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International journal of cardiology 05/2013; · 7.08 Impact Factor
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Tetsuya Saito,
Norihiko Takeda,
Eisuke Amiya,
Tomoko Nakao,
Hajime Abe,
Hiroaki Semba,
Katsura Soma,
Katsuhiro Koyama,
Yumiko Hosoya, Yasushi Imai,
Takayuki Isagawa,
Masafumi Watanabe,
Ichiro Manabe,
Issei Komuro,
Ryozo Nagai,
Koji Maemura
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ABSTRACT: Vascular endothelial growth factor-A (VEGF-A) is one of the major angiogenic factors, and its actions are primarily mediated through its two membrane receptors, VEGFR-1 and VEGFR-2. A soluble form of VEGFR-1 (sVEGFR-1) sequesters the free form of VEGF-A, and acts as a potent anti-angiogenic factor. While sVEGFR-1 is synthesized as a splice variant of VEGF-R1 gene, the interactions between VEGF-A and sVEGFR-1 remain largely unknown. Here, we show that VEGF-A upregulates sVEGF-R1 expression in human vascular endothelial cells but leaves full-length VEGF-R1 expression unchanged, and that this induction was dependent on the VEGFR-2-protein kinase C-MEK signaling pathway. The VEGF-A-induced sVEGFR-1 upregulation can operate as a negative feedback system, which if modulated can become a novel therapeutic target for regulating pathological angiogenesis. performed.
FEBS letters 05/2013; · 3.54 Impact Factor
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Eisuke Amiya,
Masafumi Watanabe,
Norihiko Takeda,
Tetsuya Saito,
Taro Shiga,
Yumiko Hosoya,
Tomoko Nakao, Yasushi Imai,
Ichiro Manabe,
Ryozo Nagai,
Issei Komuro,
Koji Maemura
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ABSTRACT: Vascular endothelial function is impaired in hypercholesterolemia partly because of injury by modified LDL. In addition to modified LDL, free cholesterol (FC) is thought to play an important role in the development of endothelial dysfunction, although the precise mechanisms remain to be elucidated. The aim of this study was to clarify the mechanisms of endothelial dysfunction induced by an FC-rich environment. Loading cultured human aortic endothelial cells with FC induced the formation of vesicular structures composed of FC-rich membranes. Raft proteins such as phospho-caveolin-1 (Tyr14) and small GTPase Rac were accumulated towards FC-rich membranes around vesicular structures. In the presence of these vesicles, angiotensin II-induced production of reactive oxygen species (ROS) was considerably enhanced. This ROS shifted endothelial NOS (eNOS) toward vesicle membranes and vesicles with a FC-rich domain trafficked toward perinuclear late endosomes/lysosomes, which resulted in the deterioration of eNOS Ser 1177 phosphorylation and NO production. Angiotensin II-induced ROS decreased the bioavailability of eNOS under the FC-enriched condition.
Journal of Biological Chemistry 04/2013; · 4.77 Impact Factor
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ABSTRACT: We report a case of aortic stenosis associated with ochronosis in a 70-year-old man who underwent biologic aortic valve replacement. Intraoperative findings included ochronosis of a severely calcified pigmented aortic valve along with pigmentation of the intima of the aorta.
The Annals of thoracic surgery 03/2013; 95(3):1076-9. · 3.74 Impact Factor
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Jun-Ichi Okada,
Teruyoshi Sasaki,
Takumi Washio,
Hiroshi Yamashita,
Taro Kariya, Yasushi Imai,
Machiko Nakagawa,
Yoshimasa Kadooka,
Ryozo Nagai,
Toshiaki Hisada,
Seiryo Sugiura
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ABSTRACT: Recent studies, supported by advances in computer science, have successfully simulated the excitation and repolarization processes of the heart, based on detailed cell models of electrophysiology and implemented with realistic morphology.
