Impact of Hemodialysis Duration on Coronary Artery Calcification Among Hemodialysis Patients Who Underwent Percutaneous Coronary Intervention.

Our study aimed to evaluate the prevalence and impact of coronary artery calcification (CAC) on hemodialysis (HD) patients with coronary artery disease (CAD) who underwent percutaneous coronary intervention (PCI). We enrolled 211 HD patients who underwent PCI (men: n = 155, age: 71 ± 1 0 years). Severe CAC was defined as calcification with an arc of 360° on intravascular ultrasound. Multivariate analysis was performed to determine the predictors of severe CAC. The impact of severe CAC on target lesion revascularization (TLR) was evaluated. Patients with severe CAC (46%) had a higher incidence of diabetes mellitus (DM) (79 vs 59%, P = .003) and longer HD duration (7.7 vs 3.4 years, P < .001) than those with non-severe CAC. Multivariate analysis demonstrated that DM, HD duration, and angiographic calcification were significant predictors for severe CAC (odds ratio 4.42, 1.13, and 6.62; P < .001, P < .001, and P < .001, respectively). After the median follow-up period of 580 days (interquartile range, 302-730 days), Kaplan-Meier curve analysis revealed that severe CAC was associated with an increased risk for TLR (χ2 12.7; P = .002). In HD patients with CAD after PCI, DM and HD duration were significant predictors for severe CAC. Furthermore, severe CAC was associated with an increased risk for TLR.

Elevated Remnant Lipoprotein Related to Adverse Events in Patients with Chronic Limb-Threatening Ischemia after Endovascular Therapy for Below-the-Knee Lesions.

BACKGROUND: The prognosis of patients with chronic limb-threatening ischemia (CLTI) is unacceptably poor, and risk factors are unknown. Serum remnant lipoprotein has been associated with cardiovascular events. The aim of our study was to test the hypothesis that remnant lipoprotein is associated with the prognosis of patients with CLTI. METHODS: This retrospective study included 67 patients with CLTI who had received endovascular therapy (EVT) for de novo below-the-knee lesions. Patients were divided into 2 groups using fasting preoperative value of remnant-like particle cholesterol (RLP-C) with a cutoff value of 5.1 mg/dL into LOW RLP-C (n = 46) and HIGH RLP-C (n = 21). We assessed the differences between the 2 groups in the prevalence of major adverse limb events (MALE), composed of target lesion revascularization and major amputation. RESULTS: At a median follow-up period of 12 months, MALE had occurred in 11 LOW RLP-C patients (23.9%) and 11 HIGH RLP-C patients (52.4%; P = 0.03). Kaplan-Meier analysis showed the prevalence of MALE was significantly higher in HIGH RLP-C than LOW RLP-C (log-rank χ2 = 5.2, P = 0.02). Multivariate analysis found HIGH RLP-C to be an independent predictor for MALE (hazard ratio, 2.6; 95% confidence interval, 1.1-6.1; P = 0.02) along with history of coronary artery disease. CONCLUSIONS: Preoperative remnant lipoprotein was associated with the prognosis of patients with CLTI who had received EVT for de novo below-the-knee lesions.

Clinical Outcomes after Endovascular Therapy Among Hemodialysis Patients with Peripheral Artery Disease Stratified by the Primary Kidney Disease.

OBJECTIVES: The objective of this study was to investigate the clinical characteristics of hemodialysis patients with peripheral artery disease (PAD) and the outcomes after endovascular therapy (EVT) in such patients stratified by the primary kidney disease. METHODS: This retrospective observational study evaluated 142 consecutive hemodialysis patients with symptomatic PAD who underwent EVT (men: n = 103, age: 74 ± 8 years). Patients were divided into 3 groups in accordance with the reason for hemodialysis: hypertensive nephrosclerosis (HTN [n = 26]), diabetic nephropathy (DN [n = 85]), and chronic glomerulosclerosis (CGN [n = 31]). The primary outcome was major adverse event(s) (MAEs), including target lesion revascularization, major amputation, and all-cause death. Clinical characteristics and outcomes were compared among the 3 groups. RESULTS: Patients with HTN were older (81 ± 6 years vs. 72 ± 8 years vs. 74 ± 8 years; P < 0.001) and had a shorter hemodialysis vintage (2.4 years vs. 6.8 years vs. 11.2 years; P < 0.001) than those with DN and CGN. Critical limb ischemia (CLI) affected 15 (58%) patients in the HTN group, 52 (61%) in the DN group, and 10 (32%) in the CGN group. Target lesion length was longer in patients with HTN than in those in the other groups (155 ± 101 mm vs. 108 ± 77 mm [DN] vs. 98 ± 76 mm [CGN]; P = 0.020). During a median follow-up period of 372 days (interquartile range, 198-730 days), Kaplan-Meier curve analysis revealed that HTN was associated with an increased risk for MAEs (χ2 11.6; P = 0.003). Furthermore, multivariate Cox regression analysis revealed that CLI, HTN, and B-type natriuretic peptide levels were independent predictors of MAE (hazard ratio 3.91, 2.88, and 1.00; P < 0.001, P < 0.001, and P = 0.001, respectively). CONCLUSIONS: Among hemodialysis patients with PAD, HTN was associated with an increased risk for MAEs after EVT.

