Daiki Akiyama

Impact of coronary plaque composition on cardiac troponin elevation after percutaneous coronary intervention in stable angina pectoris: a computed tomography analysis.

OBJECTIVES The authors used multidetector computed tomography (MDCT) to study the relation between culprit plaque characteristics and cardiac troponin T (cTnT) elevation after percutaneous coronary intervention (PCI). BACKGROUND Percutaneous coronary intervention is often complicated by post-procedural myocardial necrosis manifested by elevated cardiac biomarkers. METHODS Stable angina patients (n = 107) with normal pre-PCI cTnT levels underwent 64-slice MDCT before PCI to evaluate plaque characteristics of culprit lesions. Patients were divided into 2 groups according to presence (group I, n = 36) or absence (group II, n = 71) of post-PCI cTnT elevation ≥3 times the upper limit of normal (0.010 ng/ml) at 24 h after PCI. RESULTS Computed tomography attenuation values were significantly lower in group I than in group II (43.0 [26.5 to 75.7] HU vs. 94.0 [65.0 to 109.0] HU, p < 0.001). Remodeling index was significantly greater in group I than in group II (1.20 ± 0.18 vs. 1.04 ± 0.15, p < 0.001). Spotty calcification was observed significantly more frequently in group I than in group II (50% vs. 11%, p < 0.001). Multivariate analysis showed presence of positive remodeling (remodeling index >1.05; odds ratio: 4.54; 95% confidence interval: 1.36 to 15.9; p = 0.014) and spotty calcification (odds ratio: 4.27; 95% confidence interval: 1.30 to 14.8; p = 0.016) were statistically significant independent predictors for cTnT elevation. For prediction of cTnT elevation, the presence of all 3 variables (CT attenuation value <55 HU; remodeling index >1.05, and spotty calcification) showed a high positive predictive value of 94%, and their absence showed a high negative predictive value of 90%. CONCLUSIONS MDCT may be useful in detecting which lesions are at high risk for myocardial necrosis after PCI.

Association of contrast-induced acute kidney injury with long-term cardiovascular events in acute coronary syndrome patients with chronic kidney disease undergoing emergent percutaneous coronary intervention☆

BACKGROUND The association between contrast-induced acute kidney injury (CI-AKI) and chronic kidney disease (CKD) in patients with acute coronary syndrome (ACS) treated with percutaneous coronary intervention (PCI) has not been fully reported. We evaluated the association of CI-AKI on cardiovascular events in ACS patients with CKD. METHODS A total of 1059 ACS patients who underwent emergent PCI in our multicenter registry were enrolled (69±12 years, 804 men, 604 STEMI patients). CKD was defined as at least stage 3 CKD, and CI-AKI was defined as an increase of at least 0.5 mg/dL and/or an increase of at least 25% of pre-PCI to post-PCI serum creatinine levels within 1 week after the procedure. Primary endpoints included cardiovascular death, myocardial infarction, and cerebrovascular disorder (stroke or transient ischemic attack). RESULTS In our study, 368 (34.7%) patients had CKD. During follow-up periods (435±330 days), CI-AKI and primary endpoints occurred in 164 (15.5%) patients and 106 (10.0%) patients, respectively. Multivariate Cox proportional hazards model revealed that age, female gender, peak creatinine kinase>4000, IABP use, CI-AKI (hazard ratio [HR], 2.17; 95% confidential interval [CI], 1.52 to 4.00; P<0.001), and CKD (HR, 1.66; 95% CI, 1.01 to 2.72; P=0.046) were independent predictors of primary endpoints. Kaplan-Meier analysis showed that occurrence of primary endpoints increased significantly with an increase in CKD stage, and CI-AKI yielded worse long-term prognosis at every stage of CKD (P<0.001). CONCLUSIONS CI-AKI was revealed to be a significant incremental predictor of cardiovascular events at each stage of CKD in ACS patients.

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.

Prognostic Value of Myocardial Contrast Delayed Enhancement With 64-Slice Multidetector Computed Tomography After Acute Myocardial Infarction

OBJECTIVES This study evaluated the clinical value of myocardial contrast delayed enhancement (DE) with multidetector computed tomography (MDCT) for predicting clinical outcome after acute myocardial infarction (AMI). BACKGROUND Although some studies have described the use of MDCT for assessment of myocardial viability after AMI, clinical experience remains limited. METHODS In 102 patients with first AMI, 64-slice MDCT without iodine reinjection was performed immediately following successful percutaneous coronary intervention (PCI). We measured the size of myocardial contrast DE on MDCT and compared it with clinical outcome. Primary composite cardiac events were cardiac death or hospitalization for worsening heart failure. RESULTS Among the 102 patients (24 ± 10 months follow-up), 19 patients experienced primary composite cardiac events (cardiac death, n = 7; heart failure, n = 12). Kaplan-Meier analysis showed higher risk of cardiac events for patients in the third tertile of myocardial contrast DE size (≥ 36 g) than for those in the other 2 tertiles (p < 0.0001). Multivariable Cox proportional hazards regression analysis indicated that myocardial contrast DE size (adjusted hazard ratio [HR] for tertile 3 vs. 1: 16.1, 95% confidence interval [CI]: 1.45 to 72.4, p = 0.022; HR for tertile 3 vs. 2: 5.06, 95% CI: 1.25 to 22.7, p = 0.039) was a significant independent predictor for cardiac events after adjustment for Thrombolysis In Myocardial Infarction risk score, left ventricular ejection fraction, total defect score on single-photon emission CT with technetium tetrofosmin, and transmural extent of myocardial contrast DE on MDCT. CONCLUSIONS Myocardial contrast DE size on MDCT immediately after primary PCI may provide promising information for predicting clinical outcome in patients with AMI.

