Patients with atrial fibrillation and coronary artery disease – Double trouble

Patients with atrial fibrillation and coronary artery disease – Double trouble

Advances in Medical Sciences 63 (2018) 30–35 Contents lists available at ScienceDirect Advances in Medical Sciences journal homepage: www.elsevier.c...

415KB Sizes 1 Downloads 101 Views

Advances in Medical Sciences 63 (2018) 30–35

Contents lists available at ScienceDirect

Advances in Medical Sciences journal homepage: www.elsevier.com/locate/advms

Review article

Patients with atrial fibrillation and coronary artery disease – Double trouble _ Ewelina Michniewicza , Elzbieta Mlodawskaa , Paulina Lopatowskaa , a Anna Tomaszuk-Kazberuk , Jolanta Malyszkob,* a b

Department of Cardiology, Medical University in Bialystok, Bialystok, Poland 2nd Department of Nephrology and Hypertension with Dialysis Subunit, Medical University, M. Skłodowskiej-Curie 24A, 15-276 Białystok, Poland

A R T I C L E I N F O

Article history: Received 16 February 2017 Accepted 19 June 2017 Available online xxx Keywords: Atrial fibrillation Coronary artery disease Epidemiology Management

A B S T R A C T

Coronary artery disease (CAD) is the most common cardiovascular disease while atrial fibrillation (AF) is the most common cardiac arrhythmia. Both diseases share associated risk factors – hypertension, diabetes mellitus, sleep apnea, obesity and smoking. Moreover, inflammation plays a causative role in both diseases. The prevalence of CAD in patients with AF is from 17% to 46.5% while the prevalence of AF among patients with CAD is low and it is estimated from 0.2% to 5%. AF is a well-established factor of poor short- and long-term prognosis in patients with acute myocardial infarction (AMI) and is associated with a marked increase in overall mortality. The arrhythmia is common after cardiac surgeries and occurs in about 20 to 40% of patients after coronary artery bypass graft (CABG) surgery. It is predicted that between 5 and 15% of AF patients will require stenting at some point in their lives and will receive triple therapy with aspirin, clopidogrel or ticagrelor and oral anticoagulation (OAC). This requires careful consideration of antithrombotic therapy, balancing bleeding risk, stroke risk, and in-stent thrombosis with subsequent acute coronary syndromes. Co-prescription of OAC with antiplatelet therapy, in particular triple therapy, increases the absolute risk of major bleeding. In addition, major bleeding is associated with an up to 5-fold increased risk of death following an acute coronary syndrome. Coexistence of AF and CAD worsens the prognosis even in carefully treated patients. © 2017 Medical University of Bialystok. Published by Elsevier B.V. All rights reserved.

Contents 1.

2.

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1.1. Atrial fibrillation and myocardial infarction as co-occurring events . . . . . . . . . . . . . . . . . . . . . . . . Atrial fibrillation after coronary artery bypass surgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1.2. Angiographic findings among patients with AF . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1.3. 1.4. Antithrombotic therapy after acute coronary syndromes and percutaneous coronary intervention Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Conflict of interests . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Financial disclosure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

. . . . . . . .

. . . . . . . . .

. . . . . . . . .

. . . . . . . . .

. . . . . . . . .

. . . . . . . . .

. . . . . . . . .

. . . . . . . . .

. . . . . . . . .

. . . . . . . . .

. . . . . . . . .

. . . . . . . . .

. . . . . . . . .

. . . . . . . . .

. . . . . . . . .

. . . . . . . . .

. . . . . . . . .

. . . . . . . . .

. . . . . . . . .

. . . . . . . . .

. . . . . . . . .

. . . . . . . . .

. . . . . . . . .

. . . . . . . . .

. . . . . . . . .

. . . . . . . . .

. . . . . . . . .

. . . . . . . . .

. . . . . . . . .

30 31 31 31 32 33 33 33 33

1. Introduction

* Corresponding author. E-mail address: [email protected] (J. Malyszko).

Coronary artery disease (CAD) is the most common cardiovascular disease [1], while atrial fibrillation (AF) is the most common cardiac arrhythmia [2]. The prevalence of angina in populationbased studies increases with age, from 5 to 7% in women aged 45– 64 years to 10–12% in women aged 65–84 and from 4 to 7% in men

http://dx.doi.org/10.1016/j.advms.2017.06.005 1896-1126/© 2017 Medical University of Bialystok. Published by Elsevier B.V. All rights reserved.

E. Michniewicz et al. / Advances in Medical Sciences 63 (2018) 30–35

aged 45–64 years to 12–14% in men aged 65–84 [3]. In 2013 CAD was the most common cause of death globally, resulting in 8.14 million deaths (16.8%) up from 5.74 million deaths (12%) in 1990 [4]. Atrial fibrillation occurs in 2% of the general population and increases with age from 0.14% in those younger than 50 years old, 4% in patients between 60 and 70 years old, to 14% in population over 80 years old [2]. Both diseases share associated risk factors– hypertension, diabetes mellitus, sleep apnea, obesity and smoking. Moreover, inflammation plays a causative role in both diseases [5– 7]. The prevalence of CAD in patients with AF ranges from 17% to 46.5% [8–12]. In the ROCKET-AF (Rivaroxaban Once daily oral direct factor Xa inhibition Compared with vitamin K antagonism for prevention of stroke and Embolism Trial in atrial fibrillation) [13] and RELY (Randomized Evaluation of Long-term anticoagulant therapY with dabigatran etexilate) [14] large randomized trials CAD was present in  17% of the AF patients. Van Gelder et al. who investigated only patients with permanent AF, detected an incidence of CAD of 18% [15]. Kralev et al. in the study of AF patients undergoing coronary angiography showed that stable CAD was diagnosed in 13% of AF patients and in 21% of the patients with CAD percutaneous coronary intervention (PCI) or CABG were performed [16]. The prevalence of permanent type of AF was similar in both groups – with and without CAD (30% vs 27%, respectively) [16]. On the other hand, Lip et al. described an incidence of CAD up to 46% of the patients [10]. On the other hand, the prevalence of AF among patients with CAD is low and it is estimated from 0.2% to 5% [17–20].

