Hypertrophic cardiomyopathy is one of the most common hereditary cardiomyopathies in daily practice. The different phenotypic manifestations and hemodynamic features often make diagnosis and therapy a clinical challenge. Diagnosis and imaging follow-up of cardiomyopathies are becoming increasingly multimodal. Despite the new imaging capabilities, echocardiography continues to play a key role in the primary differential diagnostic process, in the follow-up of patients, regardless of the therapeutic approach taken, and in the screening of relatives. Therefore, good knowledge of echocardiographic methods for assessment in these patients, of practical features and possible errors during the examination, is an essential prerequisite for high quality care. Precise systematic measurements and descriptions of the fi nding in each patient are the basis of good follow-up, adequate management planning and reassessment of therapy, and of seamless team care for the patient by various specialists. Confl icting or inconsistent imaging fi ndings, discrepancies in imaging fi ndings and clinical presentation, and the need for specialized therapy are valid reasons for referring the patient for a staged evaluation to an expert center for HCM.
Patients with cancer have multiple etiological factors for the development of myocarditis. Classical or conventional chemotherapy, radiotherapy and, more recently, immunotherapy have been described as possible etiological causes of myocarditis. In addition, patients with cancer are immunosuppressed and more susceptible to bacterial and viral infections that can cause myocarditis. This review discusses the many possible causes of myocarditis in patients with cancer. Special emphasis is placed on myocarditis induced by immune checkpoint inhibitors (ICI). ICI myocarditis usually affects male patients over 50 years of age who are being treated for lung cancer, melanoma or renal cell carcinoma and have multiple comorbidities. Clinical manifestations occur early, with elevated troponin and electrocardiogram changes. The mortality rate is high. Treatment consists of discontinuation of the causative ICI and corticosteroid therapy. Myocarditis caused by cyclophosphamide, anthracyclines, 5-fl uorouracil, cisplatin, carboplatin, proteasome inhibitors, immunomodulators, tyrosine kinase inhibitors, and radiotherapy was also reviewed.
Factor VII defi ciency is a rare inherited coagulation disorder characterized by decreased activity of factor VII, leading to variable bleeding tendencies that may not correlate with measured FVII levels. While many patients remain asymptomatic, others can experience severe spontaneous hemorrhages. The condition poses signifi cant challenges during surgical or invasive procedures due to the potential for uncontrollable bleeding. Data regarding percutaneous coronary intervention (PCI) in such patients are extremely limited, mostly confi ned to isolated case reports. PCI requires anticoagulation during the procedure and dual antiplatelet therapy afterward, both of which elevate bleeding risk. Conversely, administering FVII concentrate may increase the chance of thromboembolic events. Therefore, individualized planning and a multidisciplinary approach are crucial to balance these opposing risks. We present the case of a 75-year-old Bulgarian woman with congenital FVII defi ciency and severe three-vessel coronary artery disease who underwent successful transradial PCI without FVII replacement. Drug-eluting stents were implanted in the left anterior descending and circumfl ex arteries, enabling short-term dual antiplatelet therapy. No bleeding complications occurred peri-procedurally, and only one minor episode of epistaxis was observed during follow-up. This case illustrates that, with meticulous preparation and procedural care, PCI can be a safe and effective revascularization strategy in patients with congenital FVII defi ciency.
Introduction: The EVOLUTION-HF is a prospective, multinational, real-world study designed to describe the demographic and clinical characteristics of patients initiating dapaglifl ozin for heart failure with reduced ejection fraction (HFrEF) in nine countries from the Central and Eastern Europe and Baltic Area. This manuscript presents the results of the Bulgarian cohort of the study. Methods: Enrolment period in Bulgaria was between February 2022 and October 2022, in 10 study sites. Demographic and clinical characteristics were collected at baseline (12 months before dapaglifl ozin initiation), and treatment for heart failure (HF), including guideline-directed treatment (GDMT) was collected prospectively until 12 months after dapaglifl ozin initiation. The HF treatment was administered as per routine clinical practice. Results: One hundred and fi fty patients were included in the full analysis set (mean age: 67 years, males 84%). At the time of initiation of dapaglifl ozin 10 mg/day, 69.3% of patients had treatment with renin-angiotensin-aldosterone system (RAAS) inhibitors and 35.3% all four GDMTs in HF. Almost 98% of patients remained on dapaglifl ozin at 6 months and 12 months. Seven (10.12%) dapaglifl ozin discontinuations were recorded throughout the study. The discontinuation rate of dapaglifl ozin was 4.65 per 100 patient-years and the median time-to-discontinuation was not reached. One patient stopped dapaglifl ozin between baseline and 6 month and between 6 month and 12 month-data collection, respectively. GDMT patterns were relatively stable over one year. Conclusion: A high rate of persistence of dapaglifl ozin was observed at 12-month follow-up after initiation for HFrEF. A substantial gap was noted related to GDMT strategy optimization, with only one third of patients receiving all four GDMT pillars. These results obtained in real-world practice in Bulgaria point to the unmet need for targeted efforts to improve GDMT adoption in patients with HFrEF.
