Daily Cardiology Research Analysis

BACKGROUND: The potential of mobile health (mHealth) technology combining telemonitoring and teleintervention as a non-invasive intervention to reduce the risk of cardiovascular events in patients with heart failure during the early post-discharge period (ie, the vulnerable phase) has not been evaluated to our knowledge. We investigated the efficacy of incorporating mHealth into routine heart failure management in vulnerable-phase patients. METHODS: The Heart Failure Events Reduction with Remote Monitoring and eHealth Support (HERMeS) trial was a 24-week, randomised, controlled, open-label with masked endpoint adjudication, phase 3 trial conducted in ten centres (hospitals [n=9] and a primary care service [n=1]) experienced in heart failure management in Spain. We enrolled adults (aged ≥18 years) with heart failure diagnosed according to the 2016 European Society of Cardiology criteria (then-current clinical practice guidelines at the initiation of the trial) who had recently been discharged (within the preceding 30 days of enrolment) from a hospital admission that was due to heart failure decompensation, or who were in the process of discharge planning. After discharge, participants were centrally randomly assigned (1:1) via a web-based system to mHealth, comprising telemonitoring and preplanned structured health-care follow-up via videoconference, or usual care according to each centre's heart failure care framework including a nurse-led educational programme. The primary outcome was a composite of the occurrence of cardiovascular death or worsening heart failure events during the 6-month follow-up period, assessed by time-to-first-event analysis in the full analysis set by the intention-to-treat principle. No prospective systematic collection of harms information was planned. The HERMeS trial is registered with ClinicalTrials.gov, NCT03663907, and is completed. FINDINGS: From May 15, 2018, to April 4, 2022, 506 participants (207 [41%] women and 299 [59%] men) were randomly assigned: 255 to mHealth and 251 to usual care. The mean age of participants was 73 years (SD 13). Follow-up ended prematurely in 51 (20%) of 255 participants in the mHealth group and 36 (14%) of 251 in the usual care group. During follow-up in the mHealth group, cardiovascular death or a worsening heart failure event occurred in 43 (17%) of 255 participants, compared with 102 (41%) of 251 in the usual care group (hazard ratio for time to first event 0·35 [95% CI 0·24-0·50]; p<0·0001; relative risk reduction 65% [95% CI 50-76]). No spontaneously reported harms were reported in either group during follow-up. INTERPRETATION: mHealth-based heart failure care combining teleintervention and telemonitoring reduced the risk of new fatal and non-fatal cardiovascular events compared with usual care in people with a recent hospital admission due to heart failure decompensation. The current findings could help to improve the care of patients with heart failure in the transitional post-discharge period by encouraging integration of mHealth into clinical practice guidelines. FUNDING: The HERMeS trial was funded by an unrestricted grant from Novartis.

AIMS: Thoracic aortic dissection (TAD) is a highly fatal disease lacking effective pharmacologic interventions in clinical practice. Emerging evidence indicates that the natriuretic peptide receptor C (NPR-C) plays a crucial role in the regulation of cardiovascular diseases. However, the precise involvement of NPR-C in TAD remains elusive. In this study, the role and molecular mechanisms of NPR-C in the pathogenesis of TAD were investigated. METHODS AND RESULTS: Through integrated analyses of human TAD transcriptome and single-cell sequencing data sets, we identified that NPR-C was downregulated in the aortas of acute TAD patients and in beta-aminopropionitrile (BAPN)-treated mice. Intriguingly, vascular smooth muscle cell (VSMC)-specific NPR-C knockout (NPR-CSMKO) mice, rather than endothelial cell-specific NPR-C knockout mice, developed TAD after treated with angiotensin II (Ang II) plus high salt diet (HSD), but not Ang II alone. Loss of NPR-C function promoted extracellular matrix degeneration, VSMCs apoptosis, and inflammation. RNA-sequencing analysis revealed that mitochondrial fatty acid oxidation (FAO) genes were significantly downregulated in the thoracic aortas of NPR-CSMKO mice treated with Ang II plus HSD. Notably, the expression of HADHB, a subunit of mitochondrial trifunctional protein (MTP) responsible for FAO, was obviously decreased in NPR-CSMKO mice treated with Ang II plus HSD. Mechanistically, knockdown of NPR-C activated ERK1/2 pathway, which decreased the expression and activity of peroxisome proliferator-activated receptor γ (PPARγ) and inhibited HADHB expression. Furthermore, NPR-C agonist, C-ANP4-23, mitigated the progression of TAD in BAPN-treated mice. Activation of MTP by spermidine (SPD) effectively prevented TAD formation in NPR-CSMKO mice treated with Ang II plus HSD. CONCLUSION: Our data highlight a critical role of HSD in triggering TAD and a previously unrecognized role of NPR-C that protects against TAD through regulating mitochondrial homeostasis. Therefore, NPR-C activation and SPD supplementation could be new prevention and treatment strategies for TAD.

AIM: Colchicine has recently been approved for the treatment of atherosclerotic cardiovascular disease (ASCVD). Since then, three large trials of colchicine in ASCVD have failed to reach their primary endpoints. METHOD: A systematic search of PubMed, Embase and Cochrane Central Register of Controlled Trials was performed (PROSPERO registration: CRD42024616378). The primary endpoint of major adverse cardiovascular events (MACE) was defined as a composite of myocardial infarction, stroke and cardiovascular death. The key secondary endpoint of extended MACE (eMACE) was defined as MACE plus coronary revascularisation. Pooled estimates were calculated using a random-effects model and are presented as risk ratio (95% confidence interval). RESULTS: 1624 articles were screened. 12 met inclusion criteria, yet one trial reported zero endpoint events in both arms. As such, 11 trials were included in the meta-analysis, with a total of 1983 primary endpoint events across 30,808 participants. Colchicine was associated with a 17% reduction in the incidence of MACE (0.83 [0.73, 0.95]; p=0.006) and 23% reduction in the incidence of eMACE (0.77 [0.63, 0.94]; p=0.01). This reduction was driven by a lower rate of myocardial infarction (0.78 [0.63, 0.95]; p=0.02) and coronary revascularisation (0.73 [0.55, 0.97]; p=0.03). There were also numerically fewer strokes in the colchicine treated population (0.81 [0.63, 1.04]; p=0.11). Colchicine had no effect on cardiovascular (0.96 [0.79, 1.15]; p=0.64) or non-cardiovascular mortality (1.04 [0.76, 1.41]; p=0.81). CONCLUSION: Colchicine reduces the risk of non-fatal ischaemic events in patients with ASCVD. Further studies are required to identify a population(s) who stands to benefit most from this promising therapy. In this pooled analysis of 11 randomised controlled trials, with a total of 30,808 participants, colchicine use was associated with a 17% reduction in the rate of heart attack, stroke and cardiovascular death in patients with clinically evident atherosclerotic cardiovascular disease.Colchicine predominantly reduced the risk of non-fatal cardiovascular events without improving survival. Colchicine did not significantly increase the risk of adverse effects.Further large-scale randomised trials are required to identify those patients most likely to derive the greatest benefit from this promising therapy.