Search Results (88)

Background: Both atrial cardiopathy and impaired renal function are independently associated with increased mortality, but their interrelationship and combined impact remain uncertain. Methods: We analyzed 6573 participants from NHANES-III (mean age 57 years; 50.5% women; 74.6% White) with available electrocardiograms (ECGs). Estimated glomerular filtration rate (eGFR) was calculated using the CKD-EPI equation. Atrial cardiopathy was defined by any of the following ECG markers: abnormal P-wave axis (<0° or >75°), deep terminal negativity in lead V1 (>100 µV), or prolonged P-wave duration in lead II (>120 ms). Participants with eGFR <15 mL/min/1.73 m² or major ECG abnormalities were excluded. Logistic regression assessed the association between impaired renal function (eGFR < 45 vs. ≥45 mL/min/1.73 m²) and atrial cardiopathy. Cox models evaluated independent and joint associations of impaired renal function and atrial cardiopathy with all-cause mortality. Results: About 47.9% (n = 3151) had atrial cardiopathy at baseline, of whom 161 (4.7%) had impaired renal function. Impaired renal function was associated with higher odds of atrial cardiopathy (OR 1.44; 95% CI 1.16–1.78). Over a median follow-up of 18.1 years, 3076 deaths occurred. Compared with participants without either condition, those with both had the highest mortality risk (HR 1.68; 95% CI 1.46–1.94), exceeding risks from atrial cardiopathy alone (HR 1.10; 95% CI 1.02–1.18) or impaired renal function alone (HR 1.42; 95% CI 1.18–1.70; p = 0.011 for interaction). Conclusions: Impaired renal function is associated with a greater prevalence of atrial cardiopathy. Their coexistence exerts a synergistic effect, substantially amplifying mortality risk beyond either condition alone. Full article

A significant portion of embolic strokes occurs without documented atrial fibrillation (AF), challenging the traditional paradigm of cardioembolism. This review addresses the emerging concept of “atrial cardiopathy” as a distinct clinical entity—an underlying atrial substrate abnormality, characterized by fibrosis and dysfunction, that promotes thromboembolism independent of AF. We posit that AF is often a late-stage manifestation of atrial cardiopathy, not the sole trigger for thrombosis. This paper synthesizes the growing evidence linking biomarkers of atrial cardiopathy to Embolic Stroke of Undetermined Source (ESUS). This new framework has profound clinical implications, suggesting a shift from arrhythmia detection to assessing atrial substrate health for stroke risk stratification. Recognizing atrial cardiopathy is fundamental for developing novel “upstream” therapies, such as targeted anticoagulation, aimed at preventing both AF and its devastating thromboembolic consequences. This review critically evaluates the evidence and translational gaps in the field, synthesizing the emerging role of advanced computational modeling as a key future tool for personalized risk stratification. Full article

Background: Hemodialysis (HD) patients are a highly vulnerable population with elevated mortality driven by comorbidities and dialysis-specific factors. While most studies focused on intra-pandemic outcomes, long-term effects remain underexplored. We aimed to evaluate 5-year mortality and the impact of COVID-19 vaccination in chronic HD patients. Methods: A retrospective study was conducted on 211 HD patients monitored between 2020 and 2024. Outcomes included overall and cardiovascular mortality, risk factors in COVID-19-positive patients, and vaccination impact. Logistic regression identified independent predictors. Results: The cohort had a mean age of 65.6 ± 13.3 years, with 55.9% males and mean dialysis vintage of 6.9 ± 5.5 years. Overall mortality reached 53.6%, while 38.4% were vaccinated. Predictors of all-cause mortality included age (OR = 1.078, p < 0.001), BMI (OR = 0.868, p < 0.001), hemoglobin (OR = 0.581, p < 0.001), phosphorus (OR = 1.351, p = 0.025), dialysis adequacy (OR = 0.138, p = 0.013), and ischemic cardiopathy (OR = 0.327, p = 0.009). In COVID-19-positive patients, mortality was associated with age (OR = 1.069, p = 0.002), low hemoglobin (OR = 0.642, p = 0.014), BMI (OR = 0.885, p = 0.009), CRP (OR = 1.015, p < 0.001), and coronary artery disease (OR = 5.68, p < 0.001). Cardiovascular disease was the leading cause of death (44.6% in COVID-19-positive vs. 73.3% in negatives, p = 0.006). Vaccination significantly reduced COVID-19-related mortality (OR = 0.023, p = 0.005) but did not influence overall or non-COVID mortality. Conclusions: Five-year mortality in HD patients remained high, mainly cardiovascular, and was strongly influenced by age, BMI, hemoglobin, dialysis adequacy, and comorbidities. COVID-19 vaccination substantially reduced COVID-related mortality but did not alter all-cause outcomes. These findings support vaccination and careful risk stratification in HD populations for future pandemics. Full article

