Vol 8 | Issue 3 | September-December 2022 | Page: 09-11 | David Guz, Angela Johnson, Connor McNamara
DOI: 10.13107/jaccr.2022.v08i03.207
Author: David Guz [1], Angela Johnson [2], Connor McNamara [2]
[1] Detroit Medical Center/Wayne State University, Detroit, MI 48201.
[2] University Hospitals Cleveland Medical Center, 11100 Euclid Ave., Cleveland, OH 44106.
Address of Correspondence
Dr. David Guz,
Detroit Medical Center/Wayne State University, 3990 John R St., Detroit, MI 48201.
E-mail: DGuz@dmc.org
Abstract
We describe a patient with minimal cardiac risk factors who developed transient myocardial ischemia and complete heart block demonstrated on electrocardiography in the setting of recent esophagectomy likely caused by coronary vasospasm. The ischemic changes on ECG resolved within minutes following administration of glycopyrrolate, suggesting increased vagal tone leading to coronary vasospasm as a possible etiology. Coronary vasospasm is an uncommon cause of myocardial ischemia in the perioperative period. Anesthesiologists should be aware of coronary vasospasm as a clinical entity and its management when confronted with new-onset myocardial ischemia in the perioperative period. Written informed consent was obtained from patient prior to submission of this case report for publication.
Keywords: Coronary vasospasm, Esophagectomy, Major adverse cardiac event
Introduction
Coronary vasospasm is a rarely seen and unpredictable cause of myocardial ischemia, particularly in the setting of recent non-cardiac surgery. Patients experiencing this complication typically have no significant cardiac history, and are often assessed as low risk for development for major cardiac events on common risk stratification scores [1]. We present the first reported case of coronary vasospasm successfully treated with glycopyrrolate following Ivor-Lewis esophagectomy.
Case presentation
A 59-year-old female with a past medical history of esophageal adenocarcinoma (T3 N0 M0), bipolar disorder, alcohol and tobacco use disorder, and hyperlipidemia underwent Ivor-Lewis esophagectomy. Her pre-operative cardiac risk was deemed low based on an RCRI score of 1 (awarded for high-risk thoracic surgery) and lack of subjective functional limitation. Her last alcohol exposure was one week prior to surgery. Intraoperative course was significant for the development of mild subcutaneous emphysema of the right hemithorax. Metoprolol 5 mg IV Q 4 hours was initiated per institutional policy for atrial fibrillation prophylaxis. On postoperative (POD) day 1, patient experienced sudden lightheadedness and weakness following ambulation from bed to chair. Her blood pressure was 90/70, heart rate 30-40; complete heart block with junctional escape on telemetry (Figure 1). Transcutaneous pacer pads were applied. 12-lead ECG demonstrated ST elevation in inferior leads (II, III, AVF) and reciprocal ST depression in lateral leads with persisting complete heart block (Figure 2), at this time 0.4 mg of glycopyrrolate was administered with rapid resolution of hypotension and bradycardia. Repeat ECG following glycopyrrolate administration showed interval development of an accelerated junctional rhythm (Figure 3). Serial ECGs demonstrated spontaneous resolution of ST changes and AV block within 10 minutes of the initial event (Figure 4); and the patient also endorsed resolution of symptoms. Bedside transthoracic echocardiography following the event showed no structural defects, wall motion abnormalities or impaired cardiac function. Serial troponins were negative x3 and there was no overt electrolyte derangement at the time of the event. A cardiology consult was sought at this time; per cardiology recommendations patient was placed on a low-dose nitroglycerine infusion for one day with plans for elective left heart catheterization as an outpatient. There was no recurrence of symptoms or abnormalities noted on telemetry, and the patient denied having had similar symptoms in the past. She was discharged from the ICU to telemetry floor on POD 4, and discharged from the hospital on POD 8 with home isosorbide dinitrate, smoking cessation counseling and planned outpatient cardiology for possible left heart catheterization and evaluation for ICD placement, however patient was thereafter lost to followup with cardiology.
