Hidenobu Terai

Kanazawa University, Kanazawa, Ishikawa, Japan

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Publications (31)140.27 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Although cardiovascular disease (CVD) is an important cause of death in patients on hemodialysis, evidence of a beneficial effect of percutaneous intervention (PCI) on stable heart disease is scarce. We investigated the cardiovascular outcomes of hemodialysis patients under our policy of encouraging coronary artery screening tests to the extent possible. A total of 147 hemodialysis patients have been treated in our clinic so far. In 98 of them, coronary artery screening tests were performed, three in unstable and 95 in asymptomatic patients. Significant coronary artery stenosis was detected in 29 at the first tests and in 11 during subsequent tests (40/98, 40.8%), and PCI or coronary artery bypass grafting (CABG) was performed. Multiple PCIs were needed in 21 patients. In the other 49 patients, coronary artery screening tests were not undertaken based on the nephrologist's decision or patient refusal. At the end of the study, 73 (74.5%) patients with tests, and 14 (28.6%) without tests were still outpatients (P < 0.01). Of 40 patients transferred to other hospitals for medical reasons or who died before transfer, there was cerebrovascular accident in eight, malignancy in six, congestive heart failure without CVD in four, infection in three, sudden cardiac death in one, and others 18. No patient with tests died of CVD and the only patient who died of sudden cardiac death probably due to myocardial infarction was a patient who had declined the screening tests. Coronary artery screening tests, intervention and subsequent periodic tests for asymptomatic hemodialysis patients can reduce the occurrence of cardiovascular events in this population.
    Therapeutic apheresis and dialysis: official peer-reviewed journal of the International Society for Apheresis, the Japanese Society for Apheresis, the Japanese Society for Dialysis Therapy 03/2014; · 1.53 Impact Factor
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    ABSTRACT: A 78-year-old man with unstable angina showed 90 % stenosis in the proximal left anterior descending artery. Pre-procedural intravascular ultrasound revealed ruptured plaque and attenuated plaque in the lesion. Under these conditions, two overlapping sirolimus-eluting stent (SES) implantation in this lesion resulted in slow flow which was recovered by intracoronary nitrates, nicorandil, and nitroprusside without further complications. When the patient showed up again 5 years later with recurrence of angina pectoris, angiography revealed a hazy ulcerated in-stent restenosis (ISR) at the site of the SES. Pre-procedural optical coherence tomography (OCT) imaging revealed multiple intimal ruptures, cavity formation behind the stent struts, a thin-cap fibroatheroma containing neointima surrounded by signal-poor, lipid-rich area in the proximal SES, suggesting the progression of neoatherosclerosis within SES. Importantly, there occurred slow flow again after balloon angioplasty for this lesion. We would suggest careful OCT examination is warranted to confirm development of neoatherosclerosis within the stent, and distal protection device should be considered to prevent slow flow phenomenon even in a patient with very late ISR.
    Heart and Vessels 01/2014; · 2.13 Impact Factor
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    ABSTRACT: Background: (18)F-fluoro-2-deoxyglucose (FDG) positron emission tomography (PET) is assumed to be the most useful method for evaluating the viability of the myocardium. However, there are few reports regarding serial changes in (18)F-FDG-PET images of acute myocardial infarction (AMI). We evaluated serial changes in glucose-loaded (18)F-FDG-PET, (123)I-β-methyl-p-iodophenyl-penta-decanoic acid (BMIPP) single-photon emission computed tomography (SPECT) and (99m)Tc-Tetrofosmin (TF) gated SPECT images in patients with AMI. Methods and Results: We enrolled 7 consecutive patients with first anterior AMI who successfully underwent percutaneous coronary intervention (PCI). (18)F-FDG-PET images were obtained in the acute, subacute, chronic, mid-term and long-term phases. (123)I-BMIPP and (99m)Tc-TF SPECT images were obtained in the subacute, chronic, mid-term and long-term phases. We determined the total defect score (TDS) for each image. The TDS of the glucose-loaded (18)F-FDG-PET, (123)I-BMIPP and( 99m)Tc-TF SPECT images indicated significant serial decrease (P<0.001). Comparing these images, the TDS of the glucose-loaded (18)F-FDG-PET images was larger than that of the (123)I-BMIPP and (99m)Tc-TF SPECT images, and the TDS indicated (18)F-FDG-PET>(123)I-BMIPP>(99m)Tc-TF in all phases. Conclusions: The defect areas of glucose-loaded (18)F-FDG-PET images were significantly larger than those of (123)I-BMIPP and( 99m)Tc-TF SPECT images during 9 months follow-up of patients with successful PCI for anterior AMI. Additionally, the impairment of glucose metabolism was prolonged.
