Left Ventricular Outflow Tract Tachycardia. Idiopathic ventricular tachycardia (VT) originating from the left ventricular outflow tract (LVOT) is rare. We report two patients whose QRS configuration during VT commonly showed an inferior axis and monophasic R waves in all the precordial leads. The mechanism of these VTs appeared to be triggered activity. From mapping and ablation, the origin of these VTs was determined to be in the most posterior LVOT, corresponding to the aortomitral continuity (left fibrous trigone).
There are only a few reports on successful radiofrequency catheter ablation of idiopathic right ventricular tachycardia (VT) originating from other sites than right ventricular outflow tract. We report here a case of VT which exhibited an inferior-axis and a left bundle branch block pattern and originated near the His bundle. Using the temperature-controlled ablation catheter, prudent observation of the fluoroscopy and intracardiac electrograms during pacemapping, we successfully ablated the origin of the VT without any conduction disturbance. However, further study is required to determine the effectiveness of catheter ablation and the long term prognosis for this type of VT.
In order to examine electrical and mechanical effects of hyponatremia and hypotonicity, relevant to those in patients with 'water intoxication' syndrome, Langendorff-perfused guinea pig hearts were exposed to reduced NaCl concentrations (hypotonic [NaCl](0)-reduction) under the monitoring of left ventricular developed pressure (LVDP) and epicardial ECG. In some hearts, hyponatremia (from 140 to 80 mEq/l) was compensated for by adding mannitol to maintain osmolarity at a constant level (isotonic [NaCl](0)-reduction) or tetraethylammonium chloride to maintain both osmolarity and chloride concentrations at a constant level (isotonic [Na(+)](0)-reduction). Progressive isotonic [NaCl](0)-reduction increased LVDP, which was abolished in the presence of KB-R7943, a novel inhibitor of Na(+)/Ca(2+)-exchange. LVDP was reduced in hypotonic [NaCl](0)-reduction in which myocardial water content was increased. PQ interval and QRS duration were prolonged with both hypotonic and isotonic [NaCl](0)-reduction and these changes tended to be more pronounced with hypotonic than with isotonic [NaCl](0)-reduction. Similar ECG changes were also evident with isotonic [Na(+)](0)-reduction. Gd(3+) (1-5 µM), a blocker of stretch-activated nonspecific cation channels, had no substantial effects on the electrical or mechanical changes seen with hypotonic [NaCl](0)-reduction. In conclusion, isotonic [NaCl](0)-reduction produced a positive inotropism by modulating Na(+)/Ca(2+)-exchange, whereas hypotonic [NaCl](0)-reduction led to negative inotropism, due in part to hypotonic myocardial swelling. In addition, [Na(+)](0)-reduction, irrespective of the concomitant [Cl(-)](0) or osmotic changes, depressed atrioventricular as well as intraventricular conduction.
Although the arrhythmogenic effects of interferon (IF) have been reported in clinical practice, the experimental data are limited. Therefore, these effects were investigated in in vivo and Langendorff-perfusion studies using 3 different groups of rats (ie, control, aorta-banded, and deoxycorticosterone acetate (DOCA)-salt hypertension groups) in the presence or absence of isoproterenol. In the perfusion study, human recombinant IF-α (≤15,000 U/ml) alone induced irreversible atrioventricular blockade in all groups, whereas this agent (≤1,500 U/ml) caused negative inotropism and ventricular tachyarrhythmias (arrhythmic score greater in the order of DOCA-salt>aorta-banded = control group) in the preparations pretreated with isoproterenol (10-9 mol/L). In an in vivo study, IF-α (6×10 6 U/kg) resulted in ventricular tachyarrhythmias only in the presence of isoproterenol (10 mg/kg), as in the perfusion study (arrhythmic score; DOCA-salt>aorta-banded>control). In conclusion, the arrhythmogenesis of IF-α is potentiated in pathophysiological conditions such as cardiac hypertrophy or elevated sympathetic activity. (Circ J 2002; 66: 1161 - 1167)
(1) To define the clinical and laboratory findings predictive of early mortality after myocardial infarction (AMI), 100 consecutive patients were studied. (2) To elucidate the serum potassium (K) concentration and its clinical significance after AMI, 38 patients were studied.(1) The 30-day mortality was greater for women than for men, for patients with diabetes mellitus than for those without, and for patients with previous MI than for those without. Clinical and laboratory findings predictive of early mortality were cardiogenic shock, congestive heart failure, perforation or rupture of the ventricle, and presence of bundle branch block and extensive anterior AMI on electrocardiogram. The presence of bradyarrhythmia, ventricular tachyarrhythmias, and high blood levels of peak creatinine phosphokinase (CPK) or myosin or atrial natriuretic peptide (ANP) were not independent predictors of early mortality. Patients complicated with congestive heart failure showed higher levels of peak CPK and ANP and patients with cardiogenic shock showed higher levels of ANP. (2) Serum K concentration was lower on admission than the following days, and it showed a negative correlation with plasma epinephrine. The lower serum K was accompanied with more severe ventricular arrhythmias on 24-hour electrocardiogram.(1) Early mortality after AMI is related to left ventricular function rather than to arrhythmias. (2) Serum K is lower in the early phase of AMI and is related with plasma catecholamines and severe ventricular arrhythmias.
Cardiac complications are major limiting factors regarding the success of high-dose chemotherapy supported by blood stem cell transplantation (BSCT). The cardiotoxicity of cyclophosphamide remains obscure relative to that of anthracyclines. The aim of this study was to estimate noninvasively the cardiotoxicity of cyclophosphamide administered during the pretransplant conditioning of BSCT for patients with various hematological diseases. A total of 27 consecutive patients were divided into two groups depending on the conditioning regimen, ie, group A (n=15) which received cyclophosphamide (median dose of 120 mg/kg; range 100 to 200 mg/kg) and group B (n=12) which did not. Ultrasound cardiograms (UCG) and signal-averaged electrocardiograms (SAECG) were recorded in the two groups both preceding and following the BSCT. There were no statistical intergroup or intragroup differences in left ventricular (LV) dimensions or contractile function. Significant (P<0.01) posttransplant increases in interventricular septal wall thickness and Ap/Ep ratio were noted in group A. Moreover, the filtered QRS duration as estimated by SAECG was prolonged (P<0.05) whereas the summated LV voltage (SV1+RV5) was reduced in the posttransplant period only in group A. These results suggest that early cyclophosphamide cardiotoxicity was characterized by LV diastolic rather than systolic dysfunction. These findings may contribute to acute hemodynamic deterioration observed after cyclophosphamide-containing conditioning chemotherapy.
