Although studies show that the ventricular techycardia and sudden dardiac deaths caused by ischemic heart diseases affect Japanese less than Westerners, predictive accuracy of the signal averaged ECG for ventricular tachycardia and sudden cardiac deaths are almost the same as the results for Westerners. The recent prognosis of ischemic heart diseases is showing improvements along with the development of re-perfusion therapy, which is changing the significance of the signal averaged ECG. Therefore a clinical use for signal averaged ECG should be discussed in cases of cardiomyopathy which cause sudden cardiac deaths and other heart diseases. So it is necessary to redetermine normal values of the signal averaged ECG parameters. In this article, the following was reviewed on the basis of our studies regarding the clinical significance of the signal averaged ECG of Japanese and normal signal averaged ECG values. (1) System and gender specific differences on signal averaged ECG of Japanese, (2) His-Purkinje system, pre-P deflection and atrial late potential on signal averaged ECG, (3) Ventricular late potentials of Japanese.

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The role of reactive oxygen products in myocardial damage caused by ischemia-reperfusion has been established in a number of studies performed in animals models. However, studies showing the development of increased free radicals following effective myocardial reperfusion in humans are scarce. In the present study, both the increase of lipid peroxidation (LPO) following early stage thrombolytic therapy which is the current treatment issue performed after acute myocardial infarct (AMI) and the plasma levels of vitamin E and C (chain braker antioxidants) were investigated parallel to time. Forty patients with AMI who were admitted to hospital within six hours from the beginning of symptoms were included in the study and divided into two groups; group 1 (recombinant tissue-Plasminogen Activator, rt-PA group) and group 2 (streptokinase group). Serial serum specimens were drawn before and 30, 90 minutes and 24 hours after thrombolytic therapy for the investigation of LPO, vitamin E and C levels. Echocardiographic examination was performed on the tenth day to evaluate the functions of the left ventricle. Plasma levels of lipid peroxides (LPO) were found to increase 90 minutes after thrombolytic therapy in each group, while the levels of vitamins E and C showed significant decreases. The difference between the two groups was not significant. Similar to this finding, no significant difference in the ejection fraction values was observed between the groups. Further, no correlation was observed between the ejection fraction and LPO values at the 90th minute which is considered to be the time of successful thrombolysis. In conclusion, the occurrence of a series of biochemical changes confirming an increase in free radical development of peripheral blood was observed. Although the decrease in vitamin E and C levels suggests the need for supplementation of these vitamins along with the thrombolytic therapy, the fact that at least a week is needed for an increase of tissue levels of vitamin E confirms the optinion that the daily prophylactic doses of these vitamins is suitable for the decrease of AMI risk.

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The human cytomegalovirus plays a causal role in atherosclerosis etiology, but it is discussed as controversial. We conducted a case control study to investigate whether previous infection with cytomegalovirus is associated with coronary heart disease and markers of systemic inflammation, because systemic inflammation may play a role in atherosclerosis too. We also studied the correlation between anti-cytomegalovirus antibody titer and coronary artery disease. The study involved 150 caes (45 females, mean age±SD is 58.73±7.68 years) with a documented coronary heart disease and 160 healthy volunteers (50 females, mean age±SD is 57.82±7.68, p > 0.05). Cytomegalovirus serology was performed to determine the presence of specific IgG antibodies and titers of the anti-cytomegalovirus IgG antibodies. In addition, C-Reactive protein levels were determined for each case. The prevalance of specific antibodies to cytomegalovirus was 57.30% for the patients and 56% for the controls (p=0.39). But higher levels of anti-cytomegalovirus IgG antibody titer (> 1/800) were seen in the patient group (28.6% versus 10%, p=0.0000). Mean value of C-reactive protein was higher in the patient group (2.99±0.92 mg/l versus 1.79±0.51 mg/l, p=0.0000), and there was a linar correlation with the high antibody titers and the level of C-reactive protein (r=0.35, p=0.0000) These findings support that not the seropositivity of the population but rather the titer of anti-cytomegalovirus antibody and the levels of C-reactive protein could predict patients with a high risk of coronary heart disease.

