Fast-Slow Type of Atrioventricular Nodal Reentrant Tachycardia: Horizontal Dissociation of the AV Node During Tachycardia

Two patients with recurrent supraventricular tachycardia are presented. The tachycardia was initiated and terminated by atrial extrastimulation beyond the atrial relative refractory period and the atrial activation sequence during the tachycardia was low to high. The induction of tachycardia was dependent on a critical AH interval. In patient 1 who had ventriculoatrial conduction, the tachycardia was initiated by the premature ventricular stimulation followed by double atrial response. In patient 2 the ventriculoatrial conduction was not observed. In both patients, the unchanged atrial cycle length during the tachycardia with antegrade Wenckebach AH block was observed. When AH block occurred during tachycardia the first AH interval was shorter than the subsequent HA interval. In patient 2 verapamil (5 mg) prolonged the atrial cycle length during tachycardia and rapid intravenous injection of adenosine triphosphate (10 mg) terminated the tachycardia. Oral diltiazem (280 mg/day) suppressed the tachycardia in patient 1. These findings suggest that the mechanism of tachycardia may be fast-slow type of AV nodal reentry in the upper portion of the AV node and this type of arrhythmia has tendency to show incessant form.     

Bone marrow transplantation for erythroleukemia: A case report

A 2 year old girl was diagnosed as having erythroleukemia (EL; M6 according to the French-American-British classification). After one course of low-dose cytosine arabinoside (Ara-C), complete remission was obtained. After three courses of low-dose Ara-C for consolidation, allogeneic bone marrow transplantation was performed from HLA-identical sibling. The course of post-transplantation was uneventful. Two years after transplantation, she continues to have durable engraftment and remission. In children with EL, conventional chemotherapy appears to be inadequate for producing durable long-term disease-free survival. Bone marrow transplantation should be considered in children with EL, in cases where suitable donors are available.     

Effects of Chronotropic Responsive Cardiac Pacing on Ventilatory Response to Exercise in Patients with Complete AV Block

To identify the effect of chronotropic responsive cardiac pacing on the ventilatory response to exercise, ten selected patients with complete atrioventricular block underwent paired cardiopulmonary exercise tests in fixed rate ventricular (WI) and dual chamber (DDD) or rate responsive ventricular (VVIR) pacing modes. Compared to VVI pacing, DDD or VVIR pacing increased peak oxygen uptake (P < 0.005) and augmented anaerobic threshold (P < 0.001), In eight patients, dyspnea was the major symptom limiting exercise with VAT pacing and this was markedly attenuated with DDD or VVIR pacing. In all patients, ventilation (VE) and the ratio of ventilation to CO₂ production (VE/VCO₂) were consistently higher with VVI pacing during exercise. To compare the response of the two pacing modes at the same workloads in an aerobic condition, we measured ventilatory variables 1 minute prior to the anaerobic threshold obtained with VVI pacing. When DDD or VVIR pacing was compared with VVI pacing, VE and VE/VCO₂ significantly decreased from 20.5 ± 5.3 L/min to 18.3 ± 5.0 L/min (P < 0.005) and from 35.9 ± 5.8 to 31.9 ± 5.0 (P < 0.003), respectively. Respiratory frequency rose significantly more with VVI pacing (P < 0.001) despite an unchanged tidal vohame. Although peak VE did not differ between the two pacing modes, VE/VCO₂ at the peak exercise increased significantly more with VVI pacing (P < 0.005). Respiratory frequency also rose more with VVI pacing (P < 0.005) and tidal volume did not change. This study suggests that chronotropic responsive cardiac pacing attenuates the exertional dyspnea by improving the ventilatory response to exercise as well as increasing the cardiac output in patients with complete atrioventricular block.     

Functional Communication Between Cardiac ATPSensitive K+ Channel and Na/K ATPase

K_ATP Channel and Na/K ATPase. Introduction: Functional interaction between K_ATP channel and Na/K ATPase was studied in single guinea pig ventricular myocytes because both membrane molecules are known to he involved in ischemic episodes. Methods and Results: K_ATP channel currents were recorded at 36°C by using whole cell, cell attached, inside-out, and open cell-attached modes of patch clamp techniques on enzymatically isolated ventricular myocytes. In the whole cell mode, ouabain (1 μM) reversibly inhibited the K_ATP currents induced by metabolic stress (ATP-free pipette solution and 1 mM NaCN), but not those activated by cromakalim (100 μM), a K_ATP channel opener. In the cell-attached mode, ouabain concentration dependently inhibited K_ATP, channel opening induced by metabolic suppression (5.5 μM 2-deoxyglucose and 1 mM CN). Half-inhibition concentration for ouabain was 21.0 ± 5.5 nM and the Hill coefficient was 0.8 ± 0.1 (n = 26). However, ouabain did not have an effect on the channel activity induced by cromakalim (100 μM). In the inside-out mode, ouabain applied to the internal side of membrane did not affect the channel. In the open cell-attached mode made by preincubation with streptolysin-0 (0.08 U/mL), the K_ATP channels were not activated by the metabolic inhibitors but were by reducing extracellular ATP concentrations, because subsarcolenimal ATP concentration could he controlled through tiny membrane holes. The channels thus activated were not suppressed by ouabain. Conclusion: The inhibition of Na/K ATPase by ouahain appeared to block the K_ATP channels by accumulating subsarcolemmal ATP caused by a decrease of the transition from ATP to ADP. In the presence of ischemic episodes, the administration of digitalis compounds may affect the opening of K_ATP channels, which is primarily protective against the development of irreversible myocardial damage.     