Candida parapsilosis has emerged as a prominent cause of nosocomial candidemia, particularly among critically ill patients. The increasing prevalence of fluconazole-resistant C. parapsilosis (FR-Cp) poses major therapeutic challenges, especially in resource-limited settings. We conducted a retrospective study of 144 patients with C. parapsilosis candidemia admitted to two post-surgical ICUs at a Brazilian tertiary cardiothoracic hospital between 2016 and August 2024. Demographic, clinical, microbiological, and therapeutic data were analyzed. Predictors of 30-day mortality were identified through multivariate logistic regression. The incidence density of C. parapsilosis candidemia ranged from 2.93 to 8.31 per 1000 hospitalizations. Fluconazole resistance was identified in 81% of isolates. Overall 30-day mortality was 55%. Independent risk factors for mortality included cardiopathy (OR: 19.36, p = 0.006), higher SOFA scores (OR: 1.54, p = 0.003), parenteral nutrition (OR: 29.77, p = 0.013), and dialysis (OR: 6.59, p = 0.043), while longer treatment duration was protective (OR: 0.81, p < 0.001). Fluconazole resistance was not independently associated with increased mortality. In this cohort of critically ill patients, C. parapsilosis candidemia was associated with high mortality and a high prevalence of fluconazole resistance. Clinical outcomes were mainly driven by host-related and therapeutic factors rather than antifungal resistance alone. Full article

Background: Dilated cardiomyopathy (DCM) is a major cause of heart failure and arrhythmic mortality; yet, its association with cerebrovascular events, particularly in the absence of atrial fibrillation (AF), remains insufficiently explored. Purpose: This study aimed to determine the prevalence, mechanisms, and anatomical distribution of stroke in patients with DCM and to assess the role of AF and structural remodeling in stroke risk. Methods: We retrospectively analyzed 471 patients who died with DCM at the Emergency County Clinical Hospital of Bihor between 1 January 2022 and 31 December 2024. Clinical records, neuroimaging, autopsy reports, and histopathological data were reviewed. Stroke subtypes were classified according to TOAST criteria (large artery atherosclerosis, cardioembolic, small vessel disease, other determined, undetermined) and hemorrhagic categories (intracerebral, subarachnoid). Demographic, echocardiographic, and comorbidity data were compared between patients with and without cerebrovascular events. Results: Of 471 patients with DCM, 45 (9.6%) had concomitant stroke: pure ischemic in 32 (71.1%), 7 (15.6%) showed ischemic with hemorrhagic transformation, and primary hemorrhagic in 6 (13.3%). The parietal lobe was most frequently affected. AF was present in 26 patients (57.8%) and was significantly associated with ischemic stroke (p = 0.004), though embolic strokes also occurred in sinus rhythm. Patients with stroke had significantly lower left ventricular ejection fraction (28.0 ± 13.7% vs. 34.0 ± 11.2%, p = 0.007) and larger atrial dimensions. Histopathological findings confirmed acute and chronic ischemic injury patterns, including “red neurons,” white matter vacuolization, and gliotic scarring. Conclusions: Stroke is a frequent and often underdiagnosed complication in DCM, predominantly ischemic and embolic in nature. Importantly, embolic events were observed even in patients without AF, suggesting that atrial remodeling in DCM may independently predispose to cerebrovascular risk. These results underscore the need for refined preventive strategies, including careful atrial assessment and exploration of whether anticoagulation may benefit selected high-risk DCM patients without AF, a question that requires confirmation in prospective trials. Potential embolic sources in DCM include atrial cardiopathy and left ventricular thrombus in the setting of severe systolic dysfunction; therefore, careful ventricular as well as atrial assessment is warranted in high-risk DCM. Full article

Embolic stroke of undetermined source (ESUS) was proposed in 2014 as a clinical category to subgroup non-lacunar cryptogenic ischemic strokes that appear embolic but lack an identifiable cause despite thorough investigation. The initial hypothesis was that anticoagulation might offer superior secondary prevention compared to antiplatelet therapy, prompting several large clinical trials. This review synthesizes current knowledge on ESUS. ESUS represents about 17% of ischemic strokes and often affects younger patients with fewer traditional risk factors. Although these patients lack major cardioembolic sources (e.g., atrial fibrillation) or significant arterial stenosis, many have covert embolic substrates. Major trials—NAVIGATE ESUS, RE-SPECT ESUS, and the atrial cardiopathy-focused ARCADIA—found no benefit of anticoagulants over aspirin, challenging the original ESUS framework. These results highlight the heterogeneity within ESUS and underscore the need for individualized diagnostic and therapeutic strategies. Full article

