A Case of Atrial Tachycardia Circulating around a Left Atrial Roof Scar with Diabetes Mellitus and Renal Failure on Hemodialysis

Introduction. Little is known about the effects of volume change by hemodialysis (HD) and mechanical stress caused by an anatomical structure being in contact with the left atrium on the progression of atrial remodeling. We experienced a case of atrial tachycardia (AT) in a patient who had left atrial (LA) scarring at the LA roof and a low-voltage area with slow conduction around the LA scar as components of AT circuit. Here, we present the conceivable hypothesis of the LA scar and the low-voltage area formation. Our concept can be useful in developing a strategy for ablation in a patient with chronic renal failure (CRF) on HD. Case Report. A 65-year-old man with CRF on HD was referred for AT ablation. Three-dimensional electroanatomical mapping revealed that the AT conducted around an LA scar in a counterclockwise fashion. There was a slow conduction area at the superior side of the LA scar, where the AT was terminated during the ablation. Computed tomography indicated a close relationship between the LA and the anatomical structures (ascending aorta and pulmonary artery). Conclusion. Volume change by HD and close contact of anatomical structures to the LA can promote atrial remodeling, resulting in AT occurrence

Esophageal thermal injury in catheter ablation of atrial fibrillation

Pulmonary vein isolation is an established method for the catheter ablation of atrial fibrillation. Esophageal thermal injuries, such as esophageal erosion, ulceration and periesophageal nerve injury leading to gastric hypomotility, are important complications associated with pulmonary vein isolation. In this review article, we describe the mechanisms, characteristics and the predictors of esophageal thermal injury associated with pulmonary vein isolation

Metabolic syndrome is not a predictor for cardiovascular events in Japanese patients with diabetes mellitus asymptomatic for coronary artery disease: A retrospective analysis of the J-ACCESS-2 study

Purpose: Patients with metabolic syndrome (MetS) have potentially higher risk for cardiovascular events. The aim of this study was to evaluate the effect of MetS on cardiac events in type-2 diabetic patients asymptomatic for coronary artery disease (CAD) in a Japanese population. Methods: A total of 485 patients from a J-ACCESS-2 investigation with stress-gated myocardial perfusion imaging (MPI) and quantitative-gated MPI analysis were examined. Cardiovascular hard events (cardiac death and acute coronary syndrome) and total events during a 3-year follow-up were analyzed. Results: The MetS group (n = 229) had higher incidence of hypertension, dyslipidemia, and ventricular dilatation than the non-MetS group (n = 256). The hard events were 8 and 12 for the MetS and non-MetS groups (P = n.s.), and total events were 31 and 31 for each of these groups, respectively (P = n.s.). Significant variables related to total cardiovascular events included age, current smoking, insulin use, total cholesterol, ejection fraction, summed stress score ≥ 9, and summed difference score ≥ 2. Cox proportional hazard analysis and Kaplan-Meier survival analysis showed that only the summed stress score was related to total events (P = .01), and the presence and the number of items for MetS criteria were not. Conclusion: In patients with type 2 diabetes asymptomatic for CAD, cardiovascular events and ischemia are as common in diabetic patients without MetS as in those with MetS. A high MPI defect score is related to total events including cardiac and cerebrovascular events. © 2012 American Society of Nuclear Cardiology

Vascular composition data supporting the role of N-3 polyunsaturated fatty acids in the prevention of cardiovascular disease events

AbstractN-3 polyunsaturated fatty acids (PUFAs) are thought to have protective effects against cardiovascular disease. Here, we report the relationship between serum PUFA concentrations and plaque composition, as evaluated by virtual histology-intravascular ultrasound (VH-IVUS). Consecutive patients (n=61) who underwent percutaneous coronary intervention (PCI) were pre-operatively examined using VH-IVUS to assess the composition of culprit plaques. Gray-scale IVUS and VH-IVUS data of fibrous, fibro-fatty, necrotic core, and dense calcium regions of plaques were estimated at the minimal luminal area sites of culprit lesions. Serum levels of high-sensitivity C-reactive protein (hsCRP) and PUFAs, including eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and arachidonic acid (AA), were compared between patients with (ACS, n=27) and without acute coronary syndrome (non-ACS, n=34) before PCI. Multiple logistic regression analysis of the data showed that EPA/AA under the median was more highly associated with ACS than hsCRP over the median. In addition, EPA/AA was negatively correlated with the percentage of fibrous plaque regions and EPA/AA and DHA/AA were positively correlated with the percentage of dense calcium regions in plaques. Furthermore, the correlation index of EPA/AA was the most highly (R=0.513) correlated with the percentage of dense calcium regions in plaques

