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Biomedical subjects

Taresh Taneja

Publications and source records attributed to Taresh Taneja.

4 recordsLinked to original sources

Age and gender difference in ST height at rest and after double autonomic blockade in normal adults.

BACKGROUND: ST elevation is commonly seen in young, healthy men. The exact mechanisms that cause ST height to be greater in young men are not yet completely understood. The purpose of the present study was to determine whether autonomic tone is responsible for age and gender differences in ST height. METHODS: Gender and age differences in ST height were studied at rest and after double autonomic blockade (DAB) with atropine and propranolol. Fifty healthy men and women were included (16 men, 14 women, age 23-32 years; 9 men, 11 women, age 65-79 years). Twelve-lead ECGs were registered at rest and after DAB. Leads II and V(1)-V(4) were chosen for analysis. ST height (in mm) was measured manually at the J-point, and 40 ms and 80 ms after the J-point. Values were corrected for QRS amplitude. RESULTS: Gender and age differences in ST height were seen in both rest and DAB data. Men had greater ST height compared to women at J-point, 40 and 80 ms after the J-point (P < or = 0.0001), and younger subjects had greater ST height than older subjects at J-point (P = 0.0140), 40 and 80 ms after the J-point (P < or = 0.0001). DAB did not change ST height at J-point or at 40 ms, but increased ST height at 80 ms. Women had less of an increase in ST height following DAB than men did. CONCLUSIONS: ST elevation in the absence of structural or electrical heart disease is mainly seen in young men. Age and gender difference persist after DAB and thus are not due to differences in autonomic tone.

Adult↗

Menstrual cycle and ST height.

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.

Adult↗

Is there a correlation between ventricular fibrillation cycle length and electrophysiological and anatomic properties of the canine left ventricle?

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.

Animals↗

Acute blood pressure effects at the onset of supraventricular and ventricular tachycardia.

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.

Adult↗