Left ventricular systolic dysfunction results from complex structural, cellular, and molecular disorders affecting the contractile apparatus of the myocardium and its energy homeostasis. This review discusses the key mechanisms of this process, with emphasis on myocardial contraction and its regulation by calcium dynamics and integrity of the sarcomeres. The main factors leading to the development of systolic dysfunction are presented: volume and tension overload, ischemia, infl ammation, amyloid and other deposits, neurohormonal activation and endocrine disorders, oxidative stress. In addition, cellular and molecular mechanisms are presented, such as defects in SERCA2a, and Na+/Ca2+ exchanger, pathological Ca2+ effl ux through RyR2, alterations in titin phosphorylation, myofi lament damage, proteasome dysfunction, impaired autophagy, epigenetic regulation, endoplasmic reticulum stress, and abnormalities in intercellular connectivity. The complex interaction between these processes leads to progressive myocardial remodeling, fi brosis, energy defi cit, and impaired myocardial contractility. Understanding these mechanisms is important for better understanding the pathogenesis of systolic dysfunction as well as for the development of new therapeutic strategies for its treatment.
Transcatheter aortic valve replacement (TAVR) is an effective therapeutic option for patients with severe symptomatic aortic stenosis who are at high surgical risk. Although generally safe, one of its rare but serious complications is clinical valve thrombosis, occurring in approximately 0.5% of cases. This condition can lead to prosthetic valve dysfunction, worsening heart failure, or thromboembolic events. Diagnosis usually begins with transthoracic echocardiography (TTE), while transoesophageal echocardiography (TOE) and multi-slice computed tomography (MSCT) are often required for more precise assessment. Since standardized treatment protocols are not yet established, management must be individualized according to clinical presentation and the degree of valve obstruction. Therapeutic approaches include oral anticoagulation, intravenous heparin, or, in severe cases with hemodynamic compromise, thrombolytic therapy. If conservative management fails, redo-TAVR or surgical valve explantation may be necessary. We present the case of a 78-year-old Bulgarian woman who developed progressive heart failure 12 days after TAVR. Imaging confi rmed bioprosthetic valve thrombosis. Intravenous heparin was ineffective, but thrombolytic therapy followed by oral anticoagulation led to complete thrombus resolution and restoration of valve function without bleeding complications. Clinical valve thrombosis after TAVR, though uncommon, is potentially fatal. MSCT remains the most accurate diagnostic tool, while TOE is valuable for its accessibility. Thrombolysis combined with vitamin K antagonist therapy can be an effective treatment option.
Psychogenic pseudosyncope is a state of apparent loss of consciousness, which is indistinguishable from true loss of consciousness by eyewitnesses. However, there are no hemodynamic and electroencephalographic stigmata of true syncope with real loss of consciousness. Sometimes a detailed history can raise doubts about the condition – a relatively long period of unconsciousness, unusual triggers, atypical prodromes and frequent attacks are suspicious signs, but they are far from specifi c in the population of patients presenting for differential diagnosis of syncopal episodes to the cardiologist. The gold standard for making the diagnosis is the provocation with a tilt-table test, in which psychogenic pseudosyncope is registered and simultaneously the absence of hemodynamic (and in the optimal case, electroencephalographic) signs of loss of consciousness is objectifi ed. It should be noted that the presence of psychogenic pseudosyncope does not automatically exclude the presence of true refl ex syncope in the particular patient. Treatment based primarily on a clear explanation of the condition and supportive communication with the patient can lead to a sharp reduction in the frequency of attacks. Pharmacological treatment of associated psychiatric disorders, as well as psychological support, is extremely effective. Cognitive-behavioural therapy is the most preferred approach in this patient population. In this review, we will present the diagnostic process in one patient and discuss the development of the understanding of this condition, the main clinical features and diagnostic approaches, the classifi cation and underlying pathology, as well as therapeutic methods.
