Palpitations — Symptom Overview

Table of Contents

  1. Overview and Immediate Red Flags
  2. Cardiac Arrhythmia Causes
  3. Non-Arrhythmia Cardiac Causes
  4. Metabolic and Endocrine Causes
  5. Pharmacological and Substance Causes
  6. Psychiatric and Functional Causes
  7. Diagnostic Approach
  8. Treatment by Cause
  9. Connections
  10. Key Research Papers
  11. Featured Videos

Overview and Immediate Red Flags

Palpitations are a subjective, uncomfortable awareness of the heartbeat — felt as a fast, pounding, fluttering, racing, or skipping sensation in the chest, throat, or neck. Patients describe them in many ways: "my heart was jumping out of my chest," "I felt a flip-flop," "it skipped a beat and then thudded," or "my heart was racing for no reason." The sensation can be brief (a single beat) or sustained (minutes to hours), and it may occur at rest, during exertion, or upon lying down.

Palpitations are extremely common: they account for 1–3% of all primary care visits and are among the top five presenting complaints in cardiology clinics. The vast majority of cases are benign — premature beats, sinus tachycardia from caffeine or stress, or panic — but palpitations can be the presenting symptom of a life-threatening arrhythmia. The central diagnostic challenge is that palpitations are almost always episodic, meaning the ECG is frequently normal by the time the patient reaches the clinic.

Immediate Red Flags — Do Not Wait

Palpitations combined with any of the following require immediate evaluation, including an urgent 12-lead ECG and cardiac monitoring:

A 12-lead ECG should be obtained in every patient presenting with palpitations, even if the episode has resolved. WPW pre-excitation, QTc prolongation, signs of prior MI, and resting PVCs are all visible on a resting ECG and can fundamentally redirect the workup.

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Cardiac Arrhythmia Causes

True arrhythmias are the most clinically important cause of palpitations. The sensation produced varies by arrhythmia type, and the description alone is sometimes enough to narrow the differential.

Premature Atrial Contractions (PACs)

PACs are the single most common cause of the "skipped beat" sensation. Paradoxically, the patient does not feel the PAC itself but the compensatory pause that follows it — the heart waits, then beats with extra force (post-extrasystolic potentiation), and that forceful beat is what registers as a "thump." PACs are visible on ECG as early P waves with altered morphology. They are essentially benign in the absence of structural heart disease. Common triggers include caffeine, alcohol, fatigue, stress, and nicotine. Reassurance is the primary intervention; beta-blockers can reduce frequency if symptoms are disabling.

Premature Ventricular Contractions (PVCs)

PVCs produce the same "skipped beat" or "flip-flop" sensation as PACs but arise from ventricular ectopic foci. They appear on ECG as wide, bizarre QRS complexes without a preceding P wave, followed by a compensatory pause. PVCs occurring in a regular alternating pattern with normal beats are called bigeminy; every third beat is trigeminy. PVCs are common in the general population and are benign when the PVC burden is low (<10% of total beats) and the heart is structurally normal. However, frequent PVCs — particularly those exceeding 10–20% of total beats — can themselves cause a reversible PVC-induced cardiomyopathy with reduced ejection fraction. This makes quantifying PVC burden (via Holter monitor) important in symptomatic patients.

Atrial Fibrillation (AFib)

AFib causes palpitations described as irregular, fast, and often sustained — "my heart was going completely haywire." On ECG it is characterized by absent P waves, an irregularly irregular ventricular response, and fibrillatory baseline. AFib is the most common sustained cardiac arrhythmia, affecting roughly 6 million Americans. Beyond symptoms, AFib carries substantial stroke risk from atrial thrombus formation; anticoagulation decisions are guided by the CHA₂DS₂-VASc score. Rate control (beta-blockers, calcium channel blockers) and rhythm control (antiarrhythmics, cardioversion, catheter ablation) are complementary strategies. The EAST-AFNET-4 trial demonstrated that early rhythm control improves cardiovascular outcomes compared with rate control alone in newly diagnosed AFib.

