彩色多普勒超声对急性心肌梗塞病人左房功能的分析

应用二维彩色多普勒超声技术评价急性心肌梗塞病人的左房功能。结果显示，急性心肌梗塞组与正常对照组比较其各指标均有显著性差异（Ｐ＜０．００１或Ｐ＜０．０５）。左房内径（ＬＡＤｄ）、左房容积（ＬＡＶ）、左房压力（ＬＡＰ）、左房张力（ＬＡＴ）、左房射血期（ＬＡＥＴ）、左房每搏量（ＬＡＳＶ）、左房射血分数（ＬＡＥＦ）和Ａ峰均增加，而Ｅ峰、Ｅ／Ａ比值、射血前期（ＬＡＰＥＰ）和ＬＡＰＥＰ／ＬＡＥＴ比值降低。结论：急性心肌梗塞后，左房代偿性收缩功能增强，维持一定的左房与左室间的压差（ＡＶＰＧ），对增加左室充盈量起重要作用，符合Ｆｒａｎｋ—ｓｔａｒｌｉｎｇ定律。     

超声心动图对急性心肌梗塞后左房代偿功能的分析研究

应用超声心动图分析评价急性心肌梗塞（ＡＭＩ）患者的左房功能代偿机制。结果示：ＡＭＩ组与正常对照组比较，各指标均有显著性差异。左房内径（ＬＡＤｄ）、左房容积（ＬＡＶ）、左房压力（ＬＡＰ）、左房张力（ｔＡＴ）、左房射血期（ＬＡＥＴ）、左房每搏量（ＬＡＳＶ）、左房射血分数（ＬＡＥＦ）及峰值速度Ａ（ＰｖＡ）均增加，而峰值速度Ｅ（ＰＶＥ）、ＰＶＥ／ＰＶＡ比值、射血前期（ＬＡＰＥＰ）及ＬＡＰＥＰ／ＬＡＥＴ值降低。结论：ＡＭＩ后左房代偿性收缩功能增强，维持一定的左房与左室间的压差（ＡＶＰＧ），对增加左室充盈量起重要作用，其作用机理符合Ｆｒａｎｋ－ｓｔａｒｌｉｎｇ定律。     

二维多普勒超声评价高血压病左房功能的变化

应用二维多普勒超声心动图测定４２例高血压病患者及３０例正常人的左房功能参数。结果示：高血压病组与正常对照组比较有显著性差异（Ｐ＜０．０１或Ｐ＜０．００１），高血压病组ＬＡＤ、ＬＡＶ、ＬＡＰ、ＬＡＴ、ＬＡＥＴ、ＬＡ５Ｖ、ＬＡＥＦ及Ａ峰增加；但Ｅ峰、Ｅ／Ａ比值、ＬＡＰＥＰ、ＬＡＰＥＰ／ＬＡＥＴ及ＰＦＲ降低。结论：高血压病时，左房代偿性收缩功能增强，作功增加，以维持恒定的左房室间的压差，为增加左室充盈量起重要作用，其机制符合Ｆｒａｎｋ－Ｓｔａｒｌｉｎｇ定律。     

Strain rate imaging for the assessment of preload-dependent changes in regional left ventricular diastolic longitudinal function.

BACKGROUND: Strain rate imaging is a new and intriguing way of displaying myocardial deformation properties by means of echocardiography. With high frame rate strain rate imaging we observed a spatial inhomogeneity in diastolic longitudinal strain rates in healthy persons. A base-to-apex time delay in diastolic lengthening could be seen both in early diastole and at atrial contraction. METHODS AND RESULTS: We investigated this consistent finding and its dependence on loading conditions in 20 healthy volunteers. Propagation velocities of lengthening of 91 +/- 31 cm/s (E-wave) and 203 +/- 11 cm/s (A-wave) at rest (equal to time delays of 104 +/- 29 ms and 56 +/- 24 ms, respectively) increased significantly to 101 +/- 27 cm/s (E) and 283 +/- 17 cm/s (A) with lifting the volunteers' legs. Applying nitroglycerin sublingually and sitting upright significantly decreased propagation velocities (E-wave 76 +/- 20 cm/s, A-wave 172 +/- 93 cm/s and E-wave 66 +/- 17 cm/s, A-wave 150 +/- 64 cm/s, respectively). Free lateral walls showed a lower propagation velocity than septal walls. CONCLUSION: We conclude that the propagation velocities of left ventricular lengthening waves are dependent on preload changes and increase with increasing preload.     