Discussion
Major adverse cardiac events (MACE) are responsible for significant morbidity and mortality in the perioperative period following noncardiac surgery, with incidences ranging up to 1 MACE event per 33 hospitalizations [2]. Several cardiac risk stratification models are currently used and have demonstrated efficacy in the prediction of MACE in most elective non-cardiac surgical patients [3]. Despite this, vasospasm has emerged as a possible cause of MACE in patients with low risk scores and relatively benign cardiac histories [1]. Vasospasm is considered a major cardiac event, and has been associated with cardiac arrest, myocardial infarction and the development of malignant arrhythmias [4]. Diagnostic criteria for “definite” vasospastic angina emphasize transient episodes of ischemic symptoms and ECG changes which are typically responsive to nitrates; particularly in the absence of other organic coronary artery disease [5]. Vasospasm may also be elicited utilizing provocative tests during angiography.There is a possible genetic propensity to the development of coronary vasospasm; increased incidence has been observed in the Japanese population [6, 7]. Cigarette smoking has been shown to be the only known preventable risk factor [8]. The predominant proposed mechanisms for the development of vasospasm include smooth muscular hyperreactivity and increased vagal tone [9] Episodes are commonly provoked by certain triggers which include: recent stimulant use, alcohol withdrawal, magnesium deficiency, nonselective beta-blockade and hyperventilation [10, 11]. There is a low threshold for diagnostic coronary angiography to exclude significant fixed coronary obstruction [12]. Current management emphasizes avoidance of triggers and smoking cessation [13]. Acute episodes may be treated with nitrates [14] and then prevented with low-dose calcium channel blockade [15]. Patients who have experienced cardiac arrest or unstable arrhythmia attributed to coronary vasospasm may benefit from placement of an implantable cardioverter-defibrillator [16]. In the setting of recent esophagectomy new onset atrial fibrillation is not uncommon, and has been associated with significant surgical morbidity and mortality [17]. Many institutions (including ours) include prophylactic metoprolol as part of a post-esophagectomy protocol; however, evidence regarding the efficacy and risks of this practice are limited.The etiology in our patient is multifactorial; her history of tobacco use, recent alcohol cessation and hyperactive vagal tone related to surgical dissection were likely contributing factors. Owing to its disinhibitory effects on the SA and AV nodes, glycopyrrolate has been widely used for years in the prevention and treatment of bradycardia [18]. Given the efficacy of our patient’s reaction to the administration of the anti-muscarinic drug glycopyrrolate, it is possible that vagal hyperreactivity may have played a role. This is the first reported case of coronary vasospasm after esophagectomy; additionally, we successfully utilized glycopyrrolate in treatment of the complete atrioventricular block secondary to coronary vasospasm.
References
(1) Nagayoshi Y, Kawano H, Kojima S., et al. Significance of Coronary Vasospasm in the Periopera-tive Management of Non-Cardiac Surgery. Circ J. 2012; 76(8):1965-1971. doi:10.1253/circj.cj-11-1278
(2) Smilowitz NR, Gupta N, Ramakrishna H, Guo Y, Berger JS, Bangalore S. Perioperative Major Ad-verse Cardiovascular and Cerebrovascular Events Associated With Noncardiac Surgery. JAMA Cardiol. 2017; 2(2):181-187. doi:10.1001/jamacardio.2016.4792
(3) Ford MK. Systematic Review: Prediction of Perioperative Cardiac Complications and Mortality by the Revised Cardiac Risk Index. Ann Intern Med. 2010; 152(1):26-35. doi:10.7326/0003-4819-152-1-201001050-00007
(4) Ahn J-M, Lee KH, Yoo S-Y. et al. Prognosis of Variant Angina Manifesting as Aborted Sudden Cardiac Death. J Am Coll Cardiol. 2016; 68(2):137-145.
