Prinzmetal’s angina

ECG 2A: This electrocardiogram recorded during pain shows sinus rhythm, left atrial enlargement and ST-segment elevation from V1 to V4 with minimal reciprocity in the inferior leads;

 ECG 2B: Recorded after administration of 2 puffs of sublingual nitroglycerine; this tracing shows a progressive decrease in the amplitude of the elevation concomitant with the resolution of thoracic pain;

ECG 2C: Tracing recorded in continuity of the previous ECG; disappearance of ST-segment elevation and inversion of T-waves;

Comments: This patient presented with Prinzmetal’s angina with evidence of a non-significant LAD stenosis with objectivation of a spasm induced by the injection of Methergin.

The changes in repolarization observed during a Prinzmetal’s angina attack are the result of a sudden ischemia generated by the coronary spasm.

Obtaining an electrocardiogram during pain is often difficult. Indeed, this pain is transient, resolving spontaneously within a few minutes or after administration of sublingual nitroglycerine. It is therefore difficult to capture the electrical abnormalities, since access to an electrocardiogram often requires much more time than the duration of the pain. In addition, some painful seizures may occur in the absence of electrocardiographic changes. Conversely, the recording of a long-term Holter-ECG makes it possible to demonstrate, in some patients, significant electrocardiographic changes (ST-segment elevation) in the absence of symptoms.

The inter-critical electrocardiogram of patients with Prinzmetal’s angina is usually normal or may show aspecific abnormalities of the ST-segment or of the T-wave (flat or negative T-waves in the same territory that show ST elevation during spasm).

During a painful episode, ischemia is often initially limited to subendocardial segments explaining the presence of large amplitude T-waves. The ischemia then becomes transmural for several minutes, a ST-segment elevation is thus observed after which the R wave increases in amplitude, the QRS-complex can expand, and the subepicardial lesion ultimately reaches its maximum amplitude. Possible conduction disorders or rhythm disturbances usually occur at the height of the spasm. When the spasm arises, the reperfusion phase may be accompanied by deep negative T-waves. A few minutes to a few hours after the attack, the tracing usually returns to normal or to its basal pattern.

Various abnormalities hence characterize the critical tracing of Prinzmetal’s angina:

1. The most characteristic electrocardiographic sign is the ephemeral subepicardial lesion, occurring during pain 1 to 5 minutes after the onset of the spasm. The elevation pattern of the ST-segment is remarkable for its height which has little equivalent in the initial phases of myocardial infarction. This elevation is convex upwards and may exceed 10 mm (15 mm in extreme forms) starting at the peak of the R wave, encompassing the T-wave and constituting a monophasic dome-shaped wave prolonged from 320 to 360 ms. The topography of the elevation is dependent on the coronary artery presenting the spasm. Occasionally, in the context of a multiple spasm of the right coronary artery and the LAD the territory with the elevation may alternate in the same patient between the inferior territory and the anterior territory. This subepicardial lesion current is associated with subendocardial ischemia and yields indirect images of deep ST-segment depression in the opposite leads. At the end of the spasm, at the time of ST-segment elevation resolution, a frequently deep negative T-wave often appears and can last from a few minutes to a few hours. The depth of the T-wave is dependent on the severity and duration of the previous ischemia.
2. Changes in the QRS-complex are commonly observed with an increase in amplitude of the R wave and a reduction or even disappearance of the S wave in the leads where the subepicardial lesion is maximal. Other transient changes have been described: widening of the QRS-complex, onset of a left anterior fascicular block or a right bundle branch block in the setting of a spasm of the proximal LAD.
3. A prolongation of the QT interval (may be accompanied by a negative U wave) and an increase in dispersion can be observed in a Prinzmetal’s angina attack. Similarly, an early repolarization pattern has been described with a possible negative prognostic impact and a related increased risk of ventricular rhythm disorders.
4. The sudden ischemia generated by the spasm favors the occurrence of both polymorphic rhythm and conduction disorders, often fleeting but may extend or deteriorate into ventricular torsades de pointes/ventricular fibrillation explaining the increased incidence of sudden death.

Take-home message: An elevation of significant amplitude is the characteristic electrocardiographic sign observed during a Prinzmetal’s angina attack. This elevation whose topography depends on the artery presenting the spasm, can begin at the peak of the R wave, encompass the T-wave and constitute a monophasic dome-shaped wave.