• Tuberculosis and Respiratory Diseases
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• v.64 no.2
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• pp.125-132
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• 2008

Background: In chronic obstructive pulmonary disease (COPD) patients, the serum levels of C-reactive protein (CRP) are elevated and an increase of CRP is more exaggerated in the acute exacerbation form of COPD (AECOPD) than in stable COPD. Pulmonary arterial hypertension is a common complication of COPD. An increased level of CRP is known to be associated with the risk of systemic cardio-vascular disorders. However, few findings are available on the potential role of CRP in pulmonary arterial hypertension due to COPD. Methods: This study was performed prospectively and the study population was composed of 72 patients that were hospitalized due to AECOPD. After receiving acute management for AECOPD, serum CRP levels were evaluated, arterial oxygen pressure ($PaO_2$), was measured, and the existence of pulmonary arterial hypertension under room air inhalation was determined in the patients. Results: The number of patients with pulmonary arterial hypertension was 47 (65.3%)., There was an increased prevalence of pulmonary arterial hypertension and an increase of serum CRP levels in patients with the higher stages of COPD (e.g., patients with stage 3 and stage 4 disease; P<0.05). The mean serum CRP levels of patients with pulmonary arterial hypertension and without pulmonary arterial hypertension were $37.6{\pm}7.4mg/L$ and $19.9{\pm}6.6mg/L$, respectively (P<0.05). However, there was no significant difference of the mean values of $PaO_2$ between patients with pulmonary arterial hypertension and without pulmonary arterial hypertension statistically ($77.8{\pm}3.6mmHg$ versus $87.2{\pm}6.0mmHg). Conclusion: We conclude that higher serum levels of CRP can be a sign for pulmonary arterial hypertension in AECOPD patients.

• Journal of Chest Surgery
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• v.38 no.10 s.255
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• pp.680-684
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• 2005

Background: With the increasing age of the population, coronary artery bypass grafting in the elderly patients is becoming common. Off-pump coronary artery bypass grafting (OPCAB) has been proven to be less morbidity and to facilitate early recovery. The elderly patients may have benefits by avoiding the adverse effects of the cardiopulmonary bypass. The purpose of this study is to evaluate our results of OPCAB in elderly patients. Material and Method: A retrospective chart review was carried out for 12 patients aged over 80 years who underwent isolated OPCAB from January 2001 and March 2004. Data were collected risk factors for disease, extent of coronary disease, and in-hospital outcomes. Postoperative graft patiency was evaluated in 9 patients by multi-slice computed tomography. Result: Eleven patients had triple vessel disease or left main disease. Four patients were suffered from preoperative CVA, and 4 patients had chronic obstructive pulmonary disease. Two patients had myocardial infarction (MI), among them 1 patient was suffered from pulmonary edema after preoperative MI. There was no perioperative death, perioperative MI, and no ventricular arrhythmia. Also there was no perioperative stroke and renal failure. But there was one deep sternal infection who recovered by treating of muscle flap. Atrial fibrillation was newly developed in 1 patient, but was well controlled by medication. Mean intubation time was $15.9\pm4.4(8\~20hrs)$ hrs and mean ICU stay was $2.9\pm0.8(2\~4 days)$ days. Mean hospital day was $21.6\pm14.3(13\~56 days)$ days. Postoperative mean CK-MS was $11.3\pm14.1\;ng/mL$. Early postoperative graft patency rate was $100\%(24/24)$. Follow-up was completed in all patients. In this time, there was no patients with angina or death. Conclusion: The results of this study suggest that OPCAB reduces morbidity and favors hospital outcomes. Therefore, OPCAB is safe, reasonable and might be preferable operative strategy in elderly patients.

