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Clinical manifestations of most rheumatic diseases have changed over the past few decades, largely due to advances in therapies targeting autoimmune and (auto)inflammatory pathways. Improvements in the management of rheumatic diseases have also now brought to the fore the issue of comorbidities. It has become evident that the burden of cardiovascular morbidity and mortality is increased in rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) and the spondyloarthropathies, amongst other conditions. As a result, efforts have switched toward investigating the effects of conventional antirheumatic and new biologic agents on inflammationinduced atherothrombosis. Evidence is accumulating suggesting a beneficial cardiovascular profile of some antirheumatic drugs, such as methotrexate and hydroxychloroquine, but it also indicates the possibility of a variety of adverse events developing in the short- and long-term. The aim of this review is to highlight cardiovascular adverse effects of the drugs widely used in the treatment of rheumatic diseases. The literature search was performed through PubMed, the Cochrane Library, Scopus, and Web of Science databases using the following terms: "antirheumatic drugs", "inflammation", "rheumatic diseases", "cardiovascular diseases", "adverse events", "toxicity", "drug design", and "drug interactions". Adverse events ranging from infusion-related hypertension and myocardial ischemia, to restrictive cardiomyopathy and congestive heart failure have been reported in large trials and case series on most antirheumatic drugs. Clinicians should be alert of the wide variety of cardiovascular adverse effects of individual antirheumatic drugs, and should carefully monitor blood pressure and markers of inflammation, thrombosis, myocardial ischemia, electrolytes, and lipid disturbances while administering these drugs. Future prospective studies should specifically investigate the cardiovascular safety of most antirheumatic drugs as part of mono- or combination therapy in relation to different dosage regimens, duration of therapy, age, and gender.

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Aims: It is often assumed that β-blockers, e.g. metoprolol (METO), induce erectile dysfunction (ED) in men. However, cardiovascular diseases can also induce ED and there is also the possibility that psychological factors, such as fear of the disease and side effects of the prescribed drug, may also induce ED. Thus, it is often assumed that β-blockers induce ED in a large percentage of men, but this statement is not well validated and the role of the pharmacologic effect of METO per se on the occurrence of ED is largely unknown. To get an answer we selected 114 men (age 57 ± 4.7 years) without ED but with newly diagnosed arterial hypertension, and who could be treated with METO. Methods: METO (100 mg/day) was given as a retard formulation. The hypertensive men were randomized into 3 groups. In group 1 patients were fully informed (they knew that the drug was METO and that it might induce ED). In group 2 patients were partially informed (they knew that the drug was METO, but were not informed that it might induce ED). In group 3 patients were not informed either about the drug used or about the possible occurrence of ED. The first phase of the study lasted 60 days. After 60 days the incidence of ED was 32% in group 1, 13% in group 2, and 8% in group 3 (p < 0.01). All patients with ED entered the second, cross-over, double-blind phase of the study. METO was continued at unchanged dosage, and tadalafil (20 mg) and a placebo were given to treat ED. Results: Both treatments were equally effective. Conclusion: Prejudice about the possible occurrence, i.e. the Hawthorne effect, of ED with METO facilitates the occurrence of this side effect in hypertensive men. Since the etiology of this ED is largely psychological, it is not surprising that placebo is as effective as tadalafil in reversing this side effect.