In this study, we extend these approaches to simulate the body surface electrocardiogram (ECG) of specific individuals. Patient-specific finite element models of the heart and torso are created for four patients with various heart diseases, based on clinical data including computer tomography, while the parallel multi-grid method is used to solve the dynamic bi-domain problem. Personalization procedures include demarcation of nonexcitable tissue, allocation of the failing myocyte model of electrophysiology, and modification of the excitation sequence. In particular, the adjustment of QRS morphology requires iterative computations, facilitated by the simultaneous visualization of the propagation of excitation in the heart, average QRS vector in the torso, and 12-lead ECG.
In all four cases we obtained reasonable agreement between the simulated and actual ECGs. Furthermore, we also simulated the ECGs of three of the patients under bi-ventricular pacing, and once again successfully reproduced the actual ECG morphologies. Since no further adjustments were made to the heart models in the pacing simulations, the good agreement provides strong support for the validity of the models.
These results not only help us understand the cellular basis of the body surface ECG, but also open the possibility of heart simulation for clinical applications.
Pacing and Clinical Electrophysiology 03/2013; 36(3):309-21. · 1.35 Impact Factor
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Naomi Ogawa, Yasushi Imai,
Hiroshi Nishimura,
Masayoshi Kato,
Norifumi Takeda,
Kan Nawata,
Tsuyoshi Taketani,
Tetsuro Morota,
Shinichi Takamoto,
Ryozo Nagai,
Yasunobu Hirata
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ABSTRACT: Marfan syndrome (MFS) is an inherited connective tissue disorder mainly caused by the fibrillin-1 mutation. Deficient fibrillin-1 is thought to result in the failed sequestration of transforming growth factor β (TGFβ) and subsequent activation of the TGFβ signaling pathway, suggesting that the circulating TGFβ level may be elevated in MFS, although its accurate measurement is complex due to ex vivo release from platelet stores upon platelet activation. We measured the plasma TGFβ1 levels of 32 Japanese MFS patients (22 medically untreated, 10 treated, 20 males, 30.1 ± 9.6 years old) and 30 healthy volunteers (19 males, 29.5 ± 5.8 years old) by ruthenium-based electrochemiluminescence platform (ECL). PF4 was also measured by enzyme immunoassay (EIA) as a platelet degranulation marker. There was no significant difference in the mean plasma TGFβ1 level between the MFS group (1.31 ± 0.40 ng/mL) and controls (1.17 ± 0.33 ng/mL) (P = 0.16, NS). Also, there was no significant difference between the untreated (1.24 ± 0.37 ng/mL) and treated (1.46 ± 0.45 ng/mL) MFS patients (P = 0.15, NS). We also measured PF4, which showed wide deviations but no significant difference between the two groups (P = 0.50). A difference in circulating TGFβ1 levels between MFS patients and controls was not detected in this Japanese population. Circulating TGFβ1 is not a diagnostic and therapeutic marker for Japanese MFS patients, although our findings do not eliminate the possible association of TGFβ with the pathogenesis of MFS.
International Heart Journal 01/2013; 54(1):23-6. · 1.16 Impact Factor
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ABSTRACT: Although hypertrophic cardiomyopathy (HCM) with an accessory pathway is encountered in clinical practice, there is little evidence of a coherent strategy for ablation of the accessory pathway in patients with HCM. We present the case of a 61-year-old man who had type B Wolff-Parkinson-White (WPW) syndrome with hypertrophic obstructive cardiomyopathy (HOCM). Due to paroxysmal atrial fibrillation, he underwent radiofrequency catheter ablation of the accessory pathway located in the right postero-lateral wall to prevent secondary symptomatic events. His LV dyssynchrony improved after the procedure, but the degree of the LV outflow tract (LVOT) pressure gradient was increased. To stabilize the LVOT pressure gradient, he needed additional medications. This case shows that patients with HOCM should be carefully evaluated before making a decision concerning ablation of the accessory pathway.