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The changes in the duration of atrial electrograms during different atrial activation sequences from a sinus rhythm were evaluated to test the hypothesis that the prolongation of atrial electrogram duration caused by the different atrial activation sequence is more prominent at the site of atrial fibrillation (Afib) genesis (initiation site) than other areas. In 39 patients with single retrogade left-sided accessory connection who had inducible transient atrial fibrillation during an electrophysiologic study, the site of Afib genesis was determined and classified into three groups, i.e., 1) high right atrial genesis (HRA), 2) low right atrial genesis (LRA), and 3) left atrial genesis (LA). Single premature extrastimuli after 8 basic drive trains (600 ms) were delivered at the HRA and the right ventricular apex. Three atrial electrophysiologic parameters were evaluated at three atrial sites, i.e., 1) HRA, 2) LRA, and 3) coronary sinus. The atrial vulnerability parameters were as follows; 1) %A2/A1: % prolongation of atrial electrogram duration during premature beat (A2) in comparison with basic drive (A1), 2) wavelength index (WLI): calculated as [effective refractory period]/[A2], and 3) retrograde activation index (RAI): calculated as [A1 during retrograde activation; i.e., RVA pacing/[A1 during antegrade activation, i.e., HRA pacing], shown as a percentage. The Afib genesis was HRA in 20, LRA in 12 and LA in 7 patients. At the HRA recording site, %A2/A1 and RAI were the largest and WLI the shortest in the HRA genesis group in comparison with the other two groups. Similarly, at the LRA and LA recording sites, %A2/A1 and RAI were the largest and WLI the shortest in the groups with Afib genesis at these recording sites. In patients with inducible Afib, %A2/A1 and RAI were the highest and WLI the shortest at the atrial recording site close to the site of Afib genesis. Atrial wave prolongation during retrograde atrial activation, possibly the anisotropic conduction, was considered to play a role in initiating Afib as well as a conduction delay during the atrial premature beat.

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Effective arterial elastance (Ea) is the coupling parameter between the left ventricle and peripheral circulation in normal subjects. If left ventricular end systolic pressure (Pes), contractility (Es) and Ea are known, left ventricular end diastolic volume (LVEDV) and ejection fraction of the ventricle are completely determined. The aim of this study was to give an analytical expression for Ea in patients with mitral and aortic regurgitation, and predict both LVEDV and the effect of vasodilator therapy on LVEDV. Twenty-three subjects with atypical chest pain, 15 patients with mitral insufficiency and 11 with aortic insufficiency underwent diagnostic cardiac catheterization, coronary angiography, and left ventricular cineangiography, which was analyzed quantitatively. Ea was 2.05 ± 0.63 in normal subjects, while it was 1.28 ± 0.71 and 1.57 ± 0.87 in patients with mitral and aortic insufficiency, respectively. All these groups differed with ANOVA test (p = 0.0031). We tested the ability of the analytical expressions for Ea in normal subjects, and patients with mitral insufficiency or aortic insufficiency to predict measured Ea and LVEDV. Ea and LVEDV were predicted rather accurately in every case (p < 0.0001). We used published data to test the effect of resistance modulation on LVEDV. Predicted and measured LVEDV were linearly correlated both in aortic (p < 0.0001) and mitral insufficiency (p = 0.027). Moreover, in some cases a left ventricular enlargement after vasodilator therapy could be anticipated because of an unbalanced decrease in resistance and heart rate. Ea seems to be the coupling parameter between the left ventricle and the peripheral circulation not only in normal subjects, but also in patients with mitral or aortic regurgitation; its measurement before administering vasodilating drugs may be useful in order to predict the effects on LVEDV, and achieve an optimal ventriculoarterial coupling.

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Noninvasive estimation of pulmonary arterial pressure is important for hemodynamic monitoring of patients with heart disease. In patients with tricuspid regurgitation (TR), the peak velocity of TR on continuous-wave (CW) Doppler can be used to estimate the systolic pulmonary arterial pressure (PAPs) using the simplified Bernoulli equation. We evaluated a new technique of contrast-enhanced CW Doppler for calculating PAPs in patients with trivial TR. Forty-one patients without visible TR detected by color Doppler, pulsed Doppler or CW Doppler were evaluated. Age ranged from 19 to 73 (55 ± 12) years old. Tricuspid flow signals were recorded on CW Doppler after intravenous administration of indocyanin green (ICG) or Albunex. PAPs was calculated as; PAPs = 4 × V²_TR + 10 mmHg, where V_TR is the peak velocity of TR. PAPs calculated using contrast-enhanced CW Doppler was compared with PAPs measured by the following cardiac catheterization. 1) TR signals were recorded using the contrast-enhanced CW Doppler technique in 39 of 41 patients (95%) after intravenous administration of contrast agents. 2) The error of estimate of PAPs using the contrast-enhanced CW Doppler technique was - 2.4 ± 7.5 mmHg, and the percent error was -10.7 ± 32.4% in all patients. In 20 of 39 patients (51%), the error of estimate was within ± 5 mmHg. 3) PAPs was overestimated by 12.2 ± 6.1 mmHg in patients with good contrast enhancement of TR signals. The contrast-enhanced CW Doppler technique is useful for estimating PAPs noninvasively in patients with trivial TR. It is better to assume the right atrial pressure as 3-5 mmHg, not 10 mmHg, in patients with good enhancement of trivial TR. Physiological TR may be enhanced by contrast agents in these patients.

