ABSTRACT
Previously we have demonstrated that maternal high fat diet (HF) during pregnancy increase cardiovascular risk in the offspring, and pharmacological intervention using statins in late pregnancy reduced these risk factors. However the effects of maternal HF-feeding and statin treatment during pregnancy on development of heart remain unknown. Hence we measured expression of genes involved in cell cycle progression (cyclin G1), ventricular remodelling brain natriuretic peptide (BNP), and environmental stress response small proline-rich protein 1A (SPRR 1A) in the offspring left ventricle (LV) from dams on HF with or without statin treatment. Female C57 mice were fed a HF diet (45% kcal fat) 4 weeks prior to conception, during pregnancy and lactation. From the second half of the pregnancy and throughout lactation, half of the pregnant females on HF diet were given a water-soluble statin (Pravastatin) in their drinking water (HF + S). At weaning offspring were fed HF diet to adulthood (generating dam/offspring dietary groups HF/HF and HF + S/HF). These groups were compared with offspring from dams fed standard chow (C 21% kcal fat) and fed C diet from weaning (C/C). LV mRNA levels for cyclin G1, BNP and SPRR 1A were measured by RT-PCR. Heart weights and BP in HF/HF offspring were higher versus C/C group. Maternal Pravastatin treatment reduced BP and heart weights in HF + S/HF female offspring to levels found in C/C group. LV cyclin G1 mRNA levels were lower in HF/HF versus both C/C and HF + S/HF offspring. BNP mRNA levels were elevated in HF/HF females but lower in males versus C/C. BNP gene expression in HF + S/HF offspring was similar to HF/HF. SPRR 1A mRNA levels were similar in all treatment groups. Statins given to HF-fed pregnant dams reduced cardiovascular risk in adult offspring, and this is accompanied by changes in expression of genes involved in adaptive remodelling in the offspring LV and that there is a gender difference.
Subject(s)
Diet, High-Fat , Gene Expression Regulation, Developmental/physiology , Heart/embryology , Sex Characteristics , Analysis of Variance , Animals , Blood Pressure/drug effects , Cornified Envelope Proline-Rich Proteins/metabolism , Cyclin G1/metabolism , DNA Primers/genetics , Female , Heart Ventricles/metabolism , Male , Maternal Exposure , Mice , Mice, Inbred C57BL , Natriuretic Peptide, Brain/metabolism , Organ Size/drug effects , Pravastatin/administration & dosage , Pravastatin/pharmacology , Pregnancy , Real-Time Polymerase Chain Reaction , Reverse Transcriptase Polymerase Chain ReactionABSTRACT
OBJECTIVE: Separation from cardiopulmonary bypass (CPB) requires multiple preparatory steps, during which mistakes, omissions, and human errors may occur. Checklists have been used extensively in aviation to improve performance of complex, multistep tasks. The aim of this study was to (1) develop a checklist using a modified Delphi process to identify essential steps necessary to prepare for separation from CPB, and (2) compare the frequency of completed items with and without the use of a checklist in simulation. It was hypothesized that the use of a checklist would reduce the number of omissions. DESIGN: High-fidelity simulation study. SETTING: University-affiliated tertiary care facility. PARTICIPANTS: Seven cardiac anesthesiologists created a checklist using a modified Delphi process. Ten residents participated in 4 scenarios separating from CPB in simulation. INTERVENTIONS: Each scenario was performed first without a checklist and then again with a checklist. An observer graded participants' performance. MEASUREMENTS AND MAIN RESULTS: A pre-separation checklist containing 9 tasks was created using the Delphi process. Without using this checklist, 4 tasks were completed in at least 75% of scenarios, and 8 tasks were completed at least 75% of the time when using the checklist. There was a significant improvement in completion of 5 of the 9 items (p< 0.01). CONCLUSIONS: A modified Delphi process can be used to create a checklist of steps in preparing to separate from CPB. Using this checklist during simulation resulted in increased frequency of completing designated tasks in comparison to relying on memory alone. Checklists may reduce omission errors during complex periods of anesthesiologists' perioperative workflow.
