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Abstract Background Disturbed cellular cholesterol homeostasis may lead to accumulation of cholesterol in human atheroma plaques. Cellular cholesterol homeostasis is controlled by the sterol regulatory element-binding transcription factor 2 (SREBF-2) and the SREBF cleavage-activating protein (SCAP). We investigated whole genome expression in a series of human atherosclerotic samples from different vascular territories and studied whether the non-synonymous coding variants in the interacting domains of two genes, SREBF-2 1784G>C (rs2228314) and SCAP 2386A>G, are related to the progression of coronary atherosclerosis and the risk of pre-hospital sudden cardiac death (SCD). Methods Whole genome expression profiling was completed in twenty vascular samples from carotid, aortic and femoral atherosclerotic plaques and six control samples from internal mammary arteries. Three hundred sudden pre-hospital deaths of middle-aged (33–69 years) Caucasian Finnish men were subjected to detailed autopsy in the Helsinki Sudden Death Study. Coronary narrowing and areas of coronary wall covered with fatty streaks or fibrotic, calcified or complicated lesions were measured and related to the SREBF-2 and SCAP genotypes. Results Whole genome expression profiling showed a significant (p = 0.02) down-regulation of SREBF-2 in atherosclerotic carotid plaques (types IV-V), but not in the aorta or femoral arteries (p = NS for both), as compared with the histologically confirmed non-atherosclerotic tissues. In logistic regression analysis, a significant interaction between the SREBF-2 1784G>C and the SCAP 2386A>G genotype was observed on the risk of SCD (p = 0.046). Men with the SREBF-2 C allele and the SCAP G allele had a significantly increased risk of SCD (OR 2.68, 95% CI 1.07–6.71), compared to SCAP AA homologous subjects carrying the SREBF-2 C allele. Furthermore, similar trends for having complicated lesions and for the occurrence of thrombosis were found, although the results were not statistically significant. Conclusion The results suggest that the allelic variants (SREBF-2 1784G>C and SCAP 2386A>G) in the cholesterol homeostasis regulating SREBF-SCAP pathway may contribute to SCD in early middle-aged men.

Results: In the meta-analysis, psoas muscle measurements were significantly associated with mortality among men ( p  < 0.05), with high heterogeneity in the associations across all cohorts. There was very little difference in the association between PMA and PMD and mortality (HR 0.83, 95% CI 0.69-0.99, p  = 0.002; HR 0.85, 95% CI 0.77-0.94, p  = 0.041 for one SD increase in PMA and PMD in the random effects model). Combining PMA and PMD into one composite variable by multiplying their values together showed the most robust association in terms of the magnitude of the effect size in men (HR, 0.77; 95% CI 0.73-0.87, p  < 0.001). Indexing PMA to body size did not result in any significant differences in this association. Among women, psoas muscle measurements were not associated with long-term mortality in this meta-analysis., Conclusions: Different psoas muscle measurements were significantly and very similarly associated with mortality among men but not among women. No single measurement stands out, although combining PMA and PMD seems to be a slightly stronger estimate in terms of effect size and should be considered in further studies.

Background: Despite the steady improvements in survival and operative safety, postoperative complications still remain a significant cause of morbidity and mortality after coronary artery bypass grafting (CABG). However, less is known on the impact of postoperative complications on health-related quality of life (QoL). The main objective of our study was to investigate the impact of postoperative complications on long-term QoL and survival after CABG surgery., Methods: Data of 508 patients, who underwent isolated CABG was prospectively collected. The RAND-36 Health Survey (RAND-36) was used to evaluate patients' QoL status preoperatively, 1 year and 12 years after the surgery. Predefined postoperative complications were reported during primary and secondary hospital stay. QoL and survival analysis were performed primarily on three patient groups: patients with and without complications and patients with major adverse cardiac and cerebrovascular events (MACCE)., Results: In total 205(40%) of 508 patients had at least one postoperative complication and 73 (14%) experienced MACCE. Patients' thirty-day, 1-year and 10-year survival rates were, 99, 98, 84% without complications, 97, 95, 72% with complications, and 90, 89, 64% with MACCE, respectively (log-rank p < 0.001). Patients without complications showed significant(p < 0.05) improvements in seven and patients with complications in five out of eight RAND-36 QoL dimensions. All patient groups showed significant improvements in RAND-36 summary scores compared with preoperative values. Patients with complications and especially with MACCE had more profound decline in their RAND-36 summary scores while patients without complications maintained their health status best., Conclusions: Despite the constant deterioration, both patients with and without complications showed improvements even 12 years after CABG compared with preoperative state. Postoperative complications and especially MACCE were associated with impaired long-term QoL.

