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Biomedical subjects

H Kasanuki

Publications and source records attributed to H Kasanuki.

At least 55 records · Page 3Linked to original sources
PubMed1999

A mitochondrial DNA mutation cosegregates with the pathophysiological U wave.

In a family with long QT syndrome (LQT2), some individuals who did not harbor the HERG mutation had a prolonged QTU interval on electrocardiograms after exercise. It may be determined or modified by other gene(s) or factor(s). The sequence analysis of mtDNA in these individuals of this family showed a candidate pathogenic mutation at 3394 in the ND1 gene. The cybrids (mutation at 3394) showed significantly reduced NADH-CoQ reductase (complex I) activity and O2 consumption to normal levels. These inhibitory effects on respiratory function may result in the depletion of ATP and could possibly produce an increase in Ca2+ concentration in cytosol, and it may lead to the prolongation of the QTU intervals on electrocardiograms. Therefore, we stated that the 3394 mutation in the ND1 gene is pathogenic and could be the cause of prolongation of the QTU intervals or modification of the phenotypes of not only congenital but also so-called "acquired drug-induced long QT syndrome."

Adolescent↗
PubMed1999

Clinical and angiographic outcome of stenting following suboptimal results of percutaneous transluminal coronary angioplasty in small (<2.5 mm) coronary arteries.

The purpose of the present study was to evaluate the feasibility and efficacy of stenting following suboptimal percutaneous transluminal coronary angioplasty (PTCA) in angiographically small coronary arteries. The clinical and angiographic outcome of unplanned stenting in 33 patients with coronary arteries <2.5 mm in diameter was studied. Procedural success was achieved for 97.0% with a greater initial gain (1.79 +/- 0.60 vs. 1.34 +/- 0.58 mm, P < 0.05) and larger postprocedural minimal luminal diameter (2.19 +/- 0.43 vs. 1.57 +/- 0.57 mm, P < 0.001) than that in the size-matched elective PTCA patients. Trends toward a lower restenosis rate and a significant reduction in target lesion revascularization (7.1% vs. 41.9%, P < 0.01) were observed in the stented patients, suggesting the feasibility and efficacy of stenting following suboptimal PTCA in small coronary arteries. Cathet. Cardiovasc. Intervent. 47:269-276, 1999.

Aged↗
PubMed1999

Properties of the transient outward current in rabbit sino-atrial node cells.

The electrophysiological properties of the transient outward current were investigated in voltage-clamped single cells from the rabbit sino-atrial node. To make a regional comparison, some experiments were repeated in atrial myocytes. The current-voltage relationship showed a characteristic outward rectification with an activation threshold of -30 mV. External 4-aminopyridine (0.01-5 mM) inhibited this current in a dose-dependent manner (IC50 = 0.28 mM, Hill coefficient = 1.38). The steady-state inactivation exhibited a half-maximum voltage of -35 mV and a slope factor of -.4 mV. The current density of the transient outward current was 6.3 +/- 0.5 pA/pF in sino-atrial node cells and 12.3 +/- 1.2 pA/pF in atrial cells. The inactivation time constant was faster in sino-atrial node cells (time constants 4.2 +/- 0.5 and 26.0 +/- 0.6 ms, respectively, for the fast and slow components) than in atrial cells (9.7 +/- 1.2 and 44.8 +/- 3.2 ms, respectively). Recovery from inactivation was much faster in sino-atrial node cells (time constants 44.7 +/- 9.0 ms) than in atrial cells (time constants 1.39 +/- 0.32 and 6.70 +/- 0.1 s, respectively, for the fast and slow components). These results suggest that the kinetic properties, as well as the current density, of the transient outward current differs between sino-atrial node and atrial cells. Taking the current density of Ito at +10 mV as 2.5 +/- 0.3 pA/pF gives a total Ito of approximately 100 pA at the peak of the action potential in rabbit sino-atrial node cells. The action potential duration was increased by 24.8 +/- 1.3% by 0.5 mM 4-AP. Thus, Ito may contribute significantly to the repolarization phase in mammalian sino-atrial node cells.