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Excessive neurohumoral activity remains a major burden to the circulation of patients with advanced heart failure. Prostaglandin El (PGE1), a balanced i.v. vasodilator, was shown to elicit favorable hemodynamic and clinical effects in this cohort. A prospective randomized parallel group trial was performed to evaluate acute, intermediate and chronic changes in hemodynamic, neurohumoral and renal variables in response to PGE1, dobutamine and placebo. Thirty patients with class III and IV heart failure and low cardiac index (mean 1.9 l/min/m²) two hours after oral drugs including high dose enalapril were included. A 7-day-infusion of PGE1 (16.5 ± 5 ng/kg/min, range 10 to 20 ng/kg/min, group A n = 10), dobutamine (4.5 ± 1 μg/kg/min, range 2.5 to 5 μg/kg/min, group B n = 10) or placebo (saline, group C n = 10) was administered via a central venous access line after stepwise titration until intolerable side effects developed with PGE1 or a 20% increase in cardiac index occurred with dobutamine, which was continued on this dose throughout while PGE 1 was maintained on 50% peak dose. Hemodynamic data were collected at baseline, at peak dosages, after 12 hours and after 7 days. Of neurohumoral variables plasma norepinephrine, big endothelin (Big ET) and atrial natriuretic peptide (ANP) were simultaneously evaluated using RIA methods. Renal plasma flow (by paraaminohippurate clearance) and glomerular filtration rate (by iothalamate clearance) was measured prior to and during the infusions (after 12 hours and after 7 days). At peak dose and at 12 hours significant drops from baseline of mean pulmonary artery pressure, pulmonary capillary wedge pressure and systemic vascular resistance were observed which were accompanied by a rise in cardiac output with both PGE1 and dobutamine. These changes were maintained through 7 days when pulmonary vascular resistance levels also fell with both active drugs. Blood pressure did not change throughout, but PGE1 increased heart rate slightly at 12 hrs. Both PGE1 and dobutamine enhanced renal plasma flow after 7 days, but only PGE1 decreased glomerular filtration fraction significantly. Glomerular filtration rate did not change with either drug. PGE1 decreased ANP levels at 12 hrs, and dobutamine increased big ET levels at peak, but decreased big ET at 7 days. Norepinephrine levels were unaffected throughout. Except a slight decrease in right atrial pressure after 7 days placebo did not change any measured variable significantly. Taken together, these data suggest that treatment with PGE1 is as efficacious as low-dose dobutamine in improving cardiac performance and renal perfusion in advanced heart failure. Of importance, no deleterious neurohumoral counterregulation was observed with PGE1.

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Protamine reversal of heparin anticoagulation often causes systemic hypotension by releasing nitric oxide (NO) from vascular endothelium. We investigated the hypothesis that protamine prevents severe pulmonary vasoconstriction by increasing NO. Twenty patients undergoing elective coronary artery bypass graft surgery were included in the study. Nitrite and nitrate levels -as end-metabolites of NO-were measured in blood samples obtained before and after protamine administration. Mean arterial pressure, heart rate, mean pulmonary artery pressure, central venous pressure and left atrial pressure were noted as hemodynamic data. Nitrite levels were 4.64 ± 0.67 μmol in the right atrium and 4.84 ± 0.95 μmol in the left atrium before protamine administration. The difference was insignificant statistically. These measurements were 4.85 ± 0.92 in the right atrium and 5.28 ± 0.66 μmol in the left atrium after protamine administration. This increase was significant (p < 0.05). The measurements of nitrate levels were completely parallel with those of nitrite. Mean arterial pressures were 78.9 ± 7.59 mm-Hg before protamine and 74.1 ± 8.55 mm-Hg after protamine (p = 0.03). The changes in other hemodynamic parameters were not significant. Protamine augments NO production and prevents the pulmonary circulation from possible vasoconstriction.