Subject(s)
Anesthesiology/education , Cardiopulmonary Bypass/methods , Checklist/methods , Clinical Competence/statistics & numerical data , Internship and Residency/standards , Medical Errors/prevention & control , Adult , Anesthesiology/standards , Cardiopulmonary Bypass/standards , Checklist/statistics & numerical data , Female , Humans , Internship and Residency/statistics & numerical data , Male , Patient SimulationABSTRACT
Cardiac fibromas are rare intracardiac neoplasms but represent the most common resectable tumours of childhood. They can remain asymptomatic for extended periods of time but a pertinent and unpredictable risk of sudden cardiac death and fatal ventricular arrhythmia always exists even in asymptomatic patients. We report a case of an asymptomatic two month-old with cardiac fibroma who presented with a ventricular tachycardia (VT) arrest. Here, we discuss management of cardiac fibroma in the context of occurrence of sudden VT.
Subject(s)
Fibroma/complications , Fibroma/physiopathology , Heart Neoplasms/complications , Heart Neoplasms/physiopathology , Tachycardia, Ventricular/complications , Tachycardia, Ventricular/physiopathology , Fatal Outcome , Fibroma/therapy , Heart Neoplasms/therapy , Humans , Infant , Male , Tachycardia, Ventricular/therapyABSTRACT
Severe acute respiratory distress syndrome (ARDS) in children carries a high morbidity and mortality. High frequency ventilation and extracorporeal membrane oxygenation (ECMO) are used as rescue modes of support in difficult situations. Malignancy may be considered to be a relative contraindication to ECMO support. We report a case where the decision was made to support the patient with ECMO for fulminant Epstein-Barr (EBV) infection while investigations were being done to exclude an underlying malignancy.
Subject(s)
Epstein-Barr Virus Infections/drug therapy , Extracorporeal Membrane Oxygenation , Severe Acute Respiratory Syndrome/therapy , Severe Acute Respiratory Syndrome/virology , Antibodies, Monoclonal, Murine-Derived/therapeutic use , Antiviral Agents/therapeutic use , Child, Preschool , Epstein-Barr Virus Infections/complications , Herpesvirus 4, Human , High-Frequency Ventilation , Humans , Male , RituximabABSTRACT
Tumor necrosis factor-alpha (TNF-alpha) is a potent immunomediator and proinflammatory cytokine that has been implicated in the pathogenesis of a large number of human diseases. The location of its gene within major histocompatibility complex and biological activities has raised the possibility that polymorphisms within this locus may contribute to the pathogenesis of wide range of autoimmune and infectious diseases. For example, a bi-allelic single nucleotide substitution of G (TNFA1 allele) with A (TNFA2 allele) polymorphism at -308 nucleotides upstream from the transcription initiation site in the TNF-alpha promoter is associated with elevated TNF-alpha levels and disease susceptibilities. However, it is still unclear whether TNF-alpha -308 polymorphism plays a part in the disease process, in particular whether it could affect transcription factor binding and in turn influence TNF-alpha transcription and synthesis. Several studies have suggested that TNFA2 allele is significantly linked with the high TNF-alpha-producing autoimmune MHC haplotype HLA-A1, B8, DR3, with elevated serum TNF-alpha levels and a more severe outcome in diseases. This review discusses the genetics of the TNF-alpha -308 polymorphism in selected major diseases and evaluates its common role in health and disease.
