The ratio of arterial oxygen tension to inspired oxygen fraction (PaO₂ / FiO₂) is a useful indicator for weaning patients from mechanical ventilation and a reliable predictor of pulmonary dysfunction after cardiac surgery. The aim of this study was to elucidate the patient characteristics and variables that affect the PaO₂ / FiO₂ ratio.
Between 1994-1998, 167 patients who underwent coronary artery bypass grafting (CABG) were examined retrospectively. Spearman's correlation coefficients were calculated between the PaO₂ / FiO₂ ratio and intubation period, and length of ICU stay. Patients were then divided into two groups with a PaO₂ / FiO₂ ratio < 350 and PaO₂ / FiO₂ ratio 350. Univariate analysis of the putative risk factors was performed. A logistic regression model was developed to evaluate factors that would influence the PaO₂ / FiO₂ ratio.
A significant correlation was observed between the PaO₂ / FiO₂ ratio and intubation period, and length of ICU stay. Univariate predictors of a PaO₂ / FiO₂ ratio < 350 were low body weight, low preoperative PaO₂, long operation time, high FiO₂, low postoperative PaO₂, history of smoking, hypertension and opening of pleura (p < 0.05). Excellent prediction was found with a model consisting of preoperative PaO₂ and hypertension.
Conclusion: The results of this study suggest that patients with a low preoperative PaO₂ or hypertension may need more careful peri- and postoperative management since these factors are closely associated with the PaO₂ / FiO₂ ratio.

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The aim of this study was to determine the indication for minimally invasive direct coronary artery surgery based on the operative and long-term results of conventional coronary artery bypass grafting with cardiopulmonary bypass. Operative results: The subjects included 505 patients who underwent isolated elective coronary artery bypass grafting with cardiopulmonary bypass from January 1995 through August 1999. The mean age at the time of surgery was 61.9 and the mean number of grafts per patient was 2.6. Long-term results: From January 1984 to December 1995, a total of 907 patients received coronary artery bypass grafting with cardiopulmonary bypass using the internal thoracic artery to the left anterior descending artery with or without saphenous vein grafts to other coronary arteries. The rates of complete and incomplete revascularization were 69.3% (n = 629) and 30.7% (n = 278), respectively. Mean follow-up was 5.95 ± 3.0 years. The operative results revealed low output syndrome occurred in 14 patients (2.8%), perioperative myocardial infarction with the appearance of new Q-waves in 5 (1.0%), renal failure requiring transient dialysis in 16 (3.2%), stroke with persistent sequelae in 5 (1.0%), and mediastinitis in 5 (1.0%). Two patients (0.4%) died in the hospital. The long-term results for the 907 patients revealed the 10-year actuarial survival, 10-year cardiac death free, and 10-year cardiac event free rates were 85.7%, 94.1%, and 77.3%, respectively. The 10-year survival rates was 88.4% among patients receiving complete revascularization and 79.3% among those receiving incomplete revascularization (p = 0.0334). The 10-year cardiac death free rate among patients undergoing complete revascularization was 96.3% and 88.7% among those receiving incomplete revascularization (p = 0.0016). The 10-year cardiac event free rates were 82.3% and 67.9% among patients undergoing complete and incomplete revascularization, respectively (p = 0.0118). In view of the favorable operative and long-term results of conventional coronary artery bypass grafting, especially complete revascularization, we conclude that minimally invasive direct coronary artery grafting is an appropriate treatment for multi-vessel disease in carefully selected patients at a high risk for stroke and major comorbidities due to old age.

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The purpose of this study was to investigate the diurnal variation and chronotype differences, i.e., in morning-types and evening-types, in post-exercise vagal reactivation. Twelve healthy male college students who were classified as morning-type (6) and evening-type (6), based on responses to a questionnaire, participated in this study. Post-exercise vagal reactivation was assessed as the time constant of the beat-by-beat heart rate decrease for the first 30 sec after exercise (T₃₀) at an intensity lower than the ventilatory threshold. The subjects performed 3-min cycle ergometer exercise at an intensity corresponding to 80 % of the ventilatory threshold after a 1 min warm-up exercise in the morning (7:00 - 8:00) and evening (17:00 - 18:00) to obtain the T₃₀. A significant interaction (chronotype-by-time) effect was found for T₃₀. The morning value of the T₃₀ in evening-type subjects was significantly larger than their evening value and the morning value in morning-type subjects. There was no significant interaction effect for heart rate and oxygen uptake during exercise. These results suggest that diurnal variation in post-exercise vagal reactivation is different between morning-type and evening-type, and post-exercise vagal reactivation in evening-type individuals is sluggish in the morning.