International Heart Journal 01/2013; 54(2):111-4. · 1.16 Impact Factor
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Guoqin Wang,
Masafumi Watanabe, Yasushi Imai,
Kazuo Hara,
Ichiro Manabe,
Koji Maemura,
Momoko Horikoshi,
Atsuko Ozeki,
Chikako Itoh,
Takao Sugiyama,
Takashi Kadowaki,
Tsutomu Yamazaki,
Ryozo Nagai
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ABSTRACT: Modulator recognition factor-2 (Mrf2/AT-rich interaction domain (Arid)5b) has been revealed to be involved in pathogenesis of atherosclerosis and adipogenesis. Single-nucleotide polymorphisms (SNPs) in the MRF2/ARID5B gene are associated with coronary artery disease (CAD) and has been proposed as a candidate gene for type 2 diabetes (T2D). The study was aimed to determine whether any of the four MRF2/ARID5B SNPs (rs2893880, rs10740055, rs7087507 and rs10761600) associated with susceptibility to CAD are also associated with T2D, and to determine whether SNP genotype influences the levels of adiponectin and other clinical factors. Association of MRF2/ARID5B SNPs was investigated in 500 diabetic patients from the Department of Metabolic Diseases at the University of Tokyo and 243 hospital-based nondiabetic individuals from the Institute for Adult Disease Asahi Life Foundation Hospital and 500 community-based nondiabetic individuals from the Hiroshima Atomic Bomb Casualty Council Health Management Center. Associations of haplotypes of these SNP with levels of adiponectin and other clinical factors were evaluated when the data was available. We found rs2893880C, rs10740055A, rs7087507A and rs10761600T were increasingly associated with T2D in terms of allele/genotype frequencies of each SNP and their haplotype combinations. Individuals with haplotype CAAT indicated an 1.86 times higher prevalence of diabetes compared with individuals with GCGA (OR 1.86 (95% confidence interval (CI) 1.43-2.41)). Furthermore, CAAT significantly associated with adiponectin levels and other clinical factors. In conclusion, polymorphisms on the MRF2/ARID5B gene were associated with susceptibility to T2D as well as adiponectin and other clinical factors, which was in a completely concordant way with their associations with CAD.Journal of Human Genetics advance online publication, 13 September 2012; doi:10.1038/jhg.2012.101.
Journal of Human Genetics 09/2012; · 2.57 Impact Factor
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ABSTRACT: Background: Cardiac resynchronization therapy/defibrillators (CRTD) and implantable cardioverter defibrillators (ICD) with continuous intrathoracic impedance monitoring might provide an early warning of thoracic fluid retention. In contrast, volume loss events such as dehydration and bleeding are also common events in heart failure patients treated with diuretics and anticoagulants. The correlation between intrathoracic impedance and a volume loss event is not known. Methods and Results: This study evaluated the association between intrathoracic impedance and volume loss events in 36 patients with chronic heart failure (New York Heart Association [NYHA] II, III and IV) who had received CRTD/ICD implantation. Elevation of thoracic impedance above the reference line was defined as a positive deviation of thoracic impedance (PDI). This study recorded 249 PDIs including 60 spike PDIs defined as over 5ohms elevation from the reference line and 17 large PDIs as over 5ohms elevation and continuing for at least 4 days. Clinically, 96 dehydration events and 2 bleeding events were observed over a 1-year period. The sensitivity and positive predictive value (PPV) for spike PDI was 31.6% and 51.7%, respectively, while those for large PDI were 17.3% and 100%, respectively. Conclusions: A large PDI reflected dehydration and bleeding events with a high PPV in severe heart failure patients. The large PDI criteria might therefore be useful for predicting volume loss events in chronic heart failure patients. (Circ J 2012; 76: 2592-2598).
