QR in V6 in WPW Conduction

Report:

Sinus rhythm 70/min

Left axis deviation –50o

Wolff-Parkinson-White conduction, type' A'

Comment:

The δ waves are relatively subtle and the computer reported "old inferior Mr' and "probable posterior wall involvement". This is a well-known masquerade with WPW conduction. Either type' A' or 'B' can produce inferior Q waves, usually QS complexes; only 'A', of course, can mimic posterior infarcts.

The unusual feature here is the qR morphology in lead V6; there is probably a small - invisible - primary R wave, part of the δ wave, present in what appears to be the PR interval. It can be verified by drawing a straight line down from the QRS onset in V4.

The PR interval may be normal in WPW conduction and indeed tends to get longer with age, but in most cases this is an illusion - either terminal P wave or the initial δ wave is isoelectric. The degree of preexcitation is quite variable: the tracing below (Fig 72a) had δ waves large enough for even the computer to recognise! The q wave in V6 disappeared. An example of AF with relatively slow response due to flecainide is shown in Fig 72b.

Next (Fig 72c) is a trace of a different patient that created considerable controversy until he developed SVT with narrow(er) complexes (not shown), after his AAA wound dehisced. He was a healthy 61 year old with no cardiac history. Of course, AAA is itself a marker of coronary disease. He was thought to have an old inferoposterolateral MI, even with normal Persantin thallium stress test. Interestingly, the Q wave is much larger in the SVEB near the end of the tracing.

Some call this variety of WPW type C, but I do not know much about it.

Fig 72a. More obvious WPW ‘A’.

Fig 72b. In AF, the complexes tend to be either completely normal or completely “pre-excited”. However, a few intermediate morphologies are usually present.

Fig 72c. Both q and Q waves are rare in WPW’s lead V6.

Fig 73. 81 year old in CCU with chest pain and history of remote myocardial infarction.