4-Aminopyridine↗
PubMed1999

An equation to predict the changes in peak left ventricular pressure in hypertrophic obstructive cardiomyopathy after treatment: application to the administration of disopyramide.

A theoretical equation was derived based on the time-varying elastance model to predict theoretically the relationship between the delay in the onset of left ventricular outflow obstruction and the reduction in peak left ventricular pressure (LVP) caused by treatment in hypertrophic obstructive cardiomyopathy (HOCM). ECG, LVP, and other hemodynamic parameters were measured during catheterization at a constant heart rate with atrial pacing in 16 patients with HOCM before and after intravenous administration of disopyramide (1 mg/kg). After disopyramide administration, the duration between the R wave of the ECG and the onset of obstruction (T1) was prolonged significantly (from 117 +/- 30 to 155 +/- 32 ms, P < 0.0001), and peak LVP was reduced significantly (from 222 +/- 42 to 177 +/- 39 mmHg, P < 0.0001). The relation between the prolongation of T1 and the percent reduction in peak LVP was predicted well by the theoretical equation (coefficient of determination R2 = 0.926). Our model simplifies the therapeutic strategy for reducing the left ventricular outflow pressure gradient in patients with HOCM, which is to delay the time of onset of obstruction by some methods.

Adult↗
PubMed1999

A noninvasive method of measuring wave intensity, a new hemodynamic index: application to the carotid artery in patients with mitral regurgitation before and after surgery.

Wave intensity (WI) is a new hemodynamic index, which is defined as (dP/dt)(dU/dt) at any site of the circulation, where dP/dt and dU/dt are the time derivatives of blood pressure and velocity, respectively. Arterial WI in normal subjects has two positive sharp peaks. The first peak occurs during early systole when a forward-traveling compression wave is generated by the left ventricle. The magnitude of this peak increases markedly with an increase in cardiac contractility. The second peak, which occurs towards the end of systole, is caused by generation of a forward-traveling expansion wave by the ability of the left ventricle to actively stop aortic blood flow. The interval between the R wave of the ECG and the first peak of WI (R-1st peak interval) and the interval between the first and second peaks (1st-2nd interval) are approximately equal to the preejection period and left ventricular ejection time, respectively. Using a combined Doppler and echo-tracking system, we obtained carotid arterial WI noninvasively. We examined the characteristics of WI in 11 patients with mitral regurgitation (MR) before and after surgery, and 24 normal volunteers. In the MR group before surgery, the second peak was decreased and the (1st-2nd interval)/(R-R interval) ratio was reduced, compared with the normal group (140 +/- 130 vs 750 +/- 290mmHg m/s3. P < 0.0083; 20.7% +/- 3.4% vs 26.7% +/- 2.8%, P < 0.083). There were no significant differences in the first peak between the normal group and the MR group before and after surgery. The second peak in the MR group was increased significantly (P < 0.016 vs before surgery) to 1,150 +/- 830mmHg m/s3 in the early period after surgery (stage I), and to 1,090 +/- 580mmHgm/s3 in the late period after surgery (stage II). These values did not differ significantly from that of the normal group. At stage I, the (R-1st peak interval)/ (R-R interval) ratio was increased from 13.4% +/- 2.7% to 20.6% +/- 5.6% (P < 0.016 vs before surgery). At stage II, this ratio decreased to 16.2% +/- 2.8% (P < 0.016 vs stage I). but was still significantly higher than that before surgery. The (1st-2nd interval)/(R-R interval) ratio increased significantly after surgery (P < 0.016 vs before surgery) to values (27.0% +/- 4.5% at stage I and 28.9% +/- 2.6% at stage II) which did not differ significantly from that of the normal group. The recovery of the second peak after surgery suggests that the left ventricle had recovered the ability to actively stop aortic blood flow. Wave intensity is useful for analyzing changes in the working condition of the heart.