Acenocoumarol, a vitamin K antagonist (VKA), has played a pivotal role in anticoagulant therapy for over 60 years. Derived from the coumarin family, acenocoumarol inhibits vitamin K epoxide reductase, disrupting the synthesis of vitamin K-dependent clotting factors (II, VII, IX, X) and effectively preventing thromboembolic events. Compared to warfarin, acenocoumarol offers a rapid onset and shorter half-life, providing clinicians greater therapeutic fl exibility. Despite advances and widespread adoption of direct oral anticoagulants (DOACs), acenocoumarol continues to hold clinical signifi cance, particularly in Europe, Latin America, and Asia, owing to extensive clinical experience, reversibility, and cost-effectiveness. However, its use necessitates regular monitoring of international normalized ratio (INR), with individualized dosage adjustments required due to genetic variability (CYP2C9, VKORC1 polymorphisms), drug-drug interactions, dietary infl uences, and special considerations in the elderly and patients with chronic kidney disease (CKD). Recent clinical trials have expanded our understanding of its effi cacy, safety, and optimal use. Precision dosing strategies, including genotype guidance and advanced INR monitoring based on body-surface area-adjusted estimated glomerular fi ltration rate (BSA-adjusted eGFR) dosing, promise enhanced safety and personalized treatment. Although DOACs are now widely adopted due to their predictable pharmacokinetics and lack of routine monitoring requirements, acenocoumarol remains indispensable in well-defi ned clinical scenarios such as in patients with mechanical heart valves, rheumatic mitral stenosis–associated atrial fi brillation, antiphospholipid syndrome, and other conditions in which individualized dose adjustment offers a therapeutic advantage.
Diastolic dysfunction is a condition in which ventricular fi lling is impaired, regardless of the presence of symptoms and irrespective of whether the ejection fraction is normal or reduced. Left ventricular diastolic dysfunction results from complex and interconnected biochemical and cellular mechanisms. Among them, impaired myocardial relaxation due to calcium dysregulation, altered titin phosphorylation affecting the passive elasticity of the myocardium, and extracellular matrix remodeling with the development of fi brosis mediated by signalling pathways such as TGF-β/SMAD and MAPK play a leading role. Additional contributing factors include oxidative stress and mitochondrial dysfunction, chronic infl ammation and activation of cytokine cascades, metabolic disturbances such as diabetes and obesity, as well as protein dysfunction related to endoplasmic reticulum stress and impaired proteolysis. All these processes in complex lead to impaired diastolic fi lling of the left ventricle, i.e., diastolic dysfunction. Due to its broad availability and proven clinical value, echocardiography is the primary method for diagnosing diastolic dysfunction. Invasive and other imaging modalities offer complementary information in complex or borderline cases, or when echocardiographic evaluation is diffi cult or impossible.
Marantic endocarditis, also known as nonbacterial thrombotic endocarditis (NBTE), is a rare condition typically encountered in patients with malignancy and hypercoagulable states. It is characterized by the formation of sterile fi brin–platelet vegetations on cardiac valves, which frequently lead to systemic embolic events. We report the case of an 84-year-old woman admitted with progressive exertional dyspnea and intermittent dry cough. Echocardiography revealed mobile vegetations on the mitral and aortic valves, associated with signifi cant valvular regurgitation and pulmonary hypertension. The patient remained afebrile, with persistently negative blood cultures and low infl ammatory markers. Whole-body computed tomography subsequently demonstrated pancreatic tail carcinoma with hepatic and pulmonary metastases. A diagnosis of marantic endocarditis secondary to malignancy was established. Anticoagulation and supportive therapy were initiated. Several days after discharge, the patient developed an ischemic stroke. She died a few weeks later.
Somatic mutations in hematopoietic stem cells (HSCs) are an inevitable part of human aging. When these mutations reach a certain variant allele frequency (VAF), they may confer a proliferative advantage to mutated clones, leading to clonal hematopoiesis. Once the HSCs generate over 10¹⁰-10¹² mutated cells, they can initiate various myeloid or lymphoid malignancies. In cases where the VAF exceeds 2% (roughly 10⁴ mutated blood cells) but without clinical evidence of hematologic cancer, the condition is termed clonal hematopoiesis of indeterminate potential (CHIP). Numerous studies have identifi ed that CHIP is frequently driven by mutations in genes implicated in hematologic malignancies, most notably TET2 , DNMT3A , and JAK2 . CHIP has also been strongly linked to cardiovascular diseases, particularly atherosclerosis. This dual role highlights a shared pathogenesis between cardiovascular and hematologic disorders through mutations in HSCs. CHIP-associated monocytes exhibit a pro-infl ammatory phenotype, activating infl ammasomes and overexpressing cytokines such as interleukin (IL)-1β and IL-6, as well as chemokines like Cxcl1-3 and Pf4. This leads to a chronic infl ammatory loop that contributes to endothelial dysfunction and atherosclerosis. Current data suggest that CHIP poses a cardiovascular risk comparable to traditional risk factors. Ongoing research continues to uncover the complex mechanisms underlying this association.
