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ABSTRACT: A 58-year-old man was admitted to our hospital with acute anterior myocardial infarction that occurred 4 years after single sirolimus-eluting stent (SES) implantation in the left anterior descending artery. He had been undergoing continuous dual antiplatelet therapy. Emergency coronary angiography showed total thrombotic occlusion and peri-stent contrast staining at the SES site. The lesion was evaluated using intravascular ultrasound (IVUS) and optical coherence tomography (OCT) after thrombectomy. Vessel remodeling was detected on IVUS, and multiple interstrut hollows and thrombi were observed on OCT. These findings were associated with very late stent thrombosis after SES implantation.
Cardiovascular intervention and therapeutics. 04/2013;
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ABSTRACT: A 61-year-old Japanese male was admitted to hospital due to severe congestive heart failure and pre-renal failure with middle
aortic syndrome. The patient was successfully treated with emergent aortic angioplasty and kissing stents implantation whilst
in a hemodynamically unstable state. Our experience confirms that stenosis of the descending aorta when treated with catheter
intervention may be palliative, however, it was a very effective method for life threatening clinical conditions in the short
and mid-term and may be an alternative to surgery.
KeywordsTakayasu’s arteritis-Middle aortic syndrome-Non-specific aortitis-Aortic angioplasty-Kissing stents
Cardiovascular Intervention and Therapeutics 04/2012; 25(2):117-121.
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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. · 7.08 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. · 1.50 Impact Factor
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Yoshihiro Noji,
Tohru Kojima,
Takahiko Aoyama, Masato Yamaguchi,
Tsutomu Araki,
Susumu Fujino,
Katsuaki Yokota,
Noriko Kumamoto,
Takakiyo Nakaya,
Keiichiro Takase,
Masami Shimizu,
Hiroshi Mabuchi
Circulation 07/2005; 111(24):e438-9. · 14.74 Impact Factor
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Kenji Sakata,
Masami Shimizu,
Hidekazu Ino, Masato Yamaguchi,
Hidenobu Terai,
Noboru Fujino,
Kenshi Hayashi,
Tomoya Kaneda,
Masaru Inoue,
Yoshio Oda,
Takashi Fujita,
Bunji Kaku,
Hounin Kanaya,
Hiroshi Mabuchi
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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. · 14.74 Impact Factor
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Masato Yamaguchi,
Masami Shimizu,
Hidekazu Ino,
Hidenobu Terai,
Kenshi Hayashi,
Tomoya Kaneda,
Hiroshi Mabuchi,
Ryo Sumita,
Tohru Oshima,
Naoto Hoshi,
Haruhiro Higashida
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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. · 4.61 Impact Factor
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Masaru Inoue,
Masami Shimizu,
Hidekazu Ino, Masato Yamaguchi,
Hidenobu Terai,
Noboru Fujino,
Kenji Sakata,
Akira Funada,
Ryozo Tatami,
Syozo Ishise,
Hounin Kanaya,
Hiroshi Mabuchi
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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. · 3.77 Impact Factor
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Kenshi Hayashi,
Masami Shimizu,
Hidekazu Ino, Masato Yamaguchi,
Hidenobu Terai,
Naoto Hoshi,
Haruhiro Higashida,
Nariaki Terashima,
Yoshihide Uno,
Honin Kanaya,
Hiroshi Mabuchi
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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. · 4.61 Impact Factor
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Wataru Shimizu,
Minoru Horie,
Seiko Ohno,
Kotoe Takenaka, Masato Yamaguchi,
Masami Shimizu,
Takashi Washizuka,
Yoshifusa Aizawa,
Kazufumi Nakamura,
Tohru Ohe,
Takeshi Aiba,
Yoshihiro Miyamoto,
Yasunao Yoshimasa,
Jeffrey A Towbin,
Silvia G Priori,
Shiro Kamakura
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ABSTRACT: We sought to compare the arrhythmic risk and sensitivity to sympathetic stimulation of mutations located in transmembrane regions and C-terminal regions of the KCNQ1 channel in the LQT1 form of congenital long QT syndrome (LQTS).
The LQT1 syndrome is frequently manifested with variable expressivity and incomplete penetrance and is much more sensitive to sympathetic stimulation than the other forms.
Sixty-six LQT1 patients (27 families) with a total of 19 transmembrane mutations and 29 patients (10 families) with 8 C-terminal mutations were enrolled from five Japanese institutes.
Patients with transmembrane mutations were more frequently affected based on electrocardiographic (ECG) diagnostic criteria (82% vs. 24%, p < 0.0001) and had more frequent LQTS-related cardiac events (all cardiac events: 55% vs. 21%, p = 0.002; syncope: 55% vs. 21%, p = 0.002; aborted cardiac arrest or unexpected sudden cardiac death: 15% vs. 0%, p = 0.03) than those with C-terminal mutations. Patients with transmembrane mutations had a greater risk of first cardiac events occurring at an earlier age, with a hazard ratio of 3.4 (p = 0.006) and with an 8% increase in risk per 10-ms increase in corrected Q-Tend. The baseline ECG parameters, including Q-Tend, Q-Tpeak, and Tpeak-end intervals, were significantly greater in patients with transmembrane mutations than in those with C-terminal mutations (p < 0.005). Moreover, the corrected Q-Tend and Tpeak-end were more prominently increased with exercise in patients with transmembrane mutations (p < 0.005).
