Our cells and, therefore, our organism, need energy to function at their best, which is mainly produced by mitochondria. These intracellular organelles generate energy from food macromolecules across the Krebs cycle by oxidative phosphorylation. Energy is developed by converting adenosine triphosphate (ATP) to adenosine diphosphate (ADP). It is essential, for adequate mitochondrial energy production in the form of ATP, to have the right number of well-functioning mitochondria and the right amount of oxygen (O2) available. Unfortunately, the aging process and the chronic diseases that arise over the years are associated with a reduction in the number of mitochondria and their insufficient functioning. Among the chronic diseases related to significant damage of the arteries with a reduction in the supply of O2, there is atherosclerosis, where the process of atherothrombosis occurs. To keep our organs well-functioning despite aging, we must therefore protect our mitochondria and arteries. This can be achieved by intervening early in prevention with a lifestyle correction and diet integration with effective natural substances or, in some cases, with drugs. Among the many natural substances that have good scientific support, we have chosen four that have demonstrated benefits in the absence of side effects and that we know best: quercetin and pyrroloquinoline quinone to stimulate mitochondrial biogenesis and mitophagy, while L-arginine and nattokinase to protect the arteries from atherothrombosis.
Our cells and, therefore, our organism, need energy to function at their best, which is mainly produced by mitochondria. These intracellular organelles generate energy from food macromolecules across the Krebs cycle by oxidative phosphorylation. Energy is developed by converting adenosine triphosphate (ATP) to adenosine diphosphate (ADP). It is essential, for adequate mitochondrial energy production in the form of ATP, to have the right number of well-functioning mitochondria and the right amount of oxygen (O2) available. Unfortunately, the aging process and the chronic diseases that arise over the years are associated with a reduction in the number of mitochondria and their insufficient functioning. Among the chronic diseases related to significant damage of the arteries with a reduction in the supply of O2, there is atherosclerosis, where the process of atherothrombosis occurs. To keep our organs well-functioning despite aging, we must therefore protect our mitochondria and arteries. This can be achieved by intervening early in prevention with a lifestyle correction and diet integration with effective natural substances or, in some cases, with drugs. Among the many natural substances that have good scientific support, we have chosen four that have demonstrated benefits in the absence of side effects and that we know best: quercetin and pyrroloquinoline quinone to stimulate mitochondrial biogenesis and mitophagy, while L-arginine and nattokinase to protect the arteries from atherothrombosis.
DOI: https://doi.org/10.37349/ec.2025.101268
Scientific evidence seems to indicate that, in males, intense and prolonged endurance sport can favor the onset of atrial fibrillation. A plausible explanation may be the impact that intense endurance sports produce on the three vertices of Coumel’s triangle. However, genetics is probably also involved in translating this impact into an arrhythmic phenotype. On a management level, the first task of the cardiologist is to exclude the presence of structural heart disease, channelopathy, endocrine and/or electrolyte disorders, and substance use. As for the treatment of arrhythmia, the “CARE” paradigm proposed by the latest ESC guidelines should probably be accompanied by detraining, although this suggestion is often rejected by the athlete. Anticoagulant therapy, where indicated, must take into account the risk of trauma that the sport entails, even if the particular pharmacodynamics/pharmacokinetics of DOACs should allow training/competition to take place when the anticoagulant effect of the previous administration has completely or almost completely worn off.
Scientific evidence seems to indicate that, in males, intense and prolonged endurance sport can favor the onset of atrial fibrillation. A plausible explanation may be the impact that intense endurance sports produce on the three vertices of Coumel’s triangle. However, genetics is probably also involved in translating this impact into an arrhythmic phenotype. On a management level, the first task of the cardiologist is to exclude the presence of structural heart disease, channelopathy, endocrine and/or electrolyte disorders, and substance use. As for the treatment of arrhythmia, the “CARE” paradigm proposed by the latest ESC guidelines should probably be accompanied by detraining, although this suggestion is often rejected by the athlete. Anticoagulant therapy, where indicated, must take into account the risk of trauma that the sport entails, even if the particular pharmacodynamics/pharmacokinetics of DOACs should allow training/competition to take place when the anticoagulant effect of the previous administration has completely or almost completely worn off.
DOI: https://doi.org/10.37349/ec.2025.101267
We report a rare case of non-ischemic cardiomyopathy in a 62-year-old female with mucous membrane pemphigoid following rituximab therapy. The patient presented with dyspnea and chest pain, and cardiac evaluation-including transthoracic echocardiogram and nuclear medicine stress testing-revealed left ventricular dysfunction without evidence of ischemia. Given the temporal association and absence of other etiologies, rituximab was suspected as the causative agent. This case emphasizes the importance of recognizing the potential cardiotoxic effects of biological agents used in autoimmune disease management and supports the consideration of cardiac surveillance in at-risk patients receiving rituximab.
We report a rare case of non-ischemic cardiomyopathy in a 62-year-old female with mucous membrane pemphigoid following rituximab therapy. The patient presented with dyspnea and chest pain, and cardiac evaluation-including transthoracic echocardiogram and nuclear medicine stress testing-revealed left ventricular dysfunction without evidence of ischemia. Given the temporal association and absence of other etiologies, rituximab was suspected as the causative agent. This case emphasizes the importance of recognizing the potential cardiotoxic effects of biological agents used in autoimmune disease management and supports the consideration of cardiac surveillance in at-risk patients receiving rituximab.
