We hypothesized that myocardial infarction-related alterations in ventricular fibrillation (VF) cycle length (VFCL) would correlate with changes in local cardiac electrophysiological and anatomic properties. An electrophysiological study was performed in normal, subacute, and chronic infarction mongrel dogs. VF was induced by programmed electrical stimulation and mean and minimum early and late VFCL was determined and correlated with local electrophysiological and anatomic properties. Effective refractory period (ERP), activation recovery time (ART), ERP/ART ratio, threshold, and ERP and ART dispersion were determined at 112 sites on the anterior left ventricle. Wave front progression was analyzed over a 2-s period. The extent of local tissue necrosis and of myocardial fiber disarray was also evaluated. The early mean VFCL was significantly longer in the subacute infarction (149 +/- 35 ms) and chronic infarction dogs (129 +/- 18 ms) compared with control dogs (102 +/- 15 ms; P < 0.0001 for both comparisons) as was the early minimum VFCL with similar trends seen during late VF. Complete epicardial reentrant circuits were significantly more common in normal dogs (4.3 +/- 2.4, 22.4% of cycles) than in subacute (0.75 +/- 0.96, 5.3% of cycles, P < 0.05 vs. normal) and chronic infarction dogs (1.3 +/- 1.3, 7.5% of cycles, P < 0.05 vs. normal). There was a poor correlation between the mean and minimum early and late VFCL and local electrophysiological and anatomic properties (R(2) < 0.2 for all comparisons) with a much better correlation between average mean and minimum VFCL (over the entire plaque) and global ERP and ART dispersion during early and late VF. In conclusion, VFCL in normal and infarcted myocardium shows a poor correlation with local ventricular electrophysiological and anatomic properties measured in sinus rhythm. However, there was a much better correlation between the average VFCL with global dispersion of repolarization. The lack of correlation between local VFCL and refractoriness and the infrequent occurrence of epicardial reentry suggests that intramural reentry may be the primary mechanism of VF in this model.

BACKGROUND:Sex hormones and menstrual cycle effects on ST height have not yet been clearly identified.METHODS:Twenty-two young, healthy women (aged 22-32 years) were included in this study. Twelve-lead ECGs were registered during menses, follicular and luteal phase of the menstrual cycle at baseline, and after double autonomic blockade (DAB). Chest leads V2-V4 and limb leads I and II were chosen for analysis. ST height was measured manually at J-Point and 40 ms after the J-Point, and values were corrected for QRS amplitude (J-Point/QRS, 40 ms/QRS). Repeated measure ANOVA was used to analyze differences in ST height among the three phases of the menstrual cycle. A P-value < 0.05 was considered as significant.RESULTS:At baseline, ST height, QTc, and T wave amplitude were not significantly different among the three phases of the menstrual cycle. After double autonomic blockade, ST height at 40 ms, J-Point/QRS, and 40 ms/QRS was significantly higher during follicular versus luteal phase (0.152 +/- 0.413 mm versus -0.007 +/- 0.427 mm, P = 0.0059 at 40 ms; -0.001 +/- 0.030 versus -0.015 +/- 0.032, P = 0.0039 at J-Point/QRS; 0.013 +/- 0.031 versus -0.004 +/- 0.032, P = 0.0005 at 40 ms/QRS) as was the QTc. ST height differences at J-Point were not significantly different (-0.046 +/- 0.395 mm follicular, -0.167 +/- 0.448 mm luteal, and -0.083 +/- 0.492 mm menses, P = 0.1014).CONCLUSION:ST height and QTc varied among the three phases of the menstrual cycle, predominantly after double autonomic blockade. Female sex hormones that vary throughout the menstrual cycle may modulate measures of repolarization.

