Biomedical subjects
Publications and source records attributed to Laszlo Littmann.
Deciphering the electrophysiologic mechanism of a long R-P' paroxysmal supraventricular tachycardia typically requires an invasive electrophysiologic study. We present a case where analysis of a simple surface 12-lead ECG was sufficient for the diagnosis.
In a heart failure (HF) disease management program (DMP), 4 patients with advanced HF and low ejection fractions had near full recovery within 4 to 45 months. When discharged to their primary care physicians, all 4 had severe symptom relapse and deterioration of their left ventricular function. Readmission to the HF DMP for a second time resulted in similar improvement in all parameters, as was seen the first time.
Although hyperthyroidism has many signs and symptoms, right heart failure can occasionally be the main presenting symptom. We describe the case of a previously healthy 42-year-old woman whose chief complaint was progressive bilateral lower extremity edema. The echocardiogram revealed right atrial dilatation and moderate-to-severe tricuspid regurgitation. Results of laboratory studies were consistent with hyperthyroidism. Thyroid ablation resulted in permanent resolution of symptoms and resolution of tricuspid incompetence on echocardiography. In a case of isolated, unexplained tricuspid regurgitation, it is important to consider indolent hyperthyroidism in the differential diagnosis.
Explore the source record for details and available documents.
In a 70-year-old man, without clinical suggestion of the hereditary form of the Brugada syndrome, severe flecainide overdose resulted in profound widening of the QRS complex and the development of ST-T abnormalities typical of the Brugada sign. Serial ECGs recorded over a 5-day period revealed a parallel pattern of dynamic intraventricular conduction defect and ST-segment elevation. Resolution of ST-segment elevation lagged behind resolution of the QRS widening by 16-20 hours. Despite the marked Brugada abnormality no arrhythmia occurred and the patient recovered without complications.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
BACKGROUND: Patients with the manifest Brugada syndrome have an inordinate risk of sudden death and are candidates for implantation of a defibrillator. The Brugada type electrocardiogram (ECG) abnormality (the "Brugada sign"), however, is known to be associated with a wide range of conditions, many of which may not pose such a threat. Clinicians need guidance in choosing a rational approach for the evaluation and treatment of patients with a finding of the Brugada sign. METHODS: A systematic literature search was performed to identify publications on the Brugada syndrome and the Brugada-type ECG abnormality, with special emphasis on analyzing outcomes data. In addition, the ECG database of our institution was reviewed for tracings consistent with the Brugada sign, and, when possible, clinical correlations were made. RESULTS: Patients with the Brugada sign and a family history of sudden death or a personal history of syncope are at a high risk of sudden death and therefore should be strongly considered for implantation of a defibrillator. In patients who are hospitalized and critically ill, the Brugada sign is frequently the result of severe hyperkalemia, drug toxicity, or right ventricular injury. In most individuals with no symptoms and without a family history of sudden death, the Brugada sign is likely a normal variant. CONCLUSIONS: Most patients with the Brugada sign can be risk-stratified with simple clinical tools. Specific testing for the Brugada syndrome should be reserved for questionable cases and for the research setting. A provisional diagnostic-therapeutic algorithm is offered as a means of assisting the clinician in the evaluation and treatment of patients with the Brugada sign.
Long QT syndrome (LQTS) involves both congenital and acquired predispositions toward the characteristic torsades de pointes (TP) ventricular arrhythmia. Congenital long QT syndrome generally manifests with TP, syncope, or sudden death early in life. This is a documented case of previously undiagnosed congenital LQTS in a 48-year-old woman where the first and fatal episodes of TP were provoked by hemodialysis.
OBJECTIVE: To describe 3 patients who presented with chest pain and intermittent Q waves on the electrocardiogram (ECG) and were subsequently found to have latent preexcitation. PATIENTS AND METHODS: During a span of 8 years, 3 patients were evaluated because of atypical chest pain and pathologic Q waves in the inferior leads; in all 3 patients, the Q waves were intermittent. No patient had a history of arrhythmia or had Wolff-Parkinson-White pattern on the ECG. Diagnostic and therapeutic interventions for suspected myocardial infarction included cardiac catheterization in 2 patients, intravenous thrombolytic therapy in 1 patient, and heparin in 2 patients. Ischemic heart disease was excluded in all. Patients underwent pharmacological testing and/or electrophysiologic study for suspected preexcitation. RESULTS: Despite the absence of ECG markers of preexcitation, the presence of a latent accessory atrioventricular connection was confirmed in each patient by pharmacological or electrophysiologic studies. CONCLUSION: In patients who present with intermittent noninfarction Q waves, the most likely diagnosis is latent preexcitation. Clinicians need to be educated about this clinical diagnosis and encouraged to pursue confirmatory testing. Such patients should be informed about the nature and importance of their electrocardiographic abnormality.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
In patients with narrow QRS complexes, atrioventricular block is usually localized to the AV node, and it is frequently benign. The more distal intra-His bundle blocks are rare, potentially malignant, and difficult to recognize. This case report illustrates how His bundle block can be diagnosed by analyzing the effects of certain maneuvers on the heart rate. Paradoxically, exercise and atropine tend to provoke His bundle block, whereas carotid massage may release it. Implantation of a permanent pacemaker is generally indicated.