When the resources are available, critical congenital heart diseases (CCHDs) should ideally be detected in utero; however, their later detection at birth can still reduce negative outcomes and risks. This study aimed to assess the extent of cardiac screening implementation in a national sample of hospitals within Mexico’s public health services. A cross-sectional survey was conducted to identify the barriers and facilitators to neonatal screening using a sample of 76 hospitals. The descriptive statistics and associations were analyzed, with significance set at p < 0.05. Only 12% of hospitals reported the routine implementation of CCHD screening, while 20% used variable screening criteria. A potential mandatory implementation of CCHD screening was associated with increased odds of perceiving the lack of protocols and guidelines as a barrier. The most frequently reported obstacles involved a lack of the following: equipment, designated physical space, trained personnel, and adequate training. Nevertheless, the facilitators identified suggest that when combined with standardized guidelines and protocols, routine nationwide implementation may be achievable. Full article

Background/Objectives: The maternal mortality ratio is one of the global health indicators, and cardiopathies are the leading indirect causes of maternal deaths. Proper management of pregnant women with heart disease is crucial, as the severity of these conditions can lead to complications during the perinatal period. This study aimed to evaluate the rate of severe maternal morbidity and associated factors in pregnant women with heart disease. Methods: A retrospective cohort study was conducted at a referral hospital in São Paulo from 2008 to 2017, including pregnant women with heart disease who underwent procedures in the obstetric center (n = 345). Sociodemographic, obstetric, and pre-existing conditions were analyzed, along with life-threatening conditions, near-miss events, and maternal deaths. Heart diseases were classified according to the World Health Organization (WHO) guidelines, and health indicators were calculated using WHO-recommended formulas. The Chi-square test or Likelihood Ratio test (p < 0.05) was used to compare severe maternal morbidity among women with heart disease. Results: The mean age of participants was 29.1 ± 7.29 years; most were white (58.8%), had completed high school (37.9%), and were married (71.6%). The most frequent pre-existing conditions were hypertension (9.6%) and diabetes mellitus (9.3%). The mean gestational age at admission/delivery was 37 weeks. According to the WHO classification, most women were classified as “II/III” (31.6%). Life-threatening conditions included hemorrhagic complications (13.9%), hypertensive complications (5.8%), clinical complications (19.7%), and severe management conditions (31.6%). Near-miss events occurred in 6.4% of patients, with clinical criteria in 2.9%, laboratory criteria in 4.3%, and management criteria in 3.5%. The cesarean section rate was 51%. Patients classified as WHO III and IV presented more severe management conditions (p < 0.0001), and those in WHO IV had a higher occurrence of near-miss events (p = 0.0001). Maternal mortality was 0.9% (n = 3). Conclusions: The incidence of severe maternal morbidity was 25 cases (22 near-miss events + 3 maternal deaths), equivalent to 2.86 per 1000 live births, and was significantly associated with WHO classifications III and IV. Full article

Neural crest cells (NCCs) play a significant role in the development of ventricular outflow tracts (OFTs), and cardiac neural crest cells (cNCCs) are involved in the development of the embryonic conus, suggesting that these cell lineages may be a teratogenic target for the development of cardiopathies in offspring conceived under a hyperglycemic environment. We evaluate the effect of the hyperglycemic intrauterine environment on the morphological and anatomical changes in the conal ridges along with the alterations in the spatiotemporal expression of AP2α in offspring hearts at 13, 15, and 17 DPC. The anatomical and histological analysis of the hearts in the experimental group presented smaller dimensions compared to the control group in the offspring at the three ages studied. Consequently, this resulted in a hyperglycemic environment that altered the immunostaining of AP2α in the hearts of the offspring at the three ages studied. Thus, the hyperglycemic intrauterine environment in offspring caused important morphological alterations in the development of conal ridges and promoted the generation of conotruncal heart defects in which the double outlet of the right ventricle, the atrioventricular (AV) canal, predominated. Therefore, knowing that exposing the offspring to more glucose potentially can lead to complications during organogenesis of the circulatory and central nervous systems. Full article