Usefulness of Lipoprotein (a) for Predicting Outcomes After Percutaneous Coronary Intervention for Stable Angina Pectoris in Patients on Hemodialysis.

Serum lipoprotein (a) level is genetically determined and remains consistent during a person's life. Previous studies have reported that people with high lipoprotein (a) level are at a high risk of cardiac events. We investigated the association between lipoprotein (a) levels and clinical outcomes after percutaneous coronary intervention (PCI) for stable angina pectoris (SAP) in hemodialysis (HD) patients. Serum lipoprotein (a) levels were measured on admission in 410 consecutive HD patients who underwent successful PCI for SAP. Patients were divided into 2 groups: low and high group having lipoprotein (a) level <40 mg/dL (n = 297) and ≧40 mg/dL (n = 113) respectively. After PCI, the incidence of major adverse cardiac event (MACE) including cardiac death, nonfatal myocardial infarction, necessity of a new coronary revascularization procedure (coronary bypass surgery, repeat target lesion PCI, PCI for a new non-target lesion) was analyzed. At a median follow-up of 24 months (12 to 37 months), MACE occurred in 188 patients (45.6%). The rate of MACE rate was significantly higher in the high lipoprotein (a) group than in the low lipoprotein (a) group (59.2% vs 40.7%, long-rank test chi-square = 12.3; p < 0.001). Cox analysis showed that high lipoprotein (a) level (Hazard Ratio, 1.62; 95% Confidence Interval, 1.19 to 2.20; p = 0.002) was an independent predictor for MACE after PCI. In conclusion, high lipoprotein (a) level was associated with a higher incidence of MACE after PCI for SAP in HD patients.

Aortic Plaque Distribution, and Association between Aortic Plaque and Atherosclerotic Risk Factors: An Aortic Angioscopy Study.

AIM: Knowledge of subclinical plaque morphology and plaque distribution in the aorta in vivo remains unclear. This study aimed to increase the body of knowledge in this area. METHODS: We enrolled 37 consecutive patients with stable angina pectoris patients who underwent non-obstructive angioscopy for both the coronary artery and aorta immediately after percutaneous coronary intervention. We evaluated the presence of aortic plaques and the distribution of plaque instability. Patients were allocated into two groups according to the number of vulnerable plaques in whole aorta (a low [0-11] and high [≥ 12] group). We evaluated the relationships between the two groups in terms of cardiovascular risk factors. RESULTS: Aortic plaques were identified using non-obstructive angioscopy in all patients, and the greatest number of plaques was found at the infrarenal abdominal aorta (IAA) (the aortic arch, the descending thoracic aorta, the suprarenal abdominal aorta, the IAA, and common iliac artery; 65%, 76%, 65%, 95%, and 49%, respectively; p＜0.001). The maximum yellow grade, and the number of intense yellow plaques, ruptured plaques, and thrombi were highest at the IAA (p＜0.001). The prevalence of diabetes mellitus and peripheral arterial disease was higher in the high vulnerable plaque group (83.3% vs. 40.0%, p=0.010, 50.0% vs. 8.0%, p=0.005, respectively). CONCLUSIONS: Aortic atherosclerosis was the most severe at the IAA, and aortic plaque vulnerability and distribution were associated with the prevalence of diabetes mellitus and peripheral artery disease in patients with stable angina pectoris. Non-obstructive angioscopy may identify patients at high risk of future aortic events.

