ECG Demonstrated Sinus Rhythm Research Articles

Abstract 17172: Paradoxical QRS Narrowing After Transcatheter Aortic Valve Replacement Concealing New Left Bundle Branch Block

Introduction: Left bundle branch block (LBBB) after transcatheter aortic valve replacement (TAVR) is common and is a risk factor for high-grade atrioventricular (AV) block. We report a case of paradoxical QRS narrowing after TAVR in a patient with pre-existing incomplete right bundle branch block (iRBBB). Such QRS narrowing, masquerading as improved AV conduction, may conceal the development of new LBBB. Case Presentation: An 81-year-old man with severe aortic stenosis underwent TAVR with a 29mm Medtronic Evolut transcatheter self-expanding bioprosthetic valve. Post-operative TEE showed a well-seated valve without paravalvular leak. Preoperative ECG demonstrated sinus rhythm, 1 st degree AV delay (230 ms), and iRBBB (QRS 110 ms) (Fig. 1A). Immediately after TAVR, ECG showed a narrowed QRS (90 ms) with normal morphology (Fig. 1B). A narrowed QRS was sustained on post-operative day 2, with prolongation of the PR interval (260 ms; Fig. 1C). Electrophysiology study (EPS) showed a prolonged HV interval (65 ms) but no inducible block (Fig. 1D), and an implantable loop recorder (ILR) was placed. Discussion: Damage to the infranodal cardiac conduction system after TAVR is common, and approximately 15% of post-TAVR patients require pacemaker, with a higher occurrence in self-expanding valves as compared to balloon-expandable valves. Pre-existing RBBB as well as new-onset LBBB after TAVR increase the risk for heart block. Here, QRS normalization of an iRBBB concealed the development of new LBBB, by way of balanced delay in both the right and left bundles. This balanced delay is evident in the slightly longer PR interval post-operatively. Such a finding may be falsely reassuring and requires increased scrutiny (such as EPS and ILR placement). Conclusion: This case illustrates that paradoxical normalization of AV conduction following TAVR may belie an increased risk of high-grade AV block. Structural heart teams should be aware of this potential post-operative complication.

Abstract 15244: Rapid Recognition and Implementation of Mechanical Circulatory Support in Rare Fulminant Lymphocytic Myocarditis

Case Presentation: A 65 year-old woman with heart failure, nonischemic cardiomyopathy, atrial fibrillation, hypertension, prior stroke presented with chest pain and shortness of breath for three days. She was ill-appearing, hypotensive and tachypneic, with troponins reaching greater than 125,000 ng/L. Initial ECG demonstrated sinus rhythm with inferior ST elevations and lateral T wave inversions, however emergent catheterization revealed angiographically normal coronary arteries. Repeat 2D echocardiography showed sharp decline to ejection fraction (EF) 5-10%. Patient subsequently developed cardiogenic shock and despite inotropes, vasopressors and intra-aortic balloon pump, she suffered ventricular fibrillation arrest requiring defibrillation. This prompted escalation with emergent veno-arterial extracorporeal membrane oxygenation. Endomyocardial biopsy findings taken at that time were consistent with lymphocytic myocarditis with negative viral panel. Her hospital course was also complicated by acute renal injury, respiratory failure requiring intubation, metabolic acidosis and shock liver. With treatment with high dose steroids and mechanical circulatory support, the patient's severely diminished EF improved to 20% and she is undergoing placement of a left ventricular assist device. Discussion: Fulminant lymphocytic myocarditis is a rare disease that has clinically and pathologically distinct features from subacute or acute lymphocytic myocarditis particularly in its timeline of onset and features of hemodynamic compromise. It most frequently affects young and pediatric individuals and can result in significant mortality and morbidity. This case with an older patient with severe fulminant lymphocytic myocarditis confirmed on biopsy highlights: 1) the importance of early recognition affecting survival outcome, 2) golden standard for diagnosis with endomyocardial biopsy and immunohistochemical analysis for subtype-specific evidence-based treatment, and 3) integrated medical and surgical management, including mechanical circulatory support as an essential life-saving tool.

