To compare the clinical utility of 2 methods in detecting late potentials (Lps), out method (K-method) and Simson's method (S-method) were used in 96 patients with or without ventricular tachycardia(VT). Indices of LPs were LP duration (LPd) in K-method, and mean voltage of the filtered vector magnitude for the last 40 ms of the QRS complex (V₄₀) in S-method. For patients with underlying cardiac disease (UD), LPd in patients with sustained VT (s-VT; 39.4 ± 20.1 ms) was significantly longer than that in patients with nonsustained VT (ns-VT; 16.1 ± 6.6 ms) or without VT (non-VT; 13.3 ± 5.2 ms) (p<0.01), while V₄₀ in patients with s-VT, ns-VT, and non-VT were 24.7 ± 26.4μV, 56.5 ± 31.7 μV, and 98.1 ± 75.3 μV, respectively (p<0.05>). Patients without UD had less apparent LPs in both methods. There was a significant reciprocal correlation between LPd and V₄₀ ; LPd=(378/V₄₀)+6.66 (r=0.89, p<0.001). The sensitivity and specificity with the highest predictive accuracy for s-VT in K-method were 50% and 100% and those in S-method were 50% and 97% respectively. In conclusion, despite many differences in these 2 methods, sensitivity and specificity were nearly equal and they were both useful to identify patients with s-VT.

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Body surface potential mapping (BSPM) was performed to evaluate the infarct size and the viability of myocardium in the infarct area in 20 patients with anterior myocardial infarction (MI). BSPM was performed at the early acute phase, 1 week, 1 month and 2 months after onset of the symptoms. The departure area were obtained according to the potential distribution below the mean normal range and were compared with the value for creatine phosphokinase (CPK), hemodynamic parameters, ejection fraction measured by radionuclide ventriculography, extent score (ES) and severity score (SS) of thallium-201 single photon emission computed tomogram. Two months after the infraction, the ergometer exercise were compared. With the departure map technique, the departure areas in all cases were found in the anterior region of the thorax; From 1 week to 2 months after MI, the departure areas were significantly reduced. One week after MI, the departure areas had a positive significant relation with peak CPK and ΣCPK. One month after MI the departure areas also had a positive relation with ES or SS. One week and 1 month after MI, the departure areas had a negative relation with the left ventricular stroke work index or the left ventricular ejection fraction. After exercise test in the chronic phase, the departure areas were significantly enlarged. In conclusion, the departure map is useful in evaluating the location, sequential changes of size and the left ventricular function. It is suggested that the enlarged departure areas after exercise might be the ischemic areas provoked by exercise.

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The presence and severity of ventricular premature contraction (VPC) in 35 patients with tetralogy of Fallot (TF) were studied, 5 to 10 years after intracardiac repair (ICR), using treadmill exercise testing and 24-hour ambulatory monitoring. VPCs were observed in 24 patients (68.6%). The patients were classified into two groups according to the types of VPCs: group A (23 patients) without VPCs or with VPCs of Lown's grade 1 and group B (12 patients ) with VPCs of Lown's grade 2, 3 or 4, Group B patients were found to have significantly higher right to left ventricular peak-systolic pressure ratios and higher right ventricular peak systolic pressure than those of group A. But there were no significant differences between the two groups in operative age, the time lapse between ICR and evaluation, the duration of exercise and so on, Group B patients also showed significantly decreased right ventricular regional wall motions in the right ventricular outflow tracts (ROTs), indicating akinetic or paradoxical movements than group A patients. It is thought that postoperative right ventricular hypertension and the akinetic or paradoxical wall movement of the ROT may have some effect on the genesis of postoperative VPCs after repair of TF.

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In an attempt to examine the extent to which the right heart performance can predict the left heart performance in heart diseases primarily affecting the left heart, we recorded cardiac index-venous pressure (CI-VP) plot and cardiac index-mean pulmonary artery wedge pressure (CI-PAW) plot at rest and investigated the shift of CI-VP plot and CI-PAW plot that occurred during mild dynamic exercise of the lower limbs. Six patients had normal heart function and 20 patients had heart disease primarily affecting the left heart. The sensitivity, specificity, positive predictive value and negative predictive value in the estimation of the left heart function with ΔCI/ΔVP were 80%, 100%, 89% and 100%, respectively, when ΔCI/PAW was regarded as the golden standard for the estimation of the left heart function. The sensitivity, specificity, positive predictive value and negative predictive value in estimating the left heart function with ΔCI/ΔRA were 86%, 93%, 92% and 86%, respectively. When the left heart function was estimated by ΔVP alone without measuring ΔCI, the sensitivity, specificity positive predictive value and negative predictive value were 40%, 100%, 73% and 100%, respectively. In short, it was possible to predict the left heart dysfunction with ΔCI/ΔVP or ΔCI/ΔRA, in the presence of the right heart dysfunction. It was also possible to predict a steep heart slope from normal ΔCL/ΔVP with error of 2/18 (11%), when steep left heart slope was predicted, based on the presence of steep right heart slop. In comparison, ΔVP alone was a less sensitive index of the performance of the left heart.