Circulation Journal 07/2012; 76(11):2592-8. · 3.77 Impact Factor
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Teruhiko Imamura,
Koichiro Kinugawa,
Taro Shiga,
Miyoko Endo,
Toshiro Inaba,
Hisataka Maki,
Masaru Hatano, Yasushi Imai,
Atsushi Yao,
Yasunobu Hirata,
Takashi Nishimura,
Shunei Kyo,
Minoru Ono,
Ryozo Nagai
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ABSTRACT: Refractory ventricular tachyarrhythmias are life threatening, especially in patients with stage D heart failure, and left ventricular assist device therapy is virtually the sole option to resolve the fatal conditions in many cases. The Interagency Registry for Mechanically Assisted Circulatory Support defines modifier A as complicating recurrent ventricular tachyarrhythmias. However, the optimal timing to implant a left ventricular assist device remains to be determined in less sick patients with modifier A. We experienced three patients with stage D heart failure with revised modifier A, i.e., at least two appropriate operations of implantable cardiac defibrillators within 2 weeks. Two of them were rescued by extracorporeal left ventricular assist device implantation, but one died because of an electrical storm before left ventricular assist device support was available. We would like to emphasize that we should consider implantable left ventricular assist device therapy as soon as possible for those who are assigned modifier A to prevent sudden arrhythmic death.
Journal of Artificial Organs 04/2012; 15(3):301-4. · 1.59 Impact Factor
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Naoko Kato,
Koichiro Kinugawa,
Taro Shiga,
Masaru Hatano,
Norihiko Takeda, Yasushi Imai,
Masafumi Watanabe,
Atsushi Yao,
Yasunobu Hirata,
Keiko Kazuma,
Ryozo Nagai
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ABSTRACT: Little is known about depressive symptoms in heart failure with preserved ejection fraction (HFpEF, EF ≥50%). We aimed to assess the prevalence of depression, to clarify the impact of depressive symptoms upon clinical outcomes, and to identify factors associated with these symptoms in HF with reduced EF (HFrEF, EF <50%) and HFpEF.
A total of 106 HF outpatients were enrolled. Of them, 61 (58%) had HFpEF. Most patients were male (HFrEF 80%, HFpEF 70%) and the mean of plasma B-type natriuretic peptide (BNP) level in the HFrEF group was similar to that in the HFpEF group (164.8 ± 232.8 vs. 98.7 ± 94.8 pg/mL). HFrEF patients were treated more frequently with beta-blockers compared with HFpEF patients (71% vs. 43%, p=0.004). Depressive symptoms were assessed using the Center for Epidemiologic Studies Depression Scale (CES-D). The prevalence of depression (CES-D score ≥16), and CES-D score did not significantly differ between HFrEF and HFpEF (24% vs. 25%, 14.1 ± 8.3 vs. 12.1 ± 8.3, respectively). During the 2-year follow-up, depressed patients had more cardiac death or HF hospitalization in HFrEF (55% vs. 12%, p=0.002) and HFpEF (35% vs. 11%, p=0.031). Cox proportional hazard analysis revealed that a higher CES-D score, indicating increased depressive symptoms, predicted cardiac events independent of BNP in HFrEF [hazard ratio (HR) 1.07, 95% confidence interval (CI) 1.01-1.13] and HFpEF (HR 1.09, 95% CI 1.04-1.15). Multiple regression analyses adjusted for BNP showed that independent predictors of depressive symptoms were non-usage of beta-blockers and being widowed or divorced in HFrEF. On the other hand, usage of warfarin was the only independent risk factor for depressive symptoms in HFpEF (all, p<0.05).
Depressive symptoms are common and independently predict adverse events in HFrEF/HFpEF patients. This study suggests that beta-blockers reduce depressive symptoms in HFrEF. In contrast, treatment for depression remains to be elucidated in HFpEF.