P301 FULMINANT COVID–19 RELATED MYOCARDITIS: A CASE REPORT

The caseA 58–year–old man presented to ED because of fever, non–productive cough and worsening dyspnea. The patient’s medical history was unremarkable. On examination there was a hypoxic respiratory failure and the clinical picture rapidly evolved towards a cardiogenic shock characterized by altered mental status and cool extremities. Vital parameters: peripheral blood pressure was of 60/30 mmHg, pulse rate of 126 bpm, respiratory rate of 30 breaths/min, temperature of 38 °C. Two episodes of ventricular fibrillation were resolved by electrical shocks. The nasopharyngeal swab tested positive for COVID–19 on real–time reverse transcriptase–polymerase chain reaction assay. Arterial blood gas analysis showed a severe metabolic acidosis with hyperlactacidaemia (pH 7.26, excess basis–22 mEq/L, lactates 10 mmol/dL) and hypoxaemia. Situation evolved towards an end–organ hypoperfusion associated with multisystem organ failure (MOF). High resolution chest CT demonstrated bilateral ground glass opacities consisting of COVID–19 related interstitial pneumonia. 12–leads ECG demonstrated sinus rhythm with diffuse concave ST–segment elevation. T–T echocardiogram showed: 1) severely thickened LV walls; 2) decreased LV systolic function; 3) segmental wall motion abnormalities consisting of akinesis of the LV distal segments with relatively preserved function at the base; 4) LVEF) of 25%; 5) pericardial effusion. Thickened LV walls meant myocardial inflammatory infiltration/edema and the final diagnosis was FULMINANT COVID–19 related MYOCARDITIS. Patient underwent oro–tracheal intubation+invasive ventilation. An intra–aortic balloon pump (IABP) was placed on top of adrenaline (0.07μg/kg/min), and noradrenaline (0.1μg/kg/min) was added for worsening hypotension (systolic blood pressure: 80/67/60 mmHg). Additional therapy consisted of intravenous high dose diuretics, methyprednisolone, tucilizumab, immunoglobulin, ceftriaxone, remdesivir. After 3 weeks, patient recovered a good respiratory and haemodinamic status, LV wall thicknesses decreased and EF increased to normal values. The final outcome was favorable. DiscussionThe prevalence of fulminant myocarditis among COVID–19 patients is unclear. This simultaneous presentation of fulminant myocarditis and COVID–19 pneumonia favors an alternative pathogenetic pathway with possible acute replication and direct dissemination of the virus through the blood or the lymphatic system from the respiratory tract to the myocardium.

Virus-Negative Myopericarditis in Human Coronavirus Infection: Report From an Autopsy Series.

Virus-Negative Myopericarditis in Human Coronavirus Infection: Report From an Autopsy Series.

Wide complex tachycardia with intermittent narrow beats: What is the mechanism?

A previously healthy 10-year-old male with a structurally normal heart presented in wide-complex tachycardia that terminated with intravenous adenosine. The baseline ECG demonstrated sinus rhythm with a normal PR interval (96 msec) This article is protected by copyright. All rights reserved.

