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.     

Cardiac adaptation to intensive training in prepubertal swimmers

BACKGROUND: Despite the increasing involvement of child athletes in intensive training regimens, little is known about the influence of such training on autonomic regulation and cardiac structure and function. PATIENTS AND METHODS: Twenty-five highly trained (12-14 h weekly for at least 4 years) swimmers (aged 11.9 +/- 1.6 years; 15 males, 10 females) and 20 non-training normal children who served as controls (aged 11.3 +/- 0.6 years; 14 males, 6 females) were studied. Heart rate variability analysis in the time and frequency domains was performed on 15 min resting heart rate acquisitions. Left ventricular morphology and systolic function was studied with two-dimensional guided M-mode echocardiography. The transmitral flow velocity profile was assessed with pulsed Doppler. Parameters measured included the peak early (E) and peak late (A) transmitral flow velocity and their ratio (E/A). Left atrial (LA) volumes were determined at mitral valve (MV) opening (maximal, Vmax), at onset of atrial systole (P wave of the ECG, Vp), and at MV closure (minimal, Vmin) from the apical 2- and 4-chamber views, using the biplane area-length method. LA systolic function was assessed with the LA active emptying volume (ACTEV) = Vp-Vmin and the LA active emptying fraction (ACTEF) = ACTEV/Vp. RESULTS: Average NN (967.1 +/- 141.8 vs. 768.4 +/-85.6 ms, P < 0.0001), logSDNN (1.89 +/- 0.14 vs. 1.80 +/- 0.17 ms, P < 0.05), logPNN 50% (1.66 +/- 0.23 vs. 1.46 +/- 0.35, p < 0.05), and logHF power (3.13 +/- 0.32 vs. 2.95 +/- 0.26 ms2, p < 0.05) were greater in swimmers than in controls. Left ventricular end-diastolic diameter was greater (32.3 +/- 3.3 vs. 29.5 +/- 3.3 mm m(-2), P < 0.02) in swimmers than in controls, whereas the left ventricular septal (5.9 +/- 1 vs. 5.6 +/- 0.8 mm m(-2), P = NS) and posterior wall thickness (5.7 +/-0.9 vs. 5.4 +/- 0.8 mm m(-2), P = NS) were similar in the two groups. The E/A ratio was greater (2.2 +/- 0.49 vs. 1.78 +/- 0.36, P < 0.003) whereas the A velocity was lower (0.41 +/- 0.09 vs. 0.50 +/- 0.13 m s(-1), P < or = 0.02) in swimmers than in controls. Vmax was greater (18.6 +/-4.8 vs. 14.9 +/-5.3 cm m(-2), P < 0.03), whereas ACTEF was lower (36 +/- 12% vs. 44.2 +/- 12%, P < 0.04) in swimmers than in controls. CONCLUSION: Cardiac adaptation to intensive training in prepubertal swimmers includes vagal predominance, a mild increase in left ventricular dimensions without significant changes in septal or posterior wall thickness, and increased LA size associated with depressed LA systolic function. Evaluation of LA size and systolic function may contribute to a better understanding of the characteristics of the 'athlete's heart' in children and to the differential diagnosis between left ventricular adaptive and pathologic changes.     