31

new-onset AF after AMI were almost twice more likely to have a hospital course complicated by heart failure and more than 3 times more likely to develop cardiogenic shock [34]. In a single-center data-base of 2980 consecutive patients presenting with AMI, comparing the outcomes between particular AF types, only the permanent AF and new-onset AF groups had significantly higher short- and long-term mortality than patients without AF [36,37]. Furthermore, patients with known paroxysmal AF had the lowest observed 30-day mortality (7.3%) among the subgroups, similar to that of patients without AF (5.2%). The 10-year mortality rate was high and did not differ significantly among AF subgroups [37]. Conversely, sporadic cases of thromboembolic AMI also have been reported in patients with AF [38–44]. AF is associated with systemic signs of inflammation that could promote a prothrombotic state and eventually AMI [45]. Systemic inflammation may depend on AF per se or on the concomitant presence of the classic atherosclerotic risk factors, which are typically associated with AF [46]. In addition to atherosclerosis, AMI may occur in AF by other mechanisms. For example, episodes of AF with high ventricular rates may yield type 2 MI, which is characterized by an imbalance between demand and blood supply, and is usually associated with non-ST elevation MI [47]. In the large randomized trial ROCKET-AF myocardial infarction occurred in 101 patients in the rivaroxaban group and in 126 patients in the warfarin group (0.9% and 1.1% per year, respectively) [13]. The RE-LY trial reported a lower number of myocardial infarction: 0.53% per year with warfarin and 0.72% per year with dabigatran 110 mg bid and 0.74% per year with dabigatran 150 mg bid [14]. 1.2. Atrial fibrillation after coronary artery bypass surgery

1.1. Atrial fibrillation and myocardial infarction as co-occurring events Acute myocardial infarction (AMI) is an established risk factor for an AF episode with AF occurring in 6% to 21% of patients with AMI [21]. One out of ten subjects who present with MI have a documented history of AF [22]. Moreover, one out of four subjects without prior AF will develop AF at or after MI [22]. The case control study of 2460 patients with AMI showed that coronary disease affecting the atrial branches is a predictor for the development of AF early after MI, independent of age, gender, left ventricular ejection fraction, left atrial size, time to reperfusion or TIMI flow after coronary intervention [22]. AF is a well-established marker of poor short- and long-term prognosis in patients with AMI [24–28] and is associated with a large increase in overall mortality [23]. Patients presenting with AMI and a history of AF have increased mortality rate compared with patients without AF [23]. Population-based data indicate that, one half of first-ever documented AF cases after AMI are developed in the first month post-AMI onset [29]. The risk imparted by AF varies according to its timing, with a 2-fold increase in the risk of death for AF occurring 30 days after the incident of AMI compared with patients without AF [23,27,28,30–32]. Pilgrim et al. showed that among patients with CAD undergoing revascularization with drug-eluting stent, AF confers an increased risk of ischaemic stroke and intracranial bleeding [33]. In large, community-wide study involving more than 6000 patients with AMI it was observed that new-onset AF is a common and lethal complication of AMI [34]. AF was associated with a higher risk for in-hospital death and readmission within 30 days [34]. Furthermore, there was a greaterthan 2-fold higher risk for acute stroke and death during hospitalization in patients admitted with an AMI and AF [34]. These results are consistent with those of the Global Registry of Acute Coronary Events (GRACE) study where it was observed that patients with new-onset AF had a 3-fold increased risk of death during hospitalization for an acute coronary syndrome (ACS) compared with those who did not develop AF [35]. Patients with

The arrhythmia is common after cardiac surgeries and occurs in about 20 to 40% of patients after coronary artery bypass graft (CABG) surgery [48,49]. Post-operative AF usually occurs 2–4 days after the procedure. Generally, it is well tolerated, but it can be lifethreatening, especially in the elderly and patients with left ventricular dysfunction [50]. It is also associated with an increased risk of thromboembolic events, stroke and lengthened hospital stay [48,51–53]. Aranki et al. in his study showed that the mean length of hospitalization after surgery was 15.3 +/ 28.6 days for patients with AF compared with 9.3 +/ 19.6 days for patients without AF [48]. Several studies reported association with increasing age and the risk of AF after CABG [48,49,52]. 1.3. Angiographic findings among patients with AF AF patients may present with chest pain, which can be accompanied by transient ischemic-type ST-segment changes with marginally elevated cardiac markers, thus mimicking symptoms of CAD [54]. The rapid ventricular rate is often seen in patients with AF, and ST depression occurring at these rates has been attributed to subendocardial myocardial ischemia. In the study of Tsigkas et al. ST depression was seen in 38% of the patients with rapid AF and half of them had CAD at angiography [55]. Only 4% of the patients without ST depression during rapid AF had positive noninvasive tests for myocardial ischemia and CAD at angiography [56,57]. Nevertheless ST segment depression can often occur during rapid rates, even without CAD, and is not specific for ischemia particularly if the depression is <2 mm [56,58]. Another study showed troponin release in 15% of AF patients with symptoms of myocardial ischemia, usually in the absence of CAD at angiography [59]. In a retrospectively collected database of patients presenting for selective coronary angiography, the presence or history of AF was a factor associated with non-significant coronary disease [60]. In conclusion, the presence of AF alone, without other risk factors