Supraventricular Tachycardia (SVT)

SVT presents as sudden-onset, sudden-offset rapid regular palpitations — often described as "the switch just flipped." Heart rates typically run 150–250 bpm. The most common mechanism is AV node re-entrant tachycardia (AVNRT), in which a re-entry circuit within the AV node causes rapid, regular conduction. SVT is generally not life-threatening in the absence of structural heart disease or WPW but can cause hemodynamic compromise at very high rates or with prolonged duration. Acute termination uses vagal maneuvers first: the modified Valsalva maneuver (patient strains for 15 seconds, then legs are passively elevated by 45° while supine) — the REVERT trial found this approach doubled the success rate of standard Valsalva (43% vs 17%). If vagal maneuvers fail, IV adenosine (6 mg rapid push, followed by 12 mg if needed) terminates most SVTs by transiently blocking AV node conduction. For definitive long-term management, catheter ablation of the AVNRT circuit achieves cure rates exceeding 95% and is preferred over lifelong antiarrhythmic medications in most patients.

Wolff-Parkinson-White Syndrome (WPW)

WPW results from an accessory conduction pathway (Bundle of Kent) that bypasses the AV node. On resting ECG, the signature findings are a short PR interval, a delta wave (slurred upstroke of the QRS), and a widened QRS. Most WPW patients experience SVT from re-entry involving the accessory pathway. The critical danger is atrial fibrillation in WPW: if AFib develops and conduction travels preferentially down the accessory pathway rather than the AV node, the rapid and irregular impulses can trigger ventricular fibrillation. This makes WPW with AFib a medical emergency. Critically, the standard AV node-blocking drugs — digoxin, verapamil, diltiazem, and adenosine are all contraindicated in AFib with WPW because they preferentially block the AV node, leaving the accessory pathway unopposed and potentially accelerating conduction to dangerous rates. Treatment is IV procainamide or electrical cardioversion. Curative catheter ablation of the accessory pathway is the definitive treatment for symptomatic WPW.

Ventricular Tachycardia (VT)

VT is defined as three or more consecutive ventricular beats at a rate exceeding 100 bpm. On ECG it appears as a wide-complex tachycardia (QRS >120 ms). VT in the setting of structural heart disease (post-MI scar, dilated cardiomyopathy, HCM) is potentially life-threatening and warrants aggressive evaluation and treatment, including consideration of implantable cardioverter-defibrillator (ICD) implantation. Sustained VT can cause hemodynamic collapse and degenerate into ventricular fibrillation. Not all wide-complex tachycardias are VT (SVT with aberrant conduction is the main alternative), but in a patient with structural heart disease, the safest assumption is always VT until proven otherwise.

Long QT Syndrome

Long QT syndrome (LQTS) — both congenital and acquired — predisposes to Torsades de Pointes (TdP), a distinctive polymorphic VT that can degenerate into ventricular fibrillation and sudden cardiac death. The QTc is prolonged when it exceeds 470 ms in women and 450 ms in men (Bazett formula). Congenital LQTS involves mutations in cardiac ion channel genes (KCNQ1, KCNH2, SCN5A — LQT1, LQT2, LQT3). Acquired LQTS is commonly drug-induced (antiarrhythmics, antipsychotics, antibiotics, antihistamines) — the CredibleMeds QTDrugs list is the authoritative drug interaction resource. Hypokalemia and hypomagnesemia potentiate drug-induced QT prolongation. Treatment of congenital LQTS includes beta-blockers, avoidance of QTc-prolonging drugs, and ICD for high-risk patients.

