1,720,973 research outputs found
Extended myectomy for hypertrophic obstructive cardiomyopathy after failure or contraindication of septal ablation or with combined surgical procedures
No full textBackground: Surgical correction of hypertrophic obstructive cardiomyopathy in severely symptomatic patients has been proven to be effective over the long term. The introduction of catheter-based procedures restricts surgical therapy to a subset of patients not suitable for septal ablation or requiring concomitant cardiac surgery. Methods: Between 8/2001 and 8/2003, 25 patients (58 15 years) underwent extended transaortic septal myectomy with partial excision and mobilization of the papillary muscles. Concomitant surgical procedures were performed in 40% (CABG n = 9, aortic valve replacement n = 2). In 24%, prior septal ablation was ineffective. Intraventricular gradient was 80 29 mm Hg at rest and 143 +/- 35 mm Hg during exercise. Mitral regurgitation affected 72% of patients, and 88% were NYHA functional class III or IV. Results: No hospital death, no postsurgical ventricular septal defect, and no complete atrioventricular block occurred. Severe nonfatal complications occurred in 24% of patients. Intensive care was necessary for 1.8 +/- 1.7 days; total hospital stay was 11.8 +/- 3.8 days. Early follow-up was complete in 100% (15 +/- 6 months, total of 376 months) with no late deaths, no relevant mitral regurgitation, or intraventricular gradients. Functional status was markedly improved (NYHA class 1 40%, class II 56%, class III 4%). Conclusions: Early results of extended surgical myectomy and reconstruction of the subvalvular mitral apparatus in hypertrophic obstructive cardiomyopathy remain excellent with respect to mortality, Morbidity, and functional capacity even when restricting surgery to patients earlier supposed to be at high risk
Influence of eNOS gene polymorphisms (894G/T;-786C/T) on postoperative hemodynamics after cardiac surgery
No full textBackground: Differences in vascular reactivity have been associated with variable NO release due to 894G/T and - 786C/T polymorphisms of the eNOS gene. Carriers of the 894T and - 786C alleles are known to have enhanced vascular responsiveness to vasoconstrictor stimulation due to decreased NO generation. Thus, we hypothesized that eNOS gene polymorphism could influence perioperative hemodynamics and catecholamine support in patients undergoing cardiac surgery with CPB. Methods: In 105 patients undergoing elective CABG with CPB, systemic hemodynamics, cardiac index (CI), systemic and pulmonary vascular resistance indices (SVRI, PVRI) and catecholamine support were measured at baseline and I h, 4 h, 10 h and 24 h after CPB. Genotyping for the 894G/T and - 786C/T eNOS gene polymorphisms was performed by polymerase chain reaction amplification. Patients were divided according to their genotype (894G/T: GG = group 1, GT and TT = group 2; - 786C/T: TT = group 3, CT and CC = group 4). Results: Genotype distribution for 894G/T polymorphism was 41% (GG), 52.4% (GT), 6.6% (TT) and for - 786C/T polymorphism 37.1% (TT), 41.9% (CT) and 21 % (CC). Pre- and intraciperative characteristics and systemic hemodynamics did not differ between groups. Cl, SVRI and PVRI remained unaffected by genotype distribution. Statistical analysis of postoperative data revealed no difference between groups, especially for pharmacologic inotropic or vasopressor support. Also, coexistence of the 894T and - 786C alleles had no impact on perioperative variables compared to homozygous 894G and - 786T allele carriers. Conclusions: In contrast to current suggestions, the 894G/T and - 786C/T genetic polymorphisms of the eNOS gene do not influence early perioperative hemodynamics after cardiac surgery with CPB
Postoperative Hemodynamics After Cardiopulmonary Bypass in Survived Newborn Piglets
