Left atrial systolic reserve in idiopathic vs. ischaemic-dilated cardiomyopathy

PURPOSE: There are studies indicating more pronounced left atrial (LA) systolic dysfunction at rest in idiopathic (IDDC) than in ischaemic-dilated cardiomyopathy (ISDC). It was hypothesized that the findings would be similar with regards LA systolic reserve. METHODS: Twenty-six patients with IDDC, 28 with ISDC and 25 normal controls underwent low-dose dobutamine stress echocardiography (5-10 microg kg(-1) min(-1) IV). Left atrial volumes were echocardiographically determined at rest and during stress at the mitral valve opening (maximal, Vmax), electrocardiographic P wave (onset of atrial systole, Vp) and mitral valve closure (minimal, Vmin) from the apical 4- and 2-chamber views (biplane area-length method). Left atrial systolic function was assessed with the LA-active emptying volume (ACTEV) = Vp-Vmin and fraction (ACTEF) = ACTEV/Vp. RESULTS: Vmax at rest was similar in IDDC and ISDC and greater than in the controls (54.2 +/- 12 vs. 48.5 +/- 18 vs. 27.1 +/- 6.3 cm(3) m(-2), respectively, P < 0.001) and did not change with stress (53.9 +/- 13.8 vs. 46.9 +/- 16.2 vs. 25.8 +/- 5.9 cm(3) m(-2), P < 0.001). The ACTEV at rest was similar in IDDC and ISDC and greater than in the controls (8.6 +/- 3.5 vs. 9.7 +/- 2.9 vs. 6.1 +/- 2.2 cm(3) m(-2) P < 0.01), whereas during the dobutamine infusion it remained unaltered in IDDC (10.8 +/- 4.6 cm(3) m(-2), P = NS vs. rest) and increased in ISDC (11.8 +/- 3.3 cm(3) m(-2), P < 0.05) and the controls (13.1 +/- 3.2 cm(3) m(-2), P < 0.01). The ACTEF was lower in IDDC than ISDC and the controls at rest (20 +/- 10% vs. 33 +/- 8% vs. 36 +/- 10%, P < 0.01). Dobutamine infusion was associated with no significant increase in ACTEF in IDDC (25 +/- 12%, P = NS vs. rest), and with an increase in this variable in ISDC (39 +/- 10%, P < 0.05) and the controls (49 +/- 12%, P < 0.01). CONCLUSIONS: Dobutamine infusion is associated with an increase in LA ACTEV and fraction in ISDC and no significant change in these indices in IDDC. These findings indicate a reduced LA systolic reserve in IDDC.     

Left atrial systolic function is depressed in idiopathic and preserved in ischemic dilated cardiomyopathy

BACKGROUND: Left atrial systolic dysfunction, unexplained by altered loading conditions, has been reported in idiopathic dilated cardiomyopathy suggesting left atrial involvement in the myopathic process. MATERIALS AND METHODS: Seventeen patients with idiopathic dilated cardiomyopathy, 16 with ischemic dilated cardiomyopathy and 18 normal controls were studied with transthoracic echocardiography and cardiac catheterization. Transmitral diastolic flow was evaluated with pulsed Doppler. Left atrial volume (cm3/m2) at mitral valve opening (maximal, Vmax.), onset of atrial systole (P wave of the electrocardiogram, Vp), and mitral valve closure (minimal, Vmin. ) was determined with two-dimensional echocardiography using the biplane area-length method. The left atrial active emptying fraction (ACTEF = [Vp-Vmin.] x 100/Vp) served as an index of systolic function. RESULTS: The peak early diastolic transmitral flow velocity (cm/sec) was similar in the three groups (idiopathic: 60 +/- 16, ischemic: 58 +/- 20, control: 56 +/- 22; P = NS), whereas the late diastolic transmitral flow velocity was lower but not significantly different in idiopathic compared to ischemic cardiomyopathy, and in both was lower than control (26 +/- 12 vs. 34 +/- 13 vs. 44 +/- 14, respectively; P < 0.05). Vmax. and Vp were similar in idiopathic and ischemic cardiomyopathy and greater than control (44.6 +/- 13.6 vs. 48.2 +/- 18.3 vs. 26.9 +/- 6.2; P < 0.05, and 34.6 +/- 13.4 vs. 30.8 +/- 10.9 vs. 16.7 +/- 3.7, respectively; P < 0.05). ACTEF was lower in idiopathic than in ischemic cardiomyopathy and in the latter it was similar to control (18 +/- 10% vs. 32 +/- 10% vs. 36 +/- 10%, respectively; P < 0.05). Moreover, ACTEF was inversely related to left atrial tension at end-of atrial systole both in idiopathic and in ischemic cardiomyopathy (r2 = 0.52, P = 0.001 and r2 = 0.57, P = 0.0007, respectively). However, at any given level of left atrial tension at end of atrial systole, ACTEF was lower in idiopathic than ischemic cardiomyopathy. CONCLUSION: Left atrial systolic function is depressed in idiopathic and preserved in ischemic dilated cardiomyopathy despite similar left atrial loading conditions. This finding suggests left atrial myopathy in the former, and may be related to the differences in the response to medical treatment and clinical outcome observed between the two conditions.     

