The purinergic receptor P2Y, G-protein coupled, 2 (P2RY2) gene associated with essential hypertension in Japanese men.

P2RY2 has an important function in the regulation of blood pressure by activating adenosine triphosphate (ATP). The aim of this study was to investigate the association between the human P2RY2 gene and essential hypertension (EH) through a haplotype-based case-control study that included two gender groups. The 273 EH patients and 255 age-matched controls were genotyped for five single-nucleotide polymorphisms (SNPs) of the human P2RY2 gene (rs4944831, rs1783596, rs4944832, rs4382936 and rs10898909). Data were analysed for men and women separately and then as a combined total group. For the total and the men only groups, the genotype distribution of the T allele of rs4944831 and the recessive model (GG vs TG+TT) of rs4944831 differed significantly between the EH patients and controls (P=0.028 and 0.019; P=0.009 and 0.008, respectively). Logistic regression showed that for the total and men groups, the TG+TT genotype of rs4944831 was more prevalent in EH patients than in the controls (P=0.026 and 0.011, respectively). For men, the overall distribution of the haplotype (SNP2-SNP4-SNP5) was significantly different between the EH patients and the controls (P=0.006). As compared with controls, the frequency of the T-A-G haplotype was significantly higher, whereas the T-C-G haplotype was significantly lower for the EH patients (P=0.001 and 0.014, respectively). In conclusion, the present results indicate that rs4944831 and the T-A-G haplotype of the human P2RY2 gene might be genetic markers for EH in Japanese men.

High salt diet enhances cardiovascular responses from the nucleus tractus solitarius and ventrolateral medulla of Sprague-Dawley rats.

High salt intake has been shown to augment the sensitivity of rostral ventrolateral medulla (RVLM) sympathoexcitatory neurons. We examined the effects of 4 weeks of high dietary salt (8%) on the sensitivity of nucleus tractus solitarius (NTS) and caudal ventrolateral medulla (CVLM) in controlling RVLM. In chloralose-anesthetized Sprague-Dawley rats, high salt intake did not elevate baseline arterial pressure or heart rate (HR). In high-salt group, NTS, CVLM, and RVLM responses to glutamate were greater. NTS responses to acetylcholine or serotonin, which is independent of baroreflex, also were greater. Phenylephrine or nitroprusside (i.v.) elicited similar changes in arterial pressure and heart rate, the baroreflex sensitivity also was similar in both groups of rats. These results suggest that high salt intake augments the sensitivity of NTS and CVLM sending inhibitory input to RVLM. This presumably may inhibit the RVLM, thereby inhibiting the elevation of arterial pressure.

Age and sex differences in the P-wave signal-averaged electrocardiogram in a Japanese study population.

Normal P wave signal-averaged electrocardiogram (SAE) values were determined in 120 healthy Japanese adults (56 men, 64 women), aged 44.5+/-10.2 years (mean+/-SD). The P wave trigger method was used with a Fukuda FDX6500 recorder. We used bipolar Frank leads (X,Y,Z), and recordings were made with forward and backward digital Butterworth filters [40 Hz (18 dB / oct) - 300 Hz (12 dB / oct)]. The recordings were taken for the following five parameters: forward and backward filtered P wave duration [fPd (F); tPd (B)]; bidirectionally corrected fPd [tPd (C)]; and 20 ms of the terminal portions of voltage at forward and backward filtering (RMS20). Overall, fPd (F) was 117.8-136.4 ms, fPd (B) 116.4-134.4 ms, fPd (C) 97.4-115.2 ms, RMS20 (F) 1.6-3.6 microV, and RMS20 (B) was 2.2-5.4 microV. Between the sexes, there were significant differences in fPd (F) (p<0.001) and fPd (B) (p<0.01) and in RMS20 (F) (p<0.05) and RMS20 (B) (p<0.05). Weak positive correlations were observed between fPd (F) and body surface area, fPd (F) and age, fPd (B) and body surface area, fPd (B) and age, fPd (C) and body surface area, and fPd (C) and age. There was no evident correlation, however, between either forward or backward RMS20 and body surface area or between forward or backward RMS20 and age. Differences in the normal P wave values between the sexes and age groups were evaluated in this study.

Normal limits of high-resolution signal-averaged ECG parameters of Japanese adult men and women.

