Background: Recently, several genome-wide association studies (GWAS) have independently found numerous loci at which common single-nucleotide polymorphisms (SNPs) modestly influence the risk of developing colorectal cancer. The aim of this study was to test 11 loci, reported to be associated with an increased or decreased risk of colorectal cancer: 8q23.3 (rs16892766), 8q24.21 (rs6983267), 9p24 (rs719725), 10p14 (rs10795668), 11q23.1 (rs3802842), 14q22.2 (rs4444235), 15q13.3 (rs4779584), 16q22.1 (rs9929218), 18q21.1 (rs4939827), 19q13.1 (rs10411210) and 20p12.3 (rs961253), in a Swedish-based cohort. Methods: The cohort was composed of 1786 cases and 1749 controls that were genotyped and analysed statistically. Genotype–phenotype analysis, for all 11 SNPs and sex, age of onset, family history of CRC and tumour location, was performed. Results: Of eleven loci, 5 showed statistically significant odds ratios similar to previously published findings: 8q23.3, 8q24.21, 10p14, 15q13.3 and 18q21.1. The remaining loci 11q23.1, 16q22.1, 19q13.1 and 20p12.3 showed weak trends but somehow similar to what was previously published. The loci 9p24 and 14q22.2 could not be confirmed. We show a higher number of risk alleles in affected individuals compared to controls. Four statistically significant genotype–phenotype associations were found; the G allele of rs6983267 was associated to older age, the G allele of rs1075668 was associated with a younger age and sporadic cases, and the T allele of rs10411210 was associated with younger age. Conclusions: Our study, using a Swedish population, supports most genetic variants published in GWAS. More studies are needed to validate the genotype–phenotype correlations.

Jim Fixx, the late author and jogging advocate, died of a massive heart attack while running. Several of his relatives reported that he had ignored certain signs of trouble shortness of breath, pain in the middle of the chest. How many others are ignoring similar warning signs? And what are the consequences? Statistics show that 20% of all cardiovascular disease-related deaths are due to sudden cardiac death. In some cases, there are no warning signs at all. The American Heart Association predicts that 1.5 million Americans will suffer heart attacks this year. Nearly a third will die.

Intravenous administration of 80 mg of recombinant tissue plasminogen activator (rt-PA, 40, 20, and 20 mg in successive hours) and streptokinase (SK, 1.5 million units over 1 hr) was compared in a double-blind, randomized trial in 290 patients with evolving acute myocardial infarction. These patients entered the trial within 7 hr of the onset of symptoms and underwent baseline coronary arteriography before thrombolytic therapy was instituted. Ninety minutes after the start of thrombolytic therapy, occluded infarct-related arteries had opened in 62% of 113 patients in the rt-PA and 31% of 119 patients in the SK group (p less than .001). Twice as many occluded infarct-related arteries opened after rt-PA compared with SK at the time of each of seven angiograms obtained during the first 90 min after commencing thrombolytic therapy. Regardless of the time from onset of symptoms to treatment, more arteries were opened after rt-PA than SK. The reduction in circulating fibrinogen and plasminogen and the increase in circulating fibrin split products at 3 and 24 hr were significantly less in patients treated with rt-PA than in those treated with SK (p less than .001). The occurrence of bleeding events, administration of blood transfusions, and reocclusion of the infarct-related artery was comparable in the two groups. Thus, in patients with acute myocardial infarction, rt-PA elicited reperfusion in twice as many occluded infarct-related arteries as compared with SK at each of seven serial observations during the first 90 min after onset of treatment.

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The concentration of fibrin split products (FSP) was measured, by using a modification of the staphylococcal clumping test, in 46 patients who had pulmonary angiography for suspected acute pulmonary embolism and in 12 normal control subjects. The concentration was significantly higher in 19 patients with angiographically documented pulmonary embolism (mean FSP, 158 µg/ml) than in 22 patients without (mean, 8 µg/ml; P < 0.001)—in 18 of the 19 patients the concentration was > 10 µg/ml; in 19 of the 22 patients without pulmonary embolism it was 10 µg/ml or less. The levels were highest in patients with acute symptoms (<3 days) and in those with significant increases in total pulmonary resistance, as measured at cardiac catheterization. Fibrin split products concentration seems to be increased (>10 µg/ml) in most patients with acute pulmonary embolism. We had only one false-negative finding; however, the specificity of an elevation of this variable in acute pulmonary embolism needs further assessment.

A prospective study of 50 consecutive patients undergoing cardiac valve replacement was designed to determine the incidence, types, and predisposing factors to postoperative arrhythmias. Patients were monitored continuously for the first 7 days following surgery. Thirty-seven patients (74%) experienced a total of 66 episodes of arrhythmia. Supra-ventricualr arrhythmias were the most common (43 of 66; 65%). The most frequent specific arrhythmia was atrial fibrillation (21 of 66; 32%). Arrhythmias occurred 77% of the time within the first 48 hours of surgery. Of 25 factors evaluated preoperatively in each patient, only two were found to predispose to postoperative arrhythmias. These were: (1) previous cardiac surgery; and (2) elevated blood urea nitrogen. There were four hospital deaths, representinig a hospital mortality of 8%. No deaths were due to a primary arrhythmia. It is concluded that whereas arrhythmias are a very common complication of cardiac valve replacement, early detection and treatment has lessened their significance as a cause of postoperative mortality and morbidity.