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Increased coronary sinus (CS) pressure and cardiac contraction impair coronary inflow independently. However, it has not been determined how the coronary pressure-flow relationship is strongly affected by changes in CS pressure in the beating heart compared to the non-beating heart. The purpose of this study was to evaluate the combined mechanical effects of cardiac contraction and increased CS pressure. Using isolated, perfused canine hearts, coronary perfusion pressure in the left anterior descending coronary artery (LAD) was gradually reduced in beating and non-beating conditions. Measurements were obtained with and without elevation of CS pressure to determine the mean LAD pressure-flow relationships. At normal and elevated CS pressures, the corresponding zero-flow pressures were not significantly different between the beating and non-beating hearts. A rightward shift of the mean coronary perfusion pressure-coronary flow curve for the beating heart compared to the non-beating heart was observed when CS pressure was not elevated. In contrast, the slopes for both beating and non-beating hearts were similar if the CS pressure was increased. There was a smaller increase in the mean intramyocardial pressure (IMP) at elevated CS pressures in the beating heart as compared to the non-beating heart. Moreover, the increase in diastolic IMP with increased CS pressures in the beating heart was significantly less than that in the non-beating heart. These results indicate that cardiac contraction attenuates the inhibitory effects of increased CS pressure on coronary inflow.

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The aim of this study was to obtain evidence for a transmembrane K⁺-H⁺ exchange system in Langendorff-perfused whole hearts and isolated ventricular myocytes of guinea pig. Effluent relation between K⁺ and pH in the whole hearts perfused with HEPES-buffered Tyrode's solution indicated a significant (p<0.05) functional coupling of K⁺ uptake and H⁺ extrusion that was energy-dependent and omeprazole (OPZ)-sensitive. Administration of OPZ (0.3mM) or dimethylamiloride (0.1mM), an inhibitor of Na⁺-H⁺ antiport, to whole hearts subjected to the repetitive NH₄Cl applications implied that both Na⁺-H⁺ and putative K⁺-H⁺ countertransports contribute to the regulation of intracellular pH. In isolated myocytes, voltage-dependent L-type Ca current (I_Ca) was inhibited by OPZ (0.3mM) under K⁺- and Na⁺-free condition by 11 to 14%, and was inhibited to a greater extent (i.e., by 36 to 40%) by this agent in the presence of K⁺. OPZ-induced inhibition of the putative K⁺-H⁺ exchanger likely resulted in subsarcolemmal acidification which was responsible for the rate-independent suppression of I_Ca. In conclusion, these data provide functional evidence for a myocardial transmembrane K⁺-H⁺ exchanger.

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Pseudoaneurysm of the splenic artery has been rarely reported and the Doppler echocardiographic finding seldom described. Herein we report a rare case of huge extrasplenic pseudoaneurysm, which was detected by color flow Doppler ultrasonography and successfully treated by ligation of the splenic artery and resection of the pseudoaneurysm.

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Transesophageal echocardiography combining with peripheral injection of agitated saline solution is a useful diagnostic tool to detect the intrapulmonary shunt. We performed transesophageal contrast echocardiography in a case of hepatopulmonary syndrome with normal pulmonary angiography to define the intrapulmonary right-to-left shunt bilaterally.

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A 57-year-old Japanese-Brazilian man, visiting Japan for only 9 days, was admitted to our hospital due to syncope and frequent ventricular premature beats. He grew up in a rural area of Brazil and moved to Sao Paulo in 1959 when he was 20 years old. We suspected chronic Chagas' heart disease, ie., dilated cardiomyopathy with apical ventricular aneurysm, right bundle branch block with left anterior fascicular block, and various arrhythmias including supraventricular premature beats, ventricular premature beats and non-sustained ventricular tachycardia because he showed typical echo- and electrocardiographic features of the disease. Coronary arteriograms were normal, and left ventriculogram confirmed the existence of apical ventricular aneurysm. A left ventricle biopsy specimen showed hypertrophic cardiac muscle with mild fibrosis. The diagnosis of chronic Chagas' disease was finally confirmed by the demonstration of Trypanosoma cruzi itself in the blood as well as Trypanosoma cruzi antibodies.

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