Current Diagnostic and Prognostic Assessment of Pulmonary Hypertension

Subías, Pilar Escribano; Mir, Joan; Suberviola, Verónica

doi:10.1016/s1885-5857(10)70120-1

Cited by 9 publications

(8 citation statements)

References 35 publications

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“…PAH is a rare condition with an annual incidence range of 1.1-7.6 cases per million, a prevalence range of 15-26 cases per million individuals (6,7). IPAH is a particular type of PAH, which is unexplained by any secondary cause.…”

Section: Introductionmentioning

confidence: 99%

High levels of serum lactate dehydrogenase correlate with the severity and mortality of idiopathic pulmonary arterial hypertension

Liu

et al. 2015

Experimental and Therapeutic Medicine

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Abstract. Liver dysfunction reflects the status of heart failure, and previous studies have demonstrated that serum lactate dehydrogenase (S-LDH) levels are increased in patients exhibiting heart failure and liver dysfunction. Right heart failure is a main characteristic of idiopathic pulmonary arterial hypertension (IPAH). The aim of the present study was to assess the prognostic significance of S-LDH levels in patients with IPAH. S-LDH levels were determined in 173 patients with IPAH, and these patients were subclassified into two groups according to a defined upper reference limit of S-LDH (250 IU/l). Right heart catheterization was performed in all patients. A total of 53 patients were found to have elevated S-LDH to ≥250 IU/l. In a mean follow-up period of 31.2±17.9 months, 57 patients succumbed. In the group with lower S-LDH levels (S-LDH <250 IU/l), 16.7% of the patients succumbed, compared with 69.8% of patients in the group with higher S-LDH levels (S-LDH ≥250 IU/l). The Kaplan-Meier survival curves demonstrated that patients with higher S-LDH levels had a significantly lower survival rate than did those with lower S-LDH levels (log-rank test, P<0.001). Cox proportional hazard analyses identified reduced body mass index, reduced cardiac index, elevated World Health Organization functional class, higher S-LDH and an absence of PAH-targeted therapy as significant predictors of adverse outcomes. In conclusion, elevated S-LDH is a risk factor for mortality in patients with IPAH.

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Section: Introductionmentioning

confidence: 99%

High levels of serum lactate dehydrogenase correlate with the severity and mortality of idiopathic pulmonary arterial hypertension

Liu

et al. 2015

Experimental and Therapeutic Medicine

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“…The most critical aspects of RHC are that it is performed appropriately and the data are interpreted accurately. Since end-expiratory intrathoracic pressure most closely correlates with atmospheric pressure, it is important that all RV, pulmonary artery (PA), PA occlusion pressure (PAOP), and left ventricular pressures be measured at end-expiration (specially in obese patients and patients with intrinsic lung disease in whom there can be significant variation between inspiration and end-expiratory vascular pressures) [2][3][4][5] . After determination of the presence of PH, pulmonary venous pressure should be evaluated by the PAOP.…”

Section: Parametersmentioning

confidence: 99%

“…In addition, the agreement between the Fick method and thermodilution was not affected by the severity of tricuspid regurgitation. Vasoreactivity testing is indicated in patients with idiopathic PAH, heritable PAH and associated anorexigen use to detect patients who can be treated with high doses of calcium channel blockers (class Ⅰ-level C) [1,5] . A positive response to vasoreactivity testing is defined as a reduction of mPAP ≥ 10 mmHg to reach an absolute value of mPAP ≤ 40 mmHg with an increased or unchanged CO (class Ⅰ-level C) [13] .…”

Section: Parametersmentioning

confidence: 99%

“…It has been reported that pulsatility as the ratio of pPAP to mPAP [i.e. fractional pulse pressure (fPp)] in CTEPH was larger than in PAH and that in patients with severe haemodynamic impairment (PVR > 1000-1100 dyne s/cm 5 ), fPp in addition to PVR might be useful in predicting the outcome of PEA. fPp might be low in CTEPH with inaccessible distal thrombi and/or secondary pulmonary hypertensive change [17] .…”

Section: Novel Invasive Hemodynamic Parametersmentioning

confidence: 99%

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Hemodynamic assessment of pulmonary hypertension

Grignola¹

2011

WJC

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There has been significant progress in our understanding of the pathobiology, epidemiology and prognosis of pulmonary vascular disease and, over the past few years, there has been an explosion of clinical therapeutic trials for pulmonary arterial hypertension (PAH). The increasing number of different conditions now associated with PAH and the appearance of new diagnostic techniques have led to a need for a systematic diagnostic approaches and a new disease classification, which has resulted in notable improvements in the quality and efficacy of clinical care. We appreciate traditional resting right heart catheterization techniques (which still remain the gold standard for diagnosing PAH and managing patients on therapy) and look forward to novel invasive techniques (e.g. intravascular ultrasound) that add greatly to our understanding of right ventricle and pulmonary circulation, and for the interpretation of data from clinical trials as well.

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“…Initial testing for PH has been done with an echocardiography assessment to estimate pulmonary artery pressure using tricuspid regurgitant jet velocity (TRV), 43,[45][46][47] but diagnosis requires right heart catheterization and direct measurement of the pulmonary arterial pressure and vaso-reactivity of the vessels. 43,45,50,56,337 Transient elevation in TRV has been observed during acute vaso-occlusive episodes in individuals with SCD, 51 which may not reflect baseline values or present chronic PH.…”

Section: Introductionmentioning

confidence: 99%