Aims An increase in out-of-hospital cardiac arrest (OHCA) incidence has been reported in the very early phase of the COVID-19 epidemic, but a clear demonstration of a correlation between the increased incidence of OHCA and COVID-19 is missing so far. We aimed to verify whether there is an association between the OHCA difference compared with 2019 and the COVID-19 epidemic curve. Methods and results We included all the consecutive OHCAs which occurred in the Provinces of Lodi, Cremona, Pavia, and Mantova in the 2 months following the first documented case of COVID-19 in the Lombardia Region and compared them with those which occurred in the same time frame in 2019. The cumulative incidence of COVID-19 from 21 February to 20 April 2020 in the study territory was 956 COVID-19/100 000 inhabitants and the cumulative incidence of OHCA was 21 cases/100 000 inhabitants, with a 52% increase as compared with 2019 (490 OHCAs in 2020 vs. 321 in 2019). A strong and statistically significant correlation was found between the difference in cumulative incidence of OHCA between 2020 and 2019 per 100 000 inhabitants and the COVID-19 cumulative incidence per 100 000 inhabitants both for the overall territory (ρ 0.87, P < 0.001) and for each province separately (Lodi: ρ 0.98, P < 0.001; Cremona: ρ 0.98, P < 0.001; Pavia: ρ 0.87, P < 0.001; Mantova: ρ 0.81, P < 0.001). Conclusion The increase in OHCAs in 2020 is significantly correlated to the COVID-19 pandemic and is coupled with a reduction in short-term outcome. Government and local health authorities should seriously consider our results when planning healthcare strategies to face the epidemic, especially considering the expected recurrent outbreaks.

In vitro studies suggested that glucose metabolism through the oxidative pentose phosphate pathway (oxPPP) can paradoxically feed superoxide-generating enzymes in failing hearts. We therefore tested the hypothesis that acute inhibition of the oxPPP reduces oxidative stress and enhances function and metabolism of the failing heart, in vivo. In 10 chronically instrumented dogs, congestive heart failure (HF) was induced by high-frequency cardiac pacing. Myocardial glucose consumption was enhanced by raising arterial glycemia to levels mimicking postprandial peaks, before and after intravenous administration of the oxPPP inhibitor 6-aminonicotinamide (80 mg/kg). Myocardial energy substrate metabolism was measured with radiolabeled glucose and oleic acid, and cardiac 8-isoprostane output was used as an index of oxidative stress. A group of five chronically instrumented, normal dogs served as control. In HF, raising glycemic levels from ∼ 80 to ∼ 170 mg/dL increased cardiac isoprostane output by approximately twofold, whereas oxPPP inhibition normalized oxidative stress and enhanced cardiac oxygen consumption, glucose oxidation, and stroke work. In normal hearts glucose infusion did not induce significant changes in cardiac oxidative stress. Myocardial tissue concentration of 6P-gluconate, an intermediate metabolite of the oxPPP, was significantly reduced by ∼ 50% in treated versus nontreated failing hearts, supporting the inhibitory effect of 6-aminonicotinamide. Our study indicates an important contribution of the oxPPP activity to cardiac oxidative stress in HF, which is particularly pronounced during common physiological changes such as postprandial glycemic peaks.

Key points• Whereas the effects of catecholamines on myocardial metabolism are well characterized, the potential role of the parasympathetic system is generally considered minor or absent.• We tested the hypothesis that acute stimulation of the right vagus nerve alters the balance between cardiac free fatty acid and carbohydrate oxidation and opposes the metabolic effects of beta-adrenergic stimulation.• Using a clinical-type selective stimulator of the vagal efferent fibers in dogs, we found that vagal stimulation did not significantly affect baseline cardiac performance, haemodynamics and myocardial metabolism.• During dobutamine stress, vagal stimulation attenuated the increase in left ventricular mechanical performance, cardiac oxygen consumption and myocardial glucose oxidation, while free fatty acid oxidation was affected only at low catecholamine dose.• Our results elucidate a previously unexplored parasympathetic function, indicating that selective vagal efferent stimulation antagonizes the effects of beta-adrenergic activation on myocardial metabolism. AbstractThe effects of vagal stimulation (VS) on cardiac energy substrate metabolism are unknown. We tested the hypothesis that acute VS alters the balance between free fatty acid (FFA) and carbohydrate oxidation and opposes the metabolic effects of β-adrenergic stimulation. A clinical-type selective stimulator of the vagal efferent fibres was connected to the intact right vagus in chronically instrumented dogs. VS was set to reduce heart rate by 30 beats min −1 , and the confounding effects of bradycardia were then eliminated by pacing the heart at 165 beats min −1 . [ 3 H]Oleate and [ 14 C]glucose were infused to measure FFA and glucose oxidation. The heart was subjected to β-adrenergic stress by infusing dobutamine at 5, 10 and 15 μg kg −1 min −1 before and during VS. VS did not significantly affect baseline cardiac performance, haemodynamics or myocardial metabolism. However, at peak dobutamine stress, VS attenuated the increase in left ventricular pressure-diameter area from 235.9 ± 72.8 to 167.3 ± 55.8%, and in cardiac oxygen consumption from 173.9 ± 23.3 to 127.89 ± 6.2% (both P < 0.05), and thus mechanical efficiency was not enhanced. The increase in glucose oxidation fell from 289.3 ± 55.5 to 131.1 ± 20.9% (P < 0.05), while FFA oxidation was not increased by β-adrenergic stress and fell below baseline during VS only at the lowest dose of dobutamine. The functional and in part the metabolic changes were reversed by 0.1 mg kg −1 atropine I.V. Our data show that acute right VS does not affect baseline cardiac metabolism, but attenuates myocardial oxygen consumption and glucose oxidation in response to adrenergic stress, thus functioning as a cardio-selective antagonist to β-adrenergic activation.

A total of 749 workers (males: 139 aged between 15 and 35 years, and 171 aged > 35 years; females: 176 aged between 15 and 35 years, and 263 aged > 35 years) performing tasks not at risk for work-related musculoskeletal disorders of the upper limbs (WMSDs) underwent a clinical examination using a standardized method. The 'anamnestic cases' were defined on the basis of pain or paraesthesia present for at least 1 week during the previous 12 months, or appearing at least once a month, and not subsequent to acute trauma. The anamnestic cases among the males amounted to 4.4% (age 15-35 years) and 12.3% (age > 35 years); among the females, 4.6% (age 15-35 years) and 14.2% (age > 35 years). Of the 1498 limbs examined, the prevalent diseases reported were: suspect narrow chest syndrome: 0.3% among the males > 35 years, 0.6% among the females aged 15-35 years, 1% among the females > 35 years; scapulo-humeral periarthritis: 0.3% among the males aged > 35 years, 0.3% among the females aged 15-35 years, 1.3% among the females aged > 35 years; lateral epicondylitis: 0.3% among the males aged > 35 years, 0.2% among the females aged > 35 years; trapeziometacarpal arthrosis: 0.8% among the females aged > 35 years; wrist-hand tendinitis: 0.9% among the males aged > 35 years, 0.9% among the females aged 15-35 years; carpal tunnel syndrome: 2.5% among the females aged > 35 years. No disorders were detected outside the age ranges indicated. Several workers reported more than one disorder. The number of workers with at least one WMSD was: males 0% in the 15-35 years age range, 3.5% in the > 35 years age range; females 2.3% in the 15-35 years age range, 7.2% in the > 35 year age range; 3.9% of the total sample population. The prevalences were on average quite low, particularly among the older workers, hence the authors recommend that even minimal prevalences detected in particular work environments should not be underestimated.

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