Cardiovascular, renal, and metabolic diseases are pathophysiologically interdependent, posing a significant global health challenge and being associated with a substantial increase in morbidity and mortality. In 2023, the American Heart Association (AHA) defined this complex network of interconnected health conditions as the cardiovascular–kidney–metabolic (CKM) syndrome. This syndrome is based on common pathophysiological mechanisms, including chronic inflammation, oxidative stress, hyperglycemia and insulin resistance, activation of the renin–angiotensin–aldosterone system (RAAS), and neurohormonal dysfunction, which trigger a vicious cycle where the impairment of one organ contributes to the progressive deterioration of the others. An integrated approach to these conditions, rather than treating them as separate entities, supports a holistic management strategy that helps to reduce the burden on public health and improve patients’ quality of life. Existing management focuses on lifestyle modification, glycemic and lipid control, and the use of nephroprotective and cardioprotective therapies. This narrative review aims to synthesize and contextualize existing information on the complex interactions between these systems and on diagnostic approaches, as well as to provide an overview of the available therapeutic options.

Axial spondyloarthritis (axSpA) is a chronic inflammatory disease that can lead to ankylosis by secondary ossification of inflammatory lesions, with progressive disability and a significant impact on quality of life. It is also a risk factor for the occurrence of comorbidities, especially cardiovascular diseases (CVDs), mood disorders, osteoporosis, and malignancies. Early diagnosis and treatment are needed to prevent or decrease functional decline and to improve the patient’s prognosis. In respect of axSpA, there is an unmet need for biomarkers that can help to diagnose the disease, define disease activity and prognosis, and establish personalized treatment approaches. The aim of this review was to summarize the available information regarding the most promising biomarkers for axSpA. We classified and identified six core categories of biomarkers: (i) systemic markers of inflammation; (ii) molecules involved in bone homeostasis; (iii) HLA-B27 and newer genetic biomarkers; (iv) antibody-based biomarkers; (v) microbiome biomarkers; and (vi) miscellaneous biomarkers. Unfortunately, despite efforts to validate new biomarkers, few of them are used in clinical practice; however, we believe that these studies provide useful data that could aid in better disease management.

In cancer survivors, cardiac dysfunction is the main cause of mortality. Cardiotoxicity represents a decline in cardiac function associated with cancer therapy, and the risk factors include smoking, dyslipidemia, an age of over 60 years, obesity, and a history of coronary artery disease, diabetes, atrial fibrillation, or heart failure. Troponin is a biomarker that is widely used in the detection of acute coronary syndromes. It has a high specificity, although it is not exclusively associated with myocardial ischemia. The aim of this paper is to summarize published studies and to establish the role of troponin assays in the diagnosis of cardiotoxicity associated with various chemotherapeutic agents. Troponin has been shown to be a significant biomarker in the diagnosis of the cardiac dysfunction associated with several types of chemotherapeutic drugs: anthracyclines, anti-human epidermal growth factor receptor 2 treatment, and anti-vascular endothelial growth factor therapy. Based on the data available at this moment, troponin is useful for baseline risk assessment, the diagnosis of cardiotoxicity, and as a guide for the initiation of cardioprotective treatment. There are currently clear regulations regarding the timing of troponin surveillance depending on the patient’s risk of cardiotoxicity and the type of medication administered, but data on the cut-off values of this biomarker are still under investigation.

The coexistence of heart failure (HF) and chronic obstructive pulmonary disease (COPD) presents a significant clinical challenge due to the common risk factors, overlapping symptoms, and complex pathophysiological interactions and mechanisms. This comprehensive review explores the bidirectional relationship between HF and COPD, emphasizing their combined impact on morbidity, mortality, and quality of life. Epidemiological data reveal that up to one-third of patients with HF also have COPD, complicating diagnosis and leading to suboptimal treatment strategies. We discuss the pathways through which each disease exacerbates the other, the limitations of the current staging systems, the diagnostic tools needed to differentiate cardiac from pulmonary symptoms, and the treatment choices. Therapeutic management requires careful integration of pharmacologic and non-pharmacologic strategies, with attention paid to potential drug interactions. Evidence from clinical trials confirms that beta-blockers can be safely used in patients with COPD and highlights the importance of multidisciplinary, patient-centered care models. Prevention strategies, including smoking cessation, vaccination, and patient education, play a critical role in improving outcomes. Finally, we identify key research gaps and calls for more inclusive clinical guidelines to address the needs of patients with this overlapping syndrome. A coordinated, evidence-based approach is essential for optimizing care and improving the quality of life of patients facing the dual burden of HF and COPD.

Electrocardiogram (ECG) still remains a very useful diagnostic method in modern cardiology. Its broad availability, noninvasiveness and good sensitivity explain why it plays a capital role in the very beginning of the process of diagnosis for every patient, with or without cardiac-related complaints. For the practitioner, good training in ECG interpretation is mandatory. Sometimes, the ECG trace reveals particular aspects that may cause confusion and complicate decision-making. In this article, we present several less common situations underlying the general context and ECG features. The syndromes studied have a high pathological significance and may range from acute emergencies that call for a rapid therapeutical response to chronic syndromes that require prolonged observation, monitoring and risk stratification.

Heart failure (HF) is a complex clinical syndrome characterized by impaired cardiac function and maladaptive neurohormonal activation, representing one of the leading causes of morbidity, hospitalization, and mortality worldwide. Both its incidence and prevalence continue to rise, largely as a consequence of population aging and the increasing burden of cardiovascular risk factors. The pathogenesis of HF is multifactorial, involving a dynamic interplay between inflammation and neurohormonal activation, ultimately leading to cardiac remodeling, diastolic dysfunction, and impaired cardiac output. In this context, numerous biomarkers have been investigated for diagnosis and prognosis utility in patients with HF. According to their underlying pathophysiological mechanisms, biomarkers in HF can be broadly categorized as indicators of inflammation, oxidative stress, cardiac remodeling, myocardial stress, neurohormonal activation, and cardiomyocyte injury. This review summarizes current knowledge on the pathophysiological basis of HF and highlights the diagnostic and prognostic relevance of circulating biomarkers, emphasizing their role in linking disease mechanisms with clinical management.