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Biomedical subjects

M Arita

Publications and source records attributed to M Arita.

At least 181 records · Page 10Linked to original sources
PubMed1994

Effect of temocapril on haemodynamic and humoral responses to exercise in patients with mild essential hypertension.

1. This study was carried out to evaluate the effect of temocapril on haemodynamic and humoral responses to exercise in nine patients with mild essential hypertension (WHO stages I and II). 2. After a 4-week placebo period, temocapril was administered at a dose of 1.0 mg once daily for 2-4 weeks. Graded submaximal bicycle ergometer exercise was performed before and after temocapril treatment, and the changes in arterial blood pressure, heart rate, cardiac output (CO), and systemic vascular resistance (SVR) were evaluated. In addition, the plasma norepinephrine (NE) level was determined both at rest and peak exercise before and after temocapril treatment. 3. Both the systolic and diastolic blood pressure were reduced at rest and during exercise by temocapril treatment. No significant change in the resting heart rate and CO was observed, and the exercise-induced increase of these parameters was also not affected by temocapril. In contrast, the resting SVR was significantly decreased by temocapril, although the exercise SVR was similar during both temocapril and placebo treatment. 4. Although there was no significant change in the plasma NE level with temocapril treatment, the exercise-induced increase of plasma NE was significantly suppressed by temocapril. 5. These results indicate that temocapril reduces the blood pressure without causing any significant changes in the heart rate and CO at rest, and that it does not produce any changes in the haemodynamic response to exercise.

Adult↗
PubMed1994

Immunohistochemical studies of extracellular matrix components and integrins in IgA nephropathy.

Localization of adhesive glycoproteins as the extracellular matrix and their cell surface receptors (integrins) were studied in an attempt to clarify their roles in the progression and aggravation of IgA nephropathy. The relationship between their localization and factors associated with clinical progression was then investigated in 65 patients with IgA nephropathy. The indirect immunoperoxidase method was used to study the distribution of fibronectin (FN), vitronectin (VN), fibronectin receptor (FNR) and vitronectin receptor (VNR). In all cases, FN was present in the glomeruli, mainly confined to the mesangial region, and in some cases, it was observed along the glomerular capillary loops. An expanded mesangial region accompanied higher FN distribution. FNR was present in the mesangial region and glomerular capillary loops, and was higher in the expanded mesangial region. VN was positive in 51 of 65 cases. In all cases, VNR was present in the mesangium and glomerular capillary loops, and its distribution was more predominant in and along the capillary loops than in the mesangial region. The expanded mesangium accompanied higher VNR distribution. There was a significant correlation in distribution between all factors with the exception of VN and FNR. FN, FNR and VNR increased significantly as a degree of histological damage. However, VN was not significantly associated with the degree of histological damage in positive and negative groups. The distribution of FN, FNR and VNR was associated with clinical aggravation factors although the distribution of VN was not. In conclusion, the distribution and functional alteration of FN and integrins in the glomeruli appear to be involved in the progression and exacerbation of IgA nephropathy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Monoclonal antibody raised against apoprotein of C-1027: effect on biochemical and biological activities of the holoantibiotic.

A monoclonal antibody raised against C-1027 apoprotein recognized not only the apoprotein, but also the holoantibiotic (Antibiotic C-1027) almost equally. Among the biochemical and biological activities of the holoantibiotic, the antibody inhibited the aminopeptidase activity and the cytotoxicity to Ehrlich carcinoma cells in cultures, but not the DNA-cleaving activity in vitro. The immunohistogram, using this antibody, of Ehrlich carcinoma cells that had been exposed to the holoantibiotic suggested penetration of the holoantibiotic into target cells.

Aminoglycosides↗
PubMed1994

Effects of KT-362, a new antiarrhythmic agent, on membrane ionic currents of guinea pig ventricular myocytes.

