• Journal of Chest Surgery
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• v.44 no.6
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• pp.432-436
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• 2011

We herein present a case of a successful correction of cor triatriatum associated with thrombotic pulmonary hypertension diagnosed in an adult female patient. We confirmed diagnosis using transthoracic and transesophageal echocardiography in addition to cardiac computed tomography and magnetic resonance imaging. Surgical repair comprised excision of the fibromuscular membranous septum in the left atrium, patch closure of an atrial septal defect, and reconstruction of the pulmonary arteries with a vascular graft. Cor triatriatum complicated pulmonary thrombotic hypertension with atrial septal defect is amenable to surgical correction with satisfactory results.

• Korean Circulation Journal
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• v.48 no.12
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• pp.1135-1144
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• 2018

Background and Objectives: Mitochondria play a key role in the pathophysiology of heart failure and mitochondrial permeability transition pore (MPTP) play a critical role in cell death and a critical target for cardioprotection. The aim of this study was to evaluate the protective effects of cyclosporine A (CsA), one of MPTP blockers, and morphological changes of mitochondria and MPTP related proteins in monocrotaline (MCT) induced pulmonary arterial hypertension (PAH). Methods: Eight weeks old Sprague-Dawley rats were randomized to control, MCT (60 mg/kg) and MCT plus CsA (10 mg/kg/day) treatment groups. Four weeks later, right ventricular hypertrophy (RVH) and morphological changes of right ventricle (RV) were done. Western blot and reverse transcription polymerase chain reaction (RT-PCR) for MPTP related protein were performed. Results: In electron microscopy, CsA treatment prevented MCT-induced mitochondrial disruption of RV. RVH was significantly increased in MCT group compared to that of the controls but RVH was more increased with CsA treatment. Thickened medial wall thickness of pulmonary arteriole in PAH was not changed after CsA treatment. In western blot, caspase-3 was significantly increased in MCT group, and was attenuated in CsA treatment. There were no significant differences in voltage-dependent anion channel, adenine nucleotide translocator 1 and cyclophilin D expression in western blot and RT-PCR between the 3 groups. Conclusions: CsA reduces MCT induced RV mitochondrial damage. Although, MPTP blocking does not reverse pulmonary pathology, it may reduce RV dysfunction in PAH. The results suggest that it could serve as an adjunctive therapy to PAH treatment.

• The Korean Journal of Physiology and Pharmacology
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• v.27 no.3
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• pp.209-220
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• 2023

This study is to determine the regulation of nitric oxide synthase 3 (NOS3) by edaravone in mice with hypoxic pulmonary hypertension (HPH). C57BL/6J mice were reared in a hypoxic chamber. HPH mice were treated with edaravone or edaravone + L-NMMA (a NOS inhibitor). Lung tissue was collected for histological assessment, apoptosis analysis, and detection of malondialdehyde, superoxide dismutase, tumor necrosis factor (TNF)-α, interleukin (IL)-6, and NOS3. The levels of serum TNF-α and IL-6 were also measured. Immunohistochemistry was used to visualize the expression of α-smooth muscle actin (SMA) in pulmonary arterioles. Edaravone treatment improved hemodynamics, inhibited right ventricular hypertrophy, increased NOS3 expression, and reduced pathological changes, pulmonary artery wall thickness, apoptotic pulmonary cells, oxidative stress, and the expression of TNF-α, IL-6, and α-SMA in HPH mice. L-NMMA treatment counteracted the lung protective effects of edaravone. In conclusion, edaravone might reduce lung damage in HPH mice by increasing the expression of NOS3.

• The Korean Journal of Nuclear Medicine
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• v.19 no.2
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• pp.87-89
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• 1985

Unresolved major pulmonary embolism (UMPE) is an uncommon condition which causes pulmonary hypertension, cor pulmonale and death. An accurate and prompt diagnosis of UMPE is very important in the management of such patients with pulmonary embolectomy. Follow-up lung scans can lead to earlier diagnosis of UMPE especially on patients who have a history of acute pulmonary embolism in the past and. present with pulmonary hypertension, respiratory insufficiency and cor pulmonale. We report a case of UMPE strongly suggested by follow-up lung scans and subsequently confirmed by pulmonary angiography and postmortem examination.

• Journal of Veterinary Clinics
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• v.24 no.4
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• pp.613-617
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• 2007

A 1-year-old castrated male Maltese dog(weighing 2.4 kg) was presented with primary complaints of occasional coughing, dyspnea and exercise intolerance. Based on diagnostic findings including paradoxical split S2, diastolic regurgitant murmur, marked dilation of pulmonary artery, right ventricular eccentric hypertrophy with thickening of ventricular septum, severe tricuspid and pulmonic regurgitation(5.4 m/sec and 3.4 m/sec, respectively) and the absence of any congenital intracardiac shunting, obstructive pulmonary diseases and systemic diseases associated with right ventricular pressure overload or pulmonary hyperperfusion, the case was tentatively diagnosed as primary pulmonary hypertension. The dog was treated with furosemide, aspirin and oxygen supplementation. This case report described a rare case of primary pulmonary hypertension in a Maltese dog.