Significance of pre-infarction angina for occurrence of post-infarction angina

We evaluated the factors determining the occurrence of post-infarctionangina in 41 patients who had intracoronary thrombolysis within6 h of the onset of acute myocardial infarction. Pre-infarctionangina was considered to be present if it occurred more thanone week before acute myocardial infarction. Post-infarctionangina was defined as typical chest pain occurring within 10days following the infarction. Collateral flow to the infarctzone was determined to be present if any portion of the infarct-related epicardial artery or side branches was visualized. Incases of successful thrombolysis, the prevalence of post-infarctionangina was not significantly influenced by pre-infarction anginaand the extent of collateral circulation. However, in patientswithout recanalization, pre-infarction angina and collateralblood flow supply to the area at risk caused a high prevalenceof angina after infarction. It is concluded that pre-infarctionangina indicative of myocardial ischemia is associated withpost-infarction angina especially in patients with conventionaltherapy, because the jeopardized myocardium is salvaged substantiallyby collateral circulation with a limited flow reserve     

Diastolic myocardial wall stiffness of the left ventricle in chronic pressure overload

Five dogs were instrumented with a left ventricular (LV) micromanometer,pairs of ultrasonic crystals to measure L V short axis and LV wall thickness and an inflatable cuff around the ascendingaorta. Wall stress, midwall strain and strain rate were calculatedat rest, after acute pressure elevation, and one, two and threeweeks as well as 24 h after release of aortic constriction.Myocardial wall stiffness and viscosity were determined froma viscoelastic stress-strain model. Reference values at zeropressure were determined in all five dogs. LV end-diastolic pressure increased from 7 mm Hg at rest to25 mm Hg after acute pressure elevation, to 18 mm Hg after twoweeks and decreased to 16 mm Hg after three weeks of pressureelevation, and 11 mm Hg at release of aortic constriction. LV peak systolic pressure increased from 140 mm Hg at rest to218 mm Hg after acute pressure elevation, to 227 mm Hg afterthree weeks of pressure elevation and returned to normal (143mm Hg) after cuff release. Diastolic myocardial wall stiffnessshowed no change from 23 at rest to 19 after acute pressureelevation, but increased to 47 after one and 81 after two weeks,and it decreased to 50 after three weeks and 45 after cuff release.Myocardial viscosity increased from 0.1 at rest to 3.0 afteracute pressure elevation and remained elevated during chronicpressure elevation. The reference values at zero filling pressureshowed an increase in LV short axis (creep) from 25.6 mm atrest to a maximum of 28.9 mm after one and two weeks of pressureelevation and then decreased to 27.0 mm after three weeks. LVwall thickness at zero pressure increased from 12.8 mm at restto 13.7 mm after three weeks of pressure elevation and remainedelevated after cuff release (13.8 mm). Thus, diastolic myocardial wall stiffness increased during theinitial stages of chronic pressure overload during ventriculardilatation, but decreased when dilatation regressed and concentrichypertrophy developed. Myocardial viscosity was increased duringboth acute and chronic pressure overload. It is suggested thatthe early increase in myocardial stiffness may be more importantlyrelated to ventricular dilatation with creep than to wall hypertrophyper se.     

Quantitative Relationship Between Atrial Refractoriness and the Dispersion of Refractoriness in Atrial Vulnerability

We investigated the quantitative relationship between the atrial refractory period and the dispersion of refractoriness with respect to atrial vulnerability in 19 adult mongrel dogs. The atrial effective refractory period (AERP) was measured at the sinus node area (SNA), the low posterior right atrium (LRA), and the distal coronary sinus. The study was performed under the following conditions: (1) control status; (2) hypothermia (30°C); (3) vagus nerve stimulation; and (4) a combination of (2) and (3). The subjects were separated into two groups: atrial fibrillation (AF) (+) group (n = 23), which developed AF by atrial extrastimulus due to increased vulnerability, and AF (−) group (n = 39), which did not develop AF. The mean AERP was 97 ± 23 msec (mean ± SD) in the AF (+) group and 124 ± 23 msec in the AF (−) group, with a significantly shorter refractory period seen in the former (P < 0.001). The dispersion of refractoriness was 59 ± 24 msec in the AF (+) group and 29 ± 18 msec in the AF (−) group, with a significant increase noted in the former (P < 0.001), On X-Y coordinates (where X denotes the AERP, and Y denotes the dispersion of refractoriness) the data from the AF (+) group were clustered in the upper left region of the graph while the data from the AF (−) group were clustered in the lower right region. These two groups were separated by a linear equation of Y = 0.86X - 57 with a predictability of 90.3%. No difference in the time from SNA stimulation to LRA excitation was found between the groups. On the basis of these results, we suggest that increased atria) vulnerability can be predicted from an analysis of the quantitative relationship between the atrial refractory period and the dispersion of refractoriness.