High-resolution signal-averaged electrocardiography (Hi-Res ECG) has been found useful in measuring ventricular late potentials for identifying patients prone to life-threatening ventricular arrhythmias. Several studies have reported cut-off values (normal limits) of Hi-Res ECG parameters, including sex-specific limits, for adult population. However, there are no such studies reporting such limits in the Japanese population. Hi-Res ECGs were recorded from 482 normal healthy patients (204 men; 278 women) with no cardiac disease and normal electrocardiogram. Three Hi-Res ECG parameters filtered QRS duration (FQRSD), low amplitude signal duration under 40 microV of terminal QRS (LASD), and root mean square voltage in the terminal 40 milliseconds (RMSV) were analyzed. FQRSD was longer in men than in women (P < .0001). RMSV was larger in men than in women (P < .0001). There was no significant difference in LASD between men and women. The upper limit (90th percentile) of FQRSD was 116 milliseconds for women. The upper limit of LASD was 42 milliseconds for both men and women. The lower limit (10th percentile) of the RMSV was 14 microV for both men and women. There was no significant difference in the distributions of the Hi-Res ECG parameters between our study and an earlier study on mostly whites from the United States and Europe. The upper limits (90th percentile) of FQRSD and LASD in the Japanese normal patients were nearly the same as for whites. But, the lower limit (10th percentile) of RMSV in our Japanese normals was significantly smaller than that for whites. Therefore, it may be necessary to use race-specific normal limits for late potential analysis. Criteria for abnormal late potentials (defined as abnormal values in at least 2 of the 3 Hi-Res ECG parameters) were met in 18 of 482 (3.7%) normal healthy patients. Further studies are needed to evaluate the role of these criteria in identifying cardiac patients with life-threatening arrhythmias in the Japanese population.

Analysis of the electrophysiologic effects of short-term oxybutynin on guinea pig and rabbit ventricular cells.

The objective of this study was to investigate the cardioactive properties of oxybutynin, a drug that is widely prescribed for management of voiding dysfunction. Membrane currents were recorded from whole-cell-configured guinea pig ventricular myocytes, and action potentials were recorded from guinea pig and rabbit papillary muscles. L-type Ca2+ current (I(Ca),L), inward-rectifier K+ current (I(K1)), and delayed-rectifier K+ current (I(K)) were unaffected by < or = 1 microM oxybutynin, and inhibited by higher concentrations. The concentrations that reduced the currents to one-half of predrug control amplitude (K0.5) were as follows: 1(Ca),L, 16.1 microM, I(K1), 18.2 microM, rapidly activating I(K)(I(Kr)), 11.4 microM, and slowly activating I(K)(I(Ks)), 28.7 microM. Action-potential durations at 20 and 90% repolarization (APD20, APD90) were unaffected by oxybutynin < or =3 microM in guinea pig papillary muscles driven at 1 Hz; higher concentrations selectively shortened the APD20 by as much as 25% (100 microM), and caused moderate reductions in maximal upstroke velocity. Changes in the action potentials of rabbit papillary muscles were even smaller than in the guinea pig muscles. Because the peak therapeutic plasma concentration of oxybutynin is in the 0.01-0.1 microM range, the results suggest that the drug is highly unlikely to have adverse effects on cardiac electrical activity.

Sodium-pump potentials and currents in guinea-pig ventricular muscles and myocytes.

When guinea-pig papillary muscles were depolarized to ca. -30 mV by superfusion with K+-free Tyrode's solution supplemented with Ba2+, Ni2+, and D600, addition of Cs+ transiently hyperpolarized the membrane in a reproducible manner. The size of the hyperpolarization (pump potential) depended on the duration of the preceding K+-free exposure; peak amplitudes (Epmax) elicited by 10 mM Cs+ after 5-, 10-, and 15-min K+-free exposures were 12.9, 17.7, and 23.2 mV, respectively. Pump potentials were unaffected by external Cl- but suppressed by cardiac glycosides, hyperosmotic conditions, and low-Na+ solution. Using Epmax as an indicator of Na+ pump activation, the half-maximal concentration for activation by Cs+ was 12-16.3 mM. At 6 mM, Cs+ was three times less potent than Rb+ or K+ and five times more potent than Li+. From these findings, and correlative voltage-clamp data from myocytes, we calculate that (i) a pump current of 7.8 nA/cm2 generates an Epmax of 1 mV and (ii) resting pump current in normally polarized muscle (approximately 0.16 microA/cm2) is five times smaller than previously estimated.

