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Background: Cardiovascular disease and cancer have been described as possible risk factors for COVID-19 mortality. The purpose of this study was to investigate whether a history of cardiovascular disease or cancer affects the risk of dying after a COVID-19 diagnosis in Norway., Material and Method: Data were compiled from the Norwegian Surveillance System for Communicable Diseases, the Norwegian Cardiovascular Disease Registry and the Cancer Registry of Norway. Univariable and multivariable regression models were used to calculate both relative and absolute risk., Results: In the first half of 2020, 8 809 people tested positive for SARS-CoV-2 and 260 COVID-19-associated deaths were registered. Increasing age, male sex (relative risk (RR): 1.5; confidence interval (CI): 1.2-2.0), prior stroke (RR: 1.5; CI: 1.0-2.1) and cancer with distant metastasis at the time of diagnosis (RR: 3.0; CI: 1.1-8.2) were independent risk factors for death after a diagnosis of COVID-19. After adjusting for age and sex, myocardial infarction, atrial fibrillation, heart failure, hypertension, and non-metastatic cancer were no longer statistically significant risk factors for death., Interpretation: The leading risk factor for death among individuals who tested positive for SARS-CoV-2 was age. Male sex, and a previous diagnosis of stroke or cancer with distant metastasis were also associated with an increased risk of death after a COVID-19 diagnosis.

Background: ST-elevation myocardial infarction is treated with reperfusion, either in the form of primary percutaneous coronary intervention (PCI) or thrombolytic therapy. The choice of treatment depends on transport time to the nearest PCI centre. Norway's geography means that thrombolytic therapy will be appropriate for many patients. Irrespective of treatment choice, it is important to avoid delays. We wished to compare the outcomes of primary PCI and thrombolytic therapy in our healthcare region and to examine whether reperfusion therapy was administered within the recommended time window., Material and Method: Using registry data and patient medical records, we compared the outcomes of primary PCI and thrombolytic therapy in cases of ST-elevation myocardial infarction in the Central Norway Regional Health Authority in the period 2015-16. The outcomes analysed were 30-day mortality, ejection fraction measured by echocardiography during the hospital stay, incidence of bleeding complications, and time from diagnosis to start of treatment., Results: The study population comprised 648 patients with ST-elevation myocardial infarction. Of these, 382 were treated with primary PCI and 266 received thrombolytic therapy. The 30-day mortality was 5.5 % in the primary PCI group and 5.6 % in the thrombolysis group (p = 1.0). There were no significant differences in ejection fraction and no cases of serious bleeding. In 45 % of the total population, reperfusion therapy was started later than recommended in guidelines., Interpretation: There was no statistically significant difference in mortality or ejection fraction when comparing primary PCI and thrombolytic therapy in an unselected population with ST-elevation myocardial infarction. Many patients experienced delayed start of treatment . It is important to take action to reduce delays at all stages of the therapeutic chain. Thrombolytic therapy should be considered when it is unclear whether transport time to a PCI centre will exceed that recommended in guidelines.

One of the most interesting aspects of coronary heart disease epidemiology is the gender difference: in all age groups women have lower risk of myocardial infarction compared to men. Epidemiological observations and results of recent controlled clinical trials suggest that it is not oestrogen that protects women. In this paper an alternative hypothesis is suggested: Men are at increased risk of coronary death and myocardial infarction because they are more prone than women to develop lipid-loaded, unstable coronary atherosclerotic plaques. This may be caused by gender differences in plasma levels of high density lipoprotein cholesterol, which is influenced by the blood testosterone level.