• Journal of Yeungnam Medical Science
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• v.7 no.1
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• pp.61-68
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• 1990

To assess the role of multiple factors in influencing occurrence of ventricular premature complexes after acute myocardial infarction twenty-four hour Holter electrocardiographic tape recording were made in 40 survivors of an acute myocardial infarction 10 to 20 days after attack. Ventricular premature complexes were found in 72.5percent of the patients. The incidence and grade of ventricular premature complexes in the early postinfarction period were not correlated with left ventricular function, age, sex, smoking, dibetes mellitus, previous angina, and previous myocardial infarction. The occurrence of ventricular premature complexes showed a positive correlation with the occurrence of ST-T change. The occurrence of ventricular premature complexes during sleep hours was compared to the awake state. In 22 patients. the incidence of ventricular premature complexes was reduced during sleep. If patients free of ectopic activity during 24-hour monitoring sessions are excluded from analysis, the 22 of patients, or in 76percent, sleep was associated with a lowered occurrence of ventricular extrasystoles.

• Journal of Yeungnam Medical Science
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• v.11 no.1
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• pp.186-192
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• 1994

Amiodarone has a potent suppressive effect on supraventricular and ventricular dysrhythmias, so has widely used as a class III antiarrhythmic agent. However, significant side effects were noted in over 50% of patients treated. Pulmonary toxicity represents the most serious adverse raeaction limiting the clinical efficacy of this new antidysrhythmic drug. A 66-year-old male had received amiodarone 200mg/day for 7 months to control high grade ventricular premature contraction and was admitted due to dyspnea on exertion for 1 week. At the time of admission end-inspiratory crepitant rale was heard on auscultation. The roentgenogram of his chest revealed reticular and granular radioopaque densities on both lower lung fields and high resonance CT revealed interstitial fibrosis and pneumonic consolidations on the periphery of the both middle and lower lobes. Trans-bronchoscopic lung biopsy revealed nonspecific intersitial fibrosis. The laboratory findings were non-specific. We present a case of amiodarone-induced interstitial pulmonary disease clinically improved by cortico-steroid therapy.

• Journal of Chest Surgery
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• v.29 no.1
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• pp.1-6
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• 1996

We developed an experimental model of brain death using dogs. Brain death was induced by increasing the intracranial pressure (ICP) gradually by continuous Infusion of saline through an epidural Foley catheter in 5 mongrel dogs (weight, 18~22kg). Hemodynamic and electrocardiographic changes were evaluated continuously during the process of brain death and obtained the following results. 1. The average volume and time required to induce brain death was 4.8$\pm$1.0ml and 143.0$\pm$30.9minutes respectively. 2. There was a steady rise of the ICP after starting the constant infusion of saline, and ICP rised continuously until the brain death (122.0$\pm$62.5mmHg). After reaching to the maximal value (125.0$\pm$47.7mmHg) at 30 minutes after brain death, the ICP dropped and remained approximately constant at the slightly higher level than the mean arterial pressure (MAP). 3. MAP showed no change until the establishment of brain death and it declined gradually. The peak heart rate reached to 172.6$\pm$35.3/min at 30 minutes after the brain death. 4. Even though the body temperature and all hemodynamic variables, such as cardiac output, mean pulmonary arterial pressure, left ventricular (LV) end-diastolic pressure and LV maximum + dp/dt, were slightly greater than those of basal state, at the point of brain death, there was no statistically significant change during t e process of brain death. 5. There was no remarkable arrhythmias during the experiment except ventricular premature beats which was observed transiently in one dog at the time of brain death. Hemodynamic changes in the brain death model induced by gradual ICP increment were inconspicuous, and arrhythmias were rarely seen. Hyperdynamic state, which was observed at the point of brain death in another brain death model caused by abrupt ICP increase, was not observed.

