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• W2892773780 abstract "HomeCirculationVol. 138, No. 10Abnormal ECG Findings in a Young Patient With Unexplained Shortness of Breath Free AccessCase ReportPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessCase ReportPDF/EPUBAbnormal ECG Findings in a Young Patient With Unexplained Shortness of BreathThe Apple Doesn’t Fall Far From the Tree Khalid Bakr, MD, Julia Grapsa, MD, PhD and Antonio Sorgente, MD, PhD Khalid BakrKhalid Bakr Julia Grapsa, MD, PhD, Clinical Associate Professor of Medicine, Cleveland Clinic Lerner College of Medicine, Consultant Cardiologist, Cleveland Clinic Abu Dhabi, Al Maryah Island, Abu Dhabi, United Arab Emirates 112412; or Khalid Bakr, MD, Clinical Associate, Cleveland Clinic Abu Dhabi, Al-Maryah Island, Abu Dhabi, United Arab Emirates 112412. Email E-mail Address: [email protected] or E-mail Address: [email protected] Heart and Vascular Institute, Cleveland Clinic Abu Dhabi, Al Maryah Island, United Arab Emirates. Search for more papers by this author , Julia GrapsaJulia Grapsa Julia Grapsa, MD, PhD, Clinical Associate Professor of Medicine, Cleveland Clinic Lerner College of Medicine, Consultant Cardiologist, Cleveland Clinic Abu Dhabi, Al Maryah Island, Abu Dhabi, United Arab Emirates 112412; or Khalid Bakr, MD, Clinical Associate, Cleveland Clinic Abu Dhabi, Al-Maryah Island, Abu Dhabi, United Arab Emirates 112412. Email E-mail Address: [email protected] or E-mail Address: [email protected] Heart and Vascular Institute, Cleveland Clinic Abu Dhabi, Al Maryah Island, United Arab Emirates. Search for more papers by this author and Antonio SorgenteAntonio Sorgente Heart and Vascular Institute, Cleveland Clinic Abu Dhabi, Al Maryah Island, United Arab Emirates. Search for more papers by this author Originally published4 Sep 2018https://doi.org/10.1161/CIRCULATIONAHA.118.036273Circulation. 2018;138:1060–1062ECG ChallengeA 30-year-old male patient presented reporting shortness of breath at rest for the past 6 months. He denied other symptoms or family history of heart disease. He had been a smoker for the past 10 years, but had quit recently.Baseline ECG (Figure 1) demonstrates sinus bradycardia with QR complexes in lead II, III, and aVF associated with concave ST elevation and an rs complex in aVL associated with ST depression and negative T waves. Noteworthy, as well, is the presence of RS complexes in the septal precordial leads (V2 and V3) associated with remarkable q waves and low-voltage R waves in V5 and V6. In addition, there is a notch in the middle portion of the QRS in lead II and aVF and a diphasic T wave in V2.Download figureDownload PowerPointFigure 1. ECG during the patient’s first visit. Noteworthy is the presence of RS complexes in the septal precordial leads (V2 and V3) associated with remarkable q waves and low-voltage R waves in V5 and V6. Least, but not the last, there is a notch in the middle portion of the QRS in lead II and aVF and a diphasic T wave in V2.What is the most likely underlying etiology to explain the baseline ECG findings?Please turn the page to read the diagnosis.Response to ECG ChallengeThe main abnormality in the ECG depicted in Figure 1 is the presence of prominent Q waves in the inferolateral leads. This patient shows a clear predominance of the septal forces over the lateral ones (Figure 2C and 2D).In the human heart, 4 vectors of depolarization have been reported. The first 2 vectors are related to the depolarization of the septum, conduction system (His bundle, bundle branches, and Purkinje fibers), and endomyocardial fibers of the left ventricle, and the third and fourth vectors are instead markers of the depolarization of the myocardial and epicardial free wall of the left ventricle (Figure 2A and 2B).Download figureDownload PowerPointFigure 2. Schematic representation of the biventricular depolarization in a normal heart with the correspondent QRS in lead II (A and B) in contrast to the biventricular depolarization of a heart with asymmetrical hypertrophy localized in the septum with significant changes in the QRS in the same lead (C and D). The activation of the septum in the normal heart produces a small Q wave in the inferolateral leads; the presence instead of a selective hypertrophy in the upper portion of the septum (as in this clinical scenario) creates the premise for a deeper Q wave in the same leads that is followed by a R wave and ST elevation (which should be interpreted as secondary to the depicted hypertrophy). The presence of isodiphasic QR complexes in the inferior leads is attributable to hypertrophy in the basal portion of anteroseptal wall, which is perpendicular to those leads. RS complexes in V2 and V3 go along with the finding of isolated septal hypertrophy, which explains the dampened voltages, as well, of the QRS in the lateral leads. ST elevation and correspondent depression are secondary to the reported septal hypertrophy, and the diphasic T wave in V2, as well. Last, the presence of a notch in the QRS in lead II is also a possible electric consequence of fibrosis that can be associated with hypertrophy.The presence of isodiphasic QR complexes in the inferior leads is attributable to hypertrophy in the basal portion of anteroseptal wall, which is perpendicular to those leads. RS complexes in V2 and V3 go along with the finding of isolated septal hypertrophy, which explains as well the dampened voltages of the QRS in the lateral leads.ST elevation and correspondent depression are secondary to the reported septal hypertrophy and the diphasic T wave in V2, as well.Last, the presence of a notch in the QRS in lead II is also a possible electric consequence of fibrosis that can be associated with hypertrophy.The interesting finding is that those Q waves are followed by R waves of similar amplitude. This reduces the possibility that this was related to a