To determine the number of days required to obtain 75% suppression of ventricular premature contractions (VPCs) by antiarrhythmic agents, which was expressed as t_1/4, we performed 32 in-hospital continuous all day EGG monitoring trials in four groups of 28 symptomatic patients (ages; 54±20 yearsold) with frequent VPCs. Nine patients had no organic heart disease (group 1, 11 trials), nine had valvular heart disease (group 2, 10 trials), three had dilated cardiomyopathy (group 3, 3 trials) and seven had myocardial infarction within two to four weeks onset (group 4, 8 trials). All patients were monitored by ECG telemetry with an arrhythmia analyzer, which could count hourly and daily VPCs. Class I antiarrhythmic agents were given in 18 trials, class II in two trials and class I+ class II in 12 trials. Plasma concentrations of the antiarrhythmic agents were monitored in 11 trials.
In 21 trials, t1/4 could be obtained; ten (91%), six (60%), three (100%) and two trials (25%) in the four groups, respectively (p<0.05). The value of t1/4 in the four groups was 6±6, 7±6, 14±11 and 13±2 days, respectively (mean 8±7 days; N.S.). Immediate response to the initial antiarrhythmic agent administration, expressed as percent VPC count after three hours, correlated significantly with t1/4 (r=0.696, p=0.0006), but ejection fraction, patient's age, control VPC counts or plasma antiarrhythmic agent level did not correlate with t1/4. In conclusion, t1/4 is a useful index for the evaluation of VPC suppression, revealing wide interindividual variations and can be roughly estimated from the immediate response to the initial antiarrhythmic agent administration.

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Electrophysiologic study (EPS) was performed in 68 consecutive patients with nonsustained ventricular tachycardia (VT) detected by ambulatory monitoring. The study group consisted of 11 patients with coronary artery disease, 11 patients with idiopathic cardiomyopathy or myocarditis, 2 patients with valvular heart disease, 1 patient with post atrial septal defect repair and 43 patients with a normal heart. Syncope or presyncope was found in 34 percent of these patients. EPS was performed after all antiarrhythmic drugs were withdrawn for more than 5 days. Nonsustained VT, sustained VT, and ventricular fibrillation were induced in 21%, 4%, and 4% respectively.
VT was induced more frequently in patients with organic heart diseases but it was not related to the history of syncope. Ejection fraction in the inducible patients was not different from that of the noninducible patients. During the mean follow up period of 31 months, there was no cardiac death. The results suggest that the prognosis of patients with nonsustained VT is good and the clinical significance of their EPS findings seems to be limited.

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Three ventricular inhibited mode (VVI) pacemaker implanted patients, all above 65 years, female and having sick sinus syndrome suffered from torsades de pointes; one patient after 2.5 years and the other two patients within a day of disopyramide therapy. All had hypopotassemia and plasma disopyramide was below the therapeutic range in two patients. Torsades de pointes was induced following ventricular paced beats and suppressed by cessation of disopyramide in all or by setting a higher pacing rate in one. In our department, permanent VVI pacemakers were implanted in 43 patients with sick sinus syndrome including 26 with bradycardia-tachycardia syndrome, nine of whom were treated by disopyramide. Torsades de pointes was observed only in those disopyramide treated bradycardia-tachycardia patients. Our report stresses the proarrhythmic nature of combined VVI pacing and antiarrhythmic agents in the presence of hypopotassemia.

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To evaluate prolonged diastolic dysfunction in acute coronary syndrome, mitral inflow velocities and left ventricular wall motion were examined with pulsed-wave Doppler and two-dimensional echocardiography in 14 patients with successful reperfusion, 8 patients without reperfusion after acute myocardial infarction, and in 10 patients with prolonged angina. Early peak flow velocity and the ratio of early to atrial peak flow velocity increased gradually both after the onset of acute myocardial infarction with reperfusion and cessation of angina pectoris. However, in acute myocardial infarction without reperfusion, early peak flow velocity and the ratio of early to atrial peak flow velocity decreased significantly. Atrial peak flow velocity remained unchanged in acute myocardial infarction with reperfusion, while it was decreased in angina pectoris on the seventh day. Regional systolic dysfunction abated gradually in acute myocardial infarction with successful reperfusion, and regional systolic dysfunction was not detected in angina pectoris on the third day. Thus, abnormalities in left ventricular early diastolic filling persisted for several days after reperfusion in acute myocardial infarction or cessation of angina. Left ventricular late filling remained unchanged in acute myocardial infarction, whereas, in angina pectoris, a compensatory increase in late filling diminished gradually with an increase in early filling. These results indicate that there are different types of recovery process after diastolic filling abnormalities in patients with acute coronary syndrome.