DOI: https://doi.org/10.37349/ec.2025.101266
Fungal endocarditis (FE) is still an uncommon but devastating infection, especially when immunosuppression, prosthetic valve surgery, or prolonged health care is involved. Although being only responsible for 1–6% of infective endocarditis cases, the mortality rate is higher than 40–60% due to the time lag from diagnosis and therapeutic complexity. Etiology is led by Candida species, especially Candida albicans, followed by Aspergillus, and new pathogens like multidrug-resistant Candida auris are also seen. Non-C. albicans and the biofilm-forming species also add more complexity to the manageability. Diagnosis is challenging due to the high percentage of culture-negative cases, particularly for molds, requiring sophisticated investigations such as fungal biomarkers (β-D-glucan, galactomannan), molecular tests, and imaging studies such as 18F-FDG PET/CT (fluorine-18 fluorodeoxyglucose positron emission tomography/computed tomography). Early transesophageal echocardiography is crucial in the diagnosis of vegetations, whereas histopathology of resected non-cardiac tissue offers a definitive diagnosis. Treatment requires aggressive antifungal therapy, echinocandins, amphotericin B, or azoles, in conjunction with urgent valve surgery to reduce embolic risk and enhance survival. However, drug resistance, biofilm resistance, and patient comorbidities counteract the efficacy. Novel treatments such as rezafungin and ibrexafungerp are promising but have limited clinical hands-on evidence. Risk factors of immunosuppression, indwelling devices, and IV drug use imply a need for increased clinical suspicion in high-risk groups. Although there have been minor improvements in FE survival, the grim situation of FE persists, highlighting the importance of a multidisciplinary approach, early diagnosis, and tailored antifungal therapy to control this deadly infection.
Fungal endocarditis (FE) is still an uncommon but devastating infection, especially when immunosuppression, prosthetic valve surgery, or prolonged health care is involved. Although being only responsible for 1–6% of infective endocarditis cases, the mortality rate is higher than 40–60% due to the time lag from diagnosis and therapeutic complexity. Etiology is led by Candida species, especially Candida albicans, followed by Aspergillus, and new pathogens like multidrug-resistant Candida auris are also seen. Non-C. albicans and the biofilm-forming species also add more complexity to the manageability. Diagnosis is challenging due to the high percentage of culture-negative cases, particularly for molds, requiring sophisticated investigations such as fungal biomarkers (β-D-glucan, galactomannan), molecular tests, and imaging studies such as 18F-FDG PET/CT (fluorine-18 fluorodeoxyglucose positron emission tomography/computed tomography). Early transesophageal echocardiography is crucial in the diagnosis of vegetations, whereas histopathology of resected non-cardiac tissue offers a definitive diagnosis. Treatment requires aggressive antifungal therapy, echinocandins, amphotericin B, or azoles, in conjunction with urgent valve surgery to reduce embolic risk and enhance survival. However, drug resistance, biofilm resistance, and patient comorbidities counteract the efficacy. Novel treatments such as rezafungin and ibrexafungerp are promising but have limited clinical hands-on evidence. Risk factors of immunosuppression, indwelling devices, and IV drug use imply a need for increased clinical suspicion in high-risk groups. Although there have been minor improvements in FE survival, the grim situation of FE persists, highlighting the importance of a multidisciplinary approach, early diagnosis, and tailored antifungal therapy to control this deadly infection.
DOI: https://doi.org/10.37349/ec.2025.101264
We aim to describe a unique case of a desmoplakin gene mutation with refractory ventricular arrhythmia and cardiomyopathy. We describe a 29-year-old man hospitalized for chest pain and cardiomyopathy, who subsequently developed ventricular arrhythmia that was refractory to multiple antiarrhythmic agents, ablation, immunotherapy, and sympathectomy. Diagnostic studies included coronary catheterization, cardiac MRI, and endomyocardial biopsy. He underwent placement of an Impella 5.5 temporary mechanical support device for multi-organ failure; eventually requiring a Heartmate 3 left ventricular assist device. This report details how cardiac MRI, endomyocardial biopsy, and genetic testing are crucial diagnostic modalities when assessing patients with refractory arrhythmias or myocarditis. Pathogenic variants in the desmoplakin gene can be associated with significant morbidity in patients and require multidisciplinary care from cardiology, electrophysiology, advanced heart failure, and cardiac surgery. Arrhythmogenic cardiomyopathies should be considered for patients suffering repeated episodes of myocarditis or refractory ventricular arrhythmias. We utilized various criteria of functional, electrocardiographic, arrhythmic, tissue characterization, and genetic findings to establish the diagnosis of arrhythmogenic cardiomyopathy, which will be discussed later in this paper.
We aim to describe a unique case of a desmoplakin gene mutation with refractory ventricular arrhythmia and cardiomyopathy. We describe a 29-year-old man hospitalized for chest pain and cardiomyopathy, who subsequently developed ventricular arrhythmia that was refractory to multiple antiarrhythmic agents, ablation, immunotherapy, and sympathectomy. Diagnostic studies included coronary catheterization, cardiac MRI, and endomyocardial biopsy. He underwent placement of an Impella 5.5 temporary mechanical support device for multi-organ failure; eventually requiring a Heartmate 3 left ventricular assist device. This report details how cardiac MRI, endomyocardial biopsy, and genetic testing are crucial diagnostic modalities when assessing patients with refractory arrhythmias or myocarditis. Pathogenic variants in the desmoplakin gene can be associated with significant morbidity in patients and require multidisciplinary care from cardiology, electrophysiology, advanced heart failure, and cardiac surgery. Arrhythmogenic cardiomyopathies should be considered for patients suffering repeated episodes of myocarditis or refractory ventricular arrhythmias. We utilized various criteria of functional, electrocardiographic, arrhythmic, tissue characterization, and genetic findings to establish the diagnosis of arrhythmogenic cardiomyopathy, which will be discussed later in this paper.
DOI: https://doi.org/10.37349/ec.2025.101265
We report the case of a 58-year-old patient with chronic ischemic syndrome who underwent dipyridamole stress echocardiography for the evaluation of chest pain. The stress test was negative with normal coronary flow velocity reserve, preserved chronotropic competence, and no inducible wall motion abnormalities. However, upon administration of aminophylline at the end of the test, the patient developed acute chest pain, ST-segment elevation, and severe apical wall motion abnormalities. These findings resolved with intravenous nitrates. Subsequent coronary angiography revealed a significant vasospastic stenosis in the left anterior descending artery superimposed on a mild organic stenosis of around 50% after intracoronary nitrates. The coronary stenosis was successfully treated with a drug-eluting stent. This case highlights the potential for vasospastic angina to be unmasked following vasodilator reversal, even after a negative stress echocardiography.
