CORONARY SUBCLAVIAN STEAL SYNDROME - WHEN LIFE BECOMES DEATH

Abstract

Therapeutic Area: ASCVD/CVD Risk Assessment Case Presentation: A 60-year old female with medical history notable for coronary artery disease (CAD) s/p CABG four years prior, peripheral artery disease (PAD) s/p carotid endarterectomy resulting in left vocal cord injury, three cerebrovascular accidents (CVA), poorly controlled diabetes, hypertension, dyslipidemia, continued nicotine use disorder, heart failure with reduced ejection fraction, and chronic obstructive pulmonary disease, was admitted for evaluation of multi territory CVA. During assessment, she was diagnosed with hemodynamically significant symptomatic stenosis of the left carotid artery secondary to dissection and underwent successful trans carotid artery revascularization.On the first postoperative day, a monomorphic wide complex tachycardia over 32 seconds (Figure 1) was documented. A resting electrocardiogram (EKG) showed sinus rhythm with ventricular complexes and possible premature atrial complexes with aberrant conduction, alongside nonspecific ST- segment changes (Figure 2). Transthoracic echocardiography indicated a left ventricular ejection fraction of 40-45%, with pronounced global hypokinesis, particularly affecting the septum and apex. Laboratory findings were notable for a magnesium level of 1.8 mg/dL and a troponin level peaking at 1.150 ng/mL. It was noted that she had undergone left heart catheterization (LHC) about 10 months prior to the current admission, and initially was managed for pulmonary edema and up trending troponin, with evidence of septal ischemia on Lexi scan at an outside facility. Considering the acute CVA, a decision was made for conservative medical management of her cardiac problems, and she was transferred to our facility for further management of CVA. However, due to the development of monomorphic sustained ventricular tachycardia, a repeat LHC was deemed necessary. This revealed severe native CAD including 90-95% ulcerative, calcified left main coronary artery (LMCA) stenosis with a patent SVG to obtuse marginal, occluded SVG to distal right coronary artery and a patent LIMA-LAD. Yet, due to subclavian steal syndrome, the LIMA was no longer supplying the LAD. Vascular surgery was reengaged to address the subclavian artery stenosis. In the event that intervention on the subclavian artery was not feasible, alternative measures such as Impella-assisted high-risk percutaneous coronary intervention (PCI) to the LMCA and LAD were discussed. Despite attempts at left upper extremity angiogram with stent placement, this intervention proved unsuccessful.Ultimately, the patient was discharged with plans for interval operative intervention on her subclavian artery. Background: The internal mammary artery (IMA) stands out as the primary conduit for myocardial revascularization during CABG, owing to its higher patency rate and associated survival benefit when anastomosed to a coronary artery compared to SVG's. Akin to the more commonly described phenomenon of subclavian-vertebral steal syndrome (SSS) which compromises neurological perfusion, exertion of the arm may lead to diversion of myocardial blood supply through retrograde flow up the IMA graft, to ensure perfusion to the upper extremity. This phenomenon, labeled coronary subclavian steal syndrome (CSSS) may happen in cases of significant stenosis or occlusion of the subclavian artery proximal to the ostia of the IMA. Symptoms may manifest ranging from angina up to acute coronary syndrome, acute heart failure exacerbation and malignant ventricular tachycardia, secondary to functional graft failure, despite disease-free graft. Our patient had LHC after her CABG, during which this phenomenon went unnoticed. Furthermore, there are documented reports of cyanosis of her arm, positive troponins, and pulmonary edema, which was not recognized to be secondary to CSSS. Screening for this condition is as simple as bilateral blood pressure measurement, with a blood pressure differential of >15-20 mmHg indicating the need for further investigation through advanced modalities. The prevalence of left subclavian artery stenosis (SAS) in patients with PAD and CAD requiring CABG has been reported to be 12 %, with up to 7% of these patients estimated to develop CSSS, a figure believed to have been increasing since initial reports. However, current guidelines have overlooked the importance of screening for potential SAS prior to and after CABG procedures. Conclusions: The presence of SAS in patients who have undergone CABG poses a serious risk to the myocardium supplied by the IMA conduit. Despite its significant impact on the mortality benefit offered by an IMA graft, SAS is often underestimated and overlooked. Current guidelines inadequately address this critical issue. It is essential for healthcare providers to increase their awareness and implement more rigorous screening protocols for SAS to effectively manage this potential complication.