32

E. Michniewicz et al. / Advances in Medical Sciences 63 (2018) 30–35

of CAD, should prompt to search for causes of AF other than CAD [61]. On the other hand Kralev et al. showed that in patients undergoing percutaneous coronary intervention, CAD was more frequently detected in the right coronary artery compared to controls [16]. The authors underlined that significant stenosis in the proximal right coronary artery and the circumflex artery prior to the take-off of the atrial branches increases the likelihood of AF. A retrospective analysis of 3220 consecutive patients submitted for selective coronary angiography showed that only 43% of patients with CAD and AF demonstrated a diseased right artery or circumflex artery [62]. Furthermore, in only two third of these patients the coronary stenoses were localized before the take-off of atrial branches [62]. A single-center retrospective analysis showed that CAD in AF patients seems to be associated with a higher severity. Additionally, patients with AF and myocardial infarction showed a significantly higher number of diseased coronary vessels [63]. 1.4. Antithrombotic therapy after acute coronary syndromes and percutaneous coronary intervention It is predicted that between 5 and 15% of AF patients will require stenting at some point in their lives and will receive triple therapy with aspirin, clopidogrel or ticagrelol and oral anticoagulation (OAC). This requires careful consideration of antithrombotic therapy, balancing bleeding risk, stroke risk, and risk of in-stent thrombosis with subsequent acute coronary syndromes [2,64–66]. Co-prescription of OAC with antiplatelet therapy, in particular triple therapy, increases the absolute risk of major hemorrhage [67–69]. A few retrospective and prospective analyses have compared triple therapy (OAC + dual antiplatelet) against dual therapy (DAPT; OAC + one antiplatelet), and the results are consistent in showing an increase in the risk of bleeding with triple therapy, that is 50% higher compared with dual therapy [70]. Also several large registries reported that the risk of major bleeding with triple antithrombotic therapy is 3-fold to 4-fold higher than with OAC alone or single antiplatelet therapy [71–74]. In addition, major bleeding is associated with an up to 5-fold increased risk of death following an acute coronary syndrome [75– 77]. In the trial PIONEER AF-PCI (A Study Exploring Two Strategies of Rivaroxaban and One of Oral Vitamin K Antagonist in Patients With Atrial Fibrillation Who Undergo Percutaneous Coronary Intervention) patients with non-valvular AF who had undergone PCI with stenting were assigned. The administration of either low-dose rivaroxaban (15 mg once daily) plus a P2Y12 inhibitor for 12 months or very-low-dose rivaroxaban (2.5 mg twice daily) plus dual antiplatelet therapy for 1, 6, or 12 months was associated with a lower rate of clinically significant bleeding than was standard therapy with a vitamin K antagonist (VKA) plus dual antiplatelet therapy for 1, 6, or 12 months [78]. The three groups had similar efficacy rate. Among patients with AF undergoing intracoronary stenting, administration of either rivaroxaban 15 mg daily plus P2Y12 inhibitor monotherapy or 2.5 mg rivaroxaban twice daily plus DAPT was associated with a reduced risk of all-cause mortality or recurrent hospitalization for adverse events compared with standard-of-care VKA plus DAPT [79] In the trial WOEST (What Is the Optimal Antiplatelet & Anticoagulant Therapy in Patients With Oral Anticoagulation and Coronary Stenting study), 573 patients who were receiving anticoagulation with VKAs (mostly for AF) and needed PCI were randomized to standard triple antithrombotic therapy (OAC, aspirin and clopidogrel) vs dual antithrombotic therapy (OAC and clopidogrel) [80]. The study showed that dual antithrombotic