Arrhythmogenic cardiomyopathy is a heart disease in which the heart muscle is replaced by scar tissue. This is the main substrate for the development of malignant ventricular arrhythmias. Sudden cardiac death is the most common manifestation and can often be the first sign of the disease, especially in young people. Correct stratification of arrhythmic risk is essential for the management of these patients but remains a challenge for the clinical cardiologist. In this context, the aim of our work was to review the literature and to analyse the most important studies and new developments with regard to the stratification of the risk of arrhythmia in patients suffering from arrhythmogenic cardiopathy. Full article

RASopathies are a diverse group of genetic conditions caused by hyperactivation of the RAS-MAPK signaling pathway, mainly inherited in an autosomal dominant manner. They present with variable features such as short stature, congenital heart defects, facial dysmorphisms, and neurodevelopmental delays. This study retrospectively analyzed 143 cases from 2003 to 2022, aiming to improve genotype–phenotype correlation knowledge for personalized care. Patients with genetically confirmed Noonan syndrome (NS) and related disorders were included, with molecular analysis performed via Sanger or parallel sequencing. Data from 906 previously reported cases were also reviewed. Among the 143 patients, most had NS (n = 116). PTPN11 mutations were most frequent (61%), followed by SOS1 (10.3%) and RAF1 (8.6%). Cardiac anomalies were observed in 71%, with pulmonary stenosis (PS) prevalent in NS (48.3%) and hypertrophic cardiomyopathy (HCM) in NSML (40%). PTPN11 variants were linked to PS and atrial septal defects, SOS1 to multiple cardiopathies, and RAF1 to HCM. Additional features included facial dysmorphisms (74.1%), short stature (62.0%), skeletal anomalies (43.1%), cryptorchidism (59.7%), and brain abnormalities (17.2%). JMML and other malignancies were seen in eight patients. This study emphasizes the importance of genotype-guided care, improved diagnosis of mild cases, and the underrecognized prevalence of neurological anomalies. Full article

Introduction: Hereditary transthyretin amyloidosis (ATTRv) is a severe, multisystemic, autosomal dominant disease with variable penetrance caused by mutations in the TTR gene generating protein misfolding and accumulation of amyloid fibrils. The diagnosis is usually challenging because ATTRv may initially manifest with nonspecific multisystemic symptoms. Conversely, an early diagnosis is needed to start timely appropriate therapy. Hence, screening models have been proposed to improve ATTRv diagnosis. In this study, we propose a genetic screening model based on predefined “red flags” followed by “cascading screening” on first-degree relatives of patients who tested positive. Materials and methods: After obtaining written informed consent, genetic testing on salivary swabs was performed in individuals who met at least two major red flags for ATTRv (age > 65 years old, progressive sensory or sensorimotor neuropathy not responsive to steroids or immunomodulant therapies, recent and unexplained weight loss associated with gastrointestinal signs and symptoms, diagnosis of cardiac amyloidosis, bilateral or relapsing carpal tunnel syndrome, unexplained autonomic dysfunction) or one major flag and two minor flags (family history of neuropathy, ambulation disorders or cardiopathy, sudden cardiac death, a bedridden, wheelchaired patient without specific diagnosis excluding upper motor neuron diseases, infections, juvenile cardiac disease, ocular disorders, lumbar spine stenosis, biceps tendon rupture). Results: In the first screening phase, 29 suspected cases (individuals meeting at least two major red flags or one major red flag and two minor red flags) underwent genetic testing. One patient (3.5%) was diagnosed with hereditary transthyretin amyloidosis with polyneuropathy (ATTRv-PN), carrying the Phe64Leu mutation. Then, cascade screening allowed for early recognition of two additional individuals (two pre-symptomatic carriers) among two first-degree relatives (100%). The identified patient was a 72-year-old man who had a family history of both cardiopathy, neuropathy, and a diagnosis of juvenile cardiac disease and progressive sensorimotor neuropathy unresponsive to steroids or immunomodulant therapies. Conclusions: ATTRv is a progressive and often fatal disease that should be promptly diagnosed and treated to stop progression and reduce mortality. Systematic screening for ATTRv yielded increased recognition of the disease in our neurological clinic. A focused approach for the screening of ATTRv-PN could lead to an earlier diagnosis and identification of asymptomatic carriers, enabling timely intervention through close clinical monitoring and early treatment initiation at symptom onset. Full article