No full textCardiac function and hemodynamics are frequently decreased during the first hours after heart surgery, resulting in inotropic support for treatment and prevention of further hemodynamic deterioration. The aim of this study was analysis of hemodynamics of neonatal piglets who survived early postoperative course after cardiopulmonary bypass (CPB) and cardioplegic arrest without the use of inotropic drugs. Newborn piglets (younger than 7 days) were placed on mild hypothermic CPB (32 degrees C) for 180 minutes, including 90 minutes of cardioplegic arrest. Hemodynamics were examined after, termination of CPB and none of the animals received any inotropic support. After 6 hours, survived animals were euthanized (CPB group, n = 4). For control, neonatal piglets were examined for the same time interval after surgery without CPB (control group, n = 3). Systolic left-ventricular pressure increased after CPB, mean arterial blood pressure and amplitude of left ventricular wall thickness decreased. Compared with control group, systolic left-ventricular pressure in CPB group was higher (p < 0.05). Present data demonstrated hemodynamic depression after cardiac procedures in survived neonatal animals. Although the effects may not be solely attributed to CPB and myocardial ischemia effects may be potentiate by CPB. ASAIO journal 2009; 55:93-95
Prevention of TNF alpha-associated myocardial dysfunction resulting from cardiopulmonary bypass and cardioplegic arrest by glucocorticoid treatment
No full textObjective: Cardiac surgery on cardiopulmonary bypass (CPB) results in progressive myocardial dysfunction, despite unimpaired coronary blood flow, and is associated with increased myocardial tumor necrosis factor-alpha (TNF alpha) expression. We investigated whether anti-inflammatory treatment prevents increased TNF alpha expression and myocardial dysfunction after CPB. Methods and results: Baseline systemic hemodynamics, myocardial contractile function, aortic and coronary blood flow were measured in anesthetized pigs. Then, placebo (PLA; saline; n = 7) or methylprednisolone (MP; 30 mg/kg; n = 6) was infused intravenously and CPB was instituted. Global ischemia was induced for 10 min by aortic cross-clamping, followed by 1 h of cardioplegic cardiac arrest. After declamping and reperfusion, CPB was terminated after a total of 3 h. Measurements were repeated at 15 min, 4 h, and 8 h following termination of CPB. Systemic TNF alpha-plasma concentrations and left ventricular TNF alpha expression were analyzed. With unchanged coronary blood flow in both groups, a progressive toss of myocardial contractile function to 38 +/- 2% of baseline (p < 0.01) and cardiac index to 48 +/- 6% of baseline (p < 0.01) at 8 h after CPB in PLA was attenuated in MP (myocardial function: 72 +/- 3%, p < 0.01 vs PLA; cardiac index: 78 +/- 6%, p < 0.05 vs PLA). Systemic TNFa was increased at 8 h in PLA compared to MP (243 +/- 34 vs 90 +/- 34 pg/ml, p < 0.05). Myocardial TNF alpha was increased at 8 h after CPB compared to baseline and MP (p < 0.05). Myocardial TNF alpha immunostaining was more pronounced in PLA than in MP (p < 0.05), with TNF alpha-mRNA localization predominantly to cardiomyocytes. Conclusions: Methylprednisolone attenuates both systemic and myocardial TNF alpha increases and progressive myocardial dysfunction induced by cardiac surgery, suggesting a key rote for TNF alpha. (c) 2006 Elsevier B.V. All rights reserved
Early results of extended myectomy in hypertrophic obstructive cardiomyopathy in the era of interventional septal ablation
No full textEarly results of extended myectomy in hypertrophic obstructive cardiomyopathy in the era of interventional septal ablation
No full textProgressive loss of myocardial contractile function despite unimpaired coronary blood flow after cardiac surgery
