A diagnosis of bradycardia in adults is based on a heart rate less than 60 BPM. This is determined usually either by palpation or electrocardiography.

If symptoms occur, a determination of electrolytes may be helpful in determining the underlying cause.

No formal diagnostic criteria exist. A diagnosis of Inappropriate sinus tachycardia is primarily one of exclusion and the following may be observed:

- Exclusion of all other causes of sinus tachycardia

- Common forms of supraventricular tachycardia (SVT) must be excluded

- Normal P wave morphology

- A resting sinus tachycardia is usually (but not always) present

- Nocturnal dip in heart rate

- Inappropriate heart rate response on exertion

- Mean heart rate in 24hrs >95 bpm

- Symptoms are documented to be due to tachycardia

- Hypotension is occasionally observed

- Syncope (fainting) is occasionally reported

The diagnosis of ventricular tachycardia is made based on the rhythm seen on either a 12-lead ECG or a telemetry rhythm strip. It may be very difficult to differentiate between ventricular tachycardia and a wide-complex supraventricular tachycardia in some cases. In particular, supraventricular tachycardias with aberrant conduction from a pre-existing bundle branch block are commonly misdiagnosed as ventricular tachycardia. Other rarer phenomena include ashman beats and antedromic atrioventricular re-entry tachycardias.

Various diagnostic criteria have been developed to determine whether a wide complex tachycardia is ventricular tachycardia or a more benign rhythm. In addition to these diagnostic criteria, if the individual has a past history of a myocardial infarction, congestive heart failure, or recent angina, the wide complex tachycardia is much more likely to be ventricular tachycardia.

The proper diagnosis is important, as the misdiagnosis of supraventricular tachycardia when ventricular tachycardia is present is associated with worse prognosis. This is particularly true if calcium channel blockers, such as verapamil, are used to attempt to terminate a presumed supraventricular tachycardia. Therefore, it is wisest to assume that all wide complex tachycardia is VT until proven otherwise.

Cardiac arrhythmia are often first detected by simple but nonspecific means: auscultation of the heartbeat with a stethoscope, or feeling for peripheral pulses. These cannot usually diagnose specific arrhythmia but can give a general indication of the heart rate and whether it is regular or irregular. Not all the electrical impulses of the heart produce audible or palpable beats; in many cardiac arrhythmias, the premature or abnormal beats do not produce an effective pumping action and are experienced as "skipped" beats.

The simplest "specific" diagnostic test for assessment of heart rhythm is the electrocardiogram (abbreviated ECG or EKG). A Holter monitor is an EKG recorded over a 24-hour period, to detect arrhythmias that may happen briefly and unpredictably throughout the day.

A more advanced study of the heart's electrical activity can be performed to assess the source of the aberrant heart beats. This can be accomplished in an electrophysiology study, an endovascular procedure that uses a catheter to "listen" to the electrical activity from within the heart, additionally if the source of the arrhythmias is found, often the abnormal cells can be ablated and the arrhythmia can be permanently corrected. "" (TAS) instead uses an electrode inserted through the esophagus to a part where the distance to the posterior wall of the left atrium is only approximately 5–6 mm (remaining constant in people of different age and weight). Transesophageal atrial stimulation can differentiate between atrial flutter, AV nodal reentrant tachycardia and orthodromic atrioventricular reentrant tachycardia. It can also evaluate the risk in people with Wolff–Parkinson–White syndrome, as well as terminate supraventricular tachycardia caused by re-entry.

In general, the minimal evaluation of atrial fibrillation should be performed in all individuals with AF. The goal of this evaluation is to determine the general treatment regimen for the individual. If results of the general evaluation warrant it, further studies may then be performed.

Limited studies have suggested that screening for atrial fibrillation in those 65 years and older increases the number of cases of atrial fibrillation detected.

If the person is hemodynamically unstable or other treatments have not been effective, synchronized electrical cardioversion may be used. In children this is often done with a dose of 0.5 to 1 J/Kg.