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Non-Arrhythmia Cardiac Causes

Sinus Tachycardia

Sinus tachycardia — a regular heart rate above 100 bpm driven by the sinus node — is the most common rapid heart rate overall. It is never a primary problem; it is always a physiological response to an underlying driver. The key clinical task is identifying the cause: fever, pain, hypovolemia, anemia, hyperthyroidism, pulmonary embolism, heart failure, sepsis, dehydration, anxiety, stimulants, or drugs. Sinus tachycardia should not be treated with rate-slowing agents in isolation — that would suppress the compensatory response without addressing the root problem. Patients often describe it as a persistent "racing" feeling that builds gradually rather than the sudden onset of SVT.

POTS (Postural Orthostatic Tachycardia Syndrome)

POTS is a form of dysautonomia defined by a heart rate increase of 30 bpm or more within 10 minutes of standing (or 40 bpm in adolescents), without orthostatic hypotension. Palpitations are a cardinal symptom — patients notice their heart racing whenever they stand up, often accompanied by lightheadedness, fatigue, brain fog, nausea, and near-syncope. POTS predominantly affects young women (female-to-male ratio approximately 5:1) and is increasingly recognized as a post-viral syndrome, including after COVID-19. Diagnosis is confirmed by an active stand test or tilt table test. Management includes: increased salt and fluid intake (10 g NaCl/day + 2–3 L water), compression stockings/garments, exercise reconditioning, and medications — propranolol (low-dose), fludrocortisone (volume expansion), or ivabradine (off-label, reduces heart rate without reducing contractility — useful when beta-blockers cause fatigue).

Valvular Heart Disease

Mitral valve prolapse (MVP) has historically been associated with palpitations; most MVP is benign and palpitations are caused by concomitant PACs/PVCs rather than the prolapse itself. Severe aortic regurgitation can cause prominent awareness of the heartbeat due to the large stroke volume and pounding pulse (Corrigan's pulse). Any significant valvular disease can trigger AFib, which then produces palpitations.

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Metabolic and Endocrine Causes

Hyperthyroidism

Excess thyroid hormone is a classic and important cause of palpitations. Thyroid hormone sensitizes cardiac tissue to catecholamines and directly increases heart rate, stroke volume, and cardiac output. Patients experience fast, regular palpitations often present even at rest, along with heat intolerance, excessive sweating, unintended weight loss despite increased appetite, tremor, anxiety, diarrhea, and insomnia. TSH is suppressed in hyperthyroidism and is the appropriate first-line screening test. Causes include Graves' disease (autoimmune, the most common), toxic multinodular goiter, and thyroiditis. Atrial fibrillation complicates hyperthyroidism in roughly 10–15% of cases and is a common initial presentation in older patients ("apathetic hyperthyroidism") who may lack the classic adrenergic features.

Pheochromocytoma

Pheochromocytoma — a catecholamine-secreting tumor of the adrenal medulla — classically presents with episodic palpitations, severe headache, and diaphoresis (the classic triad), often accompanied by hypertensive crises. Episodes typically last minutes to an hour and may be triggered by positional change, physical exertion, or even abdominal palpation. Sustained hypertension can also occur. Screening uses plasma free metanephrines (sensitivity >95%) or 24-hour urine fractionated metanephrines. Imaging with CT or MRI of the adrenal glands follows a positive biochemical screen. Surgical resection is curative; alpha-blockade (phenoxybenzamine or doxazosin) is essential preoperatively to prevent hypertensive crises during induction.

Hypoglycemia

When blood glucose falls, the body mounts a sympathoadrenal counter-regulatory response — epinephrine and norepinephrine surge — producing palpitations, tremor, diaphoresis, and anxiety. Patients often wake at night feeling clammy and panicked. This is most relevant in people with diabetes using insulin or sulfonylureas, but can also occur in reactive hypoglycemia after high-carbohydrate meals. Checking blood glucose during an episode (via fingerstick or CGM) is diagnostic. Treatment addresses the underlying cause: insulin dose adjustment, dietary changes, or evaluation for rare endogenous hyperinsulinism (insulinoma).

