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Right ventricular function is independently associated with poor clinical outcomes in patients with various cardiovascular diseases including pulmonary hypertension (PH). The complex geometry and mode of contractility means the right ventricle (RV) inlet and outlet are not in line; hence, 2-dimensional echocardiography fails to accurately quantify RV volumes and function in such patients. Three-dimensional echocardiography (3DE) allows for reliable and reproducible quantification of RV volumes and function by overcoming these limitations of conventional echocardiography. This review focuses on the 3DE assessment of RV function in patients with PH and discusses the following points: (1) acquiring an RV data set for 3DE imaging, including details of all available 3DE systems and software utilized in daily practice; (2) the reliability and feasibility of RV remodeling measured with 3DE with different modalities in patients with PH; and (3) the prognostic value of 3DE-derived RV function in such patients.

Pulmonary arterial hypertension (PAH) is a chronic and progressive disease that eventually leads to heart failure (HF) and subsequent fatality if left untreated. Right ventricular (RV) function has proven prognostic values in patients with a variety of heart diseases including PAH. PAH is predominantly a right heart disease; however, given the nature of the continuous circulatory system and the presence of shared septum and pericardial constraints, the interdependence of the right and left ventricles is a factor that requires consideration. Accurate and timely assessment of ventricular function is very important in the management of patients with PAH for disease outcomes and prognosis. Non-invasive modalities such as cardiac magnetic resonance (CMR) and echocardiography (two-dimensional and three-dimensional), and nuclear medicine, positron emission tomography (PET) play a crucial role in the assessment of ventricular function and disease prognosis. Each modality has its own strengths and limitations, hence this review article sheds light on (i) ventricular dysfunction in patients with PAH and RV–LV interdependence in such patients, (ii) the strengths and limitations of all available modalities and parameters for the early assessment of ventricular function, as well as their prognostic value, and (iii) lastly, the challenges faced and the potential future advancement in these modalities for accurate and early diagnosis of ventricular function in PAH.

BackgroundThe coronavirus disease 2019 (COVID-19) outbreak within China has been well controlled and stabilized since early April 2020. Therefore, the current major focus in China is to prevent the introduction of COVID into China from international arrivals. To achieve this, pre-Hospital COVID-19 Response Teams (pHCRTs) have been established.ContextThe pHRCTs were established in Xi'an, China in early 2020. During the 12 months covered in this report, there were 356 international flight arrivals with over 5,000 COVID-19 Nucleic Acid Test (NAT) positive people, 500 of them with symptomatic COVID-19 and requiring admission to special hospitals. All other arrivals were managed in dedicated facilities by pHRCTs. The outcome measure of this report was the number of positive cases among the pHRCT members.DetailsFour hundred forty-two staff worked in the pHCRTs during the reporting period. Despite multiple throat swab PCR tests during their pHRCTs tour of duty, and the subsequent mandatory 14-day quarantine required before return to the general community, no staff became NAT positive.ConclusionThe prevention of community transmission from imported cases is a vital part of the strategy to maintain the low numbers of cases in countries which have achieved control, or suppression of local internal cases. The program of pHCRTs described in this article gives successful protocols for transportation of patients who are infectious based on the minimal transmission of virus and staff safety. The strategies employed may prove useful in future pandemics.

Background: Similarities in the biology of pulmonary hypertension and cancer suggest that anticancer therapies, such as sanguinarine, may also be effective in treating pulmonary hypertension. This, along with underlying biochemical pathways, is investigated in this study.Methods: Rats were subjected to 4-week hypoxia (or control) with or without sanguinarine treatment. In addition, pulmonary artery smooth muscle cells (PASMCs) were examined after 24–48 h hypoxia (with normoxic controls) and with or without sanguinirine. Pulmonary artery pressures and plasma survivin levels were measured in vivo. Ex vivo tissues were examined histologically with appropriate staining. mRNA and protein levels of survivin, HIF-1α, TGFb1, BMPR2, Smad3, P53, and Kv 1.2, 1.5, 2.1 were determined by real-time PCR and Western blot in PASMCs and distal PAs tissue. PASMC proliferation and changes of TGFb1 and pSmad3 induced by sanguinarine were studied using MTT and Western blot. Electrophysiology for Kv functions was measured by patch-clamp experiments.Results: Four-week hypoxia resulted in an increase in serum survivin and HIF-1α, pulmonary artery pressures, and pulmonary vascular remodeling with hypertrophy. These changes were all decreased by treatment with sanguinarine. Hypoxia induced a rise of proliferation in PASMCs which was prevented by sanguinarine treatment. Hypoxic PASMCs had elevated TGFb1, pSmad3, BMPR2, and HIF1α. These increases were all ameliorated by sanguinarine treatment. Hypoxia treatment resulted in reduced expression and function of Kv 1.2, 1.5, 2.1 channels, and these changes were also modulated by sanguinarine.Conclusion: Sanguinarine is effective in modulating hypoxic pulmonary vascular hypertrophy via the survivin pathway and Kv channels.