Calcified myocardial scar seen via cardiac imaging correlating with ventricular tachycardia focus

Abstract

A 74-year-old man presented with presyncope and non-sustained monomorphic ventricular tachycardia in the setting of acute coronary syndrome. On coronary angiogram, a calcified myocardial scar was revealed, which was later identified as the ventricular tachycardia focus via electrophysiological study.

Background

Myocardial calcification is an uncommon finding on imaging that manifests as either focal deposits or diffuse myocardial involvement. In the prereperfusion era, studies concerning postmyocardial infarction ventricular tachycardia not infrequently described calcified scars; however, there are few modern-day case reports associating myocardial calcifications with symptoms of heart failure, conduction abnormalities and arrhythmias.^1–4 We describe a case of a 74-year-old man who presented with non-sustained ventricular tachycardia, which ultimately was found, via electrophysiology study, to be due to myocardial calcification in the inferolateral wall of the left ventricle.

Case presentation

A 74-year-old man with medical history of peripheral vascular disease complicated by multiple bilateral digit amputations, coronary artery disease with prior percutaneous coronary interventions in 2003 (drug-eluting stent to third obtuse marginal branch) and 2007 (bare-metal stents to right coronary and left circumflex arteries) and chronic tobacco use disorder presented to an outside hospital emergency department with several hours of chest pain. The pain was substernal, non-radiating and exacerbated by deep breaths. He had one episode of presyncope at rest associated with the chest pain. In the field, the patient was given a loading dose of aspirin and sublingual nitroglycerin with mild relief of his chest discomfort. On arrival, the patient was tachycardic and physical examination was unremarkable. An ECG demonstrated non-sustained monomorphic ventricular tachycardia with positive concordance in the precordial leads and superior axis. Frequent premature ventricular contractions, often in couplets with identical morphology to the non-sustained ventricular tachycardia, were also observed (figure 1).

Figure 1.

The12-lead ECG on admission. ECG demonstrating non-sustained monomorphic ventricular tachycardia (NSMVT) with positive concordance in the precordial leads and superior axis. Frequent premature ventricular contractions, often in couplets with identical morphology to the NSMVT, were also observed.

Investigations

Routine laboratory tests were largely unremarkable except for the initial troponin-I 0.035 ng/mL (normal range <0.03 ng/mL). He was subsequently started on acute coronary syndrome protocol with a loading dose of ticagrelor 180 mg and heparin infusion as well as amiodarone 150 mg bolus and infusion (1 mg/min) for non-sustained ventricular tachycardia. The patient was transferred to our institution for further evaluation. His troponin-I level peaked at 1.95 ng/mL. Telemetry was notable for occasional sinus bradycardia with ventricular bigeminy, however, there were no further episodes of non-sustained ventricular tachycardia. Transthoracic echocardiography demonstrated preserved left ventricular ejection fraction 55%–60% and inferolateral hypokinesis. Given concern for underlying ischaemia precipitating the ventricular tachycardia, the patient underwent coronary angiography which revealed a thrombotic lesion in the mid-left circumflex with 99% stenosis, proximal right coronary artery with 80% stenosis and 80%–90% lesion in the mid vessel (figure 2). Percutaneous coronary intervention was performed with drug-eluting stent placement to the left circumflex and right coronary arteries. Interestingly, the coronary angiogram showed a 4 cm area of focal calcification in the inferolateral wall of the left ventricle (figure 2). Additional imaging via cardiac MRI with late gadolinium enhancement demonstrated transmural infarction of the inferolateral wall with reduced myocardial signal intensity on standard cine imaging (figure 3) consistent with dystrophic myocardial calcification. The measured calcification volume was 2.28 cm³. No further episodes of ventricular tachycardia were observed on telemetry; however, the left ventricular inferolateral wall calcified scar was postulated to be the substrate of non-sustained ventricular tachycardia. Therefore, an electrophysiology study was undertaken to examine if there was a substrate for recurrent ventricular tachycardia and to determine whether secondary prevention intracardiac defibrillator placement was warranted. During the electrophysiology study, sustained ventricular tachycardia was reproducibly and easily induced with a drive train of 600 ms and a single premature extra stimulus at 320 ms. The induced ventricular tachycardia had the same morphology and cycle length as the presenting non-sustained ventricular tachycardia at admission; thus, an intracardiac defibrillator was implanted.

Figure 2.

