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SummaryThe native fibrin gel structure formed in vitro from plasma samples was examined by liquid permeation of hydrated fibrin gel networks in 38 unselected men who had suffered a myocardial infarction before the age of 45 years and in 88 age-matched population-based control men. Both the fibrin gel porosity (permeability coefficient, Ks) and the calculated fiber mass-length ratio varied considerably within the two groups, but were generally lower in the patients. Ks was 8.3 ± 5.2 cm2 × 109 (mean ± SD) in the patient group and 12.5 ± 5.7cm2 × 109 among controls (p <0.001). The corresponding figures for fiber mass-length ratio were 13.1 ± 7.7 and 16.5 ± 7.5 Dalton/ cm × 10−13, respectively (p <0.01). Around 50% of the patients had Ks values below the 10th percentile of the control group. A strong inverse correlation was seen between plasma plasminogen activator inhibitor-1 (PAI-1) activity and Ks (r = -0.603, p <0.001) or fiber mass-length ratio (r = -0.565, p <0.001) in the patient group. Corresponding weaker associations of PAI-1 with fibrin gel properties were also present in the control group. In addition, inverse relationships of very low density lipoprotein (VLDL) triglyceride concentrations to Ks (r = -0.362, p <0.001) and fiber mass-length ratio (r = -0.283, p <0.01) were found among the controls. Proneness to formation of tight and rigid fibrin gel networks with abnormal architecture in vitro is in vivo associated with myocardial infarction at a young age. Impaired fibrinolytic function secondary to a raised plasma PAI-1 activity level is associated with abnormal fibrin gel structure.

The findings of increased risk associated with β2-adrenergic agonist agents together with stress related to affective disorders emphasize the pathogenic role of sympathetic stimulation. The prognosis regarding mortality is worse than in control subjects without CAD and similar to patients with CAD emphasizing the urgent need for studies on optimal treatment of TSC.

Background: A single-nucleotide polymorphism (SNP) in the promoter region of the interleukin-6 (IL-6) gene at position ؊174 (G>C) has been reported to be associated with a variety of major diseases, such as Alzheimer disease, atherosclerosis, and cardiovascular disease, cancer, non-insulin-dependent diabetes mellitus, osteoporosis, sepsis, and systemic-onset juvenile chronic arthritis. However, authors of previous in vitro and in vivo studies have reported conflicting results regarding the functionality of this polymorphism. We therefore aimed to clarify the role of the ؊174 SNP for the induction of IL-6 in vivo. Methods: We vaccinated 20 and 18 healthy individuals homozygous for the ؊174 C and G alleles, respectively, with 1 mL of Salmonella typhii vaccine. IL-1␤, IL-6, and tumor necrosis factor-␣ (TNF-␣) were measured in the blood at baseline and up to 24 h after vaccination. Results: Individuals with the G genotype had significantly higher plasma IL-6 values at 6, 8, and 10 h after vaccination than did individuals with the C genotype (P <0.005). There were no differences between the two genotypes regarding serum concentrations of IL-1␤ and TNF-␣ before or after vaccination. Conclusions: The ؊174 G>C SNP in the promoter region of the IL-6 gene is functional in vivo with an increased inflammatory response associated with the G

Takotsubo syndrome is a recently recognized acute cardiac disease entity with a clinical presentation resembling that of an acute coronary syndrome. The typical takotsubo syndrome patient has a unique circumferential left (bi-) ventricular contraction abnormality profile that extends beyond a coronary artery supply territory and appears to follow the anatomical cardiac sympathetic innervation. The syndrome predominantly affects postmenopausal women and is often preceded by emotional or physical stress. Patients with predisposing factors such as malignancy and other chronic comorbidities are more prone to suffer from takotsubo syndrome. The pathogenesis of takotsubo syndrome is elusive. Several pathophysiological mechanisms involving myocardial ischemia (multivessel coronary artery spasm, microvascular dysfunction, aborted myocardial infarction), left ventricular outlet tract obstruction, blood-borne catecholamine myocardial toxicity, epinephrine-induced switch in signal trafficking, and autonomic nervous system dysfunction have been proposed. The syndrome is usually reversible; nevertheless, during the acute stage, a substantial number of patients develop severe complications such as arrhythmias, heart failure including pulmonary edema and cardiogenic shock, thromboembolism, cardiac arrest, and rupture. Treatment of precipitating factors, predisposing diseases, and complications is fundamental during the acute stage of the disease. The epidemiology, pathogenesis, and management of takotsubo syndrome are reviewed in this paper.

This prospective, randomised trial suggests that postconditioning does not reduce infarct size in patients with STEMI in the overall study group. The data indicate that postconditioning may be of value in patients with large areas at risk. Clinical trial registration information Karolinska Clinical Trial Registration (http://www.kctr.se). Unique identifier: CT20080014.

In the present study, we found sustained inflammation due to NF-kappaB activation in human radiated arteries. The results are supported by previous in vitro findings suggesting that deoxyribonucleic acid injury, after radiation, activates NF-kappaB. We also suggest that HOXA9 might be involved in the regulation of NF-kappaB activation. The observed sustained inflammatory response can explain cardiovascular disease years after radiation.