Subject(s)
Disease/genetics , Genetic Predisposition to Disease , Polymorphism, Genetic , Promoter Regions, Genetic , Tumor Necrosis Factor-alpha/genetics , Cytokines/metabolism , Genotype , Humans , Inflammation/immunology , Nutrigenomics , Transcriptional Activation , Tumor Necrosis Factor-alpha/metabolismABSTRACT
In rodents, adverse prenatal nutrition, such as a maternal diet rich in fat during pregnancy, enhances susceptibility of the offspring to hypertension, type 2 diabetes and other features of the human metabolic syndrome in adulthood. However, previous experimental studies were confined to short-term modifications of the maternal diet during pregnancy and/or lactation periods, a situation uncommon in humans. Moreover in humans, the offspring may also consume a high-fat diet, which may take them beyond the range to which their development has adapted them to respond healthily. We examined in C57 mice the effects on offspring of feeding their mothers a high-fat (HF) or standard chow (C) diet from weaning through pregnancy and lactation, and whether there are additive phenotypic effects of feeding the offspring an HF diet from weaning to adulthood (dam-offspring dietary group HF-HF). This group was compared with offspring from HF-fed dams fed a C diet from weaning to adulthood (HF-C) and offspring from C-fed mothers fed the C or HF diet (C-C and HF-C, respectively). HF-HF, HF-C and C-HF adult female offspring were heavier, fatter, and had raised serum cholesterol and blood pressure compared with C-C female offspring. We observed a similar trend in male offspring except for the HF-C group which was not heavier or fatter than male C-C offspring. Histology showed lipid vacuoles within hepatocytes in the HF-HF, HF-C and C-HF but not the CC offspring. Serum C-reactive protein was elevated in female (C-HF and HF-HF) but not in male offspring. Elevated blood pressure in the HF-C and C-HF groups was attenuated in the HF-HF group in males but not in females. These findings indicate that long-term consumption of an HF diet by the mother predisposes her offspring to developing a metabolic syndrome-like phenotype in adult life, although cardiovascular effects of an HF diet are related to sex specificity in the HF-HF group.
Subject(s)
Dietary Fats/administration & dosage , Fatty Liver/etiology , Hyperlipidemias/etiology , Hypertension/etiology , Lactation/physiology , Nutritional Physiological Phenomena , Adiposity , Animals , Animals, Newborn , Body Weight , C-Reactive Protein/analysis , Cholesterol/blood , Disease Susceptibility , Fatty Liver/embryology , Female , Hyperlipidemias/embryology , Hypertension/embryology , Male , Mice , Mice, Inbred C57BL , Models, Animal , Pregnancy , Prenatal Exposure Delayed Effects , Prenatal Nutritional Physiological Phenomena , Random Allocation , WeaningABSTRACT
BACKGROUND: Left ventricular hypertrophy and myocardial remodeling occur with aortic valve disease and may lead to heart failure. Although increased oxidative stress and inflammatory factors have been implicated in heart failure, their role in the progression of valve disease remains unclear. OBJECTIVES: We investigated the role of oxidative stress and inflammatory factors in valve disease whether this relates to cell death. METHODS: Blood samples were taken from 24 patients with valve disease before surgery and the results were compared with those from blood samples from 30 control healthy subjects. Myocardial biopsies from patients with valve disease were also collected before cannulation of the right atrial appendage. NF-κB activities in atrial and mononuclear cells nuclear extracts were determined by electrophoretic mobility shift assay. RESULTS: Nuclear factor kappaB activities were significantly greater in mononuclear cells from AVD patients compared with healthy controls and the antigens were detectable in atrial tissues valve disease patients. Plasma C-reactive protein, B-natriuretic peptides, plasma tumor necrosis factor alpha and soluble tumor necrosis factor receptor 1 and 3-nitrotyrosine levels were significantly higher in valve disease patients. Inducible nitric oxide and 3-nitrotyrosine antigens and cells expressing CD45 antigens were detected within atrial tissues obtained from valve disease patients suggesting oxidative stress originated from in situ leukocytes. CONCLUSION: The findings suggest that oxidative stress originating from in situ leukocytes within the atrial myocardium may be the potential trigger for excessive transcriptional activities and apoptotic cell death within the atrial myocardium of valve disease patients. This represents a potential therapeutic target.
Subject(s)
Cell Death/physiology , Heart Defects, Congenital/physiopathology , Heart Valve Diseases/physiopathology , Myocardium/pathology , Aortic Valve/physiopathology , Bicuspid Aortic Valve Disease , Female , Humans , Male , Oxidative StressABSTRACT
One of the major conceptual advances in the understanding of the pathogenesis of heart failure has been the insight that myocardial dysfunction and heart failure may progress as the result of the sustained over-expression of nitric oxide (NO) metabolites locally and in blood modulated by inducible nitric oxide synthase (iNOS). This by virtue of their deleterious effects is sufficient to contribute to disease progression by provoking left ventricular (LV) remodeling, hypertrophy and progressive LV dysfunction. Recently, tumor necrosis factor-alpha (TNF-alpha) has also been identified in this setting of heart failure. Analogous to the situation with NO, the over-expression of TNF-alpha is sufficient to contribute to disease progression in heart failure phenotype. Although important interactions between TNF-alpha and the NO have been recognized in the cardiovascular system for over a decade, the nature and importance of the interactions between these biologically active molecules in cardiac hypertrophy has become apparent only in the recent times. Therefore, we focused on the prevailing updated evidence which suggests that there is a functionally significant cross-regulation between NO and TNF-alpha signaling in blood thus playing a part in cardiac hypertrophy and failure. The discussions presented here will have a bearing on the therapeutic potential via inhibitors of these pathways in reducing cardiomyocyte hypertrophy and the LV dysfunction.