We report the case of a 58-year-old patient with chronic ischemic syndrome who underwent dipyridamole stress echocardiography for the evaluation of chest pain. The stress test was negative with normal coronary flow velocity reserve, preserved chronotropic competence, and no inducible wall motion abnormalities. However, upon administration of aminophylline at the end of the test, the patient developed acute chest pain, ST-segment elevation, and severe apical wall motion abnormalities. These findings resolved with intravenous nitrates. Subsequent coronary angiography revealed a significant vasospastic stenosis in the left anterior descending artery superimposed on a mild organic stenosis of around 50% after intracoronary nitrates. The coronary stenosis was successfully treated with a drug-eluting stent. This case highlights the potential for vasospastic angina to be unmasked following vasodilator reversal, even after a negative stress echocardiography.
DOI: https://doi.org/10.37349/ec.2025.101263
Peripartum cardiomyopathy (PPCM) is a rare condition characterized by heart failure secondary to left ventricular systolic dysfunction, occurring in women during the last trimester of pregnancy or within five months postpartum. Despite advancements in research, PPCM remains a life-threatening disorder associated with significant maternal morbidity and mortality. The primary clinical manifestations of PPCM result from heart failure due to impaired left ventricular systolic function. This article reviews the epidemiology, etiology, diagnostic criteria, management strategies, and outcomes of PPCM. Additionally, we present a case of a 34-year-old woman with PPCM who achieved full recovery within nine months, underscoring the importance of early recognition, prompt treatment, standardized medication, and regular follow-up.
Peripartum cardiomyopathy (PPCM) is a rare condition characterized by heart failure secondary to left ventricular systolic dysfunction, occurring in women during the last trimester of pregnancy or within five months postpartum. Despite advancements in research, PPCM remains a life-threatening disorder associated with significant maternal morbidity and mortality. The primary clinical manifestations of PPCM result from heart failure due to impaired left ventricular systolic function. This article reviews the epidemiology, etiology, diagnostic criteria, management strategies, and outcomes of PPCM. Additionally, we present a case of a 34-year-old woman with PPCM who achieved full recovery within nine months, underscoring the importance of early recognition, prompt treatment, standardized medication, and regular follow-up.
DOI: https://doi.org/10.37349/ec.2025.101262
This article belongs to the special issue Cardiovascular Risk for Mothers and Offspring Resulting from Complicated Pregnancy
Aim:
Coronary heart disease (CHD) has been the leading cause of death worldwide for several decades. Non-alcoholic fatty liver disease (NAFLD), the most common liver pathology, is considered a risk factor (RF) for the development of CHD and a predictor of an unfavourable prognosis. Our study aimed to compare cardiometabolic parameters in patients with CHD with and without NAFLD.
Methods:
The study prospectively included 85 patients with CHD, 61 with NAFLD (group I) and 24 without NAFLD (group II). In both groups, a comparative analysis of RF, anthropometric parameters, lipidogram, glycemic profile, brachiocephalic arteries (BCA) ultrasound (USD), and heart structural and geometric parameters according to echocardiography (EchoCG) and coronary calcium (CC) parameters was performed.
Results:
Patients with CHD and NAFLD had statistically significantly higher levels of total cholesterol, very low-density lipoproteins, triglycerides, insulin, heart structural parameters, and CC.
Conclusions:
Thus, the relationship between NAFLD and CHD is two-way, and liver diseases can exacerbate the course of cardiovascular diseases (CVD).
Aim:
Coronary heart disease (CHD) has been the leading cause of death worldwide for several decades. Non-alcoholic fatty liver disease (NAFLD), the most common liver pathology, is considered a risk factor (RF) for the development of CHD and a predictor of an unfavourable prognosis. Our study aimed to compare cardiometabolic parameters in patients with CHD with and without NAFLD.
Methods:
The study prospectively included 85 patients with CHD, 61 with NAFLD (group I) and 24 without NAFLD (group II). In both groups, a comparative analysis of RF, anthropometric parameters, lipidogram, glycemic profile, brachiocephalic arteries (BCA) ultrasound (USD), and heart structural and geometric parameters according to echocardiography (EchoCG) and coronary calcium (CC) parameters was performed.
Results:
Patients with CHD and NAFLD had statistically significantly higher levels of total cholesterol, very low-density lipoproteins, triglycerides, insulin, heart structural parameters, and CC.
Conclusions:
Thus, the relationship between NAFLD and CHD is two-way, and liver diseases can exacerbate the course of cardiovascular diseases (CVD).
DOI: https://doi.org/10.37349/ec.2025.101260
Cardiac papillary fibroelastoma (CPF) is a rare, benign cardiac tumor with a significant risk for embolic complications, most notably ischemic stroke. This paper presents a case of a 54-year-old woman with cryptogenic stroke ultimately attributed to a CPF on the aortic valve, discovered via transesophageal echocardiography (TEE) after an initial unremarkable transthoracic study. Following diagnosis, the patient was treated with anticoagulation and scheduled for surgical excision. Although often asymptomatic, CPF can present with life-threatening embolic events, underscoring the importance of timely diagnosis through high-resolution imaging, particularly TEE. Surgical excision remains the definitive treatment in symptomatic or high-risk cases, but management of incidental, asymptomatic tumors remains controversial due to the absence of formal guidelines. This paper emphasizes the need for heightened clinical suspicion of CPF in cryptogenic stroke and advocates for individualized treatment approaches based on tumor characteristics and embolic risk.
Cardiac papillary fibroelastoma (CPF) is a rare, benign cardiac tumor with a significant risk for embolic complications, most notably ischemic stroke. This paper presents a case of a 54-year-old woman with cryptogenic stroke ultimately attributed to a CPF on the aortic valve, discovered via transesophageal echocardiography (TEE) after an initial unremarkable transthoracic study. Following diagnosis, the patient was treated with anticoagulation and scheduled for surgical excision. Although often asymptomatic, CPF can present with life-threatening embolic events, underscoring the importance of timely diagnosis through high-resolution imaging, particularly TEE. Surgical excision remains the definitive treatment in symptomatic or high-risk cases, but management of incidental, asymptomatic tumors remains controversial due to the absence of formal guidelines. This paper emphasizes the need for heightened clinical suspicion of CPF in cryptogenic stroke and advocates for individualized treatment approaches based on tumor characteristics and embolic risk.
