sadgual receives salaleah
Algernon Alcala
Poor R-wave progression (PRWP) is a common ECG finding that occurs when the expected normal increase in R-wave amplitude does not appear in successive 12-lead precordial leads. Although studies show that PRWP is frequently reported by both cardiologists and computer-aided ECG interpretations, its significance is questionable, and faulty ECG lead placement likely contributes substantially to ECG misdiagnosis, unnecessary testing, and extraneous health costs.
The term PRWP arose as cardiologists attempted to describe the absence of the typical precordial R-wave height increase from V2 to V3 and the expectation of an R-wave height of at least 3 mm in V3. Definitions vary from study to study and likely from one computerized ECG analysis system to another. More recent studies use multiple criteria and typically exclude ECGs with features of LVH. The GE Marquette computerized ECG analysis system excludes LVH and uses either of the following combinations:
Some studies have also included reverse R-wave progression as a type of PRWP. Reverse R-wave progression is characterized by decreasing R-wave amplitude such that the R wave in lead V4 is smaller than the R wave in V3, or the R wave in V3 is smaller than the R wave in V2, or the R wave in V2 is smaller than the R wave in V1 (or any combination of these), provided that the R-wave amplitude in V3 was 3 mm or less.
A study published in the American Heart Journal looked at the value of several ECG criteria for the diagnosis of AMI using SPECT scintigraphy as the gold standard in a population undergoing clinical stress testing. Depending on the PRWP criteria utilized, the prevalence of PRWP was 15% to 42%. Prevalence of scintigraphy-confirmed AMI in those displaying PRWP ranged from 2% to 9% depending on the criteria.4
A study in the Journal of Electrocardiology examined the technical and constitutional factors contributing to PRWP in normal subjects. The authors identified 100 individuals at the time of a normal cardiac catheterization and found that eight of them had PRWP that was not related to any of the factors measured, including age, sex, BSA, blood pressure, and thoracic skeletal abnormalities. They prospectively analyzed the effect of precordial lead misplacement and respiratory variation in 68 hospitalized patients and were able to create false positive PRWP by superior displacement from the proper precordial lead position.5
A study in the Journal of Clinical Practice found that precordial leads V1 and V2 were often placed in the second intercostal space by physicians. The correct position of V1 in the fourth right intercostal space was identified by 90% of ECG technicians and 49% of nurses but only 31% of non-cardiologist physicians. Unexpectedly, cardiologists did most poorly, positioning the electrode properly only 16% of the time.6
Luckily, another study in the Journal of Electrocardiology demonstrated that poor lead placement could be corrected. One-hundred staff members, including doctors, nurses, and ECG technicians, were chosen at random to place sticker dots on a mannequin for assessment. Prior to an educational intervention, only 34% of lead placements across the three groups were correct, with the best performance coming from ECG technicians, who achieved perfect lead placement 55% of the time. The most common error was placement of leads V1 and V2 superiorly, an error known to create PRWP. Following an educational intervention, the proportion that achieved correct placement of any lead rose significantly, from 34% to 83%.7
False positive diagnoses of AMI based on PRWP from faulty lead placement can lead to unnecessary testing, including stress testing and cardiac catheterizations. In addition to the adverse consequences of such downstream testing, ECG misdiagnosis can also result in additional costs to the healthcare system.
The same above-mentioned article published in Cureus that estimated the incidence of PRWP also analyzed these costs. Researchers retrospectively analyzed 9,424 ECGs with AMI, LVH, LAFB, and LBBB. Ventricular pacing and low voltage were excluded, as these are known to cause PRWP, leaving 6,808 ECGs for analysis.
Of those ECGs, 7.3% met criteria for PRWP, and in 10.8% of cases, precordial lead misplacement was suspected, creating an abnormal pattern suggestive of myocardial infarction and raising suspicion of CAD. Projecting the downstream testing for CAD assessment, the authors estimated the cost to the Centers for Medicare & Medicaid Services of ECG lead mispositioning at $3.2 billion.
Given that PRWP has little or no clinical significance and can easily be created by common errors in ECG lead placement, ECG readers are probably best served by eliminating this term from their reporting vocabulary. If reading cardiologists do not eliminate the computer-generated qualifier, "cannot rule out AMI," when PRWP is present, they may generate more harm than good with their interpretations, adding to healthcare costs, anxiety in the worried well, and the potential adverse consequences of downstream testing.