• Tuberculosis and Respiratory Diseases
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• v.38 no.3
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• pp.255-261
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• 1991

Frequently patients with chronic obstructive pulmonary disease have lowered arterial oxygen saturation in daytime. During sleep, they are apt to experience additional hypoxemia. These episode of nocturnal hypoxemia are usually associated with periods of relative hypoventilation. Noctunal hypoxemia may be associated with cardiac arrhythmia and with acute increase in pulmonary arterial pressure and may be implicated in the development of chronic pulmonary hypertension and cor pulmonale. We selected 14 patients with chronic obstructive pulmonary disease, 9 with emphysema dominant type and 5 with chronic bronchitis dominant type, to examine the frequency and severity of nocturnal hypoxemia and the effect of oxygen in prevention of nocturnal hypoxemia. The results were as follows; 1) On PFT, FVC, $FEV_1$, and $FEV_1$/FVC showed no significant difference between the emphysema dominant type (pink puffers, PP) and the chronic bronchitis dominant type (blue bloaters, BB). But DLCO/VA for the PP group was $45.7{\pm}15.1%$ which was significantly different from BB group, $82.4{\pm}5.6%$. 2) The daytime arterial oxygen saturation ($SaO_2$) and the lowest $SaO_2$, during sleep for the BB group were significantly lower than for the PP group. 3) The hypoxemic episodes during sleep were more frequent in BB group and the duration of hypoxemic episode was longer in BB group. 4) In both group studied, although there was a tendency for a lower L-$SaO_2$ (the lowest $SaO_2$, during sleep), an increase in hypoxemic episodes and duration as the daytime $SaO_2$, fell lower, the only parameter which showed significant correlation was daytime $SaO_2$, and the frequency of hypoxemic episodes in the PP group (r=-0.68, P<0.05). 5) In PP group, with oxygen supplementation, L-$SaO_2$, during sleep showed significant increase, and there was a tendency for the frequency of hypoxemic episodes and duration to fall but it was not significant. 6) In BB group, oxygen supplementation significantly increased the L-$SaO_2$ during sleep and also significantly decreased the frequency and duration of hypoxemic episode. From these results, we can see that oxygen supplementation during sleep can prevent the decrease in $SaO_2$ to some extent and that this effect of oxygen can be seen more prominently in the BB group.

• Tuberculosis and Respiratory Diseases
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• v.55 no.1
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• pp.88-97
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• 2003

Background : Although smoking is a major cause of chronic obstructive pulmonary disease (COPD), only 10-20% of cigarette smokers develop symptomatic COPD, which suggests the presence of genetic susceptibility. This genetic susceptibility to COPD might depend on variations in the activities of the enzyme that detoxify hazardous chemical products, such as microsomal epoxide hydrolase (mEPHX) and glutathione-S transferase M1 subunit (GSTM1) genes. Methods : The genotypes of 58 patients with COPD, and 79 age matched control subjects, were determined by a polymerase chain reaction, followed by restriction fragment length polymorphism (PCR-RFLP) for the mEPHX, and multiplex PCR for the GSTM1. Results : GSTM1 was deleted in 53.3% of the subjects. There was no difference in GSTM1 deletion rates between the COPD patients (32/58, 55.2%) and the control subjects (41/79, 51.9%). The combination patterns of two polymorphisms of mEPHX showed slow enzyme activity in 29(21.2%), normal in 73(53.3%) and fast in 32(23.4%). The COPD group (7/57, 12.3%) showed a significantly lower incidence of slow enzyme activity compared to the control subjects (22/77, 28.6%, p<0.05). However, when the COPD and control groups were compared with smokers only, there were no significant differences in the genotypes of GSTM1 and mEPHX. Conclusion : The genotypes of GSTM1 and mEPHX were not significant risk factors of COPD in this cohort of study.

