Non-modifiable risk factors (top left box) and modifiable risk factors (bottom left box) for atrial fibrillation. The main outcomes of atrial fibrillation are in the right box. BMI=Body Mass Index. AF is linked to several forms of cardiovascular disease but may occur in otherwise normal hearts. Cardiovascular factors known to be associated with the development of AF include high blood pressure, coronary artery disease, mitral valve stenosis (e.g., due to rheumatic heart disease or mitral valve prolapse), mitral regurgitation, left atrial enlargement, hypertrophic cardiomyopathy (HCM), pericarditis, congenital heart disease, and previous heart surgery. Congenital heart disease is a strong risk factor for developing atrial fibrillation—a 20-year-old adult with congenital heart disease has a comparable lifetime risk of developing atrial fibrillation when compared to a 55-year-old adult with no history of congenital heart disease. People with congenital heart disease tend to develop atrial fibrillation at a younger age, that is more likely to be of right atrial origin (atypical) than of left origin, and have a greater risk of progressing to permanent atrial fibrillation. Additionally, lung diseases (such as pneumonia, lung cancer, pulmonary embolism, and sarcoidosis) may play a role in certain people. Sepsis also increases the risk of developing new-onset atrial fibrillation. Disorders of breathing during sleep, such as obstructive sleep apnea (OSA), are also associated with AF. Obesity is a risk factor for AF. Hyperthyroidism and subclinical hyperthyroidism are associated with AF development. Caffeine consumption does not appear to be associated with AF; excessive alcohol consumption ("binge drinking" or "holiday heart syndrome") is linked to AF. Low-to-moderate alcohol consumption also appears to be associated with an increased risk of developing atrial fibrillation, although the increase in risk associated with drinking less than two drinks daily appears to be small. Tobacco smoking and secondhand tobacco smoke exposure are associated with an increased risk of developing atrial fibrillation. Long-term endurance exercise that far exceeds the recommended amount of exercise (e.g., long-distance cycling or marathon running) appears to be associated with a modest increase in the risk of atrial fibrillation in middle-aged and elderly people. There is some evidence that night shift working may be linked to a diagnosis of AF. Genetics A family history of AF may increase the risk of AF. A study of more than 2,200 people found an increased risk factor for AF of 1.85 for those that had at least one parent with AF. Various genetic mutations may be responsible. Four<unk>  of genetic disorder are associated with atrial fibrillation: * Familial AF as a monogenic disease * Familial AF presenting in the setting of another inherited cardiac disease (hypertrophic cardiomyopathy, dilated cardiomyopathy, familial amyloidosis) * Inherited arrhythmic syndromes (congenital long QT syndrome, short QT syndrome, Brugada syndrome) * Non-familial AF associated with genetic backgrounds (polymorphism in the ACE gene) that may predispose to atrial fibrillation Family history in a first degree relative is associated with a 40% increase in risk of AF. This finding led to the mapping of different loci such as 10q22-24, 6q14-16 and 11p15-5.3 and discover mutations associated with the loci. Fifteen mutations of gain and loss of function have been found in the genes of K+ channels, including mutations in KCNE1-5, KCNH2, KCNJ5 or ABCC9 among others. Six variations in genes of Na+ channels that include SCN1-4B, SCN5A and SCN10A have also been found. All of these mutations affect the processes of polarization-depolarization of the myocardium, cellular hyper-excitability, shortening of effective refractory period favoring re-entries. Other mutations in genes, such as GJA5, affect gap junctions, generating a cellular uncoupling that promotes re-entries and a slow conduction velocity. Using genome-wide association study, which screen the entire genome for single nucleotide polymorphism (SNP), three susceptibility loci have been found for AF (4q25, 1q21 and 16q22). In these loci there are SNPs associated with a 30% increase in risk of recurrent atrial tachycardia after ablation. There are also SNPs associated with loss of function of the Pitx2c gene (involved in cellular development of pulmonary valves), responsible for re-entries. There are also SNPs close to ZFHX3 genes involved in the regulation of Ca2+. A GWAS meta-analysis study conducted in 2018 revealed the discovery of 70 new loci associated with AF. Different variants have been identified. They are associated with genes