Subject(s)
Cyclic GMP/metabolism , Heart Failure/physiopathology , Nitric Oxide/metabolism , Tumor Necrosis Factor-alpha/metabolism , Animals , Cyclic GMP/blood , Disease Progression , Heart Failure/blood , Humans , Nitric Oxide/blood , Tumor Necrosis Factor-alpha/blood , Up-RegulationABSTRACT
T cells participate in combating infection and critically determine the outcomes in any given disease process. Impaired immune response occurs in a number disease processes such as in cancer and atherosclerosis although the underlying mechanisms are still not fully understood. This article gives an up-to-date review of T cells development and functional adaptation to pathophysiological stimuli and participation in the cardiovascular disease process. In addition, we have discussed the signaling pathways controlled by the microenvironment that determine T cells function and resultant type of immune response. We have also discussed in detail how oxidative stress is a key component of the micro environmental interaction.
Subject(s)
Atherosclerosis/immunology , Immunologic Memory , Oxidative Stress/immunology , Th1 Cells/immunology , Th2 Cells/immunology , Animals , Cell Differentiation/immunology , Humans , Lymphocyte Activation , MiceABSTRACT
BACKGROUND: Atrial fibrillation (AF) is the most common arrhythmia associated with coronary artery surgery and is an important factor contributing to postoperative morbidity and mortality. Recently, there is growing evidence that dysregulation of the oxidant-antioxidant balance, inflammatory factors and discordant alteration of energy metabolites may play a significant role in its pathogenesis. DESIGN: We evaluated the link between postoperative atrial fibrillation with inflammatory factors and oxidative stress. METHODS: We searched all databases in Medline, Pubmed, ISI, the Cochrane database, and Embase. We identified more than 100 trials, multiple metaanalyses, and three sets of practice guidelines for the prevention of PAF in cardiac surgery. RESULTS: Mechanisms of postoperative AF are likely to be multifactorial and are influenced by preoperative, intraoperative and postoperative factors including a genetic basis. Electrical remodelling is thought to be related to the generation of reactive oxidant species and inflammatory factors during the ischemia-reperfusion phase of cardiac surgery. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase was found to be the primary source of superoxide within the human atrial myocardium (in patients in sinus rhythm and in those with AF) and linked with paroxysmal and chronic AF. Reactive oxidant species cause lipid peroxidation, breakdown of cell membrane, decreased mitochondrial function, calcium overload and apoptosis. This affect was shown to be reversed by exogenous nitric oxide/donors (sodium nitroprusside). Inflammatory factors such as the rise in white blood cell count, C-reactive proteins were implicated in the pathogenesis of AF. In contrast, new evidence identifies statins as having both antioxidant and anti-inflammatory properties and that their use reduces the incidence of postoperative AF (57% in the control vs. 35% in the atorvastatin group). Other antiinflammatory strategies include steroids with one study showing postoperative AF occurred in 21% in the steroid group compared with 51% in the placebo group although their use resulted in an increase in other complications. The mainstay of therapy however, remains to be beta-blockers alone which impart a modest influence on overall rates of AF with a reduction from 33.7 to 16.9% (OR: 0.37, 95% CI: 0.29-0.48). Angiotensin converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers has been shown in one study to reduce the risk of developing new-onset AF by nearly 50%, although this has not been adequately evaluated in cardiac surgery. CONCLUSION: Inflammatory factors and oxidative stress play a major role in the pathogenesis of postoperative AF. This review provides an analysis of current evidence in support of efforts directed at antiinflammatory and antioxidant agents as interventions.