Introduction: Iron defi ciency anemia (IDA) and minor thalassemia (MT) are common hematologic disorders in children that may affect cardiovascular function. Objectives: The goal of the study was to determine whether ECG abnormalities in these populations are clinically signifi cant and potentially reversible. Material and methods: This prospective, randomized clinical trial aimed to evaluate electrocardiographic (ECG) changes in 135 children aged 5-18 years, equally divided into IDA, minor thalassemia, and healthy control groups. ECG parameters such as QT interval, corrected QT interval (QTc), P-wave dispersion (PWd), Tpe interval, and Tpe/QTc ratio were assessed before and after Iron supplementation in the IDA group. Results: Pre-treatment, the IDA group showed signifi cantly lower hemoglobin, ferritin, and serum Iron levels, along with elevated TIBC and marked ECG abnormalities including prolonged QTc, P-wave dispersion, Tpe interval, and increased Tpe/QTc ratio, indicating higher arrhythmogenic risk. Following Iron supplementation, the IDA group demonstrated signifi cant improvements in hematological parameters and normalization of ECG indices. In contrast, the MT and control groups exhibited stable hematologic and ECG profi les throughout the study. Statistical analysis confi rmed signifi cant pre- to post-treatment improvements in IDA patients, while no signifi cant ECG changes were observed in MT or control groups. These fi ndings suggest that ECG abnormalities in IDA are reversible with appropriate treatment, highlighting the importance of early diagnosis and intervention to prevent cardiac complications in pediatric populations. Conclusion: These fi ndings highlight the importance of early detection and treatment of IDA to mitigate cardiac complications in pediatric populations.
Introduction: Angina with non-obstructive coronary arteries (ANOCA) is frequently encountered in clinical practice but remains poorly understood and inconsistently managed. Despite the absence of signifi cant coronary stenoses, patients often report persistent symptoms and receive extensive pharmacotherapy. Real-world data on medication use and symptom burden in ANOCA populations remain limited. Material and methods: We conducted a single-center observational study of 102 patients referred to coronary angiography due to angina, who were subsequently found to have non-obstructive coronary artery disease. Baseline medication use and symptom severity were assessed using the Canadian Cardiovascular Society (CCS) classifi cation and Seattle Angina Questionnaire (SAQ). Associations between treatment and symptoms were analyzed using non-parametric tests. Results: The mean age was 61 years; 59% were women. Over 90% of patients were on cardiovascular medications, with 22.6% receiving fi ve or more agents. The most used therapies were β-blockers (59.8%), ACE inhibitors/ARBs (70.6%), and statins (58.8%). Despite this, 54.4% were in CCS class II or higher, and SAQ scores refl ected persistent symptoms. No signifi cant associations were found between drug class or medication count and symptom severity. Trimetazidine use was associated with slightly higher CCS class (p = 0.032). Conclusion: In this ANOCA cohort, pharmacotherapy was intensive but not clearly associated with symptom control. These fi ndings highlight the need for individualized, endotype-guided treatment strategies.
Fluoropyrimidines, including 5-fluorouracil (5-FU) and its oral prodrug capecitabine, are widely used in the treatment of solid tumors. While generally well tolerated, these agents can cause cardiotoxicity, with reported incidence rates ranging from 0 to 35%. Cardiac manifestations include angina, acute coronary syndromes, hypotension, arrhythmias, myocarditis, and heart failure. The primary mechanism of toxicity is thought to involve coronary vasoconstriction and microvascular dysfunction, though direct myocardial and endothelial damage may also contribute. Risk factors remain poorly defined, and cardiotoxicity can occur even in patients without pre-existing heart disease. Diagnostic tools, including biomarkers such as NT-proBNP and troponin, as well as echocardiography and cardiac MRI, play a critical role in early detection. Management typically involves discontinuation of 5-FU and symptomatic treatment with vasodilators and beta-blockers. Prophylactic strategies remain controversial, and guideline-directed therapy is largely based on case reports and observational data. Rechallenge with 5-FU carries a high risk of recurrence and should be approached with caution. Multidisciplinary collaboration, involving cardio-oncology teams, is essential for optimizing patient outcomes and guiding individualized prevention, monitoring, and treatment strategies in patients receiving fluoropyrimidine therapy.