Echocardiographic assessment of left atrial ejection force and kinetic energy in chronic heart failure

Background There is limited information regarding left atrial (LA) systolic adaptation to chronic heart failure (HF) in humans. Therefore, the aim of our study was to determine the LA ejection force (LAEF) and kinetic energy in patients with HF. Methods and results 58 HF patients (63.8% in NYHA II) and 48 controls were studied. LA volumes were echocardiographically determined using the biplane area-length method. LA systolic function was assessed with the: (a) active emptying volume (ACTEV) and fraction (ACTEF), (b) ejection force (kdynes/m²), calculated with Manning’s method [LAEF = 0.5 * ρ * mitral orifice area * A²; ρ: blood density, Α: late transmitral flow velocity] and a modification incorporating parameters of LA function [LAEFm = 0.5 * ρ * LA volume at onset of atrial systole * ACTEF * A²/VTl_A], and (c) kinetic energy [LA-ke (kdynes.cm/m²) = 0.5 * ρ * ACTEV * A²]. LA maximal volume and ACTEV were lower (42.9 ± 14.4 vs. 59.7 ± 14.7 cm³, P < 0.0001; 10.9 ± 3.3 vs. 13 ± 3.3 cm³, P = 0.0001, respectively), whereas ACTEF (%) was higher (36.3 ± 7 vs. 29.3 ± 7.6 cm³, P < 0.0001) in controls than HF. LAEF, LAEFm, and LA-ke were lower in controls than HF (7.68 ± 5.1 vs. 10.16 ± 3.7 kdynes/m², P = 0.006; 3.63 ± 2.05 vs. 5.02 ± 1.74 kdynes/m², P = 0.0004; 2.41 ± 1.91 vs. 3.99 ± 2.1 kdynes.cm/m², P < 0.0004, respectively). Conclusion Despite the decreased LA systolic shortening, overall LA systolic performance is augmented in chronic HF due to LA dilation.     

Disturbed atrioventricular electromechanical function long after Mustard operation for transposition of great arteries: a potential contributing factor to atrial flutter.

OBJECTIVE: The objectives were to study atrial and ventricular electromechanical function in patients long after Mustard repair for transposition of great arteries and to identify possible causes and physiologic disturbances in those with recurrent atrial flutter. METHODS: Electromechanical atrial and ventricular function was assessed in 22 patients (11 women) aged 27 +/- 5 years, 10 to 29 (mean 24) years after initial Mustard operation with electrocardiography and echocardiography. The study subjects involved 12 patients with documented atrial flutter and the remaining 10 without history of atrial arrhythmia served as controls. All patients were studied while in sinus rhythm. RESULTS: There was no difference in age, gender, or age at original Mustard surgery between the 2 patient groups. The P wave and QRS duration were significantly broader in patients compared with controls (128 +/- 14 ms vs 100 +/- 10 ms, P <.05 and 120 +/- 20 ms vs 93 +/- 6 ms, P <.01). Right ventricular end diastolic dimension was not different, whereas left ventricular fraction shortening was less (20% +/- 10% vs 35% +/- 12%, P <.01) in the patient group. Left and septal total ventricular long axes amplitude were significantly lower in patients compared with controls (1.4 +/- 0.4 cm vs 1.7 +/- 0.3 cm, P <.05 and 0.6 +/- 0.2 cm vs 1.0 +/- 0.3 cm, P <.01). Right-sided total long axis excursion was equally reduced in the 2 groups (1.0 +/- 0.3 cm). Septal and right-sided but not left-sided "a" wave was smaller in the patients (1.2 +/- 1 mm vs 3 +/- 1.2 mm, P <.001 and 1 +/- 1.3 mm vs 3 +/- 0.9 mm, P <.01). Right atrial electromechanical delay was significantly longer in patients with respect to controls (110 +/- 14 ms vs 84 +/- 25 ms, P <.001), but on the left there was no difference. The P wave duration correlated closely with right atrial electromechanical delay, r = 0.79, P <.003. Significant tricuspid regurgitation was found in 9 of 12 patients but none of the controls. CONCLUSION: Right ventricular dysfunction is present long after Mustard operation for transposition of great arteries whether flutter occurs. However, in patients with history of atrial flutter, evidence of left ventricular dysfunction, significant tricuspid regurgitation, impaired right atrial electrical and mechanical function, and reversed onset of atrial systole is also present. The consistent association of the disturbed atrial and ventricular electromechanical behavior suggests a multifactorial etiology for atrial arrhythmia.     

Comparison of myocardial tissue Doppler with transmitral flow Doppler in left ventricular hypertrophy

We sought to determine the most useful echocardiographic measurements for assessment of diastolic function in patients with left ventricular hypertrophy (LVH) and normal systolic function. We compared myocardial Doppler velocities of the basal inferoposterior wall with mitral inflow pulsed wave Doppler velocities in 11 healthy volunteers (age, 36 +/- 6 years), 25 patients (age, 64 +/- 14 years) without LVH, and 37 patients (age, 67 +/- 14 years) with LVH and otherwise normal echocardiograms. The discriminatory measurements were myocardial A-wave duration (120 +/- 18 versus 98 +/- 20 and 92 +/- 12 ms, P <.0001), myocardial isovolumetric relaxation time (124 +/- 45 versus 95 +/- 48 and 78 +/- 25 ms, P =.0035), mitral A-wave velocity (0.98 +/- 0.37 versus 0.73 +/- 0.28 m/s and 0.61 +/- 0.22 m/s, P =.009), and mitral E-wave deceleration time (257 +/- 93 versus 201 +/- 85 ms and 184 +/- 83 ms, P =.015), which were significantly increased, and myocardial E-wave velocity (0.84 +/- 0.04 m/s versus 0.13 +/- 0.03 m/s and 0.14 +/- 0.03 m/s, P <.0001), which was significantly decreased, in patients with LVH compared with patients without LVH and normal volunteers, respectively. Left ventricular posterior wall thickness correlated with myocardial isovolumetric relaxation time (r = 0.52, P <.0001) and myocardial A-wave duration (r = 0.59, P <.0001), negatively with myocardial E wave (r = -0.43, P <.0001), and showed no correlation with mitral inflow parameters except mitral inflow A wave (r = 0.43, P =.002). On multivariate analysis using these variables, myocardial isovolumetric relaxation time (P =.0014) and A-wave duration (P =.001) were the only 2 variables that correlated with posterior wall thickness (multiple R = 0.71). In the presence of LVH and preserved left ventricular systolic function, myocardial relaxation time and velocities are more sensitive than mitral Doppler inflow parameters in detecting abnormal left ventricular relaxation.     