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Catheter ablation in ventricular tachycardia has achieved only limited success using direct current (DC) and radiofrequency (RF) energy, due to either high complication rates or a limited lesion size. Microwave energy represents a possible alternative source of energy for percutaneous ablation of the ventricular myocardium. However, an optimal method for titration of the dose of microwave energy to achieve the desired lesion volume has not yet been established. The safety and efficacy of microwave ablation of the atrioventricular (AV) junction were studied in 11 dogs in vivo. The relationship between lesion size following microwave ablation and the power output of or exposure duration to microwave energy was also examined at disparate sites in each superfused left ventricular epicardium in vitro. To observe the pathologic changes in the myocardium after microwave ablation, microwave ablation of the endocardium of the left ventricle was carried out in 9 dogs in vivo. Complete AV block was achieved in 10 of the above 11 dogs with a mean of 5 applications of microwave energy. The lesion volume in vitro demonstrated a parallel increase with power (r=0.76) and duration (r=0.81). The mean lesion volume at 30sec was: at 10W, 0.8±1.6; 20W, 34.7±10.3; 30W, 34.7±22.4: 40W, 64.7±64.4; 50W, 87.2±42.3; 60W, 85.8±38.1; 70W, 124.7±36.5; 80W, 134.2±49.0mm³. The mean lesion volume at 80W was: at 15sec, 32.6±37.8; 30sec, 101.2±46.4; 60sec, 180.6±80.1; 120sec, 291.8±122.7; and 180sec, 459.3±204.6mm³. The ablated lesions showed discrete, homogeneous coagulation necrosis with sharp margins from the adjacent normal myocardium. Microwave energy may thus be more effective than RF energy, and have a lower risk of complications and arrythmogenesis than DC energy when used for ablation in ventricular tachycardia.

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We examined whether total carbon dioxide content (CCO₂) estimation equations for human whole blood in the literature are applicable to canine coronary arterial and venous blood samples. PCO₂ of the tested blood samples covered 19-52mmHg; Po₂ 19-398mmHg. Three CCO₂ estimation equations developed by Kelman, Godfrey, and Douglas et al yielded CCO₂ values over a range of 26.7-54.9vol%, where plasma CCO2 values calculated by the Henderson-Hasselbalch equation ranged over 27.7-62.2vol%. The estimated blood CCO₂ values were almost identical among the three equations. They also closely correlated with plasma CCO₂ values measured after hemolysis with saponin. We conclude that the human whole blood CCO₂ estimation equations are applicable to canine coronary arterial and venous blood samples. These CCO₂ equations may be used for canine cardiac metabolic studies.

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A 6-month program of exercise with a daily swimming time of 30 minutes 3 times a week was carried out in female spontaneously hypertensive rats (SHR) to assess the roles of catecholamine and prostaglandin metabolism in the antihypertensive effect of chronic exercise conditioning. Swim training resulted in a significant reduction of mean blood pressure in SHR by 13.3mmHg as compared with sedentary controls (158.8±5.0 versus 172.1±3.3mmHg, p<0.05). The increase in plasma levels of norepinephrine and epinephrine after acute blood loss of 2% of body weight were smaller in trained than control SHR. The daily urinary excretion of thromboxane B₂, a stable metabolite of thromboxane A₂, was significantly decreased by 33% in swim trained SHR as compared with control SHR (p<0.01), while there was no difference in urinary excretion of prostaglandin E₂ or 6-keto-prostaglandin F_1α, a stable metabolite of prostacyclin. These findings indicate that both the suppression of the sympathoadrenal system and decrease in vasoconstrictory prostaglandins in the kidney may have shared in the antihypertensive effect of exercise training in SHR.

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The purpose of the present study was to evaluate the functional and biochemical effects of serum concentrations on hypothermic preservation of cardiac myocytes. Myocytes were isolated from neonatal rat ventricles and cultured for 4 days, and then incubated for 24 hrs at 4°C in media containing 0, 2, 5, 10, and 20% fetal calf serum (FCS). The myocytes were then cultured for an additional 24 hrs at 37°C to evaluate the recovery of myocyte beating rate.
The recovery ratio of myocyte beating rate after hypothermic incubation was 25.3±14.2 percent of control in the serum-free, 33.0% in 2% FCS, 30.7% in 5% FCS, 22.3% in 10% FCS, and 24.3% in 20% FCS groups. Serum-free, 10% and 20% FCS groups had lower recovery ratios compared to the other two groups. The release of CPK and LDH after hypothermic incubation were similer in the serum-free, 2% and 5% FCS groups, however, significant increases were observed for the 10% and 20% FCS groups.
It is suggested that fetal calf serum at high concentrations (>10%) might be injurious to immature myocardium under hypothermic preservation, and that the optimum concentration of FCS is two percent or less.

