92 decreasing prevalence of rheumatic fever, non-valvar causes or other valve diseases have become predominant, such as myocardial infarction, pericarditis, pulmonary embolism, chronic obstructive lung disease, hypertension, heart failure (HF), chronic coronary disease, sinus node disease, ventricular hypertrophy, atrial dilatation, non-rheumatic valvulopathies and aging itself. Currently, HF is the number one cause of AF in the elderly, diagnosed in 4% of patients in functional class I,[11] and in 10% of patients in class II–III.[12] HF evolves with structural and functional alterations which trigger and maintain AF. Atrial muscle fiber stretching is associated with a shorter refractory period and slower electrical conduction, which favor AF maintenance. Neuro- humoral alterations, such as an increase in catecholamines and renin-angiotensin system activation, also predispose to arrhythmia; on the other hand, structural and functional alterations induced by AF worsen HF. Non-cardiovascular causes may be related to AF episodes, especially in the elderly: hyperthyroidism, dehydration, electrolytic disorders, acute alcoholism, hypoxia, diabetes, postoperative period of non-cardiac surgery and stress. With regard to patients with hyperthyroidism, it is worth stressing the high prevalence of associated AF in the elderly (10% to 30%). AF risk is increased five-fold with subclinical hyperthyroidism, which may be the one and only manifestation of the disease. In general, rhythm returns to normal with hormonal disorder reversion.[13,14] The major predictive factor for AF in the elderly is the left atrium size, according to the AFFIRM study (Framingham Heart Study and Cardiovascular Health Study).[15] According to Braunwald, AF is, together with HF, the current cardiovascular pandemy.[16] This is due to longer patients’ survival, especially with regard to coronary disease. Natural AF progression starts with self- limited episodes, symptomatic or not, which increase in frequency and duration. Then, AF becomes permanent, raising the discussion of what should be done next: either maintain the rhythm with ventricular rate control and anticoagulation, or revert to sinus rhythm. The presence of cardiovascular disease with increased left atrium size is usually seen from onset of the condition. Arrhythmia chronicity causes atrial remodeling expressed through electrical, contractile and structural alterations. The decrease of the refractory period of the atrial muscle with repeated AF episodes turns them into longer- lasting episodes. Structural and contractile remodeling is represented by muscle fibers hypertrophy, normal fibers superimposed onto ill fibers and interstitial fibrosis, all leading to functional loss. The consequences of such changes are AF complications, such as intra-atrial thrombosis Franken RA et al. Atrial fibrillation in the elderly and possibly systemic, or pulmonary embolism. Another consequence seen at AF onset is the loss of atrial contraction, which in patients with left ventricular hypertrophy, may evolve to acute lung edema, especially in acute AF forms with high ventricular rate. Atrial systole is responsible for 25% of cardiac output in normal hearts and up to 50% in patients with ventricular dysfunction, especially in restrictive and hyper- trophic cardiopathies[17,18] In addition to these complications, chronic AF with a high ventricular rate evolves with ventricular dilatation and HF, called tachycardiomiopathy. AF patient mortality is twice those in sinus rhythm. Regardless of the underlying disease,[19] AF is a negative prognostic marker. In the SOLVD study,[20] AF patients had 34% mortality as compared to 24% in the ones with sinus rhythm. In the Framingham study[21] the risk of stroke in AF patients was five times greater. In patients between 50 and 59 years old, the stroke chance was of 1.5% per year, and from 80 to 89 years old 23.5% per year. According to the SPAF study,[22] the thromboembolic risks are related to systolic blood pressure above 160 mmHg, age > 75 years, recent HF, previous thrombo-embolic event, left atrial diameter > 2.5 cm/m2 and systolic shortening fraction < 25%. It also considered the presence of spontaneous atrial contrast or intra-atrial clot, confirmed by trans-esoph- ageal echocardiogram.[23] The risk for thromboembolic events is evaluated through the CHADS 2 score,[24] or more recently CHA2 DS2-VASc (Table 1).[25] The risk varies from 0% for those without any of the factors to 15.2% for those with maximum score (9 points). Table 1. CHA2 DS2-VASc score and stroke rate. Risk factors for stroke and thrombo-embolism in non-valvular AF Major risk factors Previous stroke, TIA, systemic embolism, or age > 75 years Clinically relevant non-major factors Heart failure, or moderate to severe LV systolic dysfunction (e.g., LVEF < 40%) hypertension, diabetes mellitus, female sex, age 65–74 years, vascular disease. Risk factor based approach expressed as a point based scoring system, with the acronym CHA2DS2-VASc (maximum score is 9 since age may contribute 0, 1 or 2 points Risk factor Score Congestive heart failure/LV dysfunction 1 Hypertension 1 Age > 75 2 Diabetes mellitus 1 Stroke, TIA, Thrombo-embolism 2 Vascular disease 1 Age 65–74 yaers 1 Female sex 1 Maximum score 9 LVEF: left ventricular ejection fraction; TIA: transient ischemic attack. Journal of Geriatric Cardiology | jgc@jgc301.com; http://www.jgc301.com