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.
BackgroundAcute kidney injury (AKI) has been associated with increased mortality in ST‐segment elevation myocardial infarction. We compared the mortality predictive accuracy of the 3 AKI definitions used most widely for patients with ST‐segment elevation myocardial infarction undergoing primary percutaneous coronary intervention.Methods and ResultsWe included 3771 patients with ST‐segment elevation myocardial infarction treated with primary percutaneous coronary intervention at 2 Italian hospitals. AKI incidence was evaluated according to creatinine increases of ≥25% (AKI‐25), ≥0.3 mg/dL (AKI‐0.3), and ≥0.5 mg/dL (AKI‐0.5). The primary end point was in‐hospital mortality. Overall, 557 (15%), 522 (14%), and 270 (7%) patients developed AKI‐25, AKI‐0.3, and AKI‐0.5, respectively (P<0.01). All AKI definitions independently predicted in‐hospital mortality (adjusted odds ratio 4.9 [95% CI 3.1–7.8], 5.4 [95% CI 3.3–8.6], and 8.3 [95% CI 5.1–13.3], respectively; P<0.01 for all). At receiver operating characteristic analysis, the addition of each AKI definition to combined clinical predictors of mortality (age, sex, left ventricular ejection fraction, admission creatinine, creatine kinase‐MB peak) found at stepwise analysis significantly improved mortality prognostication (area under the curve increased from 0.89 for clinical predictor combination alone to 0.92 for AKI‐25, 0.92 for AKI‐0.3, and 0.93 for AKI‐0.5; P<0.01 for all). At reclassification analysis, AKI‐0.5 added to clinical predictors, provided the highest score in mortality (net reclassification improvement +10% versus AKI‐0.3 [P=0.01] and +8% versus AKI‐25 [P=0.05]).ConclusionsEach AKI definition significantly improved the mortality prediction beyond major clinical variables. AKI‐0.5 showed a mortality discrimination advantage, suggesting it should be the preferred definition in studies addressing ST‐segment elevation myocardial infarction and focusing on short‐term mortality.
Background
Reliable preprocedural risk scores for the prediction of Contrast‐Induced Acute Kidney Injury (CI‐AKI) following Percutaneous Coronary Intervention (pPCI) in patients with ST‐elevation myocardial infarction (STEMI) are lacking. Aim of this study was to derive and validate a preprocedural Risk Score in this setting.
Methods
Two prospectively enrolled patient cohorts were used for derivation and validation (n = 3,736). CI‐AKI was defined as creatinine increase ≥0.5 mg/dl <72 h postpPCI. Odds ratios from multivariable logistic regression model were converted to an integer, whose sum represented the Risk Score.
Results
Independent CI‐AKI predictors were: diabetes, Killip class II‐III (2 points each), age > 75 years, anterior MI (3 points), Killip class IV (4 points), estimated GFR < 60 ml/min/1.73m2 (5 points). The Risk Score c‐statistic was 0.84 in both cohorts. Compared with patients with Risk Score ≤ 4, the relative risks of CI‐AKI among patients scoring 5–9 were 6.2 (derivation cohort) and 7.1 (validation cohort); among patients scoring ≥10, 19.8, and 21.4, respectively.
Conclusions
Among STEMI patients, a simple preprocedural Risk Score accurately and reproducibly predicted the risk of CI‐AKI, identifying ¼ of patients with a seven‐fold risk and 1/10 of patients with a 20‐fold risk. This knowledge may help tailored strategies, including delaying revascularization of nonculprit vessels in patients at high risk of CI‐AKI.
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