Action potentials, contraction, and membrane currents in guinea pig ventricular preparations treated with the antispasmodic agent terodiline.

Terodiline was widely prescribed for urinary incontinence before reports of adverse cardiac effects that included bradycardia, QT lengthening, and ventricular tachyarrhythmia. The present study on guinea pig papillary muscles and ventricular myocytes was undertaken to gain insight into the cardioactive properties of the drug. Clinically relevant concentrations (<10 microM) of terodiline lengthened the action potential duration by up to 12%; higher concentrations shortened the duration in a concentration-dependent manner. The drug depressed maximal upstroke velocity in a use-dependent manner; the IC(50) value was near 150 microM in muscles driven at 1 Hz, 60 microM at 3 Hz, 38 microM at 5 Hz, and 3 microM at 1 Hz in muscles depolarized with 14 mM K(+). Submicromolar terodiline frequently had a small positive inotropic effect, whereas micromolar concentrations depressed force in a frequency-dependent manner. Voltage-clamp results on myocytes indicate that terodiline inhibits three membrane currents that govern repolarization: 1) E4031-sensitive, rapidly activating K(+) current with an IC(50) value near 0.7 microM as previously reported; 2) slowly activating, delayed-rectifier K(+) current with an IC(50) value of 26 microM; and 3) L-type Ca(2+) current with an IC(50) value of 12 microM. These findings are correlated with the changes in action potential configuration and developed tension and discussed in relation to the cardiotoxic effects of the drug.

Inhibition of cardiac inward-rectifier K+ current by terodiline.

The antispasmodic agent terodiline has cardiotoxic effects that include QT lengthening. To determine whether inhibition of inwardly-rectifying K+ current (I(K1)) might be a factor in the cardiotoxicity, we measured I(K1) in guinea pig ventricular myocytes. Terodiline reduced outward I(K1) with an IC50 of 7 microM; maximal reduction was 60% with 100-300 microM concentration. Inhibition was independent of current direction, and persisted after removal of the drug. Terodiline (3-5 microM) lengthened action potentials in guinea pig papillary muscles by ca. 10%, primarily by slowing phase 3 repolarization; higher concentrations abbreviated the plateau and markedly slowed late repolarization. Terodiline washout provoked an extra lengthening, consistent with persistent inhibition of I(K1) and rapid recovery of net inward plateau current. The results suggest that inhibition of I(K1) is a likely factor in the cardiotoxicity of the drug.

[Evaluation of coronary flow velocity and coronary flow reserve before and after coronary angioplasty using transthoracic Doppler echocardiography and Doppler guide wire].

Evaluation of left anterior descending coronary (LAD) blood flow before and after coronary angioplasty was carried out non-invasively by ultrasonic Doppler echocardiography with a newly developed digital, high-frequency, high-resolution transthoracic ultrasonic Doppler flowmeter and a 7.5 MHz probe. The results were compared with those obtained using an intracoronary Doppler guide wire. Sixteen patients, 12 males and 4 females (mean age 57 +/- 14 years) with old myocardial infarction (8 patients) and angina pectoris (8 patients) were studied. Coronary flow reserve was compared following intravenous administration of adenosine triphosphate in 12 patients. The LAD blood flow was detected in 15 of 16 patients. There was a significant increase in the diastolic peak velocity from 22.2 +/- 10.6 to 29.4 +/- 14.6 cm/sec (mean +/- SD) and the coronary flow reserve from 1.8 +/- 0.3 to 2.8 +/- 0.6 (mean +/- SD). There was a good correlation between the data obtained using transthoracic flow measurement and intracoronary flow measurement (r = 0.61, p < 0.05). LAD blood flow can be easily detected parasternally using a digital, high frequency, high-resolution ultrasonic Doppler flowmeter. This method may be applicable for judging the efficacy of coronary angioplasty by measuring coronary flow reserve and for observing the clinical course of the patient non-invasively.

Potassium current and sodium pump involvement in the positive inotropy of cardiac muscle during hyperosmotic stress.

