Variant Angina Induced Life-Threatening Ventricular Arrhythmias : Does Dual Calcium Channel Blocker Eliminates the Indication for Implantable Cardioverter Defibrillator ?

C l i n M e d International Library Citation: Matar M, Chammas E, Nasr S (2016) Variant Angina Induced Life-Threatening Ventricular Arrhythmias: Does Dual Calcium Channel Blocker Eliminates the Indication for Implantable Cardioverter Defibrillator?. Clin Med Rev Case Rep 3:111 Received: May 09, 2016: Accepted: June 22, 2016: Published: June 24, 2016 Copyright: © 2016 Matar M, 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 Induced Life-Threatening Ventricular Arrhythmias: Does Dual Calcium Channel Blocker Eliminates the Indication for Implantable Cardioverter Defibrillator?


Introduction
Variant angina (Prinzmetal's angina, periodic angina) is characterized by episodic recurrent chest pain that usually occurs spontaneously and is accompanied by transient ST-segment elevation.The prognosis of variant angina is usually excellent in patients who receive medical therapy.However, a prolonged vasospasm may result in complications such as myocardial infarction (MI), high degree atrio-ventricular (AV) block, life-threatening ventricular tachycardia/ fibrillation (VT/VF), or sudden cardiac death (SCD) [1,2] challenging therefore the treatment that can range from simple calcium channel blockers with or without concomitant nitrate therapy [3] to dual calcium channel blockers of different classes [4] and ultimately to implantable cardioverter defibrillator (ICD) or pacemaker installation to prevent SCD and life-threatening arrhythmias.
The current guidelines [5] are silent with respect to use of an ICD in patients with coronary artery vasospasm.Although the results of the report of Matsue et al. [6] support the use of ICD therapy in patients with coronary artery vasospasm who have survived an episode of life-threatening VT/VF.We report a case of coronary artery spasm induced long QT with ICD terminated recurrent ventricular fibrillation, that resolved once a second calcium channel blocker was added to the treatment.coronary artery spasm, and our interventional cardiologist did not performed a stimulation test since the procedure will be risky for the patient.
Transthoracic echocardiography showed preserved left ventricular ejection fraction.Considered to have an episode of variant angina and an ICD was implanted in October 2010 for secondary prevention of ventricular tachyarrhythmia (Figure 7, Figure 8 and Figure 9).In front of the recurrent ventricular fibrillation, her medical treatment was optimized to include a combination of calcium channel blocker: amlodipine 10 mg once daily and diltiazem 300 mg once daily Since then (November 2010) no more ventricular arrhythmias occurred (Figure 10).

Discussion
So we were in front of a case of coronary artery spasm induced long QT with ICD terminated recurrent ventricular fibrillation that resolved once a second calcium channel blocker was added to the treatment.Coronary spasm-induced Ischemia by itself can cause ventricular fibrillation, and in all case we have to prevent and treat ischemia.It is important though to identify the mechanism of ventricular fibrillation; if it is due to QT prolongation, then special care should be taken to avoid all drugs that prolong QT and this will be of great importance.QT prolongation may be primary or in response to myocardial ischemia.If it is due to ischemia, then the longest QT should be present in EKG recorded at time of chest pain.This was true in our patient, where the EKG of figure 2 and figure 9, recorded at time of chest pain and showing signs of ischemia, revealed the longest QT ( 498 ms and 505 ms respectively).
The prognosis of variant angina is usually excellent but eventually MI, ventricular arrhythmias and SCD may occur.Yasue et al. [7] reported an 89% to 97% overall 5-year survival rate in a 7-year follow-up in approximately 300 patients, with 3.6 % incidence of SCD and 6.5 % incidence of MI [7].Induced ischemia may result in transient AV block or ventricular arrhythmias imposing the need for pacemaker or defibrillator respectively [4].
Sudden death and ventricular tachyarrhythmias have been well documented in patients with variant angina [8].
Previous studies demonstrated a difference between variant angina patients who die suddenly and those with uncomplicated   variant angina or other sudden death patients, and found some factors leading to this difference and permitting risk-stratification of patients and thus to important therapeutic implications [9].Miller et al. [9] and Kerin et al. [10] concluded that the degree of ischemia during attacks and therefore the degree of ST elevation was an important factor characterizing variant angina patients with serious arrhythmias and higher risk for SCD during spontaneous attacks from other variant angina patients.Other factors predicting SCD may include Severe multivessel spasm, daytime ST-segment changes, and younger age [11].
Another important factor reported in studies was the increased QTc dispersion in asymptomatic patients with variant angina reflecting a greater inhomogeneity of ventricular refractoriness, imposing a higher risk of life-threatening arrhythmias [12][13][14].An increased endogenous adenosine may be the mediator of this ventricular repolarization disparity [15].Thus, if the attacks of coronary vasospasm that provoke life threatening arrhythmias can be eliminated, sudden death should not occur, raising the importance of calcium antagonists that may resolve vasospastic episodes [16,17].
Diltiazem was associated with a decrease in angina episodes and nitroglycerin consumption, as well as reduction in ST segment deviation [18][19][20][21].Thus, it is not surprising that diltiazem would reduce the cardiovascular event rate by reducing angina frequency as was shown by the results of Schroeder et al. [18].Clinical guidelines do not recommend the implantation of an ICD because the variant angina induced arrhythmia are secondary to an acute ischemia that may be controlled by medical therapy [22].This issue can be corroborated by the finding that relapses and inefficient ICD treatments was most likely related to insufficient medical treatment and extensive ischemia [23].Observational trials of patients with coronary artery vasospasm who are receiving medical treatment with calcium antagonists report an annual cardiac arrest or sudden cardiac death risk of approximately 0.6% per year [24].
The results of Matsue et al. [6], although it has some limitations, support the use of ICD therapy in coronary artery vasospasm that survived a life threatening VT/VF.Matthijs L. Hendriks et al. indicates that a combination of calcium blocking agents and ICD implantation isthe most appropriate option, for variant angina-induced potential lethal arrhythmias [25].Our case that responded well to the combination of calcium channel blocker with cessation of the arrhythmia occurrence, leads us to re-evaluate the indication for ICD implantation if this dual therapy may abort the appearance of those life-threatening arrhythmias.Thus, It is necessary to carry out studies that evaluate the indication criteria for ICD as secondary prevention of potentially lethal arrhythmias due to coronary vasospasm [22].

Figure 4 :
Figure 4: Cardiac catheterization was done and did not reveal any significant stenosis.

Figure 5 :
Figure 5: Cardiac catheterization was done and did not reveal any significant stenosis.

Figure 6 :
Figure 6: Cardiac catheterization was done and did not reveal any significant stenosis.

Figure 7 :
Figure 7: In November 2010, she experienced an episode of chest pain and presented for evaluation.ICD records showed a recurrent ventricular fibrillation that was successfully terminated.

Figure 8 :
Figure 8: In November 2010, she experienced an episode of chest pain and presented for evaluation.ICD records showed a recurrent ventricular fibrillation that was successfully terminated.

Figure 9 :
Figure 9: EKG at that time showed long QTc (505 ms), Q wave and T wave inversion in leads III, aVF.