• Tuberculosis and Respiratory Diseases
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• v.45 no.1
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• pp.153-168
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• 1998

Background: The existing data indicate that obstructive sleep apnea syndrome contributes to the development of cardiovascular dysfunction such as systemic hypertension and cardiac arrhythmias, and the cardiovascular dysfunction has a major effect on high long-term mortality rate in obstructive sleep apnea syndrome patients. To a large extent the various studies have helped to clarify the pathophysiology of obstructive sleep apnea, but many basic questions still remain unanswered. Methods: In this study, the influence of obstructive sleep apnea on systemic blood pressure, cardiac rhythm and urinary catecholamines concentration was evaluated. Over-night polysomnography, 24-hour ambulatory blood pressure and ECG monitoring, and measurement of urinary catecholamines, norepinephrine (UNE) and epinephrine (UEP), during waking and sleep were undertaken in obstructive sleep apnea syndrome patients group (OSAS, n=29) and control group (Control, n=25). Results: 1) In OSAS and Control, UNE and UEP concentrations during sleep were significantly lower than during waking (P<0.01). In UNE concentrations during sleep, OSAS showed higher levels compare to Control (P<0.05). 2) In OSAS, there was a increasing tendency of the number of non-dipper of nocturnal blood pressure compare to Control (P=0.089). 3) In both group (n=54), mean systolic blood pressure during waking and sleep showed significant correlation with polysomnographic data including apnea index (AI), apnea-hypopnea index (AHI), arterial oxygen saturation nadir ($SaO_2$ nadir) and degree of oxygen desaturation (DOD). And UNE concentrations during sleep were correlated with AI, AHI, $SaO_2$ nadir, DOD and mean diastolic blood pressure during sleep. 4) In OSAS with AI>20 (n==14), there was a significant difference of heart rates before, during and after apneic events (P<0.01), and these changes of heart rates were correlated with the duration of apnea (P<0.01). The difference of heart rates between apneic and postapneic period (${\Delta}HR$) was significantly correlated with the difference of arterial oxygen saturation between before and after apneic event (${\Delta}SaO_2$) (r=0.223, P<0.001). 5) There was no significant difference in the incidence of cardiac arrhythmias between OSAS and Control In Control, the incidence of ventricular ectopy during sleep was significantly lower than during waking. But in OSAS, there was no difference between during waking and sleep. Conclusion : These results suggested that recurrent hypoxia and arousals from sleep in patients with obstructive sleep apnea syndrome may increase sympathetic nervous system activity, and recurrent hypoxia and increased sympathetic nervous system activity could contribute to the development of cardiovascular dysfunction including the changes of systemic blood pressure and cardiac function.

• Journal of Yeungnam Medical Science
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• v.6 no.1
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• pp.99-107
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• 1989

24-hour ambulatory ECG monitoring has been examined for the evaluation of heart rate and longest pause in 34 patients with chronic atrial fibrillation(20 patients treated with digoxin and 14 patients without treatment). Following results were obtained : 1. In 34 patients, the mean of average heart rates was $75.7{\pm}13.8$/minute, fastest heart rates $148.0{\pm}32.4$/minute, slowest heart rates $48.1{\pm}8.4$/minute, difference between fastest and slowest heart rates in individual patients $99.9{\pm}29.0$/minute and longest pauses $2.95{\pm}1.06$seconds. The longest pauses of more than 4.0 seconds occurred in 4 of the 34 patients and made an exeption of comparison groups. 2. In 27 of the 34 patients, ventricular premature contractures were developed and in 11 of 27, mainly occured less than 100/24 hours and aberrant conduction occurred in all patients. 3. In 20 patients treated with digoxin(0.25mg/day), the mean of average heart rates was $78.4{\pm}13.7$/minute, fastest heart rates $152.5{\pm}33.1$/minute, slowest heart rates $48.9{\pm}8.5$/minute, difference between fastest and slowest heart rates in individual patients $103.6{\pm}31.7$/minute and longest pauses $2.55{\pm}0.50$seconds. 4. In 10 patients without treatment, the mean of average heart rates was $78.0{\pm}10.7$/minute, fastest heart rates $154.5{\pm}26.8$/minute, slowest heart rates $50.6{\pm}7.1$/minute, difference between fastest and slowest heart rates in individual patients $103.9{\pm}22.2$/minute and longest pauses $2.66{\pm}0.39$seconds. 5. The difference of heart rates and longest pauses between patients with treatment and without treatment were statistically not significant(P>0.05). In summary, authors seemed to consider that 24-hour ambulatory ECG was useful and safe method for clinical evaluation of patients with chronic atrial fibrillation.