimally performed by a combination of techniques including echocardiography and catheterisation, which can also be used to monitor treatment efficacy. Treatment of RVF focuses on alleviating congestion, improving right ventricular contractility and right coronary artery perfusion and reducing right ventricular afterload. As part of the treatment, inhaled nitric oxide or prostacyclin effectively reduces afterload by

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“…A similar beneficial effect has been demonstrated for inhaled prostacyclins and prostacyclin analogues in RV failure. 48,49 Chronic intravenous epoprostenol infusion therapy in patients with PAH has been shown to improve RV function. 50 …”

Section: Prostacyclin (Pgi 2 ) and Prostaglandin Ementioning

confidence: 99%

Management of acute and chronic RV dysfunction

Lang

2007

European Heart Journal Supplements

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The aim of this article was to outline contemporary treatments of right ventricular (RV) dysfunction and failure. Despite the heterogeneity of disorders underlying RV failure, RV function is a main determinant of long-term prognosis. Therefore, the unique therapeutic goal is to preserve or ameliorate RV function. Although, in advanced stages of RV failure, there is a considerable overlap of pathophysiological mechanisms, the principle targets of treatment are RV contractility, RV pressure overload, and RV volume overload. Apart from surgical strategies such as pulmonary endarterectomy, lung transplantation, closure of shunt lesions, and interventional structural cardiology procedures such as closure of abnormal communications and defects, or graded blade balloon atrial septostomy, targeted pharmacological treatments have become available over the past years. In addition, global strategies such as exercise training, arrhythmia correction, and synchronization treatments may become a new standard of care in the near future. KEYWORDS Right ventricular dysfunction; Right ventricular failure DefinitionRight ventricular (RV) dysfunction has been defined as a state where stroke volume still increases in the presence of increased RV end-diastolic volume. In contrast, RV failure is present when stroke volume cannot increase any further in parallel to increased RV end-diastolic volume. The compromise of the systemic circulation by the septal shift and interventricular dependence causing a severe left ventricular (LV) filling disorder, offsets a vicious cycle. On a molecular basis, it appears that there is a recapitulation of the fetal gene pattern with a decrease in the a-myosin heavy chain gene and an increase in the expression of the fetal b-myosin heavy chain in dysfunctional or failing RV myocardium. Although excessive and longstanding elevation of RV afterload is a major and prevalent cause of RV dysfunction/ failure, evidence accumulates that RV ischemia, 2 excessive sympathetic and renin-angiotensin system stimulation, 3 and volume overload that is accelerated by tricuspid regurgitation 4 contribute. This transition from dysfunction to failure may be ongoing fast or slowly over years, with an unknown genetic component underlying the ability of the RV to resist pressure and volume overload and to maintain stroke volume. RV hypertrophy is a mechanism accounting for preserved RV function. Recent work has demonstrated that in COPD, concentric RV hypertrophy is the earliest sign of RV pressure overload. However, this early structural adaptation of the heart does not yet compromise RV and LV systolic function. 5In practice, the distinction between RV dysfunction and failure can be revealed by a short-time inhalation of NO which, because of its high pulmonary vascular selectivity, 6 will increase RV stroke volume only in the case of a predominantly pulmonary vascular alteration, i.e. in the presence of RV dysfunction.Taken together, pressure, volume, and contractility are main determinants of RV function, and as such, are ...

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Inhaled prostacyclin for treatment of pulmonary hypertension after cardiac surgery or heart transplantation: A pharmacodynamic study

Cited by 102 publications

References 18 publications

Pulmonary Vasodilation in Acute and Chronic Heart Failure: Empiricism and Evidence

Pulmonary Vasodilation in Acute and Chronic Heart Failure: Empiricism and Evidence

Acute right ventricular failure—from pathophysiology to new treatments

Management of acute and chronic RV dysfunction

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