• Tuberculosis and Respiratory Diseases
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• 제67권3호
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• pp.177-182
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• 2009

Pulmonary arterial hypertension is a progressive, symptomatic, and ultimately fatal disorder for which substantial advances in treatment have been made during the past decade. This article reviews the recent advances in the field of pulmonary arterial hypertension (PAH). Epidemiology, genetics, treatment and prognosis will be the main focus of this update.

• Journal of Chest Surgery
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• 제23권2호
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• pp.245-252
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• 1990

To see the change of pulmonary arterial pressure after mitral valve replacement, postoperative cardiac catheterization and echocardiographies were performed in 12 patients of mitral valvular disease with pulmonary hypertension[systolic pulmonary arterial pressure>50 mm Hg]. The mean follow-up duration was 35.4[range: 15-47] months per patient. The following results were obtained. 1] Preoperative systolic pulmonary arterial pressure value of 66.17\ulcorner10.73mmHg decreased significantly to 29.17\ulcorner6.86mmHg postoperatively[p<0.01]. 2] Preoperative Pp/Ps value of 0.67\ulcorner0.13 decreased significantly to 0.28\ulcorner0.06 postoperatively[p<0.01]. 3] Preoperative PAWP value of 29.00\ulcorner4.02mmHg decreased significantly to 9.92\ulcorner4.27 mmHg postoperatively[p<0.01]. 4] Preoperative LAD value of 5.58\ulcorner1.20cm decreased significantly to 4.37\ulcorner0.67cm postoperatively [p<0.01]. In conclusion, pulmonary arterial hypertension secondary to mitral valvular disease could be reduced to normal range after successful mitral valve replacement.

• Tuberculosis and Respiratory Diseases
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• 제64권1호
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• pp.28-32
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• 2008

저자들은 결핵성 파괴폐 환자에서 추적관찰 중 급성 호흡곤란을 주소로 내원하여 주폐동맥 혈전증으로 진단된 1예를 경험하였기에 문헌고찰과 함께 보고하는 바이다.

• Molecules and Cells
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• 제37권3호
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• pp.196-201
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• 2014

Pulmonary arterial hypertension (PAH) is a progressive disease characterized by the vascular remodeling of the pulmonary arterioles, including formation of plexiform and concentric lesions comprised of proliferative vascular cells. Clinically, PAH leads to increased pulmonary arterial pressure and subsequent right ventricular failure. Existing therapies have improved the outcome but mortality still remains exceedingly high. There is emerging evidence that the seven-transmembrane G-protein coupled receptor APJ and its cognate endogenous ligand apelin are important in the maintenance of pulmonary vascular homeostasis through the targeting of critical mediators, such as Kr$\ddot{u}$ppel-like factor 2 (KLF2), endothelial nitric oxide synthase (eNOS), and microRNAs (miRNAs). Disruption of this pathway plays a major part in the pathogenesis of PAH. Given its role in the maintenance of pulmonary vascular homeostasis, the apelin-APJ pathway is a potential target for PAH therapy. This review highlights the current state in the understanding of the apelin-APJ axis related to PAH and discusses the therapeutic potential of this signaling pathway as a novel paradigm of PAH therapy.

• Tuberculosis and Respiratory Diseases
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• 제64권2호
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• pp.125-132
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• 2008

