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Attilio Maseri

Publications and source records attributed to Attilio Maseri.

At least 55 records · Page 3Linked to original sources
PubMed2003

Combined role of the Lewis antigenic system, Chlamydia pneumoniae, and C-reactive protein in unstable angina.

OBJECTIVES: The goal of this study was to assess the prognostic role of the Lewis antigenic system, Chlamydia pneumoniae (CP) seropositivity (CP+), and C-reactive protein (CRP) levels in unstable angina (UA). BACKGROUND: The role of CP infection in acute coronary syndromes is contradictory. The Lewis antigenic system, a genetically determined blood group system associated with infections and several disorders, including ischemic heart disease, might influence the susceptibility to CP infection, inflammatory response, and risk of cardiac ischemic events. METHODS: The CRP levels, Lewis antigens, and CP+ were measured in 54 patients with Braunwald's class IIIB UA. All patients were followed up for one year, and the occurrence of new coronary events (coronary death, myocardial infarction, and recurrence of instability) were recorded. RESULTS: Twenty-five coronary events occurred during follow-up. At univariate analysis CRP >3 mg/l (CRP+) (p = 0.0056), Lewis antigen b (Leb+) (p = 0.028), and the combination of Leb+ and CP+ (p = 0.006) and of CRP+ and Leb+ (p = 0.003) were associated with new coronary events, while CP+ alone was not. At multivariate analysis, CRP+ (p = 0.008) and combined Leb+CP+ (p = 0.03) were independent predictors of worse outcome. The event rate was 64% in CRP+ patients, 67% in Leb+CP+ patients, and 86% in CRP+Leb+CP+ patients. Combined Leb+CP+, but not Leb+ and CP+ alone, was related to CRP levels (p = 0.03). Among CP+ patients, CRP levels were higher in Leb+ than Leb- (p = 0.028). CONCLUSIONS: Our data demonstrate that in UA the Lewis antigenic system plays an important role, probably determining individual susceptibility to the detrimental effects of CP infection and by determining an enhanced inflammatory response.

Aged↗
PubMed2003

Immunosuppressive therapy for active lymphocytic myocarditis: virological and immunologic profile of responders versus nonresponders.

BACKGROUND: The beneficial effect of immunosuppressive treatment on myocarditis is still controversial, possibly because the immunologic and virological profile of potential candidates is largely unknown. METHODS AND RESULTS: Out of 652 biopsied patients, 112 had a histological diagnosis of active lymphocytic myocarditis; 41 of these 112 patients were characterized by progressive heart failure despite conventional therapy and were treated with prednisone and azathioprine for 6 months. All were resubmitted to cardiac catheterization, angiography, and endomyocardial biopsy at 1 and 6 months and followed-up for 1 year. A total of 21 patients responded with prompt improvement in left ventricular ejection fraction from 25.7+/-4.1% to 47.1+/-4.4% and showed evidence of healed myocarditis at control biopsy. Conversely, 20 patients failed to respond and showed a histological evolution toward dilated cardiomyopathy: 12 remained stationary, 3 underwent cardiac transplantation, and 5 died. We retrospectively performed a polymerase chain reaction on frozen endomyocardial tissue for the most common cardiotropic viruses and assessed circulating serum cardiac autoantibodies. Viral genomes were present in biopsy specimens of 17 nonresponders (85%), including enterovirus (n=5), Epstein-Barr virus (n=5) adenovirus (n=4), both adenovirus and enterovirus (n=1), influenza A virus (n=1), parvovirus-B19 (n=1), and in 3 responders, who were all positive for hepatitis C virus. Cardiac autoantibodies were present in 19 responders (90%) and in none of the nonresponders. CONCLUSIONS: In patients with active lymphocytic myocarditis, those with circulating cardiac autoantibodies and no viral genome in the myocardium are the most likely to benefit from immunosuppression. The beneficial effect of immunosuppression in hepatitis C virus myocarditis suggests a relevant immunomediated component of damage.