Observation of an Asymptomatic Dissecting Aortic Aneurysm Using Non-Obstructive Angioscopy.

Non-obstructive angioscopy has become a novel method of evaluating atheromatous plaques of the aortic intimal wall. A 77-year-old man with coronary artery disease underwent percutaneous coronary intervention in the left descending artery. We subsequently used non-obstructive angioscopy to identify aortic atheromatous plaques and incidentally diagnosed an aortic dissecting aneurysm. Non-obstructive angioscopy demonstrated a great fissure in severe atheromatous plaques at the entry site of the aortic dissection identified by enhanced computed tomography. This is the first report to describe the aortic intimal findings of an aortic dissecting aneurysm in vivo by using trans-catheter angioscopy.

Intravascular Ultrasound and Angioscopy Assessment of Coronary Plaque Components in Chronic Totally Occluded Lesions.

BACKGROUND: The in vivo lesion morphologies and plaque components of coronary chronic total occlusion (CTO) lesions remain unclear.Methods and Results:We investigated 57 consecutive CTO lesions in 57 patients with stable angina pectoris undergoing elective percutaneous coronary intervention with intravascular ultrasound (IVUS) and coronary angioscopy (CAS) examination. All CTO lesions were classified according to the proximal angiographic lumen pattern; tapered-type (T-CTO) and abrupt-type (A-CTO). The differences in the intracoronary images of these lesion types were evaluated according to the location within the CTO segment. A total of 35 lesions (61.4%) were T-CTO. T-CTO lesions had higher frequencies of red thrombi (proximal 71.4%; middle 74.3%; distal 31.4%; P<0.001) and bright-yellow plaques (yellow-grade 2-3) (48.6%; 74.3%; 2.9%; P<0.001) at the proximal or middle than at the distal subsegment; A-CTO lesions showed no significant differences among the 3 sub-segments. At the middle subsegment, T-CTO lesions showed higher frequencies of positive remodeling (51.4% vs. 18.2%, P=0.01) and bright-yellow plaques (74.3% vs. 13.6%, P<0.001) compared with A-CTO lesions. Multivariate analysis identified bright-yellow plaque as an independent predictor (odds ratio, 7.25; 95% confidence interval, 1.25-42.04; P=0.03) of the occurrence of periprocedural myocardial necrosis. CONCLUSIONS: The combination of IVUS and CAS analysis may be useful for identifying lesion morphology and plaque components, which may help clarify the pathogenetic mechanism of CTO lesions.

A case of ventricular fibrillation as a consequence of capecitabine-induced secondary QT prolongation: A case report.

Capecitabine is an oral fluoropyrimidine which can prolong QT interval. However, there have been no reports that capecitabine induced ventricular fibrillation (VF) due to secondary QT prolongation in patients with no structural heart disease. A 39-year-old woman developed VF during the chemotherapy of capecitabine for colon cancer. At the administration, corrected QT interval (QTc) was prolonged to 559 ms despite no evidence of organic heart disease. Discontinuation of capecitabline normalized the QTc (414 ms). During the follow-up of eight years, neither the QTc prolongation nor the recurrent VF has been detected. We report the rare case of capecitabine-related VF without any organic heart disease. .

Impact of optical coherence tomography- and coronary angioscopy-assessed neointimal tissue characteristics on occurrence of periprocedural myonecrosis in patients with in-stent restenosis.