therapy significantly reduced the risk of bleeding and was also associated with a lower risk of death or thrombotic events than was triple antithrombotic therapy. One-year follow-up data showed that bleeding episodes were observed in 19.4% of patients receiving dual antithrombotic therapy vs 44.4% receiving triple antithrombotic therapy [80]. In the ISAR-TRIPLE study (Triple Therapy in Patients on Oral Anticoagulation After Drug Eluting Stent Implantation), in which patients were randomized to 6 weeks or 6 months of clopidogrel on top of aspirin and OAC after drug eluting stent implantation, no difference was apparent between groups in the primary endpoint of death, MI, stroke, thrombolysis in MI or major bleeding at 9month follow-up [81]. Furthermore, there were no differences in the combined secondary endpoint (cardiac death, MI or ischemic stroke). These data suggest that physicians should balance patients risk of ischemic events against their bleeding risk when selecting the shorter or longer duration of triple therapy. Another trial RE-DUAL (Evaluation of Dual Therapy With Dabigatran vs. Triple Therapy With Warfarin in Patients With AF That Undergo a PCI With Stenting) has randomized 2727 adult AF patients undergoing PCI with stenting (elective or due to an ACS) evaluates dual therapy with dabigatran vs. triple therapy. The trial is ongoing. The results will be published this year [82]. Other trials addressing various antithrombotic regimes are ongoing. The purpose of AUGUSTUS study is to determine if apixaban is safer than a vitamin K antagonist given for 6 months in terms of bleeding in patients with AF and a recent myocardial infarction or a recent PCI. All patients would also be taking P2Y12 inhibitors such as clopidogrel and be treated for up to 6 months. The primary focus will be a comparison of the bleeding risk of apixaban, with or without aspirin, versus warfarin, with or without aspirin [83]. The WOEST 2 Registry aims to improve medical care for patients with AF and/or a heart valve prosthesis ánd undergoing coronary revascularization through a better understanding of their demographics, antithrombotic management and related in-hospital and long-term outcomes. The objective is to assess the different management patterns and related in-hospital and long-term safety and efficacy outcomes of combined use of chronic oral anticoagulation and a P2Y12 inhibitor in patients with AF and/or a heart valve prosthesis undergoing coronary revascularization [84]. AF patients at risk for stroke, patients with mechanical valves, and patients with recent or recurrent deep vein thrombosis or pulmonary embolism should continue OAC during and after stenting. In general, a short period of triple therapy (OAC, aspirin, clopidogrel) is recommended, followed by a period of dual therapy (OAC plus a single anti-platelet) (Fig. 1). After elective coronary stenting for stable CAD in AF patients at risk of stroke, combination triple therapy with aspirin, clopidogrel

Fig. 1. treatment of atrial fibrillation in relation to the clinical settings.

E. Michniewicz et al. / Advances in Medical Sciences 63 (2018) 30–35

and an oral anticoagulant should be considered for 1 month to prevent recurrent coronary and cerebral ischaemic events. After an ACS with stent implantation in AF patients at risk of stroke, combination triple therapy with aspirin, clopidogrel and an oral anticoagulant should be considered for 1–6 months to prevent recurrent coronary and cerebral ischaemic events [2]. After an ACS without stent implantation in AF patients at risk of stroke, dual treatment with an oral anticoagulant and aspirin or clopidogrel should be considered for up to 12 months to prevent recurrent coronary and cerebral ischaemic events. The duration of combination antithrombotic therapy, especially triple therapy, should be kept to a limited period, balancing the estimated risk of recurrent coronary events and bleeding. Dual therapy with any oral anticoagulant plus clopidogrel 75 mg per day may be considered as an alternative to initial triple therapy in selected patients [2]. When a non-vitamin K antagonist oral anticoagulants (NOACs) is used, the consensus recommendation is that the lowest dose effective for stroke prevention in AF should be considered [2]. The recommended combination of antithrombotic therapy and duration of combination therapy for AF patients undergoing percutaneous coronary intervention is shown in Fig. 1. In patients after an ACS with a high (uncorrectable) bleeding risk,the duration of triple therapy can be shortened from 6 to 1 months, or even to immediate double therapy (with either aspirin or clopidogrel) in highly selected cases. Even longer triple therapy (up to 12 months) may be considered in individual cases receiving a first generation DES or those with a combination of very high atherothrombotic risk (as e.g. calculated by a GRACE score 118; again without existing evaluation of this value in this setting, stenting of the left main, proximal left anterior descending, proximal bifurcation, recurrent MIs etc.) and low bleeding risk according to HAS-BLED score [85]. For all CAD patients with AF, the default is to step down to anticoagulation in monotherapy after 1 year, except for those with a very high risk for coronary events and an acceptably low bleeding risk [86]. 2. Conclusions In patients with AF the overall incidence of CAD is relatively high. The number of patients with AF undergoing PCI and CABG is also high especially in elderly population >70 years. Increasing incidence of cardiovascular risk factors in the western world should lead to a careful investigation in patients presenting with AF to either definitely exclude or establish a diagnosis of CAD. This could contribute to an early and safe therapeutic strategy including also oral anticoagulation combined with antiplatelet treatment. Conflict of interests "The authors declare no conflicts of interest". Financial disclosure "The authors have no funding to disclose". References [1] Montalescot G, Sechtem U, Achenbach S, Andreotti F, Arden C, Budaj A, et al. ESC guidelines on the management of stable coronary artery disease: the Task Force on the management of stable coronary artery disease of the European Society of Cardiology. Eur Heart J 2013;34(38)2949–3003 2013. [2] Kirchhof P, Benussi S, Kotecha D, Ahlsson A, Atar D, Casadei B, et al. ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS. Europace 2016;18(11)1609–78 2016.

