• Tuberculosis and Respiratory Diseases
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• v.67 no.3
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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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• v.39 no.9 s.266
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• pp.659-667
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• 2006

Background: Experimental studies of vascular remodeling in the pulmonary arteries have been performed actively. These models required a persistent vascular insult for intimal injury induced by chronic hypoxia, monocrotaline intoxication or chronic air embolism and characterized medial hypertrophy and neointimal formation by active synthesis of the extracellular matrix protein. The purpose of this study was to determine the pattern of pulmonary vascular remodeling after obstruction of the pulmonary vein. Material and Method: Obstruction of the right pulmonary vein with a metal clip was performed in Sprague-Dawley rats $(352{\pm}18g,\;n=10)$ to cause pulmonary vascular disease. Fifteen days later, experimental studies were done and finally the both lungs and hearts were extirpated for experimental measurement. Pulmonary arterial pressure, weight ratio of right ventricle (RV) to left ventricle (LV) and ventricular septum (S) (RV/LV +S weight ratio), and pulmonary artery morphology (percent wall thickness, %WT) were evaluated and compared with normal control groups. Result: Pulmonary hypertension $(38{\pm}12mmHg\;vs\;13{\pm}4mmHg;\;p<0.05)$ and right ventricular hypertrophy (right ventricular/left ventricular and septal weight ratio, $0.52{\pm}0.07\;vs\;0.35{\pm}0.04;\;p<0.05$) with hypertrophy of the muscular layer of the pulmonary arterial wall (percent wall thickness, $22.4{\pm}6.7%\;vs\;6.7{\pm}3.4%;\;p<0.05$) were developed by 15 days after obstruction of the pulmonary vein. Conclusion: Obstruction of the pulmonary vein developed elevation of pulmonary blood pressure and medial hypertrophy of the pulmonary artery. These results are a part of the characteristic vascular remodeling. Theses results demonstrate that obstruction of the pulmonary vein can develope not only high pulmoanry blood flow of contralateral lung but also intima injury inducing vascular remodeling.

• Journal of Chest Surgery
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• v.31 no.2
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• pp.108-112
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• 1998

Experimental trials of unilateral lung transplantation in dogs have been attempted and satisfactory results were obtained without any noticeable difficulty in surgical techniques. Fourteen dogs with the body weight of around 25 kg were anesthesized by 20~30 mg/kg of intravenous Entobar,; one was sacrificed to make available blood for use during transplantation for the recipient dog. A mid-sternotomy incision was performed and 20 mg/kg of Prostaglandin E1 was infused through the pulmonary artery and Euro-Collin's(E-C) preservation solution, cooled down to 4$^{\circ}C$, was perfused at the rate of 70cc/kg by a pressure of 30 cmH2O. The heart-lung block was then resected out and promptly immersed in the prepared preservation solution at 4$^{\circ}C$. One lung preserved in the EC solution at 4$^{\circ}C$ was anastomosed to the recipient dog in the order of the pulmonary vein, bronchus then pulmomary artery and the thoracotomy incision was closed after the bleeding control and tube thoracostomy. Then the pneumonectomy in the opposite side was perfomed in the same manner and the tailored lung was transplanted in the order of the pulmonary vein, bronchus, then pulmonary artery. We conclude that in the bilateral sequential lung transplantation, the right lung transplantation should precede to better expose the operative field and to prevent reperfusion injury; also, the cardiopulmonary bypass should be consider for certain appropriate cases.

• Sleep Medicine and Psychophysiology
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• v.4 no.2
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• pp.129-139
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• 1997

The data collected to date indicate that sleep-related breathing disorders, including sleep-disordered breathing(sleep apnea) and underlying respiratory system diseases, are one of the important risk factors for cardiovascular dysfunction. Sleep-disordered breathing(sleep apnea) is now recognized as one of the leading causes of systemic hypertension, cardiac arrhythmias, coronary heart disease, pulmonary hypertension, right heart failure, and stroke. Sleep may exert a profound effect on breathing in patients with underlying respiratory system disease including bronchopumonary diseases, chest wall abnormalities, central alveolar hypoventilation syndromes or respiratory neuromuscular disorders. Chronic hypoxia and hypercapnia in these patients may accelerate the development of long term cardiovascular complications such as cardiac arrhythmias, pulmonary hypertension, and right heart failure(cor pulmonale). Several recent studies reported that sleep-related breathing disorders are associated with long-term cardiovascular morbidity and mortality. Careful assessment of respiratory and cardiovascular function in these patients is critical. Aggressive and highly effective treatment of sleep-related breathing disorders using tracheostomy, mechanical ventilation, nasal continuous positive airway pressure therapy(nCPAP), intercurrent oxygen therapy or other interventions can reduce the prevalence of cardiovascular dysfunction and the long-term mortality.

