Effect of statins on the development of renal dysfunction

Hydroxymethylglutaryl coenzyme A reductase inhibitors (statins) decrease serum cholesterol. Dyslipidemia is believed to be associated with the development of renal dysfunction. It was postulated that statins may reduce the development of renal dysfunction. The effect of statin use on the development of renal dysfunction in 197,551 patients (Department of Veterans Affairs, Veterans Integrated Service Network 16 [VISN16] database) was examined. Of these patients, 29.5% (58,332 patients) were statin users and 70.5% (139,219 patients) were not. Development of renal dysfunction was defined as doubling of baseline creatinine or increase in serum creatinine > or =0.5 mg/dl from the first to last measurement with a minimum of 90 days in between. During 3.1 years of follow-up, 3.4% of patients developed renal dysfunction. After adjustment for demographics, diabetes mellitus, smoking, hypertension, and other medications (mainly angiotensin-converting enzyme inhibitors, calcium channel blockers, and aspirin), use of statins decreased the odds of developing renal dysfunction by 13% (odds ratio [OR] 0.87, 95% confidence interval [CI] 0.82 to 0.92, p <0.0001). The beneficial effect of statins appeared to be independent of the decrease in cholesterol. Other variables that affected the development of renal dysfunction were age (OR 1.04, 95% CI 1.03 to 1.04, p <0.0001), diabetes (OR 1.77, 95% CI 1.68 to 1.86, p <0.0001), hypertension (OR 1.11, 95% CI 1.02 to 1.2, p = 0.0153), and smoking (OR 1.12, 95% CI 1.02 to 1.24, p = 0.0244). In conclusion, statin use may retard the development of renal dysfunction. The beneficial effect of statins in preventing the development of renal dysfunction appears to be independent of their lipid-lowering effect.     

A Contemporary 20-Year Cleveland Clinic Experience of Nonbacterial Thrombotic Endocarditis: Etiology,Echocardiographic Imaging,Management, and Outcomes

BackgroundNonbacterial thrombotic endocarditis, or marantic endocarditis, is rare. Contemporary data on the etiology, echocardiographic evaluation, and management of nonbacterial thrombotic endocarditis are limited.MethodsA single-center retrospective cohort study was performed. Electronic medical records and echocardiographic records were searched for patients ages ≥18 years with a confirmed diagnosis of nonbacterial thrombotic endocarditis between January 1999 and November 2019. Demographic, echocardiographic, and management data were collected.ResultsOf 600,577 transthoracic echocardiograms (TTEs) and 89,264 transesophageal echocardiograms (TEEs), 42 patients had nonbacterial thrombotic endocarditis (mean age: 54 ± 14.5 years; 66.7% were female). The median duration of follow-up was 8.2 (interquartile range 3.3-24.4) months. Seventeen patients (40.5%) had malignancy, 33.3% had systemic lupus erythematosus, and 35.7% had antiphospholipid antibody syndrome. Stroke was the most common presentation (59.5%).TTE enabled the diagnosis in 19 cases (45.2%), compared with TEE, which identified the condition in 33 of 34 (97.1%) cases in which it was utilized. Three-dimensional echocardiography was performed in 17 TEEs. The most common valves involved were mitral (61.9%), and aortic (23.8%) valves. Thirty-two patients were managed with anticoagulation. Ten patients underwent surgery. Sixteen (38.1%) patients died, most of whom had a diagnosis of advanced malignancy.ConclusionIn a contemporary 20-year cohort, TTE and TEE played important roles in diagnosis, with superior diagnostic performance of TEE for nonbacterial thrombotic endocarditis. Mortality was high, and advanced malignancy portended a worse prognosis. Management in most cases was therapeutic anticoagulation. In select cases, surgery provided favorable outcomes.     

Thyroid tuberculosis

Thyroid tuberculosis is a rare disease. Its incidence is low even in countries where prevalence of pulmonary tuberculosis is high (0.1–0.4%). In literature, there are only a few cases which were diagnosed as thyroid tuberculosis. It can be explained by a high resistance of the thyroid gland to infectious processes. However, the prevalence of tuberculosis has increased worldwide and thyroid involvement can be a primary manifestation of the disease. The incidence of extrapulmonary tuberculosis has been showing a progressive increase in the recent years(Barnes and Weatherstone, 1979). The most frequent clinical presentation is a solitary thyroid nodule that may present as a cystic nodule. It may also present as thyroid abscess with pain, fever and other non-specific signs and symptoms. ATT results in complete cure therefore it is important to differentiate it from other form of thyroiditis. Patients are usually euthyroid, but cases of hypothyroidism and hyperthyroidism are described. For accurate diagnosis of thyroid tuberculosis, clinical and radiological features are nonspecific and histological examination is required for confirmation of diagnosis. PCR may help in diagnosis. The authors encounter 3 cases of thyroid tuberculosis in last 5 year which are described in this article. The aim of this study is to review all the cases published in literature to describe clinical presentation, appropriate diagnostic method and possible treatment options of the disease.     