Journal of Cardiology 03/2012; 60(1):23-30. · 1.28 Impact Factor
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Atherosclerosis 02/2012; 221(2):602-3. · 3.79 Impact Factor
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Aiko Sakamoto,
Ryozo Nagai,
Kan Saito, Yasushi Imai,
Masao Takahashi,
Yumiko Hosoya,
Norifumi Takeda,
Kenji Hirano,
Kazuhiko Koike,
Yutaka Enomoto,
Haruki Kume,
Yukio Homma,
Daichi Maeda,
Hideomi Yamada,
Masashi Fukayama,
Yasunobu Hirata,
Nobukazu Ishizaka
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ABSTRACT: Retroperitoneal fibrosis, inflammatory aortic aneurysm, and pericardial and mediastinal fibrosis are characterized by infiltration of immuno-inflammatory cells and deposition of thickened fibrous tissues. Several recent studies suggested that an immunoglobulin-G4 (IgG4)-related immunological mechanism may play a role in these diseases. By searching the clinical database of patients admitted to our department between 2000 and 2010, we summarized the clinical data of 11 patients who were diagnosed to have these disorders. The diagnoses were idiopathic retroperitoneal fibrosis (8 cases), mediastinal and/or pericardial fibrosis (4 cases), inflammatory abdominal aneurysm (2 cases), and inflammatory coronary periarteritis (1 case). Hypertension, diabetes, and dyslipidemia were found in 45%, 36%, and 55%, respectively, in these patients, and they were all either current or former smokers. Two patients with pericardial involvement showed a rushed clinical course, resulting in in-hospital death. Serum levels of IgG were elevated in 67%, and soluble interleukin-2 receptor was elevated in 75%, when measured. Immunohistochemical analysis showed marked infiltration of IgG4-positive plasma cells in the pericardium in patients who died of constrictive pericarditis. Our data support the notion that immune-inflammatory mechanism, which might be IgG4-related sometimes, may play a role in idiopathic retroperitoneal fibrosis, inflammatory aortic aneurysm, and mediastinal/pericardial fibrosis, although clinical course may differ substantially.
Journal of Cardiology 12/2011; 59(2):139-46. · 1.28 Impact Factor
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ABSTRACT: The cardiovascular system may be involved as a target organ of multifocal fibrosclerosis, which may manifest as idiopathic retroperitoneal fibrosis, inflammatory aortic aneurysm, inflammatory periarteritis, and inflammatory pericarditis. These pathological conditions can sometimes occur concomitantly. Idiopathic retroperitoneal fibrosis and inflammatory abdominal aortic aneurysm are both characterized by the presence of fibro-inflammatory tissue around the abdominal aorta expanding into the surrounding retroperitoneal structures, and together they may be termed 'chronic periaortitis'. Cardiovascular fibrosclerosis has become non-uncommonly encountered condition since imaging modalities have made its diagnosis more feasible. In addition, recent studies have demonstrated that a certain fraction, but not all, of cardiovascular fibrosclerosis may have a link with immunoglobulin-G4 (IgG4)-related sclerosing disease (IgG4-SD). IgG4-SD is histologically characterized by dense fibrosclerosis and infiltration of lymphocytes and IgG4-positive plasma cells, and these histopathologic findings seem to be essentially similar regardless of the organs involved. In this mini review, we summarize what is known so far about multifocal fibrosclerosis of the cardiovascular system and its association with IgG4-SD, and what remains to be clarified in future investigations.
Journal of Cardiology 12/2011; 59(2):132-8. · 1.28 Impact Factor
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ABSTRACT: Immunoglobulin G4 (IgG4)-related immuno-inflammation has been suggested to play a role in the development of remodeling of arterial wall. We investigated the association between serum concentrations of IgG4 or soluble interleukin-2 receptor (sIL-2R) and coronary artery disease (CAD).
Serum concentrations of IgG4 and sIL-2R were measured in 286 patients who underwent coronary angiography.