A prevalence of diabetes is increasing among the patients undergoing coronary artery bypass grafting (CABG). Data on whether health-related quality of life improves similarly after CABG in diabetics and nondiabetics are limited. We assessed long-term mortality and changes in quality of life (RAND-36 Health Survey) after CABG. Seventy-four of the 508 patients (14.6%) operated on in a single institution had a history of diabetes and were compared with nondiabetics. The RAND-36 Health Survey was used as an indicator of quality of life. Assessments were made preoperatively and repeated 1 and 12 years later. Thirty-day mortality was 2.7 versus 1.6 ( p  = 0.511) in the diabetics and nondiabetics. One- and 10-year survival rates in the diabetics and nondiabetics were 94.6% versus 97.0% ( p  = 0.287) and 63.5% versus 81.6% ( p  < 0.001), respectively. After 1 year, diabetics improved significantly ( p  < 0.005) in seven, and nondiabetics ( p  < 0.001) in all eight RAND-36 dimensions. Despite an ongoing decline in quality of life over the 12-year follow-up, an improvement was maintained in four out of eight dimensions among diabetics and in seven dimensions among nondiabetics. Physical and mental component summary scores on the RAND-36 improved significantly ( p  < 0.001) in both groups after 1 year, and at least slight improvement was maintained during the 12-year follow-up time. Diabetics have inferior long-term survival after CABG as compared with nondiabetics. They gain similar improvement of quality of life in 1 year after surgery, but they have a stronger decline tendency over the years.

Ascending thoracic aortic aneurysm (ATAA) is a multifactorial disease with a strong inflammatory component. Surgery is often required to prevent aortic rupture and dissection. We performed gene expression analysis (Illumina HumanHT-12 version 3 Expression BeadChip) for 32 samples from ATAA (26 without/6 with dissection), and 28 left internal thoracic arteries (controls) collected in Tampere Vascular study. We compared expression profiles and conducted pathway analysis using Ingenuity Pathway Analysis (IPA) to reveal differences between ATAA and a healthy artery wall. Almost 5000 genes were differentially expressed in ATAA samples compared to controls. The most downregulated gene was homeobox (HOX) A5 (fold change, FC = -25.3) and upregulated cadherin-2 (FC = 12.6). Several other HOX genes were also found downregulated (FCs between -25.3 and -1.5, FDR < 0.05). 43, mostly inflammatory, canonical pathways in ATAA were found to be significantly (p < 0.05, FDR < 0.05) differentially expressed. The results remained essentially the same when the 6 dissected ATAA samples were excluded from the analysis. We show for the first time on genome level that ATAA is an inflammatory process, revealing a more detailed molecular pathway level pathogenesis. We propose HOX genes as potentially important players in maintaining aortic integrity, altered expression of which might be important in the pathobiology of ATAA.