Subject(s)
Atrial Fibrillation/etiology , Cardiac Surgical Procedures/adverse effects , Coronary Artery Disease/surgery , Myocardium/metabolism , Oxidative Stress , Reactive Oxygen Species/metabolism , Anti-Inflammatory Agents/therapeutic use , Antioxidants/metabolism , Antioxidants/therapeutic use , Atrial Fibrillation/genetics , Atrial Fibrillation/metabolism , Atrial Fibrillation/pathology , Atrial Fibrillation/prevention & control , Cardiovascular Agents/therapeutic use , Energy Metabolism , Genetic Predisposition to Disease , Humans , Inflammation Mediators/metabolism , Myocardium/pathology , Treatment OutcomeABSTRACT
The study compared cardiovascular risks factors, morbidity and in-hospital mortality following coronary artery bypass graft (CABG) surgery in Australian patients of different ethnic backgrounds including Aboriginal (AB), Italian (IT), Indian (IA), British Caucasians (BC), and Chinese (CH). These groups AB (n = 20), CH (n = 12), IT (n = 104), BC (n = 493), and IA (n = 16) all had first-time isolated CABG surgery at St. Vincent's Hospital, Melbourne from March 2001 to March 2007. AB patients were current or past smokers with the highest prevalence of preoperative diabetes (P = 0.001) and mostly had nonelective CABG surgery (P = 0.018). AB patients had higher incidences of postoperative respiratory failure (P = 0.001) compared with the other groups. In contrast, past history of MI (P = 0.012) was associated with IA patients. Both IA and AB groups had significantly higher acute renal failure rates requiring temporary dialysis (P = 0.025), longer ICU (P = 0.003) and hospital stays (P = 0.03) compared to BC, IT and CH groups. All groups had similar 30-day (P = 0.59) in-hospital mortality. The higher incidences of in-hospital morbidity observed in IA and AB compared to BC, IT, and CH groups suggests that ethnic lifestyle may be a strong risk factor. Larger confirmatory studies are required to verify incidents and elucidate reasons why ethnic-associated perioperative complications exist.
Subject(s)
Coronary Artery Bypass/statistics & numerical data , Coronary Disease/ethnology , Aged , Australia/epidemiology , Coronary Artery Bypass/adverse effects , Coronary Artery Bypass/mortality , Coronary Disease/mortality , Coronary Disease/surgery , Female , Hospital Mortality , Humans , Italy/ethnology , Length of Stay , Male , Middle Aged , Native Hawaiian or Other Pacific Islander/statistics & numerical data , Postoperative Complications/epidemiology , Retrospective Studies , Risk Factors , United Kingdom/ethnologyABSTRACT
PURPOSE: The aim of this study was to investigate whether the variability between individuals with coronary heart disease (CHD) is related to the prevalence of TNF-alpha gene promoter -308 variant in un-matched British Caucasian population from East Midlands. PROCEDURES: Genotypes and allele frequencies were determined using restriction fragment length polymorphism analysis of polymerase chain reaction (PCR) products. Genomic DNA prepared from peripheral blood leukocytes of patients (n=97) and healthy controls (n=95) demonstrated two alleles TNF*1 (G) and TNF*2 (A). FINDINGS: The genotype distribution in patients was GG, n=59; GA, n=36; and AA, n=2 and in controls was GG, n=41; GA, n=40; and AA, n=14 (P=0.014). The association analysis demonstrated that TNF*1 allele in patients appears to be associated with greater incidences of CHD (OR 2.15; CI, 1.36-3.39; P=0.001). CONCLUSIONS: Our results suggest that TNF*1 allele (TNF-alpha -308 GG or GA) has a high prevalence among British Caucasian population that correlates with an increased CHD risk.