Takotsubo Cardiomyopathy

63-year-old woman has had 2 hospital admissions for central chest pain occurring in the setting of emotional stress over the last 11 years. Her other medical history included anxiety, hypertension, and dyslipidemia. At 52 years of age, she presented to the hospital with central chest pain after a major argument with her mother. An ECG demonstrated sinus rhythm with 1-mm ST-segment elevation in leads I and aVL. Her serum troponin I was mildly elevated at 0.63 μg/L (normal <0.03 μg/L). A coronary angiogram demonstrated no significant flow-limiting coronary artery lesions. A left ventriculogram demonstrated severe left ventricular dysfunction resulting from a large area of akinesis involving the anterior and apical wall segments. Subsequently, she developed pulmonary edema, which was treated with diuretic therapy. A transthoracic echocardiogram performed 4 days after admission demonstrated full recovery of the patient’s left ventricular dysfunction, consistent with a diagnosis of Takotsubo cardiomyopathy. She was treated with aspirin, a statin, and a calcium channel blocker. The patient had been followed up regularly with transthoracic echocardiograms, which demonstrated normal left ventricular systolic function (Movies I and II in the online-only Data Supplement). Recently, 11 years after her first hospital admission with chest pain, the patient presented to our hospital with central chest pain after arguments with her son. She experienced significant emotional stress on learning that her son was abusing illicit recreational substances. An ECG demonstrated sinus rhythm with nonspecific T-wave flattening in the lateral leads. Her serum troponin I rapidly peaked at 1.76 μg/L (normal <0.03 μg/L). A coronary angiogram demonstrated mild atheroma in the left anterior descending artery and right coronary artery only (Figure 1). A left ventriculogram demonstrated midventricular akinesis in a noncoronary distribution. Contraction in the basal and apical segments was preserved (Figure 2 and Movie III in the online-only Data Supplement). These findings were consistent with a diagnosis of midventricular Takotsubo cardiomyopathy. She was treated with a β-blocker and angiotensin receptor blocker. She remained well after discharge with recovery of left ventricular function (Movies IV and V in the online-only Data Supplement). Discussion Takotsubo cardiomyopathy frequently occurs in the setting of significant emotional or physical stress or acute medical illnesses. Some patients develop recurrent Takotsubo cardiomyopathy in the setting of further stressors, with normal left ventricular systolic function between these episodes. The factors determining recurrence are poorly understood. One proposed mechanism is an excess of catecholamine, which results in myocardial toxicity. This theory is supported by evidence of elevated plasma catecholamine levels in patients with Takotsubo cardiomyopathy compared with patients with acute myocardial infarction. 1 Therefore, β-blockers have been used as one of the key pharmacological agents in the treatment of Takotsubo cardiomyopathy. Our patient was managed with a calcium channel blocker after her first presentation, and we hypothesize that the absence of β-blockade in the initial treatment regimen may have contributed to her recurrent presentation. What is even more enigmatic is the variable pattern of ventricular involvement in recurrent cases of Takotsubo cardiomyopathy. The first cases of midventricular variant of Takotsubo cardiomyopathy in the Western literature were described in 2006. 2 Since then, various case reports have been published describing different patterns of recurrence. 3 A consistent theme appears to emerge in the cases of recurrent Takotsubo cardiomyopathy described in literature: Recurrent Takotsubo cardiomyopathy often occurred in a different ventricular region. Our patient developed acute pulmonary edema from severe left ventricular apical involvement during her first presentation. Her recurrent presentation occurred in the midventricle only. Consequently, she was not as unwell during the recurrent presentation and did not develop pulmonary edema. We hypothesize that the previous episode of apical Takotsubo cardiomyopathy protected her left ventricular apex from being involved during the recurrent episode. The mechanisms mediating this phenomenon are unclear. It may be that the first episode protected the left ventricular apex via a phenomenon analogous to regional ischemic preconditioning. 4 Transient ischemia of the left ventricular apex during the first presentation may have imprinted memory in the apical

Treacher Collins Syndrome

The patient is a 48-year-old man with Treacher Collins syndrome (TCS) and a precordial murmur known since childhood. He was initially evaluated at 33 years of age for moderate aortic insufficiency and a noncoronary sinus of Valsalva aortic aneurysm. Over time, his aortic disease progressed. His ECG demonstrated sinus rhythm with borderline first-degree atrioventricular block, left ventricular hypertrophy with intraventricular conduction delay, and secondary repolarization abnormalities (Figure 1). His chest x-ray showed biapical pleural-parenchymal scarring with no acute cardiopulmonary abnormality (Figure 2).Transesophageal echocardiography demonstrated severe aortic insufficiency and a large noncoronary sinus of Valsalva (Movie I in the online-only Data Supplement). The aneurysm was also observed to protrude into the right atrium. Cardiac catheterization confirmed similar findings of the …

Reversal of Severe Biventricular Dysfunction From Cardiac Hemochromatosis With Iron Removal

A 47-year-old man presented with 1-week history of cough and bilateral lower extremity swelling. He had a 5-year history of diabetes mellitus and hypogonadism. His ECG demonstrated sinus rhythm with low-limb voltage and left anterior hemiblock. An echocardiogram showed severely reduced left ventricular ejection fraction 10%, restrictive diastolic filling, and severe right ventricular dysfunction (Figure 1, Movie I–IV in the online-only Data Supplement). Laboratory testing revealed brain natriuretic peptide 1849 pg/mL, ferritin 6389 µg/L, iron 108 µg/dL, transferrin 124 mg/dL, total iron binding capacity 171 µg/dL, and transferrin saturation 63%. Figure 1. Echocardiogram showed early:atrial mitral inflow velocity ratio (E/A) >2, short deceleration time (DT) …

ELECTRICAL STORM AS THE INITIAL MANIFESTATION OF AN ELDERLY PATIENT WITH ACUTE MYOCARDIAL INFARCTION (ONE CASE REPORT)

ObjectivesTo investigate the characteristics and therapeutic method of electrical storm (ES) associated with acute coronary syndrome (ACS).MethodsThe clinical data of one elderly patient with ES induced by ACS were collected...