33

[3] National Institutes of Health NH, Lung, and Blood Institute. Morbidity & Mortality:2012 Chart Book on Cardiovascular, Lung, and Blood Diseases. Bethesda, MD : National Heart, Lung, and Blood Institute. 2012. [4] GBD 2013 Mortality and Causes of Death Collaborators. Global, regional, and national age-sex specific all-cause and cause-specific mortality for 240 causes of death, 1990–2013: a systematic analysis for the Global Burden of Disease Study 2013. Lancet 2015;9963:117–71. [5] Burokiene_ N, Domarkiene_ I, Ambrozaityte_ L, Uktveryte_ I, Meškiene_ R, Kar9ciauskaite_ V, et al. Classical rather than genetic risk factors account for high cardiovascular disease prevalence in Lithuania: a cross-sectional population study. Adv Med Sci 2017;62:121–8. [6] Gensini GF, Comeglio M, Colella A. Classical risk factors and emerging elements in the risk profile for coronary artery disease. Eur Heart J 1998;19(Suppl. A): A53–61. [7] Christodoulidis G, Vittorio TJ, Fudim M, et al. Inflammation in coronary artery disease. Cardiol Rev 2014;22(6):279–88. [8] Crijns HJ, Van Gelder IC, Van Gilst WH, Hillege H, Gosselink AM, Lie KI. Serial antiarrhythmic drug treatment to maintain sinus rhythm after electrical cardioversion for chronic atrial fibrillation or atrial flutter. Am J Cardiol 1991;1 (4):335–41. [9] AFFIRM investigators atrial fibrillation follow-up investigation of rhythm management. baseline characteristics of patients with atrial fibrillation: the AFFIRM study. Am Heart J 2002;143(6):991–1001. [10] Lip GYH, Beevers DG. ABC of atrial fibrillation. History, epidemiology and importance of atrial fibrillation. BMJ 1995;18(7016):1361–3. [11] Krahn AD, Manfreda J, Tate RB, Mathewson FA, Cuddy TE. The natural history of atrial fibrillation: incidence, risk factors and prognosis in the Manitoba FollowUp Study. Am J Med 1995;98(5):476–84. [12] Hohnloser SH, Crijns HJ, van Eickels M, Gaudin C, Page RL, Torp-Pedersen C, et al. ATHENA Investigators. Effect of dronedarone on cardiovascular events in atrial fibrillation. N Engl J Med 2009;12(7):668–78. [13] Patel MR, Mahaffey KW, Garg J, Pan G, Singer DE, Hacke W, et al. ROCKET AF investigators. Rivaroxaban vs. warfarin in non-valvular atrial fibrillation. N Engl J Med 2011;365(10):883–91. [14] Connolly SJ, Ezekowitz MD, Yusuf S, Eikelboom J, Oldgren J, Parekh A, et al. RELY Steering Committee and Investigators. Dabigatran versus warfarin in patients with atrial fibrillation. N Engl J Med 2009;17(12):1139–51. [15] Van Gelder IC, Groenveld HF, Crijns HJ, Tuininga YS, Tijssen JGP, Alings AM, et al. Race II Investigators. Lenient versus strict rate control in patients with atrial fibrillation. N Engl J Med 2010;362(15):1439–41. [16] Kralev S, Schneider K, Lang S, Süselbeck T, Borggrefe M. Incidence and severity of coronary artery disease in patients with atrial fibrillation undergoing firsttime coronary angiography. PLoS One 2011;6(9):e24964. [17] Otterstad JE, Kirwan BA, Lubsen J, De Brouwer S, Fox KA, Corell P, et al. Action Investigators. Incidence and outcome of atrial fibrillation in stable symptomatic coronary disease. Scand Cardiovasc J 2006;40(3):152–9. [18] Cameron A, Schwartz MJ, Kronmal RA, Kosinski AS. Prevalence and significance of atrial fibrillation in coronary artery disease (CASS Registry). Am J Cardiol 1988;6:714–7. [19] Haddad AH, Prchkov VK, Dean DC. Chronic atrial fibrillation and coronary artery disease. J Electrocardiol 1987;11:67–9. [20] Cheng TO. Coronary artery disease as an uncommon cause of chronic atrial fibrillation. Clin Res 1974;22:268A. [21] Schmitt J, Duray G, Gersh BJ, Hohnloser SH. Atrial fibrillation in acute myocardial infarction: a systematic review of the incidence, clinical features and prognostic implications. Eur Heart J 2009;30(9):1038–145. [22] Jabre P1, Jouven X, Adnet F, Thabut G, Bielinski SJ, Weston SA, et al. Atrial fibrillation and death after myocardial infarction: a community study. Circulation 2011;17(19):2094–100. [23] Alasady M, Abhayaratna WP, Leong DP, Lim HS, Abed HS, Brooks AG, et al. Coronary artery disease affecting the atrial branches is an independent determinant of atrial fibrillation after myocardial infarction. Heart Rhythm 2011;8(7):955–60. [24] Rathore SS, Berger AK, Weinfurt KP, Schulman KA, Oetgen WJ, Gersh BJ, et al. Acute myocardial infarction complicated by atrial fibrillation in the elderly: prevalence and outcomes. Circulation 2000;101(9):969–74. [25] Crenshaw BS, Ward SR, Granger CB, Stebbins AL, Topol EJ, Califf RM. Atrial fibrillation in the setting of acute myocardial infarction: the GUSTO-I experience: global Utilization of Streptokinase and TPA for Occluded Coronary Arteries. J Am Coll Cardiol 1997;30(2):406–13. [26] Stenestrand U, Lindbäck J. RIKS-HIA Registry Anticoagulation therapy in atrial fibrillation in combination with acute myocardial infarction influences longterm outcome: a prospective cohort study from the Register of Information and Knowledge About Swedish Heart Intensive Care Admissions (RIKS-HIA). Circulation 2005;112(21):3225–31. [27] Lopes RD, Pieper KS, Horton JR, Al-Khatib SM, Newby LK, Mehta RH, et al. Short- and longterm outcomes following atrial fibrillation in patients with acute coronary syndromes with or without ST-segment elevation. Heart 2008;94(7):867–73. [28] Al-Khatib SM, Pieper KS, Lee KL, Mahaffey KW, Hochman JS, Pepine CJ, et al. Atrial fibrillation and mortality among patients with acute coronary syndromes without ST-segment elevation: results from the PURSUIT trial. Am J Cardiol 2001;1(1)76–9 A7. [29] Jabre P, Roger VL, Murad MH, Chamberlain AM, Prokop L, Adnet F, et al. Mortality associated with atrial fibrillation in patients with myocardial