应变率成像评估左心室不同舒张功能状态患者左心房功能

目的探讨应变率成像（SRI）评估左心室不同舒张功能状态下左心房功能的价值。方法128例受检者根据左心室不同舒张功能状态分成正常组、顺应性降低组、假性正常化组及限制性充盈障碍组。采集心尖四腔观、三腔观和二腔观组织速度图,SRI测量并计算左心室收缩期左心房平均峰值应变率（mSRs）、左心室舒张早期左心房平均值峰应变率（mSRe）、左心房收缩期左心房平均峰值应变率（mSRa）;测量包括二尖瓣口舒张早期前向血流峰值速度（E）与二尖瓣前瓣环纽织多普勒E比值（E／E′）及E与二尖瓣口M型彩色多普勒峰值血流速度Vp比值（E／Vp）等左心室舒张功能相关参数。将SRI所测左心房功能相关参数与反映左心室舒张功能相关参数作对比。结果E／Vp及E／E′随舒张功能障碍加重而增高,1．1±0．3vs1．6±0．2vs2．1±0．3VS2．6±0．4和7．4±2．4 vs 10．4±2．9VS17．6±4．2vs22．8±4．8（均P〈0．05）;4组患者mSRs、mSRe、mSRa差异有统计学意义（P〈0．05）;mSRe随舒张功能障碍加重而降低,（3．73±0．92）^-1 vs（2．84±0．54）^-1 vs（1.94±0．23）s^-1 vs（1．85±0．30）s。（均P〈0．05）,mSRs及mSRa在舒张功能降低组最高,而在限制性充盈障碍组中最低;E／E′、E／Vp与mSRe呈良好负相关（r=0．813,P〈0．01;r=-0．793,P〈0．01）。结论SRI可准确评价左心室不同舒张功能状态患者左心房功能。     

Myocardial velocity gradient reflects the severity of myocardial damage regardless of the presence or absence of mitral regurgitation.

Complicating mitral regurgitation (MR) apparently enhances left ventricular ejection fraction, thereby leading to the underestimation of myocardial damage by routine echocardiography. We sought to assess the significance of myocardial velocity gradient (MVG) derived from Doppler tissue imaging as an indicator of the severity of myocardial damage in the presence or absence of MR. Peak systolic and diastolic MVG was obtained from 39 participants: 12 healthy participants, 10 patients with dilated cardiomyopathy complicating moderate to severe MR [MR (+) group], and 17 patients with dilated cardiomyopathy without significant MR [MR (-) group]. MVG was compared with standard echocardiographic and Doppler transmitral flow velocity indices. Plasma brain natriuretic peptide levels were measured in all patients. Left ventricular dimension and fractional shortening was similar between MR (+) and MR (-) groups. Plasma brain natriuretic peptide levels were significantly increased in MR (+) group (440 +/- 417 pg/mL) as compared with MR (-) group (122 +/- 107 pg/mL, P <.05). Peak systolic MVG was significantly attenuated in dilated cardiomyopathy group with or without MR [MR (+) group = 1.3 +/- 0.5 seconds(-1), MR (-) group = 2.1 +/- 0.5 seconds(-1), where normal = 4.0 +/- 0.9 seconds(-1), P <.01, respectively]. Peak systolic MVG was further attenuated in MR (+) group than in MR (-) group (P <.01). Plasma brain natriuretic peptide levels were negatively correlated with peak systolic MVG (r = -0.66, P <.0005). Peak diastolic MVG was attenuated in MR (+) and also in MR (-) groups [MR (+) group = -4.5 +/- 2.0 seconds(-1), MR (-) group = -4.4 +/- 1.1 seconds(-1), where normal = -8.7 +/- 2.4 seconds(-1), P <.01, respectively], whereas transmitral flow indices failed to distinguish MR (+) group from normal as a result of pseudonormalization. MVG may reflect the severity of myocardial damage regardless of the presence or absence of complicating MR.     

Detection of early abnormalities of left ventricular function by hemodynamic, echo-tissue Doppler imaging, and mitral Doppler flow techniques in patients with coronary artery disease and normal ejection fraction.