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In present study, we investigated the fibrinolytic activities and plasma antigen levels of tissue plasminogen activator (tPA) before or after a submaximal exercise in patients with coronary artery disease (CAD). We also investigated tPA phenotypes in plasma by electrophoretic and immuno-blotting analysis. Euglobulin fractions obtained from plasma were submitted to sodium dodecylsulfate-polyacrylamide gel electrophoresis (SDS-PAGE) followed by immunoblotting analysis. There were no differences in plasma antigen levels of tPA between the study group and controls before of after the exercise, however CAD patients showed lower fibrinolytic activities after the exercise than controls. SDS-PAGE followed by immuno-blotting with an antisera against human tPA revealed two bands at molecular weights (m.w.) of 70, 000 and 120, 000. The band at m.w. of 70, 000 corresponded to free tPA and that of 120, 000 was considered to be identical to a complex of tPA with its inhibitor. Futhermore, we found a decrease in free tPA in the patients with low fibrinolytic activities. From these results it was concluded that impaired fibrinolytic activities. probably due to decreased free tPA, observed in CAD patients, might be an important factor in the pathogenesis of CAD.

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In 11 patients with common type of atrial flutter (common AF), rapid atrial pacing from the high right atrium was performed before and/or after class Ia antiarrhythmic drug administration, confirming transient entrainment by decreasing the pacing cycle length by 10ms.. In 10 patients before the drug administration, common Af was not interrupted although the pacing cycle length was decreased to 200 ms in 5 patients, accelerated atrial flutter or atrial fibrillation was induced in 4 patient. After the drug administration common AF was common Af was converted into sinus rhythm in 5 out of 6 patients. The class Ia antiarrhythmic drug prolonged the common AF cycle length (255 ± 12 ms vs. 298 ± 37 ms, p<0.005) and widened the entrainment zone (64 ± 7 ms vs. 90 ± 20 ms, p<0.05). The widening of the entrainment zone and the prolongation of the common AF cycle length facilitate the successful conversion of common Af at a longer pacing cycle length, which would not precipitate atrial fibrillation or accelerated atrial flutter. The combination therapy of rapid atrial pacing and the class Ia antiarrhythmic drug is thought to be useful in the therapy of common AF.

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Volume-pressure relationship and compliance of human systemic veins were estimated quantitatively and noninvasively using radionuclide. The effect of nitroglycerin (NTG) on these parameters was examined. Plethysmography with radionuclide (RN) was performed using the occlusion method on the forearm in 56 patients with various cardiac diseases after RN angiocardiography with ^99mT_c-RBC. The RN counts-venous pressure curve was constructed from (1) the changes in radioactivity from region of interest on the forearm that were considered to reflect the changes in the blood volume of the forearm, and (2) the changes in the pressure of the forearm vein (fv) due to venous occlusion. The specific compliance of the forearm veins (Csp, fv; 81/V)·(ΔV/ΔP) was obtained graphically from this curve at each patient's venous pressure (Pv). Csp.fv was 0.044 ± 0.012 mmHg^-1 in class I (mean ± SD; n=13), 0.033 ± 0.007 mmHg^-1 in class II (n=309, and 0.019 ± 0.007 mmHg^-1 in class III (n=13), of the previous NYHA classification of work tolerance. There were significant differences in Csp.fv among the three classes. The systemic vanous blood volume (Vsv) was determined by subtracting the central blood volume, measured by RN-angiocardiography, from total blood volume, measured by the indicator dilution method utilizing ¹³¹I-human serum albumin. Systemic venous compliance (Csv) was calculated from Csv=Csp.fv·Vsv. the Csv was 127.2 ± 24.8 ml·mmHg^-1 (mean ±SD) in class III. There were significant differences in Csv among the three classes. The class I Csv value was calculated to be 127.2 ±24.8 ml·mmHg^-1 and the Csv/body weight was calculated to be 2.3 ±0.7 ml·mmHg^-1·kg^-1 of body weight, which was very close to the values for Csv reported previously by other weight, which was very close to the values for Csv reported previously by other investigators in animal experiments. The administration of NTG caused the RN counts - venous pressure curve to become steeper and shift upward. It increased Csv significantly in all cases.