34

[30]

[31]

[32]

[33]

[34]

[35]

[36]

[37]

[38] [39]

[40]

[41]

[42]

[43]

[44]

[45] [46]

[47]

[48]

[49]

[50]

[51]

[52]

[53]

[54]

[55]

E. Michniewicz et al. / Advances in Medical Sciences 63 (2018) 30–35 infarction: a systematic review and meta-analysis. Circulation 2011;19 (15):1587–93. Goldberg RJ, Yarzebski J, Lessard D, Wu J, Gore JM. Recent trends in the incidence rates of and death rates from atrial fibrillation complicating initial acute myocardial infarction: a communitywide perspective. Am Heart J 2002;143(3):519–27. Berton G, Cordiano R, Cucchini F, Cavuto F, Pellegrinet M, Palatini P. Atrial fibrillation during acute myocardial infarction: association with all-cause mortality and sudden death after 7-year of follow-up. Int J Clin Pract 2009;63 (5):712–21. Madias JE, Patel DC, Singh D. Atrial fibrillation in acute myocardial infarction: a prospective study based on data from a consecutive series of patients admitted to the coronary care unit. Clin Cardiol 1996;19(3):180–6. Pilgrim T, Kalesan B, Zanchin T, Pulver C, Jung S, Mattle H, et al. Impact of atrial fibrillation on clinical outcomes among patients with coronary artery disease undergoing revascularization with drug-eluting stents. EuroIntervention 2013;22(9):1061–71. Kundu A, O'Day K, Shaikh AY, Lessard DM, Saczynski JS, Yarzebski J, et al. Relation of atrial fibrillation in acute myocardial infarction to in-hospital complications and early hospital readmission. Am J Cardiol 2016;15(8):1213– 8. Mehta RH, Dabbous OH, Granger CB, Kuznetsova P, Kline-Rogers EM, Anderson FA, et al. GRACE Investigators. Comparison of outcomes of patients with acute coronary syndromes with and without atrial fibrillation. Am J Cardiol 2003;1 (9):1031–6. Podolecki T, Lenarczyk R, Kowalczyk J, Kurek T, Boidol J, Chodor P, et al. Effect of type of atrial fibrillation on prognosis in acute myocardial infarction treated invasively. Am J Cardiol 2012;15(12):1689–93. Poçi D, Hartford M, Karlsson T, Edvardsson N, Caidahl K. Effect of new versus known versus no atrial fibrillation on 30-day and 10-year mortality in patients with acute coronary syndrome. Am J Cardiol 2012;15(2):217–21. Garg RK, Jolly N. Acute myocardial infarction secondary to thromboembolism in a patient with atrial fibrillation. Int J Cardiol 2007;123(1):e18–20. Van de Walle S, Dujardin K. A case of coronary embolism in a patient with paroxysmal atrial fibrillation receiving tamoxifen. Int J Cardiol 2007;123 (1):66–8. Sakai K, Inoue K, Nobuyoshi M. Aspiration thrombectomy of a massive thrombotic embolus in acute myocardial infarction caused by coronary embolism. Int Heart J 2007;48(3):387–92.  ski P, Dziewierz A, Rakowski T, et al. Cardioembolic acute myocardial Kleczyn infarction and stroke in a patient with persistent atrial fibrillation. Int J Cardiol 2012;161(3)e46–7 [PubMed: 22552166]. Hernández F, Pombo M, Dalmau R, Andreu J, Alonso M, Albarrán A, et al. Acute coronary embolism: angiographic diagnosis and treatment with primary angioplasty. Catheter Cardiovasc Interv 2002;55(4):491–4. Takenaka T, Horimoto M, Igarashi K, Yoshie H, Tsujino I, Morihira M. Multiple coronary thromboemboli complicating valvular heart disease and atrial fibrillation. Am Heart J 1996;131(1):194–6. Camaro C, Aengevaeren WR. Acute myocardial infarction due to coronary artery embolism in a patient with atrial fibrillation. Neth Heart J 2009;17(7– 8):297–9. Guo Y, Lip GY, Apostolakis S. Inflammation in atrial fibrillation. J Am Coll Cardiol 2012;4(22):2263–70. O'Neal WT, Soliman EZ, Howard G, Howard VJ, Safford MM, Cushman M, et al. Inflammation and hemostasis in atrial fibrillation and coronary heart disease: the reasons for geographic and racial differences in stroke study. Atherosclerosis 2015;243:192–7. Sandoval Y, Smith SW, Thordsen SE, Apple FS. Supply/demand type 2 myocardial infarction: should we be paying more attention. J Am Coll Cardiol 2014;63:2079–87. Aranki SF, Shaw DP, Adams DH, Rizzo RJ, Couper GS, VanderVliet M, et al. Predictors of atrial fibrillation after coronary artery surgery: current trends and impact on hospital resources. Circulation 1996;94(3):390–7. Mathew JP, Parks R, Savino JS, Friedman AS, Koch C, Mangano DT, et al. Atrial fibrillation following coronary artery bypass graft surgery: predictors, outcomes, and resource utilization. MultiCenter Study of Perioperative Ischemia Research Group. JAMA 1996;276(4):300–6. Wyse DG, Waldo AL, DiMarco JP, Domanski MJ, Rosenberg Y, Schron EB, et al. A comparison of rate control and rhythm control in patients with atrial fibrillation. N Engl J Med 2002;347(23):1825–33. Fuller JA, Adams GG, Buxton B. Atrial fibrillation after coronary artery bypass grafting. Is it a disorder of the elderly? J Thorac Cardiovasc Surg 1989;97 (6):821–5. Kowey PR, Dalessandro DA, Herbertson R, Briggs B, Wertan MA, Rials SJ, et al. Effectiveness of digitalis with or without acebutolol in preventing atrial arrhythmias after coronary artery surgery. Am J Cardiol 1997;79(8):1114–7. Mendes LA, Connelly GP, McKenney PA, Podrid PJ, Cupples LA, Shemin RJ, et al. Right coronary artery stenosis: an independent predictor of atrial fibrillation after coronary artery bypass surgery. J Am Coll Cardiol 1995;25(1):198–202. Kanjwal K, Imran N, Grubb B, Kanjwal Y. Troponin elevation in patients with various tachycardias and normal epicardial coronaries. Indian Pacing Electrophysiol J 2008;1(3):172–4. Tsigkas G, Kopsida G, Xanthopoulou I, Roussakis GN, Michaelides AP, Kartalis AN, et al. Diagnostic accuracy of electrocardiographic ST-segment depression in patients with rapid atrial fibrillation for the prediction of coronary artery disease. Can J Cardiol 2014;30(8):920–4.

