Arrhythmic Manifestation of Prinzmetal' Sangina Induced by Therapeutic Hypothermia
Abellás-Sequeiros RA*, Ocaranza-Sanchez R, García-Acuña JM and González-Juanatey JR
Department of Cardiology and Coronary Care Unit, University Clinical Hospital of Santiago de Compostela, Spain
*Corresponding author: Rosa Alba Abellás Sequeiros, Department of Cardiology and Coronary Care Unit, University Clinical Hospital of Santiago de Compostela, A Choupana s/n, CP 15706, Santiago de Compostela, A Coruña. Spain, E-mail: email@example.com
Int J Clin Cardiol, IJCC-2-048, (Volume 2, Issue 5), Case Report; ISSN: 2378-2951
Received: August 11, 2015 | Accepted: August 31, 2015 | Published: September 03, 2015
Citation: Abellás-Sequeiros RA, Ocaranza-Sanchez R, García-Acuña JM, González-Juanatey JR (2015) Arrhythmic Manifestation of Prinzmetal' Sangina Induced by Therapeutic Hypothermia. Int J Clin Cardiol 2:048. 10.23937/2378-2951/1410048
Copyright: © 2015 Abellás-Sequeiros RA, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Variant angina was first described by Prinzmetal et al.  like an episode of chest pain with transient ST-segment elevation. However, about 80% of patients course in an asymptomatic way . In other cases, syncopeor sudden cardiac death are the mainly manifestation.
We report the case of a 37-year-old Caucasian man, with prior history of smoking and DM. He had complained about multiple episodes of syncope during last year. However, the day of his hospitalization, he described a sudden and acute episode of chest pain which stopped him from sleeping. He arrived to the emergency department after 45 minutes of successful resuscitation, with VF as first cardiac rhythm detected. Admission ECG revealed sinusal rhythm with RBBB (Figure 1a) and two-dimensional echocardiogram showed a generalized hypokinetic myocardium with severe depression of LVSF. Haemogram and ionography blood tests were normal. Coronariography showed no significant lesions on epicardial coronary arteries (Figure 2a and Figure 2b). He fulfilled the entire criteria for therapeutic hypothermia. A rapid induction phase was followed by 24 hours at 32°C. During rewarming phase ECG showed transient ST-elevation followed by polymorphic ventricular tachycardia and VF (Figure 1b) and an episode of complete AV block (Figure 1c). The image of the bedside echocardiogram was not compatible with Takotsubo cardiomyopathy. This echo represent one of the main differential diagnosis in this case [3,4]. In fact, we could see a global myocardium hypokinesis with no segmentary defects in left ventricle contraction. These arrhythmic events and ST-T changes immediately disappeared after initiating parenteral nitroglycerine. Further treatment consisted in nitrates and calcium channel blockers, and an ICD was implanted to him. He was discharged after an uneventful hospital stay and, at that moment, the echocardiogram demonstrated the improvement of LVSF which was in normal range. Today, he keeps asymptomatic without electrical therapies of ICD.
Figure 1a: Control ECG
Figure 1b: ECG recordings with ventricular tachycardia during rewarming phase of hypothermia
Figure 1c: ECG recordings showing complete AV block View Figure 1
Figure 2a: Right coronary artery with no angiographically significant lesions
Figure 2b: Normal left coronary angiogram View Figure 2
Pathophysiology of variant angina remains unclear. 70% of patients have normal angiograms . Artery spasm could be the result of an inadequate tone in smooth muscle fibers of the vessels in addition to a dysfunctional endothelium . Tabaquism is a major precipitating factor of this entity , as free radicals generated by smoking can damage the endothelium and decrease NO levels. Ischemia is not always synonym of angina. In fact, 80% of patients with vasospastic angina are asymptomatic. Khisida et al.  showed 12% of patients course with history of syncope, which could be the clinical manifestation of malignant arrhythmic events, inadequate atrio-ventricular conduction, sinusal disfunction or asystolia. Provocation tests could be considered to prove coronary artery spasm (level of indication IIa C) . We decided not to perform them according to European guidelines  because of the high degree of accuracy of the diagnosis based on typical clinical presentation in a patient with acute ECG changes and no obstructive lesions on epicardial coronary arteries. Therapeutic hypothermia is worldwide used to avoid neurological damage after cardiac arrest. During rewarming phase, Firmin et al.  demonstrated an increased in catecholamine levels, which favored arterial spasm due to the activation of alfa receptors of the vessels. During induction phase of hypothermia , decreasing serum levels of magnesium are warranted with high risk of arterial spasm due to higher intracellular levels of calcium in smooth muscle fibers. Arterial spasm could be controlled by intravenous nitrates so we support hypothermia use as neurological benefits are higher than risks. According to EHRA expert consensus on ventricular arrhythmias  we inserted the patient an ICD. Matsue et al.  also suggested its use in patients with history of VT or VF and variant angina, who are in high risk of sudden cardiac death. Controversial discussion focused on patients without documented arrhythmic events, as there is a lack of evidence about ICD use in primary prevention. Nevertheless, we want to highlight medical treatment with drugs which induce vasodilatation as the cornerstone in management of patients with vasospastic angina. Medical treatment must be optimized and be continued after an ICD implantation.
Prinzmetal M, Kennamer R, Merliss R, Wada T, Bor N (1959) Angina pectoris. I. A variant form of angina pectoris; preliminary report. Am J Med 27: 375-388.
Kishida H, Tada Y, Fukuma N, Saitoh T, Kusama Y, et al. (1996) Significant characteristics of variant angina patients with associated syncope. Jpn Heart J 37: 317-326.
Katayama Y, Hifumi T, Inoue J, Koido Y (2013) A case of Takotsubo cardiomyopathy induced by accidental hypothermia and diabetic ketoacidosis. BMJ Case Rep 2013.
Davin L, Legrand V, Legrand D (2009) A frozen heart. Eur Heart J 30: 1827.
Yasue H, Kugiyama K (1997) Coronary spasm: clinical features and pathogenesis. Intern Med 36: 760-765.
Miwa K, Fujita M, Sasayama S (2005) Recent insights into the mechanisms, predisposing factors, and racial differences of coronary vasospasm. Heart Vessels 20: 1-7.
Sugiishi M, Takatsu F (1993) Cigarette smoking is a major risk factor for coronary spasm. Circulation 87: 76-79.
Task Force Members, Montalescot G, Sechtem U, Achenbach S, Andreotti F, et al. (2013) 2013 ESC guidelines on the management of stable coronary artery disease: the Task Force on the management of stable coronary artery disease of the European Society of Cardiology. Eur Heart J 34: 2949-3003.
Firmin RK, Bouloux P, Allen P, Lima RC, Lincoln JC (1985) Sympathoadrenal function during cardiac operations in infants with the technique of surface cooling, limited cardiopulmonary bypass, and circulatory arrest. J Thorac Cardiovasc Surg 90: 729-735.
Polderman KH, Herold I (2009) Therapeutic hypothermia and controlled normothermia in the intensive care unit: practical considerations, side effects, and cooling methods. Crit Care Med 37: 1101-1120.
Pedersen CT, Kay GN, Kalman J, Borggrefe M, Della-Bella P, et al. (2014) EHRA/HRS/APHRS expert consensus on ventricular arrhythmias. Heart Rhythm 11: e166-196.
Matsue Y, Suzuki M, Nishizaki M, Hojo R, Hashimoto Y, et al. (2012) Clinical implications of an implantable cardioverter-defibrillator in patients with vasospastic angina and lethal ventricular arrhythmia. J Am Coll Cardiol 60: 908-913.