ong-lasting tachyarrhythmia can result in wall motion abnormality, which is reversible if the culprit arrhythmia is treated. 1-3 Frequent isolated premature ventricular complexes (PVCs) in the absence of tachycardia can cause left ventricular (LV) dysfunction, 4,5 but this phenomenon has rarely been documented. We report resolution of apparent dilated cardiomyopathy (DCM) in a patient after the focal source of PVCs was eliminated by radiofrequency catheter ablation (RF-CA). Case ReportA 53-year-old man presented with palpitations and exertional fatigue, but without clinical or laboratory evidence of ischemic heart disease. He was diagnosed by echocardiography as having DCM with fractional shortening (FS) of the left ventricle of 25%. All 4 chambers were dilated: LV diastolic diameter 65 mm, LV systolic diameter 49 mm, and left atrial diameter 46 mm. The chest X-ray showed mild cardiomegaly (cardio thoracic ratio) (CTR) 54%, and the serum brain natrinvetic peptide (BNP) level was mildly elevated to 54 pg/ml. The electrocardiogram (ECG) did not record any abnormal findings other than frequent PVCs. Repeated Holter recordings revealed about 50,000 isolated or couplet PVCs in a 24-h period, the majority with a uniform left bundle branch block (LBBB) pattern and inferior-axis morphology. PVCs bigeminy appeared constantly throughout the day. During an exercise test, the number of PVCs decreased with the loading of exercise and increased again after the test. Tl-myocardial scintigraphy showed a mildly decreased uptake in the apicoanteroseptal wall. Cardiac magnetic resonance imaging did not show evidence of infiltration of fatty tissue.
Subepicardial aneurysm is a rare complication of acute myocardial infarction and the present case was associated with ventricular septal perforation. Echocardiography showed the subepicardial aneurysm adjoining the true apico-anteroseptal aneurysm, with the former being discontinuous with the myocardium at its neck, which was narrower than the diameter of the aneurysm. In addition, color Doppler imaging showed shunt flow from the aneurysm to the right ventricle. Coronary angiography revealed extension only of the anterior descending artery without any discernible stenosis. The apical aneurysm was excised and the defect closed with an epicardial patch. The myocardial infarction was probably caused by coronary spasm. Echocardiography was useful for diagnosing the anatomy and hemodynamic condition of the subepicardial aneurysm.
Patients with apical hypertrophic cardiomyopathy (APH) associated with paradoxic jet flow (ie, diastolic flow away from the apex) may gradually develop an apical aneurysm, which often leads to arrhythmia and mural thrombus formation. We observed systolic outward motion of the left ventricular apical myocardium in patients with APH using a magnetic resonance tagging procedure and examined the relationship of the outward motion to echocardiographic and scintigraphic findings and to cardiac events. Systolic displacement of the myocardial tags of the apical region perpendicular to the long axis in the 4-chamber view was recorded in 31 patients with APH. Of these patients, 14 showed no outward movement of tags (group A), and 17 showed outward movement (group B). In group B, apical hypertrophy was more severe (35 +/- 7 mm vs. 29 +/- 6 mm, p < 0.05), paradoxic jet flow was more frequent (64% vs. 14%, p < 0.05) and the defect score in I-123-beta-methyliodophenylpentadecanoic acid scintigraphy was higher (2.1 +/- 0.7 vs. 1.3 +/- 0.7, p < 0.01). During a mean follow-up period of 55 months, only 1 patient experienced paroxysmal atrial fibrillation in group A. In group B, 1 patient died suddenly, 1 was admitted to hospital because of congestive heart failure, 2 developed angina pectoris, 2 exhibited non-sustained ventricular tachycardia, and 1 showed multifocal premature ventricular contraction; in these 7 patients the outward movement was greater than in the 10 patients in Group B who had no cardiac events (1.00 +/- 0.59 vs. 0.52 +/- 0.40, p < 0.05). Hence, our results show that outward tag displacement is frequently associated with severe apical hypertrophy, paradoxic jet flow, apical ischemia, and cardiac events. The tagging method may be useful in assessing the severity of APH and predicting the occurrence of cardiac events at an early stage.
