Premature ventricular contraction

Premature ventricular contraction
Other names	Premature ventricular complex, ventricular premature contraction (complex or complexes) (VPC), ventricular premature beat (VPB), ventricular extrasystole (VES)
EKG, marked by the arrow
Specialty	Cardiology

A premature ventricular contraction (PVC) is a common event where the heartbeat is initiated by Purkinje fibers in the ventricles rather than by the sinoatrial node. PVCs may cause no symptoms or may be perceived as a "skipped beat" or felt as palpitations in the chest. PVCs do not usually pose any danger.^[1]

The electrical events of the heart detected by the

is therefore recommended in people with frequent PVCs.

If PVCs are frequent or troublesome, medication (beta blockers or certain calcium channel blockers) may be used. Very frequent PVCs in people with dilated cardiomyopathy may be treated with radiofrequency ablation.^[2][1]

Signs and symptoms

Although there are many possible symptoms associated with PVCs, PVCs may also have no symptoms at all. PVCs may be perceived as a skipped heart beat, a strong beat,

Premature ventricular contractions may be associated with underlying heart disease, and certain characteristics are therefore elicited routinely: the presence of signs of heart disease or a known history of heart disease (e.g. previous

Causes

Premature ventricular contractions occur in healthy persons of any age, but are more prevalent in the elderly and in men.^[3] In a very significant proportion of people they occur spontaneously with no known cause.^{[citation needed]}

Some possible underlying causes of PVCs include:

Non-cardiac causes

• Adrenaline excess
• Anemia^[4]
• Catecholamine excess
• Certain medicines such as tricyclic antidepressants,^[3] digoxin, sympathomimetics, aminophylline^[5]
• Chemical (electrolyte) abnormalities in the blood
  hypomagnesaemia
  (magnesium deficiency)).
• Contact with the carina (trachea/bronchi) when performing medical suctioning stimulates vagus nerve
• Drugs/substances such as:^[3]
  • Amphetamines^[5]
  • Alcohol^[8]
  • Caffeine^[9]
  • Cocaine
  • Nicotine
  • Theobromine^{[10][unreliable medical source?]}
• Hypercapnia (CO₂ poisoning)^[3]
• Hypertension (high blood pressure)^[11]
• Hyperthyroidism^[4]
• High blood calcium^[3]
• Hypoxia^[3] and/or hypercapnia^[5]
• exhaustion^[12]
• Sarcoidosis^[13]
• Smoking
• Stress^[12]
• Anxiety^[4]

Cardiac causes

• Any structural heart disease which alters
  electrical conduction pathways
  due to tissue alterations
• Cardiomyopathy, hypertrophic or dilated^[3]
• Myocardial infarction^[14]
• Myocarditis^[3]
• Myocardial contusion^[3]
• Mitral valve prolapse^[3]

Pathophysiology

This section needs additional citations for verification. Please help improve this article by adding citations to reliable sources in this section. Unsourced material may be challenged and removed. (May 2018) (Learn how and when to remove this template message)

left ventricle

. Ectopic foci can be located anywhere in the ventricles in the case of PVCs.

Normally, impulses pass through both ventricles almost at the same time and the depolarization waves of the two ventricles partially cancel each other out in the ECG. However, when a PVC occurs the impulse nearly always travels through only one bundle fiber, so there is no neutralization effect; this results in the high voltage QRS wave in the electrocardiograph.

There are three main physiological explanations for premature ventricular contractions: enhanced ectopic nodal automaticity, re-entry signaling, and toxic/reperfusion triggered.

Ectopic enhanced nodal automaticity suggests foci of sub-pulmonic valvular pacemaker cells that have a subthreshold potential for firing. The basic rhythm of the heart raises these cells to threshold, which precipitates an ectopic beat. This process is the underlying mechanism for arrhythmias due to excess catecholamines and some electrolyte deficiencies, particularly low blood potassium, known as hypokalemia.

Reentry occurs when an area of 1-way block in the

and a second area of slow conduction are present. This condition is frequently seen in patients with underlying heart disease that creates areas of differential conduction and recovery due to myocardial scarring or ischemia. During ventricular activation, one bundle tract's area of slow conduction activates the other tract's bundle fibers post block after the rest of the ventricle has recovered. This resulting in an extra beat. Reentry can produce single ectopic beats, or it can trigger paroxysmal tachycardia.

Triggered beats are considered to be due to after-depolarizations triggered by the preceding action potential. These are often seen in patients with ventricular arrhythmias due to digoxin toxicity and reperfusion therapy after myocardial infarction (MI).

This ectopy of the ventricles when associated with a structurally normal heart most commonly occurs from the

Molecular basis

There are a number of different molecular explanations for PVCs.

• calcium excess: One explanation is most basically due to an increased amount of
  cyclic AMP
  (cAMP) in the muscle cells of the heart's ventricles leading to increased flow of calcium ions into the cell. This may happen for the following reasons:

• Activation of the sympathetic nervous system, due to anxiety and/or physiological stress, for example
  amphetamines and cocaine
  will also cause this effect.
• Phosphodiesterase inhibitors such as caffeine directly affect the G-coupled signal transduction cascade^[18] by inhibiting the enzyme that catalyzes the breakdown of cAMP,^[15] again leading to the increased concentration of calcium ions in the cytosol.