Electrical remodeling and cardiac dimensions in patients treated by cardiac resynchronization and heart failure controls

BACKGROUND: Cardiac resynchronization therapy (CRT) reduces the left ventricular diameter (LVEDD) in heart failure (HF) patients with left bundle branch block (LBBB). The study compares structural and electrical remodeling in HF patients on CRT and matched HF controls without LBBB. METHODS: In 42 patients (64 +/- 9 years left ventricular ejection fraction [LVEF] 25 +/- 8%, 16 coronary artery disease, 26 nonischemic cardiomyopathy, 21 with LBBB and CRT indication vs 21 controls [matched for gender, age, LVEF, and underlying disease]) an unpaced electrocardiogram (ECG) and echocardiogram were recorded at baseline (bl) and after 20.6 +/- 13.8 months (fup). LVEDD, left atrial (LA) width, mitral regurgitation (MR), P-wave, PR interval, QRS width, QRS vector, and QT interval were analyzed. RESULTS: LVEDD diminished with CRT (bl 68.7 +/- 10.3 vs fup 62.0 +/- 7.7 mm, P = 0.002). Controls showed no change (bl 64.1 +/- 9.4 vs fup 64.8 +/- 8.4 mm, P = n.s.). MR improved with CRT (bl 1.2 +/- 0.6 vs fup 0.8 +/- 0.7, P = 0.02), but not among controls. LA width tended to decrease on CRT (CRT bl 48.9 +/- 4.4 vs fup 46.9 +/- 7.2 mm, P = 0.17, controls bl 48.5 +/- 5.1 vs fup 47.5 +/- 6.5 mm, P = 0.49). PR interval lengthened in both groups (CRT bl 175 +/- 29 vs fup 188 +/- 30 ms, P = 0.03, controls bl 177+/-25 vs fup 187 +/- 19 ms, P = 0.27). QRS increased in both groups (CRT bl 165 +/- 22 vs fup 171 +/- 20 ms, P = 0.07, controls bl 111 +/- 17 vs fup 118 +/- 19 ms, P = 0.01). Analyses revealed no significant association of echocardiographic and ECG parameters. CONCLUSIONS: Despite LVEDD reduction with CRT, electrical activation does not recover. Electrical remodeling does not differ between LBBB patients under CRT and matched controls without CRT indication.     

Left ventricular hypertrophy increases transepicardial dispersion of repolarisation in hypertensive patients: a differential effect on QTpeak and QTend dispersion

BACKGROUND: Ventricular arrhythmias in left ventricular hypertrophy (LVH) are related to regional electrical heterogeneity. The significance of noninvasive electrocardiographic indices of electrical heterogeneity in LVH has not been established. The aim of the study was to investigate changes in the Tpeak-Tend interval (an index of transmural dispersion of repolarisation) in addition to other traditional electrocardiographic indices of electrical dispersion in patients with hypertensive LVH. METHODS: Consecutive patients were screened for the presence of hypertensive echocardiographic LVH and compared with a control group. LVH was identified as left ventricular mass > 134 g m-2 in men and > 110 g m-2 in women. Twelve-lead ECGs were analysed in respect of various indices of electrical dispersion. RESULTS: Left ventricular mass was greater in the LVH than in the control group (174 +/- 39 vs. 101 +/- 18 g m-2, P < 0.0001). The Tpeak-Tend interval was not affected by LVH. The main effect of LVH was an increase in QTpeak dispersion (40 +/- 13 vs. 53 +/- 21 ms, P < 0.05), which resulted from an increase in the maximum QTpeak interval (337 +/- 24 vs. 358 +/- 30 ms, P < 0.04), without any change in the minimum QTpeak interval. There was a significant correlation between the left ventricular mass index and QTpeak dispersion (r = 0.40; P < 0.01). In contrast, LVH did not exert any effect on QTend dispersion (65 +/- 21 vs. 65 +/- 16 ms, ns), because LVH increased both the maximum QTend interval (430 +/- 30 vs. 449 +/- 28 ms, P < 0.05) and the minimum QTend interval (365 +/- 29 vs. 384 +/- 27 ms, P < 0.04). CONCLUSIONS: Hypertensive LVH exerts a differential effect on QTpeak and QTend interval dispersion. The most likely explanation is that these changes reflect a nonuniform prolongation of action potential duration across the epicardium, leading to an increase in transepicardial dispersion of repolarisation.     

