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Cardiovascular Diseases - Top 30 Publications

Sedation vs Intubation for Patients With Acute Stroke Undergoing Thrombectomy-Reply.

Time to Endovascular Thrombectomy for Acute Stroke-Reply.

Sedation vs Intubation for Patients With Acute Stroke Undergoing Thrombectomy.

Sedation vs Intubation for Patients With Acute Stroke Undergoing Thrombectomy.

Time to Endovascular Thrombectomy for Acute Stroke.

Medical and Interventional Therapy for Spontaneous Vertebral Artery Dissection in the Craniocervical Segment.

Background and Purpose. Spontaneous vertebral artery dissection (SVAD) is an important reason for posterior-circulation-ischemic stroke in the young and middle-aged population. Although some previous reports reveal a favorable outcome with conservative therapy, it is still controversial in the treatment of SVAD in some specific patients. Herein, we present our 10 years of clinical experience for SVAD at this location. Material and Methods. 20 patients with 20 SVADs in V2 and V3 segments were retrospectively studied. Clinical manifestations and imageology materials were collected and analyzed. All the patients underwent anticoagulation except for one patient because of contraindication. 14 patients underwent Wingspan stents implantation with general anesthesia. Results. In our sample, ischemia (infarction or transient ischemic attack, TIA) was found in all the patients. Angiographic stenosis and dissection aneurysm were the most common findings in the segments mentioned above. 19 of the patients (95%) got the excellent imageological and clinical outcomes. Conclusions. According to our experience in this group, although anticoagulation is effective in vertebral artery dissection, interventional therapy for SVADs in V2 and/or V3 segments is preferred in some specific patients. Stent with higher radial supporting and flexibility, such as Wingspan stent, is suggested.

Fluid-Structure Interaction in Abdominal Aortic Aneurysm: Effect of Modeling Techniques.

In this work, the impact of modeling techniques on predicting the mechanical behaviors of abdominal aortic aneurysm (AAA) is systematically investigated. The fluid-structure interaction (FSI) model for simultaneously capturing the transient interaction between blood flow dynamics and wall mechanics was compared with its simplified techniques, that is, computational fluid dynamics (CFD) or computational solid stress (CSS) model. Results demonstrated that CFD exhibited relatively smaller vortexes and tends to overestimate the fluid wall shear stress, compared to FSI. On the contrary, the minimal differences in wall stresses and deformation were observed between FSI and CSS models. Furthermore, it was found that the accuracy of CSS prediction depends on the applied pressure profile for the aneurysm sac. A large pressure drop across AAA usually led to the underestimation of wall stresses and thus the AAA rupture. Moreover, the assumed isotropic AAA wall properties, compared to the anisotropic one, will aggravate the difference between the simplified models with the FSI approach. The present work demonstrated the importance of modeling techniques on predicting the blood flow dynamics and wall mechanics of the AAA, which could guide the selection of appropriate modeling technique for significant clinical implications.

Hyperphosphatemia and hs-CRP Initiate the Coronary Artery Calcification in Peritoneal Dialysis Patients.

Background. Coronary artery calcification (CAC) contributes to high risk of cardiocerebrovascular diseases in dialysis patients. However, the risk factors for CAC initiation in peritoneal dialysis (PD) patients are not known clearly. Methods. Adult patients with baseline CaCS = 0 and who were followed up for at least 3 years or until the conversion from absent to any measurable CAC detected were included in this observational cohort study. Binary logistic regression was performed to identify the risk factors for CAC initiation in PD patients. Results. 70 patients recruited to our study were split into a noninitiation group (n = 37) and an initiation group (n = 33) according to the conversion of any measurable CAC during their follow-up or not. In univariate analysis, systolic blood pressure, serum phosphorus, fibrinogen, hs-CRP, serum creatinine, and triglycerides were positively associated with the initiation of CAC, while the high density lipoprotein and nPCR did the opposite function. Multivariate analysis revealed that hyperphosphatemia and hs-CRP were the independent risk factors for CAC initiation after adjustments. Conclusions. Hyperphosphatemia and hs-CRP were the independent risk factors for CAC initiation in PD patients. These results suggested potential clinical strategies to prevent the initiation of CAC in PD patients.