We studied the effects of KT-362, (5-[3[2-(3,4-dimethoxyphenyl)ethyl]amino]-1-oxopropyl]-2,3,4,5- tetrahydro-1,5-benzothiazepine fumarate), a newly synthesized vasodilating and antiarrhythmic agent, on membrane currents of single guinea pig ventricular cells, using whole-cell voltage-clamp techniques. In the steady state with a stimulation frequency of 0.5 Hz, KT-362 at concentrations of 10 and 30 microM decreased the peak sodium current (INa) in a concentration-dependent manner, i.e., by 27% and 49%, respectively. The inhibition of INa by this agent was use-dependent: KT-362 (30 microM) inhibited INa by 21% at 0.2 Hz and by 51% at 1 Hz. In addition, KT-362 (10-30 microM) decreased the L-type Ca current (ICa) in a concentration-dependent fashion. The delayed rectifier potassium current and the inward rectifier potassium current were also inhibited by KT-362. The effects of KT-362 on INa and ICa were confirmed in experiments using ventricular papillary muscle preparations and microelectrode techniques. KT-362 (10-300 microM) decreased the maximum rate of rise of action potentials provoked at normal (2.7 mM) K+ concentration and that provoked at high (20 mM) K+ concentration. KT-362 at concentrations over 100 microM significantly depolarized the resting membrane, and the action potential duration remained unaltered. From these findings, we conclude that apart from the alleged inhibitory effects of this agent on the release of calcium from sarcoplasmic reticulum (it is therefore termed "an intracellular Ca++ blocker"), KT-362 suppresses a variety of membrane ionic currents of cardiac cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Comparison of the effects of single morning and single bedtime doses of famotidine on intragastric acidity in patients with gastric ulcer.

The effects of single morning and single bedtime doses of famotidine on intragastric acidity were studied by 24-h intragastric pH monitoring in 16 patients with gastric ulcer. The patients were randomly allocated to the following regimen: one group (n = 8) received 40 mg famotidine at 8:30 AM and another group (n = 8) received the same dose at 10 PM. The morning group showed significant inhibition of gastric acidity during the 24-h and daytime measurements, compared to those of the bedtime group (p < 0.05 in 24 h, p < 0.01 in daytime). Conversely, the bedtime group showed a significant inhibition of gastric acidity during the nocturnal period compared to the morning group (p < 0.01). These results indicate that the relative importance of suppression of gastric acidity on the gastric ulcer healing process should be evaluated in a clinical trial.

Drug Administration Schedule↗
PubMed1993

Factors for transient entrainment of ventricular tachycardias by rapid atrial pacing.

Thirteen patients with sustained ventricular tachycardia (VT) were studied to elucidate predisposing factors for the development of constant and progressive fusion by rapid atrial pacing. All patients demonstrated transient entrainment by rapid ventricular pacing during VT. Constant and progressive fusion were observed in 7 patients (positive group) during rapid atrial pacing, but not in 6 (negative group). In the positive group, VT was induced by atrial pacing in 2 patients. The demonstration of constant and progressive fusion by atrial pacing was not dependent on QRS morphology or ventriculoatrial conduction during VT. VT cycle length in the positive group (363 +/- 59 ms) was longer than in the negative group (297 +/- 31 ms; p = 0.033). The maximal atrial pacing rate producing 1:1 atrioventricular (AV) conduction in the positive group was 171 +/- 18 beats/min compared with 125 +/- 22 beats/min in the negative group (p = 0.002). There were distinct differences between the positive and negative groups in the ratio of VT cycle length to minimal atrial cycle length causing 1:1 AV conduction (1.02 +/- 0.12 vs 0.61 +/- 0.12; p = 0.0001). It is concluded that AV conduction, VT cycle length and especially their ratio are important factors for the development of transient entrainment by rapid atrial pacing during VT. Therefore, atrial pacing can be used as an easy and useful method to examine transient entrainment during VT.

Adult↗
PubMed1993

A comparative study of effects of isoproterenol and dihydroouabain on calcium transients and contraction in cultured rat ventricular cells.