Effects of daily alcohol intake on glomerular filtration rate over three years

Background: The association between daily alcohol intake and changes in renal function in the Japanese general population is not well established. Methods: We analyzed data from 150 residents who underwent specific health checkups held in Mishima Town in 2016 and 2019. We divided participants on the basis of alcohol consumption: residents with daily alcohol intake of < 20 g/day (the none-to-low group, n = 104, 69.3%); those with daily alcohol intake of ≥ 20 but < 40 g/day (the intermediate group, n = 30, 20.0%); and those with daily alcohol intake of ≥ 40 g/day (the high group, n = 16, 10.7%). We compared baseline characteristics. The primary endpoint was a decrease in estimated glomerular filtration rate (eGFR), defined as the decrease in eGFR greater than the median decrease over three years. Results: The three-year changes in eGFR were +0.3 (-4.8, +3.0), -2.3 (-5.1, +1.2), and -4.9 (-8.2, -2.9) mL/min/1.73 m2 in the none-to-low, intermediate, and high groups, respectively (P = 0.007). In the multivariate logistic regression analysis, a high amount of alcohol intake was independently associated with a decrease in eGFR, with adjusted odds ratio of 11.418 (95% confidence interval 1.554-83.879, P = 0.017). Conclusion: A high average daily alcohol intake is associated with a decrease in eGFR

Senescence marker protein 30 inhibits angiotensin II-induced cardiac hypertrophy and diastolic dysfunction

AbstractBackground and objectiveSenescence marker protein 30 (SMP30) is assumed to behave as an anti-aging factor. Recently, we have demonstrated that deficiency of SMP30 exacerbates angiotensin II-induced cardiac hypertrophy, dysfunction and remodeling, suggesting that SMP30 may have a protective role in the heart. Thus, this study aimed to test the hypothesis that up-regulation of SMP30 inhibits cardiac adverse remodeling in response to angiotensin II.MethodsWe generated transgenic mice with cardiac-specific overexpression of SMP30 gene using α-myosin heavy chain promoter. Transgenic mice and wild-type littermate mice were subjected to continuous angiotensin II infusion (800ng/kg/min).ResultsAfter 14days, heart weight and left ventricular weight were lower in transgenic mice than in wild-type mice, although blood pressure was similarly elevated during angiotensin II infusion. Cardiac hypertrophy and diastolic dysfunction in response to angiotensin II were prevented in transgenic mice compared with wild-type mice. The degree of cardiac fibrosis by angiotensin II was lower in transgenic mice than in wild-type mice. Angiotensin II-induced generation of superoxide and subsequent cellular senescence were attenuated in transgenic mouse hearts compared with wild-type mice.ConclusionsCardiac-specific overexpression of SMP30 inhibited angiotensin II-induced cardiac adverse remodeling. SMP30 has a cardio-protective role with anti-oxidative and anti-aging effects and could be a novel therapeutic target to prevent cardiac hypertrophy and remodeling due to hypertension

A case of acute myocardial infarction during perioperative period of non-cardiac surgery in a patient with antiphospholipid syndrome and a history of coronary artery bypass surgery

AbstractA 65-year-old woman underwent coronary artery bypass surgery and was diagnosed with antiphospholipid syndrome (APS) at the same time in 1985. She was admitted to our hospital to undergo mastectomy for left breast cancer in 2012. She was put on intravenous infusion of heparin and stopped receiving both antiplatelet agents and warfarin. The operation was performed without complications, and antithrombotic therapy was restarted one day after the operation. On day 6 postoperative, she complained of sudden chest pain and on examination she was diagnosed with acute myocardial infarction. The culprit lesion was in a saphenous vein graft and coronary intervention was performed.<Learning objective: Antithrombotic therapy for patients with APS is complicated because of prolonged baseline activated partial thromboplastin time (aPTT). An effective perioperative antithrombotic therapy for APS patients who have a history of coronary artery disease and have undergone non-cardiac surgery has not yet been established. A safe strategy for such a therapy should therefore be discussed.

Diacylglycerol kinase ζ inhibits myocardial atrophy and restores cardiac dysfunction in streptozotocin-induced diabetes mellitus