Preserving normal ventricular activation versus atrioventricular delay optimization during pacing: the role of intrinsic atrioventricular conduction and pacing rate

The purpose of the study was to compare the effects of DDD pacing with optimal AV delay and AAI pacing on the systolic and diastolic performance at rest in patients with prolonged intrinsic AV conduction (first-degree AV block). We studied 17 patients (8 men, aged 69 +/- 9 years) with dual chamber pacemakers implanted for sick sinus syndrome in 15 patients and paroxysmal high degree AV block in 2 patients. Aortic flow and mitral flow were evaluated using Doppler echocardiography. Study protocol included the determination of the optimal AV delay in the DDD mode and comparison between AAI and DDD with optimal AV delay for pacing rate 70/min and 90/min. Stimulus-R interval during AAI (ARI) was 282 +/- 68 ms for rate 70/min and 330 +/- 98 ms for rate 90/min (P < 0.01). The optimal AV delay was 159 +/- 22 ms. AV delay optimization resulted in an increase of an aortic flow time velocity integral (AFTVI) of 16% +/- 9%. At rate 70/min the patients with ARI < or = 270 ms had higher AFTVI in AAI than in DDD (0.214 +/- 0.05 m vs 0.196 +/- 0.05 m, P < 0.01), while the patients with ARI > 270 ms demonstrated greater AFTVI under DDD compared to AAI (0.192 +/- 0.03 m vs 0.166 +/- 0.02 m, P < 0.01). At rate 90/min AFTVI was higher during DDD than AAI (0.183 +/- 0.03 m vs 0.162 +/- 0.03 m, P < 0.01). Mitral flow time velocity integral (MFTVI) at rate 70/min was higher in DDD than in AAI (0.189 +/- 0.05 m vs 0.173 +/- 0.05 m, P < 0.01), while at rate 90/min the difference was not significant in favor of DDD (0.149 +/- 0.05 m vs 0.158 +/- 0.04 m). The results suggest that in patients with first-degree AV block the relative impact of DDD and AAI pacing modes on the systolic performance depends on the intrinsic AV conduction time and on pacing rate.     

The acute effects of biatrial pacing on atrial depolarization and repolarization

Permanent biatrial and/or multisite atrial pacing may prevent atrial fibrillation (AF), but the effects on atrial electrophysiology remain incompletely understood. Acute biatrial pacing was studied in 20 patients with and 28 without (controls) a history of atrial fibrillation and/or flutter. Twelve-lead electrocardiograms were recorded during pacing from the high right atrium (RA), from the distal coronary sinus (LA), and biatrial pacing. P wave duration was measured in each lead and the difference between maximum and minimum P duration was termed P wave dispersion. Effective refractory periods (ERPs) were measured during each pacing mode. The dispersion of P wave duration was 35 +/- 14 ms in controls and 40 +/- 29 ms in AF patients (P = 0.17). Compared to RA pacing, LA pacing shortened P duration in controls (127 +/- 18 to 107 +/- 16 ms, P < 0.05) and biatrial pacing markedly shortened P duration in controls (127 +/- 18 to 93 +/- 14 ms, P < 0.05) and AF patients (114 +/- 43 to 97 +/- 21 ms, P < 0.05). P wave dispersion was unaffected. In controls, the LA ERP was longer than the RA ERP. This phenomenon was not present in AF patients, whose LA ERP was shorter than that of controls. Biatrial pacing had no effect on atrial ERPs or the dispersion of atrial refractoriness. In conclusion, acute biatrial pacing does not affect atrial repolarization but it does cause a marked shortening of global biatrial depolarization. Distal coronary sinus pacing produces a shorter P wave than RA pacing. There is substantial dispersion in the surface P wave of the electrocardiogram, the significance of which awaits further study.     

Compensatory responses of left atrial conduit flow to atrial fibrillation with acute myocardial infarction in a canine model.

The aim of this study was to examine the interaction of acute atrial fibrillation (Af) and acute myocardial infarction (AMI) on left atrial (LA) and left ventricular (LV) filling in atrioventricular (A-V) sequential paced, open chest, anesthetized dogs. Left atrial conduit function was determined from pulmonary venous flow (PVF) and detailed analysis of early diastolic flow with the use of micromanometers and transmitral Doppler echocardiography. We studied 8 dogs with regular ventricular rates to avoid the confounding effect of ventricular arrhythmia in Af. In the control stage, Af increased the diastolic PVF volume to the left atrium compared with that during regular A-V pacing (from 0.58 +/- 0.11 mL/beat to 0.70 +/- 0.13 mL/beat, P <.05), as a compensatory response to the impaired systolic PVF volume (from 0.56 +/- 0.12 mL/beat to 0.41 +/- 0.11 mL/beat, P <.05). As a result, cardiac output was maintained. However, in the AMI stage, Af decreased cardiac output (from 0.95 +/- 0.32 L/min to 0.80 +/- 0.23 L/min, P <.05 versus AMI with A-V pacing), and decreased diastolic PVF volume (from 0.46 +/- 0.13 mL/beat to 0.33 +/- 0.14 mL/beat, P <.05 versus AMI with A-V pacing). These changes were associated with a prolonged LV isovolumic pressure decay rate. Our study demonstrates that Af does not affect cardiac output in the setting of normal LV function at a controlled ventricular rate because enhanced LA conduit flow compensates for impaired LA reservoir function. In contrast, in the setting of AMI, the compensatory response to Af is attenuated because of abnormal LV relaxation, resulting in a decrease in cardiac output.     

