Frontiers in Cardiovascular Medicine最新文献

Background and aims: Conventional echocardiographic measurements like ejection fraction (EF) and global longitudinal strain (GLS) evaluate left ventricular (LV) function without considering concurrent loading conditions. A more comprehensive characterization of cardiac function and energetics can be achieved through pressure-volume analysis, but its clinical application is limited by the requirement for invasive measurements. We aimed to develop a clinically accessible, non-invasive method for pressure-volume loop analysis.

Methods: We obtained simultaneous 3-dimensional echocardiograms and invasive LV pressures with micromanometer-tipped catheters during transcatheter aortic valve replacement (TAVR) for severe aortic stenosis. Volume-time traces from the echocardiograms were combined with invasive LV pressures and non-invasive pressure estimates to construct pressure-volume loops. We used echocardiograms before and after TAVR to evaluate changes in myocardial function via non-invasive pressure-volume studies.

Results: In same-beat comparisons, stroke work calculated using non-invasive LV pressure estimations correlated well with stroke work calculated using invasive LV pressures (r = 0.95, ICC = 0.95, p < 0.0001, y = 0.90X + 1,836, mean bias -549 mmHg*mL, standard deviation 774 mmHg*mL; 95% limits of agreement: -2,006 to +967 mmHg*mL). After TAVR, stroke work fell substantially, ventricular efficiency increased, ventriculo-arterial coupling improved, and both total and resting energy consumption decreased. On the other hand, LV biplane EF and GLS remained unchanged.

Conclusions: This study confirms the validity and clinical accessibility of non-invasive pressure-volume loop analysis in patients with aortic stenosis. The method identified and characterized changes in myocardial energetics, function, and ventriculo-arterial interaction, that are not typically detected by conventional echocardiography. These findings highlight the potential of non-invasive pressure-volume analysis in clinical and research practice.

Background: Research on biological age focused on the optimization and upgrading of aging clocks, which can now prospectively predict a variety of diseases. The biological age (BA) based on clinical parameters has shown predictive value for cardiovascular disease. However, evidence linking BA and its trajectories with heart failure (HF) remained limited. This study aimed to construct a clinical-parameter-based BA and to investigate its association, along with BA trajectories, with incident heart failure.

Methods: This study utilized data from the Kailuan Study, which included 76,908 Chinese adults who underwent their first health examination between 2006 and 2007. A deep neural network model was employed to estimate BA based on 32 clinical indicators. Participants were stratified into three groups-decelerated aging, accelerated aging, and normal aging-according to their baseline BA values. Six distinct aging trajectories were subsequently identified using data from the first three follow-up examinations. Cox proportional hazard models were applied to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for the associations between aging status or BA trajectories and HF incidence.

Results: Participants exhibiting accelerated aging demonstrated a 30% higher risk of HF (HR: 1.30; 95%CI: 1.19-1.43) compared to those with normal aging. Conversely, those following a high-stable trajectory demonstrated the highest risk of HF (HR: 1.79; 95%CI: 1.48-2.17). Additionally, when compared to the high-stable trajectory, the high-descending trajectory was linked to a significantly lower risk of HF (HR: 0.74; 95%CI: 0.60-0.91).

Conclusions: Accelerated biological aging significantly increased the risk of HF, whereas decelerated biological aging was linked to a reduced risk of HF. Individuals who consistently exhibited a higher level of biological aging were at the greatest risk for HF.

Combined methylmalonic aciduria and homocystinuria, cobalamin C (cblC) type, represents the most common inborn error of cobalamin metabolism, caused by pathogenic variants in the MMACHC gene. We report the case of a 27-year-old Chinese woman who presented with dilated cardiomyopathy and renal insufficiency. Blood amino acid and acylcarnitine profiling revealed elevated ratios of propionylcarnitine (C3) to acetylcarnitine (C2) and C3 to free carnitine (C0). Genetic testing identified compound heterozygous pathogenic variants in MMACHC-c.80A > G, p. (Gln27Arg) and c.609G > A, p. (Trp203Ter)-confirming the diagnosis of cblC-type methylmalonic aciduria with homocystinuria. Despite administration of vitamin B12 and betaine, her heart function did not improve. The patient eventually succumbed to severe COVID-19 infection, which led to metabolic acidosis, renal failure, and multi-organ failure. This case underscores the challenging clinical course of late-onset cblC disorder and contributes to its expanding phenotypic spectrum.