Adolescent↗
PubMed2003

Genetic control of postoperative systemic inflammatory reaction and pulmonary and renal complications after coronary artery surgery.

BACKGROUND: Although some data suggest that the individual genetic predisposition for developing major or minor degrees of postoperative systemic inflammatory reaction may influence postoperative morbidity, this hypothesis has not been clinically tested to date. Methods and results The -174 G/C polymorphism of the promoter of the interleukin 6 gene was determined preoperatively in 111 consecutive patients submitted to primary isolated coronary artery bypass. The results of the genetic analysis were then correlated with the postoperative interleukin 6 levels and the development of postoperative renal and pulmonary complications. G homozygotes had significantly higher interleukin 6 levels postoperatively (P <.0001 for the difference between areas under the curve). These patients also had worse postoperative pulmonary and renal function. The mean perioperative difference in serum creatinine, potassium, and nitrogen was 0.82 +/- 0.34, 0.99 +/- 0.44, and 10.1 +/- 7.8 mg/dL versus 0.18 +/- 0.14, 0.15 +/- 0.48, and 2.6 +/- 4.1 mg/dL for GG versus non-GG carriers (P <.0001), respectively. The mean respiratory index at 6 and 12 hours was 2.9 +/- 0.8 and 2.8 +/- 0.3 versus 2.1 +/- 0.5 and 1.3 +/- 0.1, respectively (P <.0001). The mean duration of mechanical ventilation was 22.5 +/- 2.1 versus 12.7 +/- 6.7 hours (P <.01). A correlation was found between postoperative interleukin 6 levels and renal and pulmonary complications. CONCLUSION: The interleukin 6 -174 G/C polymorphism modulates postoperative interleukin 6 levels and is associated with the degree of postoperative renal and pulmonary dysfunction and in-hospital stay after coronary surgery.

Alleles↗
PubMed2003

4G/5G PAI-1 promoter polymorphism and acute-phase levels of PAI-1 following coronary bypass surgery: a prospective study.

BACKGROUND AND OBJECTIVE: The 4G/5G plasminogen activator inhibitor-1 (PAI-1) promoter polymorphism has been associated with basal PAI-1 levels, with ischemic heart disease, and with adverse prognosis in critically ill patients. We hypothesized it might also influence the acute-phase levels of PAI-1 following coronary bypass surgery. METHODS: In 111 consecutive patients undergoing elective coronary bypass surgery, 4G/5G genotyping and serial plasma PAI-1 activity and antigen levels were prospectively measured before surgery, daily up to 72 h, and at discharge. The inflammatory reaction was additionally assessed by white cell count, fibrinogen, interleukin-6, and C-reactive protein levels. RESULTS: PAI-1 activity and antigen concentrations increased approximately two-fold after surgery, peaking at 48 hours. Carriers of the 4G-allele, compared with 5G/5G homozygotes, showed approximately 20% higher PAI-1 activity and antigen both preoperatively ( P = 0.007 and P = 0.035) and after surgery. White cell count, fibrinogen, interleukin-6, and C-reactive protein values did not differ significantly according to genotypic groups. In multivariate analysis, the 4G/5G genotype was the only significant modulator of postoperative PAI-1 activity (P = 0.003) and the main significant modulator of postoperative PAI-1 antigen (P = 0.013). No significant interaction was found between the effects of time and genotype on postoperative PAI-1. This indicates that the association between 4G/5G and acute-phase PAI-1 levels is secondary to the genotype-related difference of baseline PAI-1. CONCLUSIONS: Postoperative PAI-1 concentrations of patients undergoing elective coronary bypass surgery are higher in carriers of the 4G-allele than in 5G/5G homozygotes as a result of higher baseline values. Knowledge of 4G/5G status may be useful to predict acute-phase PAI-1 concentrations.

Acute-Phase Reaction↗
PubMed2002

Widespread coronary inflammation in unstable angina.