Reversal of left ventricular diastolic dysfunction after kidney-pancreas transplantation in type 1 diabetic uremic patients

OBJECTIVE: Diastolic function is frequently impaired in diabetic patients. Our aim was to evaluate the effects of glycometabolic control achieved by pancreas transplantation on left ventricular function in uremic type 1 diabetic patients. RESEARCH DESIGN AND METHODS: Left ventricular systolic and diastolic functions were evaluated using radionuclide ventriculography in 42 kidney-pancreas transplant patients and 26 kidney-alone recipients who had similar clinical characteristics before transplantation. Patients were grouped according to 6, 24, and 48 months of follow-up. Control subjects consisted of 20 type 1 diabetic patients. RESULTS: The left ventricular ejection fraction was normal in all of the patients. However, kidney-pancreas transplant patients with 4 years of graft function had a higher ejection fraction (75.7 +/- 1.8%) than kidney-alone patients with 4 years of graft function (65.3 +/- 2.8%, P = 0.02) and type 1 diabetic patients (61.3 +/- 3.7%, P = 0.004). In patients with 4 years of graft function, normal diastolic parameters were evident in kidney-pancreas but not in kidney-alone or in type 1 diabetic patients (peak filling rate: 4.46 +/- 0.15 end diastolic volume (EDV)/s in kidney-pancreas patients vs. 2.73 +/- 0.24 EDV/s [P < 0.01] and 3.39 +/- 0.30 EDV/s [P < 0.01] in kidney-alone and type 1 diabetic patients, respectively; time-to-peak filling rate: 141.9 +/- 7.8 ms in kidney-alone patients vs. 209.4 +/- 13.5 ms in kidney-alone patients [P < 0.01]; peak filling rate/peak ejection rate ratio: 1.10 +/- 0.04 in kidney-pancreas patients vs. 0.81 +/- 0.08 in kidney-alone patients [P < 0.01]). A significant reduction in diastolic dysfunction rate was observed only in kidney-pancreas patients. CONCLUSIONS: Kidney-pancreas transplantation results in complete insulin independence, a better glycometabolic pattern and blood pressure control, an improvement of left ventricular function, and a reversal of diastolic dysfunction.     

Maternal cardiac systolic and diastolic function: relationship with uteroplacental resistances. A Doppler and echocardiographic longitudinal study.

OBJECTIVE: To test the hypothesis of the existence of a relationship between central and peripheral hemodynamic parameters by the longitudinal evaluation of maternal echocardiographic and uteroplacental resistance modifications during normal pregnancy. METHODS: Forty-three healthy normotensive primigravidae were evaluated at 12 +/- 1, 21 +/- 1, and 33 +/- 1 weeks of gestation with uterine artery color Doppler and maternal echocardiographic examinations to identify morphologic, systolic, and diastolic variables. RESULTS: Cardiac output and stroke volume significantly increased during pregnancy. Uterine resistance index (RI) decreased from the first to the second trimesters (0.72 +/- 0.10 versus 0.54 +/- 0.09, P < 0.001). Left atrial dimensions increased during pregnancy (33.8 +/- 1.9 cm, 38.1 +/- 1.8 cm, 39.3 +/- 2.1 cm, P < 0.001). Left atrial function also increased. Left ventricular mass increased (132 +/- 18 g, 162 +/- 16 g, 174 +/- 27 g, P < 0.001). Diastolic function parameters showed significant modifications: E wave velocity and E/A ratio decreased; A wave velocity and deceleration time of the E wave (DtE) increased; the left ventricular isovolumetric relaxation time (IVRT) decreased significantly (88.7 +/- 6.7 ms, 75.6 +/- 7.7 ms, 71.1 +/- 5.0 ms, P < 0.001) showing a correlation with left atrial dimensions and RI (r = -0.38, r = 0.47, respectively; P < 0.001). CONCLUSIONS: Diastolic cardiac function varies during pregnancy. A relationship between preload (left atrial enlargement), afterload (RI reduction), morphologic, and diastolic function modifications (IVRT reduction, DtE prolongation) appears to exist as a consequence of the hemodynamic modifications which occur during physiologic pregnancy. Diastolic function analysis maybe useful to identify women who fully adapt to pregnancy, and to understand the mechanisms that might be involved in women who show abnormal uterine artery Doppler waveforms.     

Insulin action on heart and skeletal muscle glucose uptake in essential hypertension.

Essential hypertension is characterized by skeletal muscle insulin resistance but it is unknown whether insulin resistance also affects heart glucose uptake. We quantitated whole body (euglycemic insulin clamp) and heart and skeletal muscle (positron emission tomography and 18F-fluoro-2-deoxy-D-glucose) glucose uptake rates in 10 mild essential hypertensive (age 33 +/- 1 yr, body mass index 23.7 +/- 0.8 kg/m2, blood pressure 146 +/- 3/97 +/- 3 mmHg, VO2max 37 +/- 3 ml/kg per min) and 14 normal subjects (29 +/- 2 yr, 22.5 +/- 0.5 kg/m2, 118 +/- 4/69 +/- 3 mmHg, 43 +/- 2 ml/kg per min). Left ventricular mass was similar in the hypertensive (155 +/- 15 g) and the normotensive (164 +/- 13 g) subjects. In the hypertensives, both whole body (28 +/- 3 vs 44 +/- 3 mumol/kg per min, P < 0.01) and femoral (64 +/- 11 vs 94 +/- 8 mumol/kg muscle per min, P < 0.05) glucose uptake rates were decreased compared to the controls. In contrast, heart glucose uptake was 33% increased in the hypertensives (939 +/- 51 vs 707 +/- 46 mumol/kg muscle per min, P < 0.005), and correlated with systolic blood pressure (r = 0.66, P < 0.001) and the minute work index (r = 0.48, P < 0.05). We conclude that insulin-stimulated glucose uptake is decreased in skeletal muscle but increased in proportion to cardiac work in essential hypertension. The increase in heart glucose uptake in mild essential hypertensives with a normal left ventricular mass may reflect increased oxygen consumption and represent an early signal which precedes the development of left ventricular hypertrophy.     