DOI: https://doi.org/10.37349/ec.2025.101261
Aim:
The efficacy of composite valve graft (CVG) versus stentless aortic root replacement (SARR) in patients with aortic valve and root pathologies remains a subject of debate. This study aims to analyze the in-hospital outcomes and long-term survival of these two surgical approaches.
Methods:
A retrospective analysis was conducted on 594 patients who underwent ARR between July 2003 and December 2023. Of these, 346 received a stentless aortic root and 248 CVG (100 biological and 148 mechanical). Propensity score matching (PSM) was utilized to create well-balanced cohorts based on preoperative demographics and intraoperative characteristics. Univariable and multivariable regression analyses were performed to evaluate in-hospital mortality and long-term survival rates. Kaplan-Meier curves were constructed to visualize survival outcomes.
Results:
After PSM, 212 patients in each group were well-balanced in terms of baseline characteristics. The analysis of in-hospital outcomes revealed no significant differences between the SARR and CVG groups for key outcomes except neurological complications that were consistently higher in the CVG group, with a significant difference observed in both unmatched (8.4% vs. 4.9%, P = 0.014) and matched cohorts (8.5% vs. 4.3%, P = 0.022). Long-term survival analysis in the matched cohorts demonstrated a statistically significant survival advantage for the SARR group, with a 20-year survival rate of 54% compared to 47% for the CVG group (log-rank P value of 0.047). Further analysis by specific graft type within the matched groups suggested that xenografts might offer a significant survival advantage (log-rank P value of 0.009).
Conclusions:
While SARR and CVG provided similar in-hospital outcomes, SARR, particularly xenografts, demonstrated a significant long-term survival advantage. Xenografts may be a preferable option for patients, especially those with longer life expectancies, due to their durability and reduced need for anticoagulation.
Aim:
The efficacy of composite valve graft (CVG) versus stentless aortic root replacement (SARR) in patients with aortic valve and root pathologies remains a subject of debate. This study aims to analyze the in-hospital outcomes and long-term survival of these two surgical approaches.
Methods:
A retrospective analysis was conducted on 594 patients who underwent ARR between July 2003 and December 2023. Of these, 346 received a stentless aortic root and 248 CVG (100 biological and 148 mechanical). Propensity score matching (PSM) was utilized to create well-balanced cohorts based on preoperative demographics and intraoperative characteristics. Univariable and multivariable regression analyses were performed to evaluate in-hospital mortality and long-term survival rates. Kaplan-Meier curves were constructed to visualize survival outcomes.
Results:
After PSM, 212 patients in each group were well-balanced in terms of baseline characteristics. The analysis of in-hospital outcomes revealed no significant differences between the SARR and CVG groups for key outcomes except neurological complications that were consistently higher in the CVG group, with a significant difference observed in both unmatched (8.4% vs. 4.9%, P = 0.014) and matched cohorts (8.5% vs. 4.3%, P = 0.022). Long-term survival analysis in the matched cohorts demonstrated a statistically significant survival advantage for the SARR group, with a 20-year survival rate of 54% compared to 47% for the CVG group (log-rank P value of 0.047). Further analysis by specific graft type within the matched groups suggested that xenografts might offer a significant survival advantage (log-rank P value of 0.009).
Conclusions:
While SARR and CVG provided similar in-hospital outcomes, SARR, particularly xenografts, demonstrated a significant long-term survival advantage. Xenografts may be a preferable option for patients, especially those with longer life expectancies, due to their durability and reduced need for anticoagulation.
DOI: https://doi.org/10.37349/ec.2025.101259
Aim:
Atherosclerosis and diabetes mellitus (DM) often lead to severe conditions, such as acute ischemic stroke (AIS), cardiovascular disease (CVD), and chronic kidney disease (CKD). Some cancers are also associated with atherosclerosis. Therefore, identifying novel autoantibody biomarkers associated with atherosclerosis-related conditions is crucial for improving early diagnosis and risk assessment.
Methods:
We used an array of 9,480 proteins to detect IgG antibodies in the serum of patients with atherosclerosis. Following this screening, we quantified the antibody levels using an amplified luminescent proximity homogeneous assay-linked immunosorbent assay (AlphaLISA) with recombinant antigen proteins.
Results:
Ubiquitin conjugating enzyme E2 E3 (UBE2E3) was identified as a candidate antigen recognized by IgG antibodies in the sera of individuals diagnosed with atherosclerosis. Compared with healthy donors, significantly higher serum antibody levels against UBE2E3 were found in patients with AIS, DM, CVD, CKD, esophageal cancer (EC), and gastric cancer (GC), but not in those with colorectal cancer (CRC). Receiver operating characteristic (ROC) analysis revealed that the higher areas under the ROC curves for anti-UBE2E3 antibodies were observed in DM- or nephrosclerosis-associated CKD than in the others. Spearman’s correlation analysis revealed that serum anti-UBE2E3 antibody (s-UBE2E3-Ab) levels were associated with the plaque score, maximum intima-media thickness, and cardio-ankle vascular index, which are typical indices of atherosclerosis and stenosis. In the survival analysis of GC and CRC, patients who were s-UBE2E3-Ab-positive had significantly poorer prognoses than patients who were s-UBE2E3-Ab-negative. The difference became more prominent when s-UBE2E3-Abs were combined with anti-differential screening-selected gene aberrant in neuroblastoma antibody (DAN-Ab) or sclerostin domain-containing protein 1 (SOSTDC1), which are bone morphogenetic protein (BMP) antagonists.
Conclusions:
The s-UBE2E3-Ab marker is highly associated with atherosclerosis-related diseases, such as AIS, CVD, DM, CKD, and digestive tract cancers, suggesting the involvement of BMP signals.
Aim:
Atherosclerosis and diabetes mellitus (DM) often lead to severe conditions, such as acute ischemic stroke (AIS), cardiovascular disease (CVD), and chronic kidney disease (CKD). Some cancers are also associated with atherosclerosis. Therefore, identifying novel autoantibody biomarkers associated with atherosclerosis-related conditions is crucial for improving early diagnosis and risk assessment.
