Adding the value of the Charlson Comorbidity Index to the GRACE score for mortality prediction in acute coronary syndromes.

BACKGROUND: Scarce and conflicting data still exist about the role of the Charlson Comorbidity Index (CCI) when added to the traditional Global Registry of Acute Coronary Events (GRACE) risk score for outcome prediction in patients with acute coronary syndrome (ACS). METHODS: All consecutive admissions due to ACS, from 1 January 2018 to 31 December 2020 were retrospectively reviewed from an internal database of a tertiary cardiac center in Salerno (Italy). Logistic and Cox proportional regression analyses were performed in order to assess the contribution of the CCI on 30-day and long-term mortality. The CCI adding value to the GRACE score was analyzed with several measures of improvement in discrimination: increase in the area under the receiver-operating characteristic curve (AUC), the integrated discrimination improvement (IDI), and the categorical and continuous net reclassification improvement (cNRI) more than 0. Robustness of the results was assessed through an internal validation procedure with bootstrapping. RESULTS: One thousand three hundred and ten patients were identified. The median age was 68 (58-78) years. One hundred and twenty (9.2%) and 113 (9.5%) deaths occurred, respectively, during the first 30 days from admission and during long-term follow-up (median follow-up time: 13 months; interquartile range: 9-24). After multivariate regression analysis, the CCI was not associated with short-term mortality, while it was significantly and independently associated with long-term mortality along with the GRACE score (hazard ratio: 1.34, 95% confidence interval: 1.22-1.47; P  < 0.001). An additive effect of CCI with the GRACE risk score was observed in predicting long-term mortality: AUC from 0.768 to 0.819 ( P  = 0.003), category-based NRI: 0.215, cNRI>0: 0.669 ( P  < 0.001), IDI: 0.066 ( P  < 0.001). CONCLUSION: The CCI is a predictor of long-term mortality and improves risk stratification of patients with ACS over the GRACE risk score.

[Diagnosis of cardiovascular involvement in Fabry disease]. / Diagnosi del coinvolgimento cardiovascolare nella malattia di Fabry.

Fabry disease is a rare X-linked genetic disorder, caused by partial or total loss of function of the lysosomal enzyme α-galactosidase A that induces glycosphingolipid accumulation in various organs and tissues, modifying their structure and function. Cardiovascular involvement in classic and late onset forms has emerged to be a major determinant of prognosis. In recent years, a constant evolution in imaging techniques and their mindful application has led to interesting results in the diagnostic workup, progressively reducing time required to recognize early signs of this disease. Owing to the growing awareness for diagnostic screening and the efficacy of the many therapeutic options currently available, the clinical history of Fabry patients has changed during the last decades. Therefore, an early diagnosis of Fabry disease and especially of cardiac involvement is essential to promptly adopt an adequate therapy.

Arterial hypertension in patients with takotsubo syndrome: prevalence, long-term outcome, and secondary preventive strategies: a report from the Takotsubo Italian Network register.

AIMS: The aim of this study was to investigate the long-term outcome of takotsubo syndrome (TTS) patients with and without hypertension (HT) and to evaluate the effectiveness of treatment with beta-blockers (BBs) and/or renin-angiotensin-aldosterone system inhibitors (RAASi). METHODS AND RESULTS: The study population includes a register-based, multicentre cohort of consecutive patients with TTS, divided into two groups according to the history of HT. Further stratification was performed for BB/RAASi prescription at discharge. The primary outcome was the composite of all-cause death and TTS recurrence at the longest available follow-up. The propensity score weighting technique was used to account for potential confounding. In the overall population (903 patients, mean age 70 ± 11 years), HT was reported in 66% of cases. At a median 2-year follow-up, there was no difference in the risk of the primary composite outcome between patients with and without HT. The adjusted Cox regression analysis showed a significantly lower risk for the primary outcome [adjusted hazard ratio (aHR): 0.69; 95% confidence interval (CI): 0.49-0.99] in patients who received BB vs. those who did not. Renin-angiotensin-aldosterone system inhibitors treatment was not associated with the primary study outcome. The lower risk for the primary outcome with BB treatment was confirmed in patients with HT (aHR: 0.37; 95% CI: 0.24-0.56) but not in patients without (aHR: 1.83; 95% CI: 0.92-3.64; Pinteraction < 0.001). CONCLUSION: In this TTS study, HT did not affect the long-term risk of adverse events but increased the probability of benefit from BB treatment after discharge. Owing to the favourable outcome impact of BB prescription in TTS patients with HT, a tailored pharmacological therapy should be considered in this cohort.

Although not associated with clinical outcomes, hypertension (HT) seems to modify the long-term effectiveness of pharmacological treatment in patients with takotsubo syndrome (TTS). Beta-blockers improved the overall survival of TTS patients with HT and should be considered as first-line therapy in this patient population. The effectiveness of renin­angiotensin­aldosterone system inhibitors on long-term outcome was not significant regardless of the history of HT.

Acute Coronary Syndrome in Patients with SARS-CoV-2 Infection: Pathophysiology and Translational Perspectives.

Acute coronary syndromes (ACS) may complicate the clinical course of patients with Coronavirus Disease 2019 (COVID-19). It is still unclear whether this condition is a direct consequence of the primary disease. However, several mechanisms including direct cellular damage, endothelial dysfunction, in-situ thrombosis, systemic inflammatory response, and oxygen supply-demand imbalance have been described in patients with COVID-19. The onset of a prothrombotic state may also be facilitated by the endothelial dysfunction secondary to the systemic inflammatory response and to the direct viral cell damage. Moreover, dysfunctional endothelial cells may enhance vasospasm and platelet aggregation. The combination of these factors promotes atherosclerotic plaque instability, thrombosis and, consequently, type 1 myocardial infarction. Furthermore, severe hypoxia due to extensive pulmonary involvement, in association with other conditions described in COVID-19 such as sepsis, tachyarrhythmias, anemia, hypotension, and shock, may lead to mismatch between oxygen supply and demand, and cause type 2 myocardial infarction. A deeper understanding of the potential pathophysiological mechanisms underlying ACS in patients with COVID-19 could help the therapeutic management of these very high-risk patients.