We have investigated the possibility of detecting early abnormalities of left ventricular function at the initial phase of ischemic cardiomyopathy. Sixteen normotensive patients with coronary artery disease and normal left ventricular ejection fraction and 6 control patients were studied by invasive hemodynamic techniques in combination with transmitral Doppler flow or with echo-tissue Doppler imaging. The extent of the percentage of left ventricular longitudinal shortening and the systolic peak velocity at echo-tissue Doppler were significantly higher in the control patients than in patients with ischemic cardiomyopathy (P <.01). Left ventricular end-diastolic pressure was higher (P <.05), whereas mean values of isovolumic contraction and relaxation indexes (dP/dt/P: P <.05; +dP/dt: P <.05; -dP/dt: P <.01) were lower in patients with ischemic cardiomyopathy. Tau was significantly longer in ischemic patients (42.7 +/- 8.8 versus 34.5 +/- 3.7 ms, P <.05). In the control patients, the aortic valve closure to peak E interval by transmitral Doppler flow was significantly longer than that measured by echo-tissue Doppler (P <.001), whereas in patients with ischemic cardiomyopathy, this interval difference was still present and significantly shorter (P <.05). In patients with coronary artery disease and normal ejection fraction, minor and early abnormalities of left ventricular function related to isovolumic contraction and relaxation as well as to longitudinal shortening could be detected. In addition, a suction-like effect, detected during early filling evaluation with echo-tissue Doppler, is significantly decreased but not abolished during the early stages of coronary artery disease.     

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.     

Non-invasive cardiac assessment in beta-thalassaemia major

Iron deposition in the heart occurs in beta-thalassaemia major and contributes to cardiac dysfunction. Eighteen patients with beta-thalassaemia major were assessed clinically and had non-invasive investigations. They were young (15.5 +/- 3.6 years). Two patients had clinical heart failure. Doppler echocardiography demonstrated higher transmitral peak flow velocity in early and late diastole compared with controls (e: p<0.05, a: p<0.01). Transtricuspid peak late diastolic flow velocity was higher in patients (p<0.005). Isovolumic relaxation time was shortened (p<0.001). Pulmonary venous flow velocity was higher in diastole than systole (S: 0.51 +/- 0.11 m/s, D: 0.62 +/- 0.08 m/s). Reversal of pulmonary venous flow during atrial systole was seen in eight patients. These diastolic filling abnormalities did not significantly change with blood transfusion. Left ventricular ejection fraction was normal in patients. Two patients had cardiomegaly on chest X-ray. In beta-thalassaemia with iron overload, there is a restrictive pattern of diastolic dysfunction. This is not altered by recent blood transfusion. Left ventricular function remains relatively intact.     

Noninvasive indexes of left atrial diastolic function in hypertrophic cardiomyopathy.

OBJECTIVES: Our goal was to noninvasively assess left atrial diastolic function and its relation to the impaired left ventricular filling in patients with hypertrophic cardiomyopathy. METHODS AND RESULTS: We studied 34 patients with hypertrophic cardiomyopathy, 26 patients with secondary forms of left ventricular hypertrophy (aortic stenosis, fixed subaortic stenosis, hypertension), and 21 control subjects. Left atrial diastolic function was assessed by measuring acceleration time (SAT), deceleration time (SDT), and the EF (mean deceleration rate) slope of the pulmonary venous flow systolic wave (SW). Left ventricular diastolic function assessed by transmitral Doppler included peak early left ventricular and peak atrial filling velocities, the ratio of early-to-late peak velocities, isovolumic relaxation time, deceleration time, and EF slope. In patients with hypertrophic cardiomyopathy, acceleration time was significantly reduced (P<.05), deceleration time was significantly prolonged (P<.0001), and EF slope was significantly reduced (P<.01). These indexes were similar among the other two groups. No statistically significant difference existed between the subgroups of hypertrophic cardiomyopathy in the above indexes. Patients with hypertrophic cardiomyopathy and secondary forms of left ventricular hypertrophy had evidence of left ventricular diastolic dysfunction. In patients with hypertrophic cardiomyopathy, no correlation existed between left atrial and left ventricular diastolic function indexes (r = -0.26 to 0.33). CONCLUSIONS: Echocardiographic indexes of left atrial relaxation and filling are abnormal in patients with hypertrophic cardiomyopathy but not in secondary forms of left ventricular hypertrophy. These indexes are abnormal in all forms of hypertrophic cardiomyopathy irrespective of left ventricular outflow tract obstruction and distribution of hypertrophy; they are not solely attributable to left ventricular diastolic dysfunction. The above may imply that hypertrophic cardiomyopathy is a cardiac myopathic disease that involves the heart muscle as a whole, irrespective of distribution of hypertrophy and obstruction.     