Anemia

Anemia of any cause reduces oxygen-carrying capacity. The heart compensates by increasing heart rate and stroke volume, leading to a hyperdynamic circulation with prominent palpitations, particularly during any exertion. Patients may notice their heart "pounding" even at rest in severe anemia. A complete blood count (CBC) is the key initial test; the cause (iron deficiency, B12/folate, hemolysis, chronic disease) guides treatment. Correcting the anemia resolves the palpitations.

Electrolyte Disturbances

Hypokalemia sensitizes the myocardium to arrhythmias. Low serum potassium shifts the resting membrane potential, making cardiac cells more excitable. PVCs are common; ECG classically shows flattened T waves and prominent U waves. Hypokalemia is common in patients using loop diuretics (furosemide) or thiazides, in eating disorders (purging), and in diarrheal illnesses. Potassium replacement corrects most hypokalemia-associated palpitations.

Hypomagnesemia frequently co-occurs with hypokalemia and independently predisposes to arrhythmias — particularly Torsades de Pointes. Magnesium is essential for cardiac ion channel function and for the activity of the Na/K-ATPase pump that maintains intracellular potassium. IV magnesium is the first-line treatment for TdP regardless of serum magnesium level. Common causes include diuretic use, alcoholism, malabsorption, and proton pump inhibitor use (which impairs intestinal magnesium absorption).

Fever

For every 1°C rise in core body temperature, heart rate increases by approximately 10 bpm. Any febrile illness can cause prominent palpitations through this mechanism. The clinical task is identifying and treating the infection — the palpitations resolve with defervescence.

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Pharmacological and Substance Causes

Caffeine

Caffeine is the most common dietary trigger for palpitations. It blocks adenosine receptors, increasing sympathetic tone and directly exciting cardiac tissue, precipitating PACs and PVCs in susceptible individuals. The relationship is dose-dependent: moderate caffeine intake (up to 300–400 mg/day) is generally tolerated, but individual sensitivity varies widely. Sources include coffee, tea, energy drinks, cola sodas, and dark chocolate. A structured caffeine elimination trial (2–4 weeks) is often revealing — if palpitations resolve with abstinence, the cause is identified.

Alcohol

Alcohol triggers palpitations through two distinct mechanisms. Acutely, even moderate alcohol intake can precipitate PACs and AFib in susceptible individuals. More dramatically, "Holiday Heart Syndrome" — first described by Ettinger in 1978 — refers to AFib or other atrial arrhythmias that develop after binge drinking in otherwise healthy young adults without structural heart disease. The arrhythmia typically converts to sinus rhythm spontaneously as blood alcohol clears. Chronic heavy alcohol use causes alcoholic cardiomyopathy and associated arrhythmias. Any patient with recurrent unexplained AFib should be asked carefully about alcohol intake; total abstinence significantly reduces AFib recurrence.

Stimulant Medications

Multiple over-the-counter and prescription drugs contain sympathomimetic agents that increase heart rate:

Nicotine

Nicotine stimulates nicotinic acetylcholine receptors, acutely increasing heart rate and blood pressure through catecholamine release. Both cigarette smoking and nicotine replacement products (patch, gum, vaping) can trigger palpitations, particularly in those transitioning to higher-dose nicotine replacement.

Thyroid Hormone Over-Replacement

Patients on levothyroxine for hypothyroidism who are supraphysiologically dosed will develop the palpitation pattern of hyperthyroidism — fast, regular, and present at rest. TSH suppressed below 0.1 mIU/L on thyroid supplementation should prompt dose reduction. This is commonly seen after empiric dose increases without TSH follow-up.

Beta-Agonist Bronchodilators

Albuterol, salmeterol, and other beta-2 agonists used in asthma and COPD stimulate cardiac beta-1 receptors (they are not perfectly selective), causing sinus tachycardia and palpitations. This is dose-dependent and worsens with overuse of rescue inhalers.