Evaluation of atrial thrombus formation and atrial appendage function in patients with pacemaker by transesophageal echocardiography

BACKGROUND: Physiologic pacing is claimed to be superior to ventricular pacing in as much as it entails lower risk of atrial fibrillation, stroke, and atrial remodeling. There are few data on the relation between atrioventricular (AV) synchrony and atrial clot formation. Utilizing transesophageal echocardiography (TEE), this study sought to evaluate the effect of AV synchrony loss on left atrial physiology, atrial stasis, and clot formation. METHODS: We conducted a cross-sectional study on patients with both AV and ventricular pacing with left ventricular ejection fraction (LVEF) >30%. TEE enabled us to explore atrial and pacing leads thrombi and measure left atrial appendage (LAA) flow velocity. RESULTS: A total 72 patients (mean age, 65 +/- 11.7) were enrolled in the study. The pacing mode was VVI in 53% and AV sequential in 47% of patients. LVEF (mean +/- SD; %) was 53.3 +/- 6.2% in ventricular pacing mode and 52.2 +/- 6.6 in physiologic pacing mode. Thrombus formation on pacing lead (<10 mm in 97% of patients) was observed in 32% of all the patients (23% in patients with AV sequential pacing mode and 39% with VVI mode). Left atrial appendage flow velocity (LAA-FV) was significantly higher among the patients with AV sequential pacing mode (49.44 +/- 18 cm/s vs 40.94 +/- 19.4 cm/s, P value = 0.02). LAA-FV >40 cm/s was detected in 60% of the patients, 60% of whom were in physiologic mode. Left atrial size was significantly larger among the patients with VVI pacing mode (42.3 +/- 2.3 mm vs 37.79 +/- 4.5 mm, P = 0.001). Multivariate analysis showed no relation between LAA-FV and age, hypertension, diabetes mellitus, left atrial size, and left ventricular function. Only one patient had right atrial clot. There was no thrombus in the ventricles and atrial appendage. CONCLUSION: Long-term loss of AV synchrony induced by VVI pacing is associated with the impairment of LAA contraction. Thrombus formation in the LAA is not increased by VVI pacing in patients with relatively good left ventricular (LV) function and sinus rhythm.     

Hemodynamic effects of fluid loading in acute massive pulmonary embolism

OBJECTIVE: To assess the hemodynamic effects of fluid loading in patients with acute circulatory failure caused by acute massive pulmonary embolism (AMPE). DESIGN: Prospective study. SETTING: Respiratory critical care unit of a university hospital. PATIENTS: Thirteen patients free of previous cardiopulmonary disease with angiographically proven AMPE (Miller index = 24 +/- 1), with acute circulatory failure defined by a cardiac index (CI) lower than 2.5 L/min/m2. INTERVENTION: Infusion of 500 mL of dextran 40 over 20 mins. MEASUREMENTS AND MAIN RESULTS: Fluid loading induced a substantial increase in right atrial pressure from 9 +/- 1 mm Hg to 17 +/- 1 mm Hg and in right ventricular end-diastolic volume index from 123 +/- 14 mL/m2 to 150 +/- 11 mL/m2 (p < .05 for both comparisons). The increase in right ventricular preload was associated with an increase in Cl from 1.6 +/- 0.1 to 2.0 +/- 0.1 L/min/m2 (p < .05), whereas right ventricular ejection fraction (15 +/- 3% at baseline vs. 16 +/- 3% after fluid loading) and total pulmonary vascular resistance index (1689 +/- 187 dyne x sec/cm5 x m2 at baseline vs. 1492 +/- 166 dyne x sec/ cm5 x m2 after fluid loading) remained unchanged. The increase in Cl induced by fluid loading was inversely correlated to baseline right ventricular end-diastolic volume index (r = -.89 ; p< .05). CONCLUSIONS: These results suggest that fluid loading can improve hemodynamic status in patients with acute circulatory failure caused by AMPE.     

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.     

