Feeling excessively tired, devoid of energy, demoralized, and irritable?
You may have burnout, a syndrome associated with a potentially deadly heart rhythm disturbance. That’s the conclusion of a large study published today in the European Journal of Preventive Cardiology.
“Vital exhaustion, commonly referred to as burnout syndrome, is typically caused by prolonged and profound stress at work or home,” said study author Dr. Parveen K. Garg of the University of Southern California in Los Angeles.
“It differs from depression, which is characterized by low mood, guilt, and poor self-esteem. The results of our study further establish the harm that can be caused in people who suffer from exhaustion that goes unchecked.”
Atrial fibrillation is the most common form of heart arrhythmia. It is estimated that 17 million people in Europe and 10 million people in the US will have this condition by next year, increasing their risk for heart attack, stroke, and death. Yet, what causes atrial fibrillation is not fully understood.
Psychological distress has been suggested as a risk factor for atrial fibrillation, but previous studies showed mixed results. In addition, until now, the specific association between vital exhaustion and atrial fibrillation had not been evaluated.
The researchers in this study surveyed more than 11,000 individuals for the presence of vital exhaustion, anger, antidepressant use, and poor social support. They then followed them over a period of nearly 25 years for the development of atrial fibrillation.
Participants with the highest levels of vital exhaustion were at a 20% higher risk of developing atrial fibrillation over the course of follow-up compared to those with little to no evidence of vital exhaustion.
While further study is needed to better understand the observed relationship, Dr. Garg noted that two mechanisms are likely at play. “Vital exhaustion is associated with increased inflammation and heightened activation of the body’s physiologic stress response,” he said. “When these two things are chronically triggered that can have serious and damaging effects on the heart tissue, which could then eventually lead to the development of this arrhythmia.”
Atrial fibrillation is the most common form of heart arrhythmia. It is estimated that 17 million people in Europe and 10 million people in the US will have this condition by next year, increasing their risk for heart attack, stroke, and death. Yet, what causes atrial fibrillation is not fully understood.
No connections were found between anger, antidepressant use, or poor social support and development of atrial fibrillation. “The findings for anger and social support are consistent with prior research but two previous studies did find a significant association between antidepressant use and an increased risk of atrial fibrillation. Clearly, more work still needs to be done,” said Dr. Garg.
Further research is also needed to identify concrete actions for doctors to help patients with exhaustion, said Dr. Garg.
He concluded: “It is already known that exhaustion increases one’s risk for cardiovascular disease, including heart attack and stroke. We now report that it may also increase one’s risk for developing atrial fibrillation, a potentially serious cardiac arrhythmia.
The importance of avoiding exhaustion through careful attention to – and management of – personal stress levels as a way to help preserve overall cardiovascular health cannot be overstated.”
Atrial fibrillation is the most common type of heart arrhythmia. It is due to abnormal electrical activity within the atria of the heart causing them to fibrillate. Is characterized as a tachyarrhythmia, which means that the heart rate is often fast.
This arrhythmia may be paroxysmal (less than 7 days) or persistent (more than 7 days). Due to its rhythm irregularity, blood flow through the heart becomes turbulent and has a high chance of forming a thrombus (blood clot) which can ultimately dislodge and cause a stroke. Atrial fibrillation is the leading cardiac cause of stroke.
Risk factors for atrial fibrillation include advanced age, high blood pressure, underlying heart and lung disease, congenital heart disease, and increased alcohol consumption. Symptoms vary from asymptomatic to symptoms such as chest pain, palpitations, fast heart rate, shortness of breath, nausea, dizziness, diaphoresis (severe sweating), and generalized fatigue.
Although atrial fibrillation may be a permanent disease, various treatments have been developed, and risk modifying strategies to help reduce the risk of stroke in patients that remain in atrial fibrillation exist. Treatments include anticoagulation, rate control medication, rhythm control medication, cardioversion, ablation, and other interventional cardiac procedures. [1][2][3]
Etiology
There are many causes of atrial fibrillation. Advanced age, congenital heart disease, underlying heart disease (valvular disease, coronary artery disease, structural heart disease), increased alcohol consumption, hypertension, and obstructive sleep apnea are all common causes of atrial fibrillation.