We investigated the effects of isoproterenol, a beta-adrenergic agonist, and dihydroouabain, a Na+,K(+)-pump inhibitor, on Ca2+ transients and contraction of cultured rat ventricular cells and compared the effects with those of altered external ion concentrations, with special reference to the changes in diastolic intracellular free calcium concentration ([Ca2+]i). We measured [Ca2+]i of cultured cell aggregates, stimulated at 1.0 Hz, with the use of dual-wavelength microfluorometry of fura-2, at room temperature (24-26 degrees C). The contraction was measured as a shortening of the aggregates using a photodiode array placed on a video monitor. Isoproterenol increased the magnitude of contraction and the peak amplitude of the Ca2+ transient, in a concentration (10(-9)-10(-6) M)-dependent manner, but did not change the diastolic Ca2+ level. Isoproterenol at 10(-7) M or higher significantly shortened the duration of contraction and half decay time of a Ca2+ transient yet it did not change the time to peak. Dihydroouabain (10(-7)-10(-5) M) increased the contraction and elevated both systolic and diastolic calcium levels but it did not alter the duration of contraction, the time to peak and the half decay time. The effects of dihydroouabain on Ca2+ transients were mimicked by lowering [K+]o (0.4 mM), by lowering [Na+]o (74 mM) or by elevating [Ca2+]o (3.6 or 5.4 mM). Ryanodine (10(-5) M), by itself, decreased systolic Ca2+ transient amplitude, increased diastolic Ca2+ levels and prolonged the time to peak and the half decay time. In the presence of ryanodine, isoproterenol increased both systolic and diastolic [Ca2+]i. Thus, most procedures that increased the systolic Ca2+ transient amplitude increased the diastolic Ca2+ levels as well, and enhanced the contraction. The only exception was isoproterenol that markedly increased the systolic Ca2+ transient amplitude without affecting the diastolic Ca2+ level, a finding in keeping with the observation that isoproterenol stimulates Ca2+ uptake by the sarcoplasmic reticulum.

Animals↗
PubMed1993

Differential mechanism of block of palmitoyl lysophosphatidylcholine and of palmitoylcarnitine on inward rectifier K+ channels of guinea-pig ventricular myocytes.

We investigated the effect of lysophosphatidylcholine (lysoPtdCho) and palmitoylcarnitine (PamCar), ischemia-induced amphipathic lipid metabolites, on the inward rectifier K+ channel in guinea-pig ventricular cells, under whole-cell and cell-attached configurations with patch-clamp techniques. (a) Both lysoPtdCho (10-50 microM) and PamCar (10-50 microM) depolarized the resting membrane potential (RP), retarded the repolarization of action potential, provoked spontaneous action potential discharges from oscillatory afterpotentials, and eventually caused a sudden rise of the RP to plateau levels. (b) These lysoPtdCho- or PamCar-induced depolarizations of RP were due to a decrease in the inward rectifier K+ current (IK1), and the sudden rise of the RP could be accounted for by a crossover of N-shaped current-voltage relationship on the voltage axis (zero current line) more than once. (c) Single-channel studies in the cell-attached mode revealed that lysoPtdCho (5-100 microM) decreased the conductance of the single IK1 channel with little change in its open probability, whereas PamCar (10-50 microM) did so by decreasing the open probability, with the channel conductance unaltered. (d) A short-chain acylcarnitine, l-propionylcarnitine (PpCar, 100 microM), prevented the depressant effect of lysoPtdCho (50 microM), but not of PamCar (50 microM), on the IK1. (e) Both lysoPtdCho and PamCar produced identical electrophysiological alterations on the membrane potential and IK1 in whole-cell recordings. However, molecular mechanisms involved in the effects of these toxic metabolites on single IK1 channels differ.

Animals↗
PubMed1993

Effects of elastase on contractility and morphology of elastic tissue in isolated guinea pig papillary muscles.

Elastase (ELA) is an enzyme catalyzing the digestion of elastin, an essential constituent of elastic fibers. Using isolated guinea pig papillary muscles, we examined the effect of ELA (3 x 10(-7) -3 x 10(-4) g/ml) on resting tension (RT) and twitch tension (TT). The effects of ELA on elastic fibers located in the subendocardium were examined histologically. A relatively high concentration of ELA (3 x 10(-4) g/ml) increased TT transiently, with progressive decreases in RT. In contrast, a relatively low concentration (3 x 10(-5) g/ml) decreased both TT and RT straightforwardly. Much lower concentrations (3 x 10(-6) -3 x 10(-7) g/ml) did not reveal significant effects. The ELA-induced increases in TT were unaffected in the presence of atenolol (10(-5) g/ml), ouabain (10(-7) M) or ryanodine (10(-6)M). ELA did not increase the maximum rate of rise of slow action potentials recorded using standard microelectrodes. ELA (3 x 10(-5) g/ml) decreased the maximum TT obtained at optimal RT or Lmax, and decreased the slope of the ascending and descending limbs of the TT-RT relation curve (Frank-Starling's). Electron-microscopic findings revealed that subendocardial elastin was mostly digested at ELA concentrations of 3 x 10(-5) -3 x 10(-4) g/ml. These findings suggest that the decrease of RT by ELA may be, at least in part, caused by a decomposition of the elastic fibers. On the other hand, the increase of TT by ELA could not be attributed to a release of endogenous catecholamine, an inhibition of Na+, K(+)-pump, a release of Ca2+ from sarcoplasmic reticulum, or an increase of slow inward current.