Effect of preload reduction by haemodialysis on new indices of diastolic function

Assessment of mitral annular motion diastolic velocities by M-mode or tissue Doppler imaging and the propagation velocity of early diastolic filling (Vp) by colour M-mode have been proposed as preload-independent indices of diastolic function. The aim of the present study was to determine the effects of preload reduction by haemodialysis on these new echocardiographic indices and to assess the relationship between these indices. The study group comprised 17 patients with chronic renal failure in sinus rhythm with normal left ventricular systolic function who underwent echocardiography 30 min prior to and 30 min following haemodialysis. Following dialysis there were significant reductions in weight (P<0.001), left atrial diameter (P=0.001), the peak Doppler velocity of early diastolic transmitral flow (P=0.005) and the ratio of Doppler velocities of early to late diastolic transmitral flow (P=0.02), consistent with a reduction in intravascular volume. There was no change after dialysis in early diastolic mitral annular velocity using M-mode (P=0.19) or tissue Doppler imaging from either the septal or lateral walls (P=0.88 and P=0.15 respectively), but there was a reduction in Vp after dialysis (55 to 49 cm/s; P=0.04). There were only weak correlations between Vp and the early diastolic mitral annular velocities (r<0.6 for all). We conclude that the assessment of diastolic function by the mitral annular early diastolic velocity appears to be preload-independent, that Vp may be affected by preload and that there is only a weak relationship between Vp and the early diastolic mitral annular velocity.     

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.     

Clinical relevancy of the myocardial velocity gradient: limitations of a binary response

BACKGROUND: Doppler tissue echocardiographic myocardial velocity gradient (MVG) overcomes translational or tethered motion effects. Diagnostic applications rely on MVG numeric value, an instantaneous value calculated at peak endocardial velocity. Our aim was to test the clinical relevancy of MVG for patients with dilated cardiomyopathy (CM) at rest. Efficiency of MVG, as a marker of the underlying mechanism, ischemic or nonischemic, was compared with that of mean velocities averaged over a cycle. METHODS: Peak and mean velocities were measured and MVG calculated during ejection, and early and late diastole, in the endocardium and epicardium on color M-mode Doppler tissue echocardiographic parasternal recordings of the posterior wall, simultaneously imaged with the septum. The population consisted of 34 patients with similar clinical presentation (left ventricular ejection fraction < 40%, left ventricular end-diastolic diameter > 6 cm, and proven ischemic [14] or nonischemic [20] dilated CM) and 16 control subjects. RESULTS: Doppler tissue echocardiography data significantly differed between control subjects and all patients with CM. Between patients, the only significant differences were found at the posterior wall for mean velocities at the epicardium in systole (9 +/- 4 mm/s for ischemic vs 14 +/- 5 mm/s for nonischemic, P =.002), and at both layers in early diastole (endocardium, 14 +/- 9 vs 29 +/- 12 mm/s, P =.0004; epicardium, 12 +/- 4 vs 22 +/- 11 mm/s, P =.002; ischemic vs nonischemic CM, respectively). CONCLUSION: Specific features of CM were characterized by myocardial velocity changes studied layer by layer throughout a phase. The binary response of transient peak MVG could not reach this goal.     

An integrated measure of left ventricular diastolic function based on relative rates of mitral E and A wave propagation.

