Background and Objective: In the landscape of heart failure, non-cardiac comorbidities represent a formidable challenge, imparting adverse prognostic implications. Holter ECG monitoring assumes a supplementary role in delineating myocardial susceptibility and autonomic nervous system dynamics. This study aims to explore the potential correlation between Holter ECG parameters and comorbidities in individuals with ischemic cardiomyopathy experiencing heart failure (HF), with a particular focus on the primary utility of these parameters as prognostic indicators. Materials and Methods: In this prospective inquiry, a cohort of 60 individuals diagnosed with heart failure underwent stratification into subgroups based on the presence of comorbidities, including diabetes, chronic kidney disease, obesity, or hyperuricemia. Upon admission, a thorough evaluation of all participants encompassed echocardiography, laboratory panel analysis, and 24 h Holter monitoring. Results: Significant associations were uncovered between diabetes and unconventional physiological indicators, specifically the Triangular index (p = 0.035) and deceleration capacity (p = 0.002). Pertaining to creatinine clearance, notable correlations surfaced with RMSSD (p = 0.026), PNN50 (p = 0.013), and high-frequency power (p = 0.026). An examination of uric acid levels and distinctive Holter ECG patterns unveiled statistical significance, particularly regarding the deceleration capacity (p = 0.045). Nevertheless, in the evaluation of the Body Mass Index, no statistically significant findings emerged concerning Holter ECG parameters. Conclusions: The identified statistical correlations between non-cardiac comorbidities and patterns elucidated in Holter ECG recordings underscore the heightened diagnostic utility of this investigative modality in the comprehensive evaluation of individuals grappling with HF. Furthermore, we underscore the critical importance of the thorough analysis of Holter ECG recordings, particularly with regard to subtle and emerging parameters that may be overlooked or insufficiently acknowledged.
Cardiomyopathies , Diabetes Mellitus , Heart Failure , Myocardial Ischemia , Humans , Electrocardiography, Ambulatory , Pilot Projects , Prospective Studies , Myocardial Ischemia/complications , Myocardial Ischemia/diagnosis , Heart Failure/complications , Cardiomyopathies/complications , Cardiomyopathies/diagnosis , Heart Rate
Acute heart failure (AHF) is a life-threatening condition with high morbidity and mortality. Even though this pathology has been extensively researched, there are still challenges in establishing an accurate and early diagnosis, determining the long- and short-term prognosis and choosing a targeted therapeutic strategy. The use of reliable biomarkers to support clinical judgment has been shown to improve the management of AHF patients. Despite a large pool of interesting candidate biomarkers, endothelin-1 (ET-1) appears to be involved in multiple aspects of AHF pathogenesis that include neurohormonal activation, cardiac remodeling, endothelial dysfunction, inflammation, atherosclerosis and alteration of the renal function. Since its discovery, numerous studies have shown that the level of ET-1 is associated with the severity of symptoms and cardiac dysfunction in this pathology. The purpose of this paper is to review the existing information on ET-1 and answer the question of whether this neurohormone could be a promising biomarker in AHF.
Factor V (FV) Leiden and prothrombin G20210A are the most common hereditary thrombophilias. While their role in venous thromboembolism is well known, there are still uncertainties regarding their relationship with arterial thrombotic events, especially coronary ones. Our research, based on an in-depth analysis of the available literature, provides up-to-date information on the relationship between FV Leiden and prothrombin G20210A and acute myocardial infarction. FV Leiden and prothrombin G20210A screening should be implemented only in select cases, such as acute coronary syndrome in young individuals and/or in the absence of traditional cardiovascular risk factors and/or in the absence of significant coronary artery stenosis at angiography. Their identification should be followed by the implementation of optimal control of modifiable traditional cardiovascular risk factors to reduce the risk of recurrent events and genotyping and genetic counseling of all family members of affected cases for proper prophylaxis. An extended dual antiplatelet therapy (DAPT) may be considered, given the lower risk of bleeding under DAPT conferred by FV Leiden.
