Transient unexpected improvement of AV conduction: what is the mechanism?
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Journal Article↗
Biomedical subjects
Paul Schweitzer
Publications and source records attributed to Paul Schweitzer.
Triggers of sustained monomorphic ventricular tachycardia differ among patients with varying etiologies of left ventricular dysfunction.
BACKGROUND: The mechanisms underlying the initiation of sustained ventricular tachycardia (VT) have not been fully elucidated. The extent to which reentry, abnormal automaticity, and triggered activity play a role in VT differs depending on the etiology of left ventricular dysfunction. By analyzing electrograms from implantable cardioverter defibrillator (ICD), we sought to determine whether there were differences in VT initiation patterns between patients with ischemic and nonischemic cardiomyopathy. METHODS: We analyzed ICD electrograms in patients with ejection fractions < 40% who had sustained VT over a 27-month period. The trigger for VT onset was classified as a ventricular premature beat (VPB), supraventricular tachycardia, or of "sudden onset." The baseline cycle length, VT cycle length, coupling interval, and prematurity ratio were recorded for each event. The prematurity ratio was calculated as the coupling interval of the VT initiator divided by the baseline cycle length. RESULTS: Sixty-three VT events in 14 patients met the inclusion criteria. A VPB initiated the VT in 58 episodes (92%), 1 episode (2%) was initiated by a supraventricular tachycardia, and 4 episodes (6%) were sudden onset. The prematurity ratio was significantly higher (P < 0.05) in patients with ischemic cardiomyopathy (0.751 +/- 0.068) as compared to patients with nonischemic cardiomyopathy (0.604 +/- 0.139). CONCLUSION: VPBs initiated most sustained VT episodes. A significantly higher prematurity ratio was observed in the ischemic heart disease group. This may represent different mechanisms of VT initiation in patients with ischemic versus nonischemic heart disease.
Aged↗
The initial (earliest) report of polymorphous ventricular tachycardia.
In these short historical notes, we describe the early history of polymorphic ventricular tachycardia. Polymorphous ventricular tachycardia was probably first noted in 1918 by Wilson and Robinson. In a publication describing complete heart block and ventriculophasic arrhythmia, they noted a tachyarrhythmia characterized by multiple extrasystoles of different types at a rapid rate. Also, we briefly discuss the earliest recognized torsades de pointes by Dessertenes in 1966 and the first description of catecholaminergic polymorphic ventricular tachycardia, by Reid in 1977.
History, 20th Century↗
Wide QRS tachycardia: what is the rhythm?
We report a case of an elderly man who presented to the emergency room complaining of palpitations. Electrocardiogram revealed wide QRS tachycardia with a narrow beat within the tachycardia. Most commonly, a narrow complex beat during a wide complex tachycardia suggests a capture or fusion beat in the setting of ventricular tachycardia. However, there are situations where supraventricular tachycardia can also manifest this way. In our patient a pacemaker interrogation clarified the diagnosis.
Aged, 80 and over↗
Papillary muscle masquerading as a vegetation.
We describe a case of an elderly man with an unusual post-operative complication after mitral valve replacement. The final diagnosis was discovered on reoperation. To our knowledge, this phenomenon has not been described in the literature previously.
Aged, 80 and over↗
Relation of T-wave inversion in Q-wave acute myocardial infarction to myocardial viability on resting rubidium-82 and 18-fluoro-deoxyglucose positron emission tomography imaging.
T-wave inversion in areas of Q-wave myocardial infarction has been advocated as a predictor of myocardial viability. However, the predictive value of this electrocardiographic finding in distinguishing viable from nonviable muscle is not fully defined. Thus, we correlated electrocardiographic Q waves and a measure of T-wave inversion with the results of rubidium-82 (Rb-82) and 18-fluoro-deoxyglucose-positron emission tomography (FDG-PET) imaging at rest. We analyzed 35 Q-wave myocardial infarct regions in 25 patients. Nineteen of the 35 (54%) were judged viable by Rb-82/FDG-PET. Using the Novacode T-wave score, T-wave inversion was present in 11 of 19 regions (58%) with viability and 5 of 16 regions (31%) without viability. Thus, neither Q waves nor T-wave inversion can accurately predict myocardial viability in patients with Q-wave myocardial infarction.
Acute Disease↗
Competency in electrocardiogram interpretation among internal medicine and emergency medicine residents.