• Tuberculosis and Respiratory Diseases
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• v.41 no.2
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• pp.111-119
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• 1994

Background: Because of the common etiologic factor, such as smoking, lung cancer and chronic obstructive pulmonary disease are often present in the same patient. The preoperative prediction of remaining pulmonary function after the resectional surgery is very important to prevent serious complication and postoperative respiratory failure. $^{99m}Tc$-MAA perfusion scan has been used for the prediction of postoperative pulmonary function, but it may be inaccurate in case of large V/Q mismatching. We compared $^{99m}Tc$-DTPA radioaerosol inhalation scan with $^{99m}Tc$-MAA perfusion scan in predicting postoperative lung function. Method: Preoperative inhalation scan and/or perfusion scan were performed and pulmonary function test were performed preoperatively and 2 month after operation. We predicted the postoperative pulmonary functions using the following equations. Postpneurnonectomy $FEV_1$=Preop $FEV_1x%$ of total function of lung to remain Postlobectomy $FEV_1$=Preop $FEV_1{\times}$(% of total 1-function of affected lung${\times}$$\frac{Number\;of\;segments\;to\;be\;resected}{Number\;of\;segments\;of\;affected\;lung})$ Results: 1) The inhalation scan showed good correlations between measured and predicted $FEV_1$, FVC and $FEF_{25-75%}$. (correlation coefficiency; 0.94, 0.91, 0.87 respectively). 2) The perfusion scan also showed good correlations between measured and predicted $FEV_1$, FVC and $FEF_{25-75%}$. (correlation coefficiency; 0.86, 0.72, 0.87 respectively). 3) Among three parameters, $FEV_1$ showed the best correlations in the prediction by lung scans. 4) Comparison between inhalation scan and perfusion scan in predicting pulmonary function did not show any significant differneces except FVC. Conclusion: The inhalation scan and perfusion scan are very useful in the prediction of postoperative lung function and don't make a difference in the prediction of pulmonary function a1though the former showed a better correlation in FVC.

• Tuberculosis and Respiratory Diseases
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• v.70 no.4
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• pp.293-300
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• 2011

Chronic obstructive pulmonary disease (COPD) is a substantially under-diagnosed disorder, and the diagnosis is usually delayed until the disease is advanced. However, the benefit of early diagnosis is not yet clear, and there are no guidelines in Korea for doing early diagnosis. This review highlights several issues regarding early diagnosis of COPD. On the basis of several lines of evidence, early diagnosis seems quite necessary and beneficial to patients. Early diagnosis can be approached by several methods, but it should be confirmed by quality-controlled spirometry. Compared with its potential benefit, the adverse effects of spirometry or pharmacotherapy appear relatively small. Although it is difficult to evaluate the benefit of early diagnosis by well-designed trials, several lines of evidence suggest that we should try to diagnose and manage patients with COPD at early stages of the disease.

• Journal of Chest Surgery
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• v.39 no.5 s.262
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• pp.354-358
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• 2006

Background: Pulsatile pumps for extracorporeal circulation have been known to be better for tissue perfusion than non-pulsatile pumps but be detrimental to blood corpuscles. This study is intended to examine the risks and benefits of $T-PLS^{TM}$ through the comparison of clinical effects of $T-PLS^{TM}$ (pulsatile pump) and $Bio-pump^{TM}$ (non-pulsatile pump) used for coronary bypass surgery. Material and Method: The comparison was made on 40 patients who had coronary bypass using $T-PLS^{TM}\;and\;Bio-pump^{TM}$ (20 patients for each) from April 2003 to June 2005. All of the surgeries were operated on pump beating coronary artery bypass graft using cardiopulmonary extra-corporeal circulation. Risk factors before surgery and the condition during surgery and the results were compared. Result: There was no significant difference in age, gender ratio, and risk factors before surgery such as history of diabetes, hypertension, smoking, obstructive pulmonary disease, coronary infarction, and renal failure between the two groups. Surgery duration, hours of heart-lung machine operation, used shunt and grafted coronary branch were little different between the two groups. The two groups had a similar level of systolic arterial pressure, diastolic arterial pressure and mean arterial pressure, but pulse pressure was measured higher in the group with $T-PLS^{TM}\;(46{\pm}15\;mmHg\;in\;T-PLS^{TM}\;vs\;35{\pm}13\;mmHg\;in\;Bio-pump^{TM},\;p<0.05)$. The $T-PLS^{TM}$-operated patients tended to produce more urine volume during surgery, but the difference was not statistically significant $(9.7{\pm}3.9\;cc/min\;in\;T-PLS^{TM}\;vs\;8.9{\pm}3.6\;cc/min\;in\;Bio-pump^{TM},\;p=0.20)$. There was no significant difference in mean duration of respirator usage and 24-hour blood loss after surgery between the two groups. Plasma free Hb was measured lower in the group with $T-PLS^{TM}\;(24.5{\pm}21.7\;mg/dL\;in\;T-PLS^{TM}\;versus\;46.8{\pm}23.0mg/dL\;in\;Bio-pump^{TM},\;p<0.05)$. There was no significant difference in coronary infarction, arrhythmia, renal failure and morbidity rate of cerebrovascular disease. There was a case of death after surgery (death rate of 5%) in the group tested with $T-PLS^{TM}$, but the death rate was not statistically significant. Conclusion: Coronary bypass was operated with $T-PLS^{TM}$ (Pulsatile flow pump) using a heart-lung machine. There was no unexpected event caused by mechanical error during surgery, and the clinical process of the surgery was the same as the surgery for which $Bio-pump^{TM}$ was used. In addition, $T-PLS^{TM}$ used surgery was found to be less detrimental to blood corpuscles than the pulsatile flow has been known to be. Authors of this study could confirm the safety of $T-PLS^{TM}$.

