Tetsuo Kamiishi

Sensitive Assessment of Activity of Takayasu's Arteritis by Pentraxin3, a New Biomarker

To the Editor: Takayasus arteritis (TA) is a chronic vasculitis mainly involving the aorta and its main branches ([1][1]). The erythrocyte sedimentation rate and C-reactive protein (CRP) level have generally been used to monitor disease activity. In addition to steroids and conventional

Differences in catheter ablation of paroxysmal atrial fibrillation between males and females

BACKGROUND Catheter ablation (CA) has become a standard treatment for patients with atrial fibrillation (AF). However, gender-related differences associated with CA of paroxysmal AF (PAF) remain unclear. METHODS We compared 1124 consecutive patients (mean age, 61 ± 10 years; male, n=864) with PAF scheduled for CA between the genders. RESULTS Females were significantly older (p<0.0001), and had a lower body-mass-index (p=0.02), smaller left atrial dimension (LAD; p=0.04), larger LAD indexed by the body-surface-area (LADI; p<0.0001) and better left ventricular ejection fraction (p<0.0001) at baseline. Ischemic heart disease (p=0.007) was more frequent in males, whereas hypertrophic cardiomyopathy (p=0.007) and mitral stenosis (p=0.001) were more frequent in females. More additional procedures were performed to eliminate non-pulmonary vein foci in females than males (p<0.05), but those locations were similar between the genders. The incidence of procedure-related complications was similar between genders (p=0.73). Sinus rhythm was similarly maintained between females and males after the first CA (56.4% vs. 59.3% at 5 years, p=0.24), but was significantly lower in females after the last CA (76.5% vs. 81.3% at 5 years, p=0.007). More females did refuse multiple CA procedures (especially a second one) than males (37.8% in females vs. 27.4% in males, p=0.02). The age (HR, 0.98/y, p=0.01), duration of AF (HR, 1.04/y, p=0.0001), number of failed anti-arrhythmic-drugs (HR, 1.10, p=0.03) and LADI (HR, 1.89 per 10mm/m(2), p=0.001) were significantly associated with AF-recurrence in males, but not in females. CONCLUSIONS Specific differences and similarities between the genders were observed in PAF patients undergoing CA.

Renal Function After Catheter Ablation of Atrial Fibrillation

Background— Kidney function is a known predictor of cardiovascular morbidity and mortality. Although patients with atrial fibrillation (AF) often have kidney dysfunction, less is known about the association between AF and kidney function. We sought to assess changes in kidney function after catheter ablation of AF. Methods and Results— Patients who underwent catheter ablation of AF were recruited for the present prospective study. Estimated glomerular filtration rate (eGFR) was evaluated before and 1 year after the ablation. Three hundred eighty-six patients (paroxysmal AF, 135; persistent AF, 106; longstanding persistent AF, 145) were studied. Their baseline eGFR was 68±14 mL · min−1 · 1.73 m−2. Sixty-six percent and 26% of patients had eGFR of 60 to 89 and 30 to 59 mL · min−1 · 1.73 m−2, respectively. Overall, 278 patients (72%) were arrhythmia free over a 1-year follow-up. In patients free from arrhythmia, eGFR increased 3 months later and was maintained until 1 year, whereas in patients with recurrences, eGFR had decreased over 1 year. Changes in eGFR over 1 year in patients free from arrhythmia differed significantly compared with those with recurrences (3±8 versus −2±8 mL · min−1 · 1.73 m−2; P<0.0001). In all quartiles of baseline eGFR, changes in eGFR over 1 year after the ablation were greater in patients free from arrhythmia compared with those with recurrences. Conclusion— Elimination of AF by catheter ablation was associated with improvement of kidney function over a 1-year follow-up in patients with mild to moderate kidney dysfunction.

Quantitative assessment of tissue prolapse on optical coherence tomography and its relation to underlying plaque morphologies and clinical outcome in patients with elective stent implantation.

BACKGROUND Tissue prolapse (TP) is sometimes observed after percutaneous coronary intervention (PCI), but its clinical significance remains unclear. We investigated the relationship between TP volume on optical coherence tomography (OCT) after PCI and underlying plaque morphologies and the impact of TP on clinical outcomes. METHODS We investigated 178 native coronary lesions with normal pre-PCI creatine kinase-myocardial band (CK-MB) values (154 lesions with stable angina; 24 with unstable angina). TP was defined as tissue extrusion from stent struts throughout the stented segments. All lesions were divided into tertiles according to TP volume. The differences in plaque morphologies and 9-month clinical outcomes were evaluated. RESULTS TP volume was correlated with lipid arc (r=0.374, p<0.0001) and fibrous cap thickness (r=-0.254, p=0.001) at the culprit sites. The frequency of thin-cap fibroatheroma (TCFA) was higher in the largest TP tertile (≥ 1.38 mm(3)) (p=0.015). In multivariate analysis, right coronary artery lesion (odds ratio [OR]: 2.779; p=0.005), lesion length (OR: 1.047; p=0.003), and TCFA (OR: 2.430; p=0.022) were related to the largest TP tertile. Lesions with post-PCI CK-MB elevation (>upper reference limit) had larger TP volume than those without (1.28 [0.48 to 3.97] vs. 0.70 [0.16 to 1.64] mm(3), p=0.007). The prevalence of cardiac events during the 9-month follow-up was not significantly different according to TP volume. CONCLUSIONS TP volume on OCT was related to plaque morphologies and instability, and post-PCI myocardial injury, but not to worse 9-month outcomes.