Strain-Specific Single-Nucleotide Polymorphisms in Hypertensive ISIAH Rats.

Single-nucleotide polymorphisms (SNPs) in the coding and regulatory regions of genes can affect transcription rate and translation efficiency, modify protein function, and, in some cases, cause the development of diseases. In the current study, the RNA-Seq approach has been used to discover strain-specific SNPs in ISIAH (inherited stress-induced arterial hypertension) rats, which are known as a model of stress-induced arterial hypertension. The comparison of the ISIAH SNPs with genome sequencing data available for another 42 rat strains and substrains, 11 of them known as hypertensive, showed a considerable genetic distance between the genotypes of ISIAH and all other rat strains and substrains. The study revealed 1849 novel SNPs specific for ISIAH rats and 158 SNPs present only in the genotypes of hypertensive rats. Amino acid substitutions with possible deleterious effect on protein function were detected. Several of them were found in the genes associated with hypertension. These SNPs may be considered as novel molecular targets for further studies aimed at assessing their potential in the therapy of stress-induced hypertension.

Chronic Alcohol Intoxication Is Not Accompanied by an Increase in Calpain Proteolytic Activity in Cardiac Muscle of Rats.

Enzymatic activity of Ca2+-dependent calpain proteases as well as the content and gene expression of μ-calpain (activated by micromolar calcium ion concentrations), calpastatin (inhibitor of calpains), and titin (substrate for calpains) were investigated in cardiac muscles of rats subjected to chronic alcoholization for 3 and 6 months. There was no increase in the "heart weight/body weight" parameter indicating development of heart hypertrophy in the alcoholized rats, while a decreasing trend was observed for this parameter in the rats after 6-month modeling of alcoholic cardiomyopathy, which indicated development of atrophic changes in the myocardium. Fluorometric measurements conducted using the Calpain Activity Assay Kit did not reveal any changes in total calpain activity in protein extracts of cardiac muscles of the rats alcoholized for 3 and 6 months. Western blot analysis did not show reliable changes in the contents of μ-calpain and calpastatin, and SDS-PAGE did not reveal any decrease in the titin content in the myocardium of rats after the chronic alcohol intoxication. Autolysis of μ-calpain was also not verified, which could indicate that proteolytic activity of this enzyme in myocardium of chronically alcoholized rats is not enhanced. Using Pro-Q Diamond staining, changes in phosphorylation level of titin were not detected in cardiac muscle of rats after chronic alcoholization during three and six months. A decrease in µ-calpain and calpastatin mRNA content (~1.3-fold, p ≤ 0.01 and ~1.9-fold, p ≤ 0.01, respectively) in the myocardium of rats alcoholized for 3 months and decrease in calpastatin mRNA (~1.4-fold, p ≤ 0.01) in animals alcoholized for 6 months was demonstrated using real-time PCR. These results indicate negative effect of chronic alcohol intoxication on expression of the abovementioned genes.

Multiple Myeloma: Diagnosis and Treatment.

Multiple myeloma accounts for 1.6% of all cancer cases and approximately 10% of hematologic malignancies in the United States. In 2015, an estimated 28,850 new cases of multiple myeloma were diagnosed in the United States, and the disease caused more than 11,000 deaths. Patients older than 65 years account for 85% of those diagnosed with multiple myeloma, and there is a twofold increased incidence in blacks compared with whites. Patients may present with bone pain or with symptoms that are often nonspecific, such as nausea, vomiting, malaise, weakness, recurrent infections, and weight loss. Many patients present with only laboratory abnormalities, such as anemia, renal disease, and elevated protein levels. The diagnosis of multiple myeloma requires increased numbers of immature, abnormal, or atypical plasma cells in the bone marrow; a monoclonal protein in the serum or urine; or characteristic bone lesions. The diagnostic workup in a patient with suspected multiple myeloma should include a complete blood count with differential; serum chemistries; creatinine, lactate dehydrogenase, and beta2-microglobulin tests; immunoglobulin studies; skeletal survey; and bone marrow evaluation. Initiation of chemotherapy and assessment of eligibility for autologous stem cell transplantation require referral to an oncologist. Most patients with multiple myeloma will receive thromboprophylaxis, bisphosphonate therapy, and prophylaxis against infection at some point in their treatment. Family physicians play a role in assessing these patients for infection, adverse treatment effects, and renal and thrombotic complications, and in managing issues related to pain, nutrition, and psychosocial support.