[56] Androulakis A, Aznaouridis KA, Aggeli CJ, Roussakis GN, Michaelides AP, Kartalis AN, et al. Transient ST-segment depression during paroxysms of atrial fibrillation in otherwise normal individuals: relation with underlying coronary artery disease. J Am Coll Cardiol 2007;6(19):1909–11.  ska-Loch B, [57] Wierzbowska-Drabik K, Cygulska K, Cieslik-Guerra U, Uznan  ski T, Trzos E, et al. Circumferential strain of carotid arteries does not Rechcin differ between patients with advanced coronary artery disease and group without coronary stenoses. Adv Med Sci 2016;61(2):203–6. [58] Pradhan R, Chaudhary A, Donato AA. Predictive accuracy of ST depression during rapid atrial fibrillation on the presence of obstructive coronary artery disease. Am J Emerg Med 2012;30(7):1042–7. [59] Abidov A, Hachamovitch R, Rozanski A, Hayes SW, Santos MM, Sciammarella MG, et al. Prognostic implications of atrial fibrillation in patients undergoing myocardial perfusion single-photon emission computed tomography. J Am Coll Cardiol 2004;1(5):1062–70. [60] Elabbassi W, Chowdhury MA, Brano Liska, Hatala R. Clinical profile and angiographic findings among patients with atrial fibrillation presenting for selective coronary angiography. Health (N Y) 2014;6(1):44–50. [61] Camm AJ, Kirchhof P, Lip GY, Schotten U, Savelieva I, Ernst S, et al. Guidelines for the management of atrial fibrillation: the Task Force for the Management of Atrial Fibrillation of the European Society of Cardiology (ESC). European Heart Rhythm Association; European Association for CardioThoracic Surgery. Eur Heart J 2010;31(19)2369–429 2010. [62] Lokshyn S, Mewis C, Kuhlkamp V. Atrial fibrillation in coronary artery disease. Int J Cardiol 2000;15(2):133–6. [63] Motloch LJ, Reda S, Larbig R, et al. Characteristics of coronary artery disease among patients with atrial fibrillation compared to patients with sinus rhythm. Hellenic J Cardiol 2017(March (11)) pii: S1109-9666(16)30160-9. [64] Windecker S, Kolh P, Alfonso F, Collet JP, Cremer J, Falk V, et al. ESC/EACTS Guidelines on myocardial revascularization: The Task Force on Myocardial Revascularization of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS). Developed with the special contribution of the European Association of Percutaneous Cardiovascular Interventions (EAPCI). Eur Heart J 2014;46(4):517–92. [65] Osadnik T, Strzelczyk JK, Fronczek M, Bujak K, Reguła R, Gonera M, et al. Relationship of the rs1799752 polymorphism of the angiotensin-converting enzyme gene and the rs699 polymorphism of the angiotensinogen gene to the process of in-stent restenosis in a population of Polish patients with stable coronary artery disease. Adv Med Sci 2016;61(2):276–81. [66] Łopatowska P, Tomaszuk-Kazberuk A, Młodawska E, Bachórzewska-Gajewska H, Małyszko J, Dobrzycki S, et al. Management of patients with valvular and non-valvular atrial fibrillation in Poland: results from Reference Cardiology University Center. Cardiol J 2015;22(3):296–305. [67] Dans AL, Connolly SJ, Wallentin L, Yang S, Nakamya J, Brueckmann M, et al. Concomitant use of antiplatelet therapy with dabigatran or warfarin in the Randomized Evaluation of Long-Term Anticoagulation Therapy (RE-LY) trial. Circulation 2013;5(5):634–40. [68] Vandvik PO, Lincoff AM, Gore JM, Gutterman DD, Sonnenberg FA, AlonsoCoello P, et al. American College of Chest Physicians. Primary and secondary prevention of cardiovascular disease: antithrombotic therapy and prevention of thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest 2012;141(2 Suppl):e637S–68S. [69] Rubboli A, Faxon DP, Juhani Airaksinen KE, Schlitt A, Marín F, Bhatt DL, et al. The optimal management of patients on oral anticoagulation undergoing coronary artery stenting. The 10th Anniversary Overview. Thromb Haemost 2014;112(6):1080–7. [70] Lip GY, Windecker S, Huber K, Kirchhof P, Marin F, Ten Berg JM, et al. Management of antithrombotic therapy in atrial fibrillation patients presenting with acute coronary syndrome and/or undergoing percutaneous coronary or valve interventions: a joint consensus document of the European Society of Cardiology Working Group on Thrombosis, European Heart Rhythm Association (EHRA), European Association of Percutaneous Cardiovascular Interventions (EAPCI) and European Association of Acute Cardiac Care (ACCA) endorsed by the Heart Rhythm Society (HRS) and Asia-Pacific Heart Rhythm Society (APHRS). Eur Heart J 2014;1(45):3155–79. [71] Nikolsky E, Mehran R, Dangas GD, Yu J, Parise H, Xu K, et al. Outcomes of patients treated with triple antithrombotic therapy after primary percutaneous coronary intervention for ST-elevation myocardial infarction (from the Harmonizing Outcomes With Revascularization and Stents in Acute Myocardial Infarction [HORIZONS-AMI] trial). Am J Cardiol 2012;6:831–8. [72] Andrade JG, Deyell MW, Khoo C, Lee M, Humphries K, Cairns JA. Risk of bleeding on triple antithrombotic therapy after percutaneous coronary intervention/stenting: a systematic review and meta-analysis. Can J Cardiol 2013;29(2):204–12. [73] Verheugt FW. Triple antithrombotic therapy after coronary stenting in the elderly with atrial fibrillation: necessary or too hazardous? Am Heart J 2012;163(4):531–4. [74] Lamberts M, Olesen JB, Ruwald MH, Hansen CM, Karasoy D, Kristensen SL, et al. Bleeding after initiation of multiple antithrombotic drugs, including triple therapy, in atrial fibrillation patients following myocardial infarction and coronary intervention: a nationwide cohort study. Circulation 2012;4 (10):1185–93. [75] Steg PG, Huber K, Andreotti F, Arnesen H, Atar D, Badimon L, et al. Bleeding in acute coronary syndromes and percutaneous coronary interventions: position paper by the Working Group on Thrombosis of the European Society of Cardiology. Eur Heart J 2011;32(15):1854–64.