If the symptoms are present while the person is receiving medical care (e.g., in an emergency department), an electrocardiogram (ECG/EKG) may show typical changes that confirm the diagnosis. If the palpitations are recurrent, a doctor may request a Holter monitor (24-hour or longer portable ECG) recording. Again, this will show the diagnosis if the recorder is attached at the time of the symptoms. In rare cases, disabling but infrequent episodes of palpitations may require the insertion of a small microchip-based device (e.g., Reveal Plus) under the skin that continuously record heart activity, and can be read through the skin after an episode. All these ECG-based technologies also enable the distinction between AVNRT and other abnormal fast heart rhythms such as atrial fibrillation, atrial flutter, sinus tachycardia, ventricular tachycardia and tachyarrhythmias related to Wolff-Parkinson-White syndrome, all of which may have symptoms that are similar to AVNRT.

Blood tests commonly performed in people with palpitations are:

- thyroid function tests (TFTs) - an overactive thyroid increases the risk of AVNRT

- electrolytes - disturbances in potassium, calcium and magnesium may predispose to AVNRT

- cardiac markers - if there is a concern that myocardial infarction (heart attack) has occurred either as a cause or as a result of the AVNRT; this is usually only the case if the patient has experienced chest pain

The method of cardiac rhythm management depends firstly on whether or not the affected person is stable or unstable. Treatments may include physical maneuvers, medications, electricity conversion, or electro- or cryo-cautery.

In the United States, people admitted to the hospital with cardiac arrhythmia and conduction disorders with and without complications were admitted to the intensive care unit more than half the time in 2011.

The main pumping chamber, the ventricle, is protected (to a certain extent) against excessively high rates arising from the supraventricular areas by a "gating mechanism" at the atrioventricular node, which allows only a proportion of the fast impulses to pass through to the ventricles. In Wolff-Parkinson-White syndrome, a "bypass tract" avoids this node and its protection and the fast rate may be directly transmitted to the ventricles. This situation has characteristic findings on ECG.

Ventricular tachycardia can be classified based on its "morphology":

- Monomorphic ventricular tachycardia means that the appearance of all the beats match each other in each lead of a surface electrocardiogram (ECG).

- Scar-related monomorphic ventricular tachycardia is the most common type and a frequent cause of death in patients having survived a heart attack or myocardial infarction, especially if they have a weak heart muscle.

- RVOT tachycardia is a type of monomorphic ventricular tachycardia originating in the right ventricular outflow tract. RVOT morphology refers to the characteristic pattern of this type of tachycardia on an ECG.

- The source of the re-entry circuit can be identified by evaluating the morphology of the QRS complex in the V1 lead of a surface ECG. If the R wave is dominant (consistent with a right bundle branch block morphology), this indicates the origin of the VT is the left ventricle. Conversely, if the S wave is dominant (consistent with a left bundle branch block morphology, this is consistent with VT originating from the right ventricle or interventricular septum.

- Polymorphic ventricular tachycardia, on the other hand, has beat-to-beat variations in morphology. This may appear as a cyclical progressive change in cardiac axis, previously referred to by its French name "torsades de pointes" ("twisting of the spikes"). However, at the current time, the term torsades de pointes is reserved for polymorphic VT occurring in the context of a prolonged resting QT interval.

Another way to classify ventricular tachycardias is the "duration of the episodes": Three or more beats in a row on an ECG that originate from the ventricle at a rate of more than 100 beats per minute constitute a ventricular tachycardia.

- If the fast rhythm self-terminates within 30 seconds, it is considered a non-sustained ventricular tachycardia.

- If the rhythm lasts more than 30 seconds, it is known as a sustained ventricular tachycardia (even if it terminates on its own after 30 seconds).

A third way to classify ventricular tachycardia is on the basis of its "symptoms": Pulseless VT is associated with no effective cardiac output, hence, no effective pulse, and is a cause of cardiac arrest. In this circumstance, it is best treated the same way as ventricular fibrillation (VF), and is recognized as one of the shockable rhythms on the cardiac arrest protocol. Some VT is associated with reasonable cardiac output and may even be asymptomatic. The heart usually tolerates this rhythm poorly in the medium to long term, and patients may certainly deteriorate to pulseless VT or to VF.

