Search Results (36)

Aldosterone excess, particularly in the context of primary aldosteronism, is associated with adverse cardiovascular outcomes. Historically considered a condition of resistant hypertension with hypokalaemia, patients with primary aldosteronism often experienced prolonged diagnostic delay with significant end-organ damage involving the renal, cardiovascular, and central nervous systems at diagnosis. Emerging research has revealed a wide spectrum of renin-independent aldosteronism, ranging from subclinical disease with normal or mildly elevated BP to overt disease marked by resistant hypertension and cardiovascular complications. Subclinical forms of primary aldosteronism have been identified across all age groups, and it is increasingly linked to early signs of adverse cardiac remodelling, even in young adults. Notably, adverse cardiac remodelling was independent of blood pressure. Furthermore, primary aldosteronism confers excess cardiovascular morbidity and mortality compared to blood-pressure-matched essential hypertension. Importantly, these risks can be mitigated through timely diagnosis and treatment with mineralocorticoid receptor antagonists. In this narrative review, we explore the cardiovascular consequences of aldosterone excess, discuss the pathophysiological mechanisms underlying cardiac remodelling, and examine the implications of renin-independent aldosteronism for cardiovascular risk across the lifespan. Full article

Long COVID is a persistent post-viral syndrome with the significant involvement of both the cardiovascular and pulmonary systems, often extending well beyond the acute phase of SARS-CoV-2 infection. Emerging evidence has highlighted a spectrum of chronic alterations, including endothelial dysfunction, microvascular inflammation, perivascular fibrosis, and in some cases, the persistence of viral components in the cardiac and pulmonary tissues. At the molecular level, a sustained inflammatory milieu—characterized by elevated pro-inflammatory cytokines such as interleukin 6 (IL-6)—and chronic platelet hyperreactivity contribute to a prothrombotic state. These mechanisms are implicated in microvascular damage, cardiac strain, and impaired gas exchange, correlating with clinical manifestations such as fatigue, dyspnea, chest discomfort, and reduced exercise capacity. In certain patients, especially those who were not hospitalized during the acute phase, cardiac MRI and myocardial biopsy may reveal signs of myocardial inflammation and autonomic dysregulation. These often subclinical cardiovascular alterations underscore the need for improved diagnostic strategies, integrating molecular and histopathological markers during post-COVID evaluations. Recognizing persistent inflammatory and thrombotic activity may inform risk stratification and individualized therapeutic approaches. The interdependence between pulmonary fibrosis and cardiac dysfunction highlights the importance of multidisciplinary care. In this context, molecular and tissue-based diagnostics play a pivotal role in elucidating the long-term cardio-pulmonary sequelae of long COVID and guiding targeted interventions. Early identification and structured follow-up are essential to mitigate the burden of chronic complications in affected individuals. Full article

Primary aldosteronism (PA), the most common cause of secondary hypertension, is increasingly recognized as an independent driver of adverse cardiac remodeling, mediated through mechanisms beyond elevated blood pressure alone. Chronic aldosterone excess leads to myocardial fibrosis, left ventricular hypertrophy, and diastolic dysfunction via mineralocorticoid receptor activation, oxidative stress, inflammation, and extracellular matrix dysregulation. These changes culminate in a distinct cardiomyopathy phenotype, often underrecognized in early stages. Multimodality cardiac imaging, led primarily by conventional and speckle-tracking echocardiography, and complemented by exploratory cardiac magnetic resonance (CMR) techniques such as T1 mapping and late gadolinium enhancement, enables non-invasive assessment of structural, functional, and tissue-level changes in aldosterone-mediated myocardial damage. While numerous studies have established the diagnostic and prognostic relevance of imaging in PA, several gaps remain. Specifically, the relative sensitivity of different modalities in detecting subclinical myocardial changes, the long-term prognostic significance of imaging biomarkers, and the differential impact of adrenalectomy versus medical therapy on cardiac reverse remodeling require further clarification. Moreover, the lack of standardized imaging-based criteria for defining and monitoring PA-related cardiomyopathy hinders widespread clinical implementation. This narrative review aims to synthesize current knowledge on the pathophysiological mechanisms of aldosterone-induced cardiac remodeling, delineate the strengths and limitations of existing imaging modalities, and critically evaluate the comparative effects of surgical and pharmacologic interventions. Emphasis is placed on early detection strategies, identification of imaging biomarkers with prognostic utility, and integration of multimodal imaging into clinical decision-making pathways. By outlining current evidence and highlighting key unmet needs, this review provides a framework for future research aimed at advancing personalized care and improving cardiovascular outcomes in patients with PA. Full article