Introduction: Pure coronary artery ectasia (CAE) was defi ned as segmental or diffuse coronary artery dilatation ≥ 1.5-fold the adjacent normal segment in the absence of ≥ 50% stenosis in any epicardial vessel. Previous studies on the relationship between ABO blood groups and ischemic heart disease have reported inconsistent fi ndings. This study aimed to investigate the distribution of blood groups in patients with pure CAE. Methods: This descriptive cross-sectional study included 250 patients diagnosed with pure CAE based on angiography fi ndings between 2015 and 2022 at two teaching hospitals. Data on age, gender, ABO blood group, Rh factor, white blood cell (WBC) count, lymphocyte and neutrophil percentages, and number of involved coronary vessels were collected. A control group was selected from patients undergoing coronary angiography in 2019-2020 without CAE and matched with the CAE group. Statistical analyses included Chi-square, Fisher’s Exact test, T-test, ANOVA, and logistic regression. Results: The mean age of patients was 56.2 ± 12.5 years; 160 (64%) were male and 90 (36%) were female. Rh positivity was observed in 222 (88.8%) patients, while 28 (11.2%) were Rh-negative. Blood group distribution among CAE patients was: O, 41.6%; B, 30.4%; A, 21.6%; and AB, 6.4%. Compared with the control group, a signifi cantly higher frequency of blood group O was observed among CAE patients (P < 0.001). In multivariable logistic regression adjusted for age, gender, and number of involved vessels, blood group O remained independently associated with CAE (OR = 1.78, 95% CI: 1.12–2.82, P = 0.015). Conclusion: Blood group O was signifi cantly more frequent among CAE patients compared with controls, even after adjusting for confounders.
Transcatheter aortic valve replacement (TAVR) is an established therapy for severe aortic stenosis, particularly in high-risk surgical candidates. While procedural success rates are high, valve migration remains a rare but serious complication, especially when occurring long after implantation. We report a case of late antegrade migration of a TAVR prosthesis presenting as new-onset heart failure nearly one year after successful implantation. A 77-year-old male with a history of hypertension and chronic lung disease underwent TAVR with a 27 mm NAVITOR (Abbott, USA) valve. Post-procedural recovery and early follow-up were uneventful. However, the patient later developed progressive heart failure symptoms. Transthoracic echocardiography revealed elevated transvalvular gradients, prompting further evaluation with computed tomography and fl uoroscopy, which confi rmed migration of the valve into the ascending aorta. Given the anatomic challenges and heavy native valve calcifi cation, the Heart Team opted for surgical explantation and bioprosthetic aortic valve replacement. The patient recovered well postoperatively and remained asymptomatic at three-month follow-up with normal valve function. This case underscores the importance of long-term surveillance after TAVR and highlights the potential for late mechanical complications. Early recognition through advanced imaging and individualized Heart Team decision-making are essential for optimal outcomes in such rare scenarios.
Introduction: Coronary artery ectasia (CAE) is an uncommon angiographic fi nding often associated with atherosclerosis. However, the risk profi le of patients with pure CAE (defi ned as ectasia in the absence of signifi cant obstructive coronary artery disease) remains incompletely understood. This study aimed to evaluate the association between traditional atherosclerotic risk factors and pure CAE in an Iranian population. Material and methods: In this retrospective cross-sectional study, 354 patients with pure CAE were identifi ed among 23,000 consecutive coronary angiography reports from two tertiary hospitals (2015–2022). Pure CAE was defi ned as segmental or diffuse coronary artery dilatation ≥1.5-fold the adjacent normal segment in the absence of ≥50% stenosis in any epicardial vessel. Patients with diffuse but non-obstructive atherosclerosis, history of vasculitis, autoimmune disease, congenital syndromes, or incomplete records were excluded. Demographic data and cardiovascular risk factors (hypertension, diabetes, hyperlipidemia, smoking, family history) were collected. Statistical analysis included both univariate comparisons and multivariable logistic regression to identify independent predictors of CAE. Results: The mean age was 57.5 ± 12.6 years; 64.1% were male. Hypertension (64.7%) and hyperlipidemia (57.9%) were the most prevalent risk factors. Multivariable regression identifi ed male sex (OR 1.8, 95% CI 1.1–2.9, p = 0.01), hypertension (OR 2.1, 95% CI 1.3–3.2, p = 0.002), and hyperlipidemia (OR 1.7, 95% CI 1.1–2.5, p = 0.01) as independent predictors of CAE. Diabetes mellitus and smoking were not signifi cantly associated. Family history showed borderline signifi cance (OR 1.4, p = 0.06). The most common angiographic pattern was three-vessel ectasia (37.9%). Conclusion: Pure CAE is more frequent in men and strongly associated with hypertension and hyperlipidemia, supporting a shared risk profi le with atherosclerosis. The absence of association with diabetes and smoking suggests a distinct underlying pathophysiology.
