scholarly journals 247 Relationship between the right ventricular isovolumetric relaxation time and pulmonary artery pressure in patients with pulmonary arterial hypertension

2005 ◽  
Vol 6 ◽  
pp. S26-S26
Author(s):  
Thanh Xuan Nguyen

TÓM TẮT Mục tiêu: Đánh giá áp lực động mạch phổi (ALĐMP) ở bệnh nhân Covid-19 mức độ trung bình và nặng. Đặc điểm lâm sàng, cận lâm sàng ở nhóm bệnh nhân Covid-19 mức độ trung bình và nặng có hoặc không có tăng ALĐMP. Phương pháp nghiên cứu: Nghiên cứu mô tả cắt ngang trên 200 bệnh nhân nhiễm SARS-CoV-2 đang được điều trị tại khu thoát hồi sức và khu nguy kịch trung tâm hồi sức tích cực người bệnh COVID-19 trực thuộc bệnh viện trung ương Huế tại thành phố Hồ Chí Minh từ ngày 12/8/2021 đến ngày 15/11/2021. Kết quả: Tuổi trung bình trong nhóm nghiên cứu là 57,38 ± 17,62 tuổi với 47,5% nam giới. Thời gian khởi bệnh là 6,92 ± 3,9 ngày. Qua đánh giá bằng siêu âm tim phát hiện có 28 (14%) bệnh nhân có biểu hiện tăng ALĐMP với độ tuổi trung bình là 67,04 ± 13,50 tuổi cao hơn so với nhóm không tăng ALĐMP 55,8 ± 17,75 tuổi và có các bệnh kèm theo thường xuyên hơn ĐTĐ (35,7%), THA (50%), BMV (6%), đồng thời chỉ số BMI cũng cao hơn 26,02 ± 3,68 kg/m2. Mức tăng ALDMP trung bình là 44,50 ± 8,19 mmHg, TAPSE ở bệnh nhân Tăng ALĐMP là 19,96 ± 2,36 mmHg thấp hơn ở bệnh nhân không tăng 25,51 ± 1,19 mmHg. Các đường kính đáy giữa và dọc của thất phải đều cao hơn đáng kể ở các bệnh nhân tăng ALĐMP, diện tích nhĩ phải cũng vậy 17,57 ± 2,23mm so với 13,33 ± 1,14mm ở bệnh nhân không có tăng ALĐMP. Tăng áp phổi ở các bệnh nhân đang điều trị Covid đa phần là ở mức độ nhẹ 85,7%, mức độ vừa và nặng chỉ chiếm tỷ lệ nhỏ 10,7% và 3,6%, chủ yếu ở khu vực bệnh nặng 78,6%, khu vực thoát hồi sức ít hơn chỉ có 21,4%. Bệnh nhân có tăng ALĐMP cho thấy có số lượng bạch cầu cao 16,21 ± 7,19 K/µL, D-Dimer cao 4508 ± 7208 ng/mL, Ferritin cao 1163 ± 738 ng/mL, CRP cao 111,4 ± 77,9 mg/L K/µL so với nhóm không có tăng ALĐMP. Kết luận: Siêu âm tim là phương pháp đơn giản, nhanh chóng giúp phát hiện, theo dõi và đánh giá tình trạng tăng áp phổi trong quá trình điều trị bệnh nhân COVID-19. ABSTRACT EVALUATION OF PULMONARY ARTERY PRESSURE INDEX ON ECHOCARDIOGRAPHY IN PATIENTS WITH COVID-19 Objectives: Evaluation of pulmonary artery pressure in moderate and severe Covid-19 patients. Clinical and subclinical characteristics in moderate and severe Covid-19 patients with or without pulmonary arterial hypertension. Methods: A cross - sectional descriptive study was performed on 200 Covid-19 patients who were treated in the recovery and critical areas of the COVID-19 Intensive care center of Hue Central Hospital in Ho Chi Minh City from August 12, 2021 to November 15, 2021. Results: The mean age in the study group was 57.38 ± 17.62. The time of onset was 6.92 ± 3.9 days. Underechocardiographic assessment, 28 (14%) patients showed an increase of PAP with an average age of 67.04 ± 13.50, which was higher than the group without an increase of PAP of 55.8 ± 17.75 and had comorbidities more often than diabetes (35.7%), hypertension (50%), CVD (6%), and BMI was also higher than 26.02 ± 3.68. The mean increase of PAP was 44.50 ± 8.19 mmHg, TAPSE in patients with increased PAP was 19.96 ± 2.36 lower than in patients without an increase of 25.51 ± 1.19. The medial and longitudinal basal diameters of the right ventricle were both significantly higher in patients with increased PAP, as was the area of the right atrium 17.57 ± 2.23 mm compared with 13.33 ± 1.14 mm in patients without increased PAP. Pulmonary arterial hypertension in COVID-19 patients is mostly mild at 85.7%, moderate and severe only account for a small proportion of 10.7% and 3.6%, mainly in severe illness areas. 78.6%, less in the recovery area with 21.4%. Patients with increased PAP showed a high white blood cell count of 16.21 ± 7.19 K/µL, a high D-Dimer 4508 ± 7208 ng/mL, a high Ferritin 1163 ± 738 ng/mL, a high CRP of 111.4 ± 77.9 ng/mL compared with the group without increased PAP. Conclusion: Echocardiography is a simple and quick modality to detect, monitor and evaluate pulmonary hypertension during the treatment of COVID-19 patients. Key words: SARS-CoV-2, COVID-19, Pulmonary arterial pressure.


