What is Atrial Fibrillation?
Atrial fibrillation is the most common cardiac arrhythmia, and its incidence continues to increase. It is defined as an unregulated, chaotic and ineffective contraction of the heart's top to chambers known as the atria. As a result of the ineffective contraction of the atria, ventricular (main pumping chambers of the heart) contraction can also be affected.
Whilst in most cases atrial fibrillation is asymptomatic, about two thirds of people with atrial fibrillation report having intermittent symptoms of heart palpitations, breathlessness or exercise intolerance.
Atrial fibrillation (AF) has 2 main patterns of presentation. Persistent AF where the arrhythmia is continuous, and paroxysmal AF which are intermittent periods of fibrillation that self-correct within a few hours up to a few days.
Approximately 15% of cases are known as lone AF, which is directly related to an identifiable and specific structural or electrophysiological cause for the arrhythmia. By far the most common cause for AF is related to hypertension, valve dysfunction, ischaemia heart disease, and other adaptive changes to the heart structure. Some people have a genetic predisposition to developing familial AF.
Whilst all mechanisms for the development of AF are not yet fully understood, structural changes to the connective and muscle tissues layers surrounding the atria and pulmonary veins, have been found to give rise to electrically charged groups of cells known as ectopic foci. When these foci begin to “fire”, they interrupt the normal coordinated contraction of the heart's muscle.
People diagnosed with AF have a six-fold increased risk of stroke, and a two-fold increase in all-cause mortality due to the impact AF can have on the haemodynamics of the cardiovascular system.
Markides, V. & Schilling, RJ. (2003) Atrial fibrillation: Classification, pathophysiology, mechanisms and drug treatment, Heart, 89; 939-943, http://dx.doi.org/10.1136/heart.89.8.939
Sabzwari, S., Garg, L., Lakkireddy, D. & Day, J. (2018) Ten lifestyle modification approaches to treat atrial fibrillation, Cureus, 10(5), e2682, doi:10.7759/cureus.2682
The conventional approach
Atrial fibrillation is a condition that affects the electrical conduction system of the heart causing the top two chambers of the heart (atria) to beat in a chaotic and uncoordinated way. Whilst in most people this is asymptomatic, atrial fibrillation can potentially have some serious side effects.
The conventional approach to managing atrial fibrillation is to treat it purely as a problem with cardiac electrophysiology. For uncomplicated cases this will usually mean taking daily medication to control the heart rhythm. Such medications may include beta-blockers, calcium channel blocker or specific antiarrhythmics. In most cases a person will also be prescribed an anticoagulant to prevent blood clots forming which can be a serious risk factor for people with atrial fibrillation.
In more serious cases a person may require defibrillation to shock the heart back into sinus rhythm, or radio frequency ablation if an accessory pathway is found to be the cause of the atrial fibrillation.
Main contributing factors to the development of atrial fibrillation include:
Smokers have a 2-fold increased risk for AF
Hypertension increases risk of AF by 56%
Excess alcohol consumption increases risk of AF by more than 40%
People who suffer from sleep disturbances have 3-fold increased risk of AF
Diabetes increase risk for AF by 40%
Poor diet contributing to cardiovascular and cardiometabolic disease increases the risk for developing AF
Obesity and inactive lifestyle significantly increases the risk of developing AF
Effective stress management has demonstrated 85% less arrhythmic episodes in people diagnosed with AF.
It is also important to address all of the underlying factors for the development of cardiometabolic disease.
The most common misconception about atrial fibrillation is that it is entirely caused by an “electrical” abnormality in the heart. Whilst this is true in a small number of people, for most, the underlying cause will be changes to the structure and function of the heart that are also contributors to the development of cardiometabolic disease.
There isn’t one single cause of eczema but a range of potential contributing factors that are unique to each person. These include:
Research has found people with the ‘atopic triad’ have a defective barrier of the skin and upper and lower respiratory tracts.
These genetic alterations cause a loss of function of filaggrin (filament aggregating protein), which is a protein in the skin that normally breaks down to create natural moisturisation and protect the skin from penetration by pathogens and allergens.
Filaggrin mutations are found in approximately 30 percent of people with atopic dermatitis, and also predispose people to asthma, allergic rhinitis (hayfever), keratosis pilaris (dry rough patches and bumps on the skin), and ichthyosis vulgaris (a chronic condition which causes thick, dry, scaly skin.)If one parent carries this genetic alteration, there is a 50 percent chance their child will develop atopic symptoms. And that risk increases to 80 percent if both parents are affected.
The connection between the gut microbiome and skin health is complex, however, research has found the microbiota contributes to the development, persistence, and severity of atopic dermatitis through immunologic, metabolic and neuroendocrine pathways.
Deficiency of Omega-6 essential fatty acids (EFA) has been linked with the increased incidence of atopic dermatitis, along with the inability for the body to efficiently metabolise EFA’s to gamma linoleic acids (GLA) and arachidonic acids (AA).
Changing weather conditions can certainly aggravate eczema symptoms, but the triggers are subject to change among individuals.
Mould exposure and susceptibility to mould can cause Chronic Inflammatory Response Syndrome (CIRS), of which dermatitis is a manifestation.
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