BACKGROUND AND OBJECTIVES: The mitral E wave propagation inside the left ventricle is slowed in patients with abnormal left ventricular (LV) relaxation with a prolongation of its transit time to the LV outflow tract (T(e)). On the contrary, the mitral A wave propagation is faster in those with elevated LV end-diastolic stiffness, resulting in a shortening of its transit time (T(a)). We hypothesized that the T(e)/T(a) ratio may serve an integrated measure of global LV diastolic function. METHODS AND RESULTS: The T(e)/T(a) ratio was measured with Doppler echocardiography in 94 subjects: 25 normal subjects, 38 patients with LV hypertrophy (18 with secondary LV hypertrophy and 20 with hypertrophic cardiomyopathy), and 31 patients undergoing left heart catheterization for clinical indications. The T(e)/T(a) ratio was 1. 98 +/- 0.61 in the normal subjects, 3.32 +/- 0.93 in patients with secondary LV hypertrophy (P <.0001 vs normal), and 3.18 +/- 1.36 in patients with hypertrophic cardiomyopathy (P =.0003 vs normal). In the invasive group the T(e)/T(a) ratio (range 0.56 to 3.60) correlated significantly with Tau (r = 0.76, P <.0001), peak negative dP/dt (r = -0.46, P =.01), the LV late diastolic stiffness index (r = 0.57, P =.0013), LV pre-A wave pressure (r = 0.46, P =. 0096), LV end-diastolic pressure (r = 0.58, P =.0007), and the amount of LV pressure rise with atrial systole (r = 0.52, P =.0032) but not with the heart rate. Tau and LV stiffness were its sole determinants by stepwise multiple regression (R = 0.82). CONCLUSIONS: The ratio of mitral E and A wave transit times inside the LV (T(e)/T(a) ratio) is closely related to LV relaxation, its late diastolic stiffness, and filling pressures and gives valuable insights into LV diastolic performance.     

Renal dysfunction is a confounder for plasma natriuretic peptides in detecting heart dysfunction in uremic and idiopathic dilated cardiomyopathies

BACKGROUND: The diagnostic value of natriuretic peptides in uremic cardiomyopathy has not been defined, nor has the effect of a hemodialysis (HD) session on peptides. METHODS: We performed an observational study of 100 white adult outpatients in New York Heart Association class I-II, with neither diabetes nor ischemic heart disease, 50 of whom had idiopathic dilated cardiomyopathy (DCM) and 50 of whom had uremic cardiomyopathy and were undergoing HD. We measured plasma N-terminal proB-type natriuretic peptide (NT-proBNP), BNP, and atrial natriuretic peptide (ANP) both before and after a dialysis session. Doppler echocardiograms were evaluated. We performed multiple regression analysis on the logarithm of peptide concentrations using clinical, laboratory, and echocardio-Doppler data as explanatory variables. RESULTS: Mean peptide concentrations were higher in the HD group, with an HD:DCM ratio of 25 for NT-proBNP and 5 for BNP and ANP. Peptides were correlated with each other (r > 0.85). After HD, NT-proBNP significantly increased by 14%, BNP decreased by 17%, and ANP decreased by 56%. Predialysis concentrations correlated with postdialysis values (r > 0.85). A multiple regression equation significantly fitted the observed peptide concentrations, both pre- and postdialysis, using the same set of 4 variables: disease group (DCM or HD), diastolic pattern, left atrial volume, and body mass index. CONCLUSIONS: Renal dysfunction was a confounder for natriuretic peptides, which were present in higher concentrations in the uremic patients with milder cardiac dysfunction than in those with idiopathic DCM without renal dysfunction. Left diastolic function pattern and atrial volume were cardiac determinants of peptide concentrations in DCM and HD.     