Decreased left ventricular longitudinal contraction in normotensive and normoalbuminuric patients with Type II diabetes mellitus: a Doppler tissue tracking and strain rate echocardiography study

Type II diabetes mellitus is associated with congestive heart failure with preserved ejection fraction. This group of patients has been assumed to have isolated diastolic dysfunction; however, the longitudinal systolic contraction of the left ventricle has not been studied previously. The objective of the present study was to investigate the longitudinal contraction of the left ventricle in normotensive Type II diabetes mellitus patients with normal ejection fraction. We examined 32 normotensive patients with Type II diabetes mellitus with ejection fraction >0.55 and fractional shortening >0.25. Exclusion criteria were angina pectoris, cardiac valve disease, albuminuria, retinopathy or neuropathy. Normal subjects (n =32) served as controls. A 16 segment model of motion amplitude assessed left ventricular longitudinal contraction and the average of the segments was calculated as the tissue tracking score index. Peak systolic velocity and strain rate was also obtained in each segment. Patients with Type II diabetes mellitus had a significantly lower tissue tracking score index compared with normal subjects (5.8+/-1.6 mm compared with 7.7+/-1.1 mm; P <0.001). Mean peak systolic velocity was also significantly lower (4.3+/-1.5 cm/s compared with 5.4+/-1.0 cm/s; P <0.001), as well as peak systolic strain rate (-1.2+/-0.3 s(-1) compared with -1.6+/-0.4 s(-1); P <0.001). Patients with Type II diabetes mellitus and preserved diastolic function had a significantly lower tissue tracking score index compared with normal subjects (6.6+/-1.5 mm; P <0.001), but patients with diastolic dysfunction had an even more profound decrease in tissue tracking score index compared with patients without diastolic dysfunction (4.9+/-0.9 mm; P <0.01). In conclusion, the longitudinal systolic contraction was significantly decreased in normotensive patients with Type II diabetes mellitus with normal ejection fraction, which was most profound in patients with concomitant diastolic dysfunction.     

Sequential changes in atrial pressures, dimensions, and plasma atrial natriuretic factor concentrations during volume loading in hemodynamically normal human subjects.

The effects of volume loading on atrial pressures and dimensions, plasma levels of atrial natriuretic factor (ANF), and other neurohormonal variables were studied in 11 patients with normal hemodynamics with the patients in a supine -15 degree left decubitus posture by infusing 750 ml of normal saline solution over 30 minutes. Right and left atrial areas were measured by two-dimensional echocardiography. Plasma ANF level was sampled simultaneously from the pulmonary artery, aorta, and femoral artery and vein. At 30 minutes into the infusion, pulmonary capillary wedge pressure and right atrial pressure increased from 5.6 +/- 2.8 mm Hg (mean +/- SD) and 6.4 +/- 2.2 mm Hg to 10.2 +/- 3.2 and 9.5 +/- 2.2 mm Hg, respectively (both p less than 0.01). Left atrial area increased from 12.6 +/- 2.2 cm2 to 15.0 +/- 2.1 cm2 (p less than 0.05), whereas right atrial area did not change. Plasma ANF levels from all sampling sites increased significantly (e.g., 43 +/- 21 pg/ml to 71 +/- 62 pg/ml in the femoral artery, p less than 0.05). Plasma norepinephrine and renin levels were unchanged, whereas aldosterone level declined significantly. At 30 minutes after termination of the infusion, atrial pressures declined to baseline values in all patients. However, left atrial area remained significantly increased, and a trend for systemic arterial plasma ANF level to remain increased was seen. Plasma aldosterone level remained significantly suppressed.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of atrial natriuretic peptide on left ventricular performance in conscious dogs before and after pacing-induced heart failure.