PURPOSE: Accurate interpretation of the electrocardiogram is critical, yet there are no evidence-based guidelines for assessing competency. Our study evaluated the ability of internal medicine residents and emergency medicine residents to interpret a variety of electrocardiograms. METHODS: The 120 participants included 87 internal medicine residents and 33 emergency medicine residents at two hospitals. Participants reported their sex, training level, adequacy of training, career interest in cardiology, and estimated electrocardiogram proficiency. They then took a test containing 12 electrocardiograms and recorded their diagnosis and certainty. Two cardiologists independently established the correct diagnoses. Two blinded, independent graders scored each electrocardiogram (0 = incorrect, 1 = partially correct, 2 = correct). RESULTS: The median proficiency was 6 out of 10, total electrocardiogram score was 15 of 24, and certainty was 33 of 48. There was no significant difference in overall competency between emergency medicine and internal medicine residents (14.0 vs 15.0, P = 0.239). Internal medicine residents interested in a cardiology career scored higher than those not interested in a cardiology career (17.3 vs. 14.1, P = 0.003). When analyzing the most critical diagnoses, we found that the mean score for ventricular tachycardia was 1.6 of 2.0, for myocardial infarction was 1.3 of 2.0, and for complete heart block was 0.8 of 2.0. Over half of the participants felt their electrocardiogram training was inadequate. CONCLUSION: Despite improvement in interpretation with clinical experience, overall performance was low. Research is needed to find optimal methods to improve electrocardiogram competency.
Career Choice↗
Early history of the pre-excitation syndrome.
This brief review discusses the interesting early history of the pre-excitation syndrome. In 1913 Cohn and Fraser published the first patient with a short P-R interval, wide QRS complexes, and paroxysmal tachycardia. This was followed by other cases of pre-excitation syndrome, all of which were considered to be due to bundle branch blocks. In 1930 Wolff, Parkinson, and White reported 11 patients with the syndrome, which came to bear their name. Two years later, Holzmann and Scherf suggested bypass tracts as the most likely mechanism of pre-excitation syndrome. In 1942, Wood et al. documented the first accessory connection at autopsy. Despite these early studies supporting the bypass theory, the quest for alternative mechanisms continued until the 1970s when electrophysiological studies and surgical therapy confirmed accessory connections as the mechanism of pre-excitation syndrome.
History, 20th Century↗
A troubled beginning: evolving concepts of an old arrhythmia.
The development of the sphygmograph in the nineteenth century marked the beginning of graphic registration of the arterial and venous pulse. Mackenzie, among other investigators, used this technique to study cardiac rhythm. In the early 20th century, Einthoven developed the electrocardiogram, which replaced the less sophisticated arterial and venous registrations of cardiac events and allowed for more detailed arrhythmia analysis. Interestingly, the early study of cardiac arrhythmias was obscured by misinterpretation. Specifically, atrial fibrillation stands out as a rhythm that was extensively studied though misconstrued in its early history. What follows is an in-depth consideration of the original investigations and evolving theories of this important arrhythmia.
Atrial Fibrillation↗
Measurement of QTc in patients receiving chronic methadone therapy.
Recent reports suggest that methadone may prolong the QTc interval and cause torsades de pointes. This study was conducted to evaluate the prevalence of QTc prolongation during oral methadone therapy and identify factors associated with prolongation. Patients receiving oral methadone as treatment for chronic pain or addiction were eligible for the study. One hundred four patients who were receiving > or = 20 mg methadone per day for > or = 2 weeks underwent electrocardiograms to measure QTc interval duration. Sixty-three (61%) patients were male and 63 (61%) were receiving methadone maintenance for opioid addiction. The mean (+/- SD) age was 45.3 +/- 9.4 years. The median (range) methadone dose was 110 mg/day (20-1200 mg/day); median (range) number of months on methadone was 12.5 months (1-444 months). The median (range) QTc interval was 428 msec (396-494 msec). Thirty-three percent had QTc prolongation (males 40%, females 20%; P=0.03). No patient had a QTc longer than 500 msec. Significant dose response was observed in males on methadone <12 months (rho=0.60, P=0.02). Our study suggests that methadone may prolong the QTc interval in specific subpopulations but poses little risk of serious prolongation.
Electrocardiography↗
Inhibition of cyclooxygenase-2 elicits a CB1-mediated decrease of excitatory transmission in rat CA1 hippocampus.
Cannabinoid receptor (CB1) ligands decrease excitatory and inhibitory transmission in the hippocampus, but the influence of endogenously formed cannabinoids (eCBs) on basal excitatory transmission remains uncertain. Here, we investigated the influence of eCBs on synaptic transmission in CA1 hippocampus using the slice preparation. Blockade of CB1 with the selective receptor antagonists SR141716 (rimonabant) or AM251 augmented synaptic responses evoked upon stimulation of the Schaffer collaterals. This effect persisted in the presence of bicuculline or CGP55845 to block GABA(A) or GABA(B) receptors, revealing a tonic eCB influence on excitatory transmission. Selective inhibition of cyclooxygenase-2 (COX-2) with meloxicam or NS-398 decreased excitatory responses partly in a CB1-dependent manner, independently of GABA(A) transmission. Paired-pulse paradigms suggested a presynaptic CB1 mechanism to decrease glutamate release. Inhibition of COX-1 or other routes of eCB degradation did not affect synaptic transmission. We conclude that COX-2 regulates the formation of CB1 ligands that decrease hippocampal excitatory transmission.