Several characteristics of neointimal tissues, including neoatherosclerotic progression, have been reported in lesions with in-stent restenosis (ISR). However, the effects of these characteristics on outcomes after percutaneous coronary intervention (PCI) for ISR lesions remain unclear. We assessed the relationships between neointimal tissue characteristics and the occurrence of periprocedural myonecrosis (PMN) after PCI in ISR lesions. We investigated 72 ISR lesions in 72 patients with stable angina pectoris (SAP) who underwent pre- and post-revascularization optical coherence tomography (OCT) and coronary angioscopy (CAS). All lesions were classified as with PMN, defined by an elevated peak high-sensitivity cardiac troponin-T level during the 24-h post-PCI period, and without PMN. PMN was observed in 23 (31.9 %) lesions. PMN lesions had higher frequencies of OCT-derived thin-cap fibroatheroma (26.1 vs. 6.1 %, P = 0.03), CAS-derived intensive yellow neointima (30.4 vs. 10.2 %, P = 0.04), neointima with complex surface (60.9 vs. 28.6 %, P = 0.01), and CAS-derived atheromatous appearance (CAS-AAP), defined as yellow plaque including complex thrombi underneath disrupted neointimal coverage after ballooning (47.8 vs. 16.3 %, P = 0.008) at the most stenotic sites inside stents, compared to lesions without PMN. Multivariate logistic regression analysis identified CAS-AAP (odds ratio: 3.568, 95 % confidence interval: 1.109-11.475, P = 0.033) as an independent predictor of PMN. For ISR lesions in SAP patients, an OCT- and CAS-based assessment of neointimal tissue characteristics might help to predict the occurrence of PMN.

Reversible Atrial Fibrillation with Bradycardia Associated with Primary Cardiac B-Cell Lymphoma.

Primary cardiac lymphoma (PCL) only rarely occurs and it is defined as a lymphoma in which the bulk of the tumor is located within the heart and pericardium. A 53-year-old woman was referred due to dyspnea, and an electrocardiogram exhibited atrial fibrillation (AF). Echocardiography revealed no abnormal findings. Scintigraphy and a lymph node biopsy led to a diagnosis of PCL. After the start of chemotherapy, AF was converted to atrial tachycardia prior to sinus rhythm with a first-degree atrioventricular block, which was finally restored to a normal sinus rhythm. PCL is only rarely encountered, but it should be included in the differential diagnosis as a possible cause of AF, and such AF could be reversible if the patient can be treated in a timely manner.

The anti-inflammatory mechanism of prostaglandin e2 receptor 4 activation in rat experimental autoimmune myocarditis.

Prostaglandins (PG) and their specific receptors for E type PG (EP) play an important role in inflammatory diseases. Although myocarditis results in inflammation of the heart, roles of PG and EP in its pathophysiology is still controversial. To clarify the role of PG and EP on the progression of myocarditis, we used an experimental autoimmune myocarditis model. A selective EP4 (EP4RAG) agonist was administered into both early (Day 0 to 21) and late (Day 14 to 21) -treated groups and the animals were killed on Day 21. We found that improved cardiac function was detected in the EP4RAG-treated groups in comparison to the untreated group. The infiltration area ratio in the early-treated (16.6% ± 4.6%) group was lower than those in the untreated group (32.1% ± 3.5%) (P < 0.05). The fibrosis area ratios in the early-treated (19.2% ± 6.3%) and the late-treated groups (24.4% ± 5.1%) were lower than those in the untreated group (37.4% ± 2.6%), respectively (P < 0.05). Moreover, we found that EP4RAG decreased T-cell proliferation and monocyte chemoattractant protein-1 production in vitro. We concluded that a selective EP4 agonist inactivates T-cells, which turns out to moderate the progression of experimental autoimmune myocarditis. Therefore, EP4 can be an effective target for myocarditis treatment.

Clarithromycin attenuates myocardial ischemia-reperfusion injury.

BACKGROUND: MMP activity is upregulated in the heart after myocardial ischemia reperfusion, and its activation contributes to the changes in left ventricular (LV) dysfunction. A major macrolide antibiotic, clarithromycin has many biological functions including MMP regulation. However, little is known about the effect of clarithromycin in myocardial reperfusion injury via MMPs. Our objective was to clarify the role of MMPs regulated by clarithromycin in the progression of myocardial reperfusion injury. METHODS: We administered clarithromycin to rats with ischemia-reperfusion injury twice a day for 7 days before and 14 days after reperfusion. RESULTS: Clarithromycin resulted in a significant reduction of the infarction area:area at risk ratio and preserved fractional shortening ratio after 14 days of reperfusion. Immunohistochemical analysis revealed that macrophages were the primary cellular source of MMPs. Fewer macrophages were detected in the ischemic area of the hearts following ischemia reperfusion in the clarithromycin-treated group compared with the vehicle-treated group. Although ischemia-reperfusion injury resulted in LV fibrosis with increasing MMP activities, clarithromycin significantly reduced these changes. CONCLUSION: Clarithromycin is effective for attenuating myocardial ischemia-reperfusion injury by suppressing MMPs.