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Although early total corrective repair for cyanotic tetralogy of Fallot is now safely performed at many institutions, long-term complications after surgical repair have been demonstrated. Therefore, the optimal procedure and timing for surgical treatment remain controversial. In the present study, we conducted a quantitative analysis of the hypertrophy of all four chambers of 87 autopsied hearts of cyanotic tetralogy of Fallot and 71 normal control hearts utilizing the myocardial mass index, and evaluated the progression of lesions with advancing age. In cyanotic tetralogy of Fallot, hypertrophy of the right ventricle progresses immediately after birth, with that of the right atrium developing soon after. The left side of the heart is normal or slightly atrophied which could be corrected by sufficient palliative intervention or total corrective repair. The growth curves of both ventricles were parallel to those of normal hearts for the period studied. Pulmonary atresia, palliative operation, and total corrective repair have been shown to have some influence on the morphological characteristics of hearts of cyanotic tetralogy of Fallot.

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The purpose of this study was to compare the safety and tolerability of recommended initial doses of fosinopril (FOS) with those of captopril (CAP), in diuretic-treated, salt depleted “high risk” patients with congestive heart failure. Thirty patients were randomized in a double blind fashion to receive a single dose of either FOS 10 mg, CAP 6.25 mg or placebo. CAP produced a significant early and brief fall in BP, while the first-dose hypotensive response with FOS did not differ significantly from placebo. Baseline plasma angiotensin converting enzyme (ACE) activity was similar in all groups. Only CAP showed an acute and significant fall in plasma ACE activity, whereas FOS and placebo did not change ACE activity. There was no correlation between mean arterial pressure or percentile change in mean arterial pressure and plasma ACE activity. Also no correlation was found between high or low ACE activity level and first dose hypotension. The practical importance of the results are: For patients with congestive heart failure, FOS and CAP have different effects on BP after the first dose, and this effect may be dependent on the plasma ACE activity level. FOS produces ACE inhibition and BP changes similar to placebo so it is the safer choice for the treatment of congestive heart failure.

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The aim of the present study was to investigate whether clinical doses of propofol and thiamylal affect oxygen free radical production and intracellular calcium concentration ([Ca²⁺]_i) in the post-ischemic reperfused heart. Forty-eight rat hearts were perfused with a Langendorff system and loaded with Fura-2 / AM as a [Ca²⁺]_i marker. The hearts were divided into 6 groups as follows (each group: n = 8); Group S (saline), Group TL (thiamylal 100 μM), Group TH (thiamylal 300 μM), Group I (Intralipid), Group PL (propofol 3 μM), and Group PH (propofol 10 μM). All hearts were initially perfused for 5 min as control aerobic perfusion. Afterwards, no-flow ischemia was induced for 15 min, followed by reperfusion for 20 min. The formation of hydroxyl radicals in the coronary effluent was measured with high performance liquid chromatography using salicylic acid. At the beginning of the ischemia and reperfusion periods, increases in systolic and diastolic [Ca²⁺]_i were observed in all groups except Group TH. The high dose of thiamylal significantly suppressed this initial increase in cytosolic [Ca²⁺] _i (Group S 1.30 ± 0.15; Group TL 0.99 ± 0.17; Group TH 0.70 ± 0.09, at 1 min after reperfusion; systolic [Ca²⁺]_i : p < 0.05). Total DHBAs in the coronary effluent of all groups increased significantly 1 min after reperfusion, however, there were no significant differences among the groups. Clinical doses of propofol had no significant effect on myocardial function and [Ca²⁺] _i before and after ischemia, whereas thiamylal suppressed the increase in [Ca²⁺]_i during ischemia and reperfusion. However, free radical formation during reperfusion was unaffected by thiamylal and propofol.

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The transient outward currents (I_to) play an important role in action potential repolarization in cardiac myocytes. Two components of I_to have been identified as 4-AP-sensitive but Ca²⁺-insensitive I_to carried by K⁺, and Ca²⁺-sensitive but 4-AP insensitive I_to carried by Cl^- (I_{Cl (Ca)}). It is known that the amplitudes of I_to change depending on the stimulation frequency. In this study we investigated the beat dependent alteration of ICl (Ca) during rapid stimulation using the whole cell patch clamp technique in rabbit ventricular myocytes. The cells were internally perfused with a solution containing 0.1 mM free Ca²⁺ to develop I_{Cl (Ca)} and all internal K⁺ was replaced with Cs⁺ to block 4-AP-sensitive I_to and other K⁺ currents. By applying depolarizing pulses at a high frequency of 2.5 Hz, the amplitudes of I_{Cl (Ca)} gradually increased as the number of pulses increased following a transient decrease in the 2nd pulse and reached a plateau level at the 20th pulse. The shape of the current-voltage curve of I_{Cl (Ca)} was not overly different for different numbers of preceding pulses. The recovery from inactivation of I_{Cl (Ca)}could be fitted to a single expon-ential curve and full recovery was achieved after > 1 sec with a time constant of 368 ms. The ramp clamp experiments showed that the conductance of the background I_{Cl (Ca)} increased with the preceding pulse numbers, indicating that the resting level of [Ca²⁺]_i increased with the pulses applied. From these results, we conclude that beat dependent alteration of ICl (Ca) is determined by not only its apparent kinetic property, but also the resting level of [Ca²⁺]_i during rapid stimulation.