Background/Objectives: Extracellular volume (ECV) expansion reflects myocardial fibrosis and may play a role in subjects with severe aortic stenosis (AS) receiving transcatheter aortic valve implantation (TAVI). This study aimed to assess the relationship between cardiovascular risk factors (CVRF), AS severity and left ventricular myocardial ECV measured by cardiac computed tomography (CCT). Methods: 61 patients qualified for TAVI underwent pre-procedural CCT. CVRFs were recorded, including advanced age, male gender, obesity, hypertension, hypercholesterolemia, hypertriglyceridemia, type 2 diabetes, and smoking. The CCT protocol included non-contrast (for aortic valve calcium score, AVCS), angiographic (for vascular access planning), and delayed phases (for left atrial appendage thrombus assessment). ECV was calculated from attenuation values of the interventricular septum and left ventricular cavity assessed in native and delayed phases. Patients were stratified based on the presence/absence of individual CVRFs, median AVCS, and aortic valve area (AVA). Results: Mean ECV was higher in patients with hypertension (28.01% vs. 26.93%, p = 0.03), smokers (28.71% vs. 26.52%, p = 0.01), AVCS ≥ 2975 (28.08% vs. 26.95%, p = 0.02), and AVA < 0.95 cm² (28.63% vs. 26.53%, p = 0.01). Positive correlations were found between ECV and the number of CVRFs (r = 0.49, p = 0.01), BMI (r = 0.30, p = 0.01), systolic BP (r = 0.31, p = 0.02), and AVCS (r = 0.36, p = 0.01); AVA correlated negatively (r = −0.59, p = 0.01). Regression showed that hypertension, smoking, and smaller AVA were independent predictors of higher ECV. Conclusions: Among TAVI candidates, hypertension, smoking, and more advanced AS are independently associated with increased myocardial ECV on CCT. These findings may reflect subclinical myocardial remodeling and support the added diagnostic value of ECV in pre-TAVI assessment. Full article

Subclinical chronic kidney disease (sCKD) predisposes one to acute kidney injury (AKI) and chronic kidney disease (CKD). Reduced kidney functional reserve (KFR) detects sCKD in preclinical studies and predicts AKI after cardiac surgery. We evaluated renal protection in a rat model of kidney injury where ischaemia–reperfusion injury (IRI) was induced after sCKD. Dual treatment boosting nicotinamide adenine dinucleotide (NAD) by nicotinamide riboside (NR) combined with the mitochondria-targeted antioxidant SkQR1 protected the KFR and reduced structural kidney damage, including markers of vascular integrity and the relative blood volume (rBV). The dual treatment upregulated Sirt1 and Nrf2, increased the nuclear localisation of the mitochondrial biogenesis regulator PGC-1α and the mitochondrial protein marker COX4, and upregulated the antioxidant gene NOQ1. These observations suggest mitochondrial protection and modulation of the cellular redox state provided long-term structural and functional protection against kidney injury superimposed on background sCKD. Full article