Atrial natriuretic peptide (ANP) has potent vasodilatory and natriuretic actions and may have therapeutic benefit in congestive heart failure (CHF). These benefits may be offset by a negative inotropic effect of ANP seen in isolated preparations. However, ANP's integrated effect on left ventricular (LV) contraction and relaxation, independent of loading conditions, both under normal conditions and after CHF, is not known. We studied six conscious dogs, instrumented to measure LV and left atrial pressures and to determine LV volume from three dimensions. ANP produced significant (P<.05) decreases in LV end-systolic pressure (101.2+/-11.8 versus 91.7+/-11.2 mm Hg, P<.05) in normal dogs and in dogs with CHF (93.1+/-6.4 versus 87.1+/- 4.4 mm Hg, P<.05). ANP also caused significant reductions of the slope of end-systolic pressure-end-systolic volume relation both before (7.0 +/-1.5 versus 6.3+/-1.5 mm Hg/ml) and after CHF (4.8+/-1.3 versus 4.4+/-1.2 mm Hg/ml, P<.05). Both before and after CHF, ANP slowed LV relaxation at matched end-systolic pressure. Before CHF, steady-state stroke volume and peak LV filling rate (dV/dt(max)) were reduced. However, after CHF, the fall in end-systolic pressure more than offset the load-independent LV depression, as stroke volume, the rate LV relaxation, and dV/dt(max) were increased and minimum LV pressure reduced. ANP has negative effects on LV contractility and relaxation both before and after CHF. However, after CHF, afterload reduction with ANP overcomes its negative effects, resulting in net improvement of LV ejection and relaxation. Thus, the direct cardiodepressant effects of ANP should not limit its usefulness in CHF.     

Prediction of conversion from paroxysmal to permanent atrial fibrillation

BACKGROUND: Paroxysmal atrial fibrillation (PAF) transits to permanent atrial fibrillation (PEAF). The current study was to determine whether a P wave-triggered P wave signal averaged electrocardiogram (P-SAECG) and chemoreflexsensitivity (CHRS) are useful to predict a conversion to PEAF in patients with PAF. METHODS: The filtered P wave duration (FPD) and the root mean square voltage of the last 20 ms of the P wave (RMS 20) were measured by P-SAECG. The ratio between the difference of RR intervals in the ECG and venous pO2 before and after 5-minutes oxygen inhalation is measured (ms/mmHg) for the determination of CHRS. Results: A total of 180 patients with PAF were enrolled and followed for a mean of 22.5 months. PEAF occurred in 38 patients (21%) and these patients had a significantly larger left atrial size (43.2 +/- 4.9 vs. 41.0 +/- 5.4 mm, P = 0.021), a significantly longer FPD (158.8 +/- 18.2 vs. 136.7 +/- 16.6 ms, P < 0.0001), and a significantly lower CHRS (1.96 +/- 0.99 vs. 2.44 +/- 1.19 ms/mmHg, P = 0.024) than patients with PAF. Patients with PEAF tended to have a lower RMS 20 (2.38 +/- 0.65 vs. 2.75 +/- 1.18 microV, P = 0.067) than patients with PAF. The chi(2) test showed that the combination of FPD > or = 145 ms, RMS 20 < or = 3.0 microV, left atrial size > or = 41 mm, and CHRS < or = 2.0 ms/mmHg had the best predictive power for PEAF. Patients who fulfilled these criteria had a 12-fold increased risk for a conversion from PAF to PEAF. CONCLUSIONS: Our results show that a P-SAECG, an analysis of CHRS, and left atrial enlargement are clinical predictors of a progression from PAF to PEAF.     

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.     

Long–Term Effect of VVI Pacing on Atrial and Ventricular Function in Patients with Sick Sinus Syndrome

