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Table of Contents
ECG DIAGNOSIS
Year : 2022  |  Volume : 10  |  Issue : 3  |  Page : 213-215

Salvo of Ventricular Premature Complexes in Ischemic Heart Disease


Department of General Medicine, Government Medical College and Hospital, Chandigarh, India

Date of Submission27-Aug-2021
Date of Acceptance14-Dec-2021
Date of Web Publication12-Jul-2022

Correspondence Address:
Dr. Gautam Jesrani
Department of General Medicine, Level-4, D-Block, Government Medical College and Hospital, Sector 32, Chandigarh - 160 030
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ajim.ajim_93_21

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  Abstract 


Nonsustained ventricular tachycardia can be observed in various cardiac conditions, which can be benign or life-threatening, and is commonly encountered in patients with underlying structural heart disease. Hemodynamic instability in this rhythm abnormality is uncommon, but emergency management is warranted for unstable patients to mitigate dire consequences.

Keywords: Ischemic heart disease, nonsustained ventricular tachycardia, ventricular couplets, ventricular premature complex


How to cite this article:
Jesrani G, Gupta S, Bhardwaj A, Gupta H. Salvo of Ventricular Premature Complexes in Ischemic Heart Disease. APIK J Int Med 2022;10:213-5

How to cite this URL:
Jesrani G, Gupta S, Bhardwaj A, Gupta H. Salvo of Ventricular Premature Complexes in Ischemic Heart Disease. APIK J Int Med [serial online] 2022 [cited 2022 Sep 26];10:213-5. Available from: https://www.ajim.in/text.asp?2022/10/3/213/350754




  Brief Patient History Top


A 65-year-old man was brought to our emergency department in an unconscious state for 1-h duration. He had a preexisting history of diabetes mellitus for the past 10 years and hypertension for the past 12 years, and his family members confirmed that the patient was complaining of chest discomfort 2 h before the onset of unconsciousness. On presentation, radial pulse was irregular with low volume, blood pressure was 70 mm Hg systolic, and capillary blood glucose was 110 mg/dl. Electrocardiogram (ECG) in this patient demonstrated ventricular couplets (wide QRS complex), followed by nonsustained ventricular tachycardia (NSVT) with short coupling interval and sinus beats in-between [Figure 1] and [Figure 2]. Before any procedure, his qualitative Troponin-T test was done, which came out to be positive. In view of hemodynamic instability and poor sensorium, the patient was subjected to the synchronized electrical cardioversion but failed thrice. Meanwhile, his arterial blood gas analysis depicted lactic acidosis (3.1 mmol/L) with a potassium level of 3.8 mg/dl, ionized calcium of 4.7 mg/dl (Normal 4.3–5.5), and oxygen saturation of 88%. He was intubated immediately and shifted to the intensive care unit, where echocardiography was performed and demonstrated left ventricular anterior wall hypokinesia with ejection fraction of 32% and trivial mitral regurgitation. Vasopressor (dobutamine) and reperfusion therapy in the form of two doses of 18 mg reteplase intravenously over 30 min' duration was instituted, but was not successful in achieving a stable cardiac rhythm. Hence, percutaneous intervention and temporary pacemaker insertion were planned, but the patient developed sustained ventricular tachycardia (VT). Intravenous amiodarone 300 mg in two divided doses was instituted instantly and a standard infusion was continued afterward, but unfortunately, the patient developed asystole. A total of five cycles of cardiopulmonary resuscitation were performed, but the patient could not be revived and succumbed to his illness.
Figure 1: Initial electrocardiogram demonstrating ventricular premature complexes, forming couplets (yellow stars), ventricular tachycardia (red stars), and sinus beats in between (black stars)

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Figure 2: Enlarged initial electrocardiogram demonstrating close T and subsequent R wave (a), short coupling interval (b), and atrioventricular dissociation (inverted P wave) due to ventricular premature complexes (orange arrows in part c)