In this multicenter Japanese population, LQT1 patients with transmembrane mutations are at higher risk of congenital LQTS-related cardiac events and have greater sensitivity to sympathetic stimulation, as compared with patients with C-terminal mutations.
Journal of the American College of Cardiology 07/2004; 44(1):117-25. · 14.16 Impact Factor
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Yoshihiro Noji,
Masami Shimizu,
Hidekazu Ino,
Toshinori Higashikata, Masato Yamaguchi,
Atsushi Nohara,
Takahiro Horita,
Kuniyoshi Shimizu,
Yuji Ito,
Takeshi Matsuda,
Masanobu Namura,
Hiroshi Mabuchi
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ABSTRACT: Some patients with hypertrophic cardiomyopathy (HCM) develop left ventricular (LV) wall thinning associated with LV dilatation and systolic dysfunction. Recently, matrix metalloproteinases (MMPs) and tissue inhibitors of MMPs (TIMPs) were reported to be involved in ventricular remodeling, however, little is known about MMPs and TIMPs in patients with HCM.
Enzyme-linked immunoassays were used to measure the plasma concentrations of MMP-2, MMP-3, MMP-9, TIMP-1, and TIMP-2 in 11 patients with HCM accompanied by systolic dysfunction (fractional shortening (FS) <25%, group A), 17 patients with HCM who had preserved systolic function (FS> or =25%, group B), and 50 age-matched clinically healthy control subjects (mean age: 57 years). The concentration of MMP-2 in group A was significantly higher than in group B and the control subjects (1,124 +/- 84, 792 +/- 49, 809 +/- 26 ng/ml, respectively), whereas there was no significant difference between group B and the control subjects. MMP-2 concentrations significantly increased as the New York Heart Association functional class increased in patients with HCM. TIMP-2 was also significantly higher in group A patients than in group B and the control subjects (45.3 +/- 4.7, 34.6 +/- 2.2, 33.7 +/- 1.8 ng/ml, respectively), but there was no difference between group B and control subjects. TIMP-1 was significantly higher in HCM patients than in control subjects. MMP-3 and MMP-9 concentrations did not differ among the 3 groups. Both MMP-2 and TIMP-2 correlated significantly with FS and LV dimension, negatively and positively, respectively.
These results suggest that changes in the release and activity of MMP-2 and TIMP-2 may be associated with the mechanisms responsible for cardiac remodeling in patients with HCM.
Circulation Journal 04/2004; 68(4):355-60. · 3.77 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. · 10.48 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. · 4.61 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. · 2.15 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. · 6.38 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. · 3.77 Impact Factor
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ABSTRACT: KCNQ1 is a gene encoding an alpha subunit of voltage-gated cardiac K(+) channels, with properties similar to the slowly activating delayed rectifier K(+) current, and one of the genes causing long QT syndrome (LQTS). However, genotype-phenotype correlations of the KCNQ1 gene mutations are not fully understood. The aims of this study were to identify a mutation in the KCNQ1 gene in patients with LQTS, and to characterize the clinical manifestations and electrophysiological properties of the mutation. We screened and identified mutations by PCR, single-strand conformational polymorphism analysis and DNA sequencing. We identified a novel mutation [Phe193Leu (F193L)] in the KCNQ1 gene in one family with LQTS. The patients with this mutation showed a mildly affected phenotype. The proband was a 17-year-old girl who had a prolonged QT interval. Her elder brother, father and paternal grandmother also had the mutation. None of them had any history of syncope. Sudden death was not found in this family. Next, we studied the electrophysiological characteristics of the F193L mutation in the KCNQ1 gene using the expression system in Xenopus oocytes and the two-microelectrode voltage-clamp technique. Co-expression of F193L KCNQ1 with the K(+) channel minK suppressed peak (by 23.3%) and tail (by 38.2%) currents compared with those obtained by the combination of wild-type (WT) KCNQ1 and minK. Time constants of current activation in F193L KCNQ1 and F193L KCNQ1+minK were significantly slower than those of WT KCNQ1 and WT KCNQ1+minK. This electrophysiological study indicates that F193L causes less severe KCNQ1 current suppression, and thereby this mutation may result in a mildly affected phenotype.