Any process that causes inflammation, stress, damage, and ischemia to the structure and electrical system of the heart can lead to the development of atrial fibrillation. In some cases, the cause is iatrogenic.[4]
The 3 patterns of atrial fibrillation include:
Paroxysmal AF: Here the episodes terminate spontaneously within 7 days.
Persistent AF: The episodes last more than 7 days and often require electrical or pharmacological interventions to terminate the rhythm
Long-standing persistent AD: rhythm that has persisted for more than 12 months, either because a pharmacological intervention has not been tried or cardioversion has failed.
Permanent AF where a decision has been made to abort all therapies because the rhythm is unresponsive.
Epidemiology
The prevalence of atrial fibrillation has been increasing worldwide. It is known that the prevalence of atrial fibrillation generally increases with age. It has been estimated that the number of individuals with atrial fibrillation will double or triple by the year 2050.
Although the world white prevalence of atrial fibrillation is approximately 1%, it is found in approximately 9% in individuals over the age of 75. At the age of 80, the lifetime risk of developing atrial fibrillation jumps to 22%. In addition, atrial fibrillation has more commonly been associated with males and seen more often in whites as compared to black.[5][6]
Pathophysiology
There are a wide variety of pathophysiology mechanisms that play a role in the development of atrial fibrillation. Most commonly, hypertension, structural, valvular, and ischemic heart disease illicit the paroxysmal and persistent forms of atrial fibrillation but the underlying pathophysiology is not well understood.
Some research has shown evidence of genetic causes of atrial fibrillation involving chromosome 10 (10q22-q24) that involves a mutation in the gene, alpha-subunit of the cardiac Ik5, which encodes pore formation protein. This mutation increases the function of this protein allowing for more pores, and thus, activity within the ion channels of the heart, therefore affecting the stability of the membranes and reducing its refractory time. [1]
Most cases of atrial fibrillation are non-genetic and relate to underlying cardiovascular disease. Typically, an initiating trigger excites an ectopic focus in the atria, most commonly around the area of the pulmonary veins, and allows for an unsynchronized firing of impulses and electricity leading to fibrillation of the atria.
These impulses are irregular, and pulse rates can vary tremendously. Overall, atrial fibrillation leads to a turbulent and abnormal flow of blood through the heart chamber decreasing the heart effectiveness to pump blood while increasing the likelihood of thrombus formation within the atria, most commonly the left atrial appendage.
Triggers for aF
- Atrial ischemia
- Inflammation
- Alcohol and illicit drug use
- Hemodynamic stress
- Neurological and endocrine disorders
- Advanced age
- Genetic factors
History and Physical
History and physical exam are crucial for diagnosing and risk stratifying patients with atrial fibrillation. A complete history should focus on symptoms such as palpitations, chest pain, shortness of breath, increased lower extremity swelling, dyspnea with exertion, dizziness, among others.
In addition, history is imperative in identifying risk factors such as hypertension, history of valvular, structure, or ischemic heart disease, obstructive sleep apnea, obesity hypoventilation syndrome, smoking, alcohol intake, illicit drug use, history of rheumatic fever/heart disease, history of pericarditis, hyperlipidemia, among others.
A physical exam should include the patient’s overall appearance (obese), examine the patient neck for signs of JVD, carotid bruits, circumference. A cardiovascular exam should consist of carefully auscultating all 4 cardiac posts and palpating for apical impulse. A pulmonary exam should consist of auscultation, percussion, and specialized tests, if needed, to assess pulmonary status.
Extremities should be evaluated for edema, peripheral pulses in both upper and lower extremities, and integumentary signs of PVD such as hair loss and skin breakdown. An abdominal exam should consist of palpating the aorta and listening for abdominal bruits. Depending on the severity of the atrial fibrillation, signs, and symptoms can range from none to evidence of acute heart failure.