Adult↗
PubMed1999

Effects of propafenone on K currents in human atrial myocytes.

1. The class Ic anti-arrhythmic agent, flecainide is known to inhibit the transient outward K current (Ito) selectively in human atrium. We studied the effects of propafenone, another class Ic antiarrhythmic agent, on K currents in human atrial myocytes using a whole-cell voltage-clamp method. 2. Propafenone inhibited both Ito and the sustained or ultra-rapid delayed rectifier K current (Isus or Ikur) evoked by depolarization pulses. The concentration for half-maximal inhibition (IC50) was 4.9 microM for Ito and 8.6 microM for Isus. Propafenone blocked Ito and Isus in a voltage- and use-independent fashion and accelerated the inactivation time constant of Ito [from 28.3 to 6.7 ms at 10 microM propafenone]. 3. The steady-state inactivation curve for Ito was unaffected by propafenone. Propafenone did not affect the initial current at depolarizing potentials, but it did produce a block that increased as a function of time after depolarization (time constant of 3.4 ms). This suggests that propafenone preferentially blocked Ito in the open state. 4. Propafenone had no significant effect on the rate at which Ito recovered from inactivation at -80 mV suggesting that propafenone dissociates rapidly from the channel. 5. The steady-state activation curve for Isus was not affected by propafenone. Propafenone slowed the time course of the onset of the Isus tail current. This suggests that propafenone blocked Isus in the open state. 6. The present results suggest that, unlike flecainide, propafenone blocks both Ito and Isus in human atrial myocytes in the open state at clinically relevant concentrations.

Anti-Arrhythmia Agents↗
PubMed1999

Comparison of parameters of 123I-MIBG scintigraphy for predicting prognosis in patients with dilated cardiomyopathy.

123I-metaiodobenzylguanidine (MIBG) scintigraphy has been used to predict prognosis of patients with dilated cardiomyopathy (DCM), although it is unknown which parameter of MIBG is the most useful clinically. We studied MIBG in 59 patients with DCM, and followed them up to evaluate the prognosis of DCM. Single photon emission tomography (SPET) and planar imaging were performed, both early (e) and 4 h (delayed, d) post-injection. 201Tl (TL) SPET and radionuclide-ventriculography were also investigated. The total defect score of early and delayed MIBG and 201 Tl (MIBGeDS, MIBGdDS, TLDS) was analysed visually for each SPET image. The heart to mediastinum ratio (H/M) for both the early and delayed MIBG planar images and myocardial washout rate at 4 h were analysed quantitatively. Sixteen patients died during follow-up. Cox Hazards univariate analysis selected washout rate (P < 0.0001), H/Me (P = 0.0012), H/Md (P = 0.0001) and left ventricular ejection fraction (P = 0.0004) as indices for the prediction of cardiac death. Multivariate analysis selected washout rate as the most powerful independent predictor of prognosis (P < 0.0001). Survival curves with a threshold value of 52% for washout rate were able to differentiate a negative outcome from survival (P < 0.0001). TLDS, MIBGeDS and MIBGdDS were not useful in the prediction of prognosis. The washout rate of MIBG is the most potent predictor of cardiac death and is considered clinically useful.

3-Iodobenzylguanidine↗
PubMed1999

Clinical significance of consecutive shocks in patients with left ventricular dysfunction treated with implantable cardioverter defibrillators.

