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was found after aspirin withdrawal [7], while another group reported a rebound increase in urinary thromboxane B2, a major TxA2 metabolite, after aspirin withdrawal [8]. Importantly, in contrast to our data, these studies used biochemical markers of platelet function as endpoints rather than functional platelet activity. We also found no effect on thrombin or fibrin generation, either immediately following aspirin therapy or after withdrawal. Importantly, we found no effect on fibrinolysis, which would have been expected had aspirin withdrawal resulted in the generation of a more rigid fibrin structure. Our findings are in accordance with other studies indicating that low dose aspirin, as used in clinical practice does not impact fibrinolysis [9]. Limitations of this study include the small numbers of participants and the absence of any assessment of the surface expression of activation-dependent platelet membrane receptors. We included only healthy volunteers, so we cannot rule out the existence of a rebound effect in those prescribed aspirin for underlying cardiovascular disease. In conclusion, this study of healthy volunteers demonstrated no evidence of a rebound phenomenon in healthy subjects after withdrawal of aspirin therapy using measures of platelet aggregation, nor evidence of a hypercoagulable response using global measures of coagulation. Thus we could find no biochemical evidence to support the reported clinical association between aspirin withdrawal and adverse cardiovascular events. It would seem that any observed association, is most likely to be due to recrudescence of the

prothrombotic manifestations of the underlying disease process rather than the iatrogenic upregulation of platelet activation and haemostatic function after aspirin withdrawal or interruption. References [1] Jacobs EJ, Thun MJ, Bain EB, Rodriguez C, Henley SJ, Calle EE. A large cohort study of long-term daily use of adult-strength aspirin and cancer incidence. J Natl Cancer Inst 2007;99:608–15. [2] Sambu N, Warner T, Curzen N. Clopidogrel withdrawal: is there a “rebound” phenomenon? Thromb Haemost 2011;105:211–20. [3] Hemker H, Giesen P, Al Dieri R, et al. The calibrated automated thrombogram (CAT): a universal routine test for hyper- and hypocoagulability. Pathophysiol Haemost Thromb 2002;32:249–53. [4] Reddel CJ, Curnow JL, Voitl J, et al. Detection of hypofibrinolysis in stable coronary artery disease using the overall haemostatic potential assay. Thromb Res 2013;131:457–62. [5] He S, Antovic A, Blomback M. A simple and rapid laboratory method for determination of haemostasis potential in plasma. II. Modifications for use in routine laboratories and research work. Thromb Res 2001;103:355–61. [6] Curnow JL, Morel-Kopp MC, Roddie C, Aboud M, Ward CM. Reduced fibrinolysis and increased fibrin generation can be detected in hypercoagulable patients using the overall hemostatic potential assay. J Thromb Haemost 2007;5:528–34. [7] Beving H, Zhao C, Albage A, Ivert T. Abnormally high platelet activity after discontinuation of acetylsalicylic acid treatment. Blood Coagul Fibrinolysis 1996;7:80–4. [8] Vial JH, McLeod LJ, Roberts MS. Rebound elevation in urinary thromboxane B2 and 6-keto-PGF1 alpha excretion after aspirin withdrawal. Adv Prostaglandin Thromboxane Leukot Res 1991;21A:157–60. [9] Buczko W, Mogielnicki A, Kramkowski K, Chabielska E. Aspirin and the fibrinolytic response. Thromb Res 2003;110:331–4.

http://dx.doi.org/10.1016/j.ijcard.2014.03.192 0167-5273/© 2014 Elsevier Ireland Ltd. All rights reserved.

Pacemaker, implantable cardioverter defibrillator, CRT, CRT-D, psychological difficulties and quality of life Giuseppe Mario Calvagna a,⁎, Giuseppe Torrisi a, Clea Giuffrida b, Salvatore Patanè a a b

Cardiologia Ospedale San Vincenzo - Taormina (Me) Azienda Sanitaria Provinciale di Messina, 98039 Taormina (Messina), Italy Laurea in psicologia

a r t i c l e

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Article history: Received 15 February 2014 Accepted 29 March 2014 Available online 6 April 2014 Keywords: Cardiac resynchronization therapy (CRT) CRT-D Implantable cardioverter defibrillators (ICD) Pacemaker

The use of implantable cardiac devices has increased in the last 30 years. The evolution of devices in serious cardiac rhythm pathology management has led progressively to the development of devices for the treatment of bradycardia, ventricular arrhythmia, and heart failure and for the prevention of sudden cardiac arrest [1–25] leading to delivery of pacemakers, implantable cardioverter defibrillators (ICD) and cardiac resynchronization therapy (CRT) plus ICD (CRT-D).