연구배경: COPD 환자에서 혈청 C-반응단백은 증가하는 것으로 알려져 있으며 이러한 변화는 급성 악화 시 보다 두드러진다. 폐동맥 고혈압은 COPD의 흔한 합병증 중 하나이며, C-반응단백은 전신적 심혈관계 질환 발생 위험과 밀접한 관련이 있다고 알려져 왔다. 하지만, COPD에서 이차적으로 발생하는 폐동맥 고혈압에 대한 C-반응단백의 영향에 대해서는 연구가 미비한 상태이다. 방법: 본 연구는 AECOPD에 대해 입원 치료를 시작한 72명의 환자를 대상으로 전향적으로 연구하였다. 환자들은 AECOPD에 대한 즉각적인 치료를 받았고 입원 2일 또는 3일째 실내 환기 하에서 혈청 C-반응단백, 동맥혈 산소 분압, 폐동맥 고혈압에 대한 이환 여부 등에 대한 검사를 시행 받았다. 결과: 폐동맥 고혈압에 이환된 환자는 47명으로 전체 환자 중 65.3%에 달하였다. COPD의 중증도가 심할수록 폐동맥 고혈압의 이환율과 C-반응단백 평균치가 증가하였고, C-반응단백 평균치가 증가할수록 평균 우심실 수축압 역시 증가하는 것을 관찰할 수 있었다. 폐동맥 고혈압 환자군과 비환자군에서 C-반응단백은 각각 $37.6{\pm}7.4mg/L$ 와 $19.9{\pm}6.6mg/L$ 통계적으로 의미 있게 폐동맥고혈압 환자군에서 높았지만, 동맥혈 산소분압은 양 군간 의미 있는 차이를 보이지 않았다($77.8{\pm}3.6mmHg$ vs. $87.2{\pm}6.0mmHg$). 결론: 본 연구는 COPD의 급성 악화 시 증가된 C-반응 단백은 폐동맥 고혈압의 이환 여부와 밀접한 관련이 있는 것을 보여 주고 있으며, 이는 COPD의 예후에 심혈관계 질환의 이환 여부가 중요하다는 점을 감안할 때 C-반응단백의 COPD에 대한 독립적 예후인자로서의 가능성을 시사해 준다.

• Journal of Chest Surgery
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• 제26권2호
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• pp.122-128
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• 1993

This series compromised 31 patients with pulmonary hypertension of 282 patients of ventricular septal defect(VSD) who underwent operation at the department of Thoracic and Cardiovascular Surgery in Chonnam University Hospital, from January, 1986 to December, 1991. Pulmonary hypertension was noted in 59 of 280 cases of VSD. Of them, 31 cases underwent cardiac catheterization on postoperative 8th to 77th month. Age at operation was ranged from 10 months to 29 years (mean 9.13 years). 17 patients were male and 14 patients were female. Results of follow-up studies were as follows: Cardiothoracic ratio was decreased from 0.59${\pm}$0.04 to 0.54${\pm}$0.03 (p=NS). Postoperative systolic pulmonary arterial pressure (PAPs), mean pulmonary arterial pressure (PAPm), and systolic right ventricular pressure (RVPs) were decreased significantly (p<0.001). And also Rp/Rs was decreased from 0.37${\pm}$0.21 to 0.14${\pm}$0.06 (p<0.02). However, systemic arterial pressure (SAP), right atrial pressure (RAP), and pulmonary capillary wedge pressure (PCWP) were changed insignificantly. There were significant relations of follow-up period with the decrement of PAP(p<0.005). In contrary, ther were no relations between the decrement of PAP and the age at operation. These data suggested that the long-term hemodynamic changes remained to be determined in some of the patients, even though they Were asymptomatic, with pulmonary hypertension.

• Journal of Yeungnam Medical Science
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• 제25권1호
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• pp.50-57
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• 2008

Pulmonary hypertension is an increase in blood pressure in the pulmonary artery, pulmonary vein or pulmonary capillaries. Depending on the cause, pulmonary hypertension can be a severe disease with markedly decreased exercise tolerance and right-sided heart failure. Pulmonary hypertension can present as one of five different types: arterial, venous, hypoxic, thromboembolic, or miscellaneous. Chronic obstructive pulmonary disease with severe pulmonary hypertension is a rare disease. A 52-year-old man presented with a complaint of aggravating dyspnea. The mean pulmonary arterial pressure was 61.5 mmHg by Doppler echocardiogram. The patient was prescribed diuretics, digoxin, bronchodilator, sildenafil, bosentan and an oxygen supply. However, he ultimately died of cor pulmonale. Thus, diagnosis and early combination therapy are important.