OBJECTIVE: To identify factors involved in the modification of cardiac electromechanical activity caused by hyperosmotic solution. DESIGN: Membrane potentials and contractions were recorded from isolated papillary muscles, and membrane ionic currents were measured in isolated ventricular myocytes by using the ruptured patch or perforated patch voltage clamp method. ANIMALS AND METHODS: Adult male guinea-pigs weighing 250 to 350 g were used. Normal Tyrode's solution for superfusing experimental preparations was replaced with hyperosmotic Tyrode's solution for observation periods of up to 10 mins. The hyperosmotic solution was normal Tyrode's solution supplemented with 50 or 150 mM sucrose (1.2 or 1.5 times normal osmolality). Sodium pump activity (hyperpolarization in muscles; outward current in myocytes) was activated by switching to pump-activating cation (cesium, potassium) solution from pump-inactivating potassium-free solution under conditions in which other ionic currents were suppressed. RESULTS: Hyperosmotic solution lengthened action potentials and enhanced developed tension in papillary muscles. Superfusion of myocytes with hyperosmotic solution inhibited inward L-type calcium current (ICa,L) by approximately 30% and the outward delayed rectifier potassium current (Ik) by approximately 50%. Hyperosmotic treatment also partially inhibited sodium pump-generated hyperpolarizations in papillary muscles. However, sodium pump current in myocytes was relatively small under isosmotic conditions and, therefore, unlikely to be a major factor in action potential lengthening. CONCLUSIONS: Inhibition of potassium current is a major factor in the lengthening of the action potential by hyperosmotic solution. It seems likely that the accompanying positive inotropy is due to an elevation of intracellular calcium caused by enhanced calcium influx related to action potential prolongation and sodium pump inhibition.

Protection by hypoxic preconditioning against hypoxia-reoxygenation injury in guinea-pig papillary muscles.

OBJECTIVE: Developed tension in guinea-pig papillary muscles is depressed by prolonged hypoxia; subsequent reoxygenation leads to a partial recovery that stabilizes after an early period of arrhythmia. We have investigated whether hypoxic preconditioning in these muscles (1) improves the recovery of developed tension, (2) protects against arrhythmia, and (3) causes other significant electromechanical changes. METHODS: Papillary muscles stimulated at 1 Hz were superfused with oxygenated Krebs solution for 60 min and either preconditioned (5 min of 3 Hz pacing substrate-free hypoxic conditions, 10 min of normoxic recovery) or equilibrated for an extra 15 min. Muscles were subsequently challenged with substrate-free hypoxia (1 Hz), and reoxygenated (1 Hz) for 60 min. Contractile performance, action potential parameters, and indicators of arrhythmic activity were measured in 10 preconditioned and 10 non-preconditioned muscles. RESULTS: Developed tension in preconditioned muscles declined to the same level (10-15% control) as in non-preconditioned muscles after 60 min hypoxia. A notable difference was that developed tension in the preconditioned muscles failed to rebound during mid-hypoxia, a hallmark feature in non-preconditioned muscles. The action potential duration and overshoot collapsed at a significantly faster rate in hypoxic preconditioned muscles. Action potential recovery during reoxygenation was similar in the two groups of muscles, but recovery of developed tension was significantly stronger in preconditioned (76.7 +/- 5.4%) than in non-preconditioned (42.9 +/- 1.7%) muscles (P < 0.001). Reoxygenation provoked arrhythmic activity in all muscles, but the summed average duration was shorter (5.5 +/- 1.0 vs. 9.4 +/- 1.5 min) (P < 0.05) in the preconditioned muscles. CONCLUSION: Hypoxic preconditioning can significantly enhance post-hypoxia recovery of developed tension, and significantly attenuate arrhythmic activity, in guinea-pig papillary muscles.

Force-relaxant actions of dimethyl sulfoxide on guinea-pig and rabbit papillary muscles.