Animals↗
Endocannabinoids restrict hippocampal long-term potentiation via CB1.
Cannabinoid ligands alter cognition and prevent long-term potentiation (LTP) of synaptic transmission, but the influence of endogenously formed cannabinoids (eCBs) on hippocampal LTP remains ambiguous. In the accompanying study, we showed that eCB levels regulated by cyclooxygenase-2 (COX-2) tonically decrease basal excitatory transmission. Here, we investigated the influence of eCBs on LTP in CA1 hippocampus. LTP elicited by moderate stimulations (20 or 50 pulses) was facilitated in slices treated with a CB1 antagonist, whereas LTP elicited with robust stimulations (100 or 200 pulses) was unchanged by CB1 blockade. LTP elicited with theta-burst stimulations also was facilitated with CB1 blockade, revealing a tonic inhibitory influence of eCBs on LTP induction. Conversely, inhibition of COX-2 prevented LTP elicited with theta burst stimulations. Inhibition of COX-1 or other routes of eCB degradation did not affect LTP. We conclude that COX-2 regulates the formation of CB1 ligands that negatively regulate LTP.
Animals↗
A rare, late complication after automated implantable cardioverter-defibrillator placement.
This article describes an interesting case of automated implantable cardioverter defibrillator (AICD) extrusion fifteen months after implantation. The case report is followed by a discussion of the causes and treatment of skin erosion following pacemaker/AICD insertion.
Journal Article↗
An unusual tachycardia.
The following article presents an unusual case of atrial tachycardia, initially misdiagnosed due to a lack of clear P waves. The diagnosis was eventually confirmed using the atrial electrogram from the patient's pacemaker.
Journal Article↗
gamma-hydroxybutyrate increases a potassium current and decreases the H-current in hippocampal neurons via GABAB receptors.
gamma-Hydroxybutyrate (GHB) is used for the treatment of alcoholism and to induce absence seizures in animals, but it has also recently emerged as a drug of abuse. In hippocampal neurons, GHB may activate its own putative receptor as well as GABA(B) receptors to affect synaptic transmission. We used voltage-clamp recordings of rat CA1 pyramidal neurons to characterize the postsynaptic conductances affected by GHB and to further clarify the site of GHB action. Low concentrations of GHB (0.1-1 mM) did not affect postsynaptic properties, but 10 mM GHB elicited an outward current at resting potential by augmenting an inwardly rectifying potassium current and concomitantly decreased the hyperpolarization-activated H-current (I(h)). Like GHB, the selective GABA(B)-receptor agonist baclofen (20 microM) increased a potassium current and decreased I(h). In the presence of 10 mM GHB, the baclofen effects were largely occluded. The selective GABA(B) receptor antagonist CGP 55845 [3-N[1-(S)-(3,4-dichlorophenyl)ethyl]amino-2-(S)-hydroxypropyl-p-benzyl-phosphinic acid] blocked the effects of both GHB and baclofen, whereas the putative GHB receptor antagonist NCS-382 [(2E)-(5-hydroxy-5,7,8,9-tetrahydro-6H-benzo[a][7]annulen-6-ylidene ethanoic acid] was ineffective. The GHB and baclofen effects were prevented in the presence of 200 microM barium, indicating that GHB augments a K(+) conductance, probably a G protein-coupled inwardly rectifying K(+) (GIRK) current. The decrease of I(h) by GHB and baclofen was also prevented by barium, suggesting that the diminution of I(h) is secondary to GIRK augmentation. Our results indicate that high GHB levels, which can be reached during abuse or intoxication, activate only GABA(B) receptors and not GHB receptors at the postsynaptic level to augment an inwardly rectifying K(+) current and decrease I(h).
Animals↗
Role of angiotensin-converting enzyme inhibitors in the prevention of atrial fibrillation.
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Angiotensin-Converting Enzyme Inhibitors↗
Ethanol augments GABAergic transmission in the central amygdala via CRF1 receptors.
The central amygdala (CeA) plays a role in the relationship among stress, corticotropin-releasing factor (CRF), and alcohol abuse. In whole-cell recordings, both CRF and ethanol enhanced gamma-aminobutyric acid-mediated (GABAergic) neurotransmission in CeA neurons from wild-type and CRF2 receptor knockout mice, but not CRF1 receptor knockout mice. CRF1 (but not CRF2) receptor antagonists blocked both CRF and ethanol effects in wild-type mice. These data indicate that CRF1 receptors mediate ethanol enhancement of GABAergic synaptic transmission in the CeA, and they suggest a cellular mechanism underlying involvement of CRF in ethanol's behavioral and motivational effects.
Alcohol Drinking↗