Myocardial susceptibility to ischaemia/reperfusion in obesity: a re-evaluation of the effects of age.

Reports on the effect of age and obesity on myocardial ischaemia/reperfusion (I/R) injury and ischaemic preconditioning are contradictory. The aim of this study was to re-evaluate the effects of age and diet-induced obesity (DIO) on myocardial I/R injury and preconditioning potential.

Insights for Oxidative Stress and mTOR Signaling in Myocardial Ischemia/Reperfusion Injury under Diabetes.

Diabetes mellitus (DM) displays a high morbidity. The diabetic heart is susceptible to myocardial ischemia/reperfusion (MI/R) injury. Impaired activation of prosurvival pathways, endoplasmic reticulum (ER) stress, increased basal oxidative state, and decreased antioxidant defense and autophagy may render diabetic hearts more vulnerable to MI/R injury. Oxidative stress and mTOR signaling crucially regulate cardiometabolism, affecting MI/R injury under diabetes. Producing reactive oxygen species (ROS) and reactive nitrogen species (RNS), uncoupling nitric oxide synthase (NOS), and disturbing the mitochondrial quality control may be three major mechanisms of oxidative stress. mTOR signaling presents both cardioprotective and cardiotoxic effects on the diabetic heart, which interplays with oxidative stress directly or indirectly. Antihyperglycemic agent metformin and newly found free radicals scavengers, Sirt1 and CTRP9, may serve as promising pharmacological therapeutic targets. In this review, we will focus on the role of oxidative stress and mTOR signaling in the pathophysiology of MI/R injury in diabetes and discuss potential mechanisms and their interactions in an effort to provide some evidence for cardiometabolic targeted therapies for ischemic heart disease (IHD).

Deep Venous Thrombosis and Pulmonary Embolism: Current Therapy.

Pulmonary embolism and deep venous thrombosis are the two most important manifestations of venous thromboembolism (VTE), which is the third most common life-threatening cardiovascular disease in the United States. Anticoagulation is the mainstay of VTE treatment. Most patients with deep venous thrombosis or low-risk pulmonary embolism can be treated in the outpatient setting with low-molecular-weight heparin and a vitamin K antagonist (warfarin) or direct-acting oral anticoagulants. Inpatient treatment of VTE begins with parenteral agents, preferably low-molecular-weight heparin. Unfractionated heparin is used if a patient is hemodynamically unstable or has severe renal insufficiency, high bleeding risk, hemodynamic instability, or morbid obesity. Direct-acting oral anticoagulants are an alternative; however, concerns include cost and use of reversing agents (currently available only for dabigatran, although others are in development). If warfarin, dabigatran, or edoxaban is used, low-molecular-weight or unfractionated heparin must be administered concomitantly for at least five days and, in the case of warfarin, until the international normalized ratio becomes therapeutic for 24 hours. Hemodynamically unstable patients with a low bleeding risk may benefit from thrombolytic therapy. An inferior vena cava filter is not indicated for patients treated with anticoagulation. Current guidelines recommend anticoagulation for a minimum of three months. Special situations, such as active cancer and pregnancy, require long-term use of low-molecular-weight or unfractionated heparin. Anticoagulation beyond three months should be individualized based on a risk/benefit analysis. Symptomatic distal deep venous thrombosis should be treated with anticoagulation, but asymptomatic patients may be monitored with serial imaging for two weeks and treated only if there is extension.