Introduction: Telmisartan is a long-acting angiotensin II receptor blocker (ARB) with unique pharmacologic properties, including partial PPAR-γ activation. Its comparative effectiveness against other ARBs in real-world populations remains unclear.

Methods: We conducted a retrospective cohort study using the TriNetX Global Collaborative Network, including hypertensive patients aged 55-85 years without prior stroke, heart failure, or myocardial infarction. After 1:1 propensity score matching, 41,598 patients were included in each group.

Results: Telmisartan use was associated with a significantly lower risk of stroke (HR 0.805, 95% CI 0.751-0.863), heart failure (HR 0.75, 95% CI 0.672-0.836), and all-cause mortality (HR 0.59, 95% CI 0.542-0.642) compared to other ARBs. Subgroup analyses showed consistent benefits across sex, diabetes, chronic kidney disease, and hyperlipidemia.

Conclusions: In this large real-world matched cohort of over 83,000 patients, telmisartan was associated with superior cardiovascular and cerebrovascular outcomes compared to other ARBs, supporting its potential as a preferred antihypertensive agent in high-risk populations.

Sudden cardiac death (SCD) causes 180,000-360,000 annual deaths in the United States, with mortality rates exceeding 90%. Despite advances in resuscitation science, predicting SCD remains challenging due to inconsistent definitions, subtle warning signs, and temporal variability in risk factors. While traditional cardiovascular conditions are well-integrated into risk prediction models, non-cardiovascular comorbidities remain significantly underutilized despite contributing to nearly 40% of SCD cases. This review examines evidence linking various systemic conditions to SCD risk. Neurologic disorders including epilepsy (1.6-5.89-fold increased risk), depression (1.6-2.7-fold), and anxiety (1.6-fold) elevate SCD vulnerability through autonomic dysregulation and medication effects. Respiratory conditions like COPD (1.3-3.6-fold) and obstructive sleep apnea (1.6-2.6-fold) contribute through chronic hypoxemia and inflammation. Hepatic pathology, kidney disease, anemia, and endocrine disorders (particularly diabetes with 1.7-2.4-fold risk) also demonstrate significant associations. Critically, non-cardiovascular comorbidities predict not only SCD occurrence but also initial cardiac rhythm presentation-essential for determining implantable cardioverter-defibrillator candidates, as these devices only benefit shockable rhythms. Conditions like epilepsy, depression, COPD, liver cirrhosis, and chronic kidney disease correlate with predominantly non-shockable presentations. Current prediction models incorporate few non-cardiac conditions, primarily due to historical cardiac-centric approaches, sample size constraints, complex disease interactions, and overfitting concerns. Proposed solutions include multidisciplinary research collaboration, multicenter data pooling, and advanced machine learning techniques to develop more comprehensive and accurate SCD prediction algorithms.

The management of ischemic heart disease has evolved from a narrow focus on low-density lipoprotein cholesterol (LDL-C) reduction to a comprehensive strategy targeting the regression and stabilization of coronary atherosclerotic plaque. Intravascular imaging modalities, including intravascular ultrasound (IVUS), optical coherence tomography (OCT), and near-infrared spectroscopy (NIRS), have been instrumental in characterizing the temporal sequence of plaque modification in response to lipid-lowering therapy. This review synthesizes evidence demonstrating that the effects on plaque are both time-dependent and agent-specific. Statins induce rapid plaque stabilization within weeks to months via mechanisms such asanti-inflammatory effects, fibrous cap thickening, and reduction of the lipid core. With prolonged treatment (months to years), statins promote plaque volume regression and facilitate a favorable shift in plaque composition towards a more stable, calcified phenotype. Non-statin agents further augment this regression. Ezetimibe, in combination with statins, provides synergistic LDL-C lowering and enhances plaque volume reduction. PCSK9 inhibitors, recognized as one of the most potent lipid-lowering agents currently available, have been shown in several studies to promote the regression of atherosclerotic plaques and reduce plaque volume. However, their effects on plaque composition-such as calcification, fibrous tissue, fibrofatty tissue, and necrotic core-remain controversial.

Introduction: Heart failure (HF) poses a substantial global health burden due to its high prevalence and severe clinical outcomes. Early diagnosis is critical to optimize management and reduce the economic impact of HF. This scoping review consolidates existing knowledge on strategies to improve HF diagnosis, emphasizing the utility of biomarkers, imaging techniques, artificial intelligence (AI), and care pathways.