Patent foramen ovale in a large population of ischemic stroke patients: diagnosis, age distribution, gender, and race

BACKGROUND: Patent foramen ovale (PFO) is a well-recognized risk factor for ischemic strokes. The true prevalence of PFO among stroke patients is still under debate. Transesophageal echocardiography (TEE) is the "gold standard" in diagnosing PFO but the physiology requires right-to-left atrial shunting. In this report, we evaluate the prevalence of PFO in a diverse group of ischemic stroke patients studied by TEE. METHODS: TEE of 1,663 ischemic stroke patients were reviewed for cardiac source of embolism, including PFO and atrial septal aneurysm (ASA). Agitated saline bubble injection was performed to look for right to left atrial shunting. Success of maneuvers to elevate right atrial pressure (RAP) was noted by looking at the atrial septal bulge. RESULTS: Among 1,435 ischemic stroke patients analyzed, the presence or absence of PFO could not be determined in 32.1% because bulging of the septum could not be demonstrated in patients with negative contrast study despite aggressive maneuvers to elevate RAP. Of the remaining 974 patients, 294 patients (30.2%) had a PFO. The mean age was 61.5 years in both groups, with a bimodal distribution of PFO and the highest prevalence occurring in < or =30-year-old group. Prevalence of PFO was similar in men (32.4%) and women (28.15%, P = 0.15); and in Caucasian (32.1%) and African American (27.7%; P = 0.15). ASA was present in 2.02% and hypermobile septum in 2.49% of the 1,435 patients. PFO was seen in 79.3% of the patients with ASA. CONCLUSION: Successful elevation of RAP cannot be achieved in a significant number of patients undergoing TEE and determination of PFO may be difficult. In our series, the true prevalence of PFO among ischemic stroke patients was 30.2% taking into account only those patients who showed no shunting despite bulging of the atrium septum into the left atrium (PFO absent group) during the contrast study. There was no gender or racial difference in the prevalence of PFO, but there was a bimodal distribution in prevalence with age.     

Epstein-Barr virus latent infection membrane protein 1 TRAF-binding site induces NIK/IKK alpha-dependent noncanonical NF-kappaB activation

Epstein-Barr virus (EBV) latent infection membrane protein 1 (LMP1)-induced NF-kappaB activation is important for infected cell survival. LMP1 activates NF-kappaB, in part, by engaging tumor necrosis factor (TNF) receptor-associated factors (TRAFs), which also mediate NF-kappaB activation from LTbetaR and CD40. LTbetaR and CD40 activation of p100/NF-kappaB2 is now known to be NIK/IKKalpha-dependent and IKKbeta/IKKgamma independent. In the experiments described here, we found that EBV LMP1 induced p100/NF-kappaB2 processing in human lymphoblasts and HEK293 cells. LMP1-induced p100 processing was NIK/IKKalpha dependent and IKKbeta/IKKgamma independent. Furthermore, the LMP1 TRAF-binding site was required for p100 processing and p52 nuclear localization, whereas the LMP1 death domain-binding site was not. Moreover, the LMP1 TRAF-binding site preferentially caused RelB nuclear accumulation. In murine embryo fibroblasts (MEFs), IKKbeta was essential for LMP1 up-regulation of macrophage inflammatory protein (MIP)-2, TNFalpha, I-TAC, ELC, MIG, and CXCR4 RNAs. Interestingly, in IKKalpha knockout MEFs, LMP1 hyperinduced MIP-2, TNFalpha, and I-TAC expression, consistent with a role for IKKalpha in down-modulating canonical IKKbeta activation or its effects. In contrast, LMP1 failed to up-regulate CXCR4 and MIG RNA in IKKalpha knockout MEFs, indicating a dependence on noncanonical IKKalpha activation. Furthermore, LMP1 up-regulation of MIP-2 RNA in MEFs was both IKKbeta- and IKKgamma-dependent, whereas LMP1 upregulation of MIG and I-TAC RNA was fully IKKgamma independent. Thus, LMP1 induces typical canonical IKKbeta/IKKgamma-dependent, atypical canonical IKKbeta-dependent/IKKgamma-independent, and noncanonical NIK/IKKalpha-dependent NF-kappaB activations; NIK/IKKalpha-dependent NF-kappaB activation is principally mediated by the LMP1 TRAF-binding site.     

Reduction of subacute stent thrombosis (SAT) using heparin-coated stents in a large-scale, real world registry

PURPOSE: This study was designed to compare the rates of subacute stent thrombosis (SAT) among patients receiving heparin-coated stents to patients receiving bare-metal stents in real world, contemporary coronary interventions. BACKGROUND: Controlled trials with heparin-coated coronary stents have shown a trend toward decreased rates of SAT. METHODS AND RESULTS: The data in this study were collected from a single, large cardiac center over a period of 9 months. All patients who underwent coronary stent implantation during this 9-month period were included in the study (1,288 patients; 1,366 procedures; 2,231 stents). All patients were treated with aspirin and clopidogrel (or ticlopidine) after stenting. Primary thrombotic outcome was defined as angiographically documented SAT and/or sudden unexplained cardiac death (SCD) within 30 days of the procedure. Follow-up data (1,264/1,276 patients) were obtained in 99% of patients. A total of 337 patients received 543 heparin-coated stents (BX Velocity Hepacoat) and 939 patients received bare-metal stents (1,688 stents). SAT was seen in 25/1,024 procedures (2.44%) in the bare-metal stent group and 1/342 procedures (0.29%) in the heparin-coated stent group. Primary thrombotic outcomes (SAT or SCD) were observed in 31/1,024 procedures (3.03%) in the bare-metal stent cohort and in 2/342 procedures (0.58%) in the heparin-coated stent group. The vast majority (96%) of the patients who had SAT within 30 days had initial stent placement for an acute coronary syndrome (p<0.0001). CONCLUSION: This large, single-center registry demonstrates a significant reduction of SAT using heparin-coated stents compared to bare-metal stents in real world coronary interventions.     

Impact of timing of presentation of acute pancreatitis to a tertiary care centre on the outcome

Background and objectives

Despite improvement in outcomes of acute pancreatitis (AP), some subgroups remain at increased risk. We studied the impact of onset-to-admission interval to a tertiary care centre on outcomes in AP.