    Circulation Journal 10/2012; · 3.58 Impact Factor
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    Shoichiro Daimon, Hidenobu Terai
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    ABSTRACT: Although antiplatelet medication is used in various situations, including for the prevention of ischemic and thrombotic complications, long-term antiplatelet therapy in hemodialysis patients who are at high risk of bleeding may result in a harmful bleeding tendency. We investigated bleeding events that required the cessation of the use of heparin for hemodialysis in all the hemodialysis patients treated in our clinic. This analysis revealed 111 patients, of whom 52 had been treated with antiplatelet agents (female/male, 15/37; age, 70.4±11.3years; number of days of hemodialysis treatment in our clinic, 1073±696 [31-2144]days; diabetes mellitus [DM]/non-DM, 29/23), and 59 had not been treated with them (female/male, 17/42; age, 66.7±14.0 years; number of days of hemodialysis treatment in our clinic, 917±605 [26-2102]days; DM/non-DM, 21/38). During treatment in our clinic, 21 of the 52 patients undergoing antiplatelet therapy experienced a bleeding event (gastrointestinal bleeding 16, brain stem hemorrhage 2, others 3), while 7 of the 59 patients not receiving them had a bleeding event (gastrointestinal bleeding 7) (P<0.001). Of note, diabetic patients on antiplatelet therapy had the highest incidence of bleeding events (13 of 29 patients; 44.8%), followed by non-diabetic patients on antiplatelet therapy (7 of 23 patients; 30.4%), diabetic patients not receiving antiplatelets (3 of 21 patients; 14.3%), and finally non-diabetic patients not on antiplatelets (4 of 38 patients; 10.5%). Among the patients on antiplatelet therapy, no correlations were apparent between bleeding events and the duration of such therapy or the number of agents. In conclusion, antiplatelet medications can induce bleeding events more frequently in hemodialysis patients, especially in those with DM, than in non-hemodialysis patients, and such agents should be given only under prudent consideration of the associated risks and benefits.
    Therapeutic apheresis and dialysis: official peer-reviewed journal of the International Society for Apheresis, the Japanese Society for Apheresis, the Japanese Society for Dialysis Therapy 10/2011; 15(5):454-9. · 1.53 Impact Factor
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    ABSTRACT: The restenosis rate of coronary stent has significantly decreased by implantation of the drug-eluting stent (DES). We often experienced the DES implantation for very small target vessels. The minimum size of DES in Japan and USA is 2.5 mm-diameter, but there were no reports of the expandability of DESs for the very small target vessels with reference diameter <2.2 mm. We clarify the expandable performance of 2.5 mm-DESs for very small target vessels with reference diameter <2.2 mm in vitro and vivo study. We studied 3 pieces in each kind of DES (Sirolimus-eluting stent; SES, Paclitaxel-eluting stent; PES, Zotarolimus-eluting stent; ZES and Everolimus-eluting stent; EES) in vitro and vivo study of the porcine coronary artery with reference diameter <2.2 mm. By using the delivery balloon, each stent was initially dilated with 3.5 atm. And the pressure of 0.5 atm. was applied until it reached the maximum pressure of 12 atm. The minimum pressure of the full expanded stent balloon was estimated as the minimum expandable pressure. The stent-inner diameter and area on each pressure were measured by IVUS. The average minimum expandable pressure (atm.) in vitro/vivo was 4.7/4.5 in SES, 7.2/6.8 in PES, 4.3/4.5 in ZES and 3.8/3.8 in EES. The inner diameter (mm) in vitro/vivo at minimum expandable pressure was 1.81 ± 0.07/1.84 ± 0.05 in SES, 2.31 ± 0.10/2.13 ± 0.13 in PES, 2.41 ± 0.13/1.98 ± 0.31 in ZES and 2.13 ± 0.11/1.88 ± 0.22 in EES. The stent inner-diameter (mm) of DESs at 8 atm. in vivo was 2.16/2.21/2.45/2.25 in SES/PES/ZES/EES. All kinds of DES could be delivered to very small target vessels with reference diameter <2.2 mm at the minimum expandable pressure in vivo study, but the stent which presented adequate stent inner-diameter at 8 atm. was only SES. We have to implant the 2.5 mm-DESs for very small target vessels according to the data based on this expandability of DESs to bail out threatening occlusion due to coronary dissection or elastic recoil.