Cardiovascular diseases due to atherosclerosis are the leading cause of death globally. We aimed to investigate the potentially altered gene and pathway expression in advanced peripheral atherosclerotic plaques in comparison to healthy control arteries. Gene expression analysis was performed (Illumina HumanHT-12 version 3 Expression BeadChip) for 68 advanced atherosclerotic plaques (15 aortic, 29 carotid and 24 femoral plaques) and 28 controls (left internal thoracic artery (LITA)) from Tampere Vascular Study. Dysregulation of individual genes was compared to healthy controls and between plaques from different arterial beds and Ingenuity pathway analysis was conducted on genes with a fold change (FC) > ±1.5 and false discovery rate (FDR) < 0.05. 787 genes were significantly differentially expressed in atherosclerotic plaques. The most up-regulated genes were osteopontin and multiple MMPs, and the most down-regulated were cell death-inducing DFFA-like effector C and A (CIDEC, CIDEA) and apolipoprotein D (FC > 20). 156 pathways were differentially expressed in atherosclerotic plaques, mostly inflammation-related, especially related with leukocyte trafficking and signaling. In artery specific plaque analysis 50.4% of canonical pathways and 41.2% GO terms differentially expressed were in common for all three arterial beds. Our results confirm the inflammatory nature of advanced atherosclerosis and show novel pathway differences between different arterial beds., Competing Interests: The authors declare no competing financial interests.

Objectives: To evaluate the long-term effect of perioperative myocardial infarction (PMI) on outcomes and health-related quality-of-life (QOL) after coronary artery bypass grafting (CABG)., Methods: Eighty of the 501 patients (16%) fulfilled electrocardiogram or cardiac enzyme criteria for PMI and were compared with patients with no PMI. The RAND-36 Health Survey was used as an indicator of QOL. Assessments were made preoperatively and repeated 1 year and 12 years later., Results: Thirty-day mortality was adversely affected by PMI (6.3 vs 1.0%, P = 0.001). One-year survival rates for PMI and no-PMI patients were 92.5 and 97.6%, 10-year rates being 72.5 and 79.8%. One year after the surgery, PMI patients improved in seven and no-PMI patients in all the eight RAND-36 dimensions. In the 12-year follow-up, the scores showed a general decline tendency. PMI patients still maintained a significant improvement in four and no-PMI patients in seven of eight dimensions when compared with the baseline scores. A highly significant improvement was seen in the RAND-36 mental and physical component summary scores in the no-PMI group 1 year after CABG. PMI patients improved also significantly although the magnitude of change was lower. In the 12-year follow-up, there was a general decline tendency in the scores. Both groups showed similar freedom from anginal symptoms at 12 years., Conclusions: Although PMI has a negative impact on health-related QOL 1 year after CABG, this effect is only minor in the long term. PMI increases 30-day mortality but shows no effect on later mortality.

Objectives: Improvement in quality of life (QoL) and survival benefit are the primary objectives of coronary artery bypass graft (CABG) surgery. The profile of patients undergoing isolated CABG has altered towards higher age with more preoperative comorbidities. Thus, the importance of QoL over the quantity of life among elderly patients is getting more emphasized. In this study, our main goal was to evaluate the long-term changes in QoL, overall performance status and symptomatic status after the CABG., Methods: Comprehensive data of 508 patients who underwent isolated CABG in a single institution were prospectively collected. The RAND-36 Health Survey (RAND-36) was used as an indicator of QoL. Karnofsky dependency category was used to evaluate overall performance status, and symptomatic status was assessed using New York Heart Association (NYHA) class. All assessment were made preoperatively and repeated 1 year and 12 years later. The follow-up of the study cohort was complete in 95 and 84% of the alive patients at 1 year and 12 years, respectively. Analysis was based mainly on three age groups: ≤64 years (282 patients), 65-74 years (175 patients) and ≥75 years (51 patients)., Results: Thirty-day, 1-year and 10-year survival rates were 98, 97 and 79%, respectively. Twelve years after the surgery significant improvement (P<0.05) was seen in all but one RAND-36 dimensions of the QoL (general health, P=0.76) as well as in functional capacity (P<0.001) and NYHA class. All age groups showed improvements in RAND-36 physical component summary (PCS) and mental component summary (MCS) scores compared with the preoperative values. The youngest subgroup maintained their physical and mental health status best, whereas older subgroups had more pronounced decreases in their PCS and MCS scores., Conclusions: Despite an ongoing deterioration 12 years after the CABG, there was significant improvement in most dimensions of the QoL and functional capacity in comparison with the preoperative values. The elderly gain less long-term benefit from CABG regarding the QoL and survival.