• 수면정신생리
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• 제17권2호
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• pp.69-74
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• 2010

Obstructive sleep apnea syndrome is associated with significant cardiovascular morbidity and increased mortality. However, it was controversial whether obstructive sleep apnea syndrome could cause pulmonary hypertension. The controversy was resolved by several studies that have shown pulmonary hypertension in 20% to 40% of patients with obstructive sleep apnea syndrome without underlying other cardiopulmonary diseases and reductions in pulmonary arterial pressure in patients with obstructive sleep apnea syndrome after treatment with nocturnal continuous positive airway pressure. Recent studies provide strong evidence for endothelial dysfunction in obstructive sleep apnea syndrome and pulmonary hypertension. Endothelin-1 is a 21 amino acid peptide with diverse biologic activity such as highly potent vasoconstrictor and mitogen regulator that may play a key role in obstructive sleep ap-nea syndrome and pulmonary hypertension. Continuous positive airway pressure therapy is moderately effective in reducing pulmonary arterial pressure. Further researches are needed to assess the therapeutic efficacy of pharmacologic therapy with agents that inhibit the action of endothelin-1 in obstructive sleep apnea syndrome patients with pulmonary hypertension.

• Journal of Chest Surgery
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• 제33권2호
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• pp.132-138
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• 2000

Background: Inhaled nitric oxide therapy causes selective pulmonary vasodilation in congenital heart diseases with pulmonary hypertension. However discontinuation of inhaled nitric oxide therapy may be complicated by abrupt life-threatening rebound pulmonary hypertension(RPH) The purpose of this study was to prevent by comparing group I(without RPH n=13) and group II(with RPH n=6) to determine the risk factors involved inthe development of the RPH. Material and Method: Between Januarty 6, 1998 and April 14, 1999. we studied 19 consecutive children who were treated with inhaled nitric oxide for clinically significant pulmonary hypertension after an open heart surgery for congenital heart disease. the ratio of males and females was 12:7 ranging in age from 10 days to 6040 days(16 years) To identify the effects of nitric oxide between two groups we measured heart rate mean and systolic pulmonary arterial pressure mean and systolic systemic arterial pressure central venous pressure pH paO2/FiO2 and O2 saturation before and after the initiation and just before the withdrawal of the inhaled nitric oxide. result: In 6 of 19 patients(32%) withdrawal of inhaled nitric oxide caused RPH. In the two groups inhaled nitrix oxide decreased in pulmonary arterial pressure(PAP) without decreasing the systemic arterial pressure(SAP) and increased PaO2/FiO2 Compared with patients who had no RPH(group I) patients who had RPH(group II) were older in age (1204$\pm$1688 versus 546$\pm$1654 days p<0.05) received less nitric oxide therapy(34$\pm$18 versus 67$\pm$46 hours p<0.05) has shorter weaning process(5$\pm$3 versus 15一13 hours p<0.05) and received lowerconcentration of initial nitric oxide supply(11$\pm$8 versus 17$\pm$8 ppm p>0.05) and lower concentration just before the withdrawal nitric oxide(4.2$\pm$2.6 versus 5.6$\pm$2.6 ppm, p>0.05) Conclusion : We speculate that older age shorter of nitric oxide therapy shorter weaning process are the risk factors of RPH.

• Tuberculosis and Respiratory Diseases
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• 제60권2호
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• pp.142-150
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• 2006

Pulmonary arterial hypertension (PAH) is often difficult to diagnose and challenging to treat. Untreated, it is characterized by a progressive increase in pulmonary vascular resistance leading to right ventricular failure and death. The past decade has seen remarkable improvements in therapy, driven largely by the conduct of randomized controlled trials. Still, the selection of most appropriate therapy is complex, and requires familiarity with the disease process, evidence from treatment trials, complicated drug delivery systems, dosing regimens, side effects, and complications. We tried to provide evidence-based treatment recommendations for physicians involved in the care of these complex patients. Due to the complexity of the diagnostic evaluation required, and the treatment options available, it is strongly recommended that consideration be given to referral of patients with PAH to a specialized center.