Vasospastic angina with J waves formation in patients with sudden loss of consciousness.

Vasospastic angina is caused by sudden occlusive vasoconstriction of a segment of an epicardial artery, which can present with a wide spectrum of clinical scenario. We report the cases of two patients diagnosed with vasospastic angina, with one of which presenting with sudden cardiac arrest, while the other presenting with a relatively benign syncope. But both of them have J waves formation on ECG during active ischemia. The diagnosis and management of vasospastic angina, as well as the proposed clinical significance of J waves during coronary spasm are discussed.

Introduction

Vasospastic angina (VSA) is a form of angina caused by coronary artery spasm, which consists of a sudden occlusive vasoconstriction of a segment of an epicardial artery, resulting in a significant reduction of coronary blood flow.[1] J wave, or Osborn wave, is donated by a notch or slur at the terminal part of the QRS complex, which presents in a variety of clinical situations including ischemia.[2] We report two cases presenting with sudden loss of consciousness related to VSA and J waves formation.

Case Report

Case 1

A 57-year-old male rushed to emergency room (ER) with sudden rest retrosternal burning pain. During the encounter, he lost the consciousness with no carotid pulse palpated. Cardiopulmonary resuscitation was initiated immediately and electrocardiograph (ECG) showed ventricular fibrillation. He was successfully resuscitated after 5 min and then ECG revealed intraventricular block without J waves (Figure 1). Past medical history revealed atrial fibrillation managed by metoprolol and propafenone, and sick sinus syndrome on permanent pacemaker. A 30 pack-year smoking history was noted. But there was no significant past medical history, similar episode, or chest pain in the past. We couldn't get a baseline ECG before the encounter. Laboratory test, including troponin, creatine kinase-MB (CK-MB), total CK, and echocardiogram were unremarkable. Coronary angiography showed 20%–30% stenosis of the left main coronary artery (LMCA) and 70%–80% stenosis of the posterior descending coronary artery (Figure 2). Intravascular ultrasound revealed non-stenotic plaques in the middle portion of the anterior descending coronary artery (ADCA) and the LMCA (Figure 3). During the hospitalization, he had resting chest pain and then quickly went into sudden cardiac arrest again. The resuscitation lasted for 30 min, and was successful as before. ECG during chest pain showed ST segment elevation was noted in all V2–V5, aVR and aVL, with further II, III, aVF depression, as well as J waves in V2–V6 (Figure 4), followed by ventricular fibrillation. He was presumably diagnosed with VSA treated with IV diltiazem, followed by oral formulation and atorvastatin. Heavily counseling on smoking cessation was also performed. An implantable cardioverter-defibrillator (ICD) was implanted before discharge.

Figure 1.

ECG after resuscitation.

Figure 2.

Left (A) and right (B) coronary artery angiography.

Coronary angiography showed 20%–30% stenosis at the end point of left main coronary artery and 70%–80% stenosis at the beginning of the posterior descending coronary artery.

Figure 3.

Intravascular ultrasound revealed non-stenotic plaques in the middle portion of the anterior descending (A) and the left main coronary artery (B).

Figure 4.

ECG showed ST-segment elevation with J wave formation and QRS widening in V2-V6 leads, and ST-segment depression in II, II, aVF leads.

Arrows point to ischemic J waves.

Case 2

A 53-year-old male had a 2-year history of progressive rest throat and chest tightness in the morning. Each episode lasted for 3 min and resolved spontaneously. One day, he suddenly lost his consciousness for 2 min, then regained it spontaneously, and was taken to the ER. Personal history revealed a 60 pack-year smoking history. Baseline ECG (Figure 5) was unremarkable without J waves. Laboratory test showed no abnormalities except for mild hyperlipidemia. Echocardiogram failed to show any dysfunction. He was treated with aspirin, clopidogrel and rosuvastatin. He complained rest chest pain in the morning once during hospitalization. ECG showed widening QRS complex, ST segment elevation in I, aVL, V1-V6 leads, with J waves in these leads except V1 lead, and episodes of premature ventricular complex (Figure 6). The symptom also resolved spontaneously after a couple of minutes with resolution of ECG (Figure 7). Angiography demonstrated 25%–50% stenosis of the left ADCA, 70% stenosis of the left circumflex coronary artery, and 50% stenosis of the right coronary artery (Figure 8). VSA was diagnosed. He was also counseled extensively on stopping smoking and treated with diltiazem, isosorbide mononitrate and rosuvastatin.

Figure 5.

Baseline ECG.

Figure 6.

ECG showed ST-segment elevation in I, AVL, V1-V6 leads with J wave formation and QRS widening in these leads except V1 lead.

Arrows point to ischemic J waves.

Figure 7.

ECG after the resolution of resting chest pain shows.

Figure 8.

Left (A) and right (B) coronary artery angiography.

Coronary angiography showed 25%–50% stenosis of the left anterior descending coronary artery, 70% stenosis of the left circumflex coronary artery, and 50% stenosis of the right coronary artery.

Discussion

Coronary artery spasm is defined as a condition in which a relatively large coronary artery running on the surface of the heart transiently exhibits abnormal contraction. According to the 2013 Japanese Circulation Society Guideline, the diagnosis of vasospastic angina (VSA) can be made based on the documentation of transient ST-segment elevation during resting angina episodes and normal or non-obstructive plaques on coronary angiogram, without conducting a provocative test.[1] In our cases, patients both presented with rest chest pain and transient ST segment elevation with non-obstructive plaques on coronary angiogram. The ECG pattern during the attack indicates possible either multivessel, left main artery disease or proximal left anterior descending involvement.[3] However, the extent and degree of coronary obstruction during angiography cannot explain. Normal cardiac enzyme and echocardiogram make myocardial infarction and other structural heart disease unlikely. Therefore, the loss of consciousness is highly likely from coronary spasm.

In our cases, J waves with QRS widening in the anterolateral leads coincide with ST-segment elevation during coronary spasm. It is suggested that J-wave pattern recorded in inferolateral leads is a sign of underlying electrical vulnerability that increases the risk of life threatening ventricular arrhythmias (LTVA) under favorable pathological conditions,[4] and it is reasonable to hypothesize that it also applies when J-wave pattern with QRS widening appeared in the anterolateral leads under severe coronary spasm. But one of our patients presents with sudden cardiac arrest, while the other patient only has syncope, suggesting that J wave causing loss of consciousness and arrhythmias may represent a wide spectrum of risk. The differential diagnosis of J wave and proposed pathophysiology of J waves in LTVA development are discussed in supplemental file 1.

The mainstay treatment for VSA is calcium channel blockers. Smoking cessation is also mandatory. Concomitant nitrate and statin can also be used. But unlike atherosclerotic coronary artery disease, beta-blocker should be avoided and there is no evidence that aspirin is beneficial.[1] The role of ICDs in patients with VSA is not clear. It is suggested that history of out-of-hospital cardiac arrest (OHCA), smoking, angina at rest alone, significant organic stenosis, multivessel spasm, ST elevation and beta-blocker use are poor prognostic markers of VSA, with OHCA being the most important.[5] Our case one patient has five of them, and questionable multivessel disease, with risk of major adverse cardiac event at least 13.3%,[5] so ICD was implanted.

In conclusion, VSA can be diagnosed based on the documentation of transient ST-segment elevation during a resting angina episode. Ischemic J waves can occur in VSA and may indicate a warning sign for LTVA. The standard medical treatment for VSA is calcium channel blockers. An ICD could be considered in patients with high risk features. The clinical significance of J wave in VSA needs further investigations.