In patients with CAD, the medians of serum concentrations of IgG4 (39.3 mg/dl) and sIL-2R (388 U/ml) were significantly higher than corresponding values in patients without CAD (IgG4 27.0 mg/dl, sIL-2R 312 U/ml). In receiver-operating characteristic curve analysis, the area under the curve of sIL-2R and IgG4 for the presence of CAD was 0.634 and 0.632, respectively. Age- and gender-adjusted logistic regression analysis showed that both of the fourth quartile of sIL-2R concentrations (≥509 U/ml) and that of IgG4 concentrations (≥57.7 mg/dl) were found to be associated with CAD with an odds ratio of 2.82 and 4.08, respectively, compared with the corresponding lowest quartile.
Serum concentrations of IgG4 and sIL-2R were increased in patients with angiographically-proven CAD, suggesting that IgG4-related immuno-inflammation may also have a role in the development and/or progression of coronary artery atherosclerosis.
Clinica chimica acta; international journal of clinical chemistry 11/2011; 413(5-6):577-81. · 2.54 Impact Factor
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Naomi Ogawa, Yasushi Imai,
Yuji Takahashi,
Kan Nawata,
Kazuo Hara,
Hiroshi Nishimura,
Masayoshi Kato,
Norifumi Takeda,
Takahide Kohro,
Hiroyuki Morita,
Tsuyoshi Taketani,
Tetsuro Morota,
Tsutomu Yamazaki,
Jun Goto,
Shoji Tsuji,
Shinichi Takamoto,
Ryozo Nagai,
Yasunobu Hirata
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ABSTRACT: Marfan syndrome (MS) is an inherited connective tissue disorder, and detailed evaluations of multiple organ systems are required for its diagnosis. Genetic testing of the disease-causing fibrillin-1 gene (FBN1) is also important in this diagnostic scheme. The aim of this study was to define the clinical characteristics of Japanese patients with MS and enable the efficient and accurate diagnosis of MS with mutational analysis using a high-throughput microarray-based resequencing system. Fifty-three Japanese probands were recruited, and their clinical characteristics were evaluated using the Ghent criteria. For mutational analysis, an oligonucleotide microarray was designed to interrogate FBN1, and the entire exon and exon-intron boundaries of FBN1 were sequenced. Clinical evaluation revealed more pulmonary phenotypes and fewer skeletal phenotypes in Japanese patients with MS compared to Caucasians. The microarray-based resequencing system detected 35 kinds of mutations, including 23 new mutations. The mutation detection rate for patients who fulfilled the Ghent criteria reached 71%. Of note, splicing mutations accounted for 19% of all mutations, which is more than previously reported. In conclusion, this comprehensive approach successfully detected clinical phenotypes of Japanese patients with MS and demonstrated the usefulness and feasibility of this microarray-based high-throughput resequencing system for mutational analysis of MS.
The American journal of cardiology 09/2011; 108(12):1801-7. · 3.58 Impact Factor
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ABSTRACT: Procedure-related coronary dissection is associated with an increased risk of major adverse cardiovascular events after percutaneous coronary intervention (PCI). In most patients with such an iatrogenic complication, further PCI or bypass surgery aimed at complete revascularization is performed. Moreover, conventional coronary angiography has been used as a standard modality in the follow-up of such patients. The present report describes a 70 year old female patient who was complicated by catheter-related extensive coronary dissection in the right coronary artery (RCA) when treated for an acute myocardial infarction. Although RCA flow was insufficient, we decided against revascularization and followed her medically without additional revascularization procedures. Her clinical course had been uneventful for 4 years. However, symptoms of effort angina developed and re-examinations were performed at approximately 5 years after the myocardial infarction. Although conventional coronary angiography failed to show the culprit lesion responsible for the angina symptoms, the superior spatial resolution of the coronary CT angiography clearly identified significant progression of the stenotic lesion in the true lumen of the dissected RCA. Thus, coronary CT angiography might be considered as a possible first-line follow-up modality in patients with procedure-related coronary dissection.
