Pulmonary hypertension and right ventricular failure after heart transplantation: usefulness of nitric oxide

Mosquera, Ignacio; Crespo-Leiro, María G.; Tabuyo, T; Paniagua, María; Fuente, Luis de la; Bouzas, Beatriz; Fojón, S; Pastor, J Fernandez-Armenta; Juffé-Stein, Alberto; Castro‐Beiras, Alfonso

doi:10.1016/s0041-1345(01)02713-0

Cited by 17 publications

(8 citation statements)

References 6 publications

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“…18 NO has been shown to be highly effective in reversing pulmonary hypertension after cardiac surgery, 19 including heart transplantation. 20,21 In patients with heart failure who were evaluated for heart transplantation, NO was shown to decrease TPG and PVR without reducing systemic vascular resistance or mean systemic arterial pressure. 12 Our results are similar, demonstrating a 34% decrease in TPG and a 47% decrease in PVR, without concomitant changes in systemic vascular resistance or systemic pressures.…”

Section: Discussionmentioning

confidence: 99%

Nitric Oxide Versus Prostaglandin E1 for Reduction of Pulmonary Hypertension in Heart Transplant Candidates

Radovančević

Vrtovec

Thomas

et al. 2005

The Journal of Heart and Lung Transplantation

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Section: Discussionmentioning

confidence: 99%

Nitric Oxide Versus Prostaglandin E1 for Reduction of Pulmonary Hypertension in Heart Transplant Candidates

Radovančević

Vrtovec

Thomas

et al. 2005

The Journal of Heart and Lung Transplantation

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“…iNO improves oxygenation with lower doses than those required to decrease mPAP, but it can have the opposite effect on oxygenation at higher doses [138]. Small studies have shown that iNO produces hemodynamic improvement in different settings of RVF including those caused by RV infarct, acute PE, post-surgical, post-left ventricular assist device (LVAD) implantation, and cardiac transplantation [139][140][141][142][143][144][145][146][147][148][149][150][151][152][153][154][155]. Complications encountered with the use of iNO include: accumulation of potentially toxic reactive metabolites, rebound PH, and rarely methemoglobinemia [156][157][158][159][160][161] The phosphodiesterase-5 (PDE5) inhibitors prevent the hydrolysis of cyclic guanosine monophosphate (cGMP), producing vasodilatory and antiproliferative effects in the pulmonary vasculature [170].…”

Section: Rv Afterload Reductionmentioning

confidence: 99%

Hospital and intensive care unit management of decompensated pulmonary hypertension and right ventricular failure

et al. 2015

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Pulmonary hypertension and concomitant right ventricular failure present a diagnostic and therapeutic challenge in the intensive care unit and have been associated with a high mortality. Significant co-morbidities and hemodynamic instability are often present, and routine critical care unit resuscitation may worsen hemodynamics and limit the chances of survival in patients with an already underlying poor prognosis. Right ventricular failure results from structural or functional processes that limit the right ventricle's ability to maintain adequate cardiac output. It is commonly seen as the result of left heart failure, acute pulmonary embolism, progression or decompensation of pulmonary hypertension, sepsis, acute lung injury, or in the perioperative setting. Prompt recognition of the underlying cause and institution of treatment with a thorough understanding of the elements necessary to optimize preload, cardiac contractility, enhance systemic arterial perfusion, and reduce right ventricular afterload are of paramount importance. Moreover, the emergence of previously uncommon entities in patients with pulmonary hypertension (pregnancy, sepsis, liver disease, etc.) and the availability of modern devices to provide support pose additional challenges that must be addressed with an in-depth knowledge of this disease.

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“…36 It has been reported that patients with this disorder have an increased risk of postoperative right ventricular HF after heart transplantation. 37 However, the detailed mechanisms of the condition remain to be elucidated.…”

Section: Post-capillary Ph (Left Heart Disease)mentioning

confidence: 99%

Recent Progress in the Management of Pulmonary Hypertension

Fukumoto

Shimokawa

2011

Circ J

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Pulmonary hypertension (PH) is a fatal disease caused by small pulmonary artery obstruction from vascular proliferation and remodeling. PH is characterized by elevated pulmonary arterial pressure and increased pulmonary vascular resistance, frequently leading to right-sided heart failure and death. The classification of PH has been recently updated to include 5 major categories of the disorder, are as: Group 1, pulmonary arterial hypertension (PAH); Group 2, PH due to left heart disease; Group 3, PH due to lung diseases and/or hypoxia; Group 4, chronic thromboembolic PH (CTEPH); and Group 5, others. Recently, significant progress has been made in the understanding of the pathophysiology, diagnosis and treatment of PH. Regarding the pathophysiology of the disorder, direct evidence for Rho-kinase activation in the pulmonary artery from PAH patients has been provided. Regarding diagnosis, optical coherence tomography is useful as a new differential diagnostic tool for distal type CTEPH vs. PAH. Regarding treatment, in addition to the conventional therapy, several new drugs are under clinical trial, including fasudil (a Rho-kinase inhibitor), riosiguat (a soluble guanylate cyclase activator), and imatinib (a tyrosine kinase inhibitor). In addition, pulmonary angioplasty and intensive immunosuppressive therapy may be effective for CTEPH and connective tissue disease-associated PAH, respectively. We briefly review the recent progress in the management of PH. (Circ J 2011; 75: 1801 - 1810

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Pulmonary hypertension and right ventricular failure after heart transplantation: usefulness of nitric oxide

Cited by 17 publications

References 6 publications

Nitric Oxide Versus Prostaglandin E1 for Reduction of Pulmonary Hypertension in Heart Transplant Candidates

Nitric Oxide Versus Prostaglandin E1 for Reduction of Pulmonary Hypertension in Heart Transplant Candidates

Hospital and intensive care unit management of decompensated pulmonary hypertension and right ventricular failure

Recent Progress in the Management of Pulmonary Hypertension

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