Coronary artery disease and atrial fibrillation

Coronary artery disease and atrial fibrillation

Hellenic Society of Cardiology (2017) 58, 213e214 Available online at www.sciencedirect.com ScienceDirect journal homepage: http://www.journals.else...

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Hellenic Society of Cardiology (2017) 58, 213e214

Available online at www.sciencedirect.com

ScienceDirect journal homepage: http://www.journals.elsevier.com/ hellenic-journal-of-cardiology/

EDITORIAL

Coronary artery disease and atrial fibrillation Atrial fibrillation is a very common disease that affects a large number of people in the general population.1 The incidence of the disease ranges from 0.5% to 6%, depending on the patient age.2 The clinical importance of the disease is that it increases the risk of stroke, impairs the heart function, and increases mortality. The quality of life in most cases worsens, leading to increased cost of therapy. The etiology of the disease is multi-factorial. The most frequent underlying diseases for atrial fibrillation in the past decades were rheumatic mitral disease, heart failure, and aging. Arrhythmia in such cases and persistence of the arrhythmia are due to multiple reentry wavelets moving in both the atria, perpetuating arrhythmia. This was the result of arrhythmia mapping studies in both humans and animals by Allessie et al.3 This is obviously caused by atrial fibrosis, which produces the substrate for reentry. The main cause of fibrosis seems to be the increased pressure and volume load in the atria. The last 20 years, the presence of another mechanism has been recognized, with a firing focus from the pulmonary vein ostium. This mechanism mainly contributes to the pathogenesis of the paroxysmal atrial fibrillation.4 In most cases, both mechanisms are involved to different extents, depending on the underlying disease. In normally functioning hearts, firing focus from the pulmonary veins is the most frequent etiology of arrhythmia. This has a tremendous impact on the therapy of the disease. Ablation, which includes pulmonary vein isolation, has been the main therapy for atrial fibrillation in the last 10 years. However, when mainly the substrate is involved, the therapy is rather pure because of atrial fibrosis. It must be mentioned that many other factors are involved in the pathogenesis of atrial fibrillation such as obesity, thyroid dysfunction, alcohol use, aging, smoking, diabetes, and coronary artery diseases. All these clinical situations lead to atrial fibrosis, which in turn develops reentry mechanisms and sustainable atrial fibrillation.

Peer review under responsibility of Hellenic Society of Cardiology.

Atrial fibrillation does not imply that the patient would have coronary artery disease. Vice versa, having coronary artery disease does not imply one has atrial fibrillation. Atrial fibrillation is an electrical disease of the atria, while coronary artery disease is a structural disease of blood vessels. Independent predictors of atrial fibrillation in patients with coronary artery disease seem to be similar to those in other groups of population with atrial fibrillation.5 Aging, hypertension, and left ventricular function are the main predictors of the occurrence of the atrial fibrillation. Symptoms caused during an episode of atrial fibrillation can also be confusing: atrial fibrillation can cause symptoms similar to those of coronary artery disease. Atrial fibrillation can present as chest pain, while coronary artery disease is not likely the direct reason for shortness of breath, arm, or jaw pain and near passing out; however, these symptoms are also present in both coronary artery disease and atrial fibrillation. Coronary artery disease is often an incidental finding in patients with atrial fibrillation. Another useful and important clinical information to determine whether coronary artery disease exists in a patient with atrial fibrillation is the use of the Class IC antiarrhythmic drugs flecainide and propafenone for therapy. Some studies suggest increased mortality in patients with coronary artery disease, especially in those with low ejection fraction and acute ischemia.6 Knowledge of coronary artery disease may be useful in the case of aspirin or clopidogrel therapy, in addition to the other anticoagulant regimens. Coronary artery disease can induce atrial fibrillation through two mechanisms. Acute ischemia, especially during the first hours of acute myocardial infarction, can trigger atrial fibrillation, or it can be triggered at a later phase when heart failure develops and there is increased left ventricular end diastolic pressure and increased pressure in the left atrium. This leads to fibrosis, which provides a suitable substrate for arrhythmia. In the paper by Motloch et al7 in this issue, this latter mechanism has been confirmed. The number of coronary artery disease involvement is not correlated to atrial fibrillation. The left ventricular function and mitral disease are related to atrial fibrillation. This information may have

http://dx.doi.org/10.1016/j.hjc.2017.09.002 1109-9666/ª 2017 Hellenic Society of Cardiology. Publishing services by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

214 a considerable impact in the everyday practice, i.e., when atrial fibrillation develops in a patient with known coronary artery disease, this may be due to worsening of left ventricular function. However, coronary angiography does not seem to be useful for diagnosis of patients with atrial fibrillation, except in cases with high possibility of coronary artery disease.

References 1. Tsounis D, Ioannidis A, Bouras, et al. Assessment of healthrelated quality of life in a Greek symptomatic population with atrial fibrillation: correlation with functional status and echocardiographic indices. Hellenic J Cardiol. 2014;55: 475e485. 2. Foussas S. Acute coronary syndroms and atrial fibrillation. Hellenic J Cardiology. 2016;57:141e142. 3. Janse M, Allessie M. Experimental observations in atrial fibrillation. In: Falk R, Podrid P, eds. Atrial fibrillation mechanisms. 1992:41e57.

Editorial 4. Haissaguerre M, Jais P, Shah DC, et al. Spontaneous initiation of atrial fibrillation by ectopic beats originating in the pulmonary veins. N Engl J Med. 1998;339:659e666. 5. Aranki S, Shaw D, Adams D, et al. Predictors of atrial fibrillation after coronary artery disease. Circulation. 1996;94:390e397. 6. Buxton A, Lee K, Fisher J, Josephson M, Prystowsky E, Hafly G. A randomized study of the prevention of sudden death in patients with coronary artery disease. N Eng J Med. 1999;341:1882e1890. 7. Motloch L, Reda S, Lrbig R, et al. Characteristics of coronary artery disease among patients with atrial fibrillation compared to patients with sinus rhythm. Hellenic J Cardiol. 2017;58(3):204e212.

Georgios N. Theodorakis, MD FESC FACC Electrophysiology and Pacing Unit, Onassis Cardiac Surgery Center, Greece E-mail address: [email protected] 26 June 2017 Available online 14 September 2017