Recent voltage-clamp analysis of dimethyl sulfoxide (DMSO: 0.1-10% v/v) action on membrane currents in guinea-pig ventricular myocytes (strong inhibition of delayed-rectifier K+ current, inhibition of Na+ pump current, little effect on L-type Ca2+ current) suggested that the solvent would have a strong positive inotropic effect on guinea-pig papillary muscles. In muscles driven at 1 Hz, the major effects of 30 min superfusion with hyperosmotic 10% DMSO were: (1) a 33% lengthening of the action potential duration; (2) a 23% depression of developed tension; and (3) a pronounced positive inotropy on washout of the solvent. Osmotic change in cell volume was a possible reason for these effects; however, hyperosmotic sucrose solution that shrunk myocyte volume by a DMSO-like 12% failed to elicit the DMSO response. It was postulated that DMSO has both stimulatory and inhibitory actions: during treatment the stimulatory component (Ca2+ accumulation due to action potential lengthening and Na+ pump inhibition) is masked by a concomitant inhibition of Ca(2+)-myofilament interaction; removal of the solvent reveals the Ca2+ overload. In support of this interpretation. (1) DMSO depressed developed tension by up to 85% when the stimulatory influence was attenuated by eliminating action potential lengthening (rabbit papillary muscles), relieving pump inhibition (elevated K+), or preloading Ca2+ (low-K+ or low-Na+ superfusate), and (2) DMSO relaxed Na(+)-free contractures, and nearly abolished caffeine-induced contractures, in quiescent guinea-pig muscles. These data suggest that DMSO has a reversible, powerful inhibitory action on the myofilament force-generating machinery.

Effects of atrioventricular intervals on right atrial monophasic action potential duration during pacing or reciprocating tachycardia.

We evaluated the relationship between changes in the atrioventricular (AV) intervals and right atrial monophasic action potential duration at 90% repolarization (RA-MAPD90) in humans. In 4 patients, RA-MAPD90 was measured during AV reciprocating tachycardia (AVRT, n = 2) or AV node reentrant tachycardia (AVNRT, n = 2) and atrial or ventricular pacing at similar cycle lengths. In 10 patients, RA-MAPD90 was measured during continuous atrioventricular sequential pacing at AV intervals of 0, 50, 100, 150, 200, 250, 300, 350 msec for 90 sec at a cycle length of 333-400 msec. In patients with AVRT, the RA-MAPD90 during tachycardia was shorter than RA-MAPD90 during RA or RV pacing. In patients with AVNRT, RA-MAPD90 during tachycardia was similar or longer than RA-MAPD90 during RA or RV pacing. As the AV interval was increased from 0 msec to 150 msec, the peak right atrial pressure decreased from 8-12 mmHg to 2-3 mmHg. RA-MAPD90 decreased to its minimal value at an AV interval of 150 msec. The maximal difference in the RA-MAPD90 obtained by changing the AV interval was 22.5 +/- 3.0 msec. We conclude that 1) a very short AV or VA interval causes an increase in RA-MAPD90 which correlates with an increase in RA pressure, and 2) RA-MAPD90 during supraventricular tachycardia is different from RA-MAPD90 during atrial or ventricular pacing. Thus, a contraction-excitation feedback mechanism may exist in the human atrium.

Radiofrequency catheter ablation for the treatment of common atrial flutter in humans.

Endocardial catheter ablation has been recently been proposed for the treatment of arrhythmias originating in the right atrium. In this study, we used this technique in 5 patients with paroxysmal common atrial flutter and 3 patients with paroxysmal uncommon atrial flutter. Various antiarrhythmic agents had failed to prevent the recurrence of these episodes. In each procedure, we used a large-tip 7 F quadripolar catheter electrode that was introduced via the femoral vein into the lower part of the right atrium. The two distal electrodes were used to record double-spike potentials or fragmented electrograms. A unipolar electrogram recording from a distal electrode of the same catheter was also used to identify local activation. The targets for ablation were sites which showed double-spike potential and fragmented electrogram 40-60 msec earlier than the onset of the F wave. Application of radiofrequency (RF) energy (25-40 watts) (3-17 applications) terminated atrial flutter and prevented reinduction of atrial flutter in the 5 patients with common atrial flutter. However, atrial flutter could not be terminated with the application of RF energy in the 3 patients with uncommon atrial flutter. The sites at which ablation was successful were located inferior or posterior to the coronary sinus ostium between the inferior vena cava and the tricuspid valve annulus, and were characterized by double-spike potentials and fragmented electrograms with activation times > or = 40 msec before the onset of the F wave. This area may represent the exit site from the area of slow conduction, since pacing from this site showed concealed entrainment of the F wave, and a local electrogram to the onset of the F wave coincided with the pacing spike to the onset of the F wave. Follow-up of these 5 patients (19.4 +/- 10.4 weeks) revealed recurrence of the original atrial flutter in 1 patient and a new type of atrial flutter in 1 patient. The other 3 patients have been episode-free, although an antiarrythmic agent was given for the treatment of paroxysmal atrial fibrillation in 2 patients. We conclude that the application of RF energy to the presumed critical area in the atrial flutter reentrant circuit seems to be effective in terminating and preventing common atrial flutter. Long-term follow-up is required for the recurrence of atrial flutter.