We conducted a prospective, 6–month echocardiographic study on the effect of WI pacing on left atrial and ventricular function and dimensions in patients with sick sinus syndrome. Thirty nine patients (23 women and 16 men, aged 71.7 ± 9.2 years; 30 in sinus rhythm and 9 in atrial fibrillation) who had a WI pacemaker implanted because of sick sinus syndrome were recruited in the study. In 26 patients who presented with and remained in sinus rhythm, paced left ventricular ejection fraction and stroke volume were significantly decreased (71.4%± 11.8% to 67.0%± 13.6%, and 73.9 ± 29.0 cm³ to 66.3 ±21.1 cm³, respectively, P < 0.001 for both), whereas the paced diastolic dimension of the left atrium was significantly increased (3.2 ± 0.7 cm to 3.7 ± 0.9 cm, P < 0.001) at 6 months as compared with preimplantation. In nine patients with atrial fibrillation at implantation, paced left ventricular ejection fraction at follow–up was significantly decreased (67.7%±10.1% to 64.2%± 10.6%, P = 0.003), but paced stroke volume and left atrial diastolic dimension were not significantly changed (75.1 ± 25.6 cm³ to 79.0 ± 22.7 cm³, and 4.3 ±1.2 cm to 4.6 ±1.5 cm, P = NS for both) at follow–up. Cessation of pacing and restoration of sinus rhythm in 21 patients at follow–up did not result in any significant change of ejection fraction (67.5%± 10.2% to 67.6%± 9.7%, P = NS) whereas stroke volume was increased (59.1 ± 19.6 cm³ to 69.1 ± 22.3 cm³, P < 0.0001) in comparison with paced values. However, compared with preimplantation values, ejection fraction was significantly decreased (70.4%± 10.0% to 67.6%± 9.7%, P = 0.001), whereas stroke volume was not significantly changed (68.4 ± 22.3 cm³ to 69.1 ± 22.3 cm³, P = NS) during sinus rhythm at follow–up. In 14 of those patients, discontinuation of pacing resulted in a significant increase of left atrial fractional shortening (8.1 %± 1.7% to 20.1 %± 4.3%, P < 0.001) and significant increase of left atrial diastolic dimension compared with paced and preimplantation levels (3.8 ± 0.7 cm vs 3.6 ± 0.7 cm and 3.0 ± 0.5 cm, respectively, P < 0.001). Long–term WI pacing in patients with sick sinus syndrome results in increase of the left ventricular end–systolic dimension and permanent reduction of the left ventricular ejection fraction. In the left atrium, WI pacing causes an immediate reduction of the fractional shortening as well as long–term increase of the diastolic dimension.     

Effect of right ventricular apex pacing on the Tei index and brain natriuretic peptide in patients with a dual-chamber pacemaker

BACKGROUND: Asynchronous electrical activation induced by right ventricular apex (RVA) pacing can cause various abnormalities in left ventricular (LV) function, particularly in the context of severe LV dysfunction or structural heart disease. However, the effect of RVA pacing in patients with normal LV and right ventricular (RV) function has not been fully elucidated. The aim of this study was to characterize the effects of RVA pacing on LV and RV function by assessing isovolumic contraction time and isovolumic relaxation time divided by ejection time (Tei index) and by assessing changes in plasma brain natriuretic peptide (BNP). METHODS: Doppler echocardiographic study and BNP measurements were performed at follow-up (mean intervals from pacemaker implantation, 44+/-75 months) in 76 patients with dual chamber pacemakers (sick sinus syndrome, n=30; atrioventricular block, n=46) without structural heart disease. Patients were classified based on frequency of RVA pacing, as determined by 24-hour ambulatory electrocardiogram (ECG) that was recorded just before echocardiographic study: pacing group, n=46 patients with RVA pacing>or=50% of the time, percentage of ventricular paced 100+/-2%; sensing group, n=30, patients with RVA pacing<50% of the time, percentage of ventricular paced 3+/-6%. RESULTS: There was no significant difference in mean heart rate derived from 24-hour ambulatory ECG recordings when comparing the two groups (66+/-11 bpm vs 69+/-8 bpm). LV Tei index was significantly higher in pacing group than in sensing group (0.67+/-0.17 vs 0.45+/-0.09, P<0.0001), and the RV Tei index was significantly higher in pacing group than in sensing group (0.34+/-0.19 vs 0.25+/-0.09, P=0.011). Furthermore, BNP levels were significantly higher in pacing group than in sensing group (40+/-47 pg/mL vs 18+/-11 pg/mL, P=0.017). With the exception of LV diastolic dimension (49+/-5 mm vs 45+/-5 mm, P=0.012), there were no significant differences in other echocardiographic parameters, including left atrium (LA) diameter (35+/-8 mm vs 34+/-5 mm), LA volume (51+/-27 cm3 vs 40+/-21 cm3), LV systolic dimension (30+/-6 mm vs 29+/-7 mm), or ejection fraction (66+/-9% vs 63+/-11%), when comparing the two groups. CONCLUSIONS: These findings suggest that the increase of LV and RV Tei index, LVDd, and BNP are highly correlated with the frequency of the RVA pacing in patients with dual chamber pacemakers.     

Reduced coronary flow reserve in patients with congestive heart failure assessed by transthoracic Doppler echocardiography.