BACKGROUND: Inflammation within vulnerable coronary plaques may cause unstable angina by promoting rupture and erosion. In unstable angina, activated leukocytes may be found in peripheral and coronary-sinus blood, but it is unclear whether they are selectively activated in the vascular bed of the culprit stenosis. METHODS: We measured the content neutrophil myeloperoxidase content in the cardiac and femoral circulations in five groups of patients: two groups with unstable angina and stenosis in either the left anterior descending coronary artery (24 patients) or the right coronary artery (9 patients); 13 with chronic stable angina; 13 with variant angina and recurrent ischemia; and 6 controls. Blood samples were taken from the aorta, the femoral vein, and the great cardiac vein, which selectively drains blood from the left but not the right coronary artery. RESULTS: The neutrophil myeloperoxidase content of aortic blood was similar in both groups of patients with unstable angina (-3.9 and -5.5, with negative values representing depletion of the enzyme due to neutrophil activation) and significantly lower than in the other three groups (P<0.05). Independently of the site of the stenosis, the neutrophil myeloperoxidase content in blood from the great cardiac vein was significantly decreased in both groups of patients with unstable angina (-6.4 in those with a left coronary lesion and -6.6 in those with a right coronary lesion), but not in patients with stable angina and multiple stenoses, patients with variant angina and recurrent ischemia, or controls. There was also a significant transcoronary reduction in myeloperoxidase content in both groups with unstable angina. CONCLUSIONS: The widespread activation of neutrophils across the coronary vascular bed in patients with unstable angina, regardless of the location of the culprit stenosis, challenges the concept of a single vulnerable plaque in unstable coronary syndromes.

Aged↗
PubMed2002

Celiac disease associated with autoimmune myocarditis.

BACKGROUND: Both celiac disease (CD) and myocarditis can be associated with systemic autoimmune disorders; however, the coexistence of the 2 entities has never been investigated, although its identification may have a clinical impact. METHODS AND RESULTS: We screened the serum of 187 consecutive patients with myocarditis (118 males and 69 females, mean age 41.7+/-14.3 years) for the presence of cardiac autoantibodies, anti-tissue transglutaminase (IgA-tTG), and anti-endomysial antibodies (AEAs). IgA-tTG-positive and AEA-positive patients underwent duodenal endoscopy and biopsy and HLA analysis. Thirteen of the 187 patients were positive for IgA-tTG, and 9 (4.4%) of them were positive for AEA. These 9 patients had iron-deficient anemia and exhibited duodenal endoscopic and histological evidence of CD. CD was observed in 1 (0.3%) of 306 normal controls (P<0.003). In CD patients, myocarditis was associated with heart failure in 5 patients and with ventricular arrhythmias (Lown class III-IVa) in 4 patients. From histological examination, a lymphocytic infiltrate was determined to be present in 8 patients, and giant cell myocarditis was found in 1 patient; circulating cardiac autoantibodies were positive and myocardial viral genomes were negative in all patients. HLA of the patients with CD and myocarditis was DQ2-DR3 in 8 patients and DQ2-DR5(11)/DR7 in 1 patient. The 5 patients with myocarditis and heart failure received immunosuppression and a gluten-free diet, which elicited recovery of cardiac volumes and function. The 4 patients with arrhythmia, after being put on a gluten-free diet alone, showed improvement in the arrhythmia (Lown class I). CONCLUSIONS: A common autoimmune process toward antigenic components of the myocardium and small bowel can be found in >4% of the patients with myocarditis. In these patients, immunosuppression and a gluten-free diet can be effective therapeutic options.

Adolescent↗
PubMed2002

Inflammation and atherosclerosis.

