European heart journal open最新文献

Aims: Endogenous endophthalmitis (EE) is a rarely reported complication of infective endocarditis (IE). In an international series, we sought to determine the clinical and microbiological profile, treatment, and outcome of patients presenting with IE-related EE.

Methods and results: Cases recorded from 2014 to 2023 in nine centres in Europe and the United States were collected. Results were compared to a matched control group.

Conclusion: Sixty-six patients with EE were reported, mean age of 65.2 ± 14.9 years, 71% (n = 47) male. Blood cultures were positive in 97% (64 cases) of patients, with a predominance of streptococci (46%, n = 30).As compared with the control group (n = 264), the EE group presented with more frequent diabetes (35% vs. 21%, P = 0.02), history of cirrhosis (9% vs. 3%, P = 0.04), glomerulonephritis (15% vs. 0.4%, P < 0.001), embolism before admission (92% vs. 55%, P < 0.001), and Janeway lesions (9% vs. 1%, P = 0.002). Streptococcal infection (46% vs. 26%, P = 0.001) was more frequent and Enterococcal infection (0% vs. 18%, P < 0.001) less frequent in the EE group.The main ocular symptoms were a decrease in visual acuity (96%), red eye (55%), and ocular pain (55%). Treatment of EE consisted of intravitreal antibiotic injection in 55 (83%) patients and vitrectomy in 17 (26%). Improvement of visual acuity was observed in 36 (55%) patients.

Conclusion: EE is a serious complication of IE with severe residual vision impairment. Patients with IE should be evaluated for ocular complications, since early detection of EE is crucial to prevent delays in management and to preserve visual function.

Introduction: ECG markers are associated with increased risk of sudden cardiac arrest (SCA) on the sinus rhythm ECG. A sizeable subgroup of patients at risk receives cardiac implantable electrical devices, but there are no known markers of SCA risk on the ventricular-paced (VP) ECG.

Methods and results: We conducted a case-control analysis within a community-based SCA study in Oregon USA (2002-2020; ∼1 million catchment population) with validation in an identically designed study in California USA (2015-2023; ∼850 000 catchment population). SCA cases included adults (≥18 years) with archived VP ECGs obtained prior and unrelated to their SCA. Controls met the same ECG criteria but without history of ventricular arrhythmias or SCA. The discovery analysis included 158 participants (119 SCA, 39 controls), mean age 76.9 ± 11.8 years. SCA cases had a higher ventricular rate (74.9 ± 16.0 bpm vs. 69.3 ± 12.0 bpm, P = 0.05), longer corrected QT interval (QTc; 525.9 ± 49.9 ms vs. 493.9 ± 31.0 ms, P < 0.001) and longer Tpeak-Tend (Tpe; 111.8 ± 23.3 ms vs. 95.9 ± 20.1 ms, P < 0.001). After adjustment, QTc and Tpe were significantly associated with SCA, with adjusted ORs 6.1 (95%CI: 1.4-26.2) and 7.9 (95%CI: 2.0-31.0) in the discovery population, and 6.1 (95%CI: 2.5-14.8) and 3.7 (95%CI: 1.6-8.6) in the validation population. In pooled analysis, the model combining QTc and Tpe achieved an AUC of 0.752, significantly outperforming each individually. Subjects with both prolonged QTc and Tpe had a 16-fold higher risk (adjusted OR:16.2, 95%CI: 6.0-43.6) compared to those without abnormalities.

Conclusion: Abnormal myocardial repolarization measured by QTc and Tpe was independently associated with SCA. These findings suggest that the VP ECG could also predict SCA risk.

Aims: To study the prevalence of masked uncontrolled hypertension (MUCH) in patients recently hospitalized for myocardial infarction, and to develop machine learning-based prediction models identifying MUCH.

Methods and results: Ambulatory blood pressure measurement (ABPM) was performed in 99 patients following hospitalization for a myocardial infarction. Sixty-two clinical variables were eligible for machine learning. Variable importance for the prediction of MUCH (office blood pressure <140/90 mm Hg at ABPM start but mean 24-h blood pressure ≥130/80 mm Hg) was assessed using the least absolute shrinkage and selection operator (LASSO) and the Boruta algorithms. Logistic regression, LASSO, and random forest models based on the top variables were evaluated using receiver operating characteristic area under the curve (AUC) in repeated cross-validation. Mean age was 62.1 ± 8.2 years, 73 (74%) were males. The ABPM was performed at a median of 11 weeks after discharge. Among 96 patients with valid 24-h ABPM recordings, 32 (33%) had 24-h mean blood pressure ≥130/80 mm Hg and 17 (18%) were identified with MUCH. Machine learning identified discharge diagnoses of diabetes and hypertension, and kidney dysfunction as most important predictors of MUCH. The best random forest, logistic regression, and LASSO models showed mean AUC 0.82, 0.80, and 0.80, respectively, for prediction of MUCH.