Methods:
We used an array of 9,480 proteins to detect IgG antibodies in the serum of patients with atherosclerosis. Following this screening, we quantified the antibody levels using an amplified luminescent proximity homogeneous assay-linked immunosorbent assay (AlphaLISA) with recombinant antigen proteins.
Results:
Ubiquitin conjugating enzyme E2 E3 (UBE2E3) was identified as a candidate antigen recognized by IgG antibodies in the sera of individuals diagnosed with atherosclerosis. Compared with healthy donors, significantly higher serum antibody levels against UBE2E3 were found in patients with AIS, DM, CVD, CKD, esophageal cancer (EC), and gastric cancer (GC), but not in those with colorectal cancer (CRC). Receiver operating characteristic (ROC) analysis revealed that the higher areas under the ROC curves for anti-UBE2E3 antibodies were observed in DM- or nephrosclerosis-associated CKD than in the others. Spearman’s correlation analysis revealed that serum anti-UBE2E3 antibody (s-UBE2E3-Ab) levels were associated with the plaque score, maximum intima-media thickness, and cardio-ankle vascular index, which are typical indices of atherosclerosis and stenosis. In the survival analysis of GC and CRC, patients who were s-UBE2E3-Ab-positive had significantly poorer prognoses than patients who were s-UBE2E3-Ab-negative. The difference became more prominent when s-UBE2E3-Abs were combined with anti-differential screening-selected gene aberrant in neuroblastoma antibody (DAN-Ab) or sclerostin domain-containing protein 1 (SOSTDC1), which are bone morphogenetic protein (BMP) antagonists.
Conclusions:
The s-UBE2E3-Ab marker is highly associated with atherosclerosis-related diseases, such as AIS, CVD, DM, CKD, and digestive tract cancers, suggesting the involvement of BMP signals.
DOI: https://doi.org/10.37349/ec.2025.101258
Analysis of intraventricular pressure gradients has gained interest due to the recent development of a new method of image analysis based on cardiac magnetic resonance feature tracking or echocardiographic speckle tracking. Currently, images acquired from routinely performed cardiac magnetic resonance or echocardiography can be analyzed, and the left ventricular hemodynamic forces (HDF) curves generated and displayed for measurements. This modality has been applied in clinical scenarios and normal reference values are available. However, different parameters have been derived in the available studies on HDF, and there is no standardization on which parameters should be reported. In this short review, we describe how to assess HDF and discuss the different parameters that can be derived from the HDF curves.
Analysis of intraventricular pressure gradients has gained interest due to the recent development of a new method of image analysis based on cardiac magnetic resonance feature tracking or echocardiographic speckle tracking. Currently, images acquired from routinely performed cardiac magnetic resonance or echocardiography can be analyzed, and the left ventricular hemodynamic forces (HDF) curves generated and displayed for measurements. This modality has been applied in clinical scenarios and normal reference values are available. However, different parameters have been derived in the available studies on HDF, and there is no standardization on which parameters should be reported. In this short review, we describe how to assess HDF and discuss the different parameters that can be derived from the HDF curves.
DOI: https://doi.org/10.37349/ec.2025.101257
An electrocardiogram (ECG) is a vital diagnostic tool used during cardiac imaging stress testing to evaluate the heart’s electrical activity under stress conditions. This combination of ECG and stress imaging testing provides comprehensive insights into cardiac function, particularly in detecting coronary artery disease (CAD) and assessing overall heart health. An ECG continuously monitors the heart’s electrical signals, capturing data on heart rate, rhythm, and electrical conduction patterns. The value of the ECG in this context lies in its ability to detect ischemic changes, which occur when there is insufficient blood flow to the heart muscle due to narrowed or blocked coronary arteries, but also for coronary vasospasm or coronary microvascular disease. Specific ECG changes, such as ST-segment depression or elevation, and the appearance of arrhythmias, can indicate myocardial ischemia. These findings, when correlated with symptoms like chest pain or shortness of breath during the test, may provide strong evidence for CAD even in the absence of diagnostic abnormality of cardiac imaging with regional wall motion or perfusion changes. Additionally, the ECG helps identify other conditions that may manifest under stress, such as arrhythmias or conduction abnormalities, which might not be apparent at rest. The ECG’s role extends beyond diagnosis. It helps stratify patients based on their risk of adverse cardiac events. For example, an abnormal ECG during a negative cardiac stress imaging test can suggest an increased likelihood of coronary calcification or abnormal coronary flow reserve and increased risk in the long term for cardiac events. In summary, the ECG is a valuable component of cardiac imaging stress testing. It provides real-time, non-invasive monitoring of the heart’s electrical activity under stress, aiding in the diagnosis and risk assessment of CAD and other cardiac conditions. This enhances patient management by guiding treatment decisions and preventive strategies.
An electrocardiogram (ECG) is a vital diagnostic tool used during cardiac imaging stress testing to evaluate the heart’s electrical activity under stress conditions. This combination of ECG and stress imaging testing provides comprehensive insights into cardiac function, particularly in detecting coronary artery disease (CAD) and assessing overall heart health. An ECG continuously monitors the heart’s electrical signals, capturing data on heart rate, rhythm, and electrical conduction patterns. The value of the ECG in this context lies in its ability to detect ischemic changes, which occur when there is insufficient blood flow to the heart muscle due to narrowed or blocked coronary arteries, but also for coronary vasospasm or coronary microvascular disease. Specific ECG changes, such as ST-segment depression or elevation, and the appearance of arrhythmias, can indicate myocardial ischemia. These findings, when correlated with symptoms like chest pain or shortness of breath during the test, may provide strong evidence for CAD even in the absence of diagnostic abnormality of cardiac imaging with regional wall motion or perfusion changes. Additionally, the ECG helps identify other conditions that may manifest under stress, such as arrhythmias or conduction abnormalities, which might not be apparent at rest. The ECG’s role extends beyond diagnosis. It helps stratify patients based on their risk of adverse cardiac events. For example, an abnormal ECG during a negative cardiac stress imaging test can suggest an increased likelihood of coronary calcification or abnormal coronary flow reserve and increased risk in the long term for cardiac events. In summary, the ECG is a valuable component of cardiac imaging stress testing. It provides real-time, non-invasive monitoring of the heart’s electrical activity under stress, aiding in the diagnosis and risk assessment of CAD and other cardiac conditions. This enhances patient management by guiding treatment decisions and preventive strategies.