• potassium deficiency:
  Hypercalcemia
  has a similar effect, although clinically it is of less concern.
• magnesium deficiency:
  Low blood magnesium
  therefore also makes spontaneous depolarization more likely.
• myocardium damage: Existing damage to the myocardium can also provoke PVCs. The
  cytokines
  , which can affect the electrical properties of myocytes and may be ultimately responsible for causing irritability of myocytes.

Diagnosis

EKG

PVCs may be found incidentally on cardiac tests such as a 12-lead

]

On electrocardiography (ECG or Holter) premature ventricular contractions have a specific appearance of the QRS complexes and T waves, which are different from normal readings. By definition, a PVC occurs earlier than the regular normally conducted beat. Subsequently, the time between the PVC and the next normal beat is longer as the result of a compensatory pause.[19] PVCs can be distinguished from premature atrial contractions because the compensatory pause is longer following premature ventricular contractions, in addition to a difference in QRS appearance.^[20]

In some people, PVCs occur in a predictable pattern. Two PVCs in a row are called doublets and three PVCs in a rows are triplets. Depending whether there are one, two, or three normal (sinus) beats between each PVC, the rhythm is called bigeminy, trigeminy, or quadrigeminy. If 3 or more consecutive PVCs occur in a row it may be called ventricular tachycardia.^[20] The precise shape of the QRS can give an indication as to where precisely in the heart muscle the abnormal electrical activity arises. If someone has PVCs that all have the same appearance, they are considered "monofocal", if PVC’s have different appearance, they are considerevole “multifocal”.^[2]

Treatment

Isolated PVCs with benign characteristics and no underlying heart disease require no treatment, especially if there are limited symptoms.^[2]

The most effective treatment is the elimination of triggers (particularly stopping the use of substances such as caffeine and certain drugs, like tobacco).^[21] If frequent, it’s possible to use:

• Medications
  • moricizine increased the death rate when used with diuretics, it reduced the frequency of deaths when it was used alone.^[23]
  • Beta blockers: do not directly affect or reduce the occurrence of PVCs, but reduce cardiac contractility which makes PVCs less obvious to a person; possibly reduce catecholamine induced PVCs (in catecholamine-sensitive people) due to adrenaline not reaching sinus node as much.^[14]
  • Calcium channel blockers^[14]
• Electrolytes replacement
  • Magnesium supplements (e.g. magnesium citrate, orotate, Maalox, etc.)
  • Potassium supplements (e.g. chloride potassium with citrate ion)
• tachyarrhythmia or very frequent PVC (>20% in 24 h) and normal ventricular function.^[24] This procedure is a way to destroy the area of the heart tissue that is causing the irregular contractions characteristic of PVCs using radio frequency energy.^[7]
• Implantable cardioverter-defibrillator^[22]
• Lifestyle modification
  • Frequently stressed individuals should consider therapy, or joining a support group.

Prognosis

PVCs are harmless, but frequent PVCs may increase the risk of developing cardiomyopathy, which can greatly impair heart function. On a more serious and severe scale, very frequent PVCs can accompany underlying heart disease.^[25]

People who do not have heart disease (with ejection fractions greater than 40%) have the same long-term prognoses as the minority of people without PVCs on the 24 hours. Emerging data also suggest that 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. For patients with underlying chronic structural heart disease and complex ectopy, mortality is significantly increased.^[3]

In meta-analysis of 11 studies, people with frequent PVCs (≥ once during a standard electrocardiographic recording or ≥30 times over a 1-hour recording) had risk of cardiac death twice as great as that of participants with occasional PVCs. Although most researchers attempted to exclude high-risk subjects, such as those with histories of cardiovascular disease, they did not test participants for underlying structural heart disease.^[26]

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 established by echocardiography, cardiac magnetic resonance imaging in 63 persons and Holter monitoring.^[27]

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.^[22] It was study of 70 people followed by 6.5 years on average. Healthy status was verified by extensive noninvasive cardiologic examination, although cardiac catheterization of a subgroup disclosed serious coronary artery disease in 19%. Overall survival was better than expected.^[28]

On the other hand, the

In the

In the Niigata study of 63,386 people with a 10-year follow-up period, subjects with PVC during a 10-second recording had triple the risk of atrial fibrillation of those without PVCs, independently of these risk factors: age; male sex; high simple body mass index (a possible signifier of obesity); hypertension (systolic and diastolic blood pressure within certain abnormal limits); and diabetes.^[34]

Reducing very frequent PVC (>20%) by antiarrhythmic drugs or by catheter ablation significantly improves heart performance.^[22][24]

Recent studies have shown that those subjects with extremely frequent 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 regresses.^[24][35]

Epidemiology

Single PVCs are common in healthy persons. When 24-hour ambulatory monitoring is used, up to 80 percent of apparently healthy people have occasional PVCs.

References

Further reading

• Levy, Matthew N.; Pappano, Achilles J. (2007). Cardiovascular physiology. Mosby physiology monograph series (9th ed.). Philadelphia: Mosby Elsevier.
  OCLC 63660993
  .
• Nelson, David L.; Cox, Michael M. (2008). "Biosignaling". Lehninger Principles of Biochemistry (5th ed.). New York: W.H. Freeman. pp. 419–484.
  OCLC 957377043
  – via Google Books.

External links