Black Knight In Red Square

Introduction

Black Knight in Red Square, written by Stuart M Kaminsky and published in 1984, is a crime novel set in the Soviet Union. Amongst the foreign visitors in Moscow for a film festival are an American, two Soviet citizens and a Japanese. They are killed by poison in the restaurant of the Metropole Hotel. Inspector Porfiry Rostnikov is assigned to solve the case. The challenges for Rostnikov come both from the criminals and from dealing with the rivalries and suspicions within the USSR bureaucracy.

Kaminsky's series of novels featuring Rostnikov were noted for their ability to describe and evoke the 'feel' of Moscow and life in Russia as the Soviet era was coming to its end.

The title of this novel suggests a chess game. The initial moves of a chess game are called openings, many of which are well established and have their own names. Some named openings have twenty to twenty-five recommended moves.

The evaluation of chest pain is similar to the opening stages of a chess game: the history and examination findings, the ECG change and the results of blood tests are the opening variables. Some initial findings require a specific and rapid response; an example of this is ST elevation myocardial infarct (STEMI) (Figure 1).

Figure 1

This ECG of a 64 year old woman shows a STEMI: Q waves are present in leads I, aVL and V3 to V6; ST segment elevation is present in Leads I, aVL and V2 to V6.

Other ECG changes may be less obvious but the same underlying problem (pending or developing coronary artery occlusion) is the same as found in a STEMI. The early recognition of such"high risk" (STEMI) equivalents is important, as they also need the same focus on rapid re-perfusion. 

Clinical Case

The patient is a fit 72 year old man with no risk factors for coronary artery disease. He has never smoked and is not taking any medications. While he was paddle boarding he developed chest pain that radiated into his right arm. This persisted despite rest so he went to the Emergency Department. His blood pressure was 150/85 mm Hg and physical examination was normal. An ECG taken on arrival at 1727 (less than one hour after onset of pain) is shown in Figure 2.

Figure 2 - Initial ECG at 1727

The initial 12 lead ECG (Figure 2) shows sinus rhythm with a ventricular rate of about 60 beats per minute. Left axis deviation is present.

The findings in the frontal leads are:

  • Small Q waves in Leads I and aVL
  • Slight ST segment elevation in Lead aVL
  • Slight J point depression in Lead II, and horizontal ST segments in Leads III and aVF

The findings in the praecordial leads are:

  • The transition zone is in Lead V5 (which is another way of stating there is "poor R wave progression")
  • 1-2 mm J point elevation in Leads V2 to V4, with concave ST segments in these leads
  • Tall T waves in Leads V2 to V4
  • Lead V1 probably has a rS configuration, and there are Q waves in Leads V2 and V3.

Treatment was begun with intranasal oxygen, aspirin, glyceryl trinitrate (GTN) and morphine.

A second ECG was taken at 1811 and a third ECG at 1839 hours.

The changes in the praecordial leads in the first three ECGs is shown in Figure 3.

Figure 3 - Serial Changes in Praecordial Leads

The serial changes in the praecordial leads are:

  • The J point elevation seen in Leads V2 to V4 at 1724 is only seen in Lead V2 at 1811, and is absent at 1839.
  • Tall T waves are present in Leads V2 to V4 in all the tracings. The T waves are slightly asymmetric, with the ascending (concave) limb slightly longer than the descending limb.
  • The R wave in Lead V5 has disappeared in the ECG taken at 1839, and Q waves are now seen in Leads V2 to V4

The serum troponin I concentration at 1821 was elevated.

The patient was admitted under Cardiology with a diagnosis of non-ST elevation myocardial infarction.  

The results of serial blood tests are shown in Figure 4. 

Figure 4 - Blood Results

Abnormal results are in red. The initial (high sensitivity) serum troponin I concentration was 2109 ng/L (normal < 26 ng/L) at 2000 hours, and was 45586 ng/L at 0625 hours (before coronary angiography).

A coronary angiogram the next day (Figure 5) showed an occluded left anterior descending artery (LAD)..

Figure 5 - Coronary Angiogram Showing 99% Stenosis of the LAD

Take Home Points

The patient presented with chest pain on exertion, and the initial ECG (taken less than 1 hour after the onset of chest pain) showed:

  • Poor R wave progression, with a transition zone at Lead V5
  • Probable Q waves in Leads V2 and V3. A normal ECG can have a QS complex in Lead V2, but this should not be present in Lead V3.
  • 1- 2 mm J point elevation in Leads V2 to V4, which resolved within 70 minutes after arrival.
  • Tall T waves in Leads V2 to V4

Serial ECGs within the next 70 minutes showed 

  • Resolution of the J point elevation in Leads V2to V4
  • Loss of the R wave in Lead V4, with a new Q wave in lead V4

Other causes of J point and ST elevation in the praecordial leads are left ventricular hypertrophy, left bundle branch block, previous anterior myocardial infarction or early repolarization syndrome. None of these were present in this case.

Q waves are usually seen within 9 hours of the development of an acute myocardial infarct, but may also be seen within 1 hour of the onset of symptoms.

LESSON:

The presence of the above pattern of changes in Leads V2 to V4 in a person with chest pain indicates impending or acute occlusion of the LAD; the patient needs urgent coronary angiography.

The angiogram report included the following comment: "delayed presentation of anterior STEMI".

A more accurate comment would be "delayed angiogram in occlusion of the LAD with diagnostic ECG changes on the initial ECG".

 

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