Subject(s)
Coronary Disease/epidemiology , Coronary Disease/genetics , Genetic Predisposition to Disease/epidemiology , Polymorphism, Genetic , Tumor Necrosis Factor-alpha/genetics , White People/genetics , Age Distribution , Aged , Case-Control Studies , Confidence Intervals , Coronary Angiography , Coronary Disease/diagnostic imaging , Female , Gene Frequency , Humans , Incidence , Male , Middle Aged , Odds Ratio , Pilot Projects , Probability , Prognosis , Promoter Regions, Genetic , Reference Values , Risk Assessment , Sex Distribution , United Kingdom/epidemiologyABSTRACT
There is growing evidence that altered production and/or spatio-temporal distribution of reactive oxidant species and reactive nitrosative species in blood creates oxidative and/or nitrosative stresses in the failing myocardium and endothelium. This contributes to the abnormal cardiac and vascular phenotypes that characterize cardiovascular disease. These derangements at the system level can now be interpreted at the integrated cellular and molecular levels in terms of effects on signaling elements in the heart and vasculature. The end results of nitric oxide/redox disequilibrium have implications for cardiac and vascular homeostasis and may result in the development of atherosclerosis, myocardial tissue remodelling and hypertrophy. Reactive oxygen species/reactive nitrogen species generation is also attributed to the transit from hypertrophic to apoptotic phenotypes, a possible mechanism of myocardial failure. In this review, we highlight the possible roles of altered production and/or spatio-temporal distribution of reactive oxidant species and reactive nitrosative species in blood on the pathogenesis of the failing cardiovascular system.
Subject(s)
Cardiovascular Diseases/etiology , Nitric Oxide/blood , Oxidative Stress/physiology , Reactive Nitrogen Species/blood , Reactive Oxygen Species/blood , Animals , Cardiovascular System/metabolism , Humans , Models, Biological , Nitrates/metabolism , Nitric Oxide Donors/metabolism , Nitrosation , Oxidation-Reduction , Signal Transduction/genetics , Signal Transduction/physiology , Transcription Factors/metabolismABSTRACT
The enormous progress in interventional cardiology during the last 10 years has resulted in a major change in the spectrum of patients referred for coronary artery bypass grafting. Several large retrospective analyses, meta-analyses, and the randomized trials that addressed different aspects of ONCAB and OPCAB to date have compared the two surgical strategies. It is suggested that patients may achieve an excellent outcome with either type of procedure, and individuals' outcomes more likely depend on factors other than whether they underwent ONCAB or OPCAB. Nevertheless, there appear to be trends in most studies. These trends include less blood loss and need for transfusion, less myocardial enzyme release up to 24 h, less early neurocognitive dysfunction, and less renal insufficiency after OPCAB and propensity to lower costs, thereafter proving OPCAB to be safe and clinically effective. Here, we review the physiological advantages and clinical outcomes of OPCAB for myocardial revascularization and examine whether either strategy is superior and in which patients.
Subject(s)
Coronary Artery Bypass, Off-Pump/methods , Myocardial Revascularization/methods , Humans , Meta-Analysis as Topic , Randomized Controlled Trials as Topic , Retrospective Studies , Treatment OutcomeABSTRACT
OBJECTIVES: The aim of this study was to prove that one possible statin-related protective mechanism in dams and offspring fed a high-fat diet (HFD) is the reduction in cardiovascular risk and impairment of the vasculogenic element of endothelial regeneration. METHODS: To explore this, virgin C57 BL/6 mice (n = 8/group) were fed an HFD (fat: 45% kcal) or standard chow (C; fat: 21% kcal) from weaning and throughout their pregnancy and lactation. Half of the HFD group also was given the 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor pravastatin (S) through their drinking water (5 mg/kg body weight per day) to create HF+S dam group (n = 8/group). Offspring from each group were fed HFD or C diet from weaning to adulthood, generating respective dam/offspring dietary groups (C/C, HF/HF, HF+S/HF; n = 8/group). Body weight, blood pressure, and serum lipid profile were measured in female offspring at age 24 wk, and bone marrow endothelial progenitor cells (EPCs) were cultured. RESULTS: The results indicated that in the female offspring, the statin-fed (HF+S/HF) cohort had lower total and low-density lipoprotein cholesterol concentrations, were less obese and hypertensive, and had reduced C-reactive proteins (CRPs) compared with the HF/HF phenotype. The results also showed an increased bone marrow EPCs expressing colony numbers (P < 0.001) compared with the HF/HF phenotype. CONCLUSIONS: Results from the present study demonstrated that statin administration in early life to dams fed on a HFD had a significant effect on their female offspring in terms of reduction in cardiovascular risk factors. Additionally, statin administration to female offspring on an HFD during early life was associated with reduction in circulating CRPs and an increased bone marrow EPC numbers and colony-forming characteristics.
