Life‐threatening arrhythmias leading to syncope in patients with vasospastic angina

Figures

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  Fig. 1. Dominant presenting symptom in patients without chest pain among those admitted to hospital with acute coronary syndromes [5].

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  Fig. 2. Diagnostic flowchart in patients with syncope (Japanese and Asian version) *Diagnostic ECG features suggestive of structural heart disease, Brugada syndrome, long-QT syndrome and vasospastic angina **The main examinations for the diagnosis of structural diseases and tachycardia or bradycardia. CHF, congestive heart failure; FH, family history; SCD, sudden cardiac death; ECG, electrocardiogram; UCG, ultrasonic echocardiography; CT, computed tomography; OH, orthostatic hypotension; ILR, implantable loop recorder; EPS, electrophysiological study; AMI, acute myocardial infarction; PH, pulmonary hypertension; VHD, valvular heart disease; HCM, hypertrophic cardiomyopathy; VT, ventricular tachycardia; VF, ventricular fibrillation; SSS, sick sinus syndrome; AVB, atrioventricular block; TWA, T-wave alternans; CAG, coronary arteriography; ACh, acetylcholine; HUT, head-up tilt; CSM, carotid sinus massage; NMS, neutrally mediated syncope; OMI, old myocardial infarction; DCM, dilated cardiomyopathy; LQTS, long-QT syndrome; ER: early repolarization.

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  Fig. 3. (A) ECG monitoring of a representative case during a vasospastic attack. Rapid polymorphic ventricular tachycardia (VT), which spontaneously reverted to atrial fibrillation, was recorded in the evening. Moreover, ischemic ST-segment elevation (arrow) was transiently observed in the same lead after the spontaneous termination of VT. (B) Coronary angiogram (CAG) in the right anterior oblique projection at baseline in the right coronary artery (RCA), after injection of acetylcholine (ACh) in the left coronary artery (LCA), and after injection of isosorbide dinitrate (ISDN) in both, in the same patient. Spontaneous and induced coronary artery spasms were seen in the mid-portions of the RCA and LCA, respectively.

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  Fig. 4. Coronary angiogram (CAG) and electrocardiogram (ECG) during acetylcholine (ACh) provocation test (left panel), and surface ECG and intracardiac electrograms during programmed ventricular stimulation (right upper panel), in a typical case with multivessel coronary spasm [20]. Subtotal occlusion in the mid-portion of the left anterior descending artery (LAD) and total occlusion in the distal portion of the right coronary artery (RCA) were induced by ACh. During programmed stimulation of the right ventricular apex (RVA), as the coupling interval was reduced from to 220 ms, rapid polymorphic ventricular tachycardia (VT) was induced reproducibly. After injection of isosorbide dinitrate (ISDN), only 2 ventricular responses were induced by the same mode of stimulation. The right lower panel shows changes in the ventricular response to programmed stimulation at baseline and after administration of ISDN in 14 patients. RVR, repetitive ventricular response [20].

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  Fig. 5. Patient with multiple vasospasm and macroscopic T-wave alternans (TWA) [24]. Upper panel: Coronary angiogram (CAG) at baseline and after intracoronary injection of acetylcholine (ACh). The ACh provocation test induced coronary spasm in the proximal portion of the left anterior descending (LAD) and left circumflex (LCx) coronary arteries. Diffuse coronary spasm in the right coronary artery (RCA) was also provoked by ACh injection. Lower panel: Record of ambulatory Holter monitoring of the patient during the asymptomatic phase. The patient had neither chest pain nor ST-segment elevation at the time of monitoring, but macroscopic spontaneous TWA was clearly visible on channel CM5. The maximum TWA was 78 μV. HR, heart rate; LAO, left anterior oblique; RAO, right anterior oblique; CCB, calcium channel blockers.

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  Fig. 6. Left panel: Incidence of positive T-wave alternans (TWA) in the vasospastic angina (VSA) group and control group. The black column indicates the number of patients with positive TWA and the white columns represent those with negative TWA [24]. Right panel: Maximum values of modified moving average (MMA)-TWA in patients with and without non-sustained ventricular tachycardia (NSVT). Bars indicate standard deviations and boxes indicate mean values [24].

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  Fig. 7. Kaplan–Meier survival curves for ventricular fibrillation (VF) among vasospastic angina (VSA) patients with and without day-to-day variation of early repolarization (ER) [28]. Patients with day-to-day variation in their ER pattern had a lower cumulative survival rate after VF than those without.

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  Fig. 8. A series of 12-lead ECG tracings and an intracardiac electrogram from a representative case with recurrence of ventricular fibrillation (VF) during the follow-up period [28]. (A) Twelve-lead ECG recorded 13 h after the first VF episode. Early repolarization (ER) patterns in the lateral leads are visible. (B) ECG without ER pattern 3 days after the first VF episode. (C) ECG with ER pattern 1 month before VF recurrence. (D) ECG with ER pattern after VF recurrence. (E) Intracardiac electrogram from the ICD during VF recurrence. An ICD shock successfully terminated VF.

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  Fig. 9. ECGs and coronary angiogram (CAG) from a case who developed polymorphic VT (PVT) during an acetylcholine (ACh) provocation test and ventricular fibrillation (VF) during the follow-up period. A 53-year-old man without a past history of VF or syncope experienced recurring chest pain episodes [29]. Despite taking a calcium channel blocker, he lost consciousness and was transferred to the hospital. On arrival, a J wave was observed in leads aVL and V6 (baseline). CAG showed no stenotic lesion at baseline, but diffuse coronary vasoconstriction was provoked in 3 vessels (ACh provocation in the top right corner) by ACh injection. At the same time, augmentation of ST elevation and a new J wave were observed in leads I, II, aVF, and V6, followed by the development of pulseless PVT (bottom left). Coronary vasoconstriction was relieved by isosorbide dinitrate (ISDN) injection (middle right corner). VF occurred during the follow-up period, even though the patient was taking vasodilator drugs and calcium channel blockers (bottom right). T-wave alternans (TWA) was positive at baseline (77 μV) and during the follow-up period (73 μV). Right coronary angiograms during the ACh provocation test and…

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  Fig. 10. Possible mechanism of syncope and sudden cardiac death (SCD) in patients with vasospastic angina (VSA). TWA, T-wave alternans; ER, early repolarization; EPS, electrophysiological study; AF, atrial fibrillation, PVC, premature ventricular contraction.

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  Fig. 11. Upper panel: Induction of spasm in both left and right coronary arteries by intracoronary injection of acetylcholine (ACh) in a representative case with vasospastic angina (VSA) and lethal arrhythmia [30]. (A) The left coronary artery (LCA) was normal at baseline. (B) A spasm provocation test was conducted with ACh, and severe diffuse spasm was provoked in the left anterior descending (LAD) and left circumflex (LCx) arteries. The intracoronary injection of ACh was subsequently performed for the right coronary artery (RCA), after it was confirmed that the stenotic lesions of the LCA had resolved spontaneously. (D) The RCA was shown to be normal at baseline, but (E) severe vasospasm was provoked by intracoronary injection of ACh. (C, F) After injection of isosorbide dinitrate (ISDN), all 3 vessels were released from spasm. Lower panel: Stored intracardiac ICD electrogram obtained during an arrhythmic episode in the same patient during the follow-up period [30]. Ventricular fibrillation (VF) was terminated successfully by ICD shock (arrow).