Background: Atherosclerosis is a complex disease with hundreds of genes influencing its progression. In addition, the phenotype of the disease varies significantly depending on the arterial bed., Methodology/principal Findings: We characterized the genes generally involved in human advanced atherosclerotic (AHA type V-VI) plaques in carotid and femoral arteries as well as aortas from 24 subjects of Tampere Vascular study and compared the results to non-atherosclerotic internal thoracic arteries (n=6) using genome-wide expression array and QRT-PCR. In addition we determined genes that were typical for each arterial plaque studied. To gain a comprehensive insight into the pathologic processes in the plaques we also analyzed pathways and gene sets dysregulated in this disease using gene set enrichment analysis (GSEA). According to the selection criteria used (>3.0 fold change and p-value <0.05), 235 genes were up-regulated and 68 genes down-regulated in the carotid plaques, 242 genes up-regulated and 116 down-regulated in the femoral plaques and 256 genes up-regulated and 49 genes down-regulated in the aortic plaques. Nine genes were found to be specifically induced predominantly in aortic plaques, e.g., lactoferrin, and three genes in femoral plaques, e.g., chondroadherin, whereas no gene was found to be specific for carotid plaques. In pathway analysis, a total of 28 pathways or gene sets were found to be significantly dysregulated in atherosclerotic plaques (false discovery rate [FDR] <0.25)., Conclusions: This study describes comprehensively the gene expression changes that generally prevail in human atherosclerotic plaques. In addition, site specific genes induced only in femoral or aortic plaques were found, reflecting that atherosclerotic process has unique features in different vascular beds.

Background. We studied the effect of fast induction of cardiac arrest with denosine on myocardial bax and bcl-2 expression. Methods and Results. 40 elective CABG patients were allocated into two groups. The adenosine group (n = 20) received 250 mug/kg adenosine into the aortic root followed by blood potassium cardioplegia. The control group received potassium cardioplegia in blood. Bcl-2 and bax were measured. Bax was reduced in the postoperative biopsies (1.38 versus 0.47, P = .002) in the control group. Bcl-2 showed a reducing tendency (0.14 versus 0.085, P = .07). After the adenosine treatment, the expression of both bax (0.52 versus 0.59, P = .4) and bcl-2 (0.104 versus 0.107, P = .4) remained unaltered after the operation. Conclusion. Open heart surgery is associated with rapid reduction in the expression of apoptosis regulating genes bax and bcl-2. Fast Adenosine induction abolished changes in their expression.

Background: Disturbed cellular cholesterol homeostasis may lead to accumulation of cholesterol in human atheroma plaques. Cellular cholesterol homeostasis is controlled by the sterol regulatory element-binding transcription factor 2 (SREBF-2) and the SREBF cleavage-activating protein (SCAP). We investigated whole genome expression in a series of human atherosclerotic samples from different vascular territories and studied whether the non-synonymous coding variants in the interacting domains of two genes, SREBF-2 1784G>C (rs2228314) and SCAP 2386A>G, are related to the progression of coronary atherosclerosis and the risk of pre-hospital sudden cardiac death (SCD)., Methods: Whole genome expression profiling was completed in twenty vascular samples from carotid, aortic and femoral atherosclerotic plaques and six control samples from internal mammary arteries. Three hundred sudden pre-hospital deaths of middle-aged (33-69 years) Caucasian Finnish men were subjected to detailed autopsy in the Helsinki Sudden Death Study. Coronary narrowing and areas of coronary wall covered with fatty streaks or fibrotic, calcified or complicated lesions were measured and related to the SREBF-2 and SCAP genotypes., Results: Whole genome expression profiling showed a significant (p = 0.02) down-regulation of SREBF-2 in atherosclerotic carotid plaques (types IV-V), but not in the aorta or femoral arteries (p = NS for both), as compared with the histologically confirmed non-atherosclerotic tissues. In logistic regression analysis, a significant interaction between the SREBF-2 1784G>C and the SCAP 2386A>G genotype was observed on the risk of SCD (p = 0.046). Men with the SREBF-2 C allele and the SCAP G allele had a significantly increased risk of SCD (OR 2.68, 95% CI 1.07-6.71), compared to SCAP AA homologous subjects carrying the SREBF-2 C allele. Furthermore, similar trends for having complicated lesions and for the occurrence of thrombosis were found, although the results were not statistically significant., Conclusion: The results suggest that the allelic variants (SREBF-2 1784G>C and SCAP 2386A>G) in the cholesterol homeostasis regulating SREBF-SCAP pathway may contribute to SCD in early middle-aged men.