Antiarrhythmic Proarrhythmia

A paradoxical risk of antiarrhythmic drugs is that they can cause the very arrhythmias they are meant to treat. Class IC agents — flecainide and propafenone — are particularly notable: when used for AFib, they can organize AF into atrial flutter that then conducts 1:1 to the ventricle at rates of 200–250 bpm. This is why class IC drugs for AFib are routinely combined with an AV node blocker (beta-blocker or calcium channel blocker). The CAST trial demonstrated that class IC agents increased mortality in post-MI patients — they are contraindicated in structural heart disease.

Digoxin Toxicity

Digoxin has a narrow therapeutic window (target level 0.5–0.9 ng/mL for heart failure). Toxicity — from accumulation, drug interactions (amiodarone, verapamil), or renal impairment — causes a wide range of arrhythmias: accelerated junctional rhythm, bidirectional VT (pathognomonic), and various AV blocks. Hypokalemia worsens digoxin toxicity. Management includes holding digoxin, correcting electrolytes, and digoxin-immune Fab antibodies for severe toxicity.

Recreational Drugs

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Psychiatric and Functional Causes

Panic Disorder and Panic Attacks

Panic disorder is a major cause of palpitations and one of the most important diagnoses to consider after cardiac causes have been excluded. A panic attack produces a sudden surge of autonomic nervous system activation — palpitations, shortness of breath, chest pain, dizziness, tingling, sweating, and an overwhelming sense of impending doom or death. Attacks peak at approximately 10 minutes and then subside. They can occur during the day or wake the patient from sleep (nocturnal panic attacks). Because the physical symptoms so closely mimic cardiac events, patients often present to emergency departments believing they are having a heart attack.

Important diagnostic principles: panic disorder should be diagnosed only after cardiac arrhythmias have been adequately excluded — particularly given that some patients have both a genuine arrhythmia and panic. First-line treatment is the combination of SSRIs (sertraline, escitalopram) and cognitive behavioral therapy (CBT), which together achieve remission in 70–80% of patients. Short-acting benzodiazepines (lorazepam, alprazolam) provide acute relief during attacks but should not be used as maintenance therapy due to dependence risk.

Generalized Anxiety Disorder (GAD)

Patients with GAD develop chronic autonomic hyperarousal — persistently elevated sympathetic tone that produces resting tachycardia, palpitations, muscle tension, fatigue, and difficulty concentrating. Unlike panic attacks (discrete episodes), GAD causes more continuous background somatic symptoms. Palpitations are noticed particularly during periods of heightened worry. Somatic hypervigilance amplifies awareness of normal heart beats. Beta-blockers (propranolol 10–20 mg PRN) can interrupt the palpitation-anxiety feedback loop where noticing a palpitation causes anxiety which causes more palpitations.

Somatic Symptom Disorder and Cardiac Anxiety

A subset of patients with palpitations have objectively normal Holter monitor findings — including during symptom episodes — with no correlation between symptoms and rhythm. These patients often have high levels of health anxiety focused on their heart, amplified by hypervigilance to normal cardiac sensations. Central sensitization — a phenomenon in which the perception threshold for interoceptive signals is lowered — likely plays a role. Treatment focuses on CBT targeting cardiac anxiety, psychoeducation, and low-dose beta-blockers to reduce peripheral somatic signals that feed into the anxiety loop. Avoidance of repeated cardiac testing (which reinforces illness beliefs) is part of the therapeutic approach.

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Diagnostic Approach

Clinical History

A detailed history is the most important diagnostic tool for palpitations. Key elements:

Electrocardiogram (ECG)

A 12-lead ECG should be obtained in every patient presenting with palpitations, even if asymptomatic at the time. Key findings to look for: WPW (delta wave, short PR interval — <120 ms); prolonged QTc; ST-segment changes suggesting ischemia; evidence of prior myocardial infarction (pathological Q waves); Brugada pattern (coved ST elevation in V1–V2); left ventricular hypertrophy suggesting HCM; PVCs visible at rest.

