BackgroundCoronavirus disease 2019 (COVID-19) has spread worldwide determining a dramatic impact on the healthcare system. Aim of this study is to evaluate mid-term clinical impact of COVID-19 on respiratory function.Methods379 patients were evaluated 4 months after SARS-COV-2 diagnosis. Patients were divided in two groups based on the presence of pneumonia during COVID. Clinical conditions, quality of life, symptomatology, 6-min walking test, pulmonary function test with spirometry and diffusing capacity of carbon monoxide were analysed. Data were compared to clinical evolution during COVID (development of acute respiratory distress syndrome [ARDS], needing of invasive mechanical ventilation [IMV], partial oxygen saturation/ fraction of inspired oxygen [SpO2/FiO2] ratio and pneumonia severity index [PSI]).ResultsAfter a median of 135 days, 260 (68.6%) of 379 patients referred almost one symptom. Patients who developed pneumonia during COVID-19 showed lower SpO2 at rest (p<0.001), SpO2 during 6-min walking test (p<0.001), total lung capacity (p<0.001), airway occlusion pressure after 0.1 s [P0.1] (p=0.02), P0.1/maximal inspiratory pressure [MIP] ratio (p=0.005) and higher Borg category-ratio scale (p=0.006) and modified Medical Research Council breathlessness scale (p=0.003), compared to patients without pneumonia. SpO2/FiO2 ratio and PSI during SARS-COV-2 pneumonia were directly associated with mid-term alteration of partial oxygen saturation at rest (p<0.001), SpO2 during 6-min walking test (p<0.001), residual volume (p<0.001), total lung capacity (respectively p<0.001 and p=0.003) and forced vital capacity (respectively p=0.004, p=0.03).ConclusionLung damage during COVID-19 correlates to the reduction of pulmonary function after 4 months from acute infection.

Background Coronavirus disease 2019 (COVID-19) has spread worldwide determining dramatic impacts on healthcare systems. Early identification of high-risk parameters is required in order to provide the best therapeutic approach. Coronary, thoracic aorta and aortic valve calcium can be measured from a non-gated chest computer tomography (CT) and are validated predictors of cardiovascular events and all-cause mortality. However, their prognostic role in acute systemic inflammatory diseases, such as COVID-19, has not been investigated. Objectives The aim was to evaluate the association of coronary artery calcium and total thoracic calcium on in-hospital mortality in COVID-19 patients. Methods 1093 consecutive patients from 16 Italian hospitals with a positive swab for COVID-19 and an admission chest CT for pneumonia severity assessment were included. At CT, coronary, aortic valve and thoracic aorta calcium were qualitatively and quantitatively evaluated separately and combined together (total thoracic calcium) by a central Core-lab blinded to patients’ outcomes. Results Non-survivors compared to survivors had higher coronary artery [Agatston (467.76±570.92 vs 206.80±424.13 mm 2 , p<0.001); Volume (487.79±565.34 vs 207.77±406.81, p<0.001)], aortic valve [Volume (322.45±390.90 vs 98.27±250.74 mm2, p<0.001; Agatston 337.38±414.97 vs 111.70±282.15, p<0.001)] and thoracic aorta [Volume (3786.71±4225.57 vs 1487.63±2973.19 mm2, p<0.001); Agatston (4688.82±5363.72 vs 1834.90±3761.25, p<0.001)] calcium values. Coronary artery calcium (HR 1.308; 95% CI, 1.046 - 1.637, p=0.019) and total thoracic calcium (HR 1.975; 95% CI, 1.200 - 3.251, p=0.007) resulted to be independent predictors of in-hospital mortality. Conclusion Coronary, aortic valve and thoracic aortic calcium assessment on admission non-gated CT permits to stratify the COVID-19 patients in-hospital mortality risk.