Objective: Ischemic preconditioning reduces infarct size and improves hemodynamic function. Unstable angina may be a clinical analogue to ischemic preconditioning, and involve activation of gene programs. We hypothesized that preceding unstable angina and/or ischemic preconditioning activated genes regulated by nuclear factor kappa B (NFkappaB) or hypoxia-inducible factor 1 alpha in parallel to improved cardiac function., Methods: Patients undergoing coronary artery bypass grafting with stable or unstable angina were subjected to ischemic preconditioning or sham treatment (n=10-11 in each group). Central hemodynamics were monitored. Left ventricular and atrial biopsies were harvested before cardioplegic arrest and after 25 min of reperfusion. Expression of heat shock protein 72 was evaluated by immunoblot, and activation of NFkappaB was detected by electrophoretic mobility shift assay. Real-time PCR was used to quantify expression of genes regulated by NFkappaB (inducible nitric oxide synthase, tumor necrosis factor-alpha, intercellular adhesion molecule 1) or by hypoxia-inducible factor 1 alpha (heme oxygenase-1, glucose transporter-1 and vascular endothelial growth factor-A)., Results: Ischemic preconditioning improved postoperative cardiac index and left ventricular stroke work index in both stable and unstable groups on the first postoperative day. Expression of hypoxia-inducible factor 1 alpha regulated genes was not influenced by cardioplegia and reperfusion, ischemic preconditioning or unstable angina. Expression of the NFkappaB-regulated genes increased after cardioplegia and reperfusion, but this was not influenced by ischemic preconditioning in stable patients. Inducible nitric oxide synthase and tumor necrosis factor expression were reduced after ischemic preconditioning in patients with unstable angina. There were no significant differences in gene expression between stable and unstable patients before cardioplegia and ischemic preconditioning. NFkappaB translocation at reperfusion was reduced in stable preconditioned and unstable control patients compared to stable controls. Heat shock protein 72 expression increased after preconditioning of unstable patients., Conclusion: Cardiac function was improved by ischemic preconditioning in both stable and unstable patients. Unstable angina per se had no effect. NFkappaB-regulated genes were influenced by ischemic preconditioning, but hypoxia-inducible genes were not.