2019 ◽  
Vol 10 (2) ◽  
pp. 185-191
Author(s):  
Sachin Talwar ◽  
Yatin Arora ◽  
Saurabh Kumar Gupta ◽  
Shyam Sunder Kothari ◽  
Sivasubramanian Ramakrishnan ◽  
...  

Objective: We report our experience with surgery for total anomalous pulmonary venous connection (TAPVC) beyond first decade of life. Methods: Between January 1987 and July 2017, 98 patients ≥ten years underwent TAPVC repair. Their detailed case-records were analyzed. Results: Mean age was 19.05 (± 12.8; median 18) years. Anatomic subtypes were supracardiac (n = 62), cardiac (n = 20), and mixed (n = 16). An atrial septal defect (ASD) was present in all. Severe tricuspid valve regurgitation was present in four patients and severe rheumatic mitral regurgitation was present in one. On preoperative cardiac catheterization, mean pulmonary artery pressure was 67 ± 15.6 mm Hg (median 58; range 37-96). Mean pulmonary vascular resistance was 5.6 ± 3.9 Woods units·m2 (median 4.7, range 2.9-11.8). Twenty-five patients had moderate and eight had severe pulmonary arterial hypertension. Right ventricular dysfunction was present in eight patients. At repair, a small ASD was left open in 87 patients while in 11 patients, the ASD was closed using a unidirectional valved patch. Follow-up was available for 90 (92%) patients. There were no late deaths over a mean follow-up of 163 ± 103.98 months (median 163, range 1-362). Eighty-two patients were in NYHA class I and eight were in class II. Right ventricular function normalized in 82 patients while 80 patients had reduction in pulmonary artery pressure. Event-free survival was 94.2% at 5 years, 92.3% at 10 years, and 90% at 20 and 30 years. Conclusions: Outcomes of surgical repair for TAPVC beyond first decade of life are satisfactory. Close follow-up, however, is necessary for possible persistence of pulmonary arterial hypertension.


Author(s):  
George K Istaphanous ◽  
Andreas W Loepke

Pediatric pulmonary arterial hypertension (PAH) is characterized by a pathologically elevated pulmonary artery pressure in children. The etiology of PAH is multifactorial, and while its prognosis is closely related to the reversibility of the underlying disease process, much progress has recently been made in its diagnosis and treatment, significantly decreasing the associated morbidity and mortality.


2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Yijia Xiang ◽  
Changhong Cai ◽  
Yonghui Wu ◽  
Lebing Yang ◽  
Shiyong Ye ◽  
...  

Background. Pulmonary artery remodeling is important in the development of pulmonary artery hypertension. The TGF-β1/Smads signaling pathway is activated in pulmonary arterial hypertension (PAH) in rats. Icariin (ICA) suppresses the TGF-β1/Smad2 pathway in myocardial fibrosis in rats. Therefore, we investigated the role of icariin in PAH by inhibiting the TGF-β1/Smads pathway. Methods. Rats were randomly divided into control, monocrotaline (MCT), MCT + ICA-low, and MCT + ICA-high groups. MCT (60 mg/kg) was subcutaneously injected to induce PAH, and icariin (50 or 100 mg/kg.d) was orally administered for 2 weeks. At the end of the fourth week, right ventricular systolic pressure (RVSP) was obtained and the right ventricular hypertrophy index (RI) was determined as the ratio of the right ventricular weight to the left ventricular plus septal weight (RV/LV + S). Western blots were used to determine the expression of TGF-β1, Smad2/3, P-Smad2/3, and matrix metalloproteinase-2 (MMP2) in lung tissues. Results. Compared to the control group, RVSP and RI were increased in the MCT group (ρ < 0.05). Additionally, TGF-β1, Smad2/3, P-Smad2/3, and MMP2 expressions were obviously increased (ρ < 0.01). Compared to the MCT group, RVSP and RI were decreased in the MCT + ICA group (ρ < 0.05). TGF-β1, Smad2/3, P-Smad2/3, and MMP2 expressions were also inhibited in the icariin treatment groups (ρ < 0.05). Conclusions. Icariin may suppress MCT-induced PAH via the inhibition of the TGFβ1-Smad2/3 pathway.


Medicine ◽  
2017 ◽  
Vol 96 (43) ◽  
pp. e8349 ◽  
Author(s):  
Hiroyuki Nakamura ◽  
Masaru Kato ◽  
Toshitaka Nakaya ◽  
Michihiro Kono ◽  
Shun Tanimura ◽  
...  

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