Subject(s)
Diet, High-Fat/adverse effects , Endothelial Progenitor Cells/drug effects , Hydroxymethylglutaryl-CoA Reductase Inhibitors/administration & dosage , Hypertension/prevention & control , Maternal Nutritional Physiological Phenomena , Obesity/prevention & control , Adiposity/drug effects , Animals , Blood Pressure , Body Weight , Bone Marrow , C-Reactive Protein/metabolism , Cholesterol, HDL/blood , Cholesterol, LDL/blood , Female , Hypercholesterolemia/blood , Hypertension/etiology , Mice , Mice, Inbred C57BL , Obesity/etiology , Pregnancy , Risk Factors , Triglycerides/bloodABSTRACT
BACKGROUND: Long-standing aortic stenosis (AS) causes significant progressive left ventricular dysfunction and may result in subendocardial ischaemia and conduction disorders. Though stentless bioprosthesis show better haemodynamic profiles compared with stented, yet debate exists about the differential effects of valve substitutes on the incidence of permanent pacemaker (PPM) implantation following aortic valve replacement (AVR). METHODS: 510 consecutive patients aged 65-77 years with predominant AS accepted for isolated non-emergent AVR (360 received stented and 150 stentless) were studied over three years period. A stepwise logistic regression analysis was used and statistical significance was accepted at P < 0.05. RESULTS: Mean age +/- standard deviation for the stented group was 70.43 +/- 7.2 and the stentless was 61.7 +/- 12.3. Perioperative (30-day) mortality was 1% (5 of the 510 patients). Smaller aortic prosthesis size was identified as a significant predictors of hospital mortality [univariate and multivariate analysis (P < 0.05)]. Risk factors identified for PPM by univariate analysis were: preoperative: age, left atrial enlargement (LAE), MI, left bundle branch block (LBBB), poor ejection fraction < 35% (P < 0.05), postoperative; bypass time > 100 min with x-clamp time > 70 min, concomitant aortic surgery and prosthetic valve size < or = 21 mm (P < 0.05). Multivariate analysis identified the preoperative MI (P = 0.003), poor ejection fraction < 35% (P = 0.007), LAE, (P = 0.001) and LBBB (P = 0.002), the perioperative variables; bypass time > 100 min with x-clamp time > 70 min (P < 0.001) and prosthetic valve size < or = 21 mm (P = 0.003). Test of interaction analysis identified valve type as an important predictor of PPM (P = 0.01). CONCLUSIONS: The results demonstrated that where stentless valves required longer bypass and cross clamp times, more stented valves were small (< 21 mm, P < 0.05). In précis, this suggests that prevalence of PPM seems to be dependent on the size and type of bioprosthesis used in patients undergoing isolated AVR and this incidence of PPM is twice in stentless group (18% vs. 9.1%, P = 0.01).
Subject(s)
Aortic Valve Stenosis/surgery , Aortic Valve/surgery , Bioprosthesis , Pacemaker, Artificial , Aged , Aortic Valve Stenosis/diagnostic imaging , Aortic Valve Stenosis/physiopathology , Echocardiography , Electrocardiography , Female , Hospital Mortality , Humans , Linear Models , Logistic Models , Male , Middle Aged , Risk Factors , Stents , Time Factors , Treatment OutcomeSubject(s)
Cardiac Output, Low/drug therapy , Cardiac Output, Low/therapy , Cardiac Surgical Procedures , Cardiotonic Agents/therapeutic use , Hydrazones/therapeutic use , Intra-Aortic Balloon Pumping , Pyridazines/therapeutic use , Algorithms , Cardiac Output/drug effects , Cardiac Output/physiology , Cardiotonic Agents/pharmacology , Humans , Hydrazones/pharmacology , Myocardial Stunning/complications , Preoperative Care , Pyridazines/pharmacology , Randomized Controlled Trials as Topic , Risk Assessment , SimendanABSTRACT
The enormous progress in interventional cardiology during the last 10 years has resulted in a major change in the spectrum of patients referred for coronary bypass surgery. These patients are older and sicker and frequently have had previous percutaneous coronary interventions. Consequently, cardiac surgery is responding by adding new surgical techniques: off-pump open-chest coronary bypass surgery (OPCAB), minithoracotomy bypass surgery, videothoracoscopic (robotic) procedures, etc. Several registries published to date have proved OPCAB to be safe and clinically effective. Randomized studies and meta-analysis research in this field provide scientific support and suggest that myocardial, renal, and neurological functions, amongst others, are better preserved by OPCAB than by classic techniques that use a cardiopulmonary bypass pump (CPB). Moreover, avoidance of CPB yields significantly reduced oxidative stress and systemic inflammatory response. This results in higher safety for ischemic heart disease patients undergoing revascularization, thus offsetting the propensity to lower costs. The present review examines the physiological advantages and clinical outcomes of this simple mode of myocardial revascularisation and evaluates the wider implications arising from its evolution.
