Cardiovascular (CV) diseases and cancer are the leading causes of death in Europe and the United States. Both diseases have extensive overlap and share common risk factors, symptoms, and outcomes. As the number of patients with both cancer and CV diseases continues to rise, the field of cardio-oncology is gaining increased attention. A frequent problem during anti-cancer treatment is cardiotoxicity caused by the side-effects of chemo-, immuno-, targeted, and radiation therapies. This problem may manifest as acute coronary syndrome, myocarditis, arrhythmias, or heart failure. Modern cardio-oncology spans many different research areas. While some researchers focus on treating patients that have already developed cardiotoxicity, others aim to identify new methods for preventing cardiotoxicity before, during, and after anti-cancer therapy. Both groups share the common understanding that regular monitoring of cancer patients is the basis for optimal medical treatment. Optimal treatment can only be achieved through close cooperation between cardiologists and oncologists. This review summarizes the current views on cardio-oncology and discusses the cardiotoxicities associated with commonly used chemotherapeutics.

Cardiovascular risk factors are one of the most common comorbidities in psoriasis. A higher prevalence of hypertension, insulin resistance and type 2 diabetes, dyslipidemia, obesity, metabolic syndrome, depression, as well as cardiovascular disease was confirmed in psoriatic patients in comparison to the general population. Data suggest that psoriasis and systemic inflammatory disorders may originate from the pleiotropic interactions with many genetic pathways. In this review, the authors present the current state of knowledge on the potential genetic links between psoriasis and cardiovascular risk factors. The understanding of the processes linking psoriasis with cardiovascular risk factors can lead to improvement of psoriasis management in the future.

Primary aldosteronism (PA) is a heterogeneous group of disorders caused by the autonomous overproduction of aldosterone with simultaneous suppression of plasma renin activity (PRA). It is considered to be the most common endocrine cause of secondary arterial hypertension (HT) and is associated with a high rate of cardiovascular complications. PA is most often caused by a bilateral adrenal hyperplasia (BAH) or aldosterone-producing adenoma (APA); rarer causes of PA include genetic disorders of steroidogenesis (familial hyperaldosteronism (FA) type I, II, III and IV), aldosterone-producing adrenocortical carcinoma, and ectopic aldosterone-producing tumors. Over the last few years, significant progress has been made towards understanding the genetic basis of PA, classifying it as a channelopathy. Recently, a growing body of clinical evidence suggests that mutations in ion channels appear to be the major cause of aldosterone-producing adenomas, and several mutations within the ion channel encoding genes have been identified. Somatic mutations in four genes (KCNJ5, ATP1A1, ATP2B3 and CACNA1D) have been identified in nearly 60% of the sporadic APAs, while germline mutations in KCNJ5 and CACNA1H have been reported in different subtypes of familial hyperaldosteronism. These new insights into the molecular mechanisms underlying PA may be associated with potential implications for diagnosis and therapy.

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Diastolic blood pressure, SBP × HR and DBP × HR products may be useful in subsequent heart failure exacerbation risk stratification. Moreover, DBP value may predict short-term mortality in patients with CHF.

Background Trimetazidine (TMZ) modulates cardiac metabolism, but its use in heart failure remains controversial. The aim of the study was to evaluate the effects of TMZ on exercise capacity, left ventricular ejection fraction (LVEF), mortality, and quality of life in stable patients with heart failure with reduced left ventricular ejection fraction (HFrEF). Methods Forty-five patients with stable advanced HFrEF treated with optimal medical therapy were randomized in a prospective, single-center, open-label, cross-over study of TMZ (35 mg b.i.d.) on top of standard medical therapy or standard pharmacotherapy for two periods of 30 days and one period of 6 months. Initially and at the end of each period all patients underwent the following: exercise testing, six-minute walk test (6MWT), two-dimensional-echocardiography, and quality of life assessment. Results The mean age of patients was 58.2 ± 10.6 years. Etiology of HFrEF was ischemic in 66.6% of patients. After 6 months no significant changes were observed in either group with regards to peak VO 2 uptake, 6MWT, LVEF, or quality of life. TMZ had no effect on mortality or cardiovascular events. Conclusions The additional use of TMZ on top of standard medical therapy in stable advanced HFrEF patients was not associated with significant changes in mortality, exercise capacity, LVEF, or quality of life.

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