Atherosclerosis, formerly considered a bland lipid storage disease, actually involves an ongoing inflammatory response. Recent advances in basic science have established a fundamental role for inflammation in mediating all stages of this disease from initiation through progression and, ultimately, the thrombotic complications of atherosclerosis. These new findings provide important links between risk factors and the mechanisms of atherogenesis. Clinical studies have shown that this emerging biology of inflammation in atherosclerosis applies directly to human patients. Elevation in markers of inflammation predicts outcomes of patients with acute coronary syndromes, independently of myocardial damage. In addition, low-grade chronic inflammation, as indicated by levels of the inflammatory marker C-reactive protein, prospectively defines risk of atherosclerotic complications, thus adding to prognostic information provided by traditional risk factors. Moreover, certain treatments that reduce coronary risk also limit inflammation. In the case of lipid lowering with statins, this anti-inflammatory effect does not appear to correlate with reduction in low-density lipoprotein levels. These new insights into inflammation in atherosclerosis not only increase our understanding of this disease, but also have practical clinical applications in risk stratification and targeting of therapy for this scourge of growing worldwide importance.

Aged↗
PubMed2002

Risk of myocardial infarction and angina in patients with severe peripheral vascular disease: predictive role of C-reactive protein.

BACKGROUND: Patients undergoing revascularization procedures for peripheral vascular disease (PVD) have a greatly increased risk for coronary artery disease (CAD) that is predicted only partly by clinical data and cardiovascular risk factors. We investigated whether the prognostic assessment in PVD patients could be improved by preoperative measurements of C-reactive protein (CRP). METHODS AND RESULTS: We assessed clinical and risk factors profiles, Eagle clinical scores, and preoperative CRP serum levels in 51 patients with PVD at Fontaine-Leriche stages II to IV without severe rest ventricular dysfunction or ischemia. During 24 months of follow-up, 17 patients (34%) had fatal (11) or nonfatal (6) myocardial infarction (MI). With univariate logistic regression analysis, only previous history of CAD, Eagle score, and CRP were independently related to MI. At multivariate logistic regression analysis, only CRP values in the upper tertile (<9 mg/L) were significantly associated with MI (P<0.05) and identified 65% of cases. CONCLUSIONS: The high incidence of MI in patients with PVD severe enough to require revascularization is strongly predicted by preprocedural measurements of serum CRP, independent of previous CAD, Eagle score index, and traditional cardiovascular risk factors. These patients may benefit from therapy modulating the inflammatory response.

Aged↗
PubMed2002

The linear ablation of atrial fibrillation in the right atrium: can the isthmus ablation improve its efficacy?

OBJECTIVES: The aims of this study were to compare the efficacy of a 2- versus a 3 RF lesions ablation procedure in the RA in patients with paroxysmal AF, and to map right atrial activation during AF. BACKGROUND: RF catheter-mediated ablation lines mimicking the Maze operation have been proposed as a novel curative approach for AF. The relationship between this type of ablation and right atrial mapping has not been extensively studied. METHODS: Twenty-four patients with recurrent, drug-refractory, paroxysmal AF underwent an extensive mapping of the RA before attempting linear lesion RF ablation. Patients were divided into two groups: 15 patients received two linear lesions (Group 1), 9 patients three linear lesions (Group 2). RESULTS: One-month success rate AF did not recur in 40% of Group 1 patients (6/15) and in 66% (6/9) of Group 2 patients. 27% of patients in Group 1 and 11% of patients in Group 2 had recurrences controlled by drugs. No benefit in 33% of Group 1 patients and 22% of Group 2. Long-term follow-up In the absence of any drug treatment, no AF recurrences were observed in 26% of Group 1 patients (FU: 23 to 47 months) and 55% of Group 2 (FU: 14 to 23 months). No complications were reported. CONCLUSIONS: Right atrial linear ablation is safe and may be proposed for AF treatment in selected patients.

Adult↗
PubMed2002

Prothrombotic response to coronary angioplasty in patients with unstable angina and raised C-reactive protein.