DOI: https://doi.org/10.37349/ec.2025.101256
This article belongs to the special issue Multimodality Imaging in Ischemic Heart Disease
Tuberculosis (TB) continues to pose a significant public health burden in endemic regions, remaining a leading cause of morbidity and mortality. Although TB is associated with a range of complications, the occurrence of intracardiac thrombus is an exceptionally rare manifestation. We report the case of a 62-year-old male with active pulmonary TB, who had been on anti-tubercular therapy for one month and presented with recurrent syncope and exertional dyspnea. Transthoracic 2D echocardiography revealed a large, mobile thrombus in the left ventricular apex. Evaluation for underlying hypercoagulable states was unremarkable. The patient was managed with anticoagulation therapy in conjunction with ongoing anti-tubercular treatment. This case underscores the importance of clinical vigilance for rare thrombotic complications in TB to facilitate timely diagnosis and appropriate management.
Tuberculosis (TB) continues to pose a significant public health burden in endemic regions, remaining a leading cause of morbidity and mortality. Although TB is associated with a range of complications, the occurrence of intracardiac thrombus is an exceptionally rare manifestation. We report the case of a 62-year-old male with active pulmonary TB, who had been on anti-tubercular therapy for one month and presented with recurrent syncope and exertional dyspnea. Transthoracic 2D echocardiography revealed a large, mobile thrombus in the left ventricular apex. Evaluation for underlying hypercoagulable states was unremarkable. The patient was managed with anticoagulation therapy in conjunction with ongoing anti-tubercular treatment. This case underscores the importance of clinical vigilance for rare thrombotic complications in TB to facilitate timely diagnosis and appropriate management.
DOI: https://doi.org/10.37349/ec.2025.101255
Aim:
Evaluate the role of myocardial work by echocardiography and determine its utility as an early diagnosis of cardiotoxicity.
Methods:
Single-center included 180 patients over 18 years old undergoing chemotherapy, the definition of cardiotoxicity for this study was to observe a left ventricular ejection fraction (LVEF) less than 50% and, or a global longitudinal strain (GLS) less than 16%. With these parameters, we divided the population into two groups, with cardiotoxicity and without cardiotoxicity. ROC curves were performed to determine the best cut-off point for global myocardial work to define cardiotoxicity. 2 × 2 tables were made to calculate sensitivity, specificity, positive predictive value, and negative predictive value.
Results:
Cardiotoxicity was established by obtaining cutoff points for global myocardial work index (GWI) with values lower than 1,381.5 mmHg%, Global Constructive Work (GCW) of 1,722 mmHg%, and myocardial efficiency [Global Work Efficiency (GWE)] of 88.5%, with a sensitivity (58.8%, 65.6%, and 52.9%) and specificity (91.8%, 82.1%, and 89.6%) respectively.
Conclusions:
We propose the measurement of myocardial work as a diagnostic tool for cardiotoxicity, as it has good specificity and negative predictive value, serving as an early diagnostic tool for cardiotoxicity without waiting for a decrease in LVEF and without being a marker influenced by loading conditions, in patients undergoing antineoplastic treatment.
Aim:
Evaluate the role of myocardial work by echocardiography and determine its utility as an early diagnosis of cardiotoxicity.
Methods:
Single-center included 180 patients over 18 years old undergoing chemotherapy, the definition of cardiotoxicity for this study was to observe a left ventricular ejection fraction (LVEF) less than 50% and, or a global longitudinal strain (GLS) less than 16%. With these parameters, we divided the population into two groups, with cardiotoxicity and without cardiotoxicity. ROC curves were performed to determine the best cut-off point for global myocardial work to define cardiotoxicity. 2 × 2 tables were made to calculate sensitivity, specificity, positive predictive value, and negative predictive value.
Results:
Cardiotoxicity was established by obtaining cutoff points for global myocardial work index (GWI) with values lower than 1,381.5 mmHg%, Global Constructive Work (GCW) of 1,722 mmHg%, and myocardial efficiency [Global Work Efficiency (GWE)] of 88.5%, with a sensitivity (58.8%, 65.6%, and 52.9%) and specificity (91.8%, 82.1%, and 89.6%) respectively.
Conclusions:
We propose the measurement of myocardial work as a diagnostic tool for cardiotoxicity, as it has good specificity and negative predictive value, serving as an early diagnostic tool for cardiotoxicity without waiting for a decrease in LVEF and without being a marker influenced by loading conditions, in patients undergoing antineoplastic treatment.
DOI: https://doi.org/10.37349/ec.2025.101254
Aim:
Significant tricuspid regurgitation (TR) may be a confounding factor when assessing right ventricular (RV) function with imaging techniques. Global myocardial work (GMW) has been proposed as a non-invasive surrogate of RV pressure–volume loops, and it might provide a more accurate evaluation of RV performance than standard echocardiographic parameters, accounting for both afterload and myocardial work efficiency. The aim of this study was to assess the relationship between RV GMW and hemodynamic indices of prognostic significance in pulmonary hypertension (PH) and to compare RV GMW in PH patients with or without TR.
Methods:
This was a proof-of-concept study. Thirty consecutive patients with PH undergoing diagnostic right heart catheterization (RHC) in sinus rhythm were enrolled. Echocardiography was performed in all patients within two hours of RHC.
Results:
Global work efficiency (GWE) was directly correlated (r = 0.562, p = 0.006), whereas global wasted work (GWW) was inversely correlated with stroke volume index (r = –0.447, p = 0.037). Poorer correlation was observed with tricuspid annular plane systolic excursion (TAPSE), and no correlation was observed with TAPSE/sPAP (ratio of TAPSE to systolic pulmonary artery pressure). Patients with moderate/severe TR had lower GWE [83% (77–89%) vs. 96% (94–96%), p < 0.001] and higher GWW [137% (90–179%) vs. 25% (18–89%), p = 0.002]. Similar results were obtained when the analysis was applied to subgroups of patients stratified according to either preserved or poor TAPSE/sPAP.