• Journal of Chest Surgery
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• v.43 no.3
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• pp.254-259
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• 2010

Background: Diagnosing chronic pulmonary embolism at an early stage is difficult because of the patient’s nonspecific symptoms. This condition is not prevalent in Korea, and in fact, there have been only a few case reports on this in the Korean medical literature. We analyzed the surgical outcome of performing pulmonary thromboendarterectomy in patients with chronic pulmonary embolism. Material and Method: The study subjects included those patients who underwent surgery for chronic pulmonary embolism from 1996 to 2008. For making the diagnosis, echocardiography, chest CT and a pulmonary perfusion scan were performed on the patients who complained of chronic dyspnea. Result: Pulmonary endarterectomy was performed as follows: by incision via a mid-sternal approach (7 patients); by incision via a left posterolateral approach (1 patient); using the deep hypothermic circulatory arrest technique (4 patients); under ventricular fibrillation (3 patients); and under cardioplegic arrest (1 patient). The postoperative systolic pulmonary artery blood pressure significantly decreased from a preoperative value of $78.9{\pm}14.5\;mmHg$ to $45.6{\pm}17.6\;mmHg$ postoperatively (p=0.000). The degree of tricuspid regurgitation was less than grade II after surgery. Two patients died early on, including one patient who had persistent pulmonary hypertension without improvement and right heart failure. Conclusion: Patients who have chronic pulmonary embolism are known to have a poor prognosis. However, we think that early surgical treatment along with making the proper diagnosis before the aggravation of right heart failure can help improve the quality of a patient's life.

• Tuberculosis and Respiratory Diseases
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• v.63 no.6
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• pp.475-479
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• 2007

• Sleep Medicine and Psychophysiology
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• v.17 no.2
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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.

• Tuberculosis and Respiratory Diseases
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• v.43 no.4
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• pp.600-612
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• 1996

Background : Recent studies deported that untreated patients with obstructive sleep apnea syndrome had high long-term mortality rates, and cardiovascular complications of these patients clad a major effect on mortality. Several data indicates that obstructive sheep apnea syndrome contributes to the development of diurnal systemic hypertension. But the pathophysiological mechanism of the development of systemic hypertension in these patients is still uncertain. This study was performed to evaluate the possible role of sympathetic nervous system activity for the development of systemic hypertension in patients with obstructive sleep apnea syndrome. Method : 35 patients with obstructive sleep apnea syndrome(OSAS) and 13 Control subjects(control) were included in this study. 21 patients of OSAS were normotensives(OSAS-NBP), and 14 patients of OSAS were hypertensives(OSAS-HBP). Full night polysomnography was undertaken to all subjects. We measured plasma norepinephrine(NE) and epinephrine(EP) concentrations during waking and sleep, using high performance liquid chromatography, in all patients and control subjects. Results : In OSAS, OSAS-NBP and control, plasma NE and EP concentrations during sleep were lowed than during waking(p<0.01). But, in OSAS-HBP, these was no difference between during waking and sleep. Plasma NE concentrations during sleep of OSAS, OSAS-NBP and OSAS-HBP were higher than Control(p<0.05). In OSAS-HBP, daytime systolic blood pressure correlated with plasma NE concentration during sleep(r=0.7415, p<0.01), arid correlated inversely with mean arterial oxygen saturation(r=-0.6465, p<0.05) or arterial oxygen saturation nadir(r=-0.6) 14, p<0.05) during sleep. Conclusion : The sympathetic activity during sleep of obstructive sleep apnea syndrome patients was higher than control subjects. In obstructive sleep apnea syndrome patients with systemic hypertension, there was no diurnal variation of sympathetic activity, and there was correlation between daytime systolic blood pressure and sympathetic activity during sleep. These data suggests that chronic hyperactivity of sympathetic nervous system may contribute to the development of diurnal systemic hypertension in patients with obstructive sleep apnea syndrome.

• Clinical and Experimental Pediatrics
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• v.46 no.6
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• pp.610-614
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• 2003

Pulmonary hypertension may be associated with variable conditions such as the hyperkinetic state or pulmonary vascular obstruction. In these, stenosis of the individual pulmonary veins without any cardiac or vascular malformation is very rare. We experienced stenosis of individual pulmonary veins in a 10 months old boy who was admitted with recurrent dyspnea and cyanosis and then underwent angiogram and a lung perfusion scan.

• Tuberculosis and Respiratory Diseases
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• v.59 no.2
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• pp.170-178
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• 2005

Background : Idiopathic pulmonary arterial hypertension (IPAH) and chronic thromboembolic pulmonary hypertension (CTEPH) are rare but significantly imperative in inducing chronic pulmonary hypertension. Clinically, it is difficult to distinguish between IPAH and CTEPH. However, the treatment of pulmonary hypertension is different depending on the disease. The present study was performed to analyze the similarities and differences in clinical features between IPAH and CTEPH. Methods : During a nine-year period, thirty-three patients with IPAH and twenty-two patients with CTEPH were enrolled. Symptoms, physical findings, chest radiograph, electrocardiograph, pulmonary function test, echocardiograph, perfusion lung scan, right heart catheterization results were analyzed between both the groups. Results : The median age of IPAH group was 33 (6~70) years that was lower than that (52(27~80) years) of CTEPH group. Amongst the IPAH patients, there was female predominance (76 %) and there was no sex difference between the patients with CTEPH. Both the groups exhibited similarity in the results of chest radiograph, electrocardiograph, pulmonary function test, and echocardiograph. In the perfusion lung scan, all IPAH patients exhibited findings with normal (28%) or low probability (72%) of pulmonary embolism and all CTEPH patients exhibited findings with high probability of pulmonary embolism. Conclusion : Although IPAH and CTEPH bear similarities in terms of symptoms, physical signs and general investigation results, there were differences in age distribution, sex predominance and results of perfusion lung scan.