BACKGROUND: Although coronary flow reserve (CFR) has been reported to be restricted in various conditions, there has been no report of CFR for patients with congestive heart failure (CHF). The purpose of this study was to assess coronary flow characteristics for patients with CHF. METHODS: We studied 15 patients with CHF: 8 with dilated myocardiopathy and 7 with hypertensive heart disease. Phasic coronary flow velocities were obtained in the left anterior descending coronary artery at rest and during hyperemia (0.15 mg/kg/min adenosine triphosphate infusion intravenously) by transthoracic echocardiography before and after treatment of CHF. CFR was obtained from the ratio of hyperemic/baseline diastolic mean velocity. RESULTS: CFR was significantly restricted in the condition of CHF compared with that after improvement of CHF (1.5 +/- 0.2 vs 2.0 +/- 0.3, P < .01). Baseline diastolic mean velocity in the condition with CHF was significantly greater than that after improvement of CHF (41 +/- 13 cm/s vs 33 +/- 13 cm/s, P = .04), although maximal hyperemic diastolic mean velocity was not significantly different before and after improvement of CHF (63 +/- 20 cm/s vs 61 +/- 19 cm/s, P = .68). After improvement of CHF, heart rate, along with left ventricular end-diastolic volume and dimension, were significantly decreased, and deceleration time of transmitral early filling flow was increased compared with before treatment of CHF. Blood pressure and ejection fraction were not significantly different before and after treatment of CHF. CONCLUSIONS: Restriction of CFR is demonstrated during CHF because of the elevation of baseline resting flow velocity, which might be related to increase in left ventricular preload and heart rate.     

Late improvement in ventricular performance following internal cardioversion for persistent atrial fibrillation: an argument in support of concealed cardiomyopathy

The aim of the study was to evaluate the time course of atrial and ventricular function improvement following internal atrial cardioversion in patients with structural heart disease. Twenty-nine patients with chronic persistent atrial fibrillation (AF) and underlying structural heart disease were followed by serial echocardiograms performed at 1 and 6 hours, 1 day, 1, 2, and 3 weeks, and 1, 2, 3, and 6 months after successful cardioversion. Sinus rhythm was maintained at 6 months in 24 patients. Following cardioversion the time course of left atrial mechanical function (peak A wave, percent A wave filling) differed from that of left ventricular ejection fraction: peak A wave values (cm/s) increased significantly at 1 week (51 +/- 23 vs 35 +/- 15 at 1 hour, P < 0.05), percent A wave filling (%) increased significantly at 2 weeks (34 +/- 12 vs 22 +/- 9 at 1 hour, P < 0.05), whereas left ventricular ejection fraction (%) increased later (at 1 month 60 +/- 14 vs 55 +/- 14 at baseline, P < 0.05 and at 2 months 60 +/- 14 vs 56 +/- 14 at 1 hour, P < 0.05). In conclusion, restoration of sinus rhythm results in an improvement in left ventricular ejection fraction during follow-up, even in patients with structural heart disease without fast ventricular rates at baseline. The dissociation between the time course of atrial and ventricular function improvement suggests that the latter was partly due to regression of a concealed form of cardiomyopathy and/or of a ventricular dysfunction due to chronic AF.     

Left atrial wall motion velocity measured by the velocity profile method with tissue Doppler echocardiography in normal subjects: its relation to aging

Purpose The aim of this study was to find a method for measuring left atrial wall velocity (LAWV) during atrial contraction using tissue Doppler echocardiography.Methods The velocity profile method was used to measure left atrial wall velocity at several sites in 64 healthy individuals aged 25–84 years. We attempted to find maximum left atrial wall velocity (LAWVmax) by mapping on four-chamber, two-chamber, short-axis, and long-axis views and studied the relations between maximum left atrial wall velocity, age, and peak velocity during atrial contraction in mitral or pulmonary venous flow.Results Left atrial wall velocity was varied by changing the position of the sampling volume. The velocity profile pattern was similar to the left ventricular wall velocity pattern near the mitral valve annulus in the left atrium. Left atrial wall velocity had a positive peak during atrial contraction when the sample volume was located in the cranial and dorsal area. Maximum left atrial wall velocity was obtained in 74% of cases with the two-chamber view. Maximum left atrial wall velocity in healthy subjects was 3.1 ± 0.7cm/s, and the duration of the atrial contraction was 112 ± 12ms. Maximum left atrial wall velocity increased slightly with age but was not significantly correlated with peak velocity during atrial contraction in mitral or pulmonary venous flow.Conclusions Left atrial wall velocity was measured by the velocity profile method in 64 healthy subjects aged 25–84 years. Maximum left atrial wall velocity increased slightly with age but was not significantly correlated with the peak velocity during atrial contraction in mitral or pulmonary venous flow.     