Animals↗
PubMed1993

Bepridil prolongs the action potential duration of guinea pig ventricular muscle only at rapid rates of stimulation.

1. We examined the electromechanical effects of the calcium antagonist, bepridil (1-20 microM), on isolated guinea pig ventricular muscles, driven at various stimulus frequencies (0.1, 0.5, 1, 2 and 5 Hz) in Tyrode's solution containing various K+ concentrations (1.4-43.2 mM). 2. Conventional microelectrode and tension-recording techniques were used. 3. We found that bepridil decreased the maximum upstroke velocity (Vmax) of the action potential with no change in the resting membrane potential (RMP). 4. The former effect depended on both stimulus frequency and the drug concentration used. 5. Bepridil lengthened the duration of the action potential at the level of 25% repolarization (APD25) at the highest frequency (5 Hz), but shortened it at lower frequencies (< or = 2 Hz). 6. The drug also lengthened the APD90 at the highest frequency (5 Hz) but without significant effect at lower frequencies (< or = 2 Hz). 7. Bepridil depolarized the RMP at relatively low extracellular K+ concentrations (< or = 2.7 mM), accompanied by a prolongation of APD90. 8. There were no such effects at much higher K+ concentrations (> or = 5.4 mM), and the drug markedly depressed the Vmax and the action potential amplitude. 9. The drug eliminated the positive staircase phenomenon of twitch contraction, in a concentration-dependent manner. 10. All these findings taken together suggest that bepridil prolongs the action potential duration by inhibiting outward potassium currents (IK and IK1), at rapid rates of stimulation (approximately 300/min), which is comparable to the physiological heart rate of a guinea pig. 11. The prolongation of APD seemed to be secondary to the bepridil-induced reduction of intracellular Ca2+ concentration, [Ca2+]i.

Action Potentials↗
PubMed1993

Biochemical components and myocardial performance after reversal of left ventricular hypertrophy in spontaneously hypertensive rats.

OBJECTIVE: This study was undertaken to determine the biochemical and left ventricular functional changes associated with reversal of left ventricular hypertrophy (LVH) in spontaneously hypertensive rats (SHR). DESIGN: Male SHR and normotensive Wistar-Kyoto (WKY) rats, aged 19 weeks, were treated for 3 weeks with vehicle, amlodipine (10 mg/kg), benazepril (10 mg/kg) or the combination of both agents (4 mg/kg amlodipine and 4 mg/kg benazepril). Left ventricular function was assessed while blood was infused rapidly, at pharmacologically reduced and pretreatment mean arterial pressure (MAP). RESULTS: All treatments reduced MAP and left ventricular mass significantly in SHR. Myocardial protein, RNA and myocardial collagen content were reduced proportionately in all treatment groups in SHR, but not in WKY rats. DNA remained unchanged in all groups. Increased right ventricular mass was produced by amlodipine in both SHR and WKY rats (SHR +11.3%; WKY +9.8%), but this was prevented by cotreatment with benazepril. Right ventricular protein and collagen increased significantly with amlodipine in SHR but not WKY rats, and there were no changes in right ventricular RNA and DNA contents in either strain. Amlodipine improved, benazepril impaired and the combination of both agents maintained left ventricular pumping ability when pressure was increased abruptly to pretreatment levels in WKY rats. In contrast, when afterload was increased abruptly in SHR to pretreatment levels, neither amlodipine nor benazepril affected pumping ability, although it was enhanced by the combination. CONCLUSIONS: These data demonstrate that amlodipine, benazepril and their combination reduced left ventricular mass in SHR. This reversal of LVH was associated with proportional reductions in mycotic protein, RNA and collagen, but not DNA. Therefore, it seems unlikely that LVH reversal with these agents was associated with increased fibrous tissue or impaired left ventricular performance. Finally, addition of the angiotensin converting enzyme inhibitor prevents the increase in right ventricular mass produced by the calcium antagonist.

