Premature atrial contractions (PACs) are contractions of the atria that are triggered by the atrial myocardium but have not originated from the sinoatrial node (SA node). PACs are also commonly referred to as atrial premature complexes (APCs), premature supraventricular complexes, premature supraventricular beat, and premature atrial beat. This phenomenon can be caused by an assortment of medical diseases, structural abnormalities, pharmaceuticals, and non-regulated compounds.
Triggers for PACs can be caused by a myriad of reasons and are commonly idiopathic. Idiopathic PACs, in the absence of structural cardiac disease, frequently originate from the pulmonary veins. Identifiable causes of premature atrial contractions can be stratified into structural, chemical, or as a sequela of other conditions.
Structural causes of PACs typically include coronary artery disease, hypertrophic cardiomyopathy, left atrial appendage aneurysms, left ventricular hypertrophy, valvular heart disease, septal defects, and congenital heart malformations. At the biochemical level, sodium channel malformations and BMP2 mutations, a cause of pulmonary artery hypertension, may inadvertently predispose atrial arrhythmias.
Chemical-based causes for PACs include beta-agonists, digoxin, chemotherapeutic agents, tricyclic antidepressants, sympathomimetics amines, and monoamine oxidase inhibitors. Beta-blockers have also been associated with a higher incidence of PACs.
A higher incidence of PACs is associated with many conditions and chronic states. Medical pathologies with associations for increased PACs include myocardial infarctions, congestive heart failure, hypertension, diabetes mellitus, a chronic obstructive pulmonary disorder, Coxsackie virus, and an overall higher CHA2DS2-VASC score. Additional states such as anxiety, pregnancy, fatigue, and use of alcohol or tobacco have also predisposed for PACs. Contrary to popular belief, caffeine has not been associated with an increased incidence of PACs.
PACs are prevalent amongst young and old patients, independent of many risk factors and previously known medical conditions. Newborn infants, without associated risk factors, have been found to have variations typically considered pathologic. Though still rare, elderly patients are more likely to present with abnormalities in their heart rhythm. Nevertheless, an atypical rhythm is more likely to be found with continuous monitoring, such as a Holter monitor, than on a typical electrocardiogram strip. This occurrence may be due in part to variations based on circadian rhythm. As improvements in medical devices continue, amidst increased ubiquity of low-cost ambulatory and consumer options, the prevalence of arrhythmias may increase due to the detection of otherwise covert arrhythmias.
The pathophysiology for premature atrial contractions has not been well established. This is due in part to the relatively benign nature of the condition and the unnecessary invasiveness of electrophysiologic studies on humans to find a cause. Common theoretic mechanisms for this condition are based around abnormal automaticity of the cardiac myocytes, increased eliciting events from chemical or physical instigators, and reentry of a retrograde impulse. For these causes, structural heart damage or chemical use may be found during the history and physical examination.
Genetic causes have also been studied, albeit in animals. Nevertheless, an LKB1 (cardiac-specific liver kinase B1) gene deletion has been associated with defects in ion channel formation of the atria. This has been shown to alter generation and conduction of action potentials, which predisposes the atria to remodeling, fibrosis, and ultimately atrial fibrillation. Similar studies have also examined the formation of cytoskeletons, sarcomeres, desmosomes, and other ion channels for their role in automaticity.
History findings can be occult and nonspecific for the identification of PACs. Many patients are asymptomatic, and PACs are often discovered incidentally during the workup for another disease or on routine examinations. In patients who do experience symptoms, most commonly, a skipping sensation or palpitations are noted. The patient may experience shortness of breath or anxiety, as well. If the PACs are consistent, however, patients may experience signs and symptoms of heart failure.
Physical exam findings are also indiscriminate and lack sensitivity and specificity. The major contributor to this obscurity is the intermittent nature of PACs. When present, a clinician may palpate irregular pulses or visualize a canon a wave with jugular venous mapping. Auscultation may reveal early or additional heart sounds, as well as pauses in rhythm.
The use of an electrocardiogram is standard for identifying electrical variations within the heart. PACs typically have normal QRS complex and a normal, short, or longer PR interval than sinus rhythm. Sometimes, non conducted PACs occur in which there is no QRS complex following the PAC. PACs can be unifocal arising from one location (similar P waves in all PACs) or multifocal and arising from several locations (different P wave morphologies for PACs). The P wave of the PAC typically occurs earlier than the sinus P wave and has a different morphology and axis from the sinus P wave. It appears dissimilar from a standard sinus node generation, with variations in height, length, and shape of the P wave; furthermore, the P wave may be inverted or biphasic.
Depending on the location of the generating focus, the PR interval can be shorter (<120 milliseconds if originating from low right atrium near the AV node) or longer than usual. Examination of multiple leads may be required to differentiate subtle differences. A negative P wave in the inferior leads suggests a low atrial focus and a negative P wave in the lead I and aVL suggests a left atrial origin. PACs may also appear within the preceding T wave in accelerated heart rates. If the EKG does not reveal PACs on examination, a 24-hour Holter monitor may be useful for identifying intermittent complexes.