Less common is ventricular tachycardia that occurs in individuals with structurally normal hearts. This is known as idiopathic ventricular tachycardia and in the monomorphic form coincides with little or no increased risk of sudden cardiac death. In general, idiopathic ventricular tachycardia occurs in younger individuals diagnosed with VT. While the causes of idiopathic VT are not known, in general it is presumed to be congenital, and can be brought on by any number of diverse factors.

Not required for physiologic sinus tachycardia. Underlying causes are treated if present.

Acute myocardial infarction. Sinus tachycardia can present in more than a third of the patients with AMI but this usually decreases over time. Patients with sustained sinus tachycardia reflects a larger infarct that are more anterior with prominent left ventricular dysfunction, associated with high mortality and morbidity. Tachycardia in the presence of AMI can reduce coronary blood flow and increase myocardial oxygen demand, aggravating the situation. Beta blockers can be used to slow the rate, but most patients are usually already treated with beta blockers as a routine regimen for AMI.

Practically, many studies showed that there is no need for any treatment.

IST and POTS. Beta blockers are useful if the cause is sympathetic overactivity. If the cause is due to decreased vagal activity, it is usually hard to treat and one may consider radiofrequency catheter ablation.

Usually apparent on the ECG, but if heart rate is above 140 bpm the P wave may be difficult to distinguish from the previous T wave and one may confuse it with a paroxysmal supraventricular tachycardia or atrial flutter with a 2:1 block. Ways to distinguish the three are:

- Vagal maneuvers (such as carotid sinus massage or Valsalva's maneuver) to slow the rate and identification of P waves

- administer AV blockers (e.g., adenosine, verapamil) to identify atrial flutter with 2:1 block

Adenosine, an ultra-short-acting AV nodal blocking agent, is indicated if vagal maneuvers are not effective. If unsuccessful or the PSVT recurs diltiazem or verapamil are recommended. Adenosine may be safely used during pregnancy.

SVT that does not involve the AV node may respond to other anti-arrhythmic drugs such as sotalol or amiodarone.

The treatment of bradycardia is dependent on whether or not the person is stable or unstable. If oxygen saturations are low, supplemental oxygen should be provided.

PVCs are usually diagnosed after the patient has described "skipped beats", pauses or palpitations. Typically the palpitations felt by PVC patients are very irregular and less sustained than patients with other types of arrhythmia. They are likely to have "flip flopping" sensations where it feels like the heart is flipping over or pounding due to there being a pause after the premature contraction and then a powerful contraction after the pause. There is a possibility that they might feel a ‘fluttering’ in their chest or a pounding in their neck but these two types of palpitations aren't very common in PVC patients.

A physical examination should be conducted after a full history has been taken. This is useful in determining any possible heart defects that might be causing the palpitations. For example, some cases of premature ventricular contraction have a mitral-valve prolapse which can be determined through the physical examination.

The next step in diagnosis is a 12 lead ECG which can be performed in the doctors’ office over a short period of time; however this is often non-conclusive in diagnosis because it is not very sensitive and there is only a small chance of a premature ventricular contraction occurring in the short period of time. Holter monitoring is a far better method for diagnosis as it is continuous recording of the heart’s rhythm over a period of 24 hours, or event monitoring which records noncontinuously for 30 days or indefinitely. This increases the likelihood of a premature ventricular contraction occurring during the recording period and is therefore more useful in diagnosis. Another method of detection of PVCs is a portable electrocardiogram device known as an event recorder that can be carried around for home monitoring of the heart's activity. Both the Holter monitor and the event recorder can help to identify the pattern of a PVC. The significance of a patient's PVCs can be monitored and diagnosed through exercise stress electrocardiogram. If the premature beats go away during the exercise test then they are considered to be harmless, but if the exercise provokes the extra beats than it may indicate higher risk of serious heart rhythm problems.

When looking at an electrocardiograph, premature ventricular contractions are easily spotted and therefore a definitive diagnosis can be made. The QRS and T waves look very different from normal readings. The spacing between the PVC and the preceding QRS wave is a lot shorter than usual and the time between the PVC and the following QRS is a lot longer. However, the time between the preceding and ing QRS waves stays the same as normal due to the compensatory pause.