Amlodipine↗
PubMed1993

Effect of dental metals on magnetic resonance imaging (MRI).

The aim of this research was to examine the effects of metals used in dentistry upon magnetic resonance imaging (MRI). Ten disk-shaped samples of metals have been used in this study. Each sample has been set into a volunteer who had produced a normal MR image when tested. The subject was imaged in the sagittal, frontal and coronal plane with a 0.1 T MRI device and results examined for MR defects. Au, Ag, Au-Ag-Pd and amalgam produced no defect. Ni-Cr, Co-Cr and SUS304 expressed small amounts of MR defects, but SUS405, Pd-Co-Ni and Sm-Co expressed large defects. Those metals which create MR image degradation must not be used for fixed prosthesis or orthodontic devices both of which could easily be made from other metals. If the MR image degrading metals are to be used in dentistry, their application should be restricted to removable prosthesis.

Adult↗
PubMed1993

Cibenzoline inhibits diazoxide- and 2,4-dinitrophenol-activated ATP-sensitive K+ channels in guinea-pig ventricular cells.

1. We have investigated the effects of diazoxide (a sulphonamide derivative) and cibenzoline (a class I antiarrhythmic drug) on ATP-sensitive K+ currents in guinea-pig ventricular cells, using whole-cell clamp techniques. 2. Diazoxide (50 microM) produced a marked shortening of action potential duration which was antagonized by 1 microM glibenclamide, an ATP-sensitive K+ channel blocker. 3. Diazoxide (50 microM) increased the quasi-steady state outward current elicited by a ramp voltage protocol (-20 mV s-1) at potentials positive to about -70 mV. This effect was completely prevented in the presence of glibenclamide (1 microM), thereby suggesting that diazoxide opens ATP-sensitive K+ channels. 4. Cibenzoline (5 microM) depressed the diazoxide-induced increases in the outward current and the pretreatment with this agent prevented the development of the diazoxide-induced outward current. 5. Cibenzoline (10 microM) reversed the 2,4-dinitrophenol (50 microM)-induced shortening of the action potential duration partially but significantly. 6. These results suggest that diazoxide activates ATP-sensitive K+ channels of guinea-pig ventricular cells and that cibenzoline, at therapeutic concentrations, inhibits this channel.

2,4-Dinitrophenol↗
PubMed1993

Ionic mechanisms of action potential prolongation at low temperature in guinea-pig ventricular myocytes.

1. We studied the effects of low temperature on the action potentials and membrane currents of guinea-pig ventricular myocytes, using a tight-seal whole-cell clamp technique. 2. The action potential duration at 95% repolarization was prolonged from 146 +/- 33 ms (mean +/- S.D., n = 6) at 33-34 degrees C (control temperature) to 314 +/- 83 ms at 24-25 degrees C (low temperature). 3. In whole-cell clamp experiments, low temperature decreased the calcium current (ICa), the delayed rectifier potassium current (IK), and the inwardly rectifying potassium current (IK1) with 'apparent' Q10 (temperature coefficient) values of 2.3 +/- 0.6 for ICa, 4.4 +/- 1.2 for IK tail current and 1.5 +/- 0.3 for IK1 (n = 7). 4. The effect of low temperature on IK was further studied in the presence of 0.6 microM nicardipine to block ICa. The decay phase of the IK tail consisted of two exponential components. The fast but not the slow component was highly sensitive to the temperature change with an apparent Q10 of 4.5. 5. We found that a component of time-independent current is also sensitive to the temperature. The current had a linear I-V relationship and remained almost unchanged after inhibition of Na(+) -K+ pump in K(+)-free external solution. 6. Using our mathematical model of the ventricular action potential (a modification from the DiFrancesco-Noble model), we simulated the action potential at low temperature by modifying some of the membrane currents, namely IK, IK1, ICa and a component of background current. It was shown that simultaneous changes in these currents could reproduce approximately 75% of the action prolongation induced by low temperature.

Action Potentials↗
PubMed1993

Purification and characterization of a new agarase from a marine bacterium, Vibrio sp. strain JT0107.

