Vasospastic Angina with J‐Wave Pattern and Polymorphic Ventricular Tachycardia Effectively Treated with Quinidine

Background: Myocardial ischemia during coronary spasm may generate malignant ventricular arrhythmias. The J‐wave pattern was suggested to be a marker of a disorder associated with life‐threatening arrhythmias. Results: We report the case of a patient with vasospastic angina and J‐wave pattern in inferior and lateral leads associated with polymorphic ventricular tachycardia which was effectively treated only with quinidine—vasodilating drugs were not able to prevent the arrhythmia although they were effective in preventing ischemic events. Conclusion: The J‐wave pattern in inferolateral leads may be a sign of electrical vulnerability to lethal ventricular arrhythmia in patients suffering from vasospastic angina—quinidine can effectively prevent such arrhythmias in these patients.     

Response to Atrial Extrastimulus During Supraventricular Tachycardia: What Is the Mechanism?

Arrhythmia Rounds . We describe a case illustrating the potential challenges in distinguishing AV nodal reentry tachycardia (AVNRT) from automatic junctional tachycardia (JT). While an early atrial extrastimulus advanced the next His and ventricular depolarization without tachycardia termination, suggesting JT, other features indicated the correct diagnosis of AVNRT. This teaching case demonstrates a novel exception to a recently reported diagnostic pacing maneuver and illustrates the importance of considering response to multiple maneuvers in reaching a diagnosis of SVT mechanism. (J Cardiovasc Electrophysiol, Vol. 24, pp. 359‐363, March 2013)     

Inhibitory effects of sigma‐1 ligands on handling‐induced tachycardia in conscious tethered rats

We used conscious tethered Sprague‐Dawley rats to evaluate the cardiovascular effects of four sigma‐1 (σ₁) agonists and five antagonists, given alone or in combination. All drugs were administered as a single intraperitoneal dose. The agonists were given at doses reported as efficacious in rodent cognition models, while the antagonists were administered at doses neutralizing agonist effects in vivo. Systolic blood pressure (SBP) and heart rate (HR) were continuously recorded for 20 min before and 60 min postadministration. Immediately after injection, a sudden, transitory increase in HR and SBP was noted in all animals, because of the stress induced by handling. For both parameters, a peak value (ΔHR_max and ΔSBP_max) and an area under the curve of changes from baseline over the period 5–20 min postinjection (ΔHR_AUC_{5–20 min} and ΔSBP_AUC_{5–20 min}) were calculated. Three of the four σ₁ agonists (SKF‐10,047, dehydroepiandrosterone (DHEAS), Compound 14) significantly reduced ΔHR_AUC_{5–20 min} value without changing ΔHR_max, while the fourth one, SA‐4503, had no significant effect. None of the antagonists (haloperidol, rimcazole, NE‐100, and BD1047) reduced, and even one (progesterone) enhanced the stress‐induced effects on HR. No changes in SBP were noted with any compound. When the antagonist NE‐100 was administered just before SKF‐10,047, it completely reversed the inhibitory effects of the σ₁ agonist on HR increase. In conclusion, we demonstrated for the first time the involvement of σ₁ receptors in the regulation of handling‐induced tachycardia in the conscious rat. Although additional investigations are needed to fully understand this role, it might offer new therapeutic perspectives to σ₁ ligands in the cardiovascular sphere.     

Catheter ablation for ventricular tachycardia: indications and techniques

Ventricular tachycardia (VT) may be secondary to many different underlying pathophysiologies. The nature of the underlying disorder determines amenability to catheter ablation, thus, dictating the circumstances under which it should be undertaken. The differing substrates also influence the choice of techniques that are used. The most intensively studied clinical subgroup of VT is re-entrant VT in the setting of ischemic heart disease. The approach to ablation in such patients is discussed in detail. Subsequent discussion focuses on other clinically encountered varieties of VT and the ablation methods used in each individual disease state.     

Azimilide dihydrochloride

Azimilide dihydrochloride is an antiarrhythmic drug with Vaughn Williams class III properties, which blocks both fast (IK_r) and slow (IK_s) components of the delayed rectifier cardiac potassium channel. The drug slows the heart rate slightly and, like other class III antiarrhythmic drugs, prolongs ventricular repolarization and thus, the QT interval. Unlike sotalol, another class III antiarrhythmic drug, azimilide does not exhibit reverse-use dependence, that is, its binding characteristics and effectiveness are not related to the heart rate. Azimilide is 85% bioavailable, reaches peak blood concentrations in 6–8 h and has a long elimination half-life of 114 h. Clinical trials have utilized once-daily dosing. These trials have tested the use of the drug for patients with supraventricular and ventricular arrhythmias.     