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  Discussion Top


The ECG of this case demonstrated ventricular couplets and NSVT due to acute ischemic heart disease (IHD) possibly. Ventricular couplets term is used for two consecutive ventricular ectopic beats with wide QRS complex (>120 msec), and three or more such constitute beats with a RR interval of <600 msec denote VT.[1] Further, VT can be nonsustained, if the duration of this abnormal ventricular rhythm is <30 sec, and sustained, if the duration is more than this period.[2]

The “Salvo” phrase is used for three successive ventricular discharges and was initially described by Lown et al.[3] Besides these findings, the ECG also depicted sinus beats in between with a short coupling interval [Figure 2]. This brief interval leads to R on T phenomenon, which is the superimposition of R wave of the next QRS on T wave of the previous cycle and can progress to sustained VT.[4] Moreover, the configuration of the premature ventricular beat can reveal the emergence location as the right-sided VPCs have left bundle branch block, and the left sided has right bundle branch block morphology in the ECG.

The diagnosis of NSVT by ECG is not as laborious as the etiology identification and runs of polymorphic or monomorphic ventricular premature complexes (VPCs) can be observed in the rhythm strip. Multiple etiologies for NSVT have been demonstrated, and IHD is one paramount cause in adults with age >40 years.[1] Other than this, various cardiomyopathies, hypertension, obstructive sleep apnea, and valvular heart disease-like causes have been stated in this age group.[1] For the age group <40 years, Brugada syndrome inherited channelopathies, catecholaminergic polymorphic VT, cardiomyopathies, and latent hypertension should be considered.[1]

Hemodynamic status of the patient decides the initial step of the management and underlying etiology identification is foremost in the definitive treatment. For unstable patients, synchronized electrical cardioversion is the first measure, which can lead to rhythm stability and buys time for the management of the underlying cause.[5] Revascularization therapy, either percutaneous intervention or thrombolytic drugs, remains the cornerstone in the management of rhythm abnormalities due to IHD.[5]

In stable patients, β-blockers are used for VPCs suppression, which has been associated with survival benefits and sudden cardiac death prevention.[5] Lidocaine and amiodarone are other anti-arrhythmic drugs used for this purpose, but recently, amiodarone is considered superior to lidocaine in short- and long-term mortality prevention.[5] In addition, overdrive pacing can be used if all of these measures fail, and implantable cardioverter defibrillator and radiofrequency ablation-like modalities may be used postacute event termination.[5]

Declaration of patient consent

A written consent is present, duly signed by the son of the patient. The authors obtained the consent after explaining that no identity will be revealed and the case information, including pictures will be used for education purpose only. He was also explained that journal publication will not contain any material or picture, disclosing the patient's identity.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Katritsis DG, Zareba W, Camm AJ. Nonsustained ventricular tachycardia. J Am Coll Cardiol 2012;60:1993-2004.  Back to cited text no. 1
    
2.
Zipes DP, Camm AJ, Borggrefe M, Buxton AE, Chaitman B, Fromer M, et al. ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: A report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (writing committee to develop guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death): Developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society. Circulation 2006;114:e385-484.  Back to cited text no. 2
    
3.
Lown B, Temte JV, Arter WJ. Cardiac arrhythmias. 6. Ventricular tachyarrhythmias. Clinical aspects. Circulation 1973;47:1364-81.  Back to cited text no. 3
    
4.
Gorenek B, Dogan V, Yasar B, Birdane A, Cavusoglu Y, Unalir A, et al. Initiation patterns of monomorphic ventricular tachycardia in acute myocardial infarction: Analysis of rhythm strips. Acta Cardiol 2008;63:171-4.  Back to cited text no. 4
    
5.
Bhar-Amato J, Davies W, Agarwal S. Ventricular arrhythmia after acute myocardial infarction: 'The perfect storm'. Arrhythm Electrophysiol Rev 2017;6:134-9.  Back to cited text no. 5
    


    Figures

  [Figure 1], [Figure 2]



 

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