Acute Coronary Syndrome: Current Treatment.

Acute coronary syndrome continues to be a significant cause of morbidity and mortality in the United States. Family physicians need to identify and mitigate risk factors early, as well as recognize and respond to acute coronary syndrome events quickly in any clinical setting. Diagnosis can be made based on patient history, symptoms, electrocardiography findings, and cardiac biomarkers, which delineate between ST elevation myocardial infarction and non-ST elevation acute coronary syndrome. Rapid reperfusion with primary percutaneous coronary intervention is the goal with either clinical presentation. Coupled with appropriate medical management, percutaneous coronary intervention can improve short- and long-term outcomes following myocardial infarction. If percutaneous coronary intervention cannot be performed rapidly, patients with ST elevation myocardial infarction can be treated with fibrinolytic therapy. Fibrinolysis is not recommended in patients with non-ST elevation acute coronary syndrome; therefore, these patients should be treated with medical management if they are at low risk of coronary events or if percutaneous coronary intervention cannot be performed. Post-myocardial infarction care should be closely coordinated with the patient's cardiologist and based on a comprehensive secondary prevention strategy to prevent recurrence, morbidity, and mortality.

Cannabis arteritis: ever more important to consider.

Cannabis arteritis (CA) is a major and underdiagnosed cause of peripheral arterial disease in young patients. A 34-year-old man, daily smoker of 20 cigarettes and two cannabis cigarettes for 14 years, presented with a necrotic plaque of left hallux for 3 weeks. The Doppler ultrasound and angiography were compatible with severe Buerger's disease. Submitted to a revascularisation procedure and hypocoagulation with rivaroxaban. He had ceased smoking but maintained consumption of cannabis. Owing to the persistence of distal necrosis, amputation of the hallux was performed with good evolution. CA is a subtype of Buerger's disease. It is poorly known but increasingly prevalent and manifests in cannabis users regardless of tobacco use. The drug is considered at least a cofactor of the arteriopathy. The most effective treatment is cessation of consumption. Being cannabis one of the most consumed drugs, its mandatory to ask about its use in all young patients with arteriopathy.

Anterior condylar confluence dural arteriovenous fistula: a rare cause of hoarseness.

Hoarseness secondary to an anterior condylar confluence (ACC) dural arteriovenous fistula (DAVF) has not been previously described. We present a 58-year-old patient with a 3-week history of progressive unilateral left-sided headaches and hoarseness. Nasolaryngoscopy and CT neck showed the presence of unilateral vocal cord palsy with no identifiable cause along the expected course of the recurrent laryngeal nerve. MRI revealed an incidental finding of abnormal serpiginous vessels in the left hypoglossal canal which led to a diagnostic cerebral angiogram, confirming the presence of an ACC DAVF. The patient underwent transvenous coil embolisation with subsequent resolution of arteriovenous shunting and symptoms. Follow-up MRI at 6 months showed no recurrence and there was complete resolution of clinical symptoms.

Carotid artery dissection: a rare complication of Eagle syndrome.

Carotid artery dissection is a significant cause of ischaemic stroke in all age groups and accounts for a large percentage of strokes in young patients. Carotid dissection can be caused by trauma, underlying connective tissue disease, hypertension, mechanical injury or can be spontaneous. We present an exceedingly rare case of carotid dissection caused by an elongated styloid process, causing direct mechanical damage to the carotid artery.

Increased Risk of CHD in the Presence of rs7865618 (A allele): Tehran Lipid and Glucose Study.

Recent genome-wide association studies (GWAS) in European populations have indicated that the rs12526453 polymorphism located in phosphatase and actin regulator 1 gene (PHACTR1), mapping to chromosome 6p24 and rs7865618 polymorphism in the cyclin-dependent kinase inhibitor B antisense RNA 1 gene (CDKN2B-AS1) on 9p21.3 are associated with coronary heart disease (CHD). This study was carried out to investigate the association of these polymorphisms and CHD in an Iranian population.

All-Cause and Cardiovascular Mortality following Treatment with Metformin or Glyburide in Patients with Type 2 Diabetes Mellitus.

