Serum biomarkers represent a reproducible, sensitive, minimally invasive and inexpensive method to explore possible adverse cardiovascular effects of antineoplastic treatments. They are useful tools in risk stratification, the early detection of cardiotoxicity and the follow-up and prognostic assessment of cancer patients. In this literature review, we aim at describing the current state of knowledge on the meaning and the usefulness of cardiovascular biomarkers in patients with cancer; analyzing the intricate relationship between cancer and cardiovascular disease (especially HF) and how this affects cardiovascular and tumor biomarkers; exploring the role of cardiovascular biomarkers in the risk stratification and in the identification of chemotherapy-induced cardiotoxicity; and providing a summary of the novel potential biomarkers in this clinical setting.

Systemic sclerosis is an auto-immune disease characterized by skin involvement that often affects multiple organ systems. Pulmonary hypertension is a common finding that can significantly impact prognosis. Molecular pathophysiological mechanisms underlying pulmonary hypertension in systemic sclerosis can be extremely heterogeneous, leading to distinct clinical phenotypes. In addition, different causes of pulmonary hypertension may overlap within the same patient. Since pulmonary hypertension treatment is very different for each phenotype, it is fundamental to perform an adequate diagnostic work-up to properly and promptly identify the prevalent mechanism underlying pulmonary hypertension in order to start the right therapies. When pulmonary hypertension is caused by a primary vasculopathy of the small pulmonary arteries, treatment with pulmonary vasodilators, often in an initial double-combination regimen, is indicated, aimed at reducing the mortality risk profile. In this review, we describe the different clinical phenotypes of pulmonary hypertension in the scleroderma population and discuss the utility of clinical tools to identify the presence of pulmonary vascular disease. Furthermore, we focus on systemic sclerosis-associated pulmonary arterial hypertension, highlighting the advances in the knowledge of right ventricular dysfunction in this setting and the latest updates in terms of treatment with pulmonary vasodilator drugs.

Purpose of Review: Along with population aging, the incidence of both heart failure (HF) and cancer is increasing. However, little is known about new-onset cancer in HF patients. This review aims at showing recent discoveries concerning this subset of patients.Recent Findings: Not only cancer and HF share similar risk factors but also HF itself can stimulate cancer development. Some cytokines produced by the failing heart induce mild inflammation promoting carcinogenesis, as it has been recently suggested by an experimental model of HF in mice.Summary: The incidence of new-onset cancer is higher in HF patients compared to the general population, and it significantly worsens their prognosis. Moreover, the management of HF patients developing new-onset cancer is challenging, especially due to the limited therapeutic options for patients affected by both cancer and HF and the higher risk of cardiotoxicity from anticancer drugs.

Pulmonary arterial hypertension (PAH) is a rare condition characterized by high pulmonary artery pressure leading to right ventricular dysfunction and potential life-threatening consequences. It primarily affects the pre-capillary pulmonary vascular system. The exact pathophysiological mechanisms underlying PAH are not entirely known. Environmental factors; genetic predisposition; mitochondrial and microRNA dysfunction; and inflammatory, metabolic, and hormonal mechanisms may be involved. A central role is played by the dysfunction of the pulmonary vascular endothelium. This alteration is characterized by a reduction in vasodilatory and antiproliferative factors such as prostacyclin and nitric oxide and an increase in vasoconstrictive and mitogenic substances such as endothelin and thromboxane A2. Such imbalance leads to a progressive increase in pulmonary vascular resistance. The aim of the present review is to focus on the vascular endothelium and its role as a potential therapeutic target in PAH.

Background and Objectives: Along with the ageing of the population, cancer and cardiovascular (CV) diseases more frequently coexist, complicating patients’ management. Here, we focus on elderly oncologic patients, describing clinical features and comorbidities, discussing therapeutic management CV risk factors and CV complications risen during our CV follow-up, and exploring the different items of the comprehensive geriatric assessment (CGA) and the correlation between cardiac function by means of standard 2D echocardiography and each of the CGA items. Methods: A total of 108 consecutive patients (mean age 73.55 ± 5.43 years old; 40.7% females) referred to our cardio-oncology unit were enrolled, and three different groups were identified: Group 1, patients naïve for oncologic treatments (mean age 73.32 ± 5.40; 33% females); Group 2, patients already on antineoplastic protocols (mean age 73.46 ± 5.09; 44.1% females); and Group 3, patients who had already completed cancer treatments (mean age 74.34 ± 6.23; 55% female). The correlation between CGA, performed in a subgroup of 62 patients (57.4%), and echocardiographic parameters was assessed. Results: Group 2 patients had the highest incidence of CV events (CVEs) (61.8% vs. 14.8% in Group 1, 15% in Group 3; p ≤ 0.001) and withdrawals from oncologic treatments (8.8% vs. none in Group 1; p = 0.035). Group 2 had worse 48-month survival (47.1% vs. 22.2% in Group 1, 20% in Group 3; p = 0.05), which was even more evident when focusing on patients who died during follow-up. When assessing echocardiographic parameters, physical activity showed an inverse correlation with the left ventricular mass index (p = 0.034), while the Frailty index showed a direct correlation with the E/e’ ratio (p = 0.005). Conclusions: A thorough baseline CV assessment is important in elderly oncologic patients eligible for anticancer treatment. In this population, CGA can be a simple, feasible screening tool that might help identify patients at a greater risk of developing CVEs correlating to several pivotal cardiovascular parameters.