Multiple Concealed Accessory Pathways Associate with Antegrade Triple AV Nodal Pathways and Catheter Ablation

This article describes a 54-year-old man with incessant supraven-tricular tachycardia refractory to antiarrhythmic drugs. Multiple concealed accessory pathways associated with antegrade triple AV nodal pathways were documented by a series of successful catheter ablations and detailed electrophysiological studies. After the left-wall accessory pathways were abolished with two courses of multiple low energy shocks, another two accessory pathways, one near the os of coronary sinus and the other near the site of the His bundle, were documented by programmed premature ventricular stimulation. This was followed by a third course of shocks to the os of coronary sinus for ablating posteroseptal AP and a fourth course of shock to proximal His bundle for control of SVT with a septal accessory pathway as a retrograde limb and AV nodal pathways as an antegrade limb. Without medications, the patient has remained asymptomatic even during moderate physical activity over a follow-up period of 36 months. His ECG showed sinus rhythm with persistence of right bundle branch block.     

Effects of Cimetidine on Sinus Node Function and Atrioventricular Conduction in Man

Electrophysiological effects of H2-receptor blockade 200 mg cimetidine IV on sinus node (SN) function and atrioventricular (AV) conduction were evaluated. Tests were performed in 21 people in basal state (group I), and in 14 people (group II) after autonomic blockade (AB) (propranolol 0.2 mg/kg, and atropine 0.04 mg/kg). We analyzed sinus cycle length (SCL), sinus node recovery time (SNRT), corrected sinus node recovery time (CSNRT), and secondary pause (SP) as the longest sinus pause after incremental overdrive pacing, sinoatrial conduction time (Strauss method) (SACT), Wenckebach point (WP), and blood pressure (BP). In group I, cimetidine prolonged SCL (717 ± 98 vs 860 ± 138 msec P < 0.001), SNRT (1161 ± 153 vs 1263 ± 163 msec P < 0.002), SP (943 ± 183 vs 1072 ± 187 msec P < 0.001), SACT (121 ± 20 msec vs 149 ± 21 msec P < 0.002), and lowered rate at which AV nodal Wenckebach point were observed (169 ± 24 vs 160 ± 26 beats/min P < 0.02). The drug did not produce significant change of the CSNRT (439 ± 121 vs 402 ± 107 msec. In group II, after AB cimetidine prolonged SCL (643 ± 79 vs 656 ± 86 msec P < 0.05), SP (686 ± 114 vs 717 ± 109 msec P < 0.05) and lowered WP (170 ± 19 vs 166 ± 19 beats/min P < 0.02) significantly. The effects of cimetidine, after AB on SNRT (894 ± 180 vs 920 ± 164 msec, CSNRT (243 ± 99 vs 255 ± 85 msec), SACT (85 ± 20 msec vs 90 ± 22 msec) were not significant. We conclude that H2-receptor blockade decreases SN automatically, prolongs SACT and AV conduction in man. The study suggests that histamine takes part in regulation of electrophysiological properties of the human heart in vivo.     

Electrophysiologic and histopathologic correlations in a case of permanent form of reciprocating tachycardia

A case of permanent junctional reciprocating tachycardia withpost-mortem documentation of an accessory atrioventricutar pathwayas the substrate of the arrhythmia is reported. Tachycardiahad lasted for 15 years and showed a retrograde P wave (P')and R–P' longer than P'–R interval. The tachycardiacircuit utilized a concealed posterior septal accessory pathwayas the retrograde limb. Because the arrhythmia was disablingand unresponsive to pharmacological treatment, the patient underwentclosed chest ablation of the His bundle. After the procedure,no anterograde or retrograde conduction over the normal conductionsystem was observed; anterograde conduction over the anomalouspathway showed decremental properties. Because of previous myocardialinfarction, the patient developed a ventricular aneurysm anddied suddenly 5 months after His bundle ablation. Histologicalexamination of the heart revealed a group of tiny fibromuscularbundles joining the lower rim of the coronary sinus outlet tothe summit of the interventricular septums; the anomalous atrioventricularconnection pursued a sinuous, tortuous path. The geometricaldisposition of the accessory pathway may have been responsiblefor the decremental properties of conduction observed duringlife.     

Absent right atrioventricular connexion with the left atrium connected to the morphologically right ventricle, a right-sided rudimentary left ventricle, and right juxtaposition of the atrial appendages: documentation by angiography and cross-sectional echocardiography

In this report, a 12-hr-old male infant was demonstrated to have the absent connexion variant of right atrioventricular valve atresia with the left atrium connected to the morphologically right ventricle with a right-sided rudimentary left ventricle. The aorta arose from the right ventricle and there was pulmonary atresia, the pulmonary circulation being duct-dependent. In addition there was right juxtaposition of the atrial appendages. The definitive cross-sectional echocardiographic and angiographic findings are presented.     

Unreported cardiac arrhythmias in aluminium worker

Aluminium (Al) is the third most prevalent element, representing approximately 8% of total mineral components in the earth's crust (1). Chronic exposure to Al is mainly encountered at particular work places, for example, in foundries or in the Al powder industry, as an occupational exposure. In case of occupational Al exposure, inhalation is the main route of uptake. Chronic exposure to Al is associated with skeletal, neurological, hematological and lung changes. Studies regarding the Al powder industry showed that long-term inhalative exposure to Al can induce pulmonary fibrosis (2). Although there is only one report about ventricular tachycardia as a cardiac manifestation in occupationally exposed persons (3), in this report, we presented a case that had Mobitz type I second-degree atrioventricular block and nonsustained ventricular tachycardia. To our knowledge, this is the first report in chronic poisoning.