Subject(s)
Clinical Trials as Topic , Coronary Artery Bypass, Off-Pump/methods , Coronary Artery Bypass, Off-Pump/trends , Coronary Artery Disease/surgery , Practice Patterns, Physicians'/trends , Forecasting , Humans , Practice Guidelines as Topic , Treatment OutcomeABSTRACT
BACKGROUND AND METHODS: In our earlier report, we suggested the Bonanno catheter (a 14-gauge suprapubic catheter) as a less traumatic but equally effective alternative for drainage of a variety of fluid collections, including pleural effusion. This study aims to evaluate the efficacy of the Bonanno catheter compared with closed-tube thoracostomy in draining pleural effusion in 38 patients following routine cardiac surgery between 2003 and 2004. Twenty patients were managed using the Bonanno catheter and 18 were treated with standard tube thoracostomy. Data were collected retrospectively and statistical analysis was performed using the SPSS software. P < .05 was considered significant. RESULTS: There were 20 (53%) male and 18 (47%) female patients with a mean age of 63.5 years (range, 31-83 years). Significant differences were observed with regards to the amount of lignocaine administered locally, intra-procedure pain score, post-procedure pain score after 15 minutes, and amount of analgesia used on a regular basis (P < .05 in each case). Statistically, significant differences were also noted during 2 to 3 weeks follow-up between the 2 groups with regards to pain score. In the the tube thoracostomy group, 22.2% developed infection of the procedure site, requiring antibiotic treatment, whereas no infection was reported in the Bonanno group (P < .001). CONCLUSION: This study provided evidence that smallbore drains such as the Bonanno catheter are safe and better tolerated than standard chest drains. This is consistent with the British Thoracic Society guidelines that strongly recommend small-bore drains for the drainage of pleural effusions as they are more comfortable than larger-bore tubes.
Subject(s)
Catheterization, Peripheral/instrumentation , Catheterization, Peripheral/methods , Chest Tubes , Pleural Effusion/therapy , Thoracostomy/instrumentation , Thoracostomy/methods , Adult , Aged , Aged, 80 and over , Catheterization, Peripheral/adverse effects , Equipment Failure Analysis , Female , Humans , Male , Middle Aged , Suction/adverse effects , Suction/instrumentation , Suction/methods , Thoracostomy/adverse effects , Treatment OutcomeABSTRACT
The ability to preoperatively identify patients who may require permanent pacemaker implantation is rather poorly understood. The aim of this study is to determine the current incidence of permanent pacing after valve surgery and to determine which factors place the heart valve patient at risk of requiring permanent pacemaker implantation. We audited the records of 2,392 consecutive adult patients who underwent cardiac valve surgical procedures by the same surgical team from 25 April 1998 through 31 March 2003. Of these, 118 patients (group A) required the postoperative implantation of permanent pacemakers during the same hospitalization; they were compared with 1,959 heart valve patients (group B) who did not require pacemaker placement. Multivariate logistic regression analysis showed that reoperations (odds ratio [OR], 8.23; P <0.001), longer cumulative cross-clamp times (OR, 5.9; P <0.001), multiple-valve surgical procedures (OR, 3.46; P <0.05), and absence of preoperative sinus rhythm (OR 2.52; P <0.001) were independent predictors of the need for permanent pacemaker implantation after valve surgery. These results suggest that patients who display these risk factors for arrhythmias that require permanent pacemaker implantation receive closer observation and advance counseling about the likelihood of such implantation.