Objective: Apoptosis has been considered as one of the mechanisms of cardiomyocyte loss during open heart surgery. Adenosine is cardioprotective against ischemia-reperfusion injury in experimental models. The aim of this study was to find out whether the administration of single dose adenosine added to blood cardioplegia is effective in decreasing the apoptosis process., Methods: In a double-blinded randomized control intervention study, 40 patients were enrolled for elective coronary artery bypass grafting. In the adenosine group (n=20) patients received 250 microg/kg adenosine in the aortic root after cross-clamping followed by cold blood cardioplegia. In the control group (n=20) patients had only antegrade cardioplegia. Left ventricular tissue samples (from apex) were taken before and after the bypass. The apoptotic cells were identified by dUTP nick-end labeling (TUNEL) using an apoptosis detection kit. The number of TUNEL-positive cardiomyocytes was expressed as percentage of the total number of cardiomyocytes in histological tissue sections., Results: The groups were closely identical in demographic data, cross-clamp time, cardiopulmonary bypass time and weaning time. The postoperative cardiac index and other hemodynamic parameters, including the patterns of CK-MB, did not show statistically significant differences. In the tissue samples there were an equal number of patients who developed apoptosis after the cross-clamp. Although the frequency of apoptosis in the control group was two times higher than in the adenosine group, this was statistically not significant., Conclusions: Adenosine enhanced blood cardioplegia could not prevent myocardial apoptosis completely. However, it seems to be that adenosine might influence the frequency of apoptosis and this needs to be considered in future investigations.

Background: An increasing proportion of patients undergoing coronary artery bypass grafting are diabetics who are known to carry a higher mortality and morbidity in association with operation, but data on whether health-related quality of life improves similarly after coronary artery bypass grafting in diabetic and nondiabetic patients are limited. We assessed in detail changes in health-related quality of life (RAND-36 Health Survey) during the first year after coronary artery bypass grafting., Methods: Seventy-four of the 508 patients (14.6%) operated on in a single institution had a history of diabetes and were compared to nondiabetics. The RAND-36 Health Survey was used as an indicator of quality of life. Assessments were made preoperatively and repeated 12 months later., Results: Thirty-day mortality was 2.7% versus 1.6% (p = 0.511) and one-year survival was 94.6% versus 97.0% (p = 0.287) in the diabetics and nondiabetics, respectively. Diabetics improved significantly (p < 0.005) in seven, nondiabetics (p < 0.001) in all eight RAND-36 dimensions. Physical component summary and mental component summary scores on the RAND-36 improved significantly (p < 0.001) in diabetics as well as in nondiabetics. Both groups experienced closely similar freedom from anginal symptoms at one year (86.2% vs 90.5%, p = 0.280)., Conclusions: Although diabetic patients differ from nondiabetics having slightly inferior quality of life before and one year after coronary artery bypass grafting, they gain similar improvement of quality of life in one year after surgery when compared to nondiabetics.

Objective: Perioperative myocardial infarction (PMI) is a well-described complication of coronary artery bypass grafting (CABG). Data on its effect on patients' subsequent health-related quality of life (QOL) and on other related consequences is deficient. The aim here was to evaluate in a prospective follow-up design the risk factors for and consequences of PMI and especially its possible impact on health-related QOL., Methods: Comprehensive data, including preoperative risk profile, perioperative variables and postoperative morbidity up to discharge were collected of 501 CABG patients in the Heart Center of Tampere University Hospital and in all eighteen postoperative care hospitals. Eighty patients (16%) fulfilled ECG or cardiac enzyme criteria for PMI and they were compared to patients with no PMI. The RAND-36 Health Survey (RAND-36) was used as an indicator of QOL. The primary outcomes were change in physical component summary (PCS), mental component summary (MCS) and the eight dimensions of health-related QOL from the RAND-36. Symptomatic status was estimated according to New York Heart Association (NYHA) class. Assessments were made preoperatively and repeated 12 months later., Results: Multivariate logistic regression analysis identified long cardiopulmonary bypass time (P=0.006) and high age (P=0.049) as independent predictors for PMI. Thirty-day mortality was adversely affected by PMI (6.3 vs 1.0%, P=0.001). In discharged patients, the occurrence of PMI did not affect 1-year survival adversely (98.7 vs 98.6%). The PMI patients showed significant (P<0.05) improvements in six of the eight dimensions of RAND-36, but they presented with a negative change in their 'general health' scores at the follow-up. All QOL scores improved significantly (P<0.001) among the patients without PMI. A highly significant (P<0.001) pattern of change was seen in the RAND-36 PCS and MCS scores in both groups although PMI patients showed significantly (P=0.002) smaller change in their PCS scores. Both groups showed similar freedom from anginal symptoms at 1 year (89.6 vs 90.1%) but in the PMI group later readmissions due to cardiac-related causes were more common (23 vs 10%, P=0.002)., Conclusions: PMI increases 30-day mortality and affects also adversely on later health-related QOL following CABG.