Ambulatory Cardiac Monitoring

Because palpitations are episodic, the goal of ambulatory monitoring is to capture a symptom-rhythm correlation — to record the cardiac rhythm during an episode and determine whether the patient's symptoms occur with a documented arrhythmia or with a normal rhythm.

Echocardiogram

Transthoracic echocardiography is indicated in patients with: palpitations + exertional symptoms; palpitations + syncope; any suggestion of structural heart disease on history, physical examination, or ECG; or if sustained arrhythmia is documented. It evaluates left ventricular ejection fraction, wall thickness (for HCM), valvular disease, and diastolic function.

Laboratory Tests

Specialized Testing

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Treatment by Cause

Supraventricular Tachycardia (SVT) — AVNRT

Acute termination proceeds in stepwise fashion: (1) vagal maneuvers — the Modified Valsalva (strain for 15 s then immediate passive leg raise to 45° for 15 s in supine position) is most effective; ice water facial immersion stimulates the diving reflex and is useful for children; carotid sinus massage (contraindicated if carotid bruit, recent stroke, or known carotid stenosis); (2) IV adenosine 6 mg rapid push with immediate saline flush — can be repeated at 12 mg if the first dose fails. For recurrent symptomatic SVT, catheter ablation of the re-entrant circuit achieves >95% cure rate and is preferred over chronic antiarrhythmic therapy in most guidelines.

Atrial Fibrillation

Management of AFib encompasses three parallel considerations: (1) Rate control — beta-blockers or calcium channel blockers to keep resting ventricular rate <110 bpm; (2) Rhythm control — restoration and maintenance of sinus rhythm using antiarrhythmic drugs (flecainide, propafenone in no-structural-disease; amiodarone, dofetilide broadly) or catheter ablation (pulmonary vein isolation). The EAST-AFNET-4 trial showed early rhythm control reduces major cardiovascular events compared with rate control in newly diagnosed AFib; (3) Stroke prevention — anticoagulation based on CHA₂DS₂-VASc score; direct oral anticoagulants (DOACs — rivaroxaban, apixaban, dabigatran, edoxaban) are preferred over warfarin in non-valvular AFib due to superior safety profiles.

Premature Ventricular Contractions (PVCs)

Benign low-burden PVCs (<10% of beats, structurally normal heart, asymptomatic or mildly symptomatic) require only reassurance, and trigger avoidance (caffeine, alcohol, stimulants). For symptomatic PVCs not responding to conservative measures, beta-blockers reduce PVC frequency and symptoms. For high-burden PVCs (>10–20%) — especially if ejection fraction is reduced — catheter ablation of the PVC focus can achieve dramatic reduction in burden and may reverse cardiomyopathy.

Long QT Syndrome

Core management principles: (1) avoid all QTc-prolonging medications (check CredibleMeds.org before prescribing any new drug); (2) correct electrolyte abnormalities (potassium, magnesium); (3) beta-blockers (nadolol or propranolol — specifically these two, not cardioselective agents) are first-line for LQT1 and LQT2; (4) avoid competitive sports in LQT1/2 (adrenergic triggers); (5) ICD for patients with prior cardiac arrest, syncope despite beta-blocker therapy, or high-risk genetic variants.

POTS

Non-pharmacological measures are foundational: aggressive salt loading (8–10 g NaCl/day), fluid intake of 2–3 L/day, waist-high compression garments (at least 20–30 mmHg), and a structured exercise reconditioning program (starting with recumbent exercise — swimming, rowing — to avoid the orthostatic challenge of upright exercise). Pharmacological options include: fludrocortisone (volume expansion via mineralocorticoid effect); low-dose propranolol (10–20 mg) for symptom relief; ivabradine (off-label, sinus node If current inhibitor — reduces heart rate without impairing contractility or causing the fatigue common with beta-blockers); midodrine (alpha-1 agonist vasoconstrictor, reduces venous pooling).

