A global view of pulmonary hypertension

“…Data from the INFORM study, a retrospective US-based claims analysis, suggested the proportion of PE patients developing CTEPH to be 3.8% [57], which is close to the weighted average used in this analysis. A recent review by KIM [58] estimates full incidence of CTEPH in the USA to be 4886 cases per year, based on an incidence of CTEPH after PE of 0.57%, as reported by KLOK et al [50], while the diagnosed incidence of CTEPH in Spain, the UK and Germany is reported to be 0.9, 1.75 and 4 cases per million, respectively [59]. It is clear that when calculating the full incidence of CTEPH, the rate of CTEPH following PE is highly influential on the final projection; however, irrespective of the rate of CTEPH from PE used in estimates, it appears that a large proportion of incident cases of CTEPH are undiagnosed each year.…”

Section: Discussionmentioning

confidence: 99%

An epidemiological analysis of the burden of chronic thromboembolic pulmonary hypertension in the USA, Europe and Japan

et al. 2017

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Epidemiological data for chronic thromboembolic pulmonary hypertension (CTEPH) are limited and there are conflicting reports regarding its pathogenesis.A literature review was conducted to identify CTEPH epidemiological data up to June 2014. Data were analysed to provide estimates of the incidence of CTEPH in the USA, Europe and Japan. An epidemiological projection model derived country-specific estimates of future incidence and diagnosis rates of CTEPH.Overall, 25 publications and 14 databases provided quantitative epidemiological data. In the USA and Europe, the crude annual incidence of diagnosed pulmonary embolism and crude annual full (i.e. diagnosed and undiagnosed) incidence of CTEPH were 66-104 and 3-5 cases per 100 000 population, respectively, while in Japan these rates were lower at 6.7 and 1.9 per 100 000 population, respectively. In 2013, 7-29% of CTEPH cases in Europe and the USA were diagnosed, and the majority of patients were in New York Heart Association functional class III/IV at diagnosis. The projection model indicated that incidence of CTEPH will continue to increase over the next decade.These data suggest that CTEPH is underdiagnosed and undertreated, and there is an urgent need to increase awareness of CTEPH. High-quality epidemiological studies are required to increase understanding of CTEPH.

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“…Current epidemiologic data suggests that the global prevalence of pulmonary hypertension (PH) is 1%, and this increases to 10% in individuals >65 years old (1). PH is characterized by elevated pulmonary vascular resistance, progressive right ventricle (RV) hypertrophy and, ultimately, RV failure, which is key in the development of chronic pulmonary heart disease (2).…”

Section: Introductionmentioning

confidence: 99%

Effects of 17β-estradiol and 2-methoxyestradiol on the oxidative stress-hypoxia inducible factor-1 pathway in hypoxic pulmonary hypertensive rats

Wang

Zheng

Yuan

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. The present study aimed to investigate the effects of 17β-estradiol (E2) and 2-methoxyestradiol (2ME) on the oxidative stress-hypoxia inducible factor-1 (OS-HIF-1) pathway in hypoxic pulmonary hypertensive rats. Female Sprague-Dawley rats were divided randomly into 4 groups, as follows: i) Control (Group A); ii) ovariectomy (OVX) + hypoxia (Group B); iii) OVX + hypoxia + E2 injection (Group C); and iv) 2ME injection (Group D). The rats were maintained under hypoxic conditions for 8 weeks, and mean pulmonary artery pressure (mPAP) and pulmonary arteriole morphology were measured. The reactive oxygen species, superoxide dismutase (SOD), manganese superoxide dismutase (MnSOD), and copper-zinc superoxide dismutase (Cu/ZnSOD) levels in serum were also measured. MnSOD and HIF-1α expression levels in lung tissue were determined by western blotting and reverse transcription-quantitative polymerase chain reaction. The mPAP and arterial remodeling index were significantly elevated following chronic hypoxia exposure; however, experimental data revealed a reduced response in E2 and 2ME intervention rats. Compared with Group A, Group B had significantly elevated oxidative stress levels, as illustrated by increased serum ROS levels, decreased serum SOD and MnSOD levels and decreased MnSOD mRNA and protein expression levels in lung tissue. Furthermore, HIF-1α mRNA and protein expression in Group B was significantly elevated compared with Group A. E2 and 2ME intervention significantly attenuated the aforementioned parameter changes, suggesting that E2 and 2ME partially ameliorate hypoxic pulmonary hypertension. The underlying mechanism of this may be associated with the increase in MnSOD activity and expression and reduction in ROS level, which reduces the levels of transcription and translation of HIF-1α.

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A global view of pulmonary hypertension

Cited by 583 publications

References 173 publications

Heart Disease and Stroke Statistics—2017 Update: A Report From the American Heart Association

Heart Disease and Stroke Statistics—2017 Update: A Report From the American Heart Association

An epidemiological analysis of the burden of chronic thromboembolic pulmonary hypertension in the USA, Europe and Japan

Effects of 17β-estradiol and 2-methoxyestradiol on the oxidative stress-hypoxia inducible factor-1 pathway in hypoxic pulmonary hypertensive rats

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