Left ventricular diastolic dysfunction in end-stage dilated cardiomyopathy: simultaneous Doppler echocardiography and hemodynamic evaluation

Left ventricular diastolic dysfunction is an integral component of end-stage dilated cardiomyopathy. To better characterize this disorder we studied 15 patients undergoing catheterization during cardiac transplant screening evaluation. Pulsed-wave Doppler echocardiographic recordings of mitral inflow were obtained with simultaneous high-fidelity left ventricular and phase-corrected pulmonary capillary wedge pressures. Doppler-derived isovolumic relaxation times were within normal limits, despite a prolonged coefficient of relaxation (tau), and correlated with pulmonary capillary wedge--left ventricular crossover pressure. Peak velocity of early diastolic filling was similar to that reported in normal subjects and did not correlate with crossover pressure or tau. Early diastolic acceleration and deceleration times were shortened compared with reported normal values. Acceleration time correlated with mean negative dP/dt from mitral valve opening to left ventricular minimum pressure and with crossover pressure, and deceleration time correlated with mean dP/dt from left ventricular minimum pressure to the peak of the rapid filling wave. Late diastolic filling at atrial contraction was absent in 12 patients, all of whom had a significant early diastolic rapid filling wave and an elevated end-diastolic pressure. Despite an increase in pulmonary capillary wedge pressure during atrial contraction, the failing ventricles were unable to generate detectable forward transmitral flow. Poor cardiac pump function was shown by low left ventricular stroke volume, which correlated with the diastolic flow velocity integral. Thus, in end-stage cardiomyopathy, the transmitral flow velocity pattern is characterized by normal peak early filling velocity, low normal isovolumic relaxation time, shortened acceleration and deceleration times of early diastolic flow, decreased early flow velocity integral, and absent or decreased filling during atrial contraction. This pattern reflects interaction between elevated transmitral driving pressure and the compromised relaxation and compliance of a left ventricle functioning on an elevated pressure-volume curve.     

Left and right ventricular diastolic functions in patients with rheumatoid arthritis without clinically evident cardiovascular disease

The aim of this study was to assess the prevalence of diastolic dysfunction of the left ventricle (LV) and of the right ventricle in patients with rheumatoid arthritis (RA) without clinically evident cardiovascular manifestations and to estimate whether there is a correlation between the duration of RA and the degree of LV diastolic dysfunction. The study included 81 patients (61 females and 20 males) with RA without clinically evident heart disease (group 1) and 40 healthy subjects (29 females and 11 males) who served as a control group (group 2). Both groups were matched for age and sex. Echocardiographic and Doppler studies were conducted in all patients with RA and control subjects. There were significant differences between patients with RA vs. control group with regard to early diastolic flow velocity (E), atrial flow velocity (A) and the E/A ratio (0.68 +/- 0.19 m/s vs. 0.84 +/- 0.14 m/s, p < 0.001; 0.73 +/- 0.15 m/s vs. 0.66 +/- 0.13 cm/s, p = 0.01; and 0.97 +/- 0.3 vs. 1.32 +/- 0.37, p < 0.001, respectively). There was significant difference between groups regarding the right ventricular early diastolic (Er)/atrial (Ar) flow velocities (Er/Ar ratio) (1.07 +/- 0.3 vs. 1.26 +/- 0.3, p = 0.002). There was a weak correlation between transmitral E/A ratio and the duration of RA (r = - 0.22, p = 0.001). Myocardial performance index (MPI) appeared to differ little in patients with RA as compared with control group (0.51 +/- 0.1 vs. 0.52 +/- 0.2, p = NS). In patients with RA without clinically evident cardiovascular disease, the left ventricular diastolic function and the right ventricular diastolic function are reduced. Left ventricular wall thickness, dimensions, systolic function and MPI were found to be normal. LV diastolic function had a weak correlation with the duration of RA.     