Panic Disorder

First-line treatment is the combination of an SSRI (sertraline, escitalopram, or paroxetine — noting paroxetine's higher discontinuation syndrome risk) and CBT focused on interoceptive exposure (deliberately inducing palpitation-like sensations to decondition the fear response). This combination achieves remission in 70–80% of patients. PRN short-acting benzodiazepines (lorazepam 0.5–1 mg) are appropriate for acute severe attacks but should not anchor maintenance therapy. Beta-blockers are useful for situational (performance) anxiety but are not effective for panic disorder maintenance treatment — they block peripheral symptoms without affecting the central fear circuitry.

Caffeine and Alcohol

A structured 4-week elimination trial of caffeine and/or alcohol is both diagnostic and therapeutic. If documented as a trigger, sustained avoidance is the most effective long-term intervention. For alcohol-associated AFib (Holiday Heart), recurrence rates drop substantially with abstinence — randomized data from the HOLIDAY trial showed significant AFib burden reduction with alcohol abstinence in regular drinkers.

Metabolic Causes

Hyperthyroidism is treated definitively (antithyroid drugs, radioactive iodine, or surgery) — palpitations and AFib resolve with return to euthyroid state. Beta-blockers provide rapid symptomatic relief of the adrenergic manifestations while awaiting definitive treatment. Electrolyte abnormalities are repleted (potassium orally for mild-moderate hypokalemia; IV for severe or symptomatic; IV magnesium for significant hypomagnesemia or TdP). Anemia is treated according to its etiology.

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Connections

Key Research Papers

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  3. Appelboam A, Reuben A, Mann C, et al. Postural modification to the standard Valsalva manoeuvre for emergency treatment of supraventricular tachycardias (REVERT): a randomised controlled trial. Lancet. 2015;386(10005):1747–1753. PMID: 26100142.
  4. Kirchhof P, Camm AJ, Goette A, et al. Early rhythm-control therapy in patients with atrial fibrillation (EAST-AFNET 4). N Engl J Med. 2020;383(14):1305–1316. PMID: 32865375.
  5. Blomström-Lundqvist C, Traykov V, Tabitha PA, et al. European Heart Rhythm Association (EHRA) consensus document on management of supraventricular arrhythmias. Europace. 2019;21(5):655–700. PMID: 31022100.
  6. Gorenek BC, Buber J, Georgiou S, et al. Cardiac arrhythmias in acute coronary syndromes: position paper from the joint EHRA, ACCA, and EAPCI task force. Europace. 2014;16(11):1655–1673. PMID: 24373795.
  7. Abbott AV. Diagnostic approach to palpitations. Am Fam Physician. 2005;71(4):743–750. PMID: 15742913.
  8. Orejarena LA, Vidaillet H Jr, DeStefano F, et al. Paroxysmal supraventricular tachycardia in the general population. J Am Coll Cardiol. 1998;31(1):150–157. PMID: 9426034.
  9. Brugada P, Brugada J, Mont L, Smeets J, Andries EW. A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex. Circulation. 1991;83(5):1649–1659. PMID: 2022022.
  10. Maron BJ, McKenna WJ, Danielson GK, et al. American College of Cardiology/European Society of Cardiology clinical expert consensus document on hypertrophic cardiomyopathy. J Am Coll Cardiol. 2003;42(9):1687–1713. PMID: 14607462.
  11. Priori SG, Napolitano C, Schwartz PJ. Low penetrance in the long-QT syndrome: clinical impact. Circulation. 1999;99(4):529–533. PMID: 9927399.
  12. Grubb BP. Postural tachycardia syndrome. Circulation. 2008;117(21):2814–2817. PMID: 18506020.

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