Five patients with variant angina showed alternating ST-segment elevation and contralateral ST-segment depression between the precordial and inferior leads in electrocardiographic recordings made during sequential anginal attacks. This electrocardrographic "seesaw" phenomenon was observed during ergonovine-induced attacks in 3 cases and during spontaneous attacks in I case. Another patient showed ST-segment elevation in a spontaneous attack and in other leads during hyperventilation. In all cases, the first attack was accompanied by ST-segment elevation in the inferior leads. Coronary arteriography demonstrated that in all cases, coronary arterial spasm occurred during the attacks in both coronary arterial systems. Significant organic coronary arterial stenoses (>50%) were found in both the left anterior descending branch and the right coronary artery in 2 patients. The remaining 3 patients showed no significant organic stenoses in any major coronary artery. However, pre-anginal coronary arteriography demonstrated that 13 of the 15 major coronary arteries, including all 9 of the major coronary arteries in the patients without significant stenoses, were already spastic. An exercise stress test performed in the morning induced attacks with chest pain and electrocardiographic ST-segment elevation in all 5 patients. The patients having an alternate ST-segment elevation in separate leads had vasospastic tendencies in both coronary arterial systems.

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The selective β₁ adrenoceptor agonist denopamine was studied for its effectiveness in abolishing active vasospastic angina in 10 patients without obstructive coronary artery stenosis. All patients had anginal attacks at least once a day during the 3-day placebo period. Denopamine, 40 mg/day, completely abolished the attacks in 7 patients (efficacy 70%). Denopamine reduced the mean daily number of anginal attacks and nitroglycerin consumption in comparison with placebo (0.56±1.23 vs 2.20±1.27; p<0.005 and 0.10±0.24 vs 1.60±1.93; p<0.05, respectively). Aggravation of anginal attacks was not seen in any patient. During placebo period, anginal attacks were provoked in 6 of the 10 patients who recieved exercise stress test, and in 6 of the 7 patients who recieved the cold pressor test in combination with hyperventilation. Denopamine pre-vented anginal attacks induced by exercise stress tests in 4 of the 6 patients (67%) and that induced by the cold pressor test in 4 of the 6 patients (67%). There were no severe adverse effects during denopamine therapy. These results suggest that 1) denopamine is a safe and effective medication for vasospastic angina; 2)β₁ adrenoceptors may play an important role in the prevention of coronary artery spasm.

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The relationship between the time required for reperfusion and the incidence of late potentials was studied in 94 patients who survived a first acute myocardial infarction (AMI) and who showed total occlusion of the infarct-related artery at an initial coronary arteriography. Sixty-three patients who successfully underwent direct percutaneous transluminal coronary angioplasty (PTCA), and 31 who were treated conventionally (controls), underwent signal-averaged electrocardiography. Direct PTCA patients were classified into 5 groups according to the time required for reperfusion: &lne; 4, 4-6, 6-8, 8-10, and &gne; 10 h. The incidence of late potentials in these groups was 8%, 12%, 14%, 33%, and 43%, respectively, and 48% in the controls. Late potentials were recorded more frequently as the period until successful reperfusion increased: the incidence of late potentials was significantly lower in the &lne;4 and 4-6 h groups than in the controls (p < 0.005 and p< 0.05, respectively). Therefore, reperfusion achieved within 6h reduced the incidence of late potentials in AMI patients and may be effective for preventing malignant ventricular arrhythmias.

