• Journal of Yeungnam Medical Science
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• v.25 no.1
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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.

• Journal of Veterinary Clinics
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• v.37 no.6
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• pp.311-316
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• 2020

Biomarkers used in dogs with heartworm disease include N-terminal pro B-type natriuretic peptide (NT-proBNP) and cardiac troponin I (cTnI), which are associated with damage to the myocardium. Pulmonary hypertension is one of the clinical signs of canine heartworm disease. The purpose of this study is to investigate the change in the concentration of each biomarker, severity of pulmonary hypertension and the correlation between biomarkers according to the severity of clinical signs. Five healthy dogs and 10 heartworm-infected dogs were recruited for the study. The heartworm-infected group was classified based on the history, clinical signs, and blood assay, thoracic radiography, and echocardiography after confirming the infection according to the results of the commercial ELISA kit (SNAP test, IDEXX Laboratories, Maine, USA). NT-proBNP was higher in the severely infected group than the control group (p < 0.05); cTnI was also higher in the severely infected group than the control group (p < 0.05). The pressure gradient of pulmonary hypertension was higher in the severe group than the mild group (p < 0.05). The severity of pulmonary hypertension was correlated with NT-proBNP (r = 0.818, p < 0.01), cTnI (r = 0.894, p < 0.01). When the correlation of the two serum values for each group was examined, a correlation was not found in the mild group (r = 0.707, p = 0.182), but a correlation was found in the severe group (r = 0.9, p < 0.05). NT-proBNP and cTnI were significantly increased and correlated with severe clinical signs. Pulmonary hypertension was significant higher in the severe group than in the mild group (p < 0.05). Evaluation of blood biomarker concentration and severity of pulmonary hypertension and referring to each correlation between these indicators may be helpful to assess the severity of the heartworm disease.

• Journal of Chest Surgery
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• v.7 no.1
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• pp.85-92
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• 1974

During the years 1959 to 1974, 99 patients with patent ductus arteriosus were admitted to National University Hospital. These includes 5 patients with additional cardiovascular and 5 patients with severe pulmonary hypertension. All were operated upon except three refused operation. In all instances, the diagnosis was made by history and physical, roentgenological and electrographic examinations. In addition, in 53 patients, special diagnostic procedures were carried out either for diagnosis or for evaluation of pulmonary hypertension and associated cardiovascular anomalies. Right cardiac catheterization was resorted to in 51 patients. In one of these patients catheterization was incorrectly interpreted [ventricular septal defect]. Retrograde aortogram was performed in two patients. In both cases the ductus itself was visualized on the x-ray film. An additional vascular anomaly, namely the persistent left superior vena cava, was confirmed by retrograde angiogram in one of them. In 5 cases the pulmonary arterial pressure was elevated well over 80 mmHg. In these instances,the operative mortality was 80% [4 out of 5 patients]. The management of patent ductus arteriosus when associated with severe pulmonary hypertension. and/or other cardiac anomalies is controversial. Opinions differ as to how to close the ductus and to repair the cardiac anomalies as well as to whether a one-staged or two-staged procedure should be resorted to. The author is of the that each case must be evaluated individually before any specific surgical treatment is ou.tlined. The literature on the subject is reviewed in this paper.

• Archives of Plastic Surgery
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• v.49 no.3
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• pp.369-372
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• 2022

Reduction mammaplasty is the gold standard treatment for gigantomastia. We report one female patient with juvenile gigantomastia associated with severe pulmonary hypertension where her pulmonary pressure decreased significantly after the surgery, improving her quality of life. A 22-year-old female patient with gigantomastia since 10 years old, tricuspid regurgitation, and pulmonary thromboembolism antecedent was admitted to the emergency department. Her oxygen saturation was 89%. Acute heart failure management was initiated. An echocardiogram reported left ventricle ejection fraction (LVEF) of 70% with severe right heart dilation, contractile dysfunction, and arterial pulmonary pressure (PASP) of 110 mm Hg. A multidisciplinary team considered gigantomastia could generate a restrictive pattern, so a Thorek reduction mammoplasty with Wise pattern was performed. Presurgical measurements were: sternal notch to nipple-areola complex, right 59 cm, left 56 cm. Three days after surgery, the patient could breathe without oxygen support. In the outpatient follow-up, patient referred reduction of her respiratory symptoms and marked improvement in her quality of life. Six months after surgery, a control echocardiogram showed a LVEF of 62% and PASP of 85 mm Hg. Pulmonary hypertension may be present in patients with gigantomastia. Reduction mammoplasty may be a feasible alternative to improve the cardiac signs and symptoms in patients with medical refractory management.