myocardial infarction, because it was confirmed by echocardiogram and cardiac MRI in our patient, and, as such, the abnormal Q waves were the result of an abnormal vector of depolarization. The configuration of the QRS in the inferolateral leads is indeed consequent to an asymmetrical hypertrophy of the anterior portion of the septum: the increase in the thickness in the septum obscures the depolarization forces in the lateral wall and explains the reason for the presence of a QR complex.The other interesting finding of this ECG is the lack of the classical ECG criteria for hypertrophy. Our clinical case underlines once more the overall low reliability of the ECG in detecting left ventricular hypertrophy, especially when it involves different regions of the left ventricle at a variable extent, as in this specific case. None of the 27 left ventricular hypertrophy criteria proposed in the American Heart Association/American College of Cardiology Foundation/Heart Rhythm Society Recommendations for the Standardization and Interpretation of the Electrocardiogram1 is fulfilled. This is not completely unexpected, however; asymmetrical septal hypertrophy has been associated with a reduced incidence of left ventricular hypertrophy and left atrial enlargement ECG criteria in comparison with concentric hypertrophy (as usually present in patients with aortic stenosis, for example).2 Furthermore, the presence of R/S ratio in V1 of >0.2, as is evident in our patient’s ECG, is also indicative of asymmetrical septal hypertrophy.The differential diagnosis for shortness of breath included coronary artery disease, in view of a smoking history. Yet, his baseline echocardiogram did not demonstrate any regional wall motion abnormalities; therefore, prior infarct to account for the significant Q waves was ruled out.Subsequently, cardiac magnetic resonance highlighted the disproportional septal hypertrophy and late gadolinium enhancement, confirming the diagnosis (Figure 3). Delayed enhancement demonstrated multiple small foci of contrast retention within the hypertrophic myocardium, present in the short-axis and 2-chamber views.Download figureDownload PowerPointFigure 3. Cardiac magnetic resonance. Cine evaluation of the myocardium demonstrates focal hypertrophic myocardium of the anteroseptal wall base. The anteroseptal wall measures 20 mm in diastole and thickens to 23 mm. Delayed (postcontrast) imaging demonstrates multiple small foci of contrast retention within the hypertrophic myocardium present in the short-axis and 2-chamber views. The remainder of the myocardium is normal.Cardiac magnetic resonance can be helpful when first-line imaging modalities such as echocardiography cannot fully explain symptomatology or an abnormal ECG. Parametric mapping now permits spatial visualization and quantification of changes based on changes in T1, T2, and T2*(star) relaxation times and extracellular volume. Cardiac magnetic resonance may be important in ruling out conditions such as iron overload or Anderson-Fabry disease or even extracellular myocardial disturbances such as myocardial fibrosis, cardiac amyloidosis, or myocardial edema.The patient was initially referred for possible implantation of an implantable cardioverter defibrillator, but it was deemed not indicated because of his low-risk profile, according to the European Society of Cardiology hypertrophic cardiomyopathy–risk-sudden cardiac death calculator.3 On subsequent follow-up, the patient was doing well, and his exercise capacity had improved, after having started treatment with β-blockers and angiotensin-converting enzyme inhibitors.DisclosuresNone.Footnoteshttps://www.ahajournals.org/journal/circJulia Grapsa, MD, PhD, Clinical Associate Professor of Medicine, Cleveland Clinic Lerner College of Medicine, Consultant Cardiologist, Cleveland Clinic Abu Dhabi, Al Maryah Island, Abu Dhabi, United Arab Emirates 112412; or Khalid Bakr, MD, Clinical Associate, Cleveland Clinic Abu Dhabi, Al-Maryah Island, Abu Dhabi, United Arab Emirates 112412. Email [email protected]com or [email protected]aeReferences1. Hancock EW, Deal BJ, Mirvis DM, Okin P, Kligfield P, Gettes LS, Bailey JJ, Childers R, Gorgels A, Josephson M, Kors JA, Macfarlane P, Mason JW, Pahlm O, Rautaharju PM, Surawicz B, van Herpen G, Wagner GS, Wellens H; American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; American College of Cardiology Foundation; Heart Rhythm Society. AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: part V: electrocardiogram changes associated with cardiac chamber hypertrophy: a scientific statement from the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society. Endorsed by the International Society for Computerized Electrocardiology.J Am Coll Cardiol. 2009; 53:992–1002. doi: 10.1016/j.jacc.2008.12.015CrossrefMedlineGoogle Scholar2. Engler RL, Smith P, LeWinter M, Gosink B, Johnson A. The electrocardiogram in asymmetric septal hypertropy.Chest. 1979; 75:167–173.CrossrefMedlineGoogle Scholar3. Authors/Task Force members, Elliott PM, Anastasakis A, Borger MA, Borggrefe M, Cecchi F, Charron P, Hagege AA, Lafont A, Limongelli G, Mahrholdt H, McKenna WJ, Mogensen J, Nihoyannopoulos P, Nistri S, Pieper PG, Pieske B, Rapezzi C, Rutten FH, Tillmanns C, Watkins H. 2014 ESC Guidelines on diagnosis and management of hypertrophic cardiomyopathy: the Task Force for the Diagnosis and Management of Hypertrophic Cardiomyopathy of the European Society of Cardiology (ESC).Eur Heart J2014; 35:2733–2779. doi: 10.1093/eurheartj/ehu284CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetails September 4, 2018Vol 138, Issue 10 Advertisement Article InformationMetrics © 2018 American Heart Association, Inc.https://doi.org/10.1161/CIRCULATIONAHA.118.036273PMID: 30354534 Originally publishedSeptember 4, 2018 PDF download Advertisement" @default.
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