The purpose of the present study was to determine the clinical significance of consecutive automatic shocks delivered by implantable cardioverter defibrillators (ICDs). Sixty-four patients who received ICDs at our institution between January 1990 and July 1997 were included in this study. There were 53 men and 11 women with a mean age of 50 +/- 14 years. During a follow-up period ranging between 0.2 and 73 months (mean 23 +/- 21 months), 17 patients received consecutive shocks (group A), 29 patients received single shocks (group B), and 18 patients received no ICD therapy (group C). Clinical characteristics, episodes of ICD therapy, and prognosis were compared among the three groups. There were no significant differences among the three groups with regard to clinical characteristics, time to first ICD therapy, number of antitachycardia pacing episodes, or frequency of inappropriate discharges. The mortality rate was higher in group A than in groups B and C (P = 0.0021). The sensitivity of consecutive shocks in predicting death was 70%, the specificity was 88%, and the predictive accuracy was 81% in patients with left ventricular ejection fractions < 35%. In summary, consecutive shocks are a clinically important event in patients with ICDs. Specifically, patients who receive consecutive shocks and have a depressed left ventricular function should be considered particularly high risk.

Defibrillators, Implantable↗
PubMed1999

Profiles of aprindine, cibenzoline, pilsicainide and pirmenol in the framework of the Sicilian Gambit. The Guideline Committee for Clinical Use of Antiarrhythmic Drugs in Japan (Working Group of Arrhythmias of the Japanese Society of Electrocardiology).

The Vaughan Williams classification has been used widely by clinicians, cardiologists and researchers engaged in antiarrhythmic drug development and testing in many countries throughout the world since its initial proposal in the early 1970s. However, a major criticism of the Vaughan Williams system arose from the extent to which the categorization of drugs into classes I-IV led to oversimplified views of both shared and divergent actions. The Sicilian Gambit proposed a two-dimensional tabular framework for display of drug actions to solve these problems. From April to December 1996, members of the Guideline Committee met to discuss pharmacologic profiles of 4 antiarrhythmic drugs (aprindine, cibenzoline, pilsicainide, and pirmenol) that were not included in the original spreadsheet but are used widely in clinical practice in Japan. The discussion aimed to fit the drug profiles into the Gambit framework based on all the important literature published to date regarding the actions of the 4 drugs. This report is a summary of that deliberation.

Animals↗
PubMed1999

Unsuitability of corrected QT dispersion as a marker for ventricular arrhythmias and cardiac sudden death after acute myocardial infarction.

The present study investigated whether corrected QT (QTc) dispersion could play a role as a marker of ventricular arrhythmias and sudden cardiac death after acute myocardial infarction (MI). The study included 76 males and 24 females with a mean age of 60+/-11 years. Standard 12-lead ECGs were recorded during the recovery phase (15+/-9 days) after the onset of MI. The QTc was calculated according to Bazett's formula and QTc dispersion was calculated as the difference between the maximum and minimum QTc intervals. Patients were divided into 2 groups: 21 patients (group A) had a QTc dispersion of > or =80ms, and the other 79 patients (group B) had a QTc dispersion of <80ms in the recovery stage (15+/-9 days). Clinical, angiographical, and Holter monitoring data, and prognosis (mean follow-up period 29+/-18 months) were compared between these 2 groups. The frequencies of early coronary reperfusion and recanalization of infarct-related vessels during the recovery phase were significantly higher in group B than group A. The left ventricular ejection fraction was also higher in group B than group A (51+/-12 vs 43+/-12%, p=0.0029). There were no significant differences in the number of premature ventricular contractions, the percentage of patients with repetitive ventricular arrhythmias, or in the frequency of sudden cardiac death during the follow-up period between the 2 groups. In summary, QTc dispersion in the recovery stage is not a useful marker for ventricular arrhythmias or sudden cardiac death after acute MI, although increased QTc dispersion may correlate with an ineffective early coronary reperfusion and with the degree of depressed left ventricular function.

Adult↗
PubMed1999

Clinical characteristics of amiodarone-induced thyrotoxicosis and hypothyroidism in Japan.