Diagnosis of left-ventricular diastolic dysfunction in patients with predialysis chronic renal failure

AIM: To specify effectiveness of different methods for assessment of diastolic function in patients with pre-dialysis chronic renal failure (CRF). MATERIAL AND METHODS: Forty non-diabetic pre-dialysis CRF patients (20 males and 20 females, mean age 51 +/- 11 years) were studied. Serum creatinine was 209.3 +/- 117.4 mcmol/l. 19 patients had chronic heart failure (CHF) of NYHA class I-III. M-mode echocardiography and Doppler echocardiography were performed. Transmitral and pulmonary venous flows were assessed by Doppler echocardiography and the flow propagation velocity (Vp) was estimated by color M-mode Doppler echocardiography. The ratio of peak E-wave velocity of transmitral flow to Vp (E/Vp) was calculated. All the patients had preserved systolic function (ejection fraction > 45%). RESULTS: Interpretation of transmitral flow was difficult in 16 (40.0%) patients. During Valsalva's manoeuvre the E-wave peak velocities, the A-wave velocities and the ratio E/A were decreasing. However, we did not reveal any correlation between E/A and NYHA class of heart failure (r = 0.18; p = 0.32). Interpretation of pulmonary venous flow was possible only in 24 (60.0%) patients. Vp estimation by color M-mode Doppler echocardiography improved evaluation of diastolic function in 15 of 16 patients with problems of transmitral flow assessment. A negative correlation was revealed between NYHA class and Vp (r = -0.39; p = 0.013) and a positive correlation was between NYHA class and E/Vp (r = 0.45; p = 0.004). CONCLUSION: Vp assessed by color M-mode Doppler echocardiography improves the diagnosis of diastolic dysfunction in patients with chronic renal insufficiency. This method has an advantage over pulmonary venous flow investigation. The Valsalva's manoeuvre is low-effective for differential diagnosis of transmitral flow types.     

Dual chamber pacing in hypertrophic cardiomyopathy: long-term effects on diastolic function

To assess the effects of chronic dual chamber pacing (DDD) on LV diastolic function in obstructive hypertrophic cardiomyopathy (HCM), 21 patients with obstructive HCM paced for refractory symptoms were studied at baseline and at 3 and 12 months. HCM patients were matched to 21 patients with obstructive HCM on conventional treatment. Left atrial fractional shortening was calculated by M-mode echocardiography; this index reflects LV end-diastolic pressure. LV outflow tract gradient decreased 65 +/- 21% with DDD pacing and the NYHA class improved (P = 0.033). Left atrial fractional shortening worsened with DDD pacing (P < 0.001). Patients with abnormal baseline left atrial fractional shortening (< 16%) were older, had a higher NYHA class, and had more severe mitral regurgitation. In this subgroup, left atrialfractional shortening did not worsen with DDD pacing and the NYHA class improved more than in patients with normal left atrialfractional shortening (P = 0.033). In conclusion, chronic DDD pacing reduces obstruction but impairs diastolic function in HCM. In patients with normal diastolic function, the untoward effects of pacing on diastolic function are more evident than in patients with abnormal diastolic function at baseline. This suggests that DDD pacing might be beneficial in a subgroup of patients with obstructive HCM and abnormal diastolic function.     

Effect of cardiac resynchronization therapy on left ventricular diastolic filling pattern in responder and nonresponder patients