    Cardiovascular intervention and therapeutics. 05/2011; 26(2):124-130.
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    ABSTRACT: Upper arm swelling and venous hypertension at arteriovenous fistula sites, and insufficiency of hemodialysis are induced by central venous lesions in chronic hemodialysis patients. Percutaneous transluminal angioplasty (PTA) for central venous lesions is first-choice treatment. Cardiac function can be evaluated by measuring the acute increase in venous return volume after PTA. We studied 6 cases of successful PTA for central venous stenotic or occluded lesions, and evaluated cardiac function by Swan-Ganz (SG) catheter and ultrasound echocardiography (UCG) at pre-, post-PTA, and on the following day. Ejection fraction (EF) in 6 cases was 71.0 ± 5.5% on UCG. Two cases of subclavian venous stenosis, one case of subclavian venous occlusion, and three cases of brachiocephalic venous occlusion were enrolled. The reference diameter (RD) was 10.2 ± 4.9 mm, % diameter-stenosis (%DS) was 92.2 ± 12.2% at pre-PTA, and %DS at post-PTA was 21.7 ± 20.7%. There were no significant differences in pulmonary capillary-wedge, pulmonary artery, and right ventricular end-diastolic pressure in SG at pre- and post-PTA. The pressure of right atrium (RA) and cardiac output (CO) were significantly increased by PTA (RA pressure at pre-/post-PTA, 9.7 ± 2.9/11.7 ± 3.6 mmHg, p<0.05, CO at pre-/post-PTA 5.09 ± 2.07/5.45 ± 2.25 l/min, p<0.05). There were no significant differences in serial EF, left atrial and left ventricular diameters on UCG. However, the short-diameter of right ventricle (RV) and RA were significantly increased at post-PTA and recovered on the following day (RV short-diameter at pre-/post-/following-day PTA, 26.7 ± 3.5/32.5 ± 1.9/29.1 ± 1.7 mm, p<0.05; RA short-diameter at pre-/post-/following-day PTA, 30.2 ± 4.2/36.3 ± 2.4/32.1 ± 3.6mm, p<0.05). Volume overload after PTA for central venous stenotic or occluded lesions in chronic hemodialysis patients resulted in increased RA and RV diameters. These changes were transient and completely recovered by the following day. PTA for central venous lesions in patients with normal EF can be performed without clinical cardiac problems.
    Journal of Cardiology 02/2011; 57(3):316-24. · 2.30 Impact Factor
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    ABSTRACT: Early detection in patients with hypertrophic cardiomyopathy (HCM) is very important. Integrated backscatter (IB) provides a useful noninvasive measure of the acoustic properties of the myocardium, and may detect early myocardial changes. Thirty-four carriers who had gene mutations causing HCM were studied. The patients were divided into three groups as follows: (1) 21 patients with wall hypertrophy (Group A), (2) 7 patients with ECG abnormalities but without wall hypertrophy (Group B), and (3) 6 carriers with neither ECG abnormalities nor wall hypertrophy (Group C). All subjects underwent ECG, conventional echocardiography and acoustic densitometry. In addition, we studied subjects < or =20 years old from Groups B and C (Group B-2 and Group C-2, respectively), and compared them with control subjects with no cardiac disorders who were < or =20 years old. In Group A, cyclic variations of integrated backscatter (CV-IB) in the interventricular septum and left ventricular posterior wall were significantly smaller than in Group C. The amplitude of IB in the interventricular septum and left ventricular posterior wall in Group A was significantly higher than those in Group C. Even in Group B, CV-IB in the interventricular septum was significantly smaller than those in Group C. Among patients < or =20 years old, CV-IB in the interventricular septum was significantly smaller in Group B-2 than in control subjects, while that in Group C-2 did not differ from that in control subjects. Changes in tissue characterization were found in the hearts of HCM gene carriers even in the absence of wall hypertrophy. These results suggest that tissue changes detectable by the acoustic densitometry methods may occur in the hearts of HCM gene carriers without wall hypertrophy, and that they may be detectable at the time of appearance of ECG abnormalities.