(5) Beltrame JF, Crea F, Kaski JC. et al. International standardization of diagnostic criteria for vaso-spastic angina. Eur Heart J. 2015; 38(33):2565-2568. doi:10.1093/eurheartj/ehv351
(6) Suzuki S, Yoshimura M, Nakayama M et al. A novel genetic marker for coronary spasm in women from a genome-wide single nucleotide polymorphism analysis. Pharmacogenet Genomics. 2007; 17(11):919-30.
(7) Kusama Y, Kodani E, Nakagomi A et al. Variant angina and coronary artery vasospasm: the clinical spectrum, pathophysiology, and management. J Nippon Med Sch.. 2011; 78(1):4-12.
(8) Takaoka K, Yoshimura M, Ogawa H. et al. Comparison of the risk factors for coronary artery spasm with those for organic stenosis in a Japanese population: role of cigarette smoking. Int J Cardiol. 2000; 72(2):121-126. doi:10.1016/s0167-5273(99)00172-2
(9) Yasue H, Horio Y, Nakamura N. et al. Induction of coronary artery spasm by acetylcholine in pa-tients with variant angina: possible role of the parasympathetic nervous system in the pathogenesis of coronary artery spasm. Circulation. 1986; 74(5):955-963. doi:10.1161/01.cir.74.5.955
(10) Stern S, Bayes de Luna A. Coronary Artery Spasm. Circulation. 2009; 119(18):2531-2534. doi:10.1161/CIRCULATIONAHA.108.843474
(11) Satake K, Lee J-D, Shimizu H, Ueda T, Nakamura T. Relation Between Severity of Magnesium Deficiency and Frequency of Anginal Attacks in Men With Variant Angina. J Am Coll Cardiol. 1996; 28(4):897-902. doi:10.1016/s0735-1097(96)00256-2
(12) Montalescot G, Sechtem U, Achenbach S. 2013 ESC guidelines on the management of stable coronary artery disease. Eur Heart J. 2013; 34(38):2949-3003. doi:10.1093/eurheartj/eht296
(13) Miwa K, Fujita M, Miyagi Y. Beneficial effects of smoking cessation on the short-term prog-nosis for variant angina — validation of the smoking status by urinary cotinine measurements. Int J Cardiol. 1994; 44(2):151-156. doi:10.1016/0167-5273(94)90019-1
(14) Hom GA, Brent BN. Coronary artery vasospasm during treatment with intravenous nitroglyc-erin. Cathet Cardiovasc Diagn. 1985; 11(4):423-426. doi:10.1002/ccd.1810110412
(15) Hung M-J, Hu P, Hung M-Y. Coronary Artery Spasm: Review and Update. Int J Med Sci. 2014; 11(11):1161-1171. doi:10.7150/ijms.9623
(16) Matsue Y, Suzuki M, Nishizaki M, Hojo R, Hashimoto Y, Sakurada H. Clinical Implications of an Implantable Cardioverter-Defibrillator in Patients With Vasospastic Angina and Lethal Ventricu-lar Arrhythmia. J Am Coll Cardiol. 2012; 60(10):908-913. doi:10.1016/j.jacc.2012.03.070
(17) Stawicki SP, Prosciak MP, Gerlach AT. Atrial fibrillation after esophagectomy: an indicator of postoperative morbidity. Gen Thorac Cardiovasc Surg. 2011; 59(6):399-405. doi:10.1007/s11748-010-0713-9
(18) Kongsrud F, Sponheim S. A comparison of atropine and glycopyrrolate in anesthetic practice. Acta Anesthesiol Scand. 1982; 26(6):620-5.
| How to Cite this Article: Guz D, Johnson A, McNamara C | Coronary Vasospasm with Complete Heart Block Following Ivor-Lewis Esophagectomy Treated with Glycopyrrolate: A Case Report | Journal of Anaesthesia and Critical Care Case Reports | September-December 2022; 8(3): 09-11. |