Coronary high-intensity plaque on T1-weighted magnetic resonance imaging and its association with myocardial injury after percutaneous coronary intervention

AIMS Non-contrast T1-weighted imaging (T1WI) has emerged as a novel non-invasive imaging for vulnerable coronary plaque showing a high-intensity plaque (HIP). However, the association between HIP and percutaneous coronary intervention (PCI) has not been evaluated. We investigated the association between the presence of HIP and the incidence of myocardial injury after PCI. METHODS AND RESULTS A total of 77 patients with stable angina were imaged with non-contrast T1WI by using a 1.5 T magnetic resonance system (HIP and non-HIP group, N = 31 and 46 patients, respectively). We defined HIP as a coronary plaque to myocardium signal intensity ratio (PMR) of ≥1.4. High-sensitive cardiac troponin-T (hs-cTnT) was measured at baseline and 24 h after PCI. Percutaneous coronary intervention-related myocardial injury (PMI) was defined as an elevation of hs-cTnT >5× 99th percentile upper reference limit. High-intensity plaque was associated with the characteristics of ultrasound attenuation and positive remodelling on intravascular ultrasound. Although baseline hs-cTnT was similar between the groups, increase in hs-cTnT was significantly greater in the HIP vs. non-HIP group (0.065 [0.023-0.304] vs. 0.017 [0.005-0.026], P < 0.001). Percutaneous coronary intervention-related myocardial injury occurred more frequently in the HIP than non-HIP group (58.1 vs. 10.9%, P < 0.001), and the cut-off value of PMR found to be 1.44 for predicting PMI (sensitivity 78.3% and specificity 81.5%). In multivariate analysis, a PMR of ≥1.4 was a significant predictor of PMI (odds ratio 5.63, 95% confidence interval 1.28-24.7, P = 0.022). CONCLUSION High-intensity plaque on non-contrast T1WI was characterized as vulnerable coronary plaque on IVUS and was associated with higher incidence of PMI.

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.

Effect of individual proton pump inhibitors on cardiovascular events in patients treated with clopidogrel following coronary stenting: results from the Ibaraki Cardiac Assessment Study Registry.

Objectives: The aim of this study was to evaluate whether combination therapy of clopidogrel and proton pump inhibitors (PPIs) causes higher numbers of cardiovascular events than clopidogrel alone in Japanese patients. Background: PPIs are often prescribed in combination with clopidogrel following coronary stenting. PPIs are reported to diminish the effect of clopidogrel because both are metabolized by CYP2C19. However, no reports address the effects of PPIs on cardiovascular events following coronary stenting in the Japanese population. Methods: A total of 1,887 patients treated with clopidogrel following coronary stenting were enrolled in the Ibaraki Cardiac Assessment Study (ICAS) registry. All subjects were classified into two groups according to treatment without (n = 819) or with (n = 1,068) PPI. Propensity score analysis matched 1:1 according to treatment without PPI (n = 500) or with PPI (n = 500). Primary endpoint was the composite of all‐cause death or myocardial infarction. Results: No significant difference was observed in the primary endpoint between the group without PPI and the group with PPI (4.6% vs. 4.6%, P = 0.77). In contrast, a significant difference was found between the group without PPI and with PPI in regard to the incidence of gastrointestinal bleeding at the end of the follow‐up period and the specific PPI prescribed (2.4% vs. 0.8%, adjusted HR = 0.30, 95% Confidence interval 0.08‐0.87, P = 0.026) after propensity score matching. Conclusions: No significant association between PPI use and primary endpoint was observed in the Japanese population, whereas PPI use resulted in a significant reduction in the rate of gastrointestinal bleeding.

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.

Effect of the Mehran risk score for the prediction of clinical outcomes after percutaneous coronary intervention.

BACKGROUND The association of Mehran risk score (MRS) with long-term prognosis in patients treated with percutaneous coronary intervention (PCI) has not been fully reported. We investigated the association between MRS and clinical outcomes in patients who underwent PCI. METHODS Study subjects comprised 2198 patients treated with PCI from the Ibaraki Cardiovascular Assessment Study multicenter registry, excluding patients receiving hemodialysis or who died within 7 days. We categorized them into 4 groups according to MRS (low-risk: ≤5; medium-risk: 6-10; high-risk: 11-16; and very high-risk: ≥16). Contrast-induced acute kidney injury (CI-AKI) was defined as an increase of 0.5mg/dL or 25% in pre-PCI serum creatinine within 1-week post procedure. We evaluated CI-AKI and major adverse cardiac and cerebrovascular events (MACCE), and defined as all-cause death, myocardial infarction, congestive heart failure, or cerebrovascular disorder (stroke or transient ischemic attack). RESULTS A total of 192 (8.7%) patients developed CI-AKI. At multivariate analysis, odds ratio for CI-AKI was 4.09 (95% CI: 1.72-9.17, p=0.002) in the very high-risk group, 1.49 (95% CI: 0.89-2.42, p=0.120) in the high-risk group, and 1.08 (95% CI: 0.74-1.54, p=0.693) in the medium-risk group, as compared with the low-risk group. MACCE in the very high-risk group was more than 5-fold higher [hazard ratio (HR) 5.40, 95% CI: 2.96-9.28, p<0.001] compared with the low-risk group and was also increased in the high-risk (HR 3.72, CI: 2.59-5.32, p<0.001) and medium-risk groups (HR 1.97, CI: 1.45-2.69, p<0.001). Kaplan-Meier analysis showed that increasing risk for MACCE was seen across the groups as MRS increased (p<0.001). CONCLUSION MRS might provide potentially useful information for prediction of CI-AKI and clinical outcomes after PCI.

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.