Apical hypertrophic cardiomyopathy: elegant use of contrastenhanced echocardiography in the diagnostic work-up.

A 69-year-old woman was evaluated for chest pain complaints. The ECG demonstrated sinus rhythm with deep negativeT waves from V2 to V6, in I, aVL and the inferior leads. Transthoracic echocardiography (TTE) showed suboptimal image quality and was nondiagnostic. A repeat TTE study after administration of an echo contrast agent showed normal contractile function with apical hypertrophy. This report contains two messages. First, contrast-enhanced echocardiography is an elegant bedside tool to assess left ventricular apical segments. Secondly, in patients with ECG repolarisation abnormalities without an obvious ischaemic cause, routine echocardiography without contrast may not exclude apical HCM. Defi nitive exclusion of this important diagnosis requires further imaging such as CMR or contrast echocardiography.

Bronchogenic Cyst Masquerading as Pericarditis

A 48-year-old white man was admitted 3 times within a month with symptoms of malaise, retrosternal chest pain, and fever up to 38.5°C. The chest pain increased during inspiration and was relieved by sitting up. C-reactive protein was mildly elevated during those admissions, ranging from 6.1 to 85.1 (normal range, <5.0 mg/L), and cardiac enzymes were normal. The ECG demonstrated sinus rhythm with no significant abnormalities (Figure 1). Cardiac structure and function were reported as normal by echocardiography except for a small pericardial effusion (Figure 2 and Movies I and II in the online-only Data Supplement). A presumptive diagnosis of pericarditis was made. Figure 1. ECG on admission. The patient was in sinus rhythm with no significant ECG abnormalities. Figure 2. Apical 4-chamber (A) and parasternal long-axis echocardiography (B). Initially reported as demonstrating only a pericardial effusion, on review, the echocardiography is consistent with abnormality adjacent to the left atrium. In the apical 4-chamber view, the reported small …

Catheter Ablation of Ventricular Tachycardia

Ventricular tachycardia (VT) most commonly develops in patients with structural heart disease. Myocardial infarction results in collagen replacement interspersed with surviving myocardium, which alters impulse propagation, facilitating re-entry.1 Aside from the postinfarction substrate, scar-mediated VT occurs in patients with nonischemic cardiomyopathy, Chagas disease, sarcoidosis, arrhythmogenic right ventricular cardiomyopathy, and postsurgical congenital heart disease. In structurally normal hearts, VT results from intracellular calcium overload or an abnormal response to adrenergic stimulation, promoting triggered activity or automaticity, respectively. There are 3 treatment options for VT, although many patients require a combination: an implantable cardioverter-defibrillator (ICD), antiarrhythmic medications, and catheter ablation. An ICD provides abortive “rescue” therapy but cannot prevent the heart from going into VT. Antiarrhythmic therapy has limited efficacy and has the potential for multiple side effects, including proarrhythmia.2 In this Clinician Update, we discuss 3 different VT clinical scenarios that are amenable to catheter ablation to highlight the range of substrate-specific strategies used in the electrophysiology laboratory. An 18-year-old man presented with palpitations and fatigue. Over a period of 5 months, he had been unable to play sports owing to dyspnea on exertion. A resting ECG demonstrated sinus rhythm with frequent monomorphic premature ventricular contractions. An echocardiogram revealed an ejection fraction of 35% with global hypokinesis. Previous treatment with β-blockers and flecainide was unsuccessful, and he was referred for evaluation for catheter ablation. The patient underwent electrophysiological study, and activation mapping was performed in the right and left ventricular outflow tracts to locate the earliest site of origin. A single application of radiofrequency energy at the earliest site below the left coronary cusp resulted in complete abolition of the premature ventricular contractions (Figure 1). Figure 1. A 12-lead ECG of ventricular bigeminy with left bundle-branch morphology and inferior axis with early precordial transition ( top ). Earliest site of activation ( bottom …