Both metformin and sulfonylurea (SU) drugs are among the most widely-used anti-hyperglycemic medications in patients with type 2 diabetes mellitus (T2DM). Previous studies have shown that treatment with SUs might be associated with decreased survival compared with metformin. This study aimed to evaluate all-cause and cardiovascular mortality rates between glyburide and metformin in patients diagnosed with T2DM.

Cardiovascular disease in women, is it different to men? The role of sex hormones.

Cardiovascular disease in women differs in clinical presentation, pathophysiology and prognosis from that in men. The role of estrogens and androgens may help explain such sex dimorphisms, being involved in cardiac function, endothelial function and vascular tone. In particular, the cardioprotective effect of estrogen replacement therapy is observed in postmenopausal women in a time-dependent manner, i.e. when it is initiated at their first menopausal symptoms. Postmenopausal women, beyond aged men, may also benefit from testosterone supplementation therapy. Testosterone has been found to be an effective and safe therapy for elderly women with chronic heart failure. However, further studies are needed to clarify doses and routes of administration of androgens in postmenopausal women.

Demographics and Clinical Features of Postresuscitation Comorbidities in Long-Term Survivors of Out-of-Hospital Cardiac Arrest: A National Follow-Up Study.

The outcome of patients suffering from out-of-hospital cardiac arrest (OHCA) is very poor, and postresuscitation comorbidities increase long-term mortality. This study aims to analyze new-onset postresuscitation comorbidities in patients who survived from OHCA for over one year. The Taiwan National Health Insurance (NHI) Database was used in this study. Study and comparison groups were created to analyze the risk of suffering from new-onset postresuscitation comorbidities from 2011 to 2012 (until December 31, 2013). The study group included 1,346 long-term OHCA survivors; the comparison group consisted of 4,038 matched non-OHCA patients. Demographics, patient characteristics, and risk of suffering comorbidities (using Cox proportional hazards models) were analyzed. We found that urinary tract infections (n = 225, 16.72%), pneumonia (n = 206, 15.30%), septicemia (n = 184, 13.67%), heart failure (n = 111, 8.25%) gastrointestinal hemorrhage (n = 108, 8.02%), epilepsy or recurrent seizures (n = 98, 7.28%), and chronic kidney disease (n = 62, 4.61%) were the most common comorbidities. Furthermore, OHCA survivors were at much higher risk (than comparison patients) of experiencing epilepsy or recurrent seizures (HR = 20.83; 95% CI: 12.24-35.43), septicemia (HR = 8.98; 95% CI: 6.84-11.79), pneumonia (HR = 5.82; 95% CI: 4.66-7.26), and heart failure (HR = 4.88; 95% CI: 3.65-6.53). Most importantly, most comorbidities occurred within the first half year after OHCA.

Orthostatic Intolerance and Postural Orthostatic Tachycardia Syndrome in Joint Hypermobility Syndrome/Ehlers-Danlos Syndrome, Hypermobility Type: Neurovegetative Dysregulation or Autonomic Failure?

Background. Joint hypermobility syndrome/Ehlers-Danlos syndrome, hypermobility type (JHS/EDS-HT), is a hereditary connective tissue disorder mainly characterized by generalized joint hypermobility, skin texture abnormalities, and visceral and vascular dysfunctions, also comprising symptoms of autonomic dysfunction. This study aims to further evaluate cardiovascular autonomic involvement in JHS/EDS-HT by a battery of functional tests. Methods. The response to cardiovascular reflex tests comprising deep breathing, Valsalva maneuver, 30/15 ratio, handgrip test, and head-up tilt test was studied in 35 JHS/EDS-HT adults. Heart rate and blood pressure variability was also investigated by spectral analysis in comparison to age and sex healthy matched group. Results. Valsalva ratio was normal in all patients, but 37.2% of them were not able to finish the test. At tilt, 48.6% patients showed postural orthostatic tachycardia, 31.4% orthostatic intolerance, 20% normal results. Only one patient had orthostatic hypotension. Spectral analysis showed significant higher baroreflex sensitivity values at rest compared to controls. Conclusions. This study confirms the abnormal cardiovascular autonomic profile in adults with JHS/EDS-HT and found the higher baroreflex sensitivity as a potential disease marker and clue for future research.