Lipoprotein(a) is an important factor to determine coronary artery plaque morphology in patients with acute myocardial infarction.

BackgroundLipoprotein(a) [Lp(a)] can influence the development and disruption of atherosclerotic plaques through its effect on lipid accumulation. The purpose of this study was to evaluate the relationship between serum Lp(a) levels and plaque morphology of an infarct-related lesion and non-infarct-related lesion of the coronary artery in acute myocardial infarction (AMI). Methods and resultsCoronary plaque morphology was evaluated in 68 patients (age 62.1±12.1 years, mean±SD; men n=58, women n=10) with AMI by intravascular ultrasound with radiofrequency data analysis before coronary intervention and by 64-slice computed tomography angiography within 2 weeks. Patients were divided into a group with an Lp(a) level of 25 mg/dl or more (n=20) and a group with an Lp(a) level of less than 25 mg/dl (n=48). Intravascular ultrasound with radiofrequency data analysis identified four types of plaque components at the infarct-related lesion: fibrous, fibrofatty, dense calcium, and necrotic core. The necrotic core component was significantly larger in the group with an Lp(a) level of 25 mg/dl or more than in the group with an Lp(a) level of less than 25 mg/dl (27.6±8.0 vs. 15.7±10.0%, P=0.0001). Coronary plaques were classified as calcified plaques, noncalcified plaques, mixed plaques, and low-attenuation plaques on 64-slice computed tomography angiography. Computed tomography indicated that the group with an Lp(a) level of 25 mg/dl or more had a greater number of total plaques, noncalcified plaques, and low-attenuation plaques in whole coronary arteries than did the group with an Lp(a) level of less than 25 mg/dl (5.3±1.8 vs. 3.7±2.2, P=0.0061; 4.0±2.0 vs. 1.2±1.3, P=0.0001; 2.2±2.1 vs. 0.5±0.7, P=0.0001, respectively). ConclusionElevated serum Lp(a) levels are associated with the number of plaques and plaque morphology. Patients with a high Lp(a) level during AMI require more intensive treatment for plaque stabilization.

Impact of statin use before the onset of acute myocardial infarction on coronary plaque morphology of the culprit lesion.

Statins favorably stabilize coronary plaque. We evaluated the impact of statin use before the onset of acute myocardial infarction (AMI) on culprit lesion plaque morphology. Patients (n = 127) with AMI were divided into either a statin group (n = 31) or a nonstatin group (n = 96) based on statin use before the onset of AMI. Coronary plaque morphology of the culprit lesion was evaluated using intravascular ultrasound virtual histology (IVUS-VH) with radiofrequency data analysis before coronary intervention. The IVUS-VH identified 4 types of plaque components: fibrous, fibrofatty, dense calcium, and necrotic core. The IVUS-VH showed less percentage of necrotic area, greater percentage fibrous area, and greater percentage of fibrofatty area of the culprit lesion in the statin group. In conclusion, statin use before the onset of AMI might have effects on coronary plaque morphology of the AMI culprit lesion with less necrotic core and greater fibrous and fibrofatty component.

Differential characteristics of inflammatory responses to stent implantation between de novo and intrastent restenosis lesion in patients with stable angina.

Mechanical plaque rupture of coronary atherosclerotic plaque during stent implantation can increase serum levels of high-sensitivity C-reactive protein (hsCRP). Patients with stable angina pectoris were divided into 2 groups: one group included 186 patients with de novo lesion who underwent stent implantation (de novo group); the other group included 40 patients with intrastent restenosis (ISR) undergoing stent implantation (ISR group). The de novo group had a significant increase in hsCRP levels post stenting, while the ISR group showed no increase in hsCRP post stenting. Intravascular ultrasound with radiofrequency data analysis showed that the de novo group had larger percentage of both necrotic core area and fibrofatty area at the target lesion than the ISR group, while the ISR group had a larger percentage of fibrous area. Differential inflammatory response to stent implantation between the de novo plaque and in ISR lesion is related to lesion morphology.

Response to the letter to the editor "Can statins alter coronary plaque morphology assessed by intravascular ultrasound?".

I appreciate the useful comments by Koza et al regarding our article. As mentioned in the article, our study patients received statin therapy as a primary prevention: 7 patients received pravastatin (10 mg/d), 10 patients simvastatin (5 mg/d), 5 patients fluvastatin (20 mg/d), and 9 patients atorvastatin (10 mg/d). We could not indicate the exact durations of statin treatment in all the patients. However, we can say that they all received statin treatment for 1 year before the onset of acute myocardial infarction (MI). As Dr Koza mentioned, culprit lesion of the infarct-related artery was only observed with intravascular ultrasound–virtual histology (IVUS-VH), in our study. The IVUS-VH evaluation was limited to the culprit lesions in the infarct-related artery due to emergency percutaneous coronary intervention for the acute phase of MI. I hope that this response will increase the interest in statin use before the onset of acute MI.