Stress-induced cardiomyopathy (SICM) (Takotsubo and variants) and spontaneous coronary artery dissection (SCAD) are 2 unique entities that have gained increasing recognition over the last 2 decades. Recent studies have reported cases initially diagnosed with SICM and later found to have SCAD and deemed them as SCAD misdiagnosed as SICM. Apical ballooning has been observed in patients with SCAD and regional wall motion abnormalities that do not correspond to the territory affected by the SCAD, suggestive of the coexistence of SCAD and SICM.1 Several hypotheses for their coexistence have been proposed including the mechano-cardiac disruption hypothesis (acute mechano-cardiac coronary artery disruption).2 This hypothesis suggests that mechanical stress at the hinge point between the hyperkinetic and dyskinetic segments may induce coronary vascular injury resulting in SCAD.2 In this series, we present 6 patients who were found to have concomitant SICM and SCAD, with a visible hinge point in the same plane as the proximal segment of the SCAD (Figures 1 to 7).2
FIGURE 1. Concomitant SCAD of the Left Circumflex With Apical Ballooning.
A 53-year-old female presented after developing an episode of ventricular fibrillation while getting a blood draw. Return of spontaneous circulation was accomplished after cardiopulmonary resuscitation which included unsynchronized cardioversion and 3 doses of epinephrine. An ECG showed ST-segment elevation in leads II, III, and aVF, and troponin T was elevated at 587 ng/L. TTE revealed a LVEF of 24% with RWMAs involving the apical and midventricular segments suggestive of SICM (Video 1). (A, B) Left coronary angiography illustrating type 2 SCAD3 of 2 left circumflex obtuse marginal branches in RAO and LAO projections (blue arrows/circles). (C, D) Left coronary angiography in the RAO projection illustrating the hinge point between the hypocontractile and hypercontractile myocardium (blue line) and left ventriculography showing apical ballooning. Additional angiographic and follow-up details are summarized in Supplemental Table 1. ECG = electrocardiogram; LAO = left anterior oblique; LVEF = left ventricular ejection fraction; RAO = right anterior oblique; RWMA = regional wall motion abnormality; SCAD = spontaneous coronary artery dissection; SICM = stress-induced cardiomyopathy; TTE = transthoracic echocardiogram.
FIGURE 7. Schematic Representation of the 3 Types Of SCAD According to the Yip-Saw Classification3.
Abbreviation as in Figure 1.
The acute mechano-cardiac coronary artery disruption mechanism is currently a hypothesis. Ongoing investigations of this hypothesis include the use of intravascular imaging and computational fluid dynamic analyses in SCIM patients, as well as tissue-level examination of the watershed areas in SICM rat models. Additionally, future studies incorporating strain imaging, cardiac computed tomography, and magnetic resonance imaging are essential for further validation.
Supplementary Material
FIGURE 2. Concomitant SCAD of the Mid Left Anterior Descending Artery With Apical Ballooning.
A 49-year-old female presented with acute onset of chest pain and subsequently developed ventricular fibrillation. Immediate cardiopulmonary resuscitation was performed and ROSC was achieved. Post-ROSC ECG showed sinus rhythm with subtle ST-segment elevation in anterior precordial leads and marked ST-segment depression with T-wave inversion in inferior leads. Troponin T was elevated at 2.0 ng/mL. TTE revealed a severely reduced LVEF of 26% with RWMAs involving the midventricle and apex, with preserved basal function (Video 2), consistent with SICM. (A, C) Left coronary angiography illustrating type 2 SCAD3 of the mid left anterior descending artery (blue arrow/circle). (B, D) The hinge point between the hypocontractile and hypercontractile myocardium (blue line) in RAO projection and OCT displaying intramural hematoma of the mid to distal left anterior descending artery with intraluminal narrowing. (D) The true lumen is denoted by a blue star, and the false lumen by a yellow star. Additional angiographic and follow-up details are summarized in Supplemental Table 2. OCT = optical coherence tomography; ROSC = return of spontaneous circulation; other abbreviations as in Figure 1.
FIGURE 3. Concomitant SCAD of the Left Anterior Descending Artery With Apical Ballooning.
A 57-year-old female with no significant past medical history presented with severe chest pain of 6-hour duration. ECG revealed a left anterior fascicular block, and her troponin T was mildly elevated at 0.32 ng/dL. TTE (Video 3) demonstrated RWMAs involving the apical ventricular segment, and extending beyond a single epicardial vessel distribution, indicating the co-occurrence of SICM and SCAD. (A, B) Left coronary angiography illustrating type 2 SCAD3 of the large first diagonal branch of the left anterior descending artery (blue arrows/circle) and the hinge point between the hypocontractile and hypercontractile myocardium (blue line) in RAO projection. The hinge point is below the proximal margin of SCAD. The most likely mechanism is that the SCAD extended both distally and proximally. Additional angiographic and follow-up details are summarized in Supplemental Table 3. Abbreviations as in Figure 1.
FIGURE 4. Concomitant SCAD of the Left Anterior Descending Artery With Apical Ballooning.
A 61-year-old female with a history of chronic lymphocytic leukemia who had recently received a bone marrow transplant started complaining of sudden central chest pain radiating to the shoulders and back. ECG revealed ST-segment elevation in the anterior leads V1, V2, and V3 and troponin T was elevated at 1.9 ng/mL. The wall motion abnormalities depicted in the TTE (Video 4) demonstrate akinesis of the apical and mid segments of the left ventricle with a LVEF of 27%. (A, B) Left coronary angiography illustrating type 1 SCAD3 of the mid left anterior descending artery with no distal flow (blue arrows/circle) and the hinge point between the hypocontractile and hypercontractile myocardium (blue line) in RAO projection. Additional angiographic and follow-up details are summarized in Supplemental Table 4. Abbreviations as in Figure 1.
FIGURE 5. Concomitant SCAD of the Left Circumflex With Apical Ballooning.
A 61-year-old female admitted for the management of pyelonephritis, experienced sudden onset dyspnea and pulmonary edema on day 2 of the hospitalization. ECG showed sinus rhythm with ST-segment depressions in leads V3 through V6. A TTE revealed a LVEF of 35% with RWMAs involving the apex and mid ventricular segments. Echocardiogram (Video 5) further demonstrates the wall motion abnormalities consistent with the diagnosis of SICM. (A, B) Left coronary angiography illustrating type 3 SCAD3 of the posterolateral branch of the left circumflex (blue arrows/circle) and the hinge point between the hypocontractile and hypercontractile myocardium (blue line) in LAO projection. Additional angiographic and follow-up details are summarized in Supplemental Table 5. Abbreviations as in Figure 1.
FIGURE 6. Concomitant SCAD of the Left Circumflex With Apical Ballooning.
A 59-year-old female presented with a 3-day history of chest pain accompanied by diaphoresis. ECG showed significant T-wave inversions in the anterior leads and troponin T was elevated at 2 ng/mL. TTE (Video 6) revealed RWMAs involving the anterolateral and inferior segments consistent with SICM with a LVEF of 53%. (A, B) Left coronary angiography illustrating type 3 SCAD3 of the OM2 branch of the left circumflex (blue arrows/circle) and the hinge point between the hypocontractile and hypercontractile myocardium (blue line) in RAO projection. Additional angiographic and follow-up details are summarized in Supplemental Table 6. Abbreviations as in Figure 1.
APPENDIX
For supplemental videos and tables, please see the online version of this paper.
Footnotes
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FUNDING SUPPORT AND AUTHOR DISCLOSURES
The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
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