Analysis of shape and motion of the mitral annulus in subjects with and without cardiomyopathy by echocardiographic 3-dimensional reconstruction.

The shape and dynamics of the mitral annulus of 10 patients without heart disease (controls), 3 patients with dilated cardiomyopathy, and 5 patients with hypertrophic obstructive cardiomyopathy and normal systolic function were analyzed by transesophageal echocardiography and 3-dimensional reconstruction. Mitral annular orifice area, apico-basal motion of the annulus, and nonplanarity were calculated over time. Annular area was largest in end diastole and smallest in end systole. Mean areas were 11.8 +/- 2.5 cm(2) (controls), 15.2 +/- 4.2 cm(2) (dilated cardiomyopathy), and 10.2 +/- 2.4 cm(2) (hypertrophic cardiomyopathy) (P = not significant). After correction for body surface, annuli from patients with normal left ventricular function were smaller than annuli from patients with dilated cardiomyopathy (5.9 +/- 1.2 cm(2)/m(2) vs 7.7 +/- 1.0 cm(2)/m(2); P <.02). The change in area during the cardiac cycle showed significant differences: 23.8% +/- 5.1% (controls), 13.2% +/- 2.3% (dilated cardiomyopathy), and 32.4% +/- 7.6% (hypertrophic cardiomyopathy) (P <.001). Apico-basal motion was highest in controls, followed by those with hypertrophic obstructive and dilated cardiomyopathy (1.0 +/- 0.3 cm, 0.8 +/- 0.2 cm, 0.3 +/- 0.2 cm, respectively; P <.01). Visual inspection and Fourier analysis showed a consistent pattern of anteroseptal and posterolateral elevations of the annulus toward the left atrium. In conclusion, although area changes and apico-basal motion of the mitral annulus strongly depend on left ventricular systolic function, nonplanarity is a structural feature preserved throughout the cardiac cycle in all three groups.     

Effect of the isolated left bundle branch block on systolic and diastolic functions of left ventricle.

BACKGROUND: We planned this study to evaluate the effects of left bundle branch block (LBBB) on systolic and diastolic functions of left ventricle (LV) that have not previously been investigated in detail. MATERIAL AND METHODS: Forty-five cases diagnosed as isolated LBBB according to the standard electrocardiographic criteria (group I, mean age: 60 +/- 12 years) were taken as the case group and 65 cases with normal conduction system (group II, mean age 58 +/- 14 years) were taken as the control group. Echocardiography was performed to all patients and coronary angiography was performed to 21 patients in group I and 35 patients in group II. In addition to standard systolic and diastolic function parameters, isovolumetric relaxation time (IRT), isovolumetric contraction time (ICT), and ejection time (ET) were measured by echocardiography, and the myocardial performance index (MPI) [(IRT+ICT)/ET] was calculated. LV end-diastolic pressure was calculated for the patients undergoing coronary angiography. RESULTS: In group I, LV end-systolic diameter was greater (3.1 +/- 0.4 cm vs 2.8 +/- 0.4 cm, P <.001) and ejection fraction was lower (64% +/- 6% vs 68% +/- 6%, P <.001) than those of group II. Rapid filling deceleration time and rate was markedly different in group I (respectively, 133 +/- 50 ms vs 166 +/- 24 ms, P <.001; 608 +/- 291 cm/s(2) vs 383 +/- 116 cm/s(2), P <.001). In addition, it was found that LBBB caused shortening of LV diastolic period and ET markedly (respectively, 347 +/- 116 ms vs 394 +/- 106 ms, P =.03; 255 +/- 40 ms vs 294 +/- 21 ms, P <.001) and prolongation of IRT and ICT (respectively; 124 +/- 36 ms vs 91 +/- 16 ms, 96 +/- 35 ms vs 38 +/- 9 ms, P <.001). The MPI was predominantly higher in group I (0.89 +/- 0.29 vs 0.40 +/- 0.06, P <.001). Invasively determined LV end-diastolic pressure was found higher in group I (14 +/- 3 mm Hg vs 10 +/- 3 mm Hg, P <.001). CONCLUSION: A marked elevation of the LV MPI and end-diastolic pressure, parallel to changes of conventional echocardiographic parameters, in patients with isolated LBBB points out that LBBB causes marked deterioration on LV systolic and diastolic functions.     

