Prinzmetal angina: ECG changes and clinical considerations: a consensus paper

Abstract

Background: We will focus our attention in this article in the ECG changes of classical Prinzmetal angina that occur during occlusive proximal coronary spasm usually in patients with normal or noncritical coronary stenosis.

Results: The most important ECG change during a focal proximal coronary spasm is in around 50% of cases the appearance of peaked and symmetrical T wave that is followed, if the spasm persist, by progressive ST-segment elevation that last for a few minutes, and later progressively resolve. The most frequent ECG changes associated with ST-segment elevation are: (a) increased height of the R wave, (b) coincident S-wave diminution, (c) upsloping TQ in many cases, and (d) alternans of the elevated ST-segment and negative T wave deepness in 20% of cases. The presence of arrhythmias is very frequent during Prinzmetal angina crises, especially ventricular arrhythmias. The prevalence and importance of ventricular arrhythmias were related to: (a) duration of episodes, (b) degree of ST-segment elevation, (c) presence of ST-T wave alternans, and (d) the presence of >25% increase of the R wave.

Conclusions: The incidence of Prinzmetal angina is much lower then 50 years ago for many reasons including treatment with calcium channel blocks to treat hypertension and ischemia heart disease and the decrease of smoking habits.

Keywords: Prinzmethal angina; ST elevation; coronary spasm; electrocardiography.

Figure 1

(Case 1) Electrocardioram of variant type of angina pectoris. A, during spontaneous pain; note ST elevation in leads 2 and 3 and slight depression in lead 1. B, two minutes later pain disappeared and ECG reverted to normal. (Reproduced with permission from the American Journal of Medicine. [27:375‐388, 1959]

Figure 2

(A) Surface ECG of a 65‐year‐old patient with typical crisis of Prinzmetal angina that presents in the peak of pain an ST‐segment elevation like a transmembrane action potential (TAP). This case had a transitory complete proximal occlusion of the LAD above D1 (ST‐segment elevation from V₁ to V₆, I and VL with ST‐segment depression in inferior leads especially III and ventricular fibrillation). The lack of ST‐segment elevation in VR, the small ST‐segment elevation in V₁ and the clear ST‐segment elevation in V₆—if the placement of V₆ is well done—is against that the occlusion is also above S1. (B) ECG done several hours after the resolution of the crisis with a typical pattern of prominent negative T wave in all precordial leads (reperfusion pattern). (C) One week later, the ECG was normal, even with the recovery of rS morphology in V₁–V₂.

Figure 3

Crisis of coronary spasm (Prinzmetal angina) recorded by Holter ECG. (A) Control, (B) initial pattern of a very tall T wave (subendocardial ischemia), and (C) huge pattern of ST‐segment elevation. (D–F) Resolution toward normal values. Total duration of the crisis was 2 minutes.

Figure 4

See the appearance of ST‐elevation with angina at peak exercise test, followed by junctional rhythm due to AV block after the termination of the exercise, due presumably to coronary spasm of RCA proximal to the AV nodal branch. Coronary angiography shows an evident subocclusive stenosis at this place.

Figure 5

ECG morphology: sequential changes. (A) Without pain; (B and C) with pain; (D) release of pain Note that with pain there is pseudo‐normalization of negative T wave and appearance of negative U wave. (Taken from Bayés de Luna A. Clinical ECG. Wiley‐Blackwell, 2012.)

Figure 6

Relationship between the presence of ventricular arrhythmia and the duration of the attacks (< and >5 m) (A), the ST‐elevation isolated (≤ or ≥ 4 mm) (B), and in relation to the R Clinical ECG wave (C), the presence or not of ST_QT alternans (D), and the modification of the R Clinical ECG wave in relation to the basal R Clinical ECG wave (E). Each bar graph represents one characteristic of the crises. The calculations included all the attacks that showed that characteristics.

Figure 7

Holter recording of a patient with a severe crisis of Prinzmetal angina. Observe the presence of clear ST‐segment and TQ alternans together with some premature ventricular complexes (PVCs).

Figure 8

Patient with crises of Prinzmetal angina who presented during these crises with typical ST‐elevations pattern. During the resolution of pain (Holter method recording) the ST‐elevation disappeared within a few seconds, an along the resolution starts the appearance of negative T wave.

Figure 9

In the lower part, a crisis lasting 13 s. is shown. In the upper part the amplified onset at end of the run is recorded. See after the end of ventricular tachycardia just from the first sinus complex a very evident deep negative T wave of reperfusion, that last only several minutes.

Figure 10

From A to E sequence of changes during a crisis of coronary spasm. At the moment of highest ST‐elevation (E) short runs of VF appear very frequently.

Figure 11

A crisis of supraventricular tachycardia recorded crisis in two leads device. The crisis starts when the coronary spasm presents lower ST ascent than after the crisis (see arrow). In one channel the QRS during tachycardia is seen very narrow because there is not ST‐elevation in this lead, but in the other channel looks like a ventricular flutter because coincides with highest ST‐elevation expressed in this lead.