This study was designed to assess the effects of tachycardia origin, the significance of atrial contribution, and the effects of left ventricular ejection fraction on hemodynamically tolerated ventricular tachycardia (VT) and supraventricular tachycardia (SVT). Forty-one subjects with inducible hemodynamically tolerated VT (n = 24) or SVT (n = 17) with mean ages of 60 +/- 13 and 40 +/- 16 years and mean ejection fractions of 32 +/- 15% and 59 +/- 5%, respectively, were studied. VT and SVT were induced by standard techniques, and femoral arterial blood pressure (BP) was recorded for 30 seconds. After tachycardia termination, with >/=3 minutes between conditions, ventricular overdrive pacing was performed from the right ventricular (RV) apex and then the RV outflow tract, followed by atrioventricular (AV) pacing at the tachycardia cycle length. Mean BP was measured every 5 seconds. Linear regression methods were used to model BP response for the 2 groups. There was a significant increase in BP over the 20-second interval after the induction of VT and SVT (0.55 +/- 0.21 and 1.0 +/- 0.20 mm Hg/s, respectively, p <0.05). In patients with hemodynamically tolerated VT, RV apex and RV outflow tract pacing at the tachycardia cycle length decreased BP by 6.7 +/- 2.0 (p <0.002) and 4.7 +/- 2.5 mm Hg (p = 0.06), respectively. AV pacing at the tachycardia cycle length did not improve BP compared with RV pacing alone. In patients with SVT, RV apex and RV outflow pacing at the tachycardia cycle length decreased BP by 5.6 +/- 2.9 (p = 0.05) and 4.1 +/- 2.7 mm Hg (p = 0.12), respectively. However, AV pacing at the tachycardia cycle length was associated with improved BP response over RV pacing alone. Increased age and lower ejection fraction adversely influenced BP response in the VT group and longer cycle length, and higher preinduction BP favorably influenced BP response in the SVT group. The determinants of BP response after tachycardia onset are complex and differ in patients with SVT and VT.

Although differences in patient sex in heart rate and QT interval have been well characterized, sexual differences in other cardiac electrophysiological properties have not been well defined. The study population consisted of 354 consecutive patients without structural heart disease or preexcitation who underwent clinically indicated electrophysiological testing in the drug-free state. Atrial, AV nodal, and ventricular effective refractory periods (AERP, AVNERP, VERP) were determined at a pacing cycle length of 500 ms using an 8-beat drive train and 3-second intertrain pause. There were 124 men and 230 women with a mean age of 45 +/- 19 and 47 +/- 18 years, respectively. The sinus cycle length (SCL) was longer in men than in women (864 +/- 186 and 824 +/- 172 ms, respectively, P < 0.05). The QRS duration was significantly longer in men (90 +/- 12 ms) than women (86 +/- 13 ms) (P < 0.005). The HV interval was 48 +/- 9 ms in men and 45 +/- 8 ms in women (P < 0.05). The sinus node recovery time (SNRT) was significantly longer in men than in women (1215 +/- 297 ms and 1135 +/- 214 ms, respectively, P < 0.05). AERP and VERP were similar in both sexes. Aging did not influence sexual differences in cardiac electrophysiological properties, although, it independently prolonged the SCL, PR, and QT intervals, AH and HV intervals, SNRT, AVNERP, and the AV Wenckebach cycle length. The SCL, QRS duration, HV interval, and SNRT were significantly longer in men than in women. Aging prolonged cardiac conduction and increased the SCL but the effects were similar in both sexes. AERP and VERP were unaffected by aging or sex.

BACKGROUND:Prolonged QT offset dispersion (QToD), an index of heterogeneity of ventricular repolarization, is thought to be an independent predictor of all-cause and cardiovascular mortality. However the influence of gender and autonomic tone in healthy adults on age-related changes in measures of ventricular repolarization are not well characterized.METHODS:QToD and T wave complexity were measured in 56 healthy subjects with no detectable heart disease (by echo and stress test)-38 young subjects with a mean age of 28 +/- 4 years and 18 old subjects with a mean age of 71 +/- 7 years. QToD and T wave complexity were computed from 12-lead ECGs using the GE Marquette QT Guard automated analysis program with manual overreading at rest (baseline), following exercise, and double autonomic blockade with atropine and propranolol. Data was analyzed using factorial ANOVA.RESULTS:Young males had a significantly greater QToD than young and old females at baseline (28 +/- 5 ms, 23 +/- 5 ms, and 22 +/- 5 ms, respectively, P < 0.01), an intrinsic effect independent of changes in autonomic tone. In contrast, females had significantly greater T wave complexity than males following exercise and double autonomic blockade with a definite trend at baseline. There was no correlation between T wave complexity and QToD.CONCLUSIONS:Age and gender demonstrate a complex interaction on indices of myocardial repolarization with different measures behaving differently. These findings have implications for better understanding age and gender effects on myocardial electrophysiology.