QT interval dispersion in ventricular beats: a noninvasive marker of susceptibility to sustained ventricular arrhythmias

Increased QT dispersion (QTd) calculated from sinus beats has been shown to identify patients prone to sustained VT. However, predictive accuracy of this parameter is limited. Electrophysiological properties of the myocardium may be altered by a premature ventricular beats, which is a well-established trigger for sustained VT. Therefore, the author hypothesised that QTd in spontaneous or paced ventricular beats may improve identification of patients with inducible sustained VT. In 28 consecutive patients (men, mean age 61 +/- 13 years) who underwent programmed ventricular stimulation, the values of QTd calculated in sinus and ventricular beats were compared between inducible and noninducible patients. The mean QTd values obtained using three different methods differed significantly, QTd in paced ventricular beats being the highest, QTd in spontaneous ventricular beats was intermediate, and QTd in sinus beats was the lowest (83.9 +/- 30 vs 63.0 +/- 29 ms vs 53.9 +/- 27 ms, P < 0.0001 and P < 0.004, respectively). In 13 (46%) patients sustained VT was induced. QTd values were significantly higher in inducible than noninducible patients (QTd sinus beats: 67.5 +/- 31 vs 42.1 +/- 11 ms, P = 0.02; QTd spontaneous ventricular beats: 79.3 +/- 35 vs 46.7 +/- 13 ms, P = 0.008, and QTd-paced ventricular beats: 104.8 +/- 32 vs 65.9 +/- 9 ms, P = 0.0009). The receiver operator characteristic curves showed that at a sensitivity level of 100%, the highest specificity for identification of inducible patients had QTd measured in paced ventricular beats (87%) followed by QTd in spontaneous ventricular beats (45%), and QTd in sinus beats (40%). In conclusion, (1) QTd in ventricular beats is greater than in sinus beats, and (2) QTd calculated from paced ventricular beats identifies patients with inducible sustained VT better than QTd measured during sinus rhythm.     

Effect of nebivolol on QT dispersion in hypertensive patients with left ventricular hypertrophy.

Hypertensive patients with left ventricular hypertrophy (LVH) have increased QT dispersion, which is considered an early indicator of end-organ damage and a non-invasive marker of risk for clinically important ventricular arrhythmias and cardiac mortality. The purpose of this study was to examine the effect of nebivolol antihypertensive therapy on QT dispersion in hypertensive subjects. Twenty-five subjects (15 men and 10 women, mean age 53.6 +/- 4.5 years) with essential arterial hypertension and mild-to-moderate LVH (blood pressure: 147.2 +/- 6.2/90.6 +/- 3.8 mmHg; left ventricular mass indexed: 149.1 +/- 10.7 g/m(2)) were compared with 25 age-matched healthy control subjects. All the participants underwent a complete clinical examination, including electrocardiogram for QT interval measurements. The QT dispersion was defined as the difference between the longest and the shortest QT interval occurring in the 12-lead electrocardiogram. The QT dispersion was corrected (QTc) with Bazett's formula. Hypertensive subjects were treated with 5 mg daily of nebivolol. The ECG and echocardiogram were repeated after four weeks of treatment. At baseline, hypertensive patients showed QT dispersion (56.9 +/- 6.4 vs. 31.7 +/- 8.4 ms, P < 0.001) and QTc dispersion (58.3 +/- 6.2 vs. 33.2 +/- 7.8 ms, P < 0.001) significantly higher than control subjects. Four-week nebivolol treatment reduced blood pressure from 147.2 +/- 6.2/90.6 +/- 3.6 mmHg to 136.3 +/- 3.1/83.3 +/- 2.5 mmHg (P < 0.0001), and resting heart rate from 75.3 +/- 4.7 to 64.2 +/- 3.0 bpm (P < 0.001), without significant change in left ventricular mass (LVMi: 149.1 +/- 10.7 vs. 151.4 +/- 9.8 g/m(2), ns). Nebivolol-based treatment improved QT dispersion (56.9 +/- 6.4 vs. 40.5 +/- 5.8 ms, P < 0.001) and QTc dispersion (58.3 +/- 6.2 vs. 42.2 +/- 5.6 ms, P < 0.001), which remained higher than in control subjects (P < 0.001 in both cases). The reduction of QT dispersion did not correlate with arterial BP reduction. In conclusion, nebivolol reduced increased QT dispersion in hypertensive subjects after four weeks. This effect, occurred without any change in LVM, did not seem to be related to the blood pressure lowering and could contribute to reduce arrhythmias as well as sudden cardiac death in at-risk hypertensive patients.     

Severe aortic valve stenosis with preserved and reduced systolic left ventricular function: diagnostic usefulness of the Tei index.

