• Archives of Plastic Surgery
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• 제49권3호
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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.

• The Korean Journal of Physiology and Pharmacology
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• 제22권4호
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• pp.447-456
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• 2018

Angiotensin-(1-9) [Ang-(1-9)], generated from Ang I by Ang II converting enzyme 2, has been reported to have protective effects on cardiac and vascular remodeling. However, there is no report about the effect of Ang-(1-9) on pulmonary hypertension. The aim of the present study is to investigate whether Ang-(1-9) improves pulmonary vascular remodeling in monocrotaline (MCT)-induced pulmonary hypertensive rats. Sprague-Dawley rats received Ang-(1-9) ($576{\mu}g/kg/day$) or saline via osmotic mini-pumps for 3 weeks. Three days after implantation of osmotic mini-pumps, 50 mg/kg MCT or vehicle were subcutaneously injected. MCT caused increases in right ventricular weight and systolic pressure, which were reduced by co-administration of Ang-(1-9). Ang-(1-9) also attenuated endothelial damage and medial hypertrophy of pulmonary arterioles as well as pulmonary fibrosis induced by MCT. The protective effects of Ang-(1-9) against pulmonary hypertension were inhibited by Ang type 2 receptor ($AT_2R$) blocker, but not by Mas receptor blocker. Additionally, the levels of LDH and inflammatory cytokines, such as $TNF-{\alpha}$, MCP-1, $IL-1{\beta}$, and IL-6, in plasma were lower in Ang-(1-9) co-treated MCT group than in vehicle-treated MCT group. Changes in expressions of apoptosis-related proteins such as Bax, Bcl2, Caspase-3 and -9 in the lung tissue of MCT rats were attenuated by the treatment with Ang-(1-9). These results indicate that Ang-(1-9) improves MCT-induced pulmonary hypertension by decreasing apoptosis and inflammatory reaction via $AT_2R$.

• Journal of Chest Surgery
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• 제23권1호
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• pp.32-40
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• 1990

Surgical correction of congenital cardiac defects in infants and children with an elevated pulmonary arterial pressure or pulmonary vascular resistance carries a significant early postoperative mortality. And accurate assessments of cardiac output is critically important in these patients. From April 1988 through September 1989, serial measurements of cardiac index, ratio of pulmonary-systemic systolic pressure, ratio of pulmonary-systemic resistance, central venous pressure, left atrial pressure, and urine output during the first 48 hours after the cardiac operation were made in 30 congenital cardiac defects associated with pulmonary hypertension. Cardiac index showed significant increase only after 24 hour postoperatively and this low cardiac performance in the early postoperative period should be considered when postoperative management is being planned in the risky patients. There were no variables which showed any significant correlation with cardiac index. In 12 cases[40%], pulmonary hypertensive crisis developed during the 48 hours postoperatively, and they were treated with full sedation, hyperventilation with 100 % 0y and pulmonary vasodilator infusion. In all patient with preoperative pulmonary hypertension, surgical placement of a pulmonary artery catheter is desirable to allow prompt diagnosis of pulmonary hypertensive crisis and to monitor subsequent therapy.

• Journal of Chest Surgery
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• 제25권7호
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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.

• 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.

• Journal of Chest Surgery
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• 제19권1호
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• pp.1-11
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• 1986

Using an experimental model of pulmonary hypertension, the effects of anticonstrictive drugs on the development of pulmonary vascular remodeling and right ventricular hypertrophy were studied. Male Sprague-Dawley rats weighing 200~250 gm were used. For the experimental model of pulmonary hypertension, a group of animal was given by a subcutaneous injection of monocrotaline on a dose of 20mg, 40mg, or 60mg per kg of body weight. After 4 weeks of injection, all animals were sacrificed. Another group of animal was given by a subcutaneous injection of monocrotaline in a dose of 40 mg per kg of body weight. The animals were sacrificed, in which they were kept alive for 1, 2, 3 and 4 weeks, respectively. For the effects of anticonstrictive drugs on the development of pulmonary vascular remodeling and right ventricular hypertrophy, the animals treated with monocrotaline were given daily by an intraperitoneal injection of phenoxybenzamine in a dose of 1.3mg/kg of body weight, and were given propranolol via their drinking water at a concentration of 400mg/liter. The animals were sacrificed after 4 weeks of administration. The hearts and lungs were examined histopathologically and morphometrically. The results obtained were summarized as follows: 1. The rats treated with monocrotaline showed an interstitial pneumonitis, medial thickening of the pulmonary small arteries and hypertrophy of the right ventricular wall. 2. The medial thickening of the pulmonary arteries in rats treated with monocrotaline was due to muscular hypertrophy and hyperplasia, and the right ventricular hypertrophy was due to hypertrophy of cardiac muscles. Both medial thickening of the pulmonary arteries and hypertrophy of right ventricular wall were more marked with time and with dose. 3. The daily intraperitoneal injection of phenoxybenzamine suppressed significantly the percentage medial thickness of pulmonary small arteries and the index of right ventricular hypertrophy in rats given a single subcutaneous injection of monocrotaline, but propranolol has shown no protective effect on the development of medial thickening of pulmonary arteries and right ventricular hypertrophy in treated with monocrotaline. The results described above suggested that monocrotaline is an alkaloid selectively inducing pulmonary hypertension and that a-adrenergic receptor is responsible for the pathogenesis of monocrotaline induced pulmonary hypertension in rat.

• 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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• 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.

• The Korean Journal of Physiology and Pharmacology
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• 제17권1호
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• pp.1-8
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• 2013

Understanding the cellular and molecular mechanisms involved in the development and progression of pulmonary hypertension (PH) remains imperative if we are to successfully improve the quality of life and life span of patients with the disease. A whole plethora of mechanisms are associated with the development and progression of PH. Such complexity makes it difficult to isolate one particular pathway to target clinically. Changes in intracellular free calcium concentration, the most common intracellular second messenger, can have significant impact in defining the pathogenic mechanisms leading to its development and persistence. Signaling pathways leading to the elevation of $[Ca^{2+}]_{cyt}$ contribute to pulmonary vasoconstriction, excessive proliferation of smooth muscle cells and ultimately pulmonary vascular remodeling. This current review serves to summarize the some of the most recent advances in the regulation of calcium during pulmonary hypertension.

• Tuberculosis and Respiratory Diseases
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• 제48권6호
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• pp.973-979
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• 2000

제 I 형 당원병에서 폐고혈압은 드문 합병증으로 외국 문헌에서 6예만이 보고되었으나 국내에는 아직 보고된 바가 없다. 저자들은 최근 제 Ia형 당원병으로 진단 받았던 31세 남자 환자에서 폐고혈압이 동반되었던 예를 경험하였기에 문헌 고찰과 함께 보고하는 바이다.