Jugular venous pressure mappings may also play a role in the evaluation of PACs. Though the sensitivity of this test may be suboptimal, positive findings are useful for clinical correlation. Furthermore, being a simple physical exam finding to estimate central venous pressure, there is no added expensive or invasive method. Positive findings on this maneuver would be the visualization of the typical cannon 'a' wave, which is a sizeable venous pulse, causing a prominent bulge of the jugular veins. This occurs when the atrium contracts and blood is forced upon a close ventricle, cause a pressurized backflow into the central venous system. In the setting of PACs, if the premature contraction of the atrium occurs during systole when the tricuspid valve is closed, this sign may manifest. Electrophysiologic mapping studies are not indicated for the identification of PACs.
After the identification of PACs, echocardiography is useful in determining the functional status of the heart and identifying potential underlying structural abnormalities. Evaluation for structural heart disease should always be undertaken in patients with frequent PACs because of its prognostic important and treatment requirement. Laboratory testing can be done to identify electrolyte abnormalities.
Treatment of PACs depends on the symptomatology, triggers, and associated structural heart conditions. Typically, only patients with symptomatic PACs require treatment. After appropriate identification of triggers or underlying structural cardiac conditions, therapy starts by reassuring patients that PACs are typically benign and can be controlled by avoiding triggers. In patients with persistent symptoms despite avoidance of triggers, further therapy is indicated, starting with medications.
Pharmacologic management can be achieved using:
In patients with refractory symptoms despite medical therapy or those with cardiomyopathy and heart failure linked the frequent PACs, and in those patients in whom the PACs trigger atrial arrhythmias like atrial fibrillation, further interventional therapy is indicated. Some interventional options include atrial pacing, catheter ablation thoracoscopic ablation. Of these, catheter ablation of the PAC origin is the most frequently used modality. Electrophysiologic mapping is used to identify the origin of PACs. If PACs are thought to be arising from the pulmonary veins, the pulmonary vein ostia are typically ablated to create pulmonary vein electrical isolation to prevent impulse entry into the left atrium.
Attempts should always be made to control with conservative non-pharmaceutical measures first. Primary healthcare providers may provide initial reassurance and medical treatment; however, refractory cases or use of antiarrhythmic medications should be referred to cardiologists. Percutaneous and surgical interventions are delegated to the appropriate specialists.
The differential diagnosis for PACs is broad due to its non-descript symptoms, physical exam, and imaging findings. Cardiac differentials can be categorized into arrhythmic and non-arrhythmic etiologies. Arrhythmic causes can include premature junctional contractions, premature ventricular contractions, and narrow or wide complex tachycardias. Accordingly, an EKG can be vital in the delineation of these causes. Non-arrhythmic cardiac etiologies include acute coronary syndrome, valvular disorders with a preponderance for mitral valve prolapse, pericarditis, heart failure, and pacemaker complications.
Non-cardiac causes may also mimic premature atrial contractions. A clinician should keep in mind psychiatric differentials such as panic attacks and anxiety. Alcohol, use of illicit drugs, and adverse effects of prescribed medications may cause or mimic PACs. Finally, other considerations should be given to pulmonary embolism, hyperthyroidism, and anemia.
Prognosis is dependent on the underlying cause of the PACs and the presence of structural cardiac disease. Many idiopathic PACs are relatively benign in the short term, although they can be associated with an increased risk of cardiac and all-cause mortality if they occur frequently. Similarly, frequent PACs have also been shown to be associated with a greater risk of developing atrial fibrillation and atrial flutter. Generally, underlying conditions play a more significant role in estimating prognosis.
The risk of complications from PACs should be explained in conjunction with underlying etiologies, should they exist. Complications from PACs, independent of other conditions, include:
Isolated PACs (without premature ventricular complexes) are not associated with an increased risk of sudden cardiac death.
Many times, PACs have no adverse effect on a patient’s lifestyle or outcome and may be monitored by the primary care provider. Consultations for PACs should be made based on clinical suspicion for underlying morbid etiologies or when symptoms are obstructive and overwhelming. Referral to cardiology services can assist in diagnosing underlying structural or electrical conduction abnormalities and for initiation of anti-arrhythmic therapies when appropriate.
Education is essential in providing the most up to date guidance focused on evidence-based medicine. In particular, health care providers and patients should be educated on the benign nature of isolated PACs when not associated with underlying etiologies. Education regarding possible triggers should be provided and avoidance techniques can be taught. The psychological morbidity associate with PACs should be appropriate address and patients reassured.
Healthcare practitioners should be cautious in the diagnosis and treatment of PACs. Furthermore, incidental findings should not automatically warrant extended and invasive procedures when the patient is otherwise asymptomatic. When encountered, the provider should discuss treatment options with specific emphasis on the risks versus benefits. Consultations should be considered when appropriate situations are encountered. An interprofessional approach is essential in the evaluation of prognosis and management options.
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