• Journal of Yeungnam Medical Science
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• v.37 no.2
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• pp.122-127
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• 2020

Pulmonary tumor thrombotic microangiopathy (PTTM) is a rare but fatal complication of cancer and causes pulmonary hypertension and acute/subacute right heart failure. PTTM is most commonly associated with gastric cancer and more rarely associated with pancreatic cancer. We report a case of progressive right heart failure associated with clinically diagnosed pancreatic cancer, suggesting PTTM.

• Tuberculosis and Respiratory Diseases
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• v.46 no.6
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• pp.846-855
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• 1999

Background : Secondary pulmonary hypertension is an important final endpoint in patients with chronic hypoxic lung disease, accompanied by deterioration of pulmonary hemodynamics. The clinical diagnosis of pulmonary hypertension and/or cor pulmonale could be difficult, and simple noninvasive evaluation of pulmonary artery pressures has been an relevant clinical challenge for many years. Doppler echocardiography might to be a more reliable method for evaluating pulmonary hemodynamics in such patients in terms of the accuracy, reproducibility and easiness for obtaining an appropriate echocardiographic window than M-mode echocardiography. The aim of this study was to assess echocardiographic parameters associated with pulmonary arterial hypertension, defined by increasing right ventricular systolic pressure(RVSP), calculated from trans-tricuspid gradient in patients with chronic hypoxic lungs. Method : We examined 19 patients with chronic hypoxic lung disease, suspected pulmonary hypertension under the clinical guidelines by two dimensional echocardiography via the left parasternal and subcostal approach in a supine position. Doppler echocardiography measured RVSP from tricuspid regurgitant velocity in continuous wave with 2.5MHz transducer and acceleration time(AT) on right ventricular outflow tract in pulsed wave for the estimation of pulmonary arterial pressure. Results : On echocardiography, moderate to severe degree of pulmonary arterial hypertension was defined as RVSP more than 40mmHg, presenting tricuspid regurgitation. Increased right ventricular endsystolic diameter and shortened AT were noted in the increased RVSP group. Increased RVSP was correlated negatively with the shortening of AT. Other clinical data, including pulmonary functional parameters, arterial blood gas analysis and M mode echocardiographic parameters were not changed significantly with the increased RVSP. Conclusion : These findings suggest that shortened AT on pulsed doppler can be useful when quantifying pulmonary arterial pressure with increased RVSP in patients with chronic lung disease with hypoxemia. Doppler echocardiography in pulmonary hypertension of chronic hypoxic lungs is an useful option, based on noninvasiveness under routine clinical practice.

• YAKHAK HOEJI
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• v.43 no.4
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• pp.487-493
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• 1999

Effects of Ginkgo biloba extract (EGb 761) on the anti-pulmonary hypertensive action of enalapril were evaluated in rats. Pulmonary hypertension was induced by monocrotaline treatment (60mg/kg, i.p.) in normotensive rats. In the systolic pulmonary artery pressure, the control group was 33$\pm$2 mmHg, comparing to the normal group of 19$\pm$1 mmHg. That of enalapril group(20mg/kg/day, p.o.) was 26$\pm$2 mmHg. In the isolated lung preparation, acetylcholine, which was endothelium dependent vasodilator, induced the decrease of pulmonary artery perfusion pressure(-2.0$\pm$0.7 mmHg) in normal group, but the increase of that of 3.4$\pm$0.6 and 3.0$\pm$0.9 mmHg in control and enalapril group, respectively. And that of the combined group was -0.5$\pm$0.2 mmHg. In the isolated pulmonary artery, acetylcholine(10-5M) induced the relaxation of 65$\pm$6% in normal group, but 15 and 8% in control and enalapril group, respectively. And that of the combined group was resulted 55$\pm$2%. These results suggested that co-administration of Ginkgo biloba extract(EGb 761) potentiated the anti-pulmonary hypertensive effects of enalapril through the increase of pulmonary vasodilation due to the protection of endothelial cell by antioxidant action of Ginkgo biloba extract (EGb 761).

• Tuberculosis and Respiratory Diseases
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• v.60 no.2
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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.

• Journal of Chest Surgery
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• v.23 no.4
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• pp.659-666
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• 1990

We evaluated 68 patients with mitral valve disease who underwent mitral valve replacement from April, 1986, to December, 1988. Among them 20 patients showed increased systolic pulmonary arterial pressure greater than 60 mmHg and postoperative hemodynamic data were obtained in 19 patients average 13 months after mitral valve replacement. The results were as followings. 1. Average pulmonary systolic pressure decreased from 84.8$\pm$4.5 preoperatively to 33. 0$\pm$1.9mmHg postoperatively[P<0.001]. 2. Average pulmonary vascular resistance index decreased from 1425$\pm$148 preoperatively to 287+35.8 dyne * sec * cm2 * m postoperatively[P<0.001]. 3. Average cardiac index rose from 1.927$\pm$0.169 preoperatively to 2.625$\pm$0.159 L/min/m2 postoperatively [P <0.005]. This study shows that pulmonary hypertension and the increased pulmonary vascular resistance index due to mitral valve disease can regress significantly after mitral valve replacement.