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To predict exercise tolerance in the chronic phase of myocardial infarction (MI), cardiopulmonary exercise testing was performed using a ramp treadmill protocol in 25 patients at I and 3 months after the onset of MI. Oxygen uptake, heart rate and 02 pulse were estimated at rest, during a warm-up period, and at the levels of anaerobic threshold (AT), respiratory compensation (RC) and peak exercise. Results were as follows: 1) AT and peak oxygen uptake at 3 months after the onset of MI were 14.1±2.8 and 21.8±5.2 ml/min/Kg, respectively. 2) The subjects were divided into 2 groups according to peak oxygen uptake at 3 months: one showing peak oxygen uptake >22 ml/min/Kg and the other < 22 ml/min/Kg. The former group (n=13) was referred to as the good tolerance group, and the latter group (n=12)was referred to as the poor tolerance group. Oxygen uptake at AT, RC and peak exercise was lower in the poor tolerance group than in the good tolerance group (11.2 vs 14.7, 15.1 vs 20.4, 17.1 vs 23.4 ml/min/Kg, respectively). 3) The increases in oxygen uptake from AT to RC and from AT to peak exercise were less in the poor tolerance group than in the good tolerance group. 4) O₂ pulse at rest, warm-up, AT, RC and peak exercise were also lower in the poor tolerance group. It was concluded that AT, and the increases in the oxygen uptake from AT to RC, from AT to peak exercise at I month after MI, could be used to predict exercise tolerance in the chronic phase of MI.

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To evaluate the prognostic value of exercise-induced silent ST-segment depression, 157 patients who had suffered myocardial infarction underwent symptom-limited exercise testing and coronary angiography. Patients were divided into 3 groups according to the presence or absence of ischemic ST-segment depression and angina during exercise testing. Group A patients had ST-segment depression without angina. Group B patients had both ST-segment depression and angina. Group C patients had neither ST-segment depression nor angina. A11 patients were followed without coronary artery bypass graft or percutaneous transluminal coronary angioplasty for an average of 36 months and the frequency of coronary events (cardiac death, recurrent myocardial infarction and unstable angina pectoris) was compared. Group A patients had less severe coronary artery disease, greater coronary reserve during exercise and exercised longer than group B. However, the prognosis of group A was similar to group B, and was worse than group C. Using the Cox proportional hazards model, ischemic ST-segment depression was the most useful index for predicting future coronary events among the baseline values, coronary angiographic and exercise testing variables. However, angina during exercise testing was not an independent predictor. Thus, post-infarction patients showing exercise-induced ST-segment depression should be treated carefully regardless of the presence or absence of angina.

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The purpose of this study was to objectively assess exercise tolerance before and after cardiac valve surgery by using an objectively determined ventilatory anaerobic threshold (AT). Nine patients (mean age: 38.2±8.1 years) with predominantly mitral regurgitant lesions were studied by a symptomatic maximal treadmill exercise test which included a determination of AT. The mean lengths of time from preoperative exercise testing to cardiac surgery, and from surgery to postoperative exercise testing were 5.9±4.0 and 12.1±8.3 months, respectively. The determination of AT on data plots was performed after blinding to patient identification and pre- vs postoperative status. After surgery, the clinical symptoms and NYHA class improved significantly with a decrease in the cardio-thoracic ratio and echocardiographic diastolic dimensions. The mean peak VO₂ (ml/kg/min) increased significantly from 20.2±7.1 to 29.7±7.9 (p<0.01). Together with these changes, AT (ml/kg/min in VO₂) increased from a mean of 14.8±4.8 to 22.8±5.5 (p<0.01). In conclusion, symptomatic improvement and an increase in peak oxygen uptake after cardiac valve surgery were accompanied by a significant increase in the objectively determined AT. AT determined in a blind manner provides an objective means of evaluating exercise tolerance when a double-blind intervention cannot be performed.

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We attempted nonpharmacologic treatment for common atrial flutter in 7 patients, with direct current catheter ablation (CA) in 5 cases and cryoablation in 2 cases under the guidance of transient entrainment. Transient entrainment during common atrial flutter by pacing from the mid or low lateral right atrium (LLRA) revealed a long conduction time between the LLRA and the orifice of the coronary sinus (CSo) (73% to 121% of flutter cycle length). In 2 cases, fragmented electrograms were recorded at the low right atrial septum with durations of 150 msec and 155 msec, respectively. Because these fragmented electrograms were transiently entrained by rapid atrial pacing in the same manner as other atrial electrograms and were recorded in an area of long conduction, we believe that fragmented electrograms represent critical slow conduction. In 5 cases, CA was directed at this area. Three cases were successfully treated with 3 to 4 DC shocks of 100 J (follow up periods of 11.3, 4.5 and 3 months). Two cases which received I to 2 DC shocks of 100 J had recurrence of atrial flutter 6 and 4.7 months later, respectively. Two cases which showed atrial septal defect received surgical treatment. They were successfully treated with extended cryoablation in this same area (follow up periods of 26 and 9.2 months). In conclusion, extended ablation of an area of fragmented electrograms using transient entrainment may be an effective treatment for common atrial flutter.