Diabetic cardiomyopathy (DCM) begins with a subclinical stage featuring cardiac hypertrophy, fibrosis, and disrupted signaling. These changes, especially fibrosis and stiffness, often lead to clinical heart failure. The mechanism involves metabolic dysregulation, oxidative stress, and inflammation, leading to cardiac damage and dysfunction. During the progression of the disease, the myocardium senses surrounding mechanical cues, including extracellular matrix properties, tensile tension, shear stress, and pressure load, which significantly influence the pathological remodeling of the heart through mechanotransduction. At the molecular level, the mechanisms by which mechanical cues are sensed and transduced to mediate myocardial mechanical remodeling in DCM remain unclear. The mechanosensitive transcription factors YAP and TAZ fill this gap. This article reviews the latest findings of how YAP and TAZ perceive a wide range of mechanical cues, from shear stress to extracellular matrix stiffness. We focus on how these cues are relayed through the cytoskeleton to the nucleus, where they trigger downstream gene expression. Here, we review recent progress on the crucial role of YAP and TAZ mechanotransduction in the pathological changes observed in DCM, including myocardial fibrosis, hypertrophy, inflammation, mitochondrial dysfunction, and cell death. Full article

Background and objectives: Systemic sclerosis (SSc) causes myocardial and microvascular impairment, with subclinical dysfunction and eventually permanent cardio-vascular damage. The long-term influence of SSc therapies on subclinical cardiovascular dysfunction is insufficiently investigated. We aimed to assess 2D and 4D cardiac ultrasound parameters of heart function in patients with different forms of SSc versus controls and to determine the evolution of cardiac function and arterial stiffness parameters under therapy. Materials and methods: A total of 60 subjects with SSc were studied at baseline; 30 SSc patients were compared to 30 matched controls. A total of 52 SSc subjects were reassessed after 1 year and 30 after 2 years of treatment. Cardiac function was evaluated through 2D standard echocardiography, tissue Doppler, speckle tracking and 4D auto LV quantification echo. Arterial stiffness was determined via the cardio-ankle vascular index and ankle brachial index. Results: At baseline, the standard echo parameters were normal. The 4D and myocardial work parameters, although in normal limits, were significantly altered in the SSc group vs. controls (4D ejection fraction 54.5 ± 8.5% in SSc vs. 63.8 ± 3.1% in controls; 4D longitudinal strain −14.2 ± 2.4% in SSc vs. −22.0 ± 2.7% in controls; global constructive work 2124.2 ± 449.5 mmHg% in SSc vs. 3102.8 ± 337.5 mmHg% in controls, for all p ≤ 0.02). Both at 1 year and 2 years of treatment, all echo and arterial stiffness parameters were similar to baseline, with no correlation to treatment type. Conclusions: SSc determines subclinical systolic dysfunction. Non-invasive assessment methods do not detect a functional cardiovascular decline in patients on classical therapy. Complex cardiac follow-up should be implemented in cases at risk for complications. Full article

Despite increased availability of effective drug therapy for treatment of heart failure (HF), the morbidity and mortality in chronic heart failure (CHF) are unacceptably high. Therefore, there is an urgent need to ascertain new imaging techniques to identify early sub-clinical forms of cardiac dysfunctions, to guide early relevant treatment. It seems that all the behavioral risk factors—such as tobacco, alcoholism, Western-type diet, sedentary behavior and obesity, emotional disorders, and sleep disorder are associated with early cardiac dysfunction, which may be identified by speckle-tracking echocardiography (STE). Cardiac remodeling can also occur chronologically in association with biological risk factors of CHF, such as diabetes mellitus (DM), hypertension, cardiomyopathy, valvular heart disease, and coronary artery disease (CAD). In these conditions, twisting and untwisting of the heart, cardiac fibrosis, and hypertrophy can be identified early and accurately with 2-Dimentional (2D) and 3D echocardiography (2D echo and 3D echo) with tissue Doppler imaging (TDI), strain imaging via STE, and cardiac magnetic resonance imaging (CMR). Both 2D and 3D echo with STE are also useful in the identification of myocardial damage during chemotherapy and in the presence of risk factors. It is possible that global longitudinal systolic strain (GLS) obtained by STE may be an accurate marker for early identification of the severity of CAD in patients with non-ST segment elevation MI. Left ventricular ejection fraction (LVEF) is not the constant indicator of HF and it is normal in early cardiac dysfunction. In conclusion, this review suggests that GLS can be a useful early diagnostic marker of early or pre-cardiac dysfunction which may be treated by suitable drug therapy of HF along with the causes of HF and adhere to prevention strategies for recurrence. In addition, STE may be a superior clinical tool in the identification of cardiac dysfunction in its early stages compared to ejection fraction (EF) based on conventional echocardiography. Therefore, it is suggested that the chances of either stalling or reversing HF are far better for patients who are identified at an early stage of the disease. Full article