Methods: A systematic search of PubMed/Medline and Scopus databases identified 198 relevant studies published since 2010, focusing on adult populations without a prior HF diagnosis. The inclusion criteria centered on initiatives aimed at enhancing diagnostic processes.

Results: Results indicate that biomarkers, particularly natriuretic peptides such as N-terminal prohormone of BNP (NT-proBNP), are central to early HF detection, showing high sensitivity. Emerging biomarkers, like microRNAs, offer potential for improved diagnostic accuracy. Imaging techniques, including echocardiography and lung ultrasound, remain primary tools for assessing cardiac function, while AI applications in imaging and electronic health records represent a rapidly evolving field. These tools show promising potential for early identification of HF patients, although most require further validation and standardization before routine clinical implementation. Care pathways emphasizing high-resolution consultations and integrated diagnostic tools enable prompt HF diagnosis, crucial for initiating early treatments.

Discussion: By implementing these diagnostic strategies, particularly in high-risk populations such as those with comorbid conditions, there is potential to significantly advance patient outcomes and healthcare resource management. Nevertheless, it is essential to translate these advances and discoveries into clinical practice, considering healthcare context and socioeconomic limitations, and promoting international consensus to ensure their global adoption. In conclusion, ongoing research and refinement of these diagnostic tools are imperative to effectively address the growing challenge of HF.

Background and aims: Atrial fibrillation (AF) frequently accompanies rheumatic mitral valve disease (MVD) and adversely affects postoperative outcomes. Radiofrequency ablation (RFA) and cryoablation are commonly used during mitral valve surgery, but their comparative impact on atrial remodeling in this population remains uncertain.

Methods: This retrospective cohort included 100 patients with rheumatic MVD and persistent AF who underwent mitral valve surgery with concomitant cryoablation (n = 50) or RFA (n = 50) between June 2020 and June 2024 at centers in the Almaty region, Kazakhstan. Clinical and echocardiographic parameters were assessed preoperatively, within 48 h postoperatively, and at 6 ± 2 months.

Results: Cryoablation was associated with greater left atrial (LA) volume reduction immediately and at follow-up (both p < 0.001). Multiple linear regression identified ablation modality as the only independent predictor of LA volume reduction (β = 27.9 mL, p < 0.0001), whereas duration of rheumatic disease, BMI, EuroSCORE II, and AF recurrence were not significant. At follow-up, the reduction in right atrial short-axis diameter was smaller after cryoablation (p = 0.049), and stroke volume declined less compared with RFA (-1.2 ± 17.3 mL vs. -7.3 ± 15.8 mL; p = 0.006). Cardiopulmonary bypass time, aortic cross-clamp time, and postoperative symptom improvement were comparable between groups. Freedom from AF during follow-up was also similar (log-rank p = 0.52).

Conclusions: In patients with persistent AF and rheumatic MVD undergoing mitral valve surgery, cryoablation was associated with more pronounced early atrial reverse remodeling and better preservation of stroke volume compared with RFA, without differences in operative efficiency or short-term safety. These findings should be considered hypothesis-generating, and prospective randomized studies with standardized lesion sets are required to confirm modality-specific effects.

Introduction: Two predominant pathways contribute to ischemia reperfusion injury (IRI) following donation after circulatory death (DCD): mitochondrial permeability transition pore (MPTP) opening and Calpain-1 (CPN1) activation. Each pathway has established inhibitors; Cyclosporine A (CyA) and MDL-28170 (MDL), respectively, which are effective in modulating IRI in a DCD heart with 25 min of warm ischemia time (WIT). We studied the effect of co-administering CyA and MDL during reperfusion on infarct size and graft function in DCD rat hearts with extended WIT of 35 min.

Methods: Male rats were exposed to 35 min of warm ischemia followed by 90 min of reperfusion. During reperfusion, hearts were given either 0.5 mM of CyA, 10 mM of MDL, or mixed CyA and MDL. Cardiac function and coronary flow rates were monitored throughout reperfusion and infarct size at the end of reperfusion.

Results: Infarct size in hearts treated with mixed CyA + MDL (31.59 ± 7.1%) was less than that of MDL-treated hearts (33.26 ± 4.3%) but larger than CyA-treated hearts (25.49 ± 5.9%). Graft function and coronary flow rates were variable amongst groups. CyA-treated hearts had more profound infarct size reduction when compared to MDL, and no additional synergistic effect was seen with combination treatment.

Discussion: Our results indicate that MPTP opening contributes significantly to the development of IRI in DCD hearts.