• Journal of Chest Surgery
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• v.50 no.5
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• pp.378-381
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• 2017

Patients with an atrial septal defect (ASD) and severe pulmonary arterial hypertension (PAH) are considered ineligible for defect closure surgery because of the risk of right ventricular decompensation and death after the operation. We report the case of a patient with large ASD and severe PAH who was able to undergo defect closure surgery successfully following long-term use of combined oral sildenafil and beraprost.

• Journal of Chest Surgery
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• v.31 no.7
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• pp.718-721
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• 1998

The surgical closure of VSD in patient with severe pulmonary hypertension has been considered a difficult problem for surgeons, because sudden hemodynamic change after closure of the defect could bring on high perioperative mortality. Recently, it was reported that UVP(unidirectional valve patch), which allows some blood to flow from right to left in case of acute right heart failure, is effective in improving the postoperative hemodynamics after closing septal defects. This 42-year old woman had suffered from VSD for 20 years and recently complained of worsening exertional dyspnea for three months, and was diagnosed of a large VSD(2.0 cm in diameter) with severe pulmonary hypertension(116/38 mm Hg), equal to systemic arterial pressure. We could successfully close VSD with severe pulmonary hypertension using one UVP and the other UVP for the creative ASD to be prepared against possible acute right heart failure. She was discharged on the fourteenth postoperative day and has been well for twelve months with spontanenous closure of UVP patch at the ninth postopeative month.

• Clinical and Experimental Pediatrics
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• v.53 no.1
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• pp.93-96
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• 2010

A 47-year-old male patient in whom atrial septal defect (ASD) had been diagnosed 15 years previously was admitted for cardiac catheterization. He had definite cyanotic lips and nail beds and severe pulmonary arterial hypertension (PAH). He had received medical treatment only for the last few years after being diagnosed with Eisenmenger syndrome. After cardiac catheterization, he received iloprost inhalation therapy pre and postoperation and was discharged after successful surgical closure of the ASD.

• Journal of Chest Surgery
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• v.52 no.4
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• pp.232-235
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• 2019

A 2.5-kg neonate with coarctation of the aorta and a small left ventricle experienced a severe pulmonary hypertensive crisis. An emergency pulmonary artery-to-systemic artery shunt was placed to break the positive feedback loop caused by pulmonary hypertension and functional mitral stenosis. This shunt provided immediate relief of suprasystemic pulmonary hypertension and the resultant low cardiac output.

• Journal of Chest Surgery
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• v.25 no.7
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• pp.736-738
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• 1992

We report the successful use of Nifedipine in the treatment of acute pulmonary hypertension in an young child after a cardiac operation. This patient had undergone patch closure of large ventricular septal defect. She had signs of severe pulmonary artery hypertension unresponsive to hyperventilation, oxygenation, sedation, and a myriad of vas-oactive drugs. Nifedipine, 0.3mg /kg every 4 hours, effectively treated her pulmonary artery hypertension and allowed for a smooth postoperative course and positive outcome. The drug lowered systemic diastolic pressure, but not systolic pressure.

• Journal of Yeungnam Medical Science
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• v.31 no.2
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• pp.144-147
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• 2014

Despite the necessity of surgical aortic valve replacement, many patients with symptomatic severe aortic stenosis (AS) cannot undergo surgery because of their severe comorbidities. In these high-risk patients, percutaneous transcatheter aortic valve implantation (TAVI) can be safely accomplished. However, no study has shown that TAVI can be performed for patients with severe AS accompanied by acute decompensated heart failure. In this case report, 1 patient presented a case of severe pulmonary hypertension with decompensated heart failure after diagnosis with severe AS, and was successfully treated via emergency TAVI. Without any invasive treatment, acute decompensated heart failure with severe pulmonary hypertension is common in patients with severe AS, and it can increase mortality rates. In conclusion, TAVI can be considered one of the treatment options for severe as presented as acute decompensated heart failure patients with pulmonary hypertension.