Evaluation
Aside from a detailed history and examine, the ECG is critical in making the diagnosis of atrial fibrillation. On ECG, atrial fibrillation presents with the typical narrow complex “irregularly irregular” pattern with no distinguishable p-waves. Laboratory work is required to evaluate for the causes of atrial fibrillation, for example, a complete blood count (CBC) for infection, basic metabolic panel (BMP) for electrolyte abnormalities, thyroid function tests to evaluate for hyperthyroidism, and a chest x-ray to evaluate the thorax for any abnormality.
It is imperative to evaluate the patient for pulmonary embolism (for example with d-dimer, CT scan) because right heart strain can lead to atrial malfunctioning and result in atrial fibrillation. The patient should be risk stratified for pulmonary embolism using the PERC and/or Wells criteria.
In addition, a transesophageal echocardiogram should be done for these patients to evaluate for atrial thrombus secondary to atrial fibrillation and heart structure. It is important to note that Transesophageal echocardiogram (TEE) should always be done prior to cardioversion for these patients to minimize the risk of stroke.[7][8]
Treatment / Management
The management of atrial fibrillation in the acute setting relies on patient hemodynamic stability and risk stratification. If the patient is hemodynamically unstable, immediate cardioversion with anticoagulant therapy is indicated. TEE is recommended prior to any cardioversion; however, if the patient is in hemodynamic stability due to atrial fibrillation with a rapid ventricular response, cardioversion may be performed without prior TEE.
If the patient has evidence of rapid ventricular response, rate control should be initiated using a beta-blocker or calcium-channel blocker. These medications can be used as intravenous (IV) pushes or drips. Typically, the patient is given a bolus then started on a drip if symptoms do not resolve. Digoxin can be considered as a rate control agent but is not recommended as a first-line agent due to its side-effects and tolerance.
Amiodarone can also be considered for a rhythm controlling agent but is also not first-line therapy in the acute setting. Amiodarone is also considered as a rhythm control, but cardiology should be consulted prior to use.
In the chronic setting of atrial fibrillation, the patient should be risk stratified using the CHADs-2-Vasc score which is helpful in estimate risk of CVA per year. If the patient receives a 0 score, they will be considered “low-risk” and anticoagulation is not recommended.
If the patient receives a score of 1, they are “low-moderate” risk; the physician should consider anticoagulant or antiplatelet therapy. If the patient receives a score of greater than 2, they are in the “moderate-high” risk, and anticoagulation therapy is indicated.[2] Rate or rhythm control should also be given to the patient, medications such as beta-blockers, calcium channel blockers, amiodarone, dronedarone, and digoxin.
HAS-BLED is also a scoring system that can be used to asses the risk of bleeding for the patient. This is a good indicator of bleeding risk for a patient that is considering starting anticoagulation.
Non-pharmacological therapy includes ablation therapy. Pacemaker placement is considered in severe causes resulting in heart failure in atrial fibrillation.[9][10][11]
Current guidelines
- Patients with AF and elevated CHA2DS2-VASc score of 2 or more, oral anticoagulation is recommended.
- Female sex with absence of AF risk factors and CHA2DS2-VASc of 1 or 0 in males have alow stroke risk.
- Non-vitamin K oral anticoagulants (apixaban, dabigatran, edoxaban, and rivaroxaban) are recommended over warfarin, except in those patients with moderate to severe MS with a mechanical heart valve
- In all patients with AF, the CHA2DS2-VASc score is recommended to assess stroke risk.
- Obtain renal and liver function before initiating non-vitamin K oral anticoagulants
- Aspirin is not recommended in patients with low CHA2DS2-VASc scores
- Idarucizumab is recommended for dabigatran reversal if there is an urgent procedure or bleeding. Andexanet alfa is recommended for reversal of rivaroxaban and apixaban associated bleeding.
- Percutaneous left atrial appendage occlusion is recommended in AF patients with a risk of stroke who have contraindications to long term anticoagulation.
- If AF less than 48 hours or if time unknown, start anticoagulation and maintain INR 2-3 or a factor Xa inhibitor for at least 3 weeks before and at least 4 weeks after cardioversion
- Catheter ablation is an option in patients with a low ejection fraction
- Recommend weight loss in obese patients with AF