• Tuberculosis and Respiratory Diseases
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• v.39 no.6
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• pp.511-516
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• 1992

Background: It is well known that cigarette smoking is the risk factor of lung cancer, chronic obstructive pulmonary disease and ischemic heart disease. But there are few reports about the immediate effect of cigarette smoking on the cardiopulmonary functions. The serum level of carbon monoxide increases during cigarette smoking. It is known that carbon monoxide increases respration rate, heart rate and cardiac output, with decrease in maximal oxygen consumption. So we have studied to determine the immediate effects of cigarette smoking on the cardiopulmonary function during exercise. Method: Thirteen healthy smoking male subjects were included in this study. Each subject was undertaken pulmonary function test and incremental exercise test on two separate days, one without smoking (control) and the other after smoking three cigarettes per hour for five hours. The order of the two tests was randomized. Results: 1) The mean age of the subjects was $25{\pm}4.9$ year-old and the mean smoking history was $6{\pm}5$ pack years. 2) The mean blood level of carbon monoxide on the smoking day was higher than that on the nonsmoking day ($5.97{\pm}1.34%$ vs. $1.45{\pm}0.83%$; p<0.01). 3) The mean maximal oxygen consumption on the smoking day was lower than that on the nonsmoking day ($2.09{\pm}0.32$ L/min vs. $2.39{\pm}0.32$ L/min; p<0.05). 4) The mean anaerobic threshold on the smoking day was lower than that on the nonsmoking day ($1.33{\pm}0.24$ L/min vs. $1.53{\pm}0.20$ L/min; p<0.05). 5) The mean heart rate at rest on the smoking day was higher than that on nonsmoking day ($84.38{\pm}11.06$ beats/min vs. $75.46{\pm}5.83$ beats/min; p<0.05). But the means of maximal heart rate on both days were not different. 6) The pulmonary function tests were similar on both days. Conclusion: There was no change in pulmonary function test, but the maximal oxygen consumption and anaerobic threshold were decreased on the smoking day. So it was concluded that cigarette smoking impaired the cardiovascular functions immediately during exercise.

• Tuberculosis and Respiratory Diseases
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• v.44 no.3
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• pp.583-591
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• 1997