BACKGROUND: To better understand the mechanisms linking C reactive protein (CRP) to the risk of coronary thrombosis, we investigated the relation between inflammatory state and hemostatic response to coronary angioplasty in patients with either stable or unstable angina. METHODS: Plasma levels of von Willebrand factor (vWF) antigen, vWF collagen binding activity, vWF-cleaving-protease, CRP, and whole-blood platelet reactivity were measured before and 24 h after angioplasty in 18 patients with recent unstable angina and in 17 with stable angina. Each group was divided according to preprocedural CRP levels: >or=3 mg/l (in 9 unstable and 9 stable patients) or <3 mg/l (in 9 unstable and 8 stable patients). RESULTS: Baseline hemostatic parameters did not differ significantly among the four subgroups of patients. After angioplasty, virtually all patients with unstable angina and raised preprocedural CRP showed increased vWF antigen (P = 0.01), vWF collagen-binding (P = 0.001), CRP (P = 0.008), and platelet reactivity (P = 0.0007) compared to baseline, whereas no significant change of these variables was seen within the other three sets of patients. In the overall population, the changes in vWF antigen and vWF-collagen-binding induced by angioplasty correlated with those in CRP levels (r = 0.47, P = 0.004 and r = 0.44, P = 0.008). Baseline levels of vWF cleaving protease and modifications of this enzyme with angioplasty did not differ significantly among subgroups. CONCLUSIONS: Our data suggest that high preprocedural levels of CRP predict a significant vWF rise after angioplasty in patients with unstable angina. The rise in vWF is associated with that in CRP and with enhanced platelet reactivity. Such changes may contribute to the worse prognosis of unstable patients with raised indices of inflammation.

Adult↗
PubMed2002

Normothermia does not improve postoperative hemostasis nor does it reduce inflammatory activation in patients undergoing primary isolated coronary artery bypass.

BACKGROUND: Despite its common acceptance in clinical practice, the effective benefits of normothermic systemic perfusion during coronary artery bypass operations are far from established. METHODS: A total of 113 patients undergoing primary isolated coronary artery bypass were randomly assigned to normothermic (37 degrees C) or hypothermic (26 degrees C) systemic perfusion. The clinical course of the patients was prospectively recorded, and several inflammatory and fibrinolytic markers (C-reactive protein, fibrinogen, interleukin 6, plasminogen activator inhibitor 1, prothrombin time, activated partial thromboplastin time, platelets, and white blood cell counts) were determined before surgical intervention; 24, 48, and 72 hours thereafter; and at hospital discharge. RESULTS: Postoperatively, 2 in-hospital deaths occurred in the normothermic series and none in the hypothermic series. Four patients had a myocardial infarction, 1 had respiratory insufficiency, 1 had to be reoperated on for graft malfunction, and none had renal insufficiency in the hypothermic group versus 1 patient with each of these complications in the normothermic series. Mean blood loss in the first 24 hours was 766 +/- 223 mL in the normothermic group and 740 +/- 220 mL in the hypothermic group. None of these differences was statistically significant. Similarly, no significant difference in the postoperative level of any of the measured variables at any time point was evident between the patients in the normothermic and hypothermic groups. CONCLUSION: Normothermic systemic perfusion does not influence the clinical course or the extent of inflammatory and hemostatic activation in patients undergoing primary isolated coronary artery bypass.

C-Reactive Protein↗
PubMed2002

Antibodies to 60-kilodalton heat shock protein and outer membrane protein 2 of Chlamydia pneumoniae in patients with coronary heart disease.