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.     

Doppler echocardiographic evaluation of right ventricular function in patients with right ventricular infarction.

The aim of the present study was to assess the utility of the myocardial performance index in patients with right ventricular infarction. During the study period, 120 patients were evaluated: 50 patients had a right ventricular infarction and 70 patients had an inferior left ventricular infarction without right ventricular involvement. On admission, an echocardiogram was obtained from all patients prior to the initiation of thrombolytic therapy. The right ventricular myocardial performance index was calculated, as were the Doppler-derived parameters of the right side of the heart. All patients with right ventricular infarction had undergone a right ventricular dilation, compared with 70 patients with left ventricular infarction (right ventricular end diastolic diameter 32 +/- 13 versus 26 +/- 24 mm; P < 0.01) and increased areas (diastolic area 24.8 +/- 9.9 versus 15.1 +/- 6.8 cm2; P < 0.01). Tricuspid regurgitation was detected in 26 patients. The mean peak velocity of tricuspid regurgitation was 3.8 +/- 0.8 m/s. The Doppler intervals, isovolumetric contraction times (136 +/- 30 versus 49 +/- 11 ms; P < 0.01), and relaxation times (71 +/- 28 versus 37 +/- 9 ms; P < 0.01) were prolonged in patients with right ventricular infarction, whereas the ejection time was significantly reduced (250 +/- 31 versus 330 +/- 26 ms; P < 0.001). The myocardial performance index was significantly increased in patients with right ventricular infarction (0.85 +/- 0.2 versus 0.26 +/- 0.1; P < 0.01). The inferior vena cava collapse was reduced in all patients with right ventricular infarction (35 +/- 20%). The right ventricular myocardial performance index was a useful indicator of right ventricular performance in patients with right ventricular infarction. The use of echocardiographic parameters of the right side of the heart and Doppler echocardiographic parameters of right ventricular function provides a reliable diagnosis of right ventricular infarction.     

Color-coded tissue Doppler assessment of the effects of acute ischemia on regional left ventricular function: comparison with sonomicrometry.

Echocardiographic assessment of regional left ventricular (LV) function usually consists of subjective visual inspection of endocardial movement and wall thickening. Color-coded tissue Doppler (TD) is a potential means to quantify regional LV function more objectively. Accordingly, in this study, color-coded TD was used to assess the regional effects of acute ischemia in an open-chest canine model of coronary occlusion, with implanted sonomicrometry length crystals as a standard of reference. Eight dogs were studied during baseline conditions and during left anterior descending coronary artery occlusion. Midventricular short-axis images were used to guide the color TD M-mode cursor through circumflex (septal) and left anterior descending (anterolateral) perfusion zones. Off-line conversion of endocardial time-velocity maps was performed. Peak systolic endocardial velocity by TD decreased from 4.4 +/- 1.4 cm/s to 1.8 +/- 1.5 cm/s with coronary occlusion (P < .05 versus baseline). Similar significant decreases in calculated systolic velocity by sonomicrometry occurred with ischemia from 11.1 +/- 3.8 mm/s to 8.2 +/- 1.2 mm/s (P < .05 versus baseline). Peak systolic velocity by TD was inversely correlated with end-systolic length by sonomicrometry as a measure of regional function (r = -0.77, P < .001). Time to peak systolic velocity increased with ischemia from 154 +/- 60 ms to 286 +/- 67 ms by TD and 200 +/- 60 ms to 320 +/- 30 ms by sonomicrometry (P < .05 versus baseline). The delay in time to peak systolic velocity by TD and sonomicrometry were correlated (r = 0.75, P < .001). In conclusion, color-coded TD echocardiography has the potential to quantify regional LV function during coronary ischemia.