Objective: To investigate whether novel pharmacological preconditioning with diazoxide could protect the myocardial function and decrease myocardial injury in patients undergoing coronary artery bypass grafting (CABG)., Methods: Forty patients with stable angina who were scheduled for isolated elective CABG operations were randomized into control group (n=20) and diazoxide (DZX) group (n=20). In the DZX group, 1.5 mg/kg diazoxide was infused intravenously within 5 min followed by a 5-min washout before commencing the cardiopulmonary bypass (CPB). In the control group, a time-matched period of placebo infusion was given. Hemodynamic data and biochemical markers of myocardial injury were measured perioperatively., Results: There were no adverse effects related to diazoxide. Cardiac index (CI) increased postoperatively as compared with baseline. In the DZX group, the improvement of CI was better than that in the control group (p=0.001). Left and right ventricular stroke work indexes decreased postoperatively, and recovered much faster in the DZX group (p=0.027 and p=0.049, respectively). There were no statistically significant differences in the other hemodynamic parameters. The creatine kinase cardiac isoenzyme (CK-MB) was highest in both groups on the first postoperative day (control 28.8+/-23.8 and DZX 27.3+/-19.4, N.S.). The cumulative release of CK-MB postoperatively was lower in the DZX patients as compared with the controls, but the difference remained not significant (p=0.09)., Conclusions: Pharmacological preconditioning of the human heart with diazoxide is feasible; it confers additional myocardial protection beyond that provided by the cardioplegia alone by attenuating myocardial stunning after CABG operations.

Pericardial tamponade is a feared, though rare complication during myocardial infarction. We present a case of an unusual hemorrhagic appearance of pericardial fluid accumulation during ibuprofen overdose and myocardial infarction.

Objective: Improvement in survival and quality of life are the primary indications for coronary artery bypass graft (CABG) operations. Among elderly patients the main goal of surgery is not necessarily to prolong life, but to improve the health-related quality of life. Factors associated with mortality and morbidity following CABG surgery have been well defined, but the quality of life and functional capacity in elderly patients undergoing CABG are poorly documented. The aim here was to investigate changes in health-related quality of life, overall performance status and symptomatic status during 1 year after CABG surgery., Methods: Comprehensive data on 508 CABG patients were prospectively collected, including preoperative risk factors and postoperative morbidity in a surgical center and in all eighteen secondary referral hospitals up to discharge. The RAND-36 Health Survey (RAND-36) was used as indicator of quality of life. The primary outcome was change in the physical component summary, mental component summary and General Health summary scores from the RAND-36. Karnofsky dependency category was used to assess overall performance status, and symptomatic status was estimated according to New York Heart Association (NYHA) class. All assessments were made preoperatively and repeated 12 months later. Analysis was based on three age groups: 64 years or less (282 patients), 65-74 years (175 patients), and 75 or more years (51 patients)., Results: Thirty-day and 1-year survival rates were 98.2 and 96.7%, respectively. A great majority (86.4%) of the patients recovered without major complication. In all, the present data showed significant improvement in all eight domains of QOL as well as in functional capacity and NYHA class during the 1st year after CABG. However, the mean change in RAND-36 Mental Component Summary scores among patients aged 75 years or more did not reach a statistically significant level (P=0.097) and they had significantly minor improvement as compared to younger patients (P<0.05). Moreover, their General Health score improvement was poorer and statistically insignificant (P=0.817)., Conclusions: Elderly patients not only have higher mortality and morbidity but also derive less benefit from CABG regarding certain aspects of QOL.