Tuberculous Pseudoaneurysms of the Thoracic Aorta

A 16-year-old girl from an area in Brazil where tuberculosis was endemic was admitted because of recurrent chest pain, progressive dyspnea with exertion, and inability to climb more than 1 flight of stairs. She described fatigue, weight loss, night sweats, and adenopathy of her right axilla and neck during the previous 3 months. On admission she looked distressed, with a heart rate of 76 bpm and blood pressure of 110/55 mm Hg. The ECG demonstrated sinus rhythm with first-degree heart block (Figure 1). Figure 1. First-degree atrioventricular block on ECG. Her admission chest radiograph demonstrated cardiomegaly with pulmonary edema (Figure 2). Her cardiac enzymes were negative. The patient underwent cardiac evaluation with 2-dimensional echocardiography (not shown), which revealed an interatrial septal mass, mild tricuspid regurgitation, preserved systolic function, and moderate pericardial effusion. Figure 2. Chest radiograph showing cardiomegaly and pulmonary congestive features after admission to intensive care unit. For further characterization of the mass, cardiovascular …

Survival and Prognostic Factors in Patients With an Absent Atrioventricular Connection

To identify anatomical and functional characteristics associated with survival in adult patients with an absent atrioventricular connection and to highlight the diagnostic importance of echocardiography. The clinical histories and echocardiographic and hemodynamic test results of 24 patients were recorded. Some 87.5% of patients were in New York Heart Association (NYHA) functional class I/II. In 92%, the ECG demonstrated sinus rhythm and left ventricular dilatation. Chest X-ray showed grade-II cardiomegaly in 83%. Situs solitus and an absent right atrioventricular connection were found on echocardiography in 92%. The ventriculoarterial connection was most frequently concordant (in 71%). All patients had an atrial septal defect, 21 had a ventricular septal defect and 21 had decreased pulmonary flow. The ejection fraction of the main ventricle in the whole patient group was 55% +/- 10%; 52% +/- 12% in those who did not undergo surgery and 58% +/- 8% in those who did (P=NS). Factors associated with poor survival were an ostium secundum atrial septal defect, hemoglobin <16 g/dL and a main ventricle ejection fraction <50%. Of the 54% of patients who underwent surgery, 85% are alive and the majority are in NYHA functional class I/II. Among those who did not, 82% are alive and 73% are in NYHA functional class I/II. The presence of a wide atrial septal defect, a normal hemoglobin level and a normal main ventricle ejection fraction were associated with the survival of these patients into adulthood. Echocardiography can provide clinicians and surgeons with information that is valuable for selecting treatment and monitoring follow-up.

Multiple Coronary Fistulae

A 61-year-old woman with a 3-month history of exertional chest pain was referred for further investigation. She was a smoker with a history of hypertension and hypercholesterolemia. Sublingual nitrates exacerbated her symptoms. A resting ECG demonstrated sinus rhythm with anterolateral and inferior T-wave inversion (Figure 1A). Echocardiography demonstrated normal left ventricular (LV) function with no regional wall motion abnormalities or hypertrophy. ECG stress testing was terminated early because of chest discomfort in stage 2 of the Bruce protocol. At peak exercise, there were non-diagnostic ST changes, with pseudonormalization of the resting T-wave inversion seen both at peak exercise and …

Partial Congenital Absence of the Pericardium

A 45-year-old male was admitted to the hospital with recurrent, stabbing, nonexertional chest pain. Chest x-ray showed an increased cardiothoracic ratio (Figure 1A), and ECG demonstrated sinus rhythm with incomplete right bundle-branch block and poor R-wave progression (Figure 1B). Echocardiography showed normal left ventricular dimensions and function; however, the right ventricle appeared grossly dilated with moderate to severe tricuspid regurgitation with no evidence of intracardiac shunts. These findings were confirmed by right heart catheterization, which also showed normal pulmonary and right atrial pressures without a pressure gradient over the pulmonic valve. Catheterization of the left heart showed normal ventricular pressures and function as well as normal coronary arteries. The patient was referred for cardiac magnetic resonance imaging (CMR) with suspected right ventricular cardiomyopathy. CMR showed cardiac displacement into the left hemithorax (Figure 2A). There was severe tricuspid regurgitation with marked dilatation of both the right atrium (6×8 cm) and ventricle (end-diastolic volume, 343 mL). Right ventricular function was mildly reduced (ejection fraction, 46%) without localized wall motion abnormalities. Left ventricular volumes and …

Coronary to pulmonary fistula as the primary source of pulmonary blood supply in pulmonary atresia with ventricular septal defect

