Evaluation of psychopathology in patients with paroxysmal supraventricular tachycardia

Diseases of the cardiovascular system are among the most common diseases of our population and as such represent a significant health and economic problem. The relationship between psychopathology and cardiovascular diseases has been shown to be associated with type of personality and emotional reactivity, but it can result in more severe psychopathological symptoms (1–6). More importantly, it has been shown that comorbid depression increases the risk for mortality in subjects with cardiovascular diseases (ischemic heart disease or chronic heart failure) (7). An increased risk of cardiovascular mortality has been shown in depressive subjects without cardiovascular disease; therefore, it is clear that depression is not the only marker of severity for a cardiovascular disease but it adds to the development thereof (8,9). The mechanisms explaining the relationship between depression and the cardiovascular system can be understood at the pathophysiological and behavioural levels (9,10). Specific pathophysiological changes in the cardiovascular system are caused by depression. In particular, these include an increase in platelet aggregation and heart rate, and a decrease in the variability of heart rhythm mediated by the imbalance of the autonomous nervous system (decrease in parasympathetic nervous system tone). During depression, a deficient immune system along with hypercortisolemia, which can cause the increase of insulin resistance, increase the production of steroids thereby increasing blood pressure. These factors significantly contribute to the increased risk of the development of cardiovascular diseases. Patients with depression also tend to lead unhealthy lifestyles. In the present study, the incidence of psychopathological symptoms in patients with paroxysmal supraventricular tachycardia (PSVT) was assessed. The PSVTs include several types of arrhythmias with various causal mechanisms. One of the most common PSVTs is atrioventricular nodal re-entrant tachycardia (AVNRT). Another very common PSVT is atrioventricular re-entrant tachycardia (AVRT), which arises due to the presence of an accessory pathway. The hemodynamic consequences are similar in both of these PSVTs, which include the shortening of the diastolic filling time of the ventricles, and varying degrees of impairment of synchronization of diastolic filling times of the ventricles and ventricular contraction. This may result in palpitations, dyspnea, hyperventilation, dizziness, sweating, chest pain and anxiety. From a clinical point of view it is important to note that both of the above-mentioned forms of PSVT are cured in almost 100% of cases using radiofrequency ablation (RFA). The current literature reviews provide insufficient information concerning the psychopathology of patients with PSVT. In general, the psychopathological aspects should include common prevalence of 12-month diagnosis of depressive disorder in the adult European population (7%) (11), the somatic symptoms accompanying arrhythmias and individual sensibility of each patient. In addition, the intensity of symptoms such as the frequency, timing and suddenness of episodes, which often force patients to seek emergency medical help and may resemble panic disorder (or be its trigger) (1,12–15), have to be considered. The coincidence of panic and depressive disorders is very frequent but the diagnosis of ‘pure’ depressive or panic disorder is very rare; the comorbidity among mentally ill patients is estimated to be approximately 50% (11). The facts mentioned above may play a role in the pathogenesis of psychic disorders, especially by means of activation of the vegetative nervous system (9). Currently, the role of severe somatic diseases as chronic stressors in the pathogenesis of depressive disorders is often discussed. The functional length polymorphism in the promoter of the serotonin transporter (5-HTT) gene moderates the influence of stressful life events on symptoms of depression. It was found that individuals with one or two ‘short’ alleles at this polymorphism were more stress-sensitive than those with two ‘long’ alleles (16–18). This finding may support our hypothesis that a higher incidence of depressive disorder is expected in patients with PSVT. At the same time, identification of a hypothetically presumed anxiety-depression symptomatology would provide adequate indication for psychopharmacological intervention, which may, similar to patients after acute myocardial infarction, decrease the late morbidity (19).