<p>Abstract</p> <p>Background</p> <p>Activation of the diacylglycerol (DAG)-protein kinase C (PKC) pathway has been implicated in the pathogenesis of a number of diabetic complications. Diacylglycerol kinase (DGK) converts DAG to phosphatidic acid and acts as an endogenous regulator of PKC activity. Akt/PKB is associated with a downstream insulin signaling, and PKCβ attenuates insulin-stimulated Akt phosphorylation.</p> <p>Methods and Results</p> <p>We examined transgenic mice with cardiac-specific overexpression of DGKζ (DGKζ-TG) compared to wild type (WT) mice in streptozotocin-induced (STZ, 150 mg/kg) diabetic and nondiabetic conditions. After 8 weeks, decreases in heart weight and heart weight/body weight ratio in diabetic WT mice were inhibited in DGKζ-TG mice. Echocardiography at 8 weeks after STZ-injection demonstrated that decreases in left ventricular end-diastolic diameter and fractional shortening observed in WT mice were attenuated in DGKζ-TG mice. Thinning of the interventricular septum and the posterior wall in diabetic WT hearts were blocked in DGKζ-TG mice. Reduction of transverse diameter of cardiomyocytes isolated from the left ventricle in diabetic WT mice was attenuated in DGKζ-TG mice. Cardiac fibrosis was much less in diabetic DGKζ-TG than in diabetic WT mice. Western blots showed translocation of PKCβ and δ isoforms to membrane fraction and decreased Akt/PKB phosphorylation in diabetic WT mouse hearts. However in diabetic DGKζ-TG mice, neither translocation of PKC nor changes Akt/PKB phosphorylation was observed.</p> <p>Conclusion</p> <p>DGKζ modulates intracellular signaling and improves the course of diabetic cardiomyopathy. These data may suggest that DGKζ is a new therapeutic target to prevent or reverse diabetic cardiomyopathy.</p

Cardio-protective effects of pentraxin 3 produced from bone marrow-derived cells against ischemia/reperfusion injury

AbstractBackgroundInflammation is one of major mechanisms contributing to the pathogenesis of myocardial ischemia/reperfusion (I/R) injury. Pentraxin 3 (PTX3), produced in response to inflammatory signals, acts as a humoral arm of the innate immunity. Here we investigated the role of PTX3 produced from bone marrow-derived cells in myocardial I/R injury using PTX3-deficient (PTX3KO) mice.Methods and resultsPTX3KO mice and wild-type littermate (WT) mice were lethally irradiated and injected with bone marrow (BM) cells, generating four types of mice (WTWT-BM, WTPTX3KO-BM, PTX3KOWT-BM and PTX3KOPTX3KO-BM). Six weeks after BM transplantation, the myocardial I/R procedure (45min of left descending coronary artery ligation followed by 48h of reperfusion) was performed. Infarct size was greater in WT and PTX3KO mice with BM from PTX3KO donor (WTPTX3KO-BM and PTX3KOPTX3KO-BM) compared with WT and PTX3KO mice with BM from WT donor (WTWT-BM and PTX3KOWT-BM). Localization of PTX3 was observed in neutrophils and macrophages in WT and PTX3KO mice with BM from WT donor (WTWT-BM and PTX3KOWT-BM), while only in endothelial cells in WT mice with BM from PTX3KO donor (WTPTX3KO-BM). Infiltration of neutrophils and generation of reactive oxygen species (ROS) at ischemic border zones were greater in PTX3KO mice with BM from PTX3KO donor (PTX3KOPTX3KO-BM) than PTX3KO mice with BM from WT donor (PTX3KOWT-BM). Plasma levels and cardiac expressions of interleukin-6 were higher in PTX3KO mice with BM from PTX3KO donor (PTX3KOPTX3KO-BM) than PTX3KO mice with BM from WT donor (PTX3KOWT-BM). However, no significant differences in infarct size, infiltration of neutrophils, generation of ROS and plasma and cardiac levels of interleukin-6 were observed between WT and PTX3KO mice with BM from WT donor and between WT and PTX3KO mice with BM from PTX3KO donor. These results indicated that the lack of PTX3 produced from BM-derived cells, and not from cardiac resident cells, exacerbated myocardial injury after I/R.ConclusionPTX3 produced from bone marrow-derived cells plays a crucial role in cardiac protection against myocardial I/R injury by attenuating infiltration of neutrophils, generation of ROS and inflammatory cytokine

A new method for maturity-dependent fractionation of neutrophil progenitors applicable for the study of myelodysplastic syndromes

We applied our new method, maturity-dependent fractionation of bone marrow-derived neutrophil progenitors, to a study of gene expression profiles during granulopoiesis in myelodysplastic syndromes. CD34(+) cells with low density [F1], CD11b(-)/CD16(-) [F2], CD11b(+)/CD16(-) [F3] and CD11b(+)/CD16(low) [F4] with intermediate density, CD11b(+)/CD16(int) [F5] and CD11b(+)/CD16(high) [F6] with high density were isolated from six patients. Although AML1 and C/EBP-ϵ mRNA peaked at F1 and F4, respectively, in healthy individuals, C/EBP-ϵ was maximized at F2/F3 in all patients, two of whom showed simultaneous peaks of AML1 at F2. Thus, this fractionation is useful to detect mistimed induction of granulopoiesis-regulating genes in myelodysplastic syndromes