A communication between the coronary and pulmonary arteries, so called coronary to pulmonary fistula, is a rare source of pulmonary supply in pulmonary atresia (PA) with ventricular septal defect (VSD). A 4 year old girl referred to National Cardiovascular Center Harapan Kita, Jakarta with symptoms and signs of increased pulmonary blood flow since infancy and was confirmed by the chest x-rays. Heart examination revealed normal first heart sound with single loud second heart sound and an ejection systolic murmur at the pulmonary area. ECG demonstrated sinus rhythm with normal axis and biventricular hypertrophy. Echocardiography was performed and truncus arteriosus (TA) type I was suspected with perimembranus VSD, overriding of the aorta, and dilated main pulmonary artery. But on cardiac catheterization studies, a non obstructive fistula was found between the left coronary and main pulmonary artery coexisted with PA and VSD. A successful surgery was performed subsequently and confirmed the above diagnosis. Although there were episodes of pulmonary hypertension crisis during early post operative course, she was then discharge from the hospital in a good condition. Since irreversible pulmonary vascular disease may develop in a non restrictive coronary to pulmonary fistula, early recognition of this anomaly is very important for better surgical result. (Med J Indones 2004; 13: 237-40)

Reversal of Acute Pulmonary Oedema with Beta-blockers in Hypertrophic Cardiomyopathy

A 41-year old male was admitted with dyspnoea in 1990. His ECG demonstrated sinus rhythm, voltage-criteria for left ventricular hypertrophy and Q waves in the lateral leads. Transthoracic echocardiography demonstrated asymmetrical septal hypertrophy (17 mm), partial systolic anterior movement of the anterior mitral valve leaflet, a dynamic sub-aortic gradient of 30 mmHg and the presence of diastolic dysfunction as demonstrated by a reversal of the E:A ratio. The diastolic dysfunction was thought to be responsible for the patient’s presenting symptoms. Hypertrophic cardiomyopathy (HCM) was diagnosed but the patient declined any medical treatment or follow-up. He presented in June 2000 with a right hemiparesis. The ECG on admission showed atrial fibrillation with a ventricular rate of 110 beats per minute (bpm). Computerized tomography of the brain did not reveal evidence of a haemorrhagic bleed and treatment was commenced with intravenous heparin and an oral anticoagulant. An echocardiogram on day 5 demonstrated no changes from his previous study. In the absence of a severe outflow tract gradient, he was commenced on verapamil 120 mg twice daily, for ventricular rate control and treatment of diastolic dysfunction. On day 18, the patient became acutely dyspnoeic. Examination revealed a heart rate of 65 bpm, blood pressure of 120/70 mmHg, a late systolic murmur loudest at the left sternal edge and crackles throughout the lung fields. A chest radiograph confirmed pulmonary oedema and treatment with intravenous diuretics and oxygen therapy was immediately initiated. The patient was unresponsive to therapy and so an emergency echocardiogram was performed. This revealed normal systolic function of the left ventricle, a maximum dynamic gradient of 150 mmHg in the left ventricular outflow tract and mild mitral regurgitation (Fig. 1). An intravenous bolus of esmolol was administered and within 10 min there was rapid improvement in the patient’s symptoms. Real-time echocardiography demonstrated a dramatic reduction in the outflow tract gradient to 16 mmHg (Fig. 2). An esmolol infusion was continued for a further 8 h and then replaced with oral beta-blocker therapy. The remainder of the patient’s stay was uneventful and he was discharged on oral

Diagnosis of Isolated Noncompaction of the Myocardium by Magnetic Resonance Imaging

A 15-year-old asymptomatic, physically active man, who had a history of syncope at the age of 12 and a family history of arrhythmogenic right ventricular dysplasia (father), presented for evaluation. Physical examination revealed no abnormal findings. The ECG demonstrated sinus rhythm, −20° QRS, incomplete right bundle-branch block, and left ventricular hypertrophy; the 24-hour Holter monitoring excluded ventricular arrhythmias. Normal exercise capacity (15 metabolic equivalent) without arrhythmias was confirmed by treadmill exercise testing. The echocardiogram showed apical hypertrophy of the left ventricle and an interatrial pseudo-aneurysm without shunt (Figure 1). To rule out right ventricular dysplasia, an ECG-gated cardiac MRI was performed. Surprisingly, the “black-blood” cardiac …