The functional derangement of skeletal muscles which may be attributed to chronic hypoxia has been accepted as a possible mechanism of exercise impairment in patients with chronic obstructive pulmonary disease (COPD). The metabolic changes in skeletal muscle in patients with COPD are characterized by impaired oxidative phosphorylation, early activation of anaerobic glycolysis and excessive lactate and hydrogen ion production with exercise. But the cause of exercise limitation in patients with chronic lung disease without hypoxia has not been known. In order to evaluate the change in the skeletal muscle metabolism as a possible cause of the exercise limitation in chronic lung disease patients without hypoxia, we compared the muscular metabolic data of seven male patients which had been derived from noninvasive $^{31}P$ magnetic resonance spectroscopy(MRS) with those of five age-matched normal male control persons. $^{31}P$ MRS was studied during the sustained isometric contraction of the dominant forearm flexor muscles up to the exhaustion state and the recovery period. Maximal voluntary contraction(MVC) force of the muscle was measured before the isometric exercise, and the 30% of MVC force was constantly loaded to each patient during the isometric exercise. There were no differences of intracellular pH (pHi) and inorganic phosphate/phosphocreatine(Pi/PCr) at baseline, exhaustion state and recovery period between two groups. But pHi during the exercise was lower in patients group than the control group (p < 0.05). Pi/PCr during the exercise did not show significant difference between two groups. These results suggest that the exercise limitation in chronic lung disease patients without hypoxia also could be attributed to the abnormalities in the skeletal muscle metabolism.

• Tuberculosis and Respiratory Diseases
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• v.50 no.4
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• pp.426-436
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• 2001

Background : Chronic obstructive pulmonary disease(COPD) is one of the major contributors to morbidity and mortality among the adult population. Cigarette smoking(CS) is undoubtedly the single most important factor in the pathogenesis of COPD. However, its mechanism is unclear. The current hypothesis regarding the pathogenesis of COPD postulates that an imbalance between proteases and antiproteases leads to the destructive changes in the lung parenchyma. This study had two aims. First, to evaluate the effect of CS exposure on histologic changes of the lung parenchyme, and second, to evaluate the effect of CS exposure on the expression of the gelatinolytic enzymes in BAL fluid cells in guinea pigs. Methods : Two groups of five guinea pigs were exposed to the whole smoke of 20 commercial cigarettes per day, 5 hours/day, 5 days/week, for 6weeks, and 12 weeks, respectively, using a smoking apparatus. Five age-matched guinea pigs exposed to room air were used as controls. Five or more sections were microscopically extamined(${\times}400$) and the number of cellular infiltration of the alveolar wall was measured in order to evaluate the effect of CS exposure on the histologic changes of lung parenchyme. The statistical significance was analyzed by a linear regression method. To evaluate the expression of the gelatinolytic enzymes in intraalveolar cells, BAL fluid was obtained and the intraalveolar cells were separated by centrifugation (500 g for 10 min at $4^{\circ}C$). Two sets of culture plates were loaded with $1{\times}10^6$ intraalveolar cells. One plate, contained O.1mM EDTA, a inhibitor of matrix metalloproteases(MMPs), and the other plate had no EDTA. Both plates were incubated for 48 hours at $37^{\circ}C$. After incubation, gelatinolytic protease expression in the supernatants was analyzed by gelatin zymography. Results : At the end of CS exposure, the level of blood carboxy Hb had increased significantly(4.1g/dl in control group, 24g/dl immediately after CS exposure, 18g/dl 30 min after CS exposure, 15g/dl 1 hour after CS exposure). Alveolar inflammatory cells were identified in the CS exposed guinea pigs. The number of alveolar cellular cells observed in a microscopic field ($400{\times}$) was $121.4{\pm}7.2$, $158.0{\pm}20.2$, $196.8{\pm}32.8$, in the control, the 6 weeks, and the 12 weeks group, respectively. The increased extent of inflammatory cellular infiltration of the lung parenchema showed a statistically significant linear relationship with the duration of CS exposure(p=0.001, $r^2=0.675$). Several types of gelatinolytic enzymes in the intraalveolar cells of CS exposed guinea pigs were expressed, of which some were inhibited by EDT A. However, the gelatinolytic enzymes were not expressed in the control groups. Conclusion : CS exposure increases inflammatory cellular infiltration of the alveolar wall and the expression of gelatinolytic proteases in guinea pigs. EDTA inhibits some of the gelatinolytic proteases. These findings suggest a possibility that CS exposure may increase MMP expression in the lungs of guinea pigs.