PVCs can be distinguished from premature atrial contractions because the compensatory pause is longer following premature ventricular contractions.

There are four different named patterns of regularly occurring PVCs. Depending whether there are 1, 2, or 3 normal beats between each PVC, the rhythm is called bigeminy, trigeminy, or quadrigeminy. Unifocal PVCs are triggered from a single site in the ventricle, causing the peaks on the ECG to look the same. Multifocal PVCs arise when more than one site in the ventricles initiate depolarization, causing each peak on the ECG to have a different shape. If 3 or more PVCs occur in a row it may be called ventricular tachycardia.

Subtypes of SVT can usually be distinguished by their electrocardiogram (ECG) characteristics

Most have a narrow QRS complex, although, occasionally, electrical conduction abnormalities may produce a wide QRS complex that may mimic ventricular tachycardia (VT). In the clinical setting, the distinction between narrow and wide complex tachycardia (supraventricular vs. ventricular) is fundamental since they are treated differently. In addition, ventricular tachycardia can quickly degenerate to ventricular fibrillation and death and merits different consideration. In the less common situation in which a wide-complex tachycardia may actually be supraventricular, a number of algorithms have been devised to assist in distinguishing between them. In general, a history of structural heart disease markedly increases the likelihood that the tachycardia is ventricular in origin.

- Sinus tachycardia is physiologic or "appropriate" when a reasonable stimulus, such as the catecholamine surge associated with fright, stress, or physical activity, provokes the tachycardia. It is identical to a normal sinus rhythm except for its faster rate (>100 beats per minute in adults). Sinus tachycardia is considered by most sources to be an SVT.

- Sinoatrial node reentrant tachycardia (SANRT) is caused by a reentry circuit localised to the SA node, resulting in a P-wave of normal shape and size (morphology) that falls before a regular, narrow QRS complex. It cannot be distinguished electrocardiographically from sinus tachycardia unless the sudden onset is observed (or recorded on a continuous monitoring device). It may sometimes be distinguished by its prompt response to vagal maneuvers.

- Ectopic (unifocal) atrial tachycardia arises from an independent focus within the atria, distinguished by a consistent P-wave of abnormal shape and/or size that falls before a narrow, regular QRS complex. It is caused by "automaticity", which means that some cardiac muscle cells, which have the primordial ("primitive, inborn, inherent") ability to generate electrical impulses that is common to all cardiac muscle cells, have established themselves as a 'rhythm center' with a natural rate of electrical discharge that is faster than the normal SA node.

- Multifocal atrial tachycardia (MAT) is tachycardia arising from at least three ectopic foci within the atria, distinguished by P-waves of at least three different morphologies that all fall before irregular, narrow QRS complexes. This rhythm is most commonly seen in elderly people with COPD.

- Atrial fibrillation meets the definition of SVT when associated with a ventricular response greater than 100 beats per minute. It is characterized as an "irregularly irregular rhythm" both in its atrial and ventricular depolarizations and is distinguished by its fibrillatory atrial waves that, at some point in their chaos, stimulate a response from the ventricles in the form of irregular, narrow QRS complexes.

- Atrial flutter, is caused by a re-entry rhythm in the atria, with a regular atrial rate often of about 300 beats per minute. On the ECG this appears as a line of "sawtooth" waves preceding the QRS complex. The AV node will not usually conduct 300 beats per minute so the P:QRS ratio is usually 2:1 or 4:1 pattern, (though rarely 3:1, and sometimes 1:1 where class IC antiarrhythmic drug are in use). Because the ratio of P to QRS is usually consistent, A-flutter is often regular in comparison to its irregular counterpart, atrial fibrillation. Atrial flutter is also not necessarily a tachycardia unless the AV node permits a ventricular response greater than 100 beats per minute.

- AV nodal reentrant tachycardia (AVNRT) involves a reentry circuit forming next to, or within, the AV node. The circuit most often involves two tiny pathways one faster than the other. Because the node is immediately between the atria and ventricle, the re-entry circuit often stimulates both, appearing as a backward (retrograde) conducted P-wave buried within or occurring just "after" the regular, narrow QRS complexes.