The opinions, beliefs, and viewpoints expressed in this article are solely those of the author and do not necessarily reflect the opinions, beliefs, and viewpoints of GE Healthcare. The author is a paid consultant for GE Healthcare and was compensated for creation of this article.
Impression: extensive non-acute infarct pattern, corresponding with one month of CHF symptoms. Global hypokinesis on echo with EF 25%. Cardiac MR diagnosed amyloid, which classically presents with Afib, low voltage and pseudo-infarct pattern.
Impression: LVH can produce chronic poor R wave progression and lateral T wave inversion, but here the poor R wave progression is from acute loss of R waves accompanied by new ST elevation and greater T wave inversion. So this is LVH plus occlusion MI. Cath lab activated: 95% LAD occlusion, Trop I rose from 1,800 to 9,000.
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Poor R-wave progression is a common ECG finding that is often inconclusively interpreted as suggestive, but not diagnostic, of anterior myocardial infarction (AMI). Recent studies have shown that poor R-wave progression has the following four distinct major causes: AMI, left ventricular hypertrophy, right ventricular hypertrophy, and a variant of normal with diminished anterior forces. Standard ECG criteria that identify and distinguish these causes have been developed. An interpretive approach to the ECG with poor R-wave progression is presented that has clinical relevance in the daily treatment of patients.
Poor R wave progression is a non-specific finding that is suggestive of prior anterior myocardial infarction. It is a poorly defined term that implies diminished amplitude of the R wave in the precordium. It has been defined as an R wave less than 3 mm in lead V3 or decreasing R wave amplitude from V2 to V3 or V3 to V4. Poor R wave progression has been implicated in left ventricular hypertrophy, right ventricular hypertrophy and can be a normal variant.
In other words, In lead V1, the R wave should be small. The R wave becomes larger throughout the precordial leads, to the point where the R wave is larger than the S wave in lead V4. The S wave then becomes quite small in lead V6.
Slow or poor R wave progression (PRWP) is said to be present when the R wave height does not become progressively taller from leads V1 to V3 or V4, or even remains at low amplitude across the entire precordium.
Could you please comment on poor R-wave progression seen on an ECG? I know that it is often a nonspecific finding more commonly seen in women than in men, but is it also increasingly common in athletic women?
"Poor R-wave progression (PRWP)" is a potentially problematic term. Although it is most commonly used to describe delay in the progressive increase of R-wave amplitude that is usually seen as one moves across the precordial leads, consensus is lacking even among expert electrocardiographers as to what PRWP really entails. Would deep QS complexes in leads V1 through V3 qualify as "PRWP" if a dominant R wave is then seen in lead V4? Or must the R wave remain nondominant throughout all 6 of the precordial leads, or only through 4 or 5 of the precordial leads? Can there be small R waves in leads V1, V2, V3, and/or V4, or must there be Q waves or QS complexes in these leads? And must the QRS complex be narrow?
Despite the above ambiguities in definition, perhaps the most problematic aspect inherent with use of the term "PRWP" is the diversity of potential entities that may be the cause of this ECG finding. How clinically useful can a term be when it may be caused by such diverse pathology as either left or right ventricular hypertrophy and/or pulmonary disease, myocardial infarction, conduction defects of various types, cardiomyopathy, and chest wall deformity? Or instead, it can simply reflect a normal variant or a spurious finding due to lead misplacement.
I am not aware of any predilection for PRWP among female athletes. If one exists, I would imagine body habitus would be a stronger predisposing factor than athletic prowess or female sex. Although there may still be utility for some as a descriptive term, it should be appreciated that PRWP clearly means different things to different ECG interpreters, and that there is no reliable diagnostic benefit to this term given its poor predictive value for any condition.
Rather than using PRWP, I prefer noting the zone of "transition," which indicates between which 2 leads the R wave evolves from less than to greater than the height of the S wave. Normally, transition occurs somewhere between leads V2 through V4. If there is no R wave at all in anterior precordial leads, I state this directly in my interpretation, as diagnostic implications of prior infarction are clearly much greater than if very small but still present R waves are seen in these same leads. Use of PRWP would not provide any clue to this difference.