orsade de pointes is the major tachyarrhythmia found in patients with long QT syndrome (LQTS) and several investigators report that the underlying mechanism is closely related to early afterdepolarization (EAD). 1,2 Epinephrine and isoproterenol both induce fatal arrhythmias 3 in patients with LQTS; in an electrophysiological study with catecholamine infusion, the monophasic action potential (MAP) recording often revealed an abnormal repolarization called a 'hump', which is direct evidence of EAD. 1,[3][4][5] The prolongation of the QT interval and the occurrence of hump in LQTS are generally considered to be promoted by -adrenergic effects; however, the role of -adrenergic effects on the QT interval has been relatively neglected. 6,7 In a recent case, we observed that the MAP recording showed the hump with epinephrine infusion, but not with isoproterenol infusion. The addition of -adrenergic stimulation to the -adrenergic stimulation had a greater effect on the prolongation of the QT interval and hump thanadrenergic stimulation alone. This finding suggests that in some patients with LQTS, -adrenergic stimulation has an additional role in exacerbating the arrhythmia resulting from increasing EAD amplitude and prolongation of the QT interval under -adrenergic stimulation. Case ReportA 50-year-old woman was admitted to hospital because Circulation Journal Vol.68, June 2004of a syncopal attack that occurred suddenly while she was talking to her daughter. She recovered consciousness in a few minutes; however, she was stuporous and responded very slowly on arrival in the emergency ward, but readily recovered.She had a history of occasionally feeling faint for a few minutes accompanied by palpitations, which had been diagnosed as epilepsy when she was 8 years old. There was a family history of syncopal attacks in her brother and her nephew. Her mother was suddenly died at 53 years old from an unknown cause (Fig 1).Physical examination revealed no abnormalities other than mild hypertension (166/92 mmHg). The electrocardiogram on admission revealed a marked prolongation of the QT interval up to 540 ms (QTc =530 ms) (Fig 2). Serum electrolyte concentrations were within normal limits (Na 137 mmol/L, K 3.5 mmol/L, Cl 104 mmol/L, Ca 8.2 mg/dl, Mg 2.0 mg/dl). The chest X-ray showed cardiomegaly (carCirc J 2004; 68: 587 -591 (Received July 17, 2002; revised manuscript received November 1, 2002; accepted November 14, 2002 Idiopathic Long QT Syndrome With Early Afterdepolarization Induced by Epinephrine A Case ReportNorifumi Urao, MD; Hirokazu Shiraishi, MD; Kazuya Ishibashi, MD; Masayuki Hyogo, MD; Masaki Tsukamoto, MD; Natsuya Keira, MD; Satoshi Hirasaki, MD; Takeshi Shirayama, MD*; Masao Nakagawa, MD* A patient with idiopathic long QT syndrome had repeated syncopal episodes. The QTc interval on the electrocardiogram at rest was 530 ms and was prolonged by exercise up to 740 ms with T wave alternation. Intravenous epinephrine (0.1 g/kg weight per min), but not isoproterenol (0.7 g/min), produced early afterdepolarization ...
Verapamil is widely used for the termination of parox-ysmal supraventricular tachycardia (PSVT) with little proarrhythmic effect. Wedescribe two cases of PSVTthat changed to non-sustained polymorphic ventricular tachy-cardia after administration of verapamil. Electrophysiologi-cal study revealed atrioventricular nodal reentrant tachy-cardia in the first case, and atrioventricular reentrant tachycardia due to a concealed left lateral accessory pathway in the second case. Catecholamine-induced automa-ticity was one of the possible mechanismsof VTin the first case, but the mechanism is unknownin the second case. (Internal Medicine 41: 445-448, 2002)
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.