Microwave ablation of the atrioventricular junction in vivo and ventricular myocardium in vitro and in vivo. Effects of varying power and duration on lesion volume.

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 30 sec was: at 10W, 0.8 +/- 1.6; 20 W, 34.7 +/- 10.3; 30 W, 34.7 +/- 22.4: 40 W, 64.7 +/- 64.4; 50 W, 87.2 +/- 42.3; 60 W, 85.8 +/- 38.1; 70 W, 124.7 +/- 36.5; 80 W, 134.2 +/- 49.0 mm3. The mean lesion volume at 80 W was: at 15 sec, 32.6 +/- 37.8; 30 sec, 101.2 +/- 46.4; 60 sec, 180.6 +/- 80.1; 120 sec, 291.8 +/- 122.7; and 180 sec, 459.3 +/- 204.6 mm3. 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 arrhythmogenesis than DC energy when used for ablation in ventricular tachycardia.

Effect of reperfusion by direct percutaneous transluminal coronary angioplasty on ventricular late potentials in cases of total coronary occlusion at initial coronary arteriography.

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: < or = 4, 4-6, 6-8, 8-10, and > or = 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 < or = 4 and 4-6 h groups than in the controls (p < 0.005 and p < 0.05, respectively). Therefore, reperfusion achieved within 6 h reduced the incidence of late potentials in AMI patients and may be effective for preventing malignant ventricular arrhythmias.

[Detection of ventricular late potentials comparison of 4 commercial high-resolution systems].

UNLABELLED: The purpose of this study was to evaluate the methodologic problems of noninvasive registration of ventricular late potentials. METHODS: we compared the results obtained in the same patients with four different systems which were Marquette MAC1, MAC12, ART LP101 and FUKUDA VCM 3000. Filtering was employed digital forward direction, 100-300 Hz in MAC1, digital FFT, 40-250 Hz in MAC12, digital, bidirectional, 40-250 Hz in ART and analogue, forward direction 40-300 Hz in FUKUDA VCM 3000. DEFINITION OF LATE POTENTIALS (LPs): Filtered QRS duration (FQRSD) was 120 msec or more, root mean square voltage in the last 40 msec (RMSV) was 15 microV or less in MAC12 and ART. FQRSD was 130 msec or more, RMSV was 15 microV or less in FUKUDA. FQRSD was 20 msec or more after QRS obtained from low resolution leads in MAC1. SUBJECTS: 163 patients [control 13, PVCs 23, myocardial infarction 55, others 51, IVCD (RBBB, LBBB, IVCD) 21] were included in this study. RESULTS: 17.6% of all patients (except for IVCD) showed LPs with MAC12, 20.0% with ART, 30.3% with FUKUDA, and 14.1% with MAC1. 23.1% of the control group showed LPs with MAC12 and FUKUDA, but no cases showed LPs with ART and FUKUDA. 4.3% of the PVC group showed LPs with MAC12, 13.0% with ART and FUKUDA, but no cases showed LPs with MAC1. 25.5% of the myocardial infarction group showed LPs with MAC12 and MAC1, 30.9% with ART and 36.3% with FUKUDA. All four methods gave corresponding results in 65.4% of patients, 7.0% positive and 58.4% negative findings. FQRSD of MAC12, ART and FUKUDA was 110.2 +/- 18.1 msec, 105.2 +/- 20.4 msec and 125.8 +/- 22.8 msec respectively. Correlation coefficient (r value) in FQRSD was 0.90 between ART and MAC12, 0.74 between ART and FUKUDA, and 0.75 between FUKUDA and MAC12. RMSV of MAC12, ART and FUKUDA was 49.2 +/- 30.2 microV, 43.7 +/- 37.8 microV and 22.5 +/- 10.6 microV respectively. R value in RMSV was 0.59 between ART and MAC12, 0.38 between ART and FUKUDA and 0.43 between FUKUDA and MAC12. R value in high frequency low amplitude signals duration under 40 microV of LPs positive patients in MAC1 was 0.51 between ART and MAC 12, 0.18 between MAC12 and MAC1, and 0.32 between ART and MAC1. Most of the differences result from a different interpretation of the tracings. Especially LPs far from QRS offset could be registered with neither MAC12, ART nor FUKUDA.