BACKGROUND: In patients with severe aortic valve stenosis (AS), the onset of heart failure is associated with increased mortality and higher operative risk. Heart failure may result from either systolic, diastolic, or "overall" left ventricular dysfunction. The index "isovolumic contraction time and isovolumic relaxation time divided by ejection time" was shown to be a sensitive indicator of "overall" cardiac dysfunction in patients with dilated cardiomyopathy and cardiac amyloidosis. We sought to define the role of the Tei index in patients with severe AS and to validate this index against conventional measures of systolic and diastolic LV function. PATIENTS AND METHODS: Fifty-three participants underwent left heart catheterization for invasive measurement of LV end-diastolic pressure as a marker of diastolic function: 10 AS patients (valve orifice 0.6 +/- 0.2 qcm) with depressed systolic LV function (defined by LV ejection fraction < or = 45% [mean 32% +/- 8%], 7 male/3 female, 72 +/- 10 years old, DAS group), 22 AS patients (valve orifice 0.7 +/- 0.2 qcm) with preserved systolic LV function (ejection fraction > 45% [mean 55% +/- 6%], 13 male/9 female, 71 +/- 11 years old, PAS group) and 21 asymptomatic control participants (ejection fraction > 45% [mean 62% +/- 8%], 14 male/7 female, 66 +/- 8 years old, CON group). Within 24 hours from catheterization, conventional 2-dimensional and Doppler echocardiographic examination including measurement of the Tei index was performed. RESULTS: LV end-diastolic pressure was elevated in the DAS and in the PAS group in comparison with control participants (32 +/- 6 mm Hg and 22 +/- 7 mm Hg vs 11 +/- 4 mm Hg, respectively, P <.01 for both comparisons). DAS patients were in a higher New York Heart Association functional class than PAS patients (3.2 +/- 0.4 vs 2.2 +/- 0.4, P <.001) The Tei index was easily and reproducibly obtained in all study participants. In the DAS group, isovolumic contraction time was prolonged and ejection time was shortened in comparison with the CON group (102 +/- 20 ms vs 52 +/- 15 ms, P <.01; and 235 +/- 44 ms vs 316 +/- 45 ms, P <.01), resulting in a significantly increased Tei index (0.78 +/- 0.28 vs 0.40 +/- 0.11, P <.01). In the PAS group, isovolumic relaxation time was shortened (62 +/- 18 ms vs 81 +/- 26 ms for the CON group, P <.01) and ejection time was prolonged (335 +/- 34 ms vs 316 +/- 45 ms for the CON group, P <.05), resulting in a decreased Tei index (0.29 +/- 0.12 vs 0.40 +/- 0.11, P <.05). Receiver operating characteristic curve analysis for the Tei index yielded an area under the curve of 0.98 +/- 0.03 for separating DAS and PAS patients. Using a Tei index greater than 0.42 as a cutoff, DAS patients were identified with a sensitivity of 100% and a specificity of 91%. CONCLUSION: The Tei index is significantly increased in patients with severe AS and depressed overall cardiac LV function. In AS patients with predominant diastolic dysfunction, in whom systolic function is preserved, the index is decreased in comparison with control patients. The index differentiates between symptomatic AS patients with depressed and less symptomatic AS patients with preserved systolic LV function, and may thus provide relevant information in the work-up and care of such patients.     

Influence of electrolyte abnormalities on interlead variability of ventricular repolarization times in 12-lead electrocardiography

Increased QT dispersion (QT(d)) has been associated with increased risk for ventricular arrhythmias. Pathologic extracellular electrolyte concentrations may result in ventricular arrhythmias. The aim of this study was to evaluate the effect of electrolyte abnormalities on QT(d). Ten consecutive patients with isolated electrolyte abnormalities were selected for each of the following groups: hypokalemia, hyperkalemia, hypercalcemia, hypocalcemia, hypomagnesemia, and normal controls. Standard 12-lead electrocardiography was performed for each patient and average QT, JT, and RR intervals were calculated for each lead. Dispersion of QT, JT (JT(d)), and QTc (QTc(d)) intervals were calculated as the range between the longest and shortest measurements. Compared with controls, only patients with hypokalemia had a greater QT(d) (115 +/- 31 vs. 49 +/- 15 ms), JT(d) (116 +/- 34 vs. 52 +/- 12 ms), and QTc(d) (141 +/- 40 vs. 58 +/- 1 ms), (P < 0.05). In an experimental substudy, seven rats were maintained on K(+) and seven on Mg(2+)-free diet followed by normal diet. Experimental hypokalemia significantly increased QT(d) (10 +/- 4 to 37 +/- 7 ms), and QTc(d) (32 +/- 6 to 79 +/- 27 ms) (P < 0.05), whereas hypomagnesemia did not. Restoration of serum potassium resulted in normalization of dispersion (QT(d), 14 +/- 2; QTc(d), 34 +/- 6 ms). Hypokalemia increases the dispersion of ventricular repolarization that may be responsible for arrhythmias. Even though hyperkalemia, hypocalcemia, and hypercalcemia are known to affect ventricular repolarization, our study shows that they are not associated with increased dispersion.     

Single-beat determination of Doppler-derived aortic flow measurement in patients with atrial fibrillation.

The clinical assessment of left ventricular systolic function in patients with atrial fibrillation is unreliable and difficult because of beat-to-beat variation. We initially evaluated an index that is on the basis of the ratio of preceding R-R (RR1) to pre-preceding R-R (RR2) intervals (RR1/RR2) for the measurement of Doppler aortic flow (peak flow velocity [Vp] and time-velocity integral [TVI] proportional to stroke volume) in 20 patients (aged 65 +/- 9.6 years) with atrial fibrillation. We obtained each parameter for >13 cardiac cycles, and the relationship between each parameter at a given cardiac beat and the RR1/RR2 ratio were evaluated by linear regression analysis. The value of each parameter at RR1/RR2 = 1 was calculated from the equation of linear regression line and compared with measured average value over all cardiac cycles. Both parameters showed a significant positive correlation with the RR1/RR2 ratio (Vp, r = 0.98, y = 1.01x + 0.61; TVI, r = 0.99, y = 1.01x + 0.26). The calculated value of each parameter at RR1/RR2 = 1 was quite similar to the average value (Vp, 97.4 +/- 30.8 vs 95.7 +/- 29.8 cm/s; TVI, 17.7 +/- 6.8 vs 17.3 +/- 6.7 cm, respectively). In the additional 20 patients (aged 77.4 +/- 15.2 years), Doppler aortic flow parameters of a single beat with identical RR1 and RR2 intervals were compared with measured average value over all cardiac cycles and showed similar results (Vp, r = 0.99, y = 0.99x + 3.4, P <.0001, bias -0.5 cm/s; TVI, r = 0.99, y = 0.92x + 1.5, P <.0001, bias 0.1 cm). In conclusion, the Doppler aortic flow at RR1/RR2 = 1 allows the left ventricular systolic parameters to be accurately evaluated during atrial fibrillation and obviates the less reliable process of averaging multiple irregular beats.