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The purpose of this study was to investigate the effects of the non-specific growth factor inhibitor suramin on smooth muscle cell proliferation in vitro and in vivo. Cultured vascular smooth muscle cells (VSMC) were stimulated by platelet-derived growth factor (PDGF) and cellular DNA synthesis assessed by [³H]-thymidine uptake. Suramin dose-dependently inhibited DNA synthesis in VSMC, and 100 mM of suramin completely suppressed the PDGF-AB-induced cellular DNA synthesis. Rabbit carotid arteries were injured by the balloon catheter, and then suramin locally delivered using a porous balloon catheter over ten minutes. Three weeks after the vascular injury, the extent of intimal thickening was compared between the suramin-treated and control rabbits. The neointimal formation triggered by balloon-mediated vascular injury was suppressed significantly and dose-dependently by locally infused suramin, and the intima to media area ratios of the control and 1 mM suramin-treated animals were 48.8 ± 14.9 and 12.2 ± 6.0 %, respectively (p < 0.01. n = 6 for each group). These results suggest that one time local administration of suramin was sufficient to suppress neointimal formation after balloon-mediated vascular injury, and that pharmacological intervention targeting the growth factor's signaling pathways could be a promising approach to prevent smooth muscle cell proliferation in various proliferative vascular diseases.

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The aim of the present retrospective study was to clarify the histopathologic substrates of left ventricular myocardium with transient asynergy due to acute ischemic insult in man.
Three patients who had had prolonged chest pain, new abnormal Q waves and new ST segment elevation were studied. There was no significant elevation of serum creatine phosphokinase activity in two of the three patients. Echocardiograms on admission or the next day showed severe hypokinetic or akinetic motion and thinning of the anteroseptal and apical portions of the left ventricle and regional dilatation of the same portions. Disappearance of the abnormal Q waves, ST segment elevation resolution, and early T wave inversion were observed later. Complete improvement of the echocardiographic abnormalities was confirmed after a few weeks in all patients.
Manifest ischemic lesions of subendocardial scars of the anteroseptal region of the left ventricle were detected in only one of the three cases by gross examination. However, on microscopic examination, islands of necrotic myocytes were interspersed with islands of viable cells throughout the jeopardized region in one case, although the scattered necrotic foci were restricted to the subendocardium and the trabeculae. Normal myocardium and subendocardial scars were observed in the other two cases.
In conclusion, left ventricular myocardium with transient asynergy, detected clinically during acute ischemic attack, consists of normal myocardium or small ischemic lesions primarily in the subendocardium.

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A 74-year-old Japanese male was referred to our hospital because of an abnormal electrocardiogram. The electrocardiogram revealed tall P waves in leads II, III, and aV_F. Echocardiography disclosed hypokinesis extending from the anteroseptal region to the apex. Iodine-123 15-(p-iodophenyl)-3-(R,S)-methylpentadecanoic acid (¹²³I-BMIPP) scintigraphy revealed reduced uptake from the anteroseptal region to the apex. Coronary arteriography demonstrated diffuse dilatation of the right and left coronary arteries without organic stenosis, and left ventriculography showed hypokinesis at the same area. Furthermore, the coronary flow reserve in the left anterior descending artery was decreased. He was treated with an antiplatelet agent. Ten months later, the left ventriculography, ¹²³I-BMIPP scintigraphy findings and coronary flow reserve were normalized. These findings demonstrate that antiplatelet therapy may be useful in the preservation of left ventricular function in patients with coronary artery ectasia.

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A 65-year-old Japanese woman with dilated cardiomyopathy, hypothyroidism and refractory sustained ventricular tachycardia experienced a near-death hypoglycemic syncope. The attack seemed to be induced by a high level of serum insulin, probably due to cibenzoline and by concomitant use of an angiotensin converting enzyme inhibitor (ACEI). Additionally, decreased food intake because of a severe toothache may have contributed to the deterioration of her condition. This case warns cardiologists that a combined cibenzoline and ACEI therapy can provoke serious adverse effects such as hypoglycemic syncope in the elderly. Therefore, the possibility of a hypoglycemic attack associated with these drugs should be explained to patients who are in poor condition.

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Acute infective endocarditis affecting the aortic root and valve associated with development of a fistulous communication between the aorta and pulmonary artery was presented in a young Turkish girl. Emergency surgery was required. Operation consisted initially of closure of the defect on the main pulmonary artery with a pericardial patch. This was followed by allograft aortic root replacement.

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A 53-year-old woman was hospitalized for general fatigue and palpitations. An electrocardiogram showed ST elevation and T wave inversion in leads II, III, aVF, and V4~6. Cardiac catheterization was performed since the echocardiogram demonstrated the existence of a left ventricular apical aneurysm. Left ventriculography showed an aneurysm of the apex. An endomyocardial biopsy specimen from the left ventricular apical wall demonstrated typical noncaseating granulomas with giant cells. The patient was diagnosed as having cardiac sarcoidosis. There was no evidence suggesting involvement of other systemic organs. Cardiac sarcoidosis should be considered within a spectrum of diseases that cause left ventricular aneurysm.

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