78 research outputs found

    Number of Yellow Plaques Detected in a Coronary Artery Is Associated With Future Risk of Acute Coronary Syndrome Detection of Vulnerable Patients by Angioscopy

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    ObjectivesWe sought to test whether the risk of acute coronary syndrome (ACS) can be estimated by angioscopy.BackgroundDisruption of vulnerable plaque and subsequent thrombosis is regarded as a major mechanism of ACS. Although yellow plaques are supposedly vulnerable, the association between angioscopically determined extent of coronary atherosclerosis and risk of ACS events has not been reported.MethodsPatients (n = 552) who received catheterization and angioscopic examination for the diagnosis of coronary artery diseases were prospectively included and followed up for new onset of ACS events. Yellow color intensities of all detected yellow plaques were graded as 1, 2, or 3 according to the standard colors. Number of yellow plaques (NYP) in a coronary artery and maximum color grade of detected yellow plaques (maxYP) were determined. Association between the incidence of ACS events and angioscopic findings were analyzed.ResultsFollow-up interval was 57.3 ± 22.1 months. Acute coronary syndrome events were detected in 39 patients (7.1%). Although maxYP was not statistically different (2.0 ± 0.7 vs. 1.8 ± 0.9; p = 0.18), NYP was higher in the patients with an ACS event than those without the event (3.1 ± 1.8 vs. 2.2 ± 1.5; p = 0.008). Patients with NYP ≥2 and those with NYP ≥5 had 2.2- and 3.8-fold higher event rates, respectively, than those with NYP 0 or 1 (9.0% and 15.6%, respectively, vs. 4.1%; p = 0.02). Multivariate logistic regression analysis revealed NYP and multivessel disease as the independent risk factors of ACS events.ConclusionsPatients with multiple yellow plaques per vessel have a higher risk of suffering ACS events than those with NYP 0 or 1. Angioscopy would be useful to detect vulnerable patients

    Corrigendum: Use of the index of pulmonary vascular disease for predicting longterm outcome of pulmonary arterial hypertension associated with congenital heart disease

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    Use of the index of pulmonary vascular disease for predicting long-term outcome of pulmonary arterial hypertension associated with congenital heart disease

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    AimsLimited data exist on risk factors for the long-term outcome of pulmonary arterial hypertension (PAH) associated with congenital heart disease (CHD-PAH). We focused on the index of pulmonary vascular disease (IPVD), an assessment system for pulmonary artery pathology specimens. The IPVD classifies pulmonary vascular lesions into four categories based on severity: (1) no intimal thickening, (2) cellular thickening of the intima, (3) fibrous thickening of the intima, and (4) destruction of the tunica media, with the overall grade expressed as an additive mean of these scores. This study aimed to investigate the relationship between IPVD and the long-term outcome of CHD-PAH.MethodsThis retrospective study examined lung pathology images of 764 patients with CHD-PAH aged <20 years whose lung specimens were submitted to the Japanese Research Institute of Pulmonary Vasculature for pulmonary pathological review between 2001 and 2020. Clinical information was collected retrospectively by each attending physician. The primary endpoint was cardiovascular death.ResultsThe 5-year, 10-year, 15-year, and 20-year cardiovascular death-free survival rates for all patients were 92.0%, 90.4%, 87.3%, and 86.1%, respectively. The group with an IPVD of ≥2.0 had significantly poorer survival than the group with an IPVD <2.0 (P = .037). The Cox proportional hazards model adjusted for the presence of congenital anomaly syndromes associated with pulmonary hypertension, and age at lung biopsy showed similar results (hazard ratio 4.46; 95% confidence interval: 1.45–13.73; P = .009).ConclusionsThe IPVD scoring system is useful for predicting the long-term outcome of CHD-PAH. For patients with an IPVD of ≥2.0, treatment strategies, including choosing palliative procedures such as pulmonary artery banding to restrict pulmonary blood flow and postponement of intracardiac repair, should be more carefully considered

    Complement-Related Proteins and Their Measurements: The Current Status of Clinical Investigation

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    Complement has been considered to be a factor that protects the host against invading microorganisms during infection. However, in recent years, complement-related protein deficiency has been found to be involved in the onset of various diseases, such as autoimmune and inflammatory diseases. In Japan, C3, C4, and CH50 tests were generally performed only when a complement system examination was necessary and there were not enough examinations for other complement factors. Since the complement system has a very complicated activation pathway, at present, it is not well known which molecule must be measured to understand the pathological condition or pathogenesis in complement-related diseases. Furthermore, since the frequency of complement factor gene alleles also differs depending on race, data from foreign countries cannot be directly applied to Japanese populations. Under these circumstances, the Japanese Association for Complement Research (JACR) has prepared approximately 20 items for complement-related examinations, including the 5 categories of functional analysis, complement factors, complement regulators, activation products, and autoantibodies

    Changes in Mannose-Binding Lectin and Collectin Kidney 1 Levels in Sepsis Patients With and Without Disseminated Intravascular Coagulation

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    In sepsis, systemic coagulation activation frequently causes disseminated intravascular coagulation (DIC), and the uncontrolled activation of the complement system can induce multiple organ dysfunction and poor prognosis. This study aimed to examine the association of DIC with levels of collectin kidney 1 (CL-K1), a novel collectin of the complement system, and mannose-binding lectin (MBL), a classical-type collectin in patients with sepsis. We collected blood samples prospectively from adult patients with sepsis admitted to the intensive care unit (ICU) from day 1 (admission) to day 5. The CL-K1 and MBL levels were measured by enzyme-linked immunosorbent assay, and DIC was diagnosed by using a scoring algorithm. The correlation of CL-K1 and MBL levels with other coagulation markers was analyzed. There were 37 patients with DIC (DIC group) and 15 without DIC (non-DIC group). Compared to the non-DIC group, the DIC group had more severe conditions and higher mortality. During the 5 days after ICU admission, plasma CL-K1 levels were similar between the groups, but plasma MBL levels were significantly lower in the DIC group. Plasma CL-K1 levels were weakly correlated with prothrombin time, activated partial thromboplastin time, and antithrombin levels; plasma MBL levels were weakly correlated with fibrin/fibrinogen degradation product levels and DIC score. In conclusion, during the first 5 days of ICU admission, plasma CL-K1 levels were similar between the DIC and non-DIC groups. However, plasma MBL levels were lower in the DIC group compared to the non-DIC group, and the significance of this difference grew gradually over time
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