A marine bacterial strain that decomposes the cell walls of some seaweeds, including a Laminaria sp. and Undaria pinnatifida, has been isolated from seawater. This strain has been classified to the genus Vibrio. One of the enzymes which the bacteria secreted into the culture medium was isolated and purified 45-fold from the culture fluid by a combination of ammonium sulfate precipitation and successive rounds of anion-exchange column chromatography. Purified protein migrated as a single band (M(r), 107,000) on sodium dodecyl sulfate-polyacrylamide gels. By amino acid sequence analysis, it was determined that this protein had a single N-terminal sequence that did not exhibit identity with the sequences of other agarases from marine bacteria. This novel enzyme was found to be an endo-type beta-agarase (EC 3.2.1.81) which hydrolyzes the beta-1,4 linkage of agarose to yield neoagarotetraose [O-3,6-anhydro-alpha-L-galactopyranosyl (1-->3)-O-beta-D-galactopyranosyl(1-->4)-O-3,6-anhydro-alpha-L-galactopy ranosyl (1-->3)-D-galactose] and neoagarobiose [O-3,6-anhydro-alpha-L-galactopyranosyl (1-->3)-D-galactose] at a pH of around 8. The optimum temperature was 30 degrees C. This enzyme did not decompose sodium alginate or lambda-, iota-, or kappa-carrageenan. This enzyme may be of practical application in gene technology in the isolation of DNA fragments from agarose gels after electrophoresis.

Amino Acid Sequence↗
PubMed1993

Cumulative effects of heart beat on ventricular premature contractions suggesting possible involvement of triggered activity.

We analyzed 24 h ECG recordings of 29 patients with frequent (> 2000/day) ventricular premature contractions (VPCs) to evaluate: 1) the relationship between VPC frequency and heart rate (HR); 2) the relationship between the coupling interval (CI) of VPCs and HR; 3) the time course of changes in VPC frequency following an abrupt and sustained increase in HR; and 4) the effect of oral diltiazem (90 or 180 mg/day for 4 weeks) on VPCs. Based on the patterns of relationship between VPC frequency and HR, patients were divided into 2 groups: 1) 17 patients with a positive correlation, the P group (a linear increase in VPCs with increasing HRs); and 2) 12 patients with a non-positive correlation, the NP group. The NP group showed either a linear decrease in VPCs with increased HRs (4 patients) or an increase in VPCs at low HRs and a decrease at high HRs (8 patients). In all cases, an increased HR was associated with a shortening of CI. In the P group, changes in VPCs after an abrupt increase in HR showed 2 types: 1) delayed-ascent type, in which VPCs increased as the duration of HR increase was prolonged (cumulative effects of heart beat) (7 patients); and non-delayed-ascent type (10 patients). Diltiazem reduced VPCs > or = 75% in all of the 7 delayed-ascent-type patients, compared with 3 of the 10 non-delayed-ascent-type patients (p < 0.05) and none of the 12 patients in the NP group (p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1993

Suppression of ventricular premature contractions continues after the washout of antiarrhythmic drugs.

The effects of the washout of antiarrhythmic drugs on the frequency of ventricular premature contraction (VPC) were investigated in 64 patients (VPCs > 2000/day). Included were patients on mexiletine (300-600 mg/day; 23 patients), disopyramide (300-600 mg/day; 19 patients) and atenolol (50 mg/day; 22 patients). Holter monitoring was repeated before, during and after the treatment with the above 3 drugs and the efficacies of the drugs were evaluated based on the spontaneous variability before the treatment. VPC reduction exceeding the calculated spontaneous variability during drugs therapy (drug-responders) and after the washout of the drugs (wash-responders) was noted in 17 (63%) and 3 (13%) of the mexiletine group; 11 (58%) and 5 (26%) of the disopyramide group; and 13 (59%) and 8 (36%) of the atenolol group, respectively. For the entire group of 64 patients, wash-responders were noted significantly (p < 0.05) more among drug-responders (14 of 41 patients; 34%) than drug-nonresponders (2 of 23 patients; 9%). Therefore, the antiarrhythmic effects of drugs observed during drugs therapy seem to continue even after the discontinuation of antiarrhythmic drugs in 34% of patients those whose VPC reduction exceeded the spontaneous variability (drug-responders).

Adult↗