INTRODUCTION:The existence of an excitable gap during ventricular fibrillation (VF) has been suggested in several prior studies. However, the effects of myocardial infarction on the presence and duration of an excitable gap during VF have not been evaluated. METHODS AND RESULTS:Electrophysiologic study was performed in normal dogs and in dogs with subacute and chronic infarction. Experimental infarction was produced by left anterior descending coronary ligation. The excitable gap was determined indirectly using either evaluation of intrinsic wavefronts during VF or from the shortest activation interval at individual sites using recordings from a 112-electrode plaque sutured to the epicardial surface of the left ventricle. The excitable gap also was correlated to local electrophysiologic and anatomic properties. The excitable gap using the wavefront propagation method and shortest activation method was significantly longer in subacute infarction dogs (48 +/- 17 msec and 37 +/- 18 msec, respectively) and chronic infarction dogs (41 +/- 14 msec and 35 +/- 14 msec, respectively) than normal dogs (32 +/- 13 msec and 30 +/- 11 msec, respectively; P < 0.05 normal vs subacute and chronic infarction dogs in both methods). The excitable gap occupied approximately 30% and 27% of the VF cycle length in all three groups using the wavefront propagation and shortest activation method, respectively. The excitable gap correlated better with local ventricular refractoriness determined using the wavefront propagation method than with the shortest activation method, but not at all with refractoriness determined using extrastimulus testing. Tissue necrosis was noted in subacute infarction dogs and fibrosis in chronic infarction dogs, but the gap was not highly correlated with anatomic changes. CONCLUSION:During VF, an excitable gap exists in both normal and infarcted canine ventricular myocardium. It is significantly longer in the presence of infarction. These finding have implications for understanding the pathophysiology of VF and targeting antiarrhythmic therapies.

Tiukinhoy, Susan1; Lynch, Patrick2; Blei, Andres2; Taneja, Taresh1; Abecassis, Michael2; Gheorghiade, Mihai1 Author Information

Introduction: Little information is available on the relationship between the mode of induction of ventricular fibrillation (VF) to VF characteristics.Methods and Results: VF was induced from the anterior left ventricle by programmed electrical stimulation, burst pacing, alternating current (AC), high current S2 at a site remote from S1, T wave shock, and intersecting wavefronts in seven normal dogs and seven dogs with chronic myocardial infarction, Using two electrode arrays, 112 electrograms were recorded from the anterior and lateral wall, Cycle lengths were analyzed and activation vectors were created by summing orthogonally recorded bipolar electrograms. The magnitude of the vector loops was integrated over time to produce an "ensemble vector" index (EVI) whose magnitude is high when beat-to-beat activation direction is consistent and low when activation direction is variable. T wave shock-induced VF had a significantly longer cycle length 1 to 5 seconds after VF onset than other modes of induction (P < 0.05). The frequency-corrected EVI was significantly larger for AC current and T wave shock-induced VF as opposed to all other modes of VF induction in early VF (P < 0.0001), After 10 seconds of VF, these differences persisted only on the anterior wall.Conclusion: VF induced in animals by T wave shock and AC current had different characteristics than VF induced by other methods. These findings may have implications for our understanding of VF pathophysiology.

Chronic heart failure (HF) will be the disease of the new millennium. The last decade has seen major developments in the management of HF, with beta-blockers and ACE inhibitors becoming the cornerstones of therapy by virtue of the reductions in total mortality. However, significant gaps remain. Hospitalization for exacerbations of HF are frequent and account for more than 6 million hospital days from this disease related group. Although a variety of intravenous (IV) agents are available for the management of exacerbations of HF, readmission rates are as high as 20%-47% at 6 months. Acute IV therapy for acute decompensation of chronic HF consists of inotropic agents most of which also have vasodilator properties, vasodilator, and diuretics. In addition, there are newer agents in various developmental stages, especially, calcium sensitizing drugs, vasopressin receptor antagonists, and natriuretic peptides. Despite the multiplicity of agents, there are no well designed, randomized, placebo controlled trials to guide IV inpatient therapy for HF exacerbations. (c)1999 by CHF, Inc.