Since amiodarone was introduced in Japan in 1992, the incidence of the drug-induced thyroid dysfunction has been increasing. We studied the thyroid function of 13 patients with amiodarone-induced thyrotoxicosis (AIT) and 11 patients with amiodarone-associated hypothyroidism (AAH) who had been referred to our Institute in the last 6 years. AIT and AAH developed after 39+/-21 and 20+/-16 months of amiodarone treatment, respectively. One patient developed AAH followed by AIT. The AIT ranged from subclinical to overt thyrotoxicosis. Four patients with moderate to marked AIT were treated with methimazole. Their thyrotoxicosis persisted for 3 to 9 months, despite administration of antithyroid agents. One patient with mild thyrotoxicosis was treated with prednisolone, resulting in a euthyroid state in a few months. Eight patients with asymptomatic to moderate thyrotoxicosis resolved spontaneously without any treatment. In four asymptomatic patients with AIT, serum levels of T3 and T4 were in the upper normal range or slightly high (< 12 microg/dl), accompanied by suppressed TSH (<0.1 microU/ml) and high thyroglobulin levels, suggesting destruction-induced thyrotoxicosis. Such a subclinical thyrotoxicosis developed repeatedly in one patient. Ultrasonographic studies revealed no nodular lesion in the thyroid, and color flow Doppler sonography demonstrated no hypervascularity in the thyroid gland in any AIT patient. Although it is postulated in Europe that there are two types of AIT, namely type I, which develops in patients with latent Graves' disease or toxic multinodular goiter, and type II, which develops in an apparently normal thyroid as destructive thyroiditis, all AIT patients we have seen so far had developed destructive type AIT. Sufficient intake of iodide and a very low incidence of toxic multinodular goiter may account for the rare incidence of type I AIT in our country. Mild to moderate AIT resolved spontaneously without discontinuing amiodarone, but it was discontinued in two of 13 AIT patients because of extrathyroidal adverse reactions.

Adult↗
PubMed1999

[Recent advances in radiofrequency catheter ablation for atrial fibrillation].

Failure to control the ventricular rate in atrial fibrillation (AF) can be treated by radiofrequency (RF), ablation or modification of atrioventricular (AV) node. AV nodal ablation with pacemaker and AV nodal modification are associated with significant improvement in symptoms and quality of life. But there is no evidence that these techniques influence survival, and in some cases these therapies must be followed by implantation of a permanent pacemaker (due to complete AV block), and anticoagulation (due to persistence of underlying AF). The maze operation attempts to abolish AF by channeling the atrial activation between a series of incisions. Early results are encouraging, and simultaneous surgery may be beneficial. RF ablation can be used to create long linear lesions for this purpose (catheter maze). Preliminary studies show a higher success rate when linear ablations are performed in the left atrium than in the right atrium and that arrhythmogenic foci play a significant role in atrial fibrillation. However, catheter mazes are prolonged, and it is difficult with current technology to create endocardial linear lesions consistently that act as barriers to conduction. It is required to optimize this to transform investigational technique into a routine procedure. In specific cases, focal ablation or catheter ablation of the right atrial only can prevent AF. It may be possible that different approaches of ablation may be required, depending on the etiology. Curative radiofrequency catheter ablation for patients with AF may not be far in the future.

Atrial Fibrillation↗
PubMed1999

[Significance of angiographic haziness at the distal stent edge: analysis by intravascular ultrasound and quantitative coronary angiography].