Conclusion: One in five patients had MUCH at follow-up after a myocardial infarction. The readily available variables diabetes, hypertension, and kidney dysfunction were identified as the most important predictors of MUCH, which may be implemented in a prediction model for identifying this clinically challenging blood pressure phenotype.

Previous presentation: Preliminary results were presented at the European Society of Cardiology Congress in London 2024 as an oral abstract presentation. Hellqvist H, Erlinge D, Lindahl B, et al. Prevalence and prediction of masked uncontrolled hypertension in patients recently hospitalised for an acute coronary syndrome. European Heart Journal 2024;45 (Suppl 1). doi: 10.1093/eurheartj/ehae666.2566.

Aims: Myocardial ischaemic preconditioning (IPC) increases myocardial ability to withstand ischaemic injury. Myocardial stunning is a reversible dysfunction, while necrosis results in irreversible cell death. The link between IPC, stunning, and necrosis remains unclear. This study aimed to utilize a novel 13.5-min ischaemia-reperfusion (I/R) rat model, distinct from conventional I/R models, to identify transcriptomic changes associated with IPC and investigate the role of DNA methylation in regulating these changes, particularly in relation to myocardial stunning and necrosis.

Methods and results: A novel rat model of cardiac I/R injury was used, with IPC induced by two 5-min ischaemia-reperfusion cycles followed by 13.5-min of ischaemia, and a control group undergoing 13.5-min of ischaemia without IPC. Myocardial samples were collected at early (T1) and 4-h (T2) post-reperfusion, representing stunned myocardium in the IPC group and necrosis in the control group. RNA sequencing, DNA methyltransferase (DNMT) activity assay, Chromatin immunoprecipitation (ChIP), and DNA methylation analyses were performed. IPC reprogrammed the cardiac transcriptome, with 53 genes differentially expressed at T1 and 166 at T2, including key regulators of inflammation (Nfkbia), DNA repair (Gadd45b, Parp14), and stress responses (Cebpd, Jun). IPC reduced global DNMT activity, promoting hypomethylation of protective genes like Cebpd, Nfkbia, Gadd45b, Jun, and Aplod1 at T1, while selectively hypermethylating maladaptive genes like Tmem200c and Fgfr4. ChIP assays revealed reduced Dnmt1 binding at Jun and Parp14 promoters, aligning with increased protein levels.

Conclusion: IPC re-programmes the cardiac transcriptome through dynamic DNA methylation, enhancing myocardial resilience while increasing stunning as an adaptive mechanism to limit necrosis.

Aims: Myocarditis is a potentially life-threatening condition with diverse aetiologies including viral infections, toxins, and autoimmunity. We aimed to quantify the risk factors of index myocarditis hospitalization and subsequent myocarditis recurrence.

Methods and results: We conducted a retrospective cohort study in New South Wales (NSW), Australia, using the Admitted Patient Data Collection (APDC) of all hospitalized patients. Conditions temporally associated with myocarditis within 30 days of the index admission were identified using conditional logistic regression analysis. In patients with previous myocarditis, risk factors for recurrent myocarditis admission were calculated with both Cox regression using cause-specific hazards and competing risk analysis. There were 4071 cases of index myocarditis from 2004 to 2021. Over a median of 4.8 years of follow-up, there were 124 patients whose myocarditis recurred. Two-thirds of cases were male with an average age of 42 years. Index myocarditis cases were much more common within 30 days of a hospitalization for pericarditis, heart failure, ventricular arrhythmias, COVID-19, and several other cardiac, respiratory, and autoimmune conditions, compared to the baseline risk over the preceding 12 months. Similarly, myocarditis recurrence was more common within 30 days of pericarditis, ventricular arrhythmias, COVID-19, and autoimmune disease. Recurrence was not strongly predicted by any features of the index myocarditis admission. Our analysis is solely based on administrative coding, with limited clinical validation, which introduces potential for misclassification.

Conclusion: In our cohort, myocarditis was more frequently diagnosed following presentations with acute respiratory illness (including COVID-19), autoimmune conditions, or cardiac events including ventricular arrhythmias, atrial fibrillation, and heart failure.