International Heart Journal 08/2011; 52(4):240-2. · 1.16 Impact Factor
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ABSTRACT: Hypertension is a typical modern lifestyle-related disease that is closely associated with the development of cardiovascular disorders. Elevation of angiotensin II (ANG II) is one of several critical factors for hypertension and heart failure; however, the mechanisms underlying the ANG II-mediated pathogenesis are still poorly understood. Here, we show that ANG II-mediated cardiac fibrosis, but not hypertrophy, is regulated by interferon regulatory factor 3 (IRF3), which until now has been exclusively studied in the innate immune system. In a ANG II-infusion mouse model (3.0 mg/kg/d), we compared IRF3-deficient mice (Irf3(-/-)/Bcl2l12(-/-)) with matched wild-type (WT) controls. The development of cardiac fibrosis [3.95 ± 0.62% (WT) vs. 1.41 ± 0.46% (Irf3(-/-)/Bcl2l12(-/-)); P<0.01] and accompanied reduction in left ventricle end-diastolic dimension [2.89 ± 0.10 mm (WT) vs. 3.51 ± 0.15 mm (Irf3(-/-)/Bcl2l12(-/-)); P=0.012] are strongly suppressed in Irf3(-/-)/Bcl2l12(-/-) mice, whereas hypertrophy still develops. Further, we provide evidence for the activation of IRF3 by ANG II signaling in mouse cardiac fibroblasts. Unlike the activation of IRF3 by innate immune receptors, IRF3 activation by ANG II is unique in that it is activated through the canonical ERK signaling pathway. Thus, our present study reveals a hitherto unrecognized function of IRF3 in cardiac remodeling, providing new insight into the progression of hypertension-induced cardiac pathogenesis.
The FASEB Journal 01/2011; 25(5):1531-43. · 5.71 Impact Factor
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ABSTRACT: Procedure-related coronary dissection is associated with an increased risk of major adverse cardiovascular events after percutaneous coronary intervention (PCI). In most patients with such an iatrogenic complication, further PCI or bypass surgery aimed at complete revascularization is performed. Moreover, conventional coronary angiography has been used as a standard modality in the follow-up of such patients. The present report describes a 70 year old female patient who was complicated by catheter-related extensive coronary dissection in the right coronary artery (RCA) when treated for an acute myocardial infarction. Although RCA flow was insufficient, we decided against revascularization and followed her medically without additional revascularization procedures. Her clinical course had been uneventful for 4 years. However, symptoms of effort angina developed and re-examinations were performed at approximately 5 years after the myocardial infarction. Although conventional coronary angiography failed to show the culprit lesion responsible for the angina symptoms, the superior spatial resolution of the coronary CT angiography clearly identified significant progression of the stenotic lesion in the true lumen of the dissected RCA. Thus, coronary CT angiography might be considered as a possible first-line follow-up modality in patients with procedure-related coronary dissection.
International Heart Journal 01/2011; 52(4):240-2. · 1.16 Impact Factor
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ABSTRACT: This study examines whether the serum concentration of cystatin C (Cys C) correlates with the severity of coronary artery disease (CAD) and whether it provides additional information on the risk for CAD in patients without chronic kidney disease (CKD) estimated by the creatinine-based glomerular filtration rate (GFR).
The relationship between serum Cys C and the severity of CAD in 526 patients was investigated. Based on GFR, patients were divided into those with and without CKD. The relationship of serum Cys C with the severity of CAD was examined. Serum Cys C was closely correlated with GFR in all cases and in CKD patients, but not in non-CKD patients. The average number of stenotic coronary arteries was significantly higher in the quartiles of higher concentration of Cys C as well as in those of GFR. In 348 patients (66%) the GFR was ≥60 ml · min(-1)·1.73 m(-2). Those patients with increased Cys C (>0.90 mg/L, 143 patients) had a significantly larger number of stenotic coronary arteries than those patients with normal Cys C.
Among patients considered to be at low risk based on the estimated GFR using serum creatinine, those with high concentrations of Cys C could have severe CAD. Besides CKD, Cys C might serve as a marker of CAD severity.
Circulation Journal 09/2010; 74(11):2441-7. · 3.77 Impact Factor