- Atrioventricular reciprocating tachycardia (AVRT), also results from a reentry circuit, although one physically much larger than AVNRT. One portion of the circuit is usually the AV node, and the other, an abnormal accessory pathway (muscular connection) from the atria to the ventricle. Wolff-Parkinson-White syndrome is a relatively common abnormality with an accessory pathway, the bundle of Kent crossing the AV valvular ring.

- In orthodromic AVRT, atrial impulses are conducted down through the AV node and retrogradely re-enter the atrium via the accessory pathway. A distinguishing characteristic of orthodromic AVRT can therefore be a P-wave that follows each of its regular, narrow QRS complexes, due to retrograde conduction.

- In antidromic AVRT, atrial impulses are conducted down through the accessory pathway and re-enter the atrium retrogradely via the AV node. Because the accessory pathway initiates conduction in the ventricles outside of the bundle of His, the QRS complex in antidromic AVRT is often wider than usual, with a delta wave.

- Finally, junctional ectopic tachycardia (JET) is a rare tachycardia caused by increased automaticity of the AV node itself initiating frequent heart beats. On the ECG, junctional tachycardia often presents with abnormal morphology P-waves that may fall anywhere in relation to a regular, narrow QRS complex. It is often due to drug toxicity.

Treatment is based on risk stratification of the individual, which is performed to determine which individuals with WPW are at risk for sudden cardiac death (SCD). The medical history may infrequently point to previous episodes of unexplained syncope (fainting) or, more commonly, palpitations (sudden awareness of one's own, usually irregular, heartbeat). These may have been due to earlier episodes of a tachycardia associated with the accessory pathway.

If an individual's delta waves disappear with increases in the heart rate, he or she is considered to be at lower risk of SCD. This is because the loss of the delta wave shows that the accessory pathway cannot conduct electrical impulses at a high rate (in the anterograde direction). These individuals typically do not have fast conduction down the accessory pathway during episodes of atrial fibrillation.

Risk stratification is best performed via programmed electrical stimulation (PES) in the cardiac electrophysiology laboratory. This is an invasive but generally low-risk procedure during which the atria are stimulated to try to induce tachycardia. If a tachycardia involving the accessory pathway can be triggered, the cardiologist can then assess how rapidly the accessory pathway is able to conduct. The faster it can conduct, the higher the likelihood the accessory pathway can conduct fast enough to trigger a lethal tachycardia.

High-risk features that may be present during PES include an effective refractory period of the accessory pathway less than 250 ms, multiple pathways, septal location of pathway, and inducibility of supraventricular tachycardia (AVRT, atrial fibrillation). Individuals with any of these high-risk features are generally considered at increased risk for SCD or symptomatic tachycardia, and should be treated accordingly (i.e.: catheter ablation).

It is unclear whether invasive risk stratification (with PES) is necessary in the asymptomatic individual. While some groups advocate PES for risk stratification in all individuals under 35 years old, others only offer it to individuals who have history suggestive of a tachydysrhythmia, since the incidence of sudden cardiac death is so low (less than 0.6% in some reports).

People with WPW who are experiencing tachydysrhythmias may require synchronized electrical cardioversion if they are demonstrating severe signs or symptoms (for example, low blood pressure or lethargy with altered mental status). If they are relatively stable, medication may be used.

AV nodal reentrant tachycardia (AVNRT) is the most common reentrant tachycardia. It is a regular narrow complex tachycardia that usually responds well to the Valsalva maneuver or the drug adenosine. However, unstable patients sometimes require synchronized cardioversion. Definitive care may include catheter ablation.

AV reentrant tachycardia (AVRT) requires an accessory pathway for its maintenance. AVRT may involve orthodromic conduction (where the impulse travels down the AV node to the ventricles and back up to the atria through the accessory pathway) or antidromic conduction (which the impulse travels down the accessory pathway and back up to the atria through the AV node). Orthodromic conduction usually results in a narrow complex tachycardia, and antidromic conduction usually results in a wide complex tachycardia that often mimics ventricular tachycardia. Most antiarrhythmics are contraindicated in the emergency treatment of AVRT, because they may paradoxically increase conduction across the accessory pathway.