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The present study was carried out to investigate the effects of enkephalins (methionine-enkephalin: Met-Enk, leucine-enkephalin: Leu-Enk) on the adrenergic neurotransmission in hypertension. Perfused mesenteric vasculatures were prepared in spontaneously hypertensive rats (SHR, Okamoto and Aoki strain, 7-10 weeks old) and age-matched Wistar Kyoto rats (WKY), and the effects of these peptides on vascular responsiveness as well as norepinephrine release from the sympathetic nerve endings were examined. Pressor responses to eleectrical nerve stimulation were inhibited in a does-dependent manner by Met-Enk and Leu-Enk, and the inhibition was antagonized by naloxone. Norepinephrine release during electrical nerve stimulation was also suppressed by these peptides. In SHR, stimulation-evoked pressor responses and norepinephrine release were significantly enhanced compared to those in WKY, while the suppressive magnitudes of the responses by Met-Enk and Leu-Enk were smaller in SHR than in WKY. These results demonstrate that Met-Enk and Leu-Enk affected presynaptic sites of blood vessels and caused a decrease in electrically-stimulated norepinephrine release from the sympathetic nerve endings. The lower reduction in norepinephrine release and vascular responsiveness by Met-Enk and Leu-Enk in SHR suggests an insufficient regulation of the vascular adrenergic neurotransmission by the opioid peptides in this model of hypertension.

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We studied the influence of inotropic agents on prompt and transient left ventricular (LV) diastolic relaxation dysfunction produced by superimposition of pacing tachycardia on low-flow ischemia, using an isolated, blood-perfused and isovolumic (balloon-in-LV) rabbit heart preparation. The LV balloon volume was adjusted to produce an LV end-diastolic pressure (EDP) of 15 mmHg and was held constant thereafter. Coronary perfusion pressure was adjusted to 100 mmHg during baseline and to 20 mmHg during low-flow ischemia of 6 min. At baseline, isoproterenol and ouabain were administered to cause moderate and similar rises (14 ± 3 and 16 ± 4% above baseline values, respectively) in maximum + dp/dt of LVP with no change in LVEDP. In control hearts which received no drug, superimposition of 5-min pacing tachycardia on low-flow ischemia produced a significant and transient increase in LVEDP under constant LV volume (from 13.4 ± 0.4 to 24.7± 3.3 mmHg, p<0.01). In the hearts which received isoproterenol it did not change LVEDP (from 14.0 ± 0.4 to 16.2 ± 1.0 mmHg, NS). In contrast, the ouabain hearts showed a further increase in LVEDP (from 13.7 ± 0.8 to 29.9 ± 4.6 mmHg, p<0.01). LV developed pressure, myocardial oxygen consumption or myocardial lactate production during pacing tachycardia superimposed on the low-flow ischemia did not differ significantly among the 3 groups. thus, isoproterenol markedly improved transient LV relaxation dysfunction produced by superimposition of pacing tachycardia on low-flow ischemia, in which an equipotent inotropic does of oubain exaggerated the relaxation dysfunction. These results suggest that calcium overload rather than ATP depletion per se contributes to tansiently impaired diastolic relaxation by pacing tachcardia and low-flow ischemia.

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In order to evaluate the relationship between the calcium-calmodulin system and the adenylate cyclase activity of vascular smooth muscle, we examined the effects of several calcium effectors on the basal and simulated adenylate cyclase activity. Thoracic aortae were removed from Wistar rats and the tissue were homogenated with cold homogenizing buffer containing 1 mM EDTA. Membrane protein fraction of the smooth muscle was prepared by centrifugation at 37, 000g. In this procedure, endogenous guanine nucleotides and contractile proteins remained. The protein fraction was incubated with 2 mM EGTA, 50μM trifluoperazine, 0.1μM A23187 or 25μM calmodulin under basal and stimulated (50 μM isoproterenol, 100μM GTP and 50μM forskolin) conditions. The adenylate cyclase activity was determined by a method modified in our laboratory using double isotope counting. Trifluoperazine reduced the basal adenylate cyclase activity significantly (p < 0.01) as well as the stimulated enzyme activities. A23187 did not affect the basal enzyme activity, but elevated the isoproterenol stimulated enzyme activity significantly (p < 0.02), but did not affect the stimulated enzyme activities. these results suggest that the calcium-calmodulin system is necessary for maintenance of the adenylate cyclase activity of vascular smooth muscle cells. The calmodulin acting site is considered to be the catalytic subunit, and stimulation of the enzyme is accelerated by calcium ion.

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A 24-year-old woman was admitted to our hospital with acute paracetamol poisoning, and severe hepatic injury. The peak blood level f GOT, GPT and LDH were 32, 600 U, 119, 200 U and 36, 500 U respectively. Glucagon-insulin and glutathione were administered to save the liver function. On the third hospital day, hemodialysis was administered to treat acute renal failure. On the 16th hospital day, when the liver and renal functions recovered, severe pulmonary congestion occurred and right heart catheterization revealed high pulmonary pressure. Echocardiography showed left ventricular wall motion. Multi-focal ventricular arrhythmia was frequent during this period. hemodialysis and artificial respiration were carried out for the treatment of heart failure. Three months after admission, myocardial perfusion scintigram showed patchy reduction i the uptake of T1-201 throughout the myocardium, and left ventriculography showed mild diffuse impairment of the LV wall motion (ejection fraction: 49%). in this case, acute heart failure appeared approximately 2 weeks after the severe hepatic injury. Apparently myocardial damage following paracetamol overdosage is caused not only by direct toxicity but by severe metabolic derangement.

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