E. Michniewicz et al. / Advances in Medical Sciences 63 (2018) 30–35 [76] Suh JW, Mehran R, Claessen BE, Xu K, Baber U, Dangas G, et al. Impact of inhospital major bleeding on late clinical outcomes after primary percutaneous coronary intervention in acute myocardial infarction the HORIZONS-AMI (Harmonizing Outcomes With Revascularization and Stents in Acute Myocardial Infarction) trial. J Am Coll Cardiol 2011;18(17):1750–6. [77] Pruszczyk P, Tomaszuk-Kazberuk A, Słowik A, Drwila R, Rydzewska G, Filipiak KJ, et al. Management of bleeding or urgent interventions in patients treated with direct oral anticoagulants (DOACs) – management proposals in Poland. Pol Arch Intern Med 201715(March), doi:http://dx.doi.org/10.20452/ pamw.3995. [78] Gibson CM, Mehran R, Bode C, Halperin J, Verheugt FW, Wildgoose P, et al. Prevention of bleeding in patients with atrial fibrillation undergoing PCI. N Engl J Med 2016;22(25):2423–34. [79] Gibson CM, Pinto DS, Chi G, Arbetter D, Yee M, Mehran R, et al. Recurrent hospitalization among patients with atrial fibrillation undergoing intracoronary stenting treated with 2 treatment strategies of rivaroxaban or a dose-adjusted oral vitamin K antagonist treatment strategy. Circulation 2017;135:323–33. [80] Dewilde WJ, Oirbans T, Verheugt FW, Kelder JC, De Smet BJ, Herrman JP, et al. WOEST Study Investigators. Use of clopidogrel with or without aspirin in

[81]

[82] [83] [84] [85]

[86]

35

patients taking oral anticoagulant therapy and undergoing percutaneous coronary intervention: an open-label, randomised, controlled trial. Lancet 2013;30(9872):1107–15. Fiedler KA, Maeng M, Mehilli J, Schulz-Schüpke S, Byrne RA, Sibbing D, et al. Duration of triple therapy in patients requiring oral anticoagulation after drugeluting stent implantation: the ISAR-TRIPLE Trial. J Am Coll Cardiol 2015;28 (16):1619–29. ClinicalTrials.gov Identifier: NC T02164864. ClinicalTrials.gov Identifier: NC T02415400. ClinicalTrials.gov Identifier: NCT02635230. Lopatowska P, Tomaszuk-Kazberuk A, Mlodawska E, Bachorzewska-Gajewska H, Malyszko J, Dobrzycki S, et al. Do CHA2 DS2 VASc and HAS-BLED scores influence ‘real-world' anticoagulation management in atrial fibrillation? 1556 patient registry from the reference cardiology centre, Pharmacoepidemiol. Drug Saf 2015;24(12):1297–303. Heidbuchel H, Verhamme P, Alings M, Antz M, Diener HC, Hacke W, et al. Updated European Heart Rhythm Association Practical Guide on the use of non-vitamin K antagonist anticoagulants in patients with non-valvular atrial fibrillation. Europace 2015;17(10):1467–507.