Spontaneous Coronary Artery Dissection (SCAD) and Takotsubo Syndrome (TTS) are two different entities with several shared risk factors, but their management is different. They can co-exist in patients with chest pain which affects their management. We present two cases of combined SCAD and TTS in patients presented with chest pain.
Case 1: 80F admitted with typical chest pain and dynamic ECG changes on the background of known anxiety/depression and social stresses. Her coronary angiogram showed SCAD affecting distal LAD. The left ventriculogram (LV gram) showed apical ballooning consistent with Takotsubo Syndrome (TTS). Patient was discharged on aspirin as well as angiotensin receptor blocker (ARB).
Case 2: 60F admitted with typical chest pain in the setting of emotional trauma on the background of known cardiovascular risk factors. She was found to have ST elevation in inferior leads with no reciprocal changes. Subsequently, coronary angiogram showed SCAD affecting mid-left anterior descending artery (LAD) with normal distal wrap around LAD. Her LV gram showed apical ballooning consistent with TTS. However, transthoracic echocardiogram showed akinetic left ventricular apex. She was discharged on aspirin as well as an ACE inhibitor and warfarin to prevent LV thrombus.
Spontaneous Coronary Artery Dissection (SCAD) is a rare cause of acute coronary syndrome with unknown incidence, whereas Takotsubo Syndrome (TTS) is a reversible apical ballooning syndrome. Both are associated with several physical, emotional and psychological risk factors. SCAD is managed with single or double antiplatelets therapy along with cardiovascular risk factor modifications, whereas TTS is a reversible cardiomyopathy. There are limited cases of combined SCAD and TTS in the literature and it is important to identify these cases as it may affect their ongoing management. We present two cases of combined SCAD and TTS with several shared risk factors.
An 80 years old female referred by general practitioner (GP) with typical chest pain and dynamic ECG changes. Patient reported chest pain while visiting a local doctor. She also reported being significantly stressed in last couple of months after her husband was diagnosed with cancer. She was known to have paroxysmal atrial fibrillation (pAF) causing syncope and required dual chamber permanent pacemaker (PPM) in the past. Her other comorbidities included long-term anxiety/depression, gastroesophageal reflux disease (GORD) and hypercholesterolemia. Her usual medications included sotalol and rosuvastatin. She had been a lifelong non-smoker and only drank alcohol socially. Her main cardiovascular risk factor was significant family history of cardiac disease.
On arrival to ED, she was hemodynamically stable with blood pressure of 130/70 and regular HR of 70 bpm. Her first ECG showed paced rhythm, left axis deviation (LAD), incomplete RBBB and deep TWI in anterolateral leads as shown in Fig. 1. Her T waves progressively deepened on later ECG as shown in Fig. 2.
She proceeded to have a coronary angiogram to rule out coronary obstruction. Coronary angiogram showed 2 pathologies including non-obstructive coronary artery disease affecting left and right coronaries and distal left anterior descending (LAD) type 2 Spontaneous Coronary Aartery Dissection (SCAD) as shown in Fig. 3. Patient had another coronary angiogram one year ago. The distal LAD was found to be normal on it. (Fig. 4). Left ventriculography (LV gram) on our angiogram showed apical ballooning consistent with Takotsubo Syndrome (TTS) as shown in Fig. 5. She further had transthoracic echocardiogram showing dilated LV and moderate segmental systolic dysfunction. LV appearance was consistent with Takotsubo cardiomyopathy.
Patient remained inpatient for 4 days. She remained hemodynamically stable and assessed by private psychiatrist to manage the anxiety and started on Oxazepam. She was discharged on aspirin 100 mg daily along with her usual medications including rosuvastatin 5 mg daily and sotalol 80 mg BD. She was also started on angiotensin receptor blocker (ARB) given mild left ventricular dysfunction. Her 6 months followup transthoracic echocardiogram (TTE) showed recovered LV function consistent with Takotsubo Syndrome.
She was taken to cardiac catheterization lab for coronary angiogram which showed normal right coronary artery (RCA) and mid-left anterior descending artery (LAD) had Spontaneous Coronary Artery Dissection (SCAD) with normal distal wrap around LAD as shown in Fig. 7. Her left ventriculography (LV gram) showed apical ballooning consistent with Takotsubo Syndrome as shown in Fig. 8. Post-coronary angiogram, her ECG showed TWI in anterior leads as shown in Fig. 9 and her transthoracic echocardiogram reported akinetic distal and apical segments which was consistent with LAD territory ischemia.