No full textObjective Mild to moderate transient contractile dysfunction is frequently observed after cardiac surgery on cardiopulmonary bypass (CPB) but may also lead to low-cardiac-output (LCO) failure especially in patients with unstable angina, and is often referred to represent myocardial stunning. Whether time course of contractile dysfunction after cardiac surgery is similar to that of myocardial stunning was investigated in pigs. Methods After baseline measurements of systemic hemodynamics (micromanometry), myocardial contractile function (sonomicrometry), cardiac output and coronary flow (ultrasonic probe), CPB was instituted. Control animals (n=7) were weaned after 3 h from CPB. In LCO animals (n=8), global ischemia was induced for 10 min by aortic crossclamping, followed by 1 h of cardioplegic cardiac arrest. After declamping and reperfusion, CPB was terminated after a total of 3 h. Measurements were repeated at 15 min, 4 h and 8 h after CPB. Systemic TNFalpha-plasma concentrations were measured (ELISA) and left ventricular biopsies were analyzed with respect to myocardial TNFalpha (immunohistochemistry) and irreversible cellular damage (light/electron microscopy). Results Contractile function decreased in LCO (75+/-12%) and control (83+/-17%) at 15 min compared to baseline (p<0.05). Thereafter, contractile function remained unchanged in control, but progressively decreased in LCO (52+/-12% at 4 h; 36+/-5% at 8 h; p<0.05). Coronary flow remained unchanged in both groups. Cardiac output progressively decreased to 2.8+/-0.9 l/min at 8 h in the LCO group compared to baseline (5.9+/-1.1 l/min, p<0.05) and control (5.7+/-1.4 l/min, p<0.05). There was no evidence for myocardial infarction. TNFalpha-plasma concentrations and myocardial TNFalpha-staining were increased at 8 h after CPB in the LCO group compared to baseline and control (p<0.05). Conclusions The progressive pattern of myocardial dysfunction apart from ongoing ischemia after cardiac surgery suggested underlying mechanisms at least partially different from those of myocardial stunning
Effects of preoperative statin therapy on cytokines after cardiac surgery
No full textIntroduction: In addition to their lipid-lowering action, it has been demonstrated that statins can exert direct anti-inflammatory effects. We investigated the effect of preoperative statin therapy on systemic inflammatory markers and myocardial NF-kappa B inhibitor I kappa B-alpha after cardiac surgery. Methods: Thirty-six patients undergoing elective coronary artery bypass grafting with cardiopulmonary bypass (CPB) with cardioplegia were divided into two groups (statin group, n = 18; control group, n = 18). Plasma concentrations of pro-inflammatory cytokines (tumor necrosis factor alpha [TNF alpha], interleukin [IL]-6, IL-8) and anti-inflammatory IL-10 were measured before and 1, 4, 10, and 24 hours (h) after CPB. Phosphorylated I kappa B-alpha/total IKB-alpha ratio was assessed before and after CPB in right atrial biopsies. Results: Baseline and operative data did not differ between groups. Statin therapy was associated with lower preoperative low-density lipoprotein levels compared to control (73 +/- 6 vs. 92 +/- 6 mg/dL; p = 0.03). Release of IL-6 was attenuated in the statin group at 4 h (2270 +/- 599 vs. 5120 +/- 656 pg/ml; p<0.01) and 10 h (1295 +/- 445 vs. 3116 +/- 487 pg/ml; p<0.05) compared to the control group. IL-10 increased after surgery in both groups (p < 0.05), but was higher in the statin group at 1 h (66 +/- 15 vs. 26 +/- 16 pg/ mL; p < 0.01). Phosphorylated I kappa B-alpha/total I kappa B-alpha ratio before CPB did not differ between groups, but was elevated after CPB in both groups (p < 0.05), indicating enhanced degradation of I kappa B-alpha. Statin therapy had no effect on TNF alpha and IL-8. Conclusions: Preoperative statin therapy attenuates the release of pro-inflammatory IL-6 and up-regulates anti-inflammatory IL-10 after cardiac surgery with cardioplegia, but fails to inhibit phosphorylation of myocardial I kappa B-alpha
Methylprednisolone Fails to Preserve Pulmonary Surfactant and Blood-Air Barrier Integrity in a Porcine Cardiopulmonary Bypass Model