    International Journal of Cardiology 10/2005; 104(2):170-5. · 6.18 Impact Factor
  • Circulation 09/2005; 112(7):e96-7. · 15.20 Impact Factor
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    ABSTRACT: We report regression of the abnormal Q waves of an inferior old myocardial infarction after an additional anterior acute myocardial infarction, and demonstrate the scintigraphic correlation and chronological course of this phenomenon. Scintigraphic findings in the present case here may contribute to an interpretation of regression of abnormal Q waves in myocardial infarction.
    Annals of Nuclear Medicine 08/2005; 19(5):407-9. · 1.41 Impact Factor
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    ABSTRACT: PRKAR1A gene encodes the type 1A regulatory subunit of protein kinase A. The mutation of this gene causes Carney complex which is an autosomal dominant multiple neoplasia syndrome characterized by spotty pigmentations, endocrine overactivity and cardiac myxoma. We hypothesized that cardiac myxoma may be associated with PRKAR1A gene mutation and determined whether mutation in the PRKAR1A gene is the cause of familial and sporadic cardiac myxoma. We studied seven patients (three males and four females) with cardiac myxoma. Two of them had familial cardiac myxoma complicated with Carney complex. The other five patients were characterized as sporadic cardiac myxomas. We analyzed the PRKAR1A gene of all patients by the polymerase chain reaction (PCR)-single-strand conformation method, followed with direct sequence analysis. We identified a novel mutation (494delTG) in exon 4A of the PRKAR1A gene in the patients with Carney complex. A 16-year-old proband had a left atrial myxoma, pituitary adenoma and skin pigmentation. His father also had left atrial myxoma and skin pigmentation. In contrast, no mutations in the PRKAR1A gene were identified in the other five patients with sporadic cardiac myxomas. These results suggest that mutation of the PRKAR1A gene may be associated with familial cardiac myxoma in Carney complex but may not be associated with sporadic cardiac myxoma.
    International Journal of Cardiology 08/2005; 102(2):273-7. · 6.18 Impact Factor
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    ABSTRACT: The STA gene encodes emerin and is one of the genes that is affected in Emery-Dreifuss muscular dystrophy (EDMD). Although it has been reported that EDMD caused by the STA gene mutation is associated with X-linked recessive inheritance, the genotype-phenotype correlations, with special reference to cardiac manifestations, are not well defined. We identified 16 carriers (7 male and 9 female) with a nonsense mutation in exon 6 of the STA gene in 2 EDMD families. Pacemakers were required for treatment of bradyarrhythmias in all 7 male carriers and in 2 of the 9 female carriers. In addition, 2 of the 9 female carriers displayed atrial fibrillation. In these 2 families, 3 males without pacemaker implantation, who were not tested genetically, had died suddenly. In these family members, the majority of carriers with the mutation had not been clinically diagnosed as having EDMD before genetic testing because of extremely mild or nonexistent skeletal myopathy. EDMD caused by this mutation is characterized by atypical clinical features and incomplete penetrance of the clinical phenotype and may result in serious cardiac complications, including sudden death. Approaches to preventing possible sudden death in carriers with the STA gene mutation require further study.