Introduction and objectives: Multivessel disease (MVD) occurs in approximately half of non–ST elevation myocardial infarction (NSTEMI) patients and is associated with an increased risk of cardiovascular events. However, current recommendation for complete revascularization in NSTEMI is based in observational and non-randomized studies suggesting a possible benefi t regarding mortality and major cardiovascular events. This study aimed to retrospectively evaluate the prognostic impact of complete percutaneous revascularization in a population of patients with NSTEMI and MVD. Material and methods: This was a national multicentre retrospective study of patients hospitalized for NSTEMI with MVD, included on the Portuguese Registry for Acute Coronary Syndromes (ProACS). The impact of complete percutaneous revascularization on in-hospital and one-year mortality rates, as well as on the probability of cardiovascular re-hospitalization was evaluated. Results: A total of 3084 patients were included in this analysis. We found no signifi cant differences between groups regarding in-hospital complications and mortality, as well as median hospitalization length. Nevertheless, complete revascularization showed a signifi cant impact on the primary endpoint of all-cause mortality or cardiovascular re-hospitalization (11.9% vs. 20.4%, p < 0.001), mainly driven by a major reduction in unplanned cardiovascular re-hospitalizations at one year of follow-up (9.3 vs. 16.8%, p < 0.001). Conversely, one-year mortality rate was once again similar between groups (4.2 vs. 5.0%, p = 0.536). Conclusions: In our population, complete revascularization during hospitalization was associated with lower risk of the primary endpoint of all-cause mortality or cardiovascular re-hospitalization, mainly driven by a major reduction in cardiovascular re-hospitalizations, with similar rate of intra-hospital complications.
Background: HDL is decisive for reverse cholesterol transport, enabling the removal of cholesterol from macrophages in atherosclerotic plaques. Although HDL-C has long been allied to CVS protection, recent evidence suggests that CEC may more accurately reflect HDL’s functional efficacy. However, studies exploring the relationship between CEC and CAD risk have produced inconsistent results. Objectives: The association between CEC and CAD risk was assessed, along with its potential to predict MACE, including cardiac mortality, all-cause mortality, and non-fatal MI, in this systematic review and meta-analysis. Material and methods: A comprehensive search of PubMed, Scopus, Web of Science, and The Cochrane Library was conducted to identify studies published up to January 2025. Observational studies comparing CEC levels between individuals with and without CAD were included. Results: Twenty-three studies met the inclusion criteria. The pooled SMD of – 0.40 (95% CI: -0.53−-0.26), with a p-value < 0.0001, revealed significantly lower CEC levels in CAD patients compared to non-CAD individuals. Higher CEC was strongly allied with a reduced risk of CAD – OR = 0.57; 95% CI: 0.48−0.67, P < 0.00001, and a pooled risk ratio (RR) of 0.64; 95% CI: 0.48−0.86, p = 0.003. Impaired CEC was associated with an increased risk of cardiac mortality – OR = 3.94; 95% CI: 2.63−5.90, p < 0.00001, and all-cause mortality – OR = 2.84; 95% CI: 2.01−4.00, p < 0.00001. However, insignificant association was found between CEC and non-fatal MI (OR = 3.47; 95% CI: 0.41−29.22, p = 0.25). Conclusion: This meta-analysis underscores the probability of CEC as a biomarker for the assessment of CVS risk. Higher CEC levels are linked to a reduced risk of CAD, cardiac mortality, and all-cause mortality, but no significant relationship was observed with non-fatal MI. Future research should prioritize standardizing CEC measurement methods and investigating its therapeutic potential for preventing atherosclerotic CVS disease.