No full textBACKGROUND: Pulmonary inflammation after cardiac surgery with cardiopulmonary bypass (CPB) has been linked to respiratory dysfunction and ultrastructural injury. Whether pretreatment with methylprednisolone (MP) can preserve pulmonary surfactant and blood-air barrier, thereby improving pulmonary function, was tested in a porcine CPB-model. MATERIALS AND METHODS: After randomizing pigs to placebo (PLA; n = 5) or MP (30 mg/kg, MP; n = 5), animals were subjected to 3 h of CPB with 1 h of cardioplegic cardiac arrest. Hemodynamic data, plasma tumor necrosis factor-alpha (TNF-alpha, ELISA), and pulmonary function parameters were assessed before, 15 min after CPB, and 8 h after CPB. Lung biopsies were analyzed for TNF-alpha (Western blot) or blood-air barrier and surfactant morphology (electron microscopy, stereology). RESULTS: Systemic TNF-alpha increased and cardiac index decreased at 8 h after CPB in PLA (P < 0.05 versus pre-CPB), but not in MP (P < 0.05 versus PLA). In both groups, at 8 h after CPB, PaO(2) and PaO(2)/FiO(2) were decreased and arterio-alveolar oxygen difference and pulmonary vascular resistance were increased (P < 0.05 versus baseline). Postoperative pulmonary TNF-alpha remained unchanged in both groups, but tended to be higher in PLA (P = 0.06 versus MP). The volume fraction of inactivated intra-alveolar surfactant was increased in PLA (58 +/- 17% versus 83 +/- 6%) and MP (55 +/- 18% versus 80 +/- 17%) after CPB (P < 0.05 versus baseline for both groups). Profound blood-air barrier injury was present in both groups at 8 h as indicated by an increased blood-air barrier integrity score (PLA: 1.28 +/- 0.03 versus 1.70 +/- 0.1; MP: 1.27 +/- 0.08 versus 1.81 +/- 0.1; P < 0.05). CONCLUSION: Despite reduction of the systemic inflammatory response and pulmonary TNF-alpha generation, methylprednisolone fails to decrease pulmonary TNF-alpha and to preserve pulmonary surfactant morphology, blood-air barrier integrity, and pulmonary function after CPB
Cardiopulmonary and systemic effects of methylprednisolone in patients undergoing cardiac surgery
No full textBackground. Cardiopulmonary bypass (CPB)-related inflammatory response can be attenuated by glucocorticoid treatment, but its impact on postoperative cardiopulmonary function remains controversial. It was investigated whether the systemic and myocardial anti-inflammatory effects of glucocorticoids are associated with improved cardiopulmonary function in cardiac surgery patients. Methods. Eighty patients undergoing elective coronary artery bypass grafting were randomly assigned to receive a single shot of methylprednisolone ( 15 mg/kg) or placebo before CPB. Variables of myocardial and pulmonary function and systemic hemodynamics were measured before and 1, 4, 10, and 24 hours after CPB. Blood was sampled for measurement of proinflammatory ( tumor necrosis factor-alpha, interleukin 6, interleukin 8) and antiinflammatory ( interleukin 10) cytokines ( by enzyme-linked immunoassay), troponin T, and C-reactive protein. Phosphorylation of inhibitory kappa-B alpha and p38 mitogen-activated protein kinase was determined in right atrial biopsies before and after CPB ( phosphoprotein assay). Results. Preoperative and intraoperative characteristics of patients were not different between groups. Methylprednisolone attenuated postoperative tumor necrosis factor-alpha, interleukin 6, interleukin 8, and C-reactive protein levels while increasing interleukin 10 release. Myocardial inhibitory kappa-B alpha was preserved with methylprednisolone ( p < 0.05 versus placebo), but p38 mitogen-activated protein kinase activation occurred in both groups after CPB ( p < 0.05 versus before CPB). Methylprednisolone improved postoperative cardiac index and was associated with decreased troponin T when compared with placebo ( p < 0.05). Postoperative blood glucose, oxygen delivery index, and pulmonary shunt flow were increased in the methylprednisolone group ( p < 0.05). There was no difference in postoperative oxygenation index, ventilation time, and clinical outcome between treatment groups. Conclusions. Glucocorticoid treatment before CPB attenuates perioperative release of systemic and myocardial inflammatory mediators and improves myocardial function, suggesting potential cardioprotective effects in patients undergoing cardiac surgery
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