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In this study, we evaluated cardiac myocyte viability and function under hypothermic conditions using three types of storage solutions; saline solution (SS), Euro-Collins solution (ECS) and MCDB 107 medium (MM). Cardiac myocytes were isolated from neonatal rat ventricles by collagenase dispersion and cultured for 4 days with MCDB 107 medium. A total of 12.5×10⁵ myocytes/culture dish were used and the myocytes were incubated at 4°C for 6, 12, 18 and 24 hrs in the various storage solutions. After each incubation time, CPK and LDH were measured in the storage solutions. The myocytes were then cultured in MCDB 107 medium and incubated for 24 hrs at 37°C to evaluate the recovery of the myocyte beating rate. In group MM (n=7), the recovery ratio of the myocyte beating rate was 99.2 percent of control (beating rate prior to hypothermic incubation) at 6 hours, 104.6% at 12 hrs and 44.8% at 24 hrs. Groups SS and ECS (n=7 each) had significantly lower recovery ratios than the MM group (at 6 hrs: 74.3, 34.0; at 12 hrs: 61.0, 32.2; at 24 hrs: 0.0, 0.0 percent of control, respectively). Release of CPK and LDH in the MM group gradually increased and at 24 hrs was 28.6IU/l and 93.6IU/l, respectively. However, the SS group had significantly increased CPK and LDH values at 24 hrs (CPK: 66.9, LDH: 164.2). The ECS group showed the greatest increase in both markers (CPK: 317.5, LDH: 421.2). In summary, saline solution showed a beneficial effect on recovery of myocyte viability at 12 hours compared to Euro-Collins solution, however MCDB 107 medium had the best overall protective effect on cultured myocytes. Accordingly, alternate hypothermic storage solutions, such as cell-culture medium, may have protective characteristics that are suitable for cardiac preservation.

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A patient who developed acute myocardial infarction secondary to spontaneous coronary artery dissection and cerebral infarction is described, and possible mechanisms for the association of the diseases are discussed.

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We report a patient with atrioventricular (AV) nodal reentry in which a 2:1 infra-His conduction block was demonstrated during tachycardia. The electrocardiogram (EGG) at the time of attack showed two types of supraventricular tachycardias. The first type was a narrow QRS tachycardia associated with 1:1 AV conduction at a rate of 170 beats/minute. The second type was a narrow QRS associated with 2:1 AV block at a rate of 85 beats/minute. Electrophysiological study revealed AV nodal reentry based on AV nodal triple pathways. The AV conduction curve obtained by atrial premature stimulation showed two discontinuous points at two different basic cycle lengths (500msec, 400msec) and from two different pacing sites (high right atrium, distal coronary sinus). These two types of tachycardias were induced by both atrial premature and overdrive stimulation. In the first type, the impulse conducted in the slow pathway antegradely with 1:1 AV conduction and in the fast pathway retrogradely. In the second type, the impulse was conducted beatto-beat by either a slow pathway or a very slow pathway antegradely with the retrograde limb being the fast pathway and 2:1 infra-His conduction block. Only when the impulse was conducted in the slow pathway antegradely was the infra-His conduction block observed during the tachycardia. The tachycardia in this patient was drug refractory and controlled by an anti-tachycardia pacemaker.

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A 65-year-old male with Wolff-Parkinson-White syndrome presented with atrial fibrillation. The patient was found at the electrophysiological study to have two accessory pathways, a Kent fiber and an atrioventricular accessory pathway with decremental properties. The latter pathway conducted exclusively in the antegrade conduction and the ventricular insertion site was the tricuspid annulus. Both accessory pathways were successfully abolished by radiofrequency catheter ablations at the tricuspid annulus. We propose that an atrioventricular accessory pathway with decremental conduction may have various forms concerning not only sites of origin, but also sites of insertion.

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A patient with complete atrioventricular block and an implanted permanent pacemaker died of colon cancer at the age of 64 years. At autopsy, a cardiac tumor in the region of the atrioventricular node (mesothelioma of the atrioventricular node) was found. The origin of this type of tumor is controversial. Histochemical findings suggested that the tumor in this case was of endodermal origin.

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