Background: Systemic lupus erythematosus (SLE) is characterized by inflammation and cardiovascular complications. Our study aimed to investigate subclinical and early indicators of systolic myocardial dysfunction in SLE patients using advanced echocardiographic methods and biomarkers. Methods: In this cross-sectional study, we enrolled 102 SLE patients without known cardiac impairment and 51 healthy controls. Demographics, disease characteristics, laboratory results, disease activity (SLEDAI), and organ damage (SDI) indices were recorded. Left ventricular global longitudinal strain (GLS) and myocardial work indices were assessed by utilizing speckle tracking echocardiography. In addition, high-sensitivity C-reactive protein (hsCRP), high-sensitivity troponin (hsTn), and N-terminal-pro B-type natriuretic peptide (NT-proBNP) levels were measured in blood samples. Results: In comparison with controls, SLE patients had significantly higher GLS (−19.94 ± 2.71% vs. −21.15 ± 1.55%, p < 0.001) and global wasted work (GWW) (94 ± 71 mmHg% vs. 71 ± 49 mmHg%, p = 0.025). Notably, NT-proBNP and hsTn were threefold and twofold higher in the SLE group compared with the control group, respectively (p < 0.001). Within the SLE cohort, in patients with at least moderate disease activity (SLEDAI ≥ 4), both biomarkers were significantly more elevated than those with low disease activity (SLEDAI < 4). Notably, hsTn levels remained within the normal range. Conclusions: Advanced echocardiographic parameters combined with specific biomarkers have a promising role in detecting systolic dysfunction in SLE patients, potentially enabling timely interventions to mitigate cardiovascular risk Full article

Background/Objectives: Severe aortic stenosis (AS) is the most frequent valvular heart disease. Models for stratifying cardiac damage associated with aortic stenosis have been developed to predict outcomes following valve replacement. However, evidence regarding morphological and functional evolution, as well as potential changes in the degree of cardiac damage, is limited. We aim to provide information on the evolution of cardiac morphology and the function of patients undergoing transcatheter aortic valve replacement (TAVR) who have been classified using a cardiac damage staging system. Methods: In total, 496 patients were included in the analysis, and were classified into four stages based on the extent of cardiac damage as follows: Stage 0, no cardiac damage: left ventricle global longitudinal strain (LV-GLS) < −17%; right ventricular–arterial coupling (RVAc) ≥ 0.35), and absence of significant mitral regurgitation (MR). Stage 1, left-sided subclinical damage: LV-GLS ≥ −17%. Stage 2, left-sided damage: significant MR. Stage 3, right-sided damage: RVAc < 0.35. Results: The mean age was 82.1 ± 5.9 years, and 53.0% were female. In total, 24.5% of patients met the criteria for Stage 0, and Stage 1 included 42.8% of patients, Stage 2 included 16.5%, and Stage 3 comprised 16.2% of patients. Mortality was 8.4% for stage 0, 17.4% for stage 1, 25.6% for stage 2, and 28.6% for stage 3 patients (p = 0.004). Diabetes mellitus (DM) (p = 0.047) and chronic kidney disease (CKD) (p = 0.024) were the only clinical predictors of no change or worsening in the stage of cardiac damage. Regarding echocardiographic variables, concomitant tricuspid, and mitral regurgitation, ≥ 2 were both significantly associated with no change or worsening, also (p < 0.001). Conclusions: Cardiac damage that is secondary to severe aortic stenosis has morphological and functional repercussions that, even after valve replacement, persist and might worsen the prognosis. Full article

