BackgroundThe circadian clock influences a number of cardiovascular (patho)physiological processes including the incidence of acute myocardial infarction. A circadian variation in infarct size has recently been shown in rodents, but there is no clinical evidence of this finding. Objective To determine the impact of time-of-day onset of ST segment elevation myocardial infarction (STEMI) on infarct size. Methods A retrospective single-centre analysis of 811 patients with STEMI admitted between 2003 and 2009 was performed. Infarct size was estimated by peak enzyme release. The relationship between peak enzyme concentrations and time-of-day were characterised using multivariate regression splines. Time of STEMI onset was divided into four 6-hour periods in phase with circadian rhythms. Results Model comparisons based on likelihood ratio tests showed a circadian variation in infarct size across time-of-day as evaluated by peak creatine kinase (CK) and troponin-I (TnI) concentrations (p¼0.015 and p¼0.012, respectively). CK and TnI curves described similar patterns across time, with a global maximum in the 6:00enoon period and a local minimum in the noone18:00 period. Infarct size was largest in patients with STEMI onset in the dark-to-light transition period (6:00enoon), with an increase in peak CK and TnI concentrations of 18.3% (p¼0.031) and 24.6% (p¼0.033), respectively, compared with onset of STEMI in the 18:00emidnight period. Patients with anterior wall STEMI also had significantly larger infarcts than those with STEMI in other locations. Conclusions Significant circadian oscillations in infarct size were found in patients according to time-of-day of STEMI onset. The infarct size was found to be significantly larger with STEMI onset in the dark-to-light transition period (6:00enoon). If confirmed, these results may have a significant impact on the interpretation of clinical trials of cardioprotective strategies in STEMI.

Dysnatremia is associated with increased mortality in patients with community-acquired pneumonia. SARS-COV2 (Severe-acute-respiratory syndrome caused by Coronavirus-type 2) pneumonia can be fatal. The aim of this study was to ascertain whether admittance dysnatremia is associated with mortality, sepsis, or intensive therapy (IT) in patients hospitalized with SARS-COV2 pneumonia. This is a retrospective study of the HOPE-COVID-19 registry, with data collected from January 1th through April 31th, 2020. We selected all hospitalized adult patients with RT-PCR-confirmed SARS-COV2 pneumonia and a registered admission serum sodium level (SNa). Patients were classified as hyponatremic (SNa <135 mmol/L), eunatremic (SNa 135–145 mmol/L), or hypernatremic (SNa >145 mmol/L). Multivariable analyses were performed to elucidate independent relationships of admission hyponatremia and hypernatremia, with mortality, sepsis, or IT during hospitalization. Four thousand six hundred sixty-four patients were analyzed, median age 66 (52–77), 58% males. Death occurred in 988 (21.2%) patients, sepsis was diagnosed in 551 (12%) and IT in 838 (18.4%). Hyponatremia was present in 957/4,664 (20.5%) patients, and hypernatremia in 174/4,664 (3.7%). Both hyponatremia and hypernatremia were associated with mortality and sepsis. Only hyponatremia was associated with IT. In conclusion, hyponatremia and hypernatremia at admission are factors independently associated with mortality and sepsis in patients hospitalized with SARS-COV2 pneumonia.Clinical Trial Registrationhttps://clinicaltrials.gov/ct2/show/NCT04334291, NCT04334291.

Background Coronavirus disease 2019 (COVID-19) is a disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Despite its international aggressive extension, with a significant morbidity and mortality, the impact of renal function on its prognosis is uncertain. Methods Analysis from the international HOPE-Registry (NCT04334291). The objective was to evaluate the association between kidney failure severity on admission with the mortality of patients with SARS-CoV-2 infection. Patients were categorized in 3 groups according to the estimated glomerular filtration rate on admission (eGFR > 60 mL/min/1.73 m 2 , eGFR 30-60 mL/min/1.73 m 2 and eGFR < 30 mL/min/1.73 m 2 ). Results 758 patients were included: mean age was 66 ± 18 years, and 58.6% of patient were male. Only 8.5% of patients had a history of chronic kidney disease (CKD); however, 30% of patients had kidney dysfunction upon admission (eGFR < 60 mL/ min/1.73 m 2 ). These patients received less frequently pharmacological treatment with hydroxychloroquine or antivirals and had a greater number of complications such as sepsis (11.9% vs 26.4% vs 40.8%, p < 0.001) and respiratory failure (35.4% vs 72.2% vs 62.0%, p < 0.001) as well as a higher in-hospital mortality rate (eGFR > 60 vs eGFR 30-60 vs and eGFR < 30, 18.4% vs 56.5% vs 65.5%, p < 0.001). In multivariate analysis: age, hypertension, renal function, 0 2 saturation < 92% and lactate dehydrogenase elevation on admission independently predicted all-cause mortality. Conclusions Renal failure on admission in patients with SARS-CoV-2 infection is frequent and is associated with a greater number of complications and in-hospital mortality. Our data comes from a multicenter registry and therefore does not allow to have a precise mortality risk assessment. More studies are needed to confirm these findings.

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The readmission burden after TAVR in an all-comers population was high. Nearly one-fifth of the patients were readmitted early after hospital discharge, increasing the risk of mortality at follow-up. Reasons for readmission were split between noncardiac and cardiac causes, with respiratory causes and heart failure as the main diagnoses in each group, respectively. Whereas early readmissions were mainly related to periprocedural bleeding events, most late readmissions were secondary to baseline patient comorbidities. These results underscore the importance of and provide the basis for implementing specific preventive measures to reduce readmission rates after TAVR.

CMD decreases the diagnostic performance of QFR. However, even in the presence of CMD, QFR remains superior to angiography alone in ascertaining functional stenosis severity.

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Background The coronavirus disease 2019 (COVID-19) is characterized by poor outcomes and mortality, particularly in older patients. Methods Post-hoc analysis of the international, multicentre, “real-world” HOPE COVID-19 registry. All patients aged ≥65 years hospitalised for COVID-19 were selected. Epidemiological, clinical, analytical and outcome data were obtained. A comparative study between two age subgroups, 65–74 and ≥75 years, was performed. The primary endpoint was all cause in-hospital mortality. Results 1,520 patients aged ≥65 years (60.3% male, median age of 76 [IQR 71–83] years) were included. Comorbidities such as hypertension (69.2%), dyslipidemia (48.6%), cardiovascular diseases (any chronic heart disease in 38.4% and cerebrovascular disease in 12.5%), and chronic lung disease (25.3%) were prevalent, and 49.6% were on ACEI/ARBs. Patients aged 75 years and older suffered more in-hospital complications (respiratory failure, heart failure, renal failure, sepsis) and a significantly higher mortality (18.4 vs. 48.2%, P &lt; 0.001), but fewer admissions to intensive care units (11.2 vs. 4.8%). In the overall cohort, multivariable analysis demonstrated age ≥75 (OR 3.54), chronic kidney disease (OR 3.36), dementia (OR 8,06), peripheral oxygen saturation at admission &lt;92% (OR 5.85), severe lymphopenia (&lt;500/mm3) (OR 3.36) and qSOFA (Quick Sequential Organ Failure Assessment Score) &gt;1 (OR 8.31) to be independent predictors of mortality. Conclusion Patients aged ≥65 years hospitalised for COVID-19 had high rates of in-hospital complications and mortality, especially among patients 75 years or older. Age ≥75 years, dementia, peripheral oxygen saturation &lt;92%, severe lymphopenia and qSOFA scale &gt;1 were independent predictors of mortality in this population.