Left ventricular thrombosis (LVT) is one of the most feared complications of both ischemic and non-ischemic cardiopathy, and despite its incidence having decreased over the years (mostly due to novel reperfusion therapies in acute coronary syndromes), it is still not negligible. If transthoracic echocardiography, possibly with the adjunction of echo contrast, represents the cornerstone in LVT diagnosis, sometimes it is found to be nonconclusive and advanced cardiovascular imaging, namely cardiac magnetic resonance, needs to be performed to fully exclude intraventricular masses or to better characterize them. Vitamin K antagonists always represented the anticoagulant of choice for the treatment of LVT; however, the recent spread of direct oral anticoagulants (DOACs) pushed clinicians to adopt them also in this setting despite the absence of robust evidence in their favor. If the optimal duration of anticoagulation for the treatment of LVT in non-ischemic cardiopathy is still a matter of debate, an initial treatment of 3–6 months seems to be reasonable in the setting of ischemic cardiopathy, with possible extension according to the follow-up findings. High-quality randomized studies are strongly needed to evaluate the potential role of prophylactic anticoagulation in high-risk patients and provide conclusive evidence for the use of DOACs in LVT treatment. Full article

Sodium-glucose co-transporter type 2 inhibitors (SGLT2i) have emerged as a class of agents relevant for managing diabetic nephropathy and cardiopathy. In a previous report, we noticed that these drugs share, with other drugs with “nephroprotective” effects, the ability to reduce the glomerular filtration rate (GFR), thus suggesting the kidney hemodynamic effect as a proxy for optimal drug dosage. We also noticed that all known nephroprotective drugs exert cardioprotective functions, suggesting the possibility of activities not mediated by the kidney. Finally, we observe that nephroprotective drugs can be grouped according to their effects on hemoglobin levels, thus suggesting their mechanism of action. While the primary mechanism of SGLT2i involves glycosuria and natriuria, growing evidence suggests broader therapeutic effects beyond hemodynamic modulation. Specifically, the evidence that SGLT2 can be expressed in several atypical regions under pathological conditions, supports the possibility that its inhibition has several extratubular effects. Evidence supports the hypothesis that SGLT2i influence mitochondrial function in various cell types affected by diabetes, particularly in the context of diabetic nephropathy. Notably, in SGLT2i-treated patients, the extent of albumin-creatinine ratio (ACR) reduction post-treatment may be correlated with mitochondrial staining intensity in glomerular endothelial cells. This implies that the anti-proteinuric effects of SGLT2i could involve direct actions on glomerular endothelial cell. Our investigation into the role of SGLT2 inhibitors (SGLT2i) in endothelial function suggests that the aberrant expression of SGLT2 in endothelial cells in T2DM would lead to intracellular accumulation of glucose; therefore, SGLT2i are the first type of endothelial protective drugs available today, with potential implications for ageing-related kidney disease. The review reveals two major novel findings: SGLT2 inhibitors are the first known class of endothelial-protective drugs, due to their ability to prevent glucose accumulation in endothelial cells where SGLT2 is aberrantly expressed in Type 2 Diabetes. Additionally, the research demonstrates that SGLT2 inhibitors share a GFR-reducing effect with other nephroprotective drugs, suggesting both a mechanism for optimal drug dosing and potential broader applications in ageing-related kidney disease through their effects on mitochondrial function and glomerular endothelial cells. Full article

Background: Hereditary transthyretin amyloidosis (ATTRv) is an autosomal-dominant systemic disease, where amyloid fibrils accumulate especially in the peripheral and autonomic nervous systems and in the heart. The aim of the present work was to outline the follow-up and type of management received by asymptomatic carriers (ACs) and Coutinho stage 1 ATTRv patients in Spain. Methods: A cross-sectional, non-interventional study was conducted throughout seven experienced hospitals in Spain. A total of 86 ACs without neurological symptoms and 19 Coutinho stage 1 ATTRv patients diagnosed 12 months before their enrollment were included. Clinical and demographic data, red flags, and neurological and cardiological evaluations were gathered. In addition, site variables were collected from four centers to describe the clinical management of ATTRv. Results: ATTRv clinical management varied depending on the center setting but was primarily overseen by neurology and internal medicine, which were responsible for the holistic follow-up of ACs and patients. Routinely, neurologists, neurophysiologists, cardiologists, and internal medicine conducted the follow-up. Specialties involved in initial AC assessment were neurophysiologists and cardiologists in 100% of cases, neurologists (75%), internists and geneticists (50%), and ophthalmologists (25%). A review of the medical tests performed proved an exhaustive management of the study population. Stable patients were followed up every 6 months, while those under evolution were monitored every 3–6 months. The frequency of monitoring of ACs was annual, and carriers classified with doubtful disease onset were visited every 3–6 months. Conclusions: The EMPATIa study provides valuable insights into the management of ATTRv in a real-world clinical setting in highly experienced hospitals in Spain. It demonstrates that multidisciplinary practice and enhanced disease awareness may lead to a reduction in diagnostic delay. Full article