Conclusions:
RV myocardial work is more strongly associated with hemodynamic indicators of prognosis in PH than standard echocardiographic parameters. Patients with moderate/severe TR have significantly lower values of work efficiency and higher values of wasted work as compared to those without significant TR.
Aim:
Significant tricuspid regurgitation (TR) may be a confounding factor when assessing right ventricular (RV) function with imaging techniques. Global myocardial work (GMW) has been proposed as a non-invasive surrogate of RV pressure–volume loops, and it might provide a more accurate evaluation of RV performance than standard echocardiographic parameters, accounting for both afterload and myocardial work efficiency. The aim of this study was to assess the relationship between RV GMW and hemodynamic indices of prognostic significance in pulmonary hypertension (PH) and to compare RV GMW in PH patients with or without TR.
Methods:
This was a proof-of-concept study. Thirty consecutive patients with PH undergoing diagnostic right heart catheterization (RHC) in sinus rhythm were enrolled. Echocardiography was performed in all patients within two hours of RHC.
Results:
Global work efficiency (GWE) was directly correlated (r = 0.562, p = 0.006), whereas global wasted work (GWW) was inversely correlated with stroke volume index (r = –0.447, p = 0.037). Poorer correlation was observed with tricuspid annular plane systolic excursion (TAPSE), and no correlation was observed with TAPSE/sPAP (ratio of TAPSE to systolic pulmonary artery pressure). Patients with moderate/severe TR had lower GWE [83% (77–89%) vs. 96% (94–96%), p < 0.001] and higher GWW [137% (90–179%) vs. 25% (18–89%), p = 0.002]. Similar results were obtained when the analysis was applied to subgroups of patients stratified according to either preserved or poor TAPSE/sPAP.
Conclusions:
RV myocardial work is more strongly associated with hemodynamic indicators of prognosis in PH than standard echocardiographic parameters. Patients with moderate/severe TR have significantly lower values of work efficiency and higher values of wasted work as compared to those without significant TR.
DOI: https://doi.org/10.37349/ec.2025.101252
Preterm birth, defined as delivery before 37 weeks of gestation, represents a global health concern linked to substantial cardiovascular risk later in life. Individuals born preterm, especially at earlier gestational ages, exhibit increased rates of hypertension, heart failure, and ischemic heart disease. The underlying mechanisms include disrupted fetal programming, impaired vascular remodeling, chronic neonatal inflammation, neuroendocrine immaturity, and epigenetic alterations. This review synthesizes current epidemiological evidence from large cohort studies and meta-analyses, integrating mechanistic insights from developmental biology. We discuss distinct prematurity categories—extremely preterm (< 28 weeks), very preterm (28–32 weeks), and moderate to late preterm (33–37 weeks)—highlighting their association with graded cardiovascular risk. Recent findings emphasize the role of non-transmitted parental genes and prenatal environmental toxic metal exposure as additional critical factors influencing fetal cardiovascular programming. A total of 57 articles, identified through a systematic search of PubMed, Embase, and Cochrane databases, were included to address these topics comprehensively. Early identification of preterm-born individuals as a high-risk cardiovascular group is essential for targeted screening, prevention, and interventions from childhood into adulthood. Future studies leveraging multi-omics and epigenetic approaches will further clarify these mechanisms, informing evidence-based guidelines to reduce cardiovascular morbidity associated with preterm birth.
Preterm birth, defined as delivery before 37 weeks of gestation, represents a global health concern linked to substantial cardiovascular risk later in life. Individuals born preterm, especially at earlier gestational ages, exhibit increased rates of hypertension, heart failure, and ischemic heart disease. The underlying mechanisms include disrupted fetal programming, impaired vascular remodeling, chronic neonatal inflammation, neuroendocrine immaturity, and epigenetic alterations. This review synthesizes current epidemiological evidence from large cohort studies and meta-analyses, integrating mechanistic insights from developmental biology. We discuss distinct prematurity categories—extremely preterm (< 28 weeks), very preterm (28–32 weeks), and moderate to late preterm (33–37 weeks)—highlighting their association with graded cardiovascular risk. Recent findings emphasize the role of non-transmitted parental genes and prenatal environmental toxic metal exposure as additional critical factors influencing fetal cardiovascular programming. A total of 57 articles, identified through a systematic search of PubMed, Embase, and Cochrane databases, were included to address these topics comprehensively. Early identification of preterm-born individuals as a high-risk cardiovascular group is essential for targeted screening, prevention, and interventions from childhood into adulthood. Future studies leveraging multi-omics and epigenetic approaches will further clarify these mechanisms, informing evidence-based guidelines to reduce cardiovascular morbidity associated with preterm birth.
DOI: https://doi.org/10.37349/ec.2025.101253
Age-related atrial fibrillation (AF) is a common condition that has yet to be fully understood, with mechanisms to explain its development under investigation. Notably, cellular senescence, cardiac fibrosis, coronary ischemia, cardiac valvular disease, autonomic dysfunction, channelopathies, and immune system remodeling are processes that have been seen to occur with aging and ample evidence has shown their association with the development of AF. Despite robust therapeutic approaches, the incidence of AF continues to rise, suggesting that the dynamic, multi-faceted interactions leading to AF are incompletely understood. One of the newer mechanisms currently being investigated is the gut microbiome. Although more research is needed to understand its impact on the development of age-related AF and targets for therapies, the gut microbiome is a promising new avenue of research that may provide future benefits in AF prophylaxis or enhanced management. As the field works towards developing this knowledge, there are important questions to answer as to the optimal role of potential gut microbiome targeting therapies and their potential risks versus the benefits they provide. This commentary first summarizes the currently understood mechanisms contributing to age-related AF, which is then followed by an analysis of the current work investigating the role of the gut microbiome in the development of age-related AF, and concludes by highlighting notable questions to consider in future work on the role of the gut microbiome and its relationship to age-related AF.