⁎ Corresponding author at: Cardiologia Ospedale San Vincenzo - Taormina (Me) Azienda Sanitaria Provinciale di Messina, 98039 Taormina (Messina), Italy. Tel.: + 39 3474800260. E-mail address: [email protected] (G.M. Calvagna).

Despite the success of these medical innovations, nowadays there is a growing demand, not only to improve overall patients' mortality and safety, but also to improve patient quality of life [26–29]. Pacemaker implantation causes anxiety disorders [30] and depression of patients up to first month [31]. A better functional class due to pacemaker is associated with a better quality of life [32]. Reduction of anxiety is observed at sixth month due to cardiac symptoms' improvement and to rehabilitation but a slight increase of depression is observed too [31]. A recent study suggests a significant association between the serotonin transporter gene 5-HTTLPR (serotonin-transporter-linked polymorphic region) polymorphism and the new onset of depression after pacemaker implantation, especially in smokers or in women [33]. Increased health-related quality of life is observed not only shortly after pacemaker implantation for bradycardia, but also after long-term 7.5 year follow-up period [34]. Infectious complications leading also to endocarditis [35–37] and non-infectious complications affect patients' wellbeing [1,8,9,21–27,38–47] often necessitating removal [1,3,25,26,38,41–47] and leading to psychological difficulty increase [26]. Implantable cardioverter defibrillators (ICD) are associated not only to precedent complications but also with a scenario of psychological sequelae often incompletely addressed at the time of implantation [47–51]. During the first 12 months, patients with primary prevention indication and older age have a protective effect against deterioration in

Letters to the Editor

psychological functioning while patients with type D personality (vulnerability to chronic psychological distress) [52], atrial fibrillation, and left ventricular dysfunction are at risk of poor psychological adaptation [53] as well as the comorbidity burden was a significant predictor of poorer psychological well-being and physical health status [54]. Patients with genetic heart diseases can experience psychological difficulties, including anxiety, depression and posttraumatic stress [55]. Phantom shocks (ICD sensation discharge without an actual discharge) are experienced by about one in ten ICD patients [56,57]. CRT improves cardiac, functional, and QoL (quality of life) outcomes. CRT-D patients have better mental component and disease-specific QoL than CRT patients; however, they have worse QoL, worse mental component QoL at baseline, and worse device acceptance at 9-month follow-up than patients with ICDs [58]. ICD discharge, whether appropriate or inappropriate, represents a particularly challenging psychological event [48]. Severe psychological distress (anxiety, panic, adjustment and post-traumatic stress disorders) due to the so-called “multiple ICD shocks” has been described [59]. Research suggests that the early finding and management of negative emotional response in ICD patients might prevent the development of depression. Unlikely no effect of a short-term psychoeducational intervention has been proven [60]. The role of the attending physician and the patient-to-health-careprovider relationship is crucial for the following aspects: information, participation, organization, and behavior [26,39,43,44,61,62]. Research suggests that an integrative, multidisciplinary approach to treating anxiety disorders can result in sustained improvements in physical, psychological, and functional status of ICD patients [46]. Evidence of low QoL, psychological functioning, and device acceptance need new researches relating to CRT-D in heart failure patients [58]. Future investigations may further point to the differential predictive value of emotional distress factors and on their relations to mortality [63]. The authors of this manuscript have certified that they adhere to the statement of ethical publishing as appears in International Journal of Cardiology. Author contributions: Salvatore Patanè wrote the introduction; Giuseppe Mario Calvagna wrote ICD, CRT-therapy and CRT-D therapy; Clea Giuffrida wrote severe psychological distress and short-term psychoeducational intervention fail in ICD patients; Giuseppe Torrisi wrote the conclusions and prepared the references.

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Pacemaker, implantable cardioverter defibrillator, CRT, CRT-D, psychological difficulties and quality of life.

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