    Circulation 07/2005; 111(25):3352-8. · 15.20 Impact Factor
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    ABSTRACT: LQTS (long QT syndrome) is an inherited cardiac disorder characterized by prolongation of QT interval, torsades de pointes and sudden death. We have identified two heterozygous missense mutations in the KCNQ1 and KCNH2 (also known as HERG) genes [Asp611-->Tyr (D611Y) in KCNQ1 and Asp609-->Gly (D609G) in KCNH2] in a 2-year-old boy with LQTS. The aim of the present study was to characterize the contributions of the mutations in the KCNQ1 and KCNH2 genes relative to the clinical manifestations and electrophysiological properties of LQTS. Six of 11 carriers of D611Y in KCNQ1 had long QT intervals. D609G in KCNH2 was detected only in the proband. Studies on the electrophysiological alterations due to the two missense mutations revealed that the D611Y mutation in KCNQ1 did not show a significant suppression of the currents compared with wild-type, but the time constants of current activation in the mutants were increased compared with that in the wild-type. In contrast, the D609G mutation in KCNH2 showed a dominant-negative suppression. Our results suggest that the mild phenotype produced by the D611Y mutation in KCNQ1 became more serious by addition of the D609G mutation in KCNH2 in the proband.
    Clinical Science 03/2005; 108(2):143-50. · 4.86 Impact Factor
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    ABSTRACT: There has not been a comparison of the electrocardiographic (ECG) finding of ST-segment elevation in the precordial leads in patients with takotsubo cardiomyopathy (TC) and those with anterior acute myocardial infarction (AMI), with regard to the location of the culprit lesion. The present study evaluated 18 patients with TC, and 85 with anterior AMI who were divided into 3 groups: group A had the culprit lesion proximal to both the first septal branch (S1) and the first diagonal branch (D1), group B had the culprit lesion proximal to either S1 or D1, and group C had the culprit lesion distal to both S1 and D1. In patients with TC, reciprocal ST-segment depression in the inferior leads was observed less frequently than in patients in groups A (p<0.0001) and B (p=0.0002), and abnormal Q waves and ST-segment elevation in the inferior leads were observed more frequently than in group A (p=0.0007, p=0.0057, respectively). The ECG findings in TC did not differ from those in group C. Electrocardiographic findings may differentiate TC from AMI with a proximal lesion of left anterior descending coronary artery, but not those with distal lesions.
    Circulation Journal 01/2005; 69(1):89-94. · 3.58 Impact Factor
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    ABSTRACT: Patients with LQTS (long QT syndrome) with a mutation in a cardiac ion channel gene, leading to mild-to-moderate channel dysfunction, may manifest marked QT prolongation or torsade de pointes only upon an additional stressor. A 59-year-old woman had marked QT prolongation and repeated torsade de pointes 3 months after initiation of probucol, a cholesterol-lowering drug. We identified a single base substitution in the HERG gene by genetic analysis. This novel missense mutation is predicted to cause an amino acid substitution of Met(124)-->Thr (M124T) in the N-terminus. Three other relatives with this mutation also had QT prolongation and one of them had a prolonged QT interval and torsade de pointes accompanied by syncope after taking probucol. We expressed wild-type HERG and HERG with M124T in Xenopus oocytes and characterized the electrophysiological properties of these HERG channels and the action of probucol on the channels. Injection of the M124T mutant cRNA into Xenopus oocytes resulted in expression of functional channels with markedly smaller amplitude. In both HERG channels, probucol decreased the amplitude of the HERG tail current, decelerated the rate of channel activation, accelerated the rate of channel deactivation and shifted the reversal potential to a more positive value. The electrophysiological study indicated that QT lengthening and cardiac arrhythmia in the two present patients were due to inhibition of I(Kr) (rapidly activating delayed rectifier K(+) current) by probucol, in addition to the significant suppression of HERG current in HERG channels with the M124T mutation.