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We investigated the roles of the endothelium in the hypoxic responses of the isolated main pulmonary artery (PA) in the rat. Hypoxia was induced by gas-sing an organ chamber with 95% N₂+5% CO₂ (P02=34.6±3.1 Torr) instead of 16% O₂+5% CO₂+balance N2 (PO₂=92.8±3.0 Torr). Vascular rings were precontracted with 2×10^-8 M phenylephrine. A transient hypoxic contraction and a subsequent relaxation were observed in the endothelium-intact rings. The hypoxic contraction was reduced in the endothelium-denuded rings. In contrast, there were no significant differences between the hypoxic relaxation in the endothelium-intact and endothelium-denuded rings. Inhibitors of endothelium-derived relaxing factor (EDRF) activity, 2×10^-6 M N^G-monomethyl-L-arginine (L-NMMA) and 10^-6 M methylene blue, produced 53% and 66% reductions in hypoxic contraction, respectively, Furthermore, the amount of cyclic GMP in the endothelium-intact PA rings which had been precontracted with phenylephrine decreased from 2. 10±0.45 pmol/mg protein during normoxia to 0.90±0.18 pmol/mg protein during hypoxia. Indomethacin and OKY-046 did not influence hypoxic contraction or relaxation. These results suggest that hypoxic contraction of the isolated pulmonary artery in the rat is partially induced by inhibition of the release of EDRF.

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Maximum deactivation of the contractile elements using Ca^lt;2+> minimizes oxygen requirements during global ischemia, Ca^lt;2+> antagonists and Ca^lt;2+>-free cardioplegia solutions are methods by which the Ca^lt;2+> flux can be manipulated. This study was performed with 5 experimental groups: 1) Standard cardioplegia (with Ca^lt;2+>), 2) Ca^lt;2+>-free cardioplegia, 3) Ca^lt;2+>-free cardioplegia plus verapamil (0.5 mg/L), 4) Verapamil cardioplegia (with Ca^lt;2+>), and 5) Ca^lt;2+>-free cardioplegia, in which verapamil was administered at the onset of reperfusion (0.5 mg/L). Cardiac functions, heart rate, edema formation, and creatine kinase concentration were measured before and after 70 min of ischemia at a myocardial temperature of 20 °C. Ca^lt;2+>-free cardioplegia may be beneficial under hypothermic conditions, but the " Ca^lt;2+> paradox" was still a matter of concern. Reperfusion with verapamil did not protect from reperfusion-related injuries. However, the use of verapamil provided more protection than did standard or Ca^lt;2+>-free cardioplegic solutions. Since verapamil did not maintain membrane integrity during ischemia when combined with Ca^lt;2+>-free cardioplegic solutions (prominent edema formation was observed), its combination with Ca^lt;2+> containing cardioplegic solutions is recommended.

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A 42-year-old female with cardiomegaly showed bradycardia without syncope. Clinical data showed that she had an isolated levocardia with interruption of the inferior vena cava. Isolated levocardia was defined as a normally placed heart associated with situs ambiguus of other viscera. She did not have intracardiac anomalies. Isolated levocardia without intracardiac anomalies, as in this case, has only been reported in 13 other cases. Isolated levocardia is often accompanied by severe complex intracardiac anomalies and, therefore, most of the patients have a short life span. Situs ambiguus, especially left isomerism, is frequently associated with deteriorated sinus node function, and an interruption of the inferior vena cava may also be an indication of this phenomenon. Therefore, the patient's sinus node function was examined using an electrophysiological study and a 24-hour ambulatory electrocardiogram. Sick sinus syndrome was finally confirmed.

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