Clinical Science 05/2003; 104(4):377-82. · 4.61 Impact Factor
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Tetsuo Konno,
Masami Shimizu,
Hidekazu Ino,
Toru Matsuyama, Masato Yamaguchi,
Hidenobu Terai,
Kenshi Hayashi,
Tomohito Mabuchi,
Masaru Kiyama,
Kenji Sakata,
Tatsumi Hayashi,
Masaru Inoue,
Tomoya Kaneda,
Hiroshi Mabuchi
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ABSTRACT: We studied the clinical features of hypertrophic cardiomyopathy (HCM) caused by a novel mutation in the myosin binding protein-C (MyBP-C) gene in patients and family members of Japanese descent.
Previous reports have demonstrated that the clinical features of HCM associated with mutations in the MyBP-C gene include late onset and a favorable clinical course. Recently, some mutations in genes encoding sarcomeric proteins have been reported to be a cause of dilated cardiomyopathy (DCM), as well as HCM. However, mutations of the MyBP-C gene have not been reported as a cause of DCM up to now.
We analyzed MyBP-C gene mutations in 250 unrelated probands with HCM and in 90 with DCM. We used electrocardiography (ECG) and echocardiography to determine clinical phenotypes.
We identified 17 individuals in 8 families (7 HCM, 1 DCM) with an Arg820Gln mutation in the MyBP-C gene. Overall, 2 (40%) of 5 carriers age >70 years displayed "burnt-out" phase HCM, and one of them had been diagnosed as having DCM before genetic identification. The disease penetrance in subjects age >50 years was 70% by echocardiography and 100% by ECG, and that in those age <50 years was 40% and 50%, respectively.
Elderly patients with Arg820Gln mutation may show "burnt-out" phase HCM, and patients with this mutation may be included among those diagnosed as having DCM. Screening of patients with DCM, as well as HCM, for this mutation is of significant importance because patients with this mutation may be diagnosed clinically as having DCM.
Journal of the American College of Cardiology 03/2003; 41(5):781-6. · 14.16 Impact Factor
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ABSTRACT: An abnormal blood pressure response (BPR) during exercise has been proposed as a risk factor for sudden cardiac death in patients with hypertrophic cardiomyopathy (HCM). Some patients with HCM show systolic dysfunction during exercise.
The aim of this study was to clarify the hemodynamic response during exercise and prognosis in patients with HCM and abnormal BPR.
Sixty-five patients with HCM underwent radionuclide monitoring of left ventricular function and measurement of blood pressure during supine ergometer exercise. Thereafter, cardiac events were recorded for an average period of 76 months.
Seven of 65 patients had abnormal BPR, while the others had normal BPR. Changes of heart rate and systemic vascular resistance during exercise did not differ between the two groups. Stroke volume did not increase in the abnormal BPR group but did in the normal BPR group. During a mean follow-up period of 76 months, three of the seven patients (43%) with abnormal but only one patient (2%) with normal BPR suffered a malignant arrhythmia.
Abnormal BPR occurred in about 11% of patients with nonobstructive HCM and was associated with a high prevalence of cardiac events. The predictor of abnormal BPR during exercise may not be an abnormal response of systemic vascular resistance and heart rate, but the lack of an appropriate increase in stroke volume.
Clinical Cardiology 03/2003; 26(2):71-6. · 2.15 Impact Factor
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Kotaro Oe,
Masami Shimizu,
Hidekazu Ino, Masato Yamaguchi,
Hidenobu Terai,
Kenshi Hayashi,
Masaru Kiyama,
Kenji Sakata,
Tatsumi Hayashi,
Masaru Inoue,
Tomoya Kaneda,
Hiroshi Mabuchi
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ABSTRACT: Very elderly patients have higher mortality rates than younger patients after acute coronary syndrome (ACS). However, the mechanism by which increasing age contributes to such mortality remains unclear. In addition, the efficacy and safety of invasive coronary procedures for octogenarians with ACS have not been well established. We compared the clinical characteristics and in-hospital outcome of 193 octogenarians (mean age, 83 years) with those of 1,462 younger patients (mean age, 64 years) with ACS who underwent emergent coronary angiography. Octogenarians included a greater number of females, had higher rates of cerebrovascular disease and multivessel disease, a higher Killip class, a higher Forrester class, and lower rates of smoking, diabetes, and hypercholesterolemia than the younger subjects. Interventions, including percutaneous transluminal coronary angioplasty (PTCA) and coronary artery bypass grafting (CABG), were performed less frequently in octogenarians than in younger patients (88.0% versus 90.8%). The procedural success rate in octogenarians did not differ from that in younger patients. However, the in-hospital mortality rate for the octogenarians was about three times higher than for the younger patients (19.2% versus 6.9%). Multivariate analysis revealed that the predictors of in-hospital mortality in the octogenarians were a higher Killip class and a higher Forrester class. Octogenarians with ACS had fewer coronary risk factors and a similar success rate for the intervention, but had more greatly impaired hemodynamics and higher in-hospital mortality than the younger patients. Therefore, impaired myocardial reserve may contribute to a large portion of in-hospital deaths in octogenarians with ACS.
Japanese Heart Journal 02/2003; 44(1):11-20. · 0.40 Impact Factor
