Cases reported "Heart Block"

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1/291. Unusual evidence of myocardial involvement during a hypersensitivity reaction to oral penicillin.

    A hypersensitivity reaction to orally administered phenoxymethyl penicillin is reported. The manifestations of the reaction included fever, arthralgia, urticaria and an irregular pulse. Serial ECG showed second-degree atrioventricular block with junctional escape beats, an atypical Wenckebach pattern and, finally, first-degree atrioventricular block with gradually decreasing PR intervals. A normal tracing was recorded on the sixth day despite the persistence of the rash and joint pains.
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2/291. Junctional ectopic tachycardia evolving into complete heart block.

    Transition from congenital junctional ectopic tachycardia to complete AV block was observed in an 8 month old girl, over a 36 hour period, during initial hospital admission. Two years later she had evidence of a rapidly increasing left ventricular end diastolic diameter, associated with lowest heart rates during sleep of < 30 beats/min. A transvenous permanent pacemaker was therefore implanted. This finding supports the idea that a pathological process in the area of the AV junction, initially presenting as junctional ectopic tachycardia may later extend to sudden complete atrioventricular block.
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3/291. Pseudo second degree atrioventricular block with bradycardia. Successful treatment with quinidine.

    Pseudo second degree atrioventricular block resulting from blocked His premature beats was successfully treated with quinidine. The diagnosis was proved by His bundle electrogam which showed both blocked and conducted His premature beats. The blocked His prematures produced second degree atrioventricular block by making the atrioventricular junction refractory. quinidine abolished both conducted and blocked His extrasystoles. There has been no recurrence of arrhythmia during a one-year follow-up.
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4/291. adenosine-induced cardiac pause for endovascular embolization of cerebral arteriovenous malformations: technical case report.

    OBJECTIVE: Extremely high flow through arteriovenous malformations (AVMs) may limit the safety and effectiveness of endovascular glue therapy. To achieve a more controlled deposition of glue, we used transient but profound systemic hypotension afforded by an intravenously administered bolus of adenosine to induce rapidly reversible high-degree atrioventricular block. methods AND CASE REPORT: A patient with a large high-flow occipital AVM fed primarily by the posterior cerebral artery underwent n-butyl cyanoacrylate glue embolization. nitroprusside-induced systemic hypotension did not adequately reduce flow through the nidus, as determined by contrast injection in the feeding artery. In a dose-escalation fashion, boluses of adenosine were administered to optimize the dose and verify that there was no flow reversal in the AVM and no other unexpected hemodynamic abnormalities by arterial pressure measurements and transcranial Doppler monitoring of the posterior cerebral artery feeding the AVM. Thereafter, 64 mg of adenosine was rapidly injected as a bolus to provide 10 to 15 seconds of systemic hypotension (approximately 20 mm Hg). Although there were conducted beats and some residual forward flow through the AVM during this time, the mean systemic and feeding artery pressures were roughly similar and remained relatively constant. A slow controlled injection of n-butyl cyanoacrylate glue was then performed, with excellent filling of the nidus. CONCLUSION: adenosine-induced cardiac pause may be a viable method of partial flow arrest in the treatment of cerebral AVMs. Safe, deep, and complete embolization with a permanent agent may increase the likelihood of endovascular therapy's being curative or may further improve the safety of microsurgical resection.
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5/291. Electrophysiologic characteristics of accessory atrioventricular connections in an inherited form of wolff-parkinson-white syndrome.

    INTRODUCTION: A familial form of wolff-parkinson-white syndrome (WPW) occurs in association with hypertrophic cardiomyopathy and intraventricular conduction abnormalities. This syndrome, demonstrating autosomal dominant inheritance and segregating with a high degree of penetrance but variable expressivity, has been genetically linked to chromosome 7q3. The purpose of this study is to detail the electrophysiologic characteristics of accessory atrioventricular connections (AC) in four members of a kindred with this syndrome. methods AND RESULTS: We clinically evaluated 32 members of a single kindred and identified 20 individuals with ventricular preexcitation, abnormal intraventricular conduction including complete AV block and/or ventricular hypertrophy. genetic linkage analysis mapped the disease gene in this kindred to the chromosome 7q3 locus (maximum logarithm of the odds score = 6.88, theta = 0); recombination events in affected individuals reduced the genetic interval from 7 centimorgans (cM) to 5 cM. Electrophysiologic study of four individuals with preexcitation, identified seven AC (1 right sided, 3 septal, and 3 left sided). All four individuals had inducible orthodromic tachycardia; while three had multiple AC. Bidirectional conduction was demonstrated in 6 of 7 AC. Successful ablation was accomplished in 5 of 7 AC. CONCLUSION: The electrophysiologic characteristics and location of AC in family members having this complex cardiac phenotype are similar to those seen in individuals with isolated WPW. Identification of WPW in more than one family member should prompt clinical evaluation of relatives for additional findings of ventricular hypertrophy or conduction abnormalities.
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keywords = complex
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6/291. Reciprocal beats initiated by artificial pacemaker.