Coronary angiogram. right anterior oblique (RAO) caudal view highlighting diseased left circumflex artery (white arrowhead) and inferolateral calcifications (white arrows).

Figure 3.

Cardiovascular MRI cine imaging (balanced steady state free precession) acquired in short axis (A) and three-chamber (C) views demonstrates regional thinning of the inferolateral wall with reduced signal intensity compared with remote myocardium (white arrows). Late gadolinium enhancement (LGE) imaging in short-axis (B) and three-chamber (D) views shows a region of avid transmural enhancement in the inferolateral wall indicative of myocardial infarction with discrete areas of low signal (red arrows). Low signal regions within areas of infarction on LGE imaging are indicative of either microvascular obstruction or dystrophic myocardial calcification, which can be differentiated by the acuity of the presentation. in this instance, the presence of a thin/remodelled inferolateral wall and modest troponin elevation are consistent with an existing transmural infarct with dystrophic myocardial calcification.

Outcome and follow-up

The patient was discharged 4 days after admission. Three weeks after discharge, the patient was readmitted for intracardiac defibrillator firing. Interrogation of his device demonstrated multiple episodes of ventricular tachycardia terminated by antitachycardia pacing or defibrillation. He received an intravenous loading dose of amiodarone and was discharged on maintenance therapy.

Discussion

Aetiologies of myocardial calcifications are broadly classified as either dystrophic, secondary to tissue damage or cellular necrosis, or metastatic, due to imbalances in calcium homeostasis. Dystrophic myocardial calcifications are typically seen in patients who had prior myocardial infarctions.⁵

The most common aetiology of monomorphic ventricular tachycardia is macro reentrant pathways and is usually scar mediated as seen in our patient. Despite the known association between scar and ventricular tachycardia, the relationship between calcium within the scar and ventricular tachycardia is still uncertain. Alyesh et al attempted to provide insight into this knowledge gap by comparing postinfarction patients who received cardiac CT prior to undergoing ventricular tachycardia ablation to a control group of postinfarction patients without a history of ventricular tachycardia that had CT performed for other indications. The authors demonstrated that myocardial calcifications seen via preprocedural cardiac imaging were present in approximately 70% of patients with postinfarction ventricular tachycardia. Additionally, among patients with calcifications, a myocardial calcification volume of 0.538 cm³ differentiated patients with calcification-associated ventricular tachycardia from patients without calcification-associated ventricular tachycardia.⁶ Correlating these findings with our case, given the magnitude of calcification seen on low sensitivity fluoroscopy, we appropriately identified this area as a suspected source of ventricular tachycardia. Furthermore, it raises the question whether myocardial calcifications can be a potential predictor to risk stratify patients at higher risk of sudden cardiac death.

A notable aspect of our case was the rationale to pursue an electrophysiology study despite the patient’s preserved left ventricular systolic function. Per current guidelines, an electrophysiology study can be used to risk stratify patients after a myocardial infarction if their left ventricular ejection fraction is <40% and non-sustained ventricular tachycardia is present.⁷ In our patient, despite the preserved ejection fraction and recent revascularisation, the presence of a large area of scar and calcification led to a high index of suspicion for future episodes of sustained ventricular tachycardia. This suspicion was confirmed during the electrophysiology study where sustained ventricular tachycardia was induced with a nonaggressive protocol, and the ventricular tachycardia morphology suggested an origin in the inferior wall of the left ventricle. Additionally, Buxton et al devised a predictive multivariable model incorporating left ventricular ejection fraction to risk stratify patients with coronary artery disease susceptible to sudden cardiac death and all-cause mortality. The authors noted multiple variables had similar prognostic value to left ventricular ejection fraction.⁸ This study further substantiates the limitations of using left ventricular ejection fraction as a sole indicator for sudden cardiac death risk assessment and intracardiac defibrillator placement. Our patient received an intracardiac defibrillator after considering the overall clinical picture of a history of presyncope, presence of myocardial calcification and inducible sustained ventricular tachycardia.

Learning points.

• Myocardial calcification secondary to prior infarction is an uncommon finding on fluoroscopic imaging which may be associated with risk for ventricular arrhythmia.

• To understand the various underlying causes of monomorphic ventricular tachycardia.

• To examine the impact of electrophysiology testing on diagnosing high-risk arrhythmias.

• To understand the limitations of left ventricular ejection fraction as an indicator for risk of sudden cardiac death and/or and all-cause mortality.