[Show abstract][Hide abstract] 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; 30(3). DOI:10.1007/s00380-014-0477-8 · 2.07 Impact Factor
[Show abstract][Hide abstract] 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.
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.
[Show abstract][Hide abstract] 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.
[Show abstract][Hide abstract] 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.
[Show abstract][Hide abstract] 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. DOI:10.1016/j.jjcc.2011.01.004 · 2.78 Impact Factor
[Show abstract][Hide abstract] 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. DOI:10.1016/j.ijcard.2004.11.009 · 4.04 Impact Factor
[Show abstract][Hide abstract] 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. DOI:10.1007/BF03027406 · 1.68 Impact Factor
[Show abstract][Hide abstract] 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. DOI:10.1016/j.ijcard.2004.05.053 · 4.04 Impact Factor
[Show abstract][Hide abstract] 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.
[Show abstract][Hide abstract] 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.
[Show abstract][Hide abstract] 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.
[Show abstract][Hide abstract] 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.
[Show abstract][Hide abstract] 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. DOI:10.1016/j.ehj.2003.10.031 · 15.20 Impact Factor