Aims: To examine the association between a personal history of cancer and the likelihood of a cardiovascular diagnosis among patients presenting with chest pain.

Methods and results: We analyzed data from consecutive adult patients hospitalized with a primary diagnosis of chest pain between 2007 and 2022, excluding those with active cancer or ST-elevation myocardial infarction. Patients were categorized into two groups: cancer survivors and other patients. The primary outcome was a cardiovascular probable diagnosis, defined as a composite of non-ST-segment elevation myocardial infarction, pulmonary embolism, new-onset atrial fibrillation, or mortality within 30 days. The final cohort included 37 819 patients with a median age of 65 years (Q1-Q3: 55-75), of whom 24 644 (65%) were men. Among these, 1838 (5%) had a history of cancer. A multivariable logistic regression model demonstrated that cancer survivors were 70% more likely to reach the study primary endpoint compared with other patients (P < 0.001). A propensity score matching model consistently demonstrated that cancer survivors were 40% more likely to meet the study endpoint (95% CI 1.2-1.7, P < 0.001). Over a median follow-up of 4.3 years (Q1-Q3: 2.1-7.3), 7035 (19%) patients died. Kaplan-Meier survival analysis indicated a cumulative probability of death of 29% ± 22% for cancer survivors vs. 12% ± 9% for other patients (P < 0.001, Log rank).

Conclusion: Among patients admitted to the hospital with chest pain, a personal history of cancer is independently associated with a significantly higher likelihood of receiving a final cardiovascular diagnosis.

Aims: Aetiologies of sudden death (SD) have been reported in autopsied case series and less frequently in resuscitated patients, but large series are scarce and if causes are similar between deceased and surviving patients is unknown.

Methods and results: All successive adult patients with resuscitated SD (n = 283) and autopsied SD cases (n = 1258) over the last 10 years at our centre were included. Causes were detailed and compared between resuscitated and autopsied cases. Coronary artery disease was present in 87% of resuscitated patients and in 48% of autopsied subjects (P < 0.0001). In coronary artery disease patients, an acute coronary event was present in 85% of resuscitated patients vs. 22% of autopsied cases (P < 0.0001).No coronary artery disease was present in 13% of resuscitated patients (42% cardiomyopathy, 58% primary electrical disease) and noncardiac causes were absent. In autopsied cases, some cardiomyopathy was present in 19%, noncardiac causes were noted in 16% (pulmonary embolisms, aortic dissections/aortic aneurysm ruptures or strokes, and brain/meningeal haemorrhages) and no apparent cardiac or noncardiac cause for explaining SD was present in 15% (sudden arrhythmic death syndrome).

Conclusion: In this large series of resuscitated and autopsied SD cases, coronary artery disease remains the main aetiology but was significantly less frequent in autopsied cases, with a majority of acute coronary events in resuscitated patients vs. a majority of remote myocardial infarction without fresh thrombus in autopsied cases. Noncardiac causes were present in 15% of autopsies but never in surviving patients.

Introduction: Coronary no-reflow phenomenon occurs when cardiac tissue fails to perfuse normally despite opening of the occluded vessel. It is one of the manifestations of reperfusion injury, a series of pathological conditions associated with an increase in infarct size and adverse clinical outcomes. While there is currently no specific treatment to limit or prevent reperfusion injury, preclinical models have shown promising results with iSGLT2 inhibitors in this regard. However, there are no human studies specifically designed to evaluate the effects of empagliflozin on the no-reflow phenomenon or reperfusion injury.

Methods and analysis: The EMPA-PCI is a single-centre, open-label, randomized clinical trial that compares the use of empagliflozin vs. standard treatment in reducing reperfusion injury in patients with STEMI. A total of 162 patients will be randomized to receive either 25 mg of Empagliflozin as a loading dose before angioplasty followed by 10 mg per day for three doses in the treatment group, or standard treatment in the control group. The incidence of the no-reflow phenomenon during PCI, infarct size by magnetic resonance imaging, myocardial injury biomarkers will be compared. Clinical follow-up will be conducted for 3 months following patient enrollment.

Conclusion: Empagliflozin administered prior to PCI in patients with STEMI may contribute to prevent the no-reflow phenomenon and limit reperfusion injury. This could provide new insights into the cardiovascular benefits already known for SGLT2 inhibitors.

Trial registration: ClinicalTrials registry. NCT06342141.