Hellenic Journal of Cardiology最新文献

Objective: Remote ischemic preconditioning (RIPC) reduces periprocedural myocardial injury (PMI) after percutaneous coronary intervention (PCI) through various pathways, including an adenosine-triggered pathway. Ticagrelor inhibits adenosine uptake, thus may potentiate the effects of RIPC. This randomized trial tested the hypothesis that ticagrelor potentiates the effect of RIPC and reduces PMI, assessed by post-procedural troponin release.

Methods: Patients undergoing PCI for non-ST elevation acute coronary syndromes were 1:1 randomized to ticagrelor (TG-Group) or clopidogrel (CL-Group). Within each treatment, patients were 1:1 randomized to a RIPC (RIPC-Group) or a control group (CTRL-Group). The primary endpoint was the difference between post- and pre-procedural troponin at 24 h following PCI, termed deltaTnI.

Results: During a 12-month period, 138 patients were included in the study (34 in the CL-CTRL group, 34 in the TG-CTRL group, 35 in the CL-RIPC group, and 35 in the TG-CTRL group). There was a significant difference in deltaTnI between the study groups [ TG-RIPC:0.04 (0-0.16), CL-CTRL:0.10 (0.03-0.43), CLRIPC:0.11 (0.03-0.89), and TG-CTRL:0.24 (0.06-0.47); p = 0.007]. Eight patients (22.9%) in the TG-RIPC group developed type 4a myocardial infarction (MI), compared to 14 (40%) in the CL-RIPC group, 13 (38.2%) in the CL-CTRL group, and 19 (55.9%) in the TG-CTRL group (p = 0.048). A significant interaction between antiplatelet group allocation and RIPC on deltaTnI was observed [F (1,134) = 7.509; p = 0.007]. In multivariate analysis, the interaction between RIPC and ticagrelor treatment was independently associated with a lower incidence of Type 4a MI.

Conclusion: Our results demonstrate an interaction between ticagrelor and RIPC, which may potentiate the cardioprotective effects of RIPC during PCI by reducing PMI.

Objective: Neurohumoral alterations in heart failure (HF) affect blood pressure variability (BPV) and vascular compliance, but little is known about this subject among patients admitted to the hospital with decompensated HF. This study sought to investigate in-hospital 24-h blood pressure monitoring (BPM)-derived BPV parameters and vascular compliance in patients with decompensated HF and explore the association of these parameters with hospitalization length and in-hospital adverse events.

Methods: A 24-h BPM was applied during the first 6 h of admission to the hospital in patients with decompensated HF. Circadian patterns were determined by the study patients. Average real variability (ARV), pulse pressure index (PPI), pulse stiffening ratio (PSR), and ambulatory arterial stiffness index (AASI) values were calculated from in hospital 24-h BPM recordings. Admission and discharge N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels, length of hospitalization, and in-hospital adverse events were recorded.

Results: A total of 167 patients with decompensated HF were included in the study. The dipper group exhibited a greater NT-proBNP decrease with the treatment than the non-dipper group and reverse dipper group. Hospitalization length was shorter in the dipper group than in the non-dipper and reverse dipper groups. Although ARV, AASI, and PSR were independently associated with the length of hospitalization, ARV, AASI, and PPI were independently associated with in-hospital adverse events.

Conclusion: The post-admission in hospital 24-h BPM-derived parameters (dipper pattern, ARV, PPI, PSR, and AASI) of patients admitted to hospital with decompensated HF provide important prognostic information and predict the length of hospital stay.

Aortic dissection (AD) is a catastrophic life-threatening cardiovascular emergency with a 1-2% per hour mortality rate post-diagnosis, characterized physiologically by the separation of aortic wall layers. AD initially presents as intense pain that can then radiate to the back, arms, neck, or jaw along with neurological deficits like difficulty in speaking, and unilateral weakness in some patients. This spectrum of clinical features associated with AD is often confused with acute myocardial infarction, hence leading to a delay in AD diagnosis. Cardiac and vascular biomarkers are structural proteins and microRNAs circulating in the bloodstream that correlate to tissue damage and their levels become detectable even before symptom onset. Timely diagnosis of AD using biomarkers, in combination with advanced imaging diagnostics, will significantly improve prognosis by allowing earlier vascular interventions. This comprehensive review aims to investigate emerging biomarkers in the diagnosis of AD, as well as provide future directives for creating advanced diagnostic tools and imaging techniques.

