Phycotoxins are marine toxins produced by phytoplankton that can get accumulated in filter feeding shellfish. Human intoxication episodes occur due to contaminated seafood consumption. Okadaic acid (OA) and dynophysistoxins (DTXs) are phycotoxins responsible for a severe gastrointestinal syndrome called diarrheic shellfish poisoning (DSP). Yessotoxins (YTXs) are marine toxins initially included in the DSP class but currently classified as a separated group. Food safety authorities from several countries have regulated the content of DSPs and YTXs in shellfish to protect human health. In mice, OA and YTX have been associated with ultrastructural heart damage in vivo. Therefore, this study explored the potential of OA, DTX-1 and YTX to cause acute heart toxicity. Cardiotoxicity was evaluated in vitro by measuring hERG (human èter-a-go-go gene) channel activity and in vivo using electrocardiogram (ECG) recordings and cardiac damage biomarkers. The results demonstrated that these toxins do not exert acute effects on hERG channel activity. Additionally, in vivo experiments showed that these compounds do not alter cardiac biomarkers and ECG in rats acutely. Despite the ultrastructural damage to the heart reported for these toxins, no acute alterations of heart function have been detected in vivo, suggesting a functional compensation in the short term.

Electrocardiographic reference values were established on apparently healthy buzzards (Buteo buteo) in Lugo (Spain) from March 1997 to June 1999. All birds were anesthetized with isofluorane and placed in dorsal recumbence. The standard and augmented unipolar limb leads electrocardiograms were recorded in 65 buzzards. The wave forms were analyzed in lead II at 50 mm/sec and at 1 cm = 1 mV to determine P, PR, QRS, T and QT durations and P, QRS and T amplitudes. The polarity of each wave form was tabulated in all leads. The mean electrical axis (MEA) for the frontal plane was calculated using leads II and III. The mean heart rate was 325.2 +/- 52.9 beats/min. In lead II, the P wave was positive, the dominant pattern of QRS complex was QS and the T wave was always positive. The average value of the MEA was -99.2 +/- 7.7 degrees. Establishment of normal electrocardiogram (EKG) values will facilitate a better understanding of EKG changes seen in many diseases of these birds.

Electrocardiographic parameters were measured in 28 free-ranging roe deer (Capreolus capreolus). The electrocardiograms (ECGs) were recorded in base-apex lead, standard bipolar limb leads (I, II, III), and augmented unipolar limb leads (aVR, aVL, aVF). Morphology and amplitude of P waves, QRS complexes, and T waves were analyzed in all seven leads. Cardiac rhythm, heart rate, and durations of P, QRS, and T waves, PR interval, QTc interval, and ST segment were calculated in the base-apex lead. The mean electrical axis for each individual was determined from the net amplitude of the QRS complex in leads I and II. All of the animals had a sinus rhythm. Heart rates ranged from 60-180 beats per minute, with a mean +/- SD of 104.8 +/- 44.1. The electrical axis was 100 degrees-220 degrees, with a mean +/- SD of 169.5 degrees +/- 40.8 degrees. The base-apex lead provided the most uniform ECG patterns and higher mean amplitudes than did standard leads.

Background/Objectives: Traditionally, risk stratification in heart failure with reduced ejection fraction (HFrEF) patients has been a static process. This study aims to identify clinical predictors and causes of mortality at different stages of the disease, distinguishing between early mortality (≤1 year) and late mortality (>1 year), as well as cardiovascular and non-cardiovascular causes. Methods: This is an observational, longitudinal study of a cohort of 1510 patients with HFrEF followed up in a specialist heart failure unit between 2011 and 2023. Patients were categorized into three groups: alive (n = 1093), early mortality (n = 55) and late mortality (n = 362). Multivariate Cox regression models were used to identify mortality independent predictors in each period. Results: During the first year, cardiovascular and non-cardiovascular mortality showed a relatively balanced distribution, with a slight predominance of non-cardiovascular causes (52.8%). Progression of heart failure remained the leading individual cause of early death (38.2%). Independent predictors of early cardiovascular death included ischemic etiology (HR 2.78; 95% CI: 1.20–6.40; p = 0.01), NYHA functional class (HR 4.38; 95% CI: 2.18–8.81; p < 0.001) and renal function (HR 0.60; 95% CI: 0.44–0.84; p = 0.002). In contrast, late mortality (>1 year) was predominantly due to non-cardiovascular causes (59.7%), notably cancer (24.3%) and infections (7.5%). Late all-cause mortality was independently associated with age (HR 1.35; 95% CI: 1.17–1.56; p < 0.001), hypertension (HR 1.38; 95% CI: 1.06–1.81; p = 0.015) and ischemic etiology (HR 1.45; 95% CI: 1.16–1.80; p < 0.001). In the follow-up, the improvement of left ventricular ejection fraction (LVEF) emerged as a protective factor against long-term all-cause mortality (HR 0.77; 95% CI: 0.63–0.94; p = 0.01) and, even more markedly, against late cardiovascular mortality (HR 0.47; 95% CI: 0.33–0.66; p < 0.001), whereas baseline LVEF at diagnosis lacked significant predictive value in either model. Conclusions: Mortality in HFrEF is a dynamic process. Early survival is determined by hemodynamic stability, renal function and functional severity, whilst late survival is predominantly driven by non-cardiovascular comorbidities, biological aging, and ventricular remodeling trajectory. The improvement of LVEF during follow-up is a more reliable prognostic marker than the baseline measurement, suggesting that clinical management should shift from early pharmacological optimization towards a multidisciplinary approach focused on long-term non-cardiovascular risk.

In collaboration with the American College of Veterinary Radiology

Background/Objectives: Sex-related differences in prognosis among patients with heart failure with reduced ejection fraction (HFrEF) have been described, but their association with long-term all-cause and cardiovascular mortality remains incompletely characterised. This study investigated these associations in a real-world HFrEF cohort, accounting for non-cardiovascular death as a competing event. Methods: We conducted a single-centre, retrospective, longitudinal observational study of 1510 consecutive patients with HFrEF followed between 2011 and 2023; 1158 (76.7%) were men and 352 (23.3%) were women. All-cause mortality was assessed using Kaplan–Meier methods and Cox regression. Multivariable models used a complete-case approach. Cardiovascular mortality was analysed using cause-specific Cox regression and the Fine–Gray model, with non-cardiovascular death and death of unknown cause treated as competing events. Interaction terms between sex and year of inclusion were used to assess potential changes in the association across the study period. Results: No statistically significant between-sex difference in cumulative all-cause mortality was detected at one year (3.7% in men vs. 3.8% in women; p = 0.95). Exploratory pointwise comparisons showed higher cumulative mortality in men at five years (24.8% vs. 16.0%; p = 0.002) and ten years (49.3% vs. 39.8%; p = 0.046). After multivariable adjustment, male sex was associated with higher all-cause mortality (HR, 1.95; 95% CI, 1.47–2.59; p < 0.001). Male sex was also associated with cardiovascular mortality in the cause-specific analysis (HR, 2.46; 95% CI, 1.54–3.92; p < 0.001) and after accounting for non-cardiovascular death as a competing event (subdistribution HR, 2.12; 95% CI, 1.32–3.39; p = 0.002). No significant interaction was observed between sex and year of inclusion. Conclusions: In this real-world HFrEF cohort, male sex remained associated with higher all-cause and cardiovascular mortality after adjustment for measured baseline covariates. The association with cardiovascular mortality persisted in competing-risk analysis. These observational findings do not establish a causal or time-varying effect of sex.