Myocardial ischemia is a pathophysiological state characterized by inadequate perfusion of the myocardium, resulting in an imbalance between myocardial oxygen demand and supply. It is most commonly caused by coronary artery disease, in which atherosclerotic plaques lead to luminal narrowing and reduced blood flow to the heart. Myocardial ischemia can manifest as angina pectoris or silent myocardial ischemia and can progress to myocardial infarction or heart failure if left untreated. Diagnosis of myocardial ischemia typically involves a combination of clinical evaluation, electrocardiography and imaging studies. Electrocardiographic parameters, as assessed by 24 h Holter ECG monitoring, can predict the occurrence of major adverse cardiovascular events in patients with myocardial ischemia, independent of other risk factors. The T-waves in patients with myocardial ischemia have prognostic value for predicting major adverse cardiovascular events, and their electrophysiological heterogeneity can be visualized using various techniques. Combining the electrocardiographic findings with the assessment of myocardial substrate may offer a better picture of the factors that can contribute to cardiovascular death.
Despite the improvements in the treatment of coronary artery disease (CAD) and acute myocardial infarction (MI) over the past 20 years, ischemic heart disease (IHD) continues to be the most common cause of heart failure (HF). In clinical trials, over 70% of patients diagnosed with HF had IHD as the underlying cause. Furthermore, IHD predicts a worse outcome for patients with HF, leading to a substantial increase in late morbidity, mortality, and healthcare costs. In recent years, new pharmacological therapies have emerged for the treatment of HF, such as sodium-glucose cotransporter-2 inhibitors, angiotensin receptor-neprilysin inhibitors, selective cardiac myosin activators, and oral soluble guanylate cyclase stimulators, demonstrating clear or potential benefits in patients with HF with reduced ejection fraction. Interventional strategies such as cardiac resynchronization therapy, cardiac contractility modulation, or baroreflex activation therapy might provide additional therapeutic benefits by improving symptoms and promoting reverse remodeling. Furthermore, cardiac regenerative therapies such as stem cell transplantation could become a new therapeutic resource in the management of HF. By analyzing the existing data from the literature, this review aims to evaluate the impact of new HF therapies in patients with IHD in order to gain further insight into the best form of therapeutic management for this large proportion of HF patients.
Given the possible pathophysiological links between myocardial ischemia and SARS-CoV-2 infection, several studies have focused attention on acute coronary syndromes in order to improve patients' morbidity and mortality. Understanding the pathophysiological aspects of myocardial ischemia in patients infected with SARS-CoV-2 can open a broad perspective on the proper management for each patient. The electrocardiogram (ECG) remains the easiest assessment of cardiac involvement in COVID-19 patients, due to its non-invasive profile, accessibility, low cost, and lack of radiation. The ECG changes provide insight into the patient's prognosis, indicating either the worsening of an underlying cardiac illnesses or the acute direct injury by the virus. This indicates that the ECG is an important prognostic tool that can affect the outcome of COVID-19 patients, which important to correlate its aspects with the clinical characteristics and patient's medical history. The ECG changes in myocardial ischemia include a broad spectrum in patients with COVID-19 with different cases reported of ST-segment elevation, ST-segment depression, and T wave inversion, which are associated with severe COVID-19 disease.
Constant and intense physical activity causes physiological adaptive changes in the human body, but it can also become a trigger for adverse events, such as sudden cardiac arrest or sudden cardiac death. Our main objective was to assess the use of combined cardiopulmonary exercise testing (CPET) and cardiac biomarker determinants in young professional athletes. We conducted a study which involved the full examination of 19 football players, all male, aged between 18 and 20 years old. They underwent standard clinical and paraclinical evaluation, a 12-lead electrocardiogram (ECG), and transthoracic echocardiography (TTE). Afterwards, a tailored CPET was performed and peripheral venous blood samples were taken before and 3 h after the test in order to determine five biomarker levels at rest and post-effort. The measured biomarkers were cardiac troponin I (cTnI), myoglobin (Myo), the MB isoenzyme of creatine-kinase (CK-MB), the N-terminal prohormone of brain natriuretic peptide (NT-proBNP) and D-dimers. While cTnI and NT-proBNP levels were undetectable both at rest and post-effort in all subjects, the variations in Myo, CK-MB and D-dimers showed significant correlations with CPET parameters. This highlights the potential use of combined CPET and biomarker determinants to evaluate professional athletes, and encourages further research on larger study groups.