    Clinical Science 09/2004; 107(2):175-82. · 4.86 Impact Factor
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    ABSTRACT: There are currently no established diagnostic criteria for the identification of abnormal Q waves in patients with hypertrophic cardiomyopathy (HCM), resulting in various definitions being applied in each previous study. The aim of this study was to determine the most accurate diagnostic definition of abnormal Q waves for HCM based on a molecular genetic diagnosis, and also to apply abnormal Q waves to the identification of preclinical carriers. We applied three different criteria used in previous reports for abnormal Q waves in 148 genotyped subjects. Of the three criteria, Criterion 3 (Q wave >3mm in depth and/or >0.04s in duration in at least two leads except aVR) showed the highest sensitivity (50% in the young, 29% in adults) while retaining a high specificity (90% in the young, 97% in adults), resulting in the highest accuracy (69% in the young, 52% in adults). Using Criterion 3, abnormal Q waves were present 27.6% of preclinical carriers, and in 5.4% of non-carriers (P<0.01). These findings suggest that Criterion 3 may be the most accurate diagnostic definition for HCM. Understanding the diagnostic value of abnormal Q waves may be useful in screening preclinical carriers of HCM.
    European Heart Journal 02/2004; 25(3):246-51. · 14.10 Impact Factor
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    ABSTRACT: QT dispersion (QTD) on 12-lead ECGs has been proposed as a marker of malignant ventricular tachyarrhythmias, and increased QTD has been reported in long QT syndrome (LQTS). On the other hand, it has been demonstrated that transmural dispersion is associated with ventricular tachyarrhythmias in an experimental model. However, the precise type of QTD or transmural dispersion that contributes most to ventricular tachyarrhythmias in patients with LQTS remains unclear. We evaluated 27 patients with acquired LQTS. These patients were divided into two groups: group A (n =12), patients with polymorphic ventricular tachycardia [torsades de pointes (TdP)], and group B (n =15), patients without TdP. The QT intervals were corrected using Bazett's formula. QTD was measured as the difference between the maximum and the minimum QT intervals, and T wave peak-to-end interval divided by the QT interval (Tpe) in the V5 lead was measured as a new index. Both the corrected QTD (QTDc) and Tpe were significantly larger in group A than in group B. Logistic regression analysis revealed that a reliable predictor for TdP in the QT variables in these patients was not QTDc but Tpe. Cumulative frequency distributions revealed that a Tpe of 0.28 is a good cut-off point for TdP. Tpe did not correlate with the corrected maximum QT interval, whereas the QTDc did correlate with this parameter. In conclusion, Tpe may be the best predictor for TdP in patients with acquired LQTS.
    Clinical Science 01/2004; 105(6):671-6. · 4.86 Impact Factor
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    ABSTRACT: Hypertrophic cardiomyopathy (HCM) is caused by mutations in the genes that encode sarcomeric proteins. Although some patients with HCM have shown dilated cardiomyopathy (DCM)-like features, the relationship between genotype and histologic findings is not well known. Family members with the same gene mutation may show the same histopathologic changes and clinical manifestations. Siblings with HCM caused by an Arg92Trp mutation in the cardiac troponin T gene, showing DCM-like features, were examined. The patients were a 69-year-old woman and her 57-year-old brother who both died from congestive heart failure. Their autopsies revealed the same histopathologic findings in the heart. The anterior walls and interventricular septa of their hearts were replaced with extensive fibrosis and showed thinning. Myocyte hypertrophy, disarray, and thickened medial walls of the intramural coronary arteries were found. On electron microscopy, the number of mitochondria was seen to be increased and they formed many clusters. Patients with HCM caused by an Arg92Trp mutation in the cardiac troponin T gene may have the same histopathologic findings, which may result in DCM-like features.
