Clinical efficacy of sildenafil in primary pulmonary hypertension. A randomized, placebo-controlled, double-blind, crossover study

Sastry, B.K.S.; Narasimhan, Chitra; Reddy, N K

doi:10.1016/j.accreview.2004.06.025

Cited by 165 publications

(218 citation statements)

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“…[7][8][9]15 Sildenafil has been shown to be beneficial in pulmonary hypertension and cardiac hypertrophy. 22,23,12 Tadalafil and sildenafil have also been shown to improve endothelial dysfunction in patients with high cardiovascular risk, chronic heart failure, diabetes and in smokers. 11,[24][25][26] There is evidence that PDE5 inhibitors may have cardioprotective effects.…”

Section: Discussionmentioning

confidence: 99%

The phosphodiesterase-5 inhibitor tadalafil reduces myocardial infarct size

et al. 2006

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The aim of this study was to determine, in an animal model, the effects of tadalafil on myocardial infarct size (IS), hemodynamics and regional myocardial blood flow after myocardial ischemia and reperfusion. Patients with erectile dysfunction (ED) often have risk factors for coronary artery disease. Tadalafil, a long-acting inhibitor of the enzyme phosphodiesterase-5 (PDE5), is used for the treatment of ED; there are no previous data regarding tadalafil in the setting of coronary artery occlusion (CAO). Sprague-Dawley male rats were treated with tadalafil or vehicle (10 mg/kg, by gastric gavage), 2 h before a 30 min CAO. Heart rate was comparable between tadalafil and control groups. Tadalafil reduced mean arterial pressure (P ¼ 0.009), systolic (P ¼ 0.035) and diastolic (P ¼ 0.009) blood pressures during ischemia/reperfusion. Tadalafil significantly reduced IS (4272%) versus controls (5473%) (P ¼ 0.006). For the first time, we showed that the PDE5 inhibitor, tadalafil, was well tolerated and cardioprotective in the setting of an experimental myocardial infarction, by substantially reducing ischemic cell death.

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Section: Discussionmentioning

confidence: 99%

The phosphodiesterase-5 inhibitor tadalafil reduces myocardial infarct size

et al. 2006

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“…11,12 In adults with PH, sildenafil has improved survival rates, exhibited low toxicity, and is available as an enteral preparation that is more practical for long-term, outpatient therapy. [13][14][15][16][17][18][19][20] Early clinical experience indicates that sildenafil treatment may be efficacious for infants with BPD-PH, with evidence suggesting that sildenafil normalizes lung development and may improve outcomes. [21][22][23][24][25] However, practice patterns for sildenafil treatment in infants with BPD-PH have not been fully reported; these patterns include variables associated with exposure, timing of initiation, length of treatment, and interhospital variation in use.…”

mentioning

confidence: 99%

Sildenafil Treatment of Infants With Bronchopulmonary Dysplasia–Associated Pulmonary Hypertension

Backes

Reagan

Smith

et al. 2016

Hospital Pediatrics

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OBJECTIVE: This study had 2 goals: (1) to identify clinical and demographic characteristics associated with sildenafil exposure for infants with bronchopulmonary dysplasia (BPD)-associated pulmonary hypertension (PH); and (2) to characterize hospital-specific treatment frequency, age at first administration, and length of sildenafil treatment. METHODS: This retrospective cohort study used data from the Pediatric Health Information System to determine variables associated with sildenafil exposure and between-hospital variations in sildenafil utilization patterns. The study included infants with BPD-PH who were discharged between January 1, 2006, and December 31, 2013. RESULTS: Within 36 US pediatric hospitals, 3720 infants were diagnosed with BPD, of whom 598 (16%) also had a diagnosis of PH (BPD-PH). Among infants with BPD-PH, 104 infants (17%) received sildenafil. The odds for sildenafil treatment among infants born between 25 and 26 weeks’ gestational age (GA) and <24 weeks’ GA, respectively, were 2.26 (95% confidence interval [CI]: 1.20–4.24) and 3.21 (95% CI: 1.66–6.21) times those of infants born at 27 to 28 weeks’ GA. Severity of BPD correlated with sildenafil exposure, with adjusted odds ratios (ORs) for moderate BPD (OR: 3.03 [95% CI: 1.03–8.93]) and severe BPD (OR: 7.56 [95% CI: 2.50–22.88]), compared with mild BPD. Greater rates of sildenafil exposure were observed among small for GA neonates (OR: 2.32 [95% CI: 1.21–4.46]). The proportion of infants with BPD-PH exposed to sildenafil varied according to hospital (median: 15%; 25th–75th percentile: 0%–25%), as did the median duration of therapy (52 days; 25th–75th percentile: 28–109 days). CONCLUSIONS: The odds of sildenafil treatment were greatest among the most premature infants with severe forms of BPD. The frequency and duration of sildenafil exposure varied markedly according to institution. Patient-centered trials for infants with BPD-PH are needed to develop evidence-based practices.

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“…70 The initial randomised controlled cross over trial carried out in 22 patients showed improvement in treadmill time, quality of life and cardiac output. 71 Similar study by Bharani and colleagues also reported significant improvement in exercise capacity, but no significant improvement was found in the NYHA functional class. 72 Similar results are reported in 20 patients in another study, also from India.…”

Section: Sildenafilmentioning

confidence: 68%

“…There is genetic anticipation in familial PAH, i.e. the onset of disease occurs at an Indian Heart Journal 6401 (2012) [60][61][62][63][64][65][66][67][68][69][70][71][72][73] earlier age in successive generations. 8,9 Group 1 of Dana Point classification also includes drugs and toxins associated with development of PAH; the most notorious of these include the appetite suppressants fenfluramine and dexfenfluramine.…”

Section: Epidemiologymentioning

confidence: 99%

Pulmonary hypertension—“state of the art” management in 2012

Saxena

2012

Indian Heart Journal

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A B S T R A C TPulmonary artery hypertension (PAH) is a pathological condition of small pulmonary arteries, characterised by vascular proliferation and remodelling. The pulmonary artery pressure and pulmonary vascular resistance progressively rise, leading to right heart failure and death. Pulmonary artery hypertension may be secondary to various conditions, or it may be idiopathic where no underlying cause is identifiable. Earlier, only symptomatic treatment was available for such patients which did not change the natural history of the disease. However, over the years, improvement in understanding the pathogenesis has resulted in the development of targeted approaches to the treatment of PAH. Survival advantage has also been shown with some of the pharmacologic agents. This review article discusses the current management strategy for PAH with special emphasis on an idiopathic variety, in an Indian context.

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Clinical efficacy of sildenafil in primary pulmonary hypertension. A randomized, placebo-controlled, double-blind, crossover study

Cited by 165 publications

References 0 publications

The phosphodiesterase-5 inhibitor tadalafil reduces myocardial infarct size

The phosphodiesterase-5 inhibitor tadalafil reduces myocardial infarct size

Sildenafil Treatment of Infants With Bronchopulmonary Dysplasia–Associated Pulmonary Hypertension

Pulmonary hypertension—“state of the art” management in 2012

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