Evidence linking Chlamydia pneumoniae infection to atherosclerosis and to atherothrombotic events has recently emerged. A primary candidate implicated in these pathogenetic events is the 60-kDa chlamydial heat shock protein (HSP60). Another putative candidate to activate a potential proinflammatory mechanism is the chlamydial outer membrane protein 2 (OMP2). We have generated both HSP60 and OMP2 recombinant antigens in a nondenatured form and shown that (i) the two antigens were highly immunogenic in mice and (ii) murine antisera thus generated recognized the native C. pneumoniae proteins. We measured by enzyme linked immunosorbent assay (ELISA) and immunoblot assay antibody titers to the recombinant antigens in samples from 219 patients with coronary heart disease (CHD), 179 patients with unstable angina (UA), 40 patients with acute myocardial infarction (AMI), and 100 age-, sex-, and risk factor-matched healthy controls. We also examined whether anti-HSP60 and/or anti-OMP2 antibodies correlated with anti-C. pneumoniae antibodies assessed by a commercial microimmunofluorescence (MIF) assay. Immunoglobulin G (IgG), but neither IgA nor IgM, antibodies against the two recombinant proteins were detected by ELISA. In particular, anti-HSP60 antibodies were detected in >99% of CHD patients versus 0% of the controls, whereas the proportions of anti-OMP2 positive subjects were >70 and 27%, respectively. Nonetheless, among CHD patients, similar frequencies of positive subjects and titers of anti-HSP60 or anti-OMP2 antibodies were present in UA and AMI subjects. The anti-OMP2, but not the anti-HSP60, antibodies showed high specificity. Consistently, high serological correlation was observed between IgG MIF titers and IgG ELISA reactivity to OMP2 but not to HSP60. Overall, the results of this study demonstrate a strong correlation between CHD and anti-HSP60 IgG levels, as measured by our in-house ELISA. They also suggest that recombinant OMP2 ELISA, because of its high specificity and strong correlation with MIF assay, could be a candidate diagnostic marker for C. pneumoniae infection, which would be of potential usefulness for its specificity and nonsubjective nature.

Adult↗
PubMed2002

Lone hepatitis C virus myocarditis responsive to immunosuppressive therapy.

OBJECTIVES: This study analyzes the causal role of hepatitis C virus (HCV) in patients with lone myocarditis, and its susceptibility to immunosuppression. BACKGROUND: Prevalence of HCV in lone myocarditis, its mechanism of damage, and possible treatment are still unknown. METHODS: Among 48 consecutive patients with myocarditis serologically screened for HCV and other cardiotropic viruses, 3 patients had anti-HCV antibodies. Clinical manifestation was heart failure in two cases, and left bundle-branch block with moderate cardiac dysfunction was present in patient 3. The three patients underwent two-dimensional echocardiography, coronary angiography, and endomyocardial biopsy. Nested polymerase chain reaction (PCR) for positive and negative strands of HCV on sera and myocardial samples, and PCR for the most common cardiotropic viruses were performed. HCV in the myocardium was detected by TORDJI-22 antibody. RESULTS: At histology, a lymphocytic myocarditis associated with myocytes positively stained by TORDJI-22 was shown in all. Cardiac autoantibodies were detected in all cases. Nested PCR showed both positive and negative strands of HCV RNA in serum and myocardium; other viral genomes were absent. Patients were treated with prednisone and azathioprine for 6 months, with recovery of cardiac volumes and function. At 4-week control biopsy, myocarditis progressed to a healed phase, though HCV RNA was still detectable in the serum and myocardium. Cardiac improvement was maintained at the 12-month overall follow-up. CONCLUSIONS: HCV can be detected in the myocardium of as many as 6% of patients with lone myocarditis; HCV myocarditis can benefit from immunosuppression despite persistence of viral genome, suggesting an immunomediated mechanism of damage.

Adult↗
PubMed2002

[Role of clopidogrel in acute coronary syndromes without ST-segment elevation].