She had an uncomplicated admission and was discharged on aspirin 100 mg daily and atorvastatin 40 mg daily. She was also prescribed cardio-selective beta blocker and an ACE inhibitor for her LV dysfunction. Due to akinetic left ventricular apex, she was discharged on warfarin with bridging therapeutic clexane to prevent LV thrombus. Patient decided to be reviewed privately and lost the followup.
Management of both SCAD and TTS is different. Management of SCAD involves modification of cardiovascular risk factors with or without standard acute coronary syndrome (ACS) management. Cerrato et al. reported that dual antiplatelet therapy (DAPT) in the management of SCAD was independently associated with higher cardiovascular complication in comparison with single-agent antiplatelet therapy at 1 year [9]. However, TTS is considered as reversible cardiomyopathy and has a good prognosis. Hospital mortality associated with TTS is reported to be as low as 2% [3, 4].
The similarities between SCAD and TTS presentation and causes can lead to missing the diagnosis and future management altogether. Therefore, it is extremely important to look closely for any SCAD in patients with the findings of apical ballooning on LV gram as it might change the treatment goals. Additionally, since SCAD is associated with several medical conditions hence knowing its existence might help identify those medical problems.
Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit
In our SFIA Assessments in serveral organizations, we lacked a way to adequately represent the topic of Identity and Access Management. We find IAM partially in the SCAD, but this leads to a mixing of security operations and IAM, which can result in incorrect / incomplete reports and conclusions. We suggest an dedicated Identity and Access Management Skill. The skill could include tasks like:
I agree that we should split this out, with one skill for Security operations (SCAD) and a separate skill for Identify and access management. In some organisations these activities are done by the same people, but not all - so they need to be separated in SFIA.
I have had similar experiences with the lack of a dedicated IAM skill. Stakeholders have opted to add in 2-4 other skills to 'cover' what would be defined in a dedicated skill for IAM. In favour of this addition.
Spontaneous coronary artery dissection (SCAD) is an increasingly recognized cause of myocardial infarction (MI), particularly affecting young women. It is defined as a non-traumatic, non-iatrogenic, and non-atherosclerotic separation of the coronary arterial wall by intramural hematoma, resulting in a false lumen with or without intimal tear. Intramural hematoma can accumulate between any arterial layer (intima, media, or adventitia) and cause compression of the arterial lumen. In turn, this can compromise antegrade coronary perfusion and result in myocardial ischemia or infarction.1
SCAD was previously thought to be rare and frequently associated with pregnancy. However, under-diagnosis of SCAD and under-recognition of its angiographic variants made the prevalence difficult to estimate. SCAD primarily affects young to middle-aged women. In recent studies, women accounted for >90% of patients with SCAD.4-8 SCAD was the underlying cause in 22-43% of MI in women
The majority of patients with SCAD presents with MI. In CanSCAD, 69.9% had non-ST-segment elevation MI, and 29.7% had ST-segment elevation MI; the most common presenting symptom was chest discomfort (91.5%). A small proportion (8.1%) presented with more dramatic and life-threatening ventricular tachycardia or fibrillation.3 Less frequently, patients may present with cardiogenic shock (
Conditions that increase intracoronary shear stress, such as increase in thoracoabdominal pressure or catecholamines, may precipitate SCAD. The most common precipitating factor in the CanSCAD cohort was emotional stress, reported in 50.3% of patients (rated as high to severe stress). Another important stressor is intense physical stress, reported in 29%, with isometric activities lifting >50 lb in 10%.3 These have management implications because changes in lifestyle or psychological well-being may impact SCAD recurrence.
In terms of predisposing arteriopathy, fibromuscular dysplasia (FMD) is most commonly observed in patients with SCAD (co-prevalence reported from 52 to 86%). Non-coronary FMD can be diagnosed on catheter-based angiography of renal and iliac arteries during coronary angiographies or with computed tomography angiography.4,5,14 In CanSCAD, only 31% of patients had concomitant non-coronary FMD; however, this was underestimated because 45% of patients did not yet undergo any FMD screening or had incomplete screening. Non-coronary FMD can affect the renal, iliac, and cerebrovascular arteries. Other causes of SCAD were much less frequent, including peripartum SCAD in
c01484d022