that encode transcription factors, such as TBX3 and TBX5, NKX2-5 or PITX2, involved in the regulation of cardiac conduction, modulation of ion channels and in cardiac development. Have been also identified new genes involved in tachycardia (CASQ2) or associated with an alteration in cardiomyocyte communication (PKP2). Rare mutations in the cardiomyopathy gene TTN may also increase the risk of AF, even in individuals without signs of heart failure. Small genetic deletions on the X chromosome around the STS (steroid sulfatase) gene are associated with increased rates of AF in males Sedentary lifestyle A sedentary lifestyle increases the risk factors associated with AF, such as obesity, hypertension, or diabetes mellitus. This favors remodeling processes of the atrium due to inflammation or alterations in the depolarization of cardiomyocytes by elevation of sympathetic nervous system activity. A sedentary lifestyle is associated with an increased risk of AF compared to physical activity. In both men and women, the practice of moderate exercise reduces the risk of AF progressively; intense sports may increase the risk of developing AF, as seen in athletes. It is due to a remodeling of cardiac tissue, and an increase in vagal tone, which shortens the effective refractory period (ERP) favoring re-entries from the pulmonary veins. Tobacco The rate of AF in smokers is 1.4 times higher than in non-smokers. However, snus consumption, which delivers nicotine at a dose equivalent to that of cigarettes and is debated as a harm-reduction product, is not correlated with AF. Alcohol Acute alcohol consumption can directly trigger an episode of atrial fibrillation. Regular alcohol consumption also increases the risk of atrial fibrillation in several ways. The long-term use of alcohol alters the physical structure and electrical properties of the atria. Alcohol consumption does this by repeatedly stimulating the sympathetic nervous system, increasing inflammation in the atria, raising blood pressure, lowering the levels of potassium and magnesium in the blood, worsening obstructive sleep apnea, and by promoting harmful structural changes (remodeling) in the atria and ventricles of the heart. This remodeling leads to abnormally increased pressure in the left atrium, inappropriately dilates it, and increases scarring (fibrosis) in the left atrium. The aforementioned structural changes increase the risk of developing atrial fibrillation when paired with the harmful changes in how the left atrium conducts electricity. High blood pressure According to the CHARGE Consortium, both systolic and diastolic blood pressure are predictors of the risk of AF. Systolic blood pressure values close to normal limit the increase in the risk associated with AF. Diastolic dysfunction is also associated with AF, which increases left atrial pressure, left atrial volume, size, and left ventricular hypertrophy, characteristic of chronic hypertension. All atrial remodeling is related to heterogeneous conduction and the formation of re-entrant electric conduction from the pulmonary veins. Other diseases There is a relationship between risk factors such as obesity and hypertension, with the appearance of diseases such as diabetes mellitus and sleep apnea-hypopnea syndrome, specifically, obstructive sleep apnea (OSA). These diseases are associated with an increased risk of AF due to their remodeling effects on the left atrium. Medications Several medications are associated with an increased risk of developing atrial fibrillation. Few studies have examined this phenomenon, and the exact incidence of medication-induced atrial fibrillation is unknown. Medications that are commonly associated with an increased risk of developing atrial fibrillation include dobutamine and the chemotherapy agent cisplatin. Agents associated with a moderately increased risk include nonsteroidal anti-inflammatory drugs (e.g., ibuprofen), bisphosphonates, and other chemotherapeutic agents such as melphalan, interleukin 2, and anthracyclines. Other medications that rarely increase the risk of developing atrial fibrillation include adenosine, aminophylline, corticosteroids, ivabradine, ondansetron, and antipsychotics. This form of atrial fibrillation occurs in people of all ages but is most common in the elderly, in those with other atrial fibrillation risk factors, and after heart surgery.
types of Supraventricular tachycardia
medical cause of Ventricular tachycardia
medical cause of Ventricular fibrillation
symptoms of Brugada syndrome
medical cause of Supraventricular tachycardia
symptom of Brugada syndrome
complications of Atrial fibrillation
symptom of Catecholaminergic polymorphic ventricular tachycardia