Transoesophageal echocardiography (TOE) is a well-established and valid imaging modality, providing more accurate and of higher quality information than transthoracic echocardiography (TTE) for several specific diagnoses and recently a useful guide of an increasing number of catheter-based and surgical interventions. The present paper represents an effort by the Echocardiography Working Group (WG) of the Hellenic Society of Cardiology to state the essential steps of the TOE exam performed beyond the echo lab: a) in the operating rooms intraoperatively during either transcatheter interventions, or cardiothoracic surgery and b) in the intensive care unit for critically ill patients' monitoring. This paper includes information and tips and tricks about the pre-procedural evaluation, the procedural echocardiographic guidance, and post-procedural evaluation of the result and potential complications.

Background: A couple of cardiac magnetic resonance (CMR) attributes strongly predict adverse remodeling after ST-segment elevation myocardial infarction (STEMI); however, the value of incorporating high-risk CMR attributes, particularly, in patients with non-reduced ejection fraction, remains undetermined. This study sought to evaluate the independent and incremental predictive value of a multiparametric CMR approach for adverse remodeling after STEMI across left ventricular ejection fraction (LVEF) categories.

Methods: A total of 157 patients with STEMI undergoing primary percutaneous coronary intervention were prospectively enrolled. Adverse remodeling was defined as ≥20% enlargement in left ventricular end-diastolic volume from index admission to 3 months of follow-up.

Results: Adverse remodeling occurred in 23.6% of patients. After adjustment for clinical risk factors, a stroke volume index <29.6 mL/m², a global longitudinal strain >-7.5%, an infarct size >39.2%, a microvascular obstruction >4.9%, and a myocardial salvage index <36.4 were independently associated with adverse remodeling. The incidence of adverse remodeling increased with the increasing number of high-risk CMR attributes, regardless of LVEF (LVEF ≤ 40%: P = 0.026; 40% < LVEF < 50%: P = 0.001; LVEF ≥ 50%: P < 0.001). The presence of ≥4 high-risk attributes was an independent predictor of LV adverse remodeling (70.0% vs. 16.8%, adjusted OR 9.68, 95 CI% 3.25-28.87, P < 0.001). Furthermore, the number of high-risk CMR attributes had an incremental predictive value over reduced LVEF and baseline clinical risk factors (AUC: 0.81 vs. 0.68; P = 0.002).

Conclusions: High-risk CMR attributes showed a significant association with adverse remodeling after STEMI across LVEF categories. This imaging-based model provided incremental value for adverse remodeling over traditional clinical factors and LVEF.

Objective: Atherosclerosis is closely related to cardiovascular disease risk. The present study aims to evaluate the association between metabolic dysfunction-associated fatty liver disease (MAFLD) and the presence of coronary atherosclerotic plaques and plaques burden, as detected by computed tomography angiography (CTA), and further test the screening value of MAFLD on the presence of coronary atherosclerotic plaques and plaques burden.

Methods: We used data from the PolyvasculaR Evaluation for Cognitive Impairment and vaScular Events study, a community-based cohort. Hepatic steatosis was assessed using the fatty liver index. Coronary atherosclerotic plaques and burden were detected by CTA. The association of MAFLD with the presence of coronary atherosclerotic plaques and burden was assessed by binary and ordinal logistic regression models, respectively.

Results: Among the 3029 participants (mean age 61.2 ± 6.7 years), 47.9% (1452) presented with MAFLD. MAFLD was associated with an increased odds of the presence of coronary atherosclerotic plaques (OR, 1.27; 95% CI: 1.03-1.56), segment involvement score [cOR (common odds ratio), 1.25; 95% CI, 1.03-1.51], and segment stenosis score (cOR, 1.29; 95% CI, 1.06-1.57). Participants with severe fibrosis or diagnosed as DM-MAFLD subtypes had with higher odds for the presence of coronary atherosclerotic plaques and plaques burden. In addition, MAFLD demonstrated a higher sensitivity for detecting the presence of coronary atherosclerotic plaques and plaque burden (54%-64%) than conventional CVD risk factors (such as diabetes, obesity, and dyslipidemia).

Conclusion: MAFLD is associated with higher odds of having coronary atherosclerotic plaques and plaque burden. Moreover, MAFLD may offer better screening potential for coronary atherosclerosis than established CVD risk factors.