Cell-Based Models for Development of Antiatherosclerotic Therapies.

The leading cause of death worldwide is cardiovascular disease. Among the conditions related to the term, the most prominent one is the development of atherosclerotic plaques in the walls of arteries. The situation gets even worse with the fact that the plaque development may stay asymptomatic for a prolonged period of time. When it manifests as a cardiovascular disorder, it is already too late: the unfortunate individual is prescribed with a plethora of synthetic drugs, which are of debatable efficacy in the prevention of atherosclerotic lesions and safety. Cell models could be useful for the purpose of screening substances potentially effective against atherosclerosis progression and effective in reduction of already present plaques. In this overview, we present studies making use of in vitro and ex vivo models of atherosclerosis development that can prove valuable for clinical applications.

Phase I and Phase II Therapies for Acute Ischemic Stroke: An Update on Currently Studied Drugs in Clinical Research.

Acute ischemic stroke is a devastating cause of death and disability, consequences of which depend on the time from ischemia onset to treatment, the affected brain region, and its size. The main targets of ischemic stroke therapy aim to restore tissue perfusion in the ischemic penumbra in order to decrease the total infarct area by maintaining blood flow. Advances in research of pathological process and pathways during acute ischemia have resulted in improvement of new treatment strategies apart from restoring perfusion. Additionally, limiting the injury severity by manipulating the molecular mechanisms during ischemia has become a promising approach, especially in animal research. The purpose of this article is to review completed and ongoing phases I and II trials for the treatment of acute ischemic stroke, reviewing studies on antithrombotic, thrombolytic, neuroprotective, and antineuroinflammatory drugs that may translate into more effective treatments.

Bioinformatics Analysis Reveals MicroRNAs Regulating Biological Pathways in Exercise-Induced Cardiac Physiological Hypertrophy.

Exercise-induced physiological cardiac hypertrophy is generally considered to be a type of adaptive change after exercise training and is beneficial for cardiovascular diseases. This study aims at investigating exercise-regulated microRNAs (miRNAs) and their potential biological pathways. Here, we collected 23 miRNAs from 8 published studies. MirPath v.3 from the DIANA tools website was used to execute the analysis, and TargetScan was used to predict the target genes. Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) analyses were performed to identify potential pathways and functional annotations associated with exercise-induced physiological cardiac hypertrophy. Various miRNA targets and molecular pathways, such as Fatty acid elongation, Arrhythmogenic right ventricular cardiomyopathy (ARVC), and ECM-receptor interaction, were identified. This study could prompt the understanding of the regulatory mechanisms underlying exercise-induced physiological cardiac hypertrophy.

Aneurysms of Peripancreatic Arterial Arcades Coexisting with Celiac Trunk Stenosis or Occlusion: Single Institution Experience.

Introduction. True aneurysms of peripancreatic arterial arcades (PAAAs) are rare. Most of them coexist with celiac axis stenosis/occlusion due to median arcuate ligament (MAL) compression or atherosclerosis. The aim of this study was to evaluate the cause of celiac axis lesion and characterize the anatomy of the aneurysms. These findings may have important management implications. Material and Methods. A retrospective analysis of 15 patients with true PAAAs was performed. The diagnosis was established by contrast-enhanced CT, using a 64-MDCT scanner. We evaluated the most probable cause of celiac axis lesion. Aneurysms were characterized by their number, location, size, and morphology. Location of the aneurysms was classified either as pancreaticoduodenal arteries (PDA) or as dorsal pancreatic arteries (DPA) as they may represent different collateral pathways between superior mesenteric artery and celiac trunk. Results. A total of 32 true PAAAs were identified. Celiac trunk was occluded in 12 patients and critically narrowed in 3 patients. Celiac axis lesion was categorized as secondary to MAL compression in 14 cases and due to atherosclerosis in 1 case. The most common location of the aneurysms was inferior pancreaticoduodenal arteries. Only in 1 case aneurysms involved both PDA and DPA. Conclusions. Coexistence of PAAAs with celiac axis compression as well as involvement of either PDAs or DPAs has important therapeutic implications. The uninvolved collateral pathway may be sufficient to preserve effective circulation in celiac trunk branches in case of resection or embolization of the aneurysms. However, further studies are crucial to confirm our findings.