Haziness on coronary angiograms has been interpreted as thrombogenic morphologies such as dissection or thrombus. Haziness is often seen at distal sites following stent deployment. To clarify the pathophysiology of distal haziness of coronary stenting, we performed intravascular ultrasonography (3.5F, 30 MHz) after implantation of 48 Palmaz-Schatz stents in 45 patients. Haziness was defined visually as a reduction in contrast density or an indistinct vessel border. The luminal diameter and videodensitometry score were measured at the distal edge of the stent and distal adjacent segment by quantitative coronary angiography. Luminal diameter and lumen area were measured by intravascular ultrasound. The distal/in-stent ratio was calculated for each measurement to assess the magnitude of the vessel tapering and the reduction in contrast density. Haziness was found in 18 vessels. Qualitative intravascular ultrasound determined dissections (n = 5) and irregular shapes of the lumen compressed by heavy calcium (n = 3) in the hazy vessels. There were no specific morphologies in the other 10 cases. Distal/in-stent ratio of the videodensitometry score was significantly smaller in hazy vessels, but quantitative coronary angiography could not distinguish hazy arteries with dissection or calcium from arteries without specific morphologies. The distal/in-stent ratio of the lumen area (< 0.8) and lumen area at the distal segment (< 5 mm2) were markedly smaller in the 'hazy' group without specific morphologies. Dissection, heavy calcium, and luminal reduction can cause a hazy appearance at the distal stent edge. Quantitative coronary angiography could quantify the haziness, but could not distinguish the morphologies of the vessel wall. Only intravascular ultrasound could assess the pathophysiology of hazy vessels after coronary stenting.

Calcium↗
PubMed1998

Possible mechanism of ECG features in patients with idiopathic ventricular fibrillation studied by heart model and computer simulation.

The possible contribution of localized conduction delay and abnormal action potentials to ventricular fibrillation (VF) was studied by applying an anisotropic cardiac computer model to clinical cases of the Brugada-type electrocardiogram (ECG), which shows right bundle branch block (RBBB), a normal QT interval, ST-segment elevation, and late r' in leads V1 and V2. The anisotropic heart model was composed of 50,000 discrete units with a spatial resolution of 1.5 mm and was mounted in a human torso model. The longitudinal/transverse conduction velocity ratio was 3:1. For the normal ECG, a conduction velocity of 0.75 m/s was required. In the abnormal area of the right anterior epicardial wall, the conduction velocity was set at 0.2 m/s, with decreasing action potential amplitude and 10% prolonged action potential duration. The ECG features of ST-segment elevation and Brugada-type right bundle branch block pattern were simulated. The action potential duration was able to change dynamically with coupling interval of stimulation, with a ratio of 9% for normal ventricular muscle and 50% for Purkinje fibers. Five successive stimuli were applied to the left lateral epicardium 300 ms after the first sinus excitation, and sustained VF was induced with the transmural conduction delay at the right anterior ventricle as a block increasing the vulnerability. At the initiation of VF, reentry circuits were shown around the border zone of the right epicardium and were very heterogeneous around the conduction delayed area and septal area. In an area with the characteristics of nontransmural conduction delay, sustained VF was prevented, and the pattern of transient right bundle branch block appeared on the simulated ECG and body surface potential maps. The late r' wave was calculated in the precordial leads and right anterior site on the body surface potential maps. These results suggest that increased multipolarity in the border zone between the Purkinje fibers and delayed conduction area in the right ventricle might play an important role as a functional block for the persistence of VF.

Action Potentials↗
PubMed1998

Amiodarone-induced thyrotoxicosis associated with thyrotropin receptor antibody.

Since amiodarone was first marketed in 1992 in Japan, the incidence of amiodarone-induced thyrotoxicosis (AIT) has been increasing. Among 12 thyrotoxic patients, a patient with arrhythmogenic right ventricular dysplasia, who had been taking amiodarone for 4 years, developed thyrotoxicosis with subacute onset, accompanied by transiently positive thyrotropin (TSH) receptor antibody (TRAb), or thyrotropin-binding inhibiting immunoglobulin (TBII). The immunoglobulin G (IgG) obtained from the TRAb-positive serum of the patient elicited no thyroid hormone-releasing activity in cultured human thyroid follicles, whereas all IgGs obtained from untreated Graves' disease elicited positive results. These in vitro findings and clinical course suggest that TRAb/TBII without thyroid-stimulating activity may develop in patients with amiodarone-induced destructive thyroiditis, as reported in patients with destructive thyroiditis, such as subacute and silent thyroiditis.

Adult↗