Most recently, the possible impact of transitions to and from daylight saving time (DST) on the increased incidence of acute myocardial infarction (AMI) has been suggested. The goal of this report was to analyze independent influence of DST transitions on the incidence of AMI with simultaneous control for the confounding presence of situational triggers such as physical exertion, emotional stress, heavy meals, and sexual intercourse, as well as for other clinical factors. Detailed information was obtained from 2412 patients and included baseline characteristics, working status, exact time of AMI, possible external triggers, cardiovascular risk factors, and prehospital medication. AMI incidence on days after the DST was compared with incidence during control periods and patient characteristics, cardiovascular medication, and circumstances of AMI were evaluated to identify potential risk modifiers. Relative risks of AMI and differences in patient characteristics were expressed through incidence ratios and odds ratios, respectively, with 95% confidence intervals (CIs). Multivariate analysis was performed by using a stepwise multiple regression to assess the independent predictive significance of the characteristics of patients for the AMI occurring in the posttransitional period. The incidence ratio for AMI for the first four workdays after the spring DST transition was 1.29 (95% CI: 1.09–1.49) and the excess was particularly prominent on Monday. In autumn, the incidence ratio for AMI for this 4-d period was 1.44 (95% CI: 1.19–1.69), with peaks on Tuesday and Thursday. The independent predictors for AMI during this period in spring were male sex (p = 0.03) and nonengagement in physical activity (p = 0.02) and there was a trend for the lower risk of incident among those taking calcium antagonists (p = 0.07). In autumn, the predictors were female sex (p = 0.04), current employment (p = 0.006), not taking β-blocker (p = 0.03), and nonengagement in physical activity (p = 0.02). The present report supports the possibility that DST transitions represent additional chronobiological feature of AMI, and that risk of an onset varies according to sex, employment status, and the taking of cardiovascular medication. (Author correspondence: viktor.culic@st.t-com.hr)

Background: Hyponatremia, a marker of disease severity and prognosis, has been associated with various clinical factors and drug use, especially diuretics. Methods: This observational prospective cohort study enrolled patients hospitalized at the University Hospital Center Split because of heart failure (HF). We investigated the association of clinical variables and cardiovascular drugs, including furosemide, hydrochlorothiazide, spironolactone, and their doses, with the presence of hyponatremia at admission. Results: Of the 565 included patients, 32.4% were hyponatremic, 62.6% were males, and the mean age was 73.1 ± 10.6 years. In the univariate analysis, hyponatremic patients were more often current smokers (p = 0.01), alcohol consumers (p = 0.01), receiving spironolactone (p = 0.004) or combination of furosemide and spironolactone (p = 0.003). Patients who received 50 and 100 mg of spironolactone, compared to those receiving 25 mg (p < 0.0001), as well as patients who received 250 to 500 mg of furosemide compared to ≤240 mg (p = 0.001), were significantly more often hyponatremic. In the multivariate analysis, when diuretic doses were accounted for, furosemide doses of 250 to 500 mg (p = 0.009), spironolactone doses of 50 to 100 mg (p = 0.0003), increasing age (p = 0.03), diabetes mellitus (p = 0.02) and alcohol consumption (p = 0.04) were independently associated with hyponatremia. Conclusion: High doses of furosemide and spironolactone, or concomitant use of these diuretics, seem to be an important cause of hyponatremia in HF patients, particularly in combination with advanced age, diabetes and alcohol consumption. Diuretic dose reduction may help avoid hyponatremia and improve clinical status and prognosis in such patients.

COVID-19-associated vascular disease complications are primarily associated with endothelial dysfunction; however, the consequences of disease on vascular structure and function, particularly in the long term (>7 weeks post-infection), remain unexplored. Individual pre- and post-infection changes in arterial stiffness as well as central and systemic hemodynamic parameters were measured in patients diagnosed with mild COVID-19. As part of in-laboratory observational studies, baseline measurements were taken up to two years before, whereas the post-infection measurements were made 2–3 months after the onset of COVID-19. We used the same measurement protocol throughout the study as well as linear and mixed-effects regression models to analyze the data. Patients (N = 32) were predominantly healthy and young (mean age ± SD: 36.6 ± 12.6). We found that various parameters of arterial stiffness and central hemodynamics—cfPWV, AIx@HR75, and cDBP as well as DBP and MAP—responded to a mild COVID-19 disease. The magnitude of these responses was dependent on the time since the onset of COVID-19 as well as age (p_{regression_models} ≤ 0.013). In fact, mixed-effects models predicted a clinically significant progression of vascular impairment within the period of 2–3 months following infection (change in cfPWV by +1.4 m/s, +15% in AIx@HR75, approximately +8 mmHg in DBP, cDBP, and MAP). The results point toward the existence of a widespread and long-lasting pathological process in the vasculature following mild COVID-19 disease, with heterogeneous individual responses, some of which may be triggered by an autoimmune response to COVID-19.