As an overall medical condition PVCs are normally not very harmful to patients that experience them, but frequent PVCs may put patients at increased risk of developing arrhythmias or cardiomyopathy, which can greatly impact the functioning of the heart over the span of that patient's life. On a more serious and severe scale, frequent PVCs can accompany underlying heart disease and lead to chaotic, dangerous heart rhythms and possibly sudden cardiac death.

Asymptomatic patients that do not have heart disease have long-term prognoses very similar to the general population, but asymptomatic patients that have ejection fractions greater than 40% have a 3.5% incidence of sustained ventricular tachycardia or cardiac arrest. One drawback comes from emerging data that suggests very frequent ventricular ectopy may be associated with cardiomyopathy through a mechanism thought to be similar to that of chronic right ventricular pacing associated cardiomyopathy. Patients that have underlying chronic structural heart disease and complex ectopy, mortality is significantly increased.

In meta-analysis of 11 studies, people with frequent PVC (≥1 time during a standard electrocardiographic recording or ≥30 times over a 1-hour recording) had risk of cardiac death 2 times higher than persons without frequent PVC. Although most studies made attempts to exclude high-risk subjects, such as those with histories of cardiovascular disease, they did not test participants for underlying structural heart disease.

In a study of 239 people with frequent PVCs (>1000 beats/day) and without structural heart disease (i.e. in the presence of normal heart function) there were no serious cardiac events through 5.6 years on average, but there was correlation between PVC prevalence and decrease of ejection fraction and increase of left ventricular diastolic dimension. In this study absence of heart of disease was excluded by echocardiography, cardiac magnetic resonance imaging in 63 persons and Holter monitoring.

Another study has suggested that in the absence of structural heart disease even frequent (> 60/h or 1/min) and complex PVCs are associated with a benign prognosis. It was study of 70 people followed by 6.5 years on average. Healthy status was confirmed by extensive noninvasive cardiologic examination, although cardiac catheterization of a subgroup disclosed serious coronary artery disease in 19%. Overall survival was better than expected.

On the other hand, the Framingham Heart Study reported that PVCs in apparently healthy people were associated with a twofold increase in the risk of all-cause mortality, myocardial infarction and cardiac death. In men with coronary heart disease and in women with or without coronary heart disease, complex or frequent arrhythmias were not associated with an increased risk. The at-risk people might have subclinical coronary disease. These Framingham results have been criticised for the lack of rigorous measures to exclude the potential confounder of underlying heart disease.

In the ARIC study of 14,783 people followed for 15 to 17 years those with detected PVC during 2 minute ECG, and without hypertension or diabetes on the beginning, had risk of stroke increased by 109%. Hypertension or diabetes, both risk factors for stroke, did not change significantly risk of stroke for people with PVC. It is possible that PVCs identified those at risk of stroke with blood pressure and impaired glucose tolerance on a continuum of risk below conventional diagnostic thresholds for hypertension and diabetes. Those in ARIC study with any PVC had risk of heart failure increased by 63% and were >2 times as likely to die due to coronary heart disease (CHD). Risk was also higher for people with or without baseline CHD.

In the Niigata study of 63,386 people with 10-year follow-up period those with PVC during a 10-second recording had risk of atrial fibrillation increased nearly 3 times independently from risk factors: age, male sex, body mass index, hypertension, systolic and diastolic blood pressure, and diabetes.

Reducing frequent PVC (>20%) by antiarrhythmic drugs or by catheter ablation significantly improves heart performance.

Recent studies have shown that those subjects who have an extremely high occurrence of PVCs (several thousand a day) can develop dilated cardiomyopathy. In these cases, if the PVCs are reduced or removed (for example, via ablation therapy) the cardiomyopathy usually regresses.

Also, PVCs can permanently cease without any treatment, in a material percentage of cases.

IST has been treated both pharmacologically and invasively, with varying degrees of success. IST, in and of itself, is not indicative of higher rates of mortality, and non-treatment is an option chosen by many if they have minimal symptoms.