Objectives: The aim of the present study was to evaluate the performance of three different preoperative risk models in the prediction of postoperative morbidity and mortality in coronary artery bypass (CAB) surgery., Methods: Data on 1132 consecutive CAB patients were prospectively collected, including preoperative risk factors and postoperative morbidity and in-hospital mortality. The preoperative risk models CABDEAL, EuroSCORE and Cleveland model were used to predict morbidity and mortality. A C statistic (receiver operating characteristic (ROC) curve) was used to test the discrimination of these models., Results: The area under the ROC curve for morbidity was 0.772 for the CABDEAL, 0.694 for the EuroSCORE and 0.686 for the Cleveland model. Major morbidity due to postoperative complications occurred in 268 patients (23.6%). The mortality rate was 3.4% (n=38 patients). The ROC curve areas for prediction of mortality were 0.711 for the CABDEAL, 0.826 for the EuroSCORE and 0.858 for the Cleveland model., Conclusions: The CABDEAL model was initially developed for the prediction of major morbidity. Thus, it is not surprising that this model evinced the highest predictive value for increased morbidity in this database. Both the Cleveland and the EuroSCORE models were better predictive of mortality. These results have implications for the selection of risk indices for different purposes. The simple additive CABDEAL model can be used as a hand-held model for preoperative estimation of patients' risk of postoperative morbidity, while the EuroSCORE and Cleveland models are to be preferred for the prediction of mortality in a large patient sample.

Faunistic information shows that Denmark, Norway, Sweden and Finland were colonized by an average of 2.8 species (winners) and lost 0.6 species (losers) per decade and country in 1850-1970. The smallest passerines had best changes of colonization, but body size and colonization success were not related in nonpasserines; extinctions were fairly common among the largest species. Turnover was highest in a faunal group derived from steppe regions and in widely but often patchily distributed species. Population trends were generally similar over a larger region. Species turnover has changed the total number of breeding pairs only a little, but the colonization rate has been highest after 1950, when quantitative population changes have also been extensive.Extinction was most often caused by persecution and/or habitat changes by man (e.g. destruction of old forests). As large nonpasserines are often hunted or persecuted, they were frequent among the losers, many of which have specialized habitat requirements and usually migrate to the tropics.Over 50 of the 88 winners have been favoured by man's direct measures, such as introductions (3 spp.), relaxed persecution, or improved food conditions. Habitat changes (eutrophication, reduced grazing, and conifer plantations) stand out as major factors and may subtly interact with population parameters. Perturbation of tropical habitats in this century may have benefitted many Palearctic winter visitors: the frequency of tropical migrants among the winners has increased from 10% before 1900 to 38% after 1900. Population changes in central parts of the range probably led to several colonizations and extinctions at the periphery.In theoretical terms, r-selected species (small body size, large clutch size) were often winners, while K-species comprised the bulk of the losers, but this is no more than a general trend. Judged by their faunal origin, species adapted to effective dispersal were often winners, but also seemed vulnerable to environmental deterioration. Because many winners have invaded habitats that have been available for a long time, North European bird communities are probably often unsaturated.

European data from 15 long-term censuses of breeding land bird communities were analysed in order to measure community stability. Stability was here operationally defined as year-to-year persistence of community structure (total density, number of species, diversity, evenness of the species-abundance distribution, species list, and frequencies of species). Central Europe and southern Scandinavia formed a zone of fairly stable communities, but more northern communities were fairly unstable. This result contrasts with several recent arguments, but accords well with the classic dogma that instability of biological communities increases northwards in the northern hemisphere.Three theoretical explanations for the difference in stability between northern and southern communities were explored, and causal mechanisms underlying the hypotheses were specified and tested. Considerable evidence supported the hypothesis that environmental (climatic) unpredictability increases northwards and mainly causes the phenomenon observed. Gradients in productivity may, perhaps in interaction with unpredictability, also contribute to geographical differences in stability, but tests suggested that low diversity is not an important cause of northern instability.