Background and aims The potential impact of coronary atherosclerosis, as detected by coronary artery calcium, on clinical outcomes in COVID-19 patients remains unsettled. We aimed to evaluate the prognostic impact of clinical and subclinical coronary artery disease (CAD), as assessed by coronary artery calcium score (CAC), in a large, unselected population of hospitalized COVID-19 patients undergoing non-gated chest computed tomography (CT) for clinical practice. Methods SARS-CoV 2 positive patients from the multicenter (16 Italian hospitals), retrospective observational SCORE COVID-19 (calcium s core for CO VID-19 R isk E valuation) registry were stratified in three groups: (a) “clinical CAD” (prior revascularization history), (b) “subclinical CAD” (CAC >0), (c) “No CAD” (CAC = 0). Primary endpoint was in-hospital mortality and the secondary endpoint was a composite of myocardial infarction and cerebrovascular accident (MI/CVA). Results Amongst 1625 patients (male 67.2%, median age 69 [interquartile range 58–77] years), 31%, 57.8% and 11.1% had no, subclinical and clinical CAD, respectively. Increasing rates of in-hospital mortality (11.3% vs. 27.3% vs. 39.8%, p < 0.001) and MI/CVA events (2.3% vs. 3.8% vs. 11.9%, p < 0.001) were observed for patients with no CAD vs. subclinical CAD vs clinical CAD, respectively. The association with in-hospital mortality was independent of in-study outcome predictors (age, peripheral artery disease, active cancer, hemoglobin, C-reactive protein, LDH, aerated lung volume): subclinical CAD vs. No CAD: adjusted hazard ratio (adj-HR) 2.86 (95% confidence interval [CI] 1.14–7.17, p= 0.025); clinical CAD vs. No CAD: adj-HR 3.74 (95% CI 1.21–11.60, p= 0.022). Among patients with subclinical CAD, increasing CAC burden was associated with higher rates of in-hospital mortality (20.5% vs. 27.9% vs. 38.7% for patients with CAC score thresholds≤100, 101–400 and > 400, respectively, p < 0.001). The adj-HR per 50 points increase in CAC score 1.007 (95%CI 1.001–1.013, p= 0.016). Cardiovascular risk factors were not independent predictors of in-hospital mortality when CAD presence and extent were taken into account. Conclusions The presence and extent of CAD are associated with in-hospital mortality and MI/CVA among hospitalized patients with COVID-19 disease and they appear to be a better prognostic gauge as compared to a clinical cardiovascular ri...

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The relationship between arterial stiffness, measured as pulse wave velocity (PWV), and the left ventricle is confounded by the effects of blood pressure. We evaluated the relationship between carotid-femoral PWV and cardio-ankle vascular index (CAVI), a less pressure-dependent measurement of the stiffness constant (β) of the aorta and the iliac, femoral and tibial arteries, and obtained prognostically relevant measurements of left ventricular structure and systolic function. CAVI, carotid-femoral PWV and echocardiographic left ventricular mass and systolic function were determined in 133 subjects with either hypertension or high-normal blood pressure (33% treated; 56 ± 16 years, blood pressure 145/89 ± 21/12 mm Hg). Carotid-femoral PWV exhibited a direct relationship with systolic and diastolic blood pressure (r = 0.33/0.26, P < 0.001/0.014), whereas CAVI demonstrated no such relationship (r = 0.12/-0.05, both P > 0.1). Both CAVI and PWV correlated significantly with left ventricular mass index (r = 0.31, P<0.001; r = 0.21, P = 0.014). Subjects with inappropriately high left ventricular masses for a given cardiac workload (n = 44) had higher CAVI values (9.1 ± 2.0 vs. 7.9 ± 1.6, P < 0.001), but not higher PWV values (8.5 ± 2.5 vs. 8.7 ± 2.4, P>0.1). In a multivariate regression model, CAVI was independently associated with inappropriate left ventricular mass (β = 0.40, P < 0.001), along with body mass index. CAVI also demonstrated a negative relationship with left ventricular midwall fractional shortening (r = -0.41, P = 0.001) that was independent of age, sex, blood pressure and left ventricular mass in a multivariate analysis. In conclusion, a high CAVI is associated with inappropriately high left ventricular mass and low midwall systolic function. As a marker of arterial diastolic-to-systolic stiffening, CAVI may have a relationship with left ventricular structure and function that is independent of blood pressure levels.