Some types of medication tried by cardiologists and other physicians include: beta blockers, selective sinus node I channel inhibitors (ivabradine), calcium channel blockers and antiarrhythmic agents. Some SSRI drugs are also occasionally tried and also treatments more commonly used to treat postural orthostatic tachycardia syndrome such as fludrocortisone. This approach is very much "trial-and-error". Patients with IST are often intolerant to beta blockers. A new selective sinus node inhibitor ivabradine is also being used to treat IST.

Invasive treatments include forms of catheter ablation such as sinus node modification (selective ablation of the sinus node), complete sinus node ablation (with associated implantation of a permanent artificial pacemaker) and AV node ablation in very resistant cases (creation of iatrogenic complete heart block, necessitating implantation of a permanent artificial pacemaker).

However invasive treatments can also make the symptoms worse, not cure it. Treatment should be chosen with care as the patient could become in need of a pacemaker or have more extensive symptoms.

There are no specific diagnostic criteria for TIC, and it can be difficult to diagnose for a number of reasons. First, in patients presenting with both tachycardia and cardiomyopathy, it can be difficult to distinguish which is the causative agent. Additionally, it can occur in patients with or without underlying structural heart disease. Previously normal left ventricular ejection fraction or left ventricular systolic dysfunction out of proportion to a patient’s underlying cardiac disease can be important clues to possible TIC. The diagnosis of TIC is made after excluding other causes of cardiomyopathy and observing resolution of the left ventricular systolic dysfunction with treatment of the tachycardia.

Specific tests that can be used in the diagnosis and monitoring of TIC include:

- electrocardiography (EKG)

- Continuous cardiac rhythm monitoring (e.g. Holter monitor)

- echocardiography

- Radionuclide imaging

- Endomyocardial biopsy

- Cardiac magnetic resonance imaging (CMR)

- N-terminal pro-B-type natriuretic peptide (NT-pro BNP)

Cardiac rhythm monitors can be used to diagnose tachyarrhythmias. The most common modality used is an EKG. A continuous rhythm monitor such as a Holter monitor can be used to characterize the frequency of a tachyarrhythmia over a longer period of time. Additionally, some patients may not present to the clinical setting in an abnormal rhythm, and continuous rhythm monitor can be useful to determine if an arrhythmia is present over a longer duration of time.

To assess cardiac structure and function, echocardiography is the most commonly available and utilized modality. In addition to decreased left ventricular ejection fraction, studies indicate that patients with TIC may have a smaller left ventricular end-diastolic dimension compared to patients with idiopathic dilated cardiomyopathy. Radionuclide imaging can be used as a non-invasive test to detect myocardial ischemia. Cardiac MRI has also been used to evaluate patients with possible TIC. Late-gadolinium enhancement on cardiac MRI indicates the presence of fibrosis and scarring, and may be evidence of cardiomyopathy not due to tachycardia. A decline in serial NT-pro BNP with control of tachyarrhythmia indicates reversibility of the cardiomyopathy, which would also suggest TIC.

People with TIC display distinct changes in endomyocardial biopsies. TIC is associated with the infiltration of CD68 macrophages into the myocardium while CD3 T-cells are very rare. Furthermore, patients with TIC display significant fibrosis due to collagen deposition. The distribution of mitochondria has found to be altered as well, with an enrichment at the intercalated discs (EMID-sign).

TIC is likely underdiagnosed due to attribution of the tachyarrhythmia to the cardiomyopathy. Poor control of the tachyarrhythmia can result in worsening of heart failure symptoms and cardiomyopathy. Therefore, it is important to aggressively treat the tachyarrhythmia and monitor patients for resolution of left ventricular systolic dysfunction in cases of suspected TIC.

Treatment depends on the origin of the automatic tachycardia, however the mainstay of treatment is either antidysrhythmic medication or cardiac pacing. Specifically overdrive pacing may be used for all forms of automatic tachycardia; a pacemaker assumes control of the heart rhythm in overdrive pacing. In some cases ablation of the ectopic focus may be necessary.