Unstable angina and no ST-segment elevation myocardial infarction are acute coronary syndromes (ACS) typically characterized by minimal or little myocardial damage, but often heralding "classical" infarction or coronary death in the short or medium term. Coronary thrombi, mainly composed by platelets, are the major pathogenetic component of ACS and an effective therapeutic target. The hemostatic balance can be shifted towards an antithrombotic state in the clinical setting. Although the thrombogenic stimuli acting in each individual patient, their intensity as well as the prothrombotic factors that may contribute to an inappropriate thrombus growth, remain largely unknown. To this purpose the modulation of platelet aggregation is a particularly effective and practical therapeutic target. The availability of a new antiplatelet agent, clopidogrel, with a proven efficacy in the prevention of cardiovascular events, suggests the opportunity of reviewing the mechanisms of instability and the therapeutic strategies in patients with ACS. In this review we analyze: 1) the composition of coronary thrombi in patients with ACS, 2) the mechanisms of thrombus development and growth, 3) the mechanisms of platelet adhesion and aggregation, 4) the characteristics of clopidogrel, 5) the efficacy of the various therapeutic strategies, 6) the possible implications of the adjunctive therapy with clopidogrel for the treatment and prevention of cardiovascular events in ACS with no ST-segment elevation.

Acute Disease↗
PubMed2002

Scintigraphic results in asymptomatic myocardial infarction patients with exercise-induced ST segment elevation.

BACKGROUND: The mechanism responsible for exercise-induced ST segment elevation is debated, but heterogeneous patients were likely included in previous studies. This study was specifically aimed at investigating the clinical meaning of isolated exercise-induced ST segment elevation in asymptomatic patients with a recent acute myocardial infarction (MI). METHODS: We studied 30 patients (28 males, 2 females, mean age 62 +/- 9 years) with a recent MI who developed ST segment elevation in leads with a Q/QS wave pattern, and who did not develop angina or ST segment depression during exercise testing and did not have any history of post-infarction angina. Patients underwent bicycle 99m-Tc-sestamibi (MIBI) myocardial scintigraphy for the assessment of myocardial perfusion and of left ventricular function. RESULTS: Only 7 patients (23.3%) showed reversible perfusion defects on stress MIBI myocardial scintigraphy, which were mild and of limited extension in all. There were no statistically significant differences in the main exercise variables between groups with or without stress-related perfusion defects. Signs of exercise-related left ventricular dysfunction were detected in 6 patients (20%), 3 of whom also showed reversible perfusion defects. Again, no significant differences in the main exercise variables were found between patients with or without stress-induced scintigraphic abnormalities. CONCLUSIONS: In asymptomatic MI patients, isolated exercise-induced ST segment elevation in leads with a Q/QS wave pattern is unlikely to represent clinically relevant residual myocardial ischemia during exercise, thus suggesting that further diagnostic investigations are not necessary in these patients.

Aged↗
PubMed2002

[Inflammatory and fibrinolytic activation after coronary artery bypass with extracorporeal circulation].

BACKGROUND: The aim of this study was to determine the course of the main inflammatory and fibrinolytic markers in patients undergoing primary elective coronary artery bypass graft with extracorporeal circulation. METHODS: One hundred and thirteen patients (105 males, 8 females) undergoing primary isolated coronary artery bypass with normo- (37 degrees C) or hypothermic (26 degrees C) systemic perfusion were prospectively studied. The clinical course of the patients was recorded and inflammatory and fibrinolytic markers (C-reactive protein, fibrinogen, interleukin-6, plasminogen activator inhibitor-1, prothrombin time, activated partial thromboplastin time, platelets and white blood cell counts) were determined before surgery, 24, 48 and 72 hours thereafter, and at hospital discharge. RESULTS: Two patients died (mortality 1.7%) and 6 had a major complication (event free survival > 94%). Interleukin-6, lymphocyte, neutrophil and monocyte levels increased after surgery but returned to normal at hospital discharge. C-reactive protein levels increased after 24 hours and remained high at hospital discharge. Plasminogen activator inhibitor-1, prothrombin time, and activated partial thromboplastin time increased from few hours postoperatively and returned to normal before discharge. Platelets decreased immediately after surgery and normalized only at hospital discharge. Fibrinogen decreased in the first 24 postoperative hours, raised later and remained elevated at hospital discharge. CONCLUSIONS: Cardiopulmonary bypass activates inflammatory response and hemostatic/fibrinolytic balance in patients undergoing primary isolated coronary artery bypass.

Aged↗