Background: The sulfide–hydrogen sulfide brine balneotherapy (HSBB), including a combination of dissolved hydrogen sulfide (H₂S) gas, inorganic sulfur ions (S²⁻), and hydrosulfide ions (HS⁻), is one of the most important and most effective forms of spa treatment in patients with osteoarticular disorders (OADs). Some cardiovascular diseases (CVDs) are often considered to be contraindications to HSBB since the presence of thiol groups may lead to an increased quantity of reactive oxygen species (ROS), which damage the vascular endothelium, and endothelial dysfunction is considered to be the main cause of atherosclerosis. However, there are a number of literature reports suggesting this theory to be false. H₂S is a member of the endogenous gaseous transmitter family and, since it is a relatively recent addition, it has the least well-known biological properties. H₂S–NO interactions play an important role in oxidative stress in CVDs. The general objective of this study was to assess the cardiovascular safety of HSBB and analyze the effect of HSBB on selected cardiovascular risk markers. Methods: A total of 100 patients at the age of 76.3 (±7.5) years from the Włókniarz Sanatorium in Busko-Zdrój were initially included in the study. The following parameters were assessed: age, sex, height, body weight, body surface area (BSA), body mass index (BMI), systolic (SBP) and diastolic blood pressure (DBP), heart rate, the diagnosis of OAD that was the indication for balneotherapy, creatinine (CREAT), glomerular filtration rate (GFR), lipid panel, C-reactive protein (CRP), uric acid (UA), and fibrinogen (FIBR) and cardiovascular markers: (cardiac troponin T (cTnT), N-terminal pro-B-type natriuretic peptide (NT-proBNP). Results: A significant decrease in DBP and a trend towards SBP reduction were observed over the course of the study. A significant decrease was observed in CRP levels decreasing from 2.7 (±3.6) mg/L to 2.06 (±1.91) mg/L, whereas FIBR rose significantly from 2.95 (±0.59) g/L to 3.23 (±1.23) g/L. LDL-C levels decreased slightly, statistically significant, from 129.36 (±40.67) mg/dL to 123.74 (±36.14) mg/dL. HSBB did not affect the levels of evaluated cardiovascular biomarkers, namely NT-proBNP (137.41 (±176.52) pg/mL vs. 142.89 (±182.82) pg/mL; p = 0.477) and cTnT (9.64 (±4.13) vs. 9.65 (±3.91) ng/L; p = 0.948). A multiple regression analysis of pre-balneotherapy and post-balneotherapy values showed cTnT levels to be independently correlated only with CREAT levels and GFR values. None of the assessed parameters independently correlated with the NT-proBNP level. Conclusions: HSBB resulted in a statistically significant improvement in a subclinical pro-inflammatory state. HSBB has a beneficial effect in modifying key cardiovascular risk factors by reducing LDL-C levels and DBP values. HSBB has a neutral effect on cardiovascular ischemia/injury. Despite slightly elevated baseline levels of the biochemical marker of HF (NT-proBNP), HSBB causes no further increase in this marker. The use of HSBB in patients with OAD has either a neutral effect or a potentially beneficial effect on the cardiovascular system, which may constitute grounds for further studies to verify the current cardiovascular contraindications for this form of therapy. Full article

Chronic aortic regurgitation (AR) leads to volume overload in the left ventricle (LV), which is well tolerated for years. In this condition, the LV usually dilates with minimal reduction in the ejection fraction (EF), even in the absence of symptoms. Echocardiography is the primary imaging test used to quantify AR. However, no single assessment of Doppler measures is accurate and precise in individual patients; therefore, the integration of multiple parameters is necessary. Recent guidelines recommend surgical treatment for severe AR in patients who are symptomatic or have an LVEF < 55% and an end-systolic diameter > 50 mm. Nevertheless, advances in imaging technology have improved the quantification of AR and the assessment of LV subclinical dysfunction. It is widely recognized that patients who undergo aortic valve replacement/repair (AVR) due to symptoms or a low LVEF experience worse outcomes than those undergoing AVR for non-Class I indications. In fact, subclinical irreversible myocardial damage may occur in clinically well-compensated and closely monitored patients while awaiting formal surgical indications. This condition could be prevented by the use of multimodal imaging parameters, in particular longitudinal LV strain and magnetic resonance imaging. In addition, better cut-off values for mortality predictors should be established. This review aims to identify simple models that integrate several echocardiographic and cardiac magnetic resonance-derived parameters to predict the optimal timing of surgical treatment in asymptomatic patients with chronic severe AR. Full article