    Clinical Cardiology 12/2003; 26(11):536-9. · 1.83 Impact Factor
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    ABSTRACT: Left ventricular (LV) systolic function in hypertrophic cardiomyopathy (HCM) is usually normal. Late in the disease, however, LV systolic dysfunction and dilatation are recognized. Although abnormalities in cardiac sympathetic nerve activity in patients with HCM have been demonstrated using (123)I-metaiodobenzylguanidine (MIBG) myocardial scintigraphy, the changes of cardiac sympathetic nerve activity throughout the clinical course from typical to end-stage HCM are unclear. The objective of this study was to evaluate the relationship between abnormalities on (123)I-MIBG myocardial scintigraphy and pathophysiologic changes in patients with HCM. We performed (123)I-MIBG scintigraphy on 46 patients with HCM and 18 age-matched control subjects. The patients were categorized into 3 groups: 28 patients with normal LV systolic function (group A), 9 patients with LV systolic dysfunction (group B), and 9 patients with LV systolic dysfunction and dilatation (group C). With planar (123)I-MIBG imaging, the heart-to-mediastinum ratio for early and delayed acquisitions and the washout rate were calculated. With SPECT, polar maps of the LV myocardium were divided into 20 segments. The regional uptake and washout rate were calculated from semiquantitative 20-segment bull's-eye analysis. The early uptake was significantly lower in group C than in the control group (P < 0.01). The washout rate was progressively higher in group A, group B, and group C (P < 0.01). Reduced regional early uptake was found in 2.9 +/- 3.4 (group A), 4.1 +/- 4.7 (group B), and 7.4 +/- 4.3 (group C) segments, respectively. In group C, regional early uptake was significantly reduced, predominantly in the interventricular septal wall, and regional washout rate was increased in the apex and lateral wall. These results suggest that cardiac sympathetic nerve abnormalities in patients with HCM may advance with development of LV systolic dysfunction and dilatation and that (123)I-MIBG myocardial scintigraphy may be a useful tool for the evaluation of pathophysiologic changes in HCM.
    Journal of Nuclear Medicine 10/2003; 44(10):1612-7. · 5.77 Impact Factor
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    ABSTRACT: To evaluate the relation between QT variables and disproportion of left ventricular wall hypertrophy in patients with hypertrophic cardiomyopathy. Retrospective analysis of the results of echocardiography and electrocardiography. University hospital (tertiary referral centre). 70 patients with hypertrophic cardiomyopathy were divided into four groups according to the distribution of left ventricular wall hypertrophy on cross sectional echocardiography: group A--hypertrophy confined to the interventricular septum; group B--hypertrophy confined to the interventricular septum and left ventricular anterior wall; group C--hypertrophy confined to the interventricular septum, left ventricular anterior wall, and lateral free wall; group D--hypertrophy involving all portions of the left ventricle. QT intervals and QT dispersion in precordial six lead ECGs. There were no significant differences in the maximum left ventricular wall thickness among the four groups, and maximum and minimum QTc intervals also did not differ. QTc dispersion was increased significantly in groups A and B compared with groups C and D. Dispersions of the interval from the J point to the end of the T wave (JTc dispersions) in groups A and B were also increased significantly compared with groups C and D. By linear regression analysis, QTc and JTc dispersions correlated with the ratio of the interventricular septal thickness to left ventricular posterior wall thickness (p = 0.0152 and p = 0.0075, respectively). QT dispersion may be affected by not only electrical inhomogeneity but also by morphological inhomogeneity of the left ventricle in patients with hypertrophic cardiomyopathy.
    Heart (British Cardiac Society) 09/2003; 89(8):882-6. · 5.01 Impact Factor
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    ABSTRACT: Congenital long QT syndrome (LQTS) is caused by mutations in various cardiac potassium or sodium channel genes, with 6 different genotypes thus far identified. However, it is unknown whether these genotypes can be differentiated by QT variables. The electrocardiograms obtained from 16 patients with a mutation in KCNQ1 (LQT1), 7 patients with a mutation in HERG (LQT2) and 20 control subjects were analyzed. The corrected QT interval (QTc), Q-T peak interval (QTpc) and dispersion of QTc or QTpc were measured in 6 precordial leads. The corrected interval from T peak to T end (Tpec) was measured in lead V(5). The maximum QTc, QTc dispersion, and Tpec were significantly increased in the LQT1 and LQT2 patients than in the controls. However, there were no significant differences in these indices between the LQT1 and LQT2 patients. In contrast, QTpc dispersion was significantly increased in the LQT2 patients (78+/-25 ms) compared with the LQT1 patients (29+/-15 ms) and controls (26+/-19 ms). These results suggest that increased lag of the peak of the T wave in each precordial lead (QTpc dispersion) may be a possible index to differentiate LQTS patients with HERG mutation from those with KCNQ1 mutation.
    Circulation Journal 07/2003; 67(6):495-8. · 3.58 Impact Factor