Premature ventricular contraction natural history, complications and prognosis
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Premature ventricular contraction Microchapters |
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Differentiating Premature Ventricular Contraction from other Disorders |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mugilan Poongkunran M.B.B.S [2] Radwa AbdElHaras Mohamed AbouZaied, M.B.B.S[3]
Overview
Premature ventricular contraction caries no risk of mortality in the absence of any underlying heart disease. Heart rate turbulence is a phenomenon representing the return to equilibrium of the heart rate after a PVC. These parameters correlate significantly with mortality after myocardial infarction.
Natural History, Complications and Prognosis
- In the absence of ischemic heart disease (CAD) or hypertension (HTN), there is no excess risk of mortality in patients with PVCs.
- On the other hand, PVCs in the presence of structural cardiac abnormalities or hypertension is associated with twice the expected mortality.
- The development of sustained ventricular tachycardia (VT) is most likely among those patients with greater than 12 PVCs/min, couplets, and multifocal PVCs.
- Complex ventricular ectopic activity (VEA) during acute phase of STEMI does not have any prognostic significance.
- Their presence 2 to 3 weeks after acute MI is associated with a 3 fold increase in the risk of sudden death.
- Healthy patients
- The most common arrhythmia in patients with and without CAD.
- Less common in infants and children, more common in the elderly.
- Usually originate from the RV.
- In normal patients, they may be either precipitated or suppressed by exercise.
- No relationship to coffee or smoking has been established.
- Frequency decreases with sleep.
- Coronary artery disease
- Routine ECGs demonstrate PVCs in 10% of patients with CAD.
- Incidence inreases to 60 to 88% when the monitoring is increased to 12 to 24 hours.
- The frequency of complex VEA increases with increasing numbers of vessels involved. (40% with one, 53% with two, and 78% with three vessels involved has VEA).
- Patients with CAD are more prone to develop VEA with exercise (incidence 4 times higher than age matched controls).
- Reported incidence in acute MI varies, but is near 100%.
- After the initial 6 hours, the frequency decreases.
- Persistence of VEA is associated with larger infarct size.
- In one study, patients with EFs of greater than 50% had no persistent VEA, and patients with EFs of less than 30% had frequent PVCs.
- Other Organic Heart Diseases:
- Occur on routine EKG in 1/3rd of patients.
- 12% of patients with congested cardiomyopathy have PVC on routine tracings.
- 1.6% of patients with IHSS have PVCs on routine EKG.
- Drugs:
- PVCs are the most common arrhythmia in patients with digoxin toxicity.
- Other drugs that cause PVCs are quinidine, PCA, norpace, phenothiazines and tricyclic antidepressants.
- Electrolyte Imbalance:
- Hypokalemia, hypomagnesemia, and hypercalcemia are frequently associated with the appearance of ventricular arrhythmias.[1] [2]
Overview
There is insufficient evidence to recommend routine screening for [disease/malignancy].
OR
According to the [guideline name], screening for [disease name] is not recommended.
OR
According to the [guideline name], screening for [disease name] by [test 1] is recommended every [duration] among patients with [condition 1], [condition 2], and [condition 3].
Screening
There is insufficient evidence to recommend routine screening for [disease/malignancy].
OR
According to the [guideline name], screening for [disease name] is not recommended.
OR
According to the [guideline name], screening for [disease name] by [test 1] is recommended every [duration] among patients with:
- [Condition 1]
- [Condition 2]
- [Condition 3]