The role of the gut microbiome (GM) and oral microbiome (OM) in cardiovascular disease (CVD) has been increasingly being understood in recent years. It is well known that GM is a risk factor for various CVD phenotypes, including hypertension, dyslipidemia, heart failure and atrial fibrillation. However, its role in valvular heart disease (VHD) is less well understood. Research shows that, direct, microbe-mediated and indirect, metabolite-mediated damage as a result of gut dysbiosis and environmental factors results in a subclinical, chronic, systemic inflammatory state, which promotes inflammatory cell infiltration in heart valves and subsequently, via pro-inflammatory molecules, initiates a cascade of reaction, resulting in valve calcification, fibrosis and dysfunction. This relationship between GM and VHD adds a pathophysiological link to the pathogenesis of VHD, which can be aimed therapeutically, in order to prevent or regress any risk for valvular pathologies. Therapeutic interventions include dietary modifications and lifestyle interventions, in order to influence environmental factors that can promote gut dysbiosis. Furthermore, the combination of probiotics and prebiotics, as well as fecal m transplantation and targeted treatment with inducers or inhibitors of microbial enzymes have showed promising results in animal and/or clinical studies, with the potential to reduce the inflammatory state and restore the normal gut flora in patients. This review, thus, is going to discuss the pathophysiological links behind the relationship of GM, CVD and VHD, as well as explore the recent data regarding the effect of GM-altering treatment in CVD, cardiac function and systemic inflammation. Full article

Cardiac troponin serum concentration is the primary marker used for the diagnosis of acute coronary syndrome. Moreover, the measurement of cardiac troponin concentration is important for risk stratification in patients with pulmonary embolism. The cardiac troponin level is also a general marker of myocardial damage, regardless of etiology. The purpose of this study is to conduct a literature review and present the most important information regarding the current state of knowledge on the cardiac troponin serum concentration in patients with chronic cardiovascular disease (CVD), as well as on the relationships between cardiac troponin serum concentration and features of subclinical cardiovascular dysfunction. According to research conducted to date, patients with CVDs, such as chronic coronary syndrome, chronic lower extremities’ ischemia, and cerebrovascular disease, are characterized by higher cardiac troponin concentrations than people without a CVD. Moreover, the literature data indicate that the concentration of cardiac troponin is correlated with markers of subclinical dysfunction of the cardiovascular system, such as the intima–media thickness, pulse wave velocity, ankle–brachial index, coronary artery calcium index (the Agatston score), and flow-mediated dilation. However, further research is needed in various patient subpopulations and in different clinical contexts. Full article

Anderson–Fabry disease (AFD) is a lysosome storage disorder resulting from an X-linked inheritance of a mutation in the galactosidase A (GLA) gene encoding for the enzyme alpha-galactosidase A (α-GAL A). This mutation results in a deficiency or absence of α-GAL A activity, with a progressive intracellular deposition of glycosphingolipids leading to organ dysfunction and failure. Cardiac damage starts early in life, often occurring sub-clinically before overt cardiac symptoms. Left ventricular hypertrophy represents a common cardiac manifestation, albeit conduction system impairment, arrhythmias, and valvular abnormalities may also characterize AFD. Even in consideration of pleiotropic manifestation, diagnosis is often challenging. Thus, knowledge of cardiac and extracardiac diagnostic “red flags” is needed to guide a timely diagnosis. Indeed, considering its systemic involvement, a multidisciplinary approach may be helpful in discerning AFD-related cardiac disease. Beyond clinical pearls, a practical approach to assist clinicians in diagnosing AFD includes optimal management of biochemical tests, genetic tests, and cardiac biopsy. We extensively reviewed the current literature on AFD cardiomyopathy, focusing on cardiac “red flags” that may represent key diagnostic tools to establish a timely diagnosis. Furthermore, clinical findings to identify patients at higher risk of sudden death are also highlighted. Full article