Preoperative Antihypertensive Medication in Relation to Postoperative Atrial Fibrillation in Patients Undergoing Cardiac Surgery: A Meta-Analysis.

Background. We undertake a systematic review and meta-analysis to evaluate the effect of preoperative hypertension and preoperative antihypertensive medication to postoperative atrial fibrillation (POAF) in patients undergoing cardiac surgery. Methods. We searched PubMed, Embase, and Cochrane Library (from inception to March 2016) for eligible studies. The outcomes were the effects of preoperative hypertension, preoperative calcium antagonists regimen, preoperative ACE inhibitors regimen, and preoperative beta blocking agents regimen with POAF. We calculated pooled risk ratios (OR) and 95% CIs using random- or fixed-effects models. Results. Twenty-five trials involving 130087 patients were listed. Meta-analysis showed that the number of preoperative hypertension patients in POAF group was significantly higher (P < 0.05), while we found that there are no significant differences between two groups in Asia patients by subgroup analysis, which is in contrast to other outcomes. Compared with the Non-POAF group, the number of patients who used calcium antagonists and ACE inhibitors preoperatively in POAF group was significantly higher (P < 0.05). And we found that there were no significant differences between two groups of preoperative beta blocking agents used (P = 0.08). Conclusions. Preoperative hypertension and preoperative antihypertensive medication in patients undergoing cardiac operations seem to be associated with higher risk of POAF.

The Impact of tagSNPs in CXCL16 Gene on the Risk of Myocardial Infarction in a Chinese Han Population.

CXCL16 has been demonstrated to be involved in the development of atherosclerosis and myocardial infarction (MI). Nonetheless, the role of the CXCL16 polymorphisms on MI pathogenesis is far to be elucidated. We herein genotyped four tagSNPs in CXCL16 gene (rs2304973, rs1050998, rs3744700, and rs8123) in 275 MI patients and 670 control subjects, aimed at probing into the impact of CXCL16 polymorphisms on individual susceptibility to MI. Multivariate logistic regression analysis showed that C allele (OR = 1.31, 95% CI = 1.03-1.66, and P = 0.029) and CC genotype (OR = 1.84, 95% CI = 1.11-3.06, and P = 0.018) of rs1050998 were associated with increased MI risk; and C allele (OR = 0.77, 95% CI = 0.60-0.98, and P = 0.036) of rs8123 exhibited decreased MI risk, while the other two tagSNPs had no significant effect. Consistently, the haplotype rs2304973T-rs1050998C-rs3744700G-rs8123A containing the C allele of rs1050998 and A allele of rs8123 exhibited elevated MI risk (OR = 1.41, 95% CI = 1.02-1.96, and P = 0.037). Further stratified analysis unveiled a more apparent association with MI risk among younger subjects (≤60 years old). Taken together, our results provided the first evidence that CXCL16 polymorphisms significantly impacted MI risk in Chinese subjects.

Usage of 3D models of tetralogy of Fallot for medical education: impact on learning congenital heart disease.

Congenital heart disease (CHD) is the most common human birth defect, and clinicians need to understand the anatomy to effectively care for patients with CHD. However, standard two-dimensional (2D) display methods do not adequately carry the critical spatial information to reflect CHD anatomy. Three-dimensional (3D) models may be useful in improving the understanding of CHD, without requiring a mastery of cardiac imaging. The study aimed to evaluate the impact of 3D models on how pediatric residents understand and learn about tetralogy of Fallot following a teaching session.