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Background The burden of cardiovascular (CV) complications in patients hospitalised for community-acquired pneumonia (CAP) is still uncertain. Available studies used different designs and different criteria to define CV complications. We assessed the cumulative incidence of acute of CV complications during hospitalisation for CAP in Internal Medicine Units (IMUs). Methods This was a prospective study carried out in 26 IMUs, enrolling patients consecutively hospitalised for CAP. Defined CV complications were: newly diagnosed heart failure, acute coronary syndrome, new onset of supraventricular or ventricular arrhythmias, new onset hemorrhagic or ischemic stroke or transient ischemic attack. Outcome measures were: in-hospital and 30-day mortality, length of hospital stay and rate of 30-day re-hospitalisation. Results A total of 1266 patients were enrolled, of these 23.8% experienced at least a CV event, the majority (15.5%) represented by newly diagnosed decompensated heart failure, and 75% occurring within 3 days. Female gender, a history of CV disease, and more severe pneumonia were predictors of CV events. In-hospital (12.2% vs 4.7%, p p = 0.0001) mortality was higher in patients with CV events, as well as the re-hospitalisation rate (13.3% vs 9.3%, p = 0.002), and mean hospital stay was 11.4 ± 6.9 vs 9.5 ± 5.6 days (p p = 0.009). Conclusion Cardiovascular events are frequent in CAP, and their occurrence adversely affects outcome. A strict monitoring might be useful to intercept in-hospital CV complications for those patients with higher risk profile. Trial registration NCT03798457 Registered 10 January 2019 - Retrospectively registered

Heart failure (HF) is characterized by a high prevalence and hospitalization rate with considerable health and social impact; the knowledge of its epidemiological features remains the mainstay to assess adequacy of the health care needs. The aim of this study was to evaluate the prevalence of HF in Internal Medicine Units of the Campania region (Italy) and patients’ characteristics. We recruited all patients with HF admitted between April 1 and June 30, 2014, in 23 Units of Internal Medicine: 975 patients (19.5% of 5000 admissions), 518 women and 457 men, mean age 76.9±9.9 (range 34-100) with 741 (76%) older than 70 years. The mean age was higher in women than men; 35.8% of patients had atrial fibrillation, with higher prevalence in women than in men. Coronary artery disease represented the leading etiology while prevalence of non-ischemic heart failure was higher in women. New York Heart Association class was indicated in 926 patients. Left ventricular ejection fraction (LVEF) was measured in 503 patients; 18.4% of patients had a severely reduced LVEF40%. At least one hospital admission in the previous 12 months was registered in 39.6% of patients. One, two and more than two relevant comorbidities were present in 8.6%, 24.7% and 64.8% of patients, respectively. Arterial hypertension and coronary artery disease were more frequent in female. In conclusion, advanced age and clinical complexity were the main characteristics of HF patients hospitalized in the Internal Medicine Units in Campania. Gender differences also emerged from the analysis of demographic parameters and etiopathogenetic features. Some diagnostic and therapeutic aspects not in line with that recommended by the most recent HF international guidelines were registered.

The role of atenolol, a non-vasodilating beta-blocker drug, on long-term mortality in hypertensive older adults is still unclear. The aim of the present study was to evaluate long-term mortality in community-dwelling hypertensive older adults taking atenolol.Long-term mortality after 12-year follow up in isolated hypertensive older adults (n = 972) was analyzed. The patients were stratified in the presence and absence of atenolol use. Systolic, diastolic and pulse arterial pressure were measured.Older adults taking atenolol showed a greater mortality and higher pulse arterial pressure values than those not taking atenolol (73.9% vs 55.0%; P = 0.047 and 74.7 ± 14.1 vs 63.0 ± 14.2 mmHg, P 0.001, respectively). Cox regression analysis showed that atenolol use (hazard risk 1.91; 95% confidence interval 1.04-4.31; P = 0.04) and pulse arterial pressure (hazard risk 1.02; 95% confidence interval 1.01-1.03; P = 0.032) were predictive of long-term mortality.Atenolol use was related to increased mortality in community-dwelling hypertensive Older adults. This increase in mortality risk seems to be related to an increase of pulse arterial pressure.

OBJECTIVE Elderly subjects are characterized by a high prevalence of OA and clinical frailty. This study aimed to examine the predictive role of clinical frailty on long-term mortality in elderly subjects with and without OA. METHODS Mortality was evaluated after a 12-year follow-up in 698 subjects with and 590 subjects without OA recruited in 1992. Clinical frailty was assessed according to the Frailty Staging System and stratified in tertiles. RESULTS After a 12-year follow-up, mortality was 42.2% in subjects without and 55.8% in subjects with OA (P = 0.256). With increasing frailty, mortality increased by 30.5% (P for trend < 0.001) in subjects without and by 45.6% in subjects with OA (P for trend < 0.001). Multivariate analysis showed that frailty [hazard ratio (HR) = 1.49 for each unit of increase, 95% CI 1.32, 1.94, P < 0.001) but not OA (HR = 1.28, 95% CI 0.987, 1.39, P = 0.412) was predictive of long-term mortality. Moreover, when Cox regression analysis was performed, frailty enhanced the risk of long-term mortality for each unit of increase by 32% (HR = 1.32, 95% CI 1.06, 1.65, P = 0.03) in the absence of OA and by 98% in the presence (HR = 1.98, 95% CI 1.63, 2.95, P < 0.01) of OA. CONCLUSION Clinical frailty significantly predicts mortality in subjects without OA and even more in those with OA. Thus clinical frailty may be considered a new prognostic factor to identify subjects with OA at high risk of mortality.