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Biomedical subjects

M Shenasa

Publications and source records attributed to M Shenasa.

94 records · Page 6Linked to original sources

Role of retrograde His Purkinje block in the initiation of supraventricular tachycardia by ventricular premature stimulation in the Wolff-Parkinson-White syndrome.

The precise mechanisms for paroxysmal reentrant supraventricular tachycardia (PSVT) initiation during right ventricular premature stimulation (V(2) method) were analyzed in 14 consecutive patients with Wolff-Parkinson-White Syndrome in whom the PSVT was inducible during retrograde refractory period studies. 9 patients had left-sided and the remaining 5 of 14 had right-sided ventriculo-atrial (VA) accessory pathway (AP). At the basic cycle lengths (V(1)V(1)) ranging from 550 to 900 ms (mean, 657.1+/-139.5), closely coupled V(2) (mean V(1)V(2), 357.3+/-59.2 ms, range 320-500) produced retrograde His bundle (H(2)) activation via the bundle branches and retrograde atrial (A(2)) activation via the AP. As the V(1)V(2) were further shortened, the V(2) showed a retrograde block in the His Purkinje system (HPS) and conducted to the atria via AP in 9 of 14 cases. Subsequently, the A(2) impulse conducted anterograde over the atrioventricular node-HPS to initiate a PSVT or an atrial echo response in all nine cases. In none of the patients was a PSVT induced by V(2) when the latter produced retrograde H(2) activation via the bundle branches. In 10 of 14 cases, however, the retrograde H(2) was followed by a V(3), due to macroreentry in the HPS. The V(3) in turn blocked retrogradely in the HPS while producing A(3) via the AP to initiate a PSVT or an atrial echo response in 9 of 10 cases. Retrograde block of V(2) and/or V(3) in the HPS resulted in PSVT initiation in 13 of 14 cases, whereas in the remaining 1 case the exact mechanism was not clear. In none of the patients in this series was the PSVT initiated with a retrograde block of V(2) in the atrioventricular node with or without concomitant retrograde A(2) activation via the AP. We conclude that within the ranges of cycle lengths tested, a retrograde block of V(2) and/or V(3) in the HPS is the most common mechanism for initiation of PSVT during ventricular premature stimulation in patients with the Wolff-Parkinson-White Syndrome.

Bundle of His↗

Anisotropic conduction characteristics in ischemia-reperfusion induced chronic myocardial infarction.

OBJECTIVES: Anisotropic properties of cardiac tissue play an important role in initiation and perpetuation of ventricular tachycardia. However, anisotropic conduction properties in different morphologic types of chronic myocardial infarctions as well as frequency dependency still need to be elucidated. In the present study, the characteristics of anisotropic conduction were investigated in situ in the setting of ischemia-reperfusion induced chronic myocardial infarction. METHODS: Myocardial infarction was induced in 12 dogs by a percutaneous transcatheter left anterior descending coronary artery occlusion-reperfusion technique. Four additional dogs served as normal controls. After 14 to 20 days, epicardial mapping was performed using simultaneous unipolar recordings from 240 electrodes of a plaque electrode array placed on the epicardial border zone overlying the infarctions. Constant rate pacing with five cycle lengths (CL) ranging from 500 to 200 ms as well as programmed electrical stimulation (PES) with four basic cycle lengths (BCL) ranging from 430 to 300 ms and single extrastimuli (S2) were performed. RESULTS: Two anatomically different patterns of epicardial surface morphology were analyzed, designated as type I and type II. In seven animals, there was a continuous thin layer of surviving epicardial muscle fibers overlying the infarction (type I). During pacing with CL of 500 vs 200 ms, conduction velocity longitudinal to fiber orientation (theta L) decreased significantly in the infarcted animals compared to control group (10.9% vs 5.2%, p < 0.05) whereas conduction velocity transverse to fiber axis (theta T) decreased to a similar degree in control and infarcted animals (6.9 vs 7.4%, n.s.). After premature stimulation, there was considerably greater reduction in theta L in infarcted animals than in controls (39.8% vs 31.5%, p < 0.05) whereas theta T decreased to a similar extend in infarcted and control animals (22.2% vs 21.4%, n.s.). During constant rate pacing and premature stimulation, no functional conduction block was induced in type I infarctions. In five animals, the transmural infarctions clearly extended to the epicardial surface, but continuous strands of surviving epicardial muscle fibers traversed the area of necrosis (type II). During PES with S2, functional conduction block and areas of very slow conduction were observed in each case. CONCLUSIONS: In ischemia-reperfusion induced chronic myocardial infarctions, different epicardial patterns of morphology were observed. Anisotropic conduction was frequency dependent in the longitudinal but not in the transverse direction. In type I infarctions, functional conduction block was not inducible during PES whereas in type II infarctions, prerequisites for reentrant arrhythmias like functional conduction block and very slow conduction were induced in each case by single extrastimuli.

Animals↗

Vasovagal syncope: management with atrioventricular sequential pacing and beta-blockade.

A case of vasovagal syncope in an otherwise healthy 74-year-old woman is described. Attempts to prevent symptoms with ventricular and atrioventricular sequential temporary pacing (documented by continuous monitoring of heart rate and intra-arterial recording of blood pressure during spontaneous episodes) proved inadequate. However, the addition of a beta-blocker to permanent DDD pacing was clinically successful in markedly diminishing symptoms. The mechanisms of action of this treatment modality is discussed.

Adrenergic beta-Antagonists↗

Termination of sustained ventricular tachycardia with a new antitachycardia pacemaker: role of the nonautomatic mode to follow pacemaker function.

The use of an antitachycardia pacemaker for the treatment of recurrent, drug resistant nonsyncopal sustained ventricular tachycardia in a 28-year-old patient is described. The report emphasizes the role of electrocardiographic recording during manual activation of the tachycardia response in an outpatient setting. The follow-up covers 12 months with 26 spontaneous tachycardia episodes forcing the patient to go to an emergency room to monitor tachycardia termination. Mean ventricular tachycardia cycle length was 340 +/- 21 ms. Tachycardias were terminated either by the primary or secondary modality without acceleration or degeneration to ventricular fibrillation. Thus, it was possible to assess the efficacy and the safety of the termination programs. Unlike during intensive in-hospital testing, restoration of stable sinus rhythm was complicated by re-emergence of ventricular tachycardia. It is concluded that manual activation with medical supervision provides safe management of selected patients with ventricular tachycardia. However, in-hospital testing overestimated, in this case, the efficacy of tachycardia response modalities to terminate spontaneous tachycardia episodes. The customization of an antitachycardia pacemaker with an automatic implantable cardioverter/defibrillator may increase the quality of life as it would allow switching to automatic pace termination.

Adult↗