Stefano Coiro

Aims: Acute heart failure (AHF) and respiratory infection (RI) frequently coexist, with the latter commonly regarded as a trigger of AHF decompensation. However, the independent and combined prognostic impact of these conditions on survival is not well studied. We therefore assessed the association of AHF and RI, both separately and in combination, with subsequent mortality. Methods: Patients discharged with diagnoses of AHF, RI, or both were identified from the PARADISE study, a large cohort of patients hospitalized for acute dyspnoea. Associations with in-hospital and post-discharge mortality were assessed using multivariable binomial logistic regression and Cox proportional hazards models, respectively. Results: Among 11 679 patients, 4349 (37%) had AHF alone, 5091 (44%) had RI alone, and 2239 (19%) had both AHF and RI. In-hospital mortality was highest in patients with concomitant AHF and RI (21.9%), whereas post-discharge mortality was highest among those with AHF (55.2%). After multivariable adjustment, the coexistence of AHF and RI was associated with higher in-hospital mortality compared with AHF alone (adjusted OR [aOR]: 1.62, 1.33–1.98, P < .001), but not with higher post-discharge mortality (adjusted HR [aHR]: 0.99, 0.88–1.11, P = .9). Compared with AHF alone, RI alone was not associated with a higher risk of death both during hospitalization (aOR 1.11, 0.89–1.39, P = .3) and after discharge (aHR 1.07, 0.97–1.17, P = .2). Results from sensitivity analyses including natriuretic peptides confirmed those results. Conclusion: Patients with concomitant AHF and RI showed an increased in-hospital risk but no excess post-discharge risk compared with AHF alone, whereas RI alone is not associated with increased mortality both in-hospital and post-discharge.

Lung ultrasound (LUS) is an effective tool for diagnosing acute heart failure (AHF). However, several imaging protocols currently exist and how to best use LUS remains undefined. We aimed at developing a lung ultrasound-based model for AHF diagnosis using machine learning. Random forest and decision trees were generated using the LUS data (via an 8-zone scanning protocol) in patients with acute dyspnea admitted to the Emergency Department (PLUME study, N = 117) and subsequently validated in an external dataset (80 controls from the REMI study, 50 cases from the Nancy AHF cohort). Using the random forest model, total B-line sum (i.e., in both hemithoraces) was the most significant variable for identifying AHF, followed by the difference in B-line sum between the superior and inferior lung areas. The decision tree algorithm had a good diagnostic accuracy [area under the curve (AUC) = 0.865] and identified three risk groups (i.e., low 24%, high 70%, and very high-risk 96%) for AHF. The very high-risk group was defined by the presence of 14 or more B-lines in both hemithoraces while the high-risk group was described as having either B-lines mostly localized in superior points or in the right hemithorax. Accuracy in the validation cohort was excellent (AUC = 0.906). Importantly, adding the algorithm on top of a validated clinical score and classical definition of positive LUS scanning for AHF resulted in a significant improvement in diagnostic accuracy (continuous net reclassification improvement = 1.21, P < 0.001). Our simple lung ultrasound-based machine learning algorithm features an excellent performance and may constitute a validated strategy to diagnose AHF.

Background Diagnosis of heart failure with preserved ejection fraction (HFpEF) remains challenging despite the use of scores/algorithms. This study intended to assess the diagnostic value of exercise lung ultrasound (LUS) for HFpEF diagnosis. Methods We studied two independent case–control studies of HFpEF patients and control subjects undergoing different exercise protocols: (i) submaximal exercise stress echocardiography (ESE) with LUS performed by expert cardiologists (N = 116, HFpEF = 65.5%), and (ii) maximal cycle ergometer test (CET) (N = 54, HFpEF = 50%) with LUS performed by unexperienced physicians shortly trained for the study. B-line kinetics (i.e. peak values and their changes from rest) were assessed. Results In the ESE cohort, the C-index (95% CI) of peak B-lines for HFpEF diagnosis was 0.985 (0.968–1.000), whereas the C-index of rest and exercise HFA-PEFF scores (i.e. including stress echo findings) were < 0.90 (CI 0.823–0.949), and that of H2FPEF score was < 0.70 (CI 0.558–0.764). The C-index increase of peak B-lines on top of the above-mentioned scores was significant (C-index increase > 0.090 and P-value < 0.001 for all). Similar results were observed for change B-lines. Peak B-lines > 5 (sensitivity = 93.4%, specificity = 97.5%) and change B-lines > 3 (sensitivity = 94.7%, specificity = 87.5%) were the best cutoffs for HFpEF diagnosis. Adding peak or change B-lines on top of HFpEF scores and BNP significantly improved diagnostic accuracy. Peak B-lines showed a good diagnostic accuracy in the LUS beginner-led CET cohort (C-index = 0.713, 0.588–0.838). Conclusions Exercise LUS showed excellent diagnostic value for HFpEF diagnosis regardless of different exercise protocols/level of expertise, with additive diagnostic accuracy on top of available scores and natriuretic peptides. Graphical abstract

Background Loop diuretics are the mainstay of congestion treatment in patients with heart failure (HF). We assessed the association between baseline loop diuretic use and outcome. We also compared the increment in risk related to diuretic dose with conventional prognostic enrichment criteria used in the EMPHASIS-HF trial, which included patients with systolic HF and mild symptoms, such as prior hospitalization and elevated natriuretic peptides. Methods Individual analyses were performed according to baseline loop diuretic usage (furosemide-equivalent dose > 40 mg, 1–40 mg, and no furosemide), and according to enrichment criteria adopted in the trial [i.e. recent hospitalization (< 30 days or 30 to 180 days prior to randomization) due to HF or other cardiovascular cause, or elevated natriuretic peptides]. The primary endpoint was a composite of cardiovascular death or HF hospitalization. Results Loop diuretic usage at baseline (HR for > 40 mg furosemide-equivalent dose = 3.16, 95% CI 2.43–4.11; HR for 1–40 mg = 2.06, 95% CI 1.60–2.65) was significantly associated with a higher risk for the primary endpoint in a stepwise manner when compared to no baseline loop diuretic usage. In contrast, the differences in outcome rates were more modest when using history of hospitalization and/or BNP: all HR ranged from 1 (reference, non-HF related CV hospitalization > 30 days) to 2.04 (HF hospitalization < 30 days). The effect of eplerenone on the primary endpoint was consistent across subgroups in both analyses (P for interaction ≥ 0.2 for all). Conclusions Loop diuretic usage (especially at doses > 40 mg) identified patients at higher risk than history of HF hospitalization and/or high BNP blood concentrations. Graphic abstract

Pneumonia is the most commonly described manifestation of Legionella pneumophila infection (legionellosis), and extrapulmonary manifestations are uncommon. There are a few descriptions of acute myocarditis associated with legionellosis. We present a case of acute myocarditis in a patient admitted for legionellosis with multisystemic involvement (lung, heart, and kidney). Left ventricular (LV) dysfunction was documented by cardiac magnetic resonance (CMR) and two-dimensional speckle-tracking echocardiography; layer-specific strain analyses were performed, which allowed to differentiate subendocardial or subepicardial contractile impairment. Layer-specific strain analyses by echocardiography demonstrated impairment of subepicardial deformation in the inferolateral wall, which mirrored CMR findings, showing late gadolinium enhancement in the subepicardium of the same LV segments. After initiation of appropriate antibiotic therapy with levofloxacin, LV systolic function rapidly improved as assessed by both CMR and strain analyses, with concomitant normalization of both clinical and biochemical abnormalities. The basic mechanisms of myocardial involvement during legionellosis are unclear; we discussed our findings according to the limited available evidence.