    In conclusion, the underlying mechanism for this rhythm disturbance in our patient is the re-entry phenomenon, which is dependent upon a localized unidirectional block in the A-V junction. The predisposing factors, including digoxin and Inderal which tend to prolong A-V conduction, are considered for the mechanism of the production of the reciprocal beats in our case. Upon temporary withdrawal of digoxin and Inderal, the re-entry phenomenon has disappeared.
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7/291. Wide QRS complex tachycardia: ECG differential diagnosis.

    Wide QRS complex tachycardias (WCT) present significant diagnostic and therapeutic challenges to the emergency physician. WCT may represent a supraventricular tachycardia with aberrant ventricular conduction; alternatively, such a rhythm presentation may be caused by ventricular tachycardia. Other clinical syndromes may also demonstrate WCT, such as tricyclic antidepressant toxicity and hyperkalemia. Patient age and history may assist in rhythm diagnosis, especially when coupled with electrocardiographic (ECG) evidence. Numerous ECG features have been suggested as potential clues to origin of the WCT, including ventricular rate, frontal axis, QRS complex width, and QRS morphology, as well as the presence of other characteristics such as atrioventricular dissociation and fusion/capture beats. Differentiation between ventricular tachycardia and supraventricular tachycardia with aberrant conduction frequently is difficult despite this clinical and electrocardiographic information, particularly in the early stages of evaluation with an unstable patient. When the rhythm diagnosis is in question, resuscitative therapy should be directed toward ventricular tachycardia.
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ranking = 1.3394112977041
keywords = beat, supraventricular, complex
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8/291. Prominent bifid T waves observed in the QT prolongation caused by complete atrioventricular blockade in a hypokalemic diabetic patient.

    A 63-year-old diabetic man was admitted with general fatigue. Electrocardiogram (ECG) on admission showed complete atrioventricular (AV) blockade associated with prominent bifid T waves. The second component of the bifid T waves was distinguished from U waves by the beat-to-beat varying bifidity and the nadir between the two components located at > or = 1 mm above the isoelectric line. Range of absolute QT interval was 535 to 650 ms. hypokalemia (3.6 mEq/L) was noted at admission. Partial restoration of the potassium level (3.9 mEq/L) prior to temporary ventricular demand pacing obscured the bifid T waves and attenuated the QT prolongation and dispersion to some extent (absolute QT interval ranging 520 to 620 ms). It was concluded that marked bradycardia caused by complete AV blockade (ie, a junctional escaped rhythm at a rate of 42 beats/min), hypokalemia, and underlying diabetes mellitus contributed in concert to the QT prolongation and dispersion leading to the prominent bifid T waves.
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9/291. Pseudo A-V block. Part I.

    An example of junctional premature beats with concealed conduction has been presented. The arrhythmia mimics Mobitz Type II second-degree A-V block. awareness of this arrhythmia when added to the fact that Mobitz Type II block is rarely seen with IWMI will prevent an improper or hasty diagnosis. Cardiac arrhythmias should be interpreted and managed in context of the clinical setting.
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10/291. Fetal treatment of congenital heart block ascribed to anti-SSA antibody: case reports with observation of cardiohemodynamics and review of the literature.

    PROBLEM: Maternal anti-SSA(B) antibody crosses the placenta and causes fetal myocarditis, congenital heart block (CHB), hydrops fetalis, and intrauterine fetal death. The aim of this study was to evaluate corticosteroids' efficacy as a treatment for CHB. METHOD OF STUDY: One fetus with complete CHB and one fetus with incomplete CHB due to anti-SSA(B) antibody received maternal prednisolone (PSL) and dexamethasone (DEXA) treatments. heart rate, cardiothoracic ratio (CTR), left ventricular fractional shortening (FS), and preload index (PLI) were longitudinally measured by serial fetal echocardiograms. RESULTS: In the former case, after maternal PSL/DEXA administration, improvement of cardiohemodynamics, i.e., the reduction of PLI from 1.7 to 0.4, CTR from 70 to 52%, and FS from 63 to 54% were observed. In the latter case, second degree 2:1 block was converted to 3:2 block/sinus rhythm, resulting in the increase of the fetal heart rate from 65 to 116 beats per minute (bpm). CONCLUSIONS: We disclosed for the first time the beneficial effects of corticosteroids in the fetal cardiohemodynamics and conduction system of affected fetuses with the presence of maternal anti-SSA(B) antibodies.
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