Age-related atrial fibrillation (AF) is a common condition that has yet to be fully understood, with mechanisms to explain its development under investigation. Notably, cellular senescence, cardiac fibrosis, coronary ischemia, cardiac valvular disease, autonomic dysfunction, channelopathies, and immune system remodeling are processes that have been seen to occur with aging and ample evidence has shown their association with the development of AF. Despite robust therapeutic approaches, the incidence of AF continues to rise, suggesting that the dynamic, multi-faceted interactions leading to AF are incompletely understood. One of the newer mechanisms currently being investigated is the gut microbiome. Although more research is needed to understand its impact on the development of age-related AF and targets for therapies, the gut microbiome is a promising new avenue of research that may provide future benefits in AF prophylaxis or enhanced management. As the field works towards developing this knowledge, there are important questions to answer as to the optimal role of potential gut microbiome targeting therapies and their potential risks versus the benefits they provide. This commentary first summarizes the currently understood mechanisms contributing to age-related AF, which is then followed by an analysis of the current work investigating the role of the gut microbiome in the development of age-related AF, and concludes by highlighting notable questions to consider in future work on the role of the gut microbiome and its relationship to age-related AF.
DOI: https://doi.org/10.37349/ec.2025.101251
This article belongs to the special issue Molecular Mechanisms of Cardiovascular Aging
L-Carnitine (LC) is integral to energy production and fatty acid metabolism, facilitating the transport of long-chain fatty acids into mitochondria for β-oxidation. It modulates metabolic pathways, including pyruvate dehydrogenase activity, proteolysis, and protein synthesis, while also having anti-inflammatory and antioxidant characteristics. LC can be commonly applied to win the battle against HIV and cancer cachexia. Also, it can be recruited with the aim of improving physical and cognitive functions in athletes and the elderly. Despite these benefits, long-term LC administration has been associated to cardiovascular risks due its conversion to trimethylamine-N-oxide (TMAO) by the gut microbiota. Elevated TMAO levels are linked to atherosclerosis, oxidative stress, and an increased risk of cardiovascular disease, diabetes, and chronic kidney disease. Managing TMAO levels using dietary treatments and gut microbiota-targeting techniques, such as probiotics, may reduce these risks. This comprehensive review presents the state-of-the-art information on LC’s dual role, emphasizing the balance between its therapeutic potential and the risks of prolonged supplementation. It aims to guide clinicians and researchers in optimizing LC’s benefits while addressing its long term cardiovascular safety concerns.
L-Carnitine (LC) is integral to energy production and fatty acid metabolism, facilitating the transport of long-chain fatty acids into mitochondria for β-oxidation. It modulates metabolic pathways, including pyruvate dehydrogenase activity, proteolysis, and protein synthesis, while also having anti-inflammatory and antioxidant characteristics. LC can be commonly applied to win the battle against HIV and cancer cachexia. Also, it can be recruited with the aim of improving physical and cognitive functions in athletes and the elderly. Despite these benefits, long-term LC administration has been associated to cardiovascular risks due its conversion to trimethylamine-N-oxide (TMAO) by the gut microbiota. Elevated TMAO levels are linked to atherosclerosis, oxidative stress, and an increased risk of cardiovascular disease, diabetes, and chronic kidney disease. Managing TMAO levels using dietary treatments and gut microbiota-targeting techniques, such as probiotics, may reduce these risks. This comprehensive review presents the state-of-the-art information on LC’s dual role, emphasizing the balance between its therapeutic potential and the risks of prolonged supplementation. It aims to guide clinicians and researchers in optimizing LC’s benefits while addressing its long term cardiovascular safety concerns.
DOI: https://doi.org/10.37349/ec.2025.101250
Aim:
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), or COVID-19, infection resulting in acute respiratory distress syndrome (ARDS) requiring veno-venous or veno-arterial extracorporeal membrane oxygenation (VV or VA-ECMO) support is a life-threatening disease process that requires prolonged intubation and has a high risk of mortality.
Methods:
In this retrospective, observational, single-center cohort study, we attempt to better understand the role of extubation in the course of treatment by dichotomizing groups into those extubated early while remaining on ECMO treatment (group A), compared to patients who remained intubated for the entirety of their ECMO treatment (group B).
Results:
The data indicate that early extubation of patients with COVID-19-associated ARDS requiring ECMO support leads to improved survival rates for group A (93%) compared to prolonged intubation (group B) throughout the course of ECMO therapy (64%) (p = 0.13). Additionally, patients extubated earlier (19 days vs. 59 days; p = 0.012) required significantly fewer vasoactive drugs (norepinephrine dosing: 0.03 mcg/kg/min vs. 0.093 mcg/kg/min; p = 0.04), and were less likely to require a tracheostomy (0 vs. 4, p = 0.026).
Conclusions:
Although the utility of ECMO in severe ARDS patients remains a contentious topic, early extubation seems to increase survival rates and overall patient outcomes in patients with COVID-19-associated ARDS requiring ECMO support.
Aim:
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), or COVID-19, infection resulting in acute respiratory distress syndrome (ARDS) requiring veno-venous or veno-arterial extracorporeal membrane oxygenation (VV or VA-ECMO) support is a life-threatening disease process that requires prolonged intubation and has a high risk of mortality.
Methods:
In this retrospective, observational, single-center cohort study, we attempt to better understand the role of extubation in the course of treatment by dichotomizing groups into those extubated early while remaining on ECMO treatment (group A), compared to patients who remained intubated for the entirety of their ECMO treatment (group B).
Results:
The data indicate that early extubation of patients with COVID-19-associated ARDS requiring ECMO support leads to improved survival rates for group A (93%) compared to prolonged intubation (group B) throughout the course of ECMO therapy (64%) (p = 0.13). Additionally, patients extubated earlier (19 days vs. 59 days; p = 0.012) required significantly fewer vasoactive drugs (norepinephrine dosing: 0.03 mcg/kg/min vs. 0.093 mcg/kg/min; p = 0.04), and were less likely to require a tracheostomy (0 vs. 4, p = 0.026).
Conclusions:
Although the utility of ECMO in severe ARDS patients remains a contentious topic, early extubation seems to increase survival rates and overall patient outcomes in patients with COVID-19-associated ARDS requiring ECMO support.
DOI: https://doi.org/10.37349/ec.2025.101249