BACKGROUND: The aim of this study was to investigate the short- and long-term effects of cardiac resynchronization therapy (CRT) on left ventricular (LV) diastolic filling pattern and the relation between the diastolic filling pattern and the response to CRT. METHODS: Twenty-three patients with systolic heart failure and complete left bundle-branch block underwent implantation of biventricular pacemaker devices. In order to follow the changes in diastolic function, mitral inflow, pulmonary venous flow, and LV flow propagation (Vp) velocities were measured with pulsed-wave and color M-mode Doppler echocardiography 1 week before and 1 and 6 months after pacemaker implantation. At the 6-month follow-up, patients were divided into two groups according to their response to CRT defined as a relative increase in LV ejection fraction (LVEF) > or =25% versus baseline. RESULTS: After biventricular pacemaker implantation, significant clinical improvement was observed in all patients. Compared to baseline, the ratio of early-to-late peak velocities (E/A) decreased significantly at the 6th month (E/A ratio: from 1.5 +/- 0.9 to 0.8 +/- 0.5 at the 6th month (P = 0.02)). Pulmonary systolic flow to diastolic flow ratio (PVs/PVd) increased with CRT after 6 months (PVs/PVd ratio: from 0.9 +/- 0.4 to 1.3 +/- 0.7 at the 6th month (P = 0.02)). E/Vp ratio decreased significantly at the 1st and 6th month (E/Vp ratio: from 2.7 +/- 0.8 to 2 +/- 0.8 at the 1st (P < 0.002) and to 1.9 +/- 0.7 at the 6th month (P < 0.02)). In responders (n: 17, 74%), E wave and PVra velocity decreased, E-wave deceleration time increased, and E/Vp ratio improved significantly, whereas in nonresponders, changes in LV diastolic parameters remained insignificant. However, diastolic filling pattern improved significantly at the 1st and 6th month of CRT in both responders and nonresponders. CONCLUSION: CRT enhances diastolic filling patterns in both responder and nonresponder patients. This may be related to improvement in symptoms even in nonresponders who have a relative increase in LVEF <25%.     

Intramyocardial analysis of regional systolic and diastolic function in ischemic heart disease with Doppler tissue imaging: role of the different myocardial layers.

BACKGROUND: Preliminary experimental data have shown a nonuniform distribution of myocardial velocities (MVs) across the myocardial wall in normal conditions. However, after ischemic damage to the myocardium, a different pattern of reduction in the myocardial layers has been reported. The aim of this study is to analyze the spatial distribution of MVs and the resultant myocardial velocity gradients (MVGs) during the systolic and diastolic time periods. Doppler tissue imaging (DTI) in color M-mode was used to evaluate 3 different myocardial layers (endocardium, mesocardium, and epicardium) and their changes as a result of ischemia. METHODS: Thirty-two consecutive patients were studied with DTI color M-mode: 18 patients with a history of previous or ongoing myocardial infarction and 14 healthy subjects. Postprocessing of images was accomplished with proprietary software. MV and MVG values of all layers along both systolic and diastolic time were calculated. For temporal analysis, systole was subdivided in 3 equal periods. Early- and late-diastolic times were also identified. RESULTS: In ischemic patients, the mean MV and maximum MV throughout systole decreased significantly in the endocardium and mesocardium, whereas only slightly in the epicardium. The mean MVG was less in ischemic patients (0.66 +/- 0.11 vs 0.23 +/- 0.15, P <.03). Temporal analysis showed a decrease in the maximal MV and MVG in all layers over the 3 systolic periods. This decrease was the more consistent in mesocardium. In diastole, there was a decrease in maximal MV in all layers, being more pronounced in endocardium and mesocardium. Diastolic mean MVG was shown to be different between control and ischemic groups (-0.2 +/- 0.05 vs -0.10 +/- 0.04, P <.06). A significant decrease of the maximal MV in endocardium and mesocardium was reported in the temporal analysis during early diastole. No change was reported in the epicardium. The MVG value also showed a significant decrease (-2.69 +/- 0.29 vs -1.59 +/- 0.89, P <.02). In ischemic patients in late diastole, the maximum MV was increased in all layers of the myocardium, and this increase was observed mainly in the endocardium. An increase in the MVG (-0.78 +/- 0.18 vs -1.47 +/- 0.85, P = NS) was also reported during late diastole. CONCLUSION: There is a nonuniform distribution of velocities in the different myocardial layers under normal conditions. This distribution of velocities undergoes a significant change in patients with ischemic myocardial damage. Intramyocardial wall motion analysis could have clinical applications in both the early detection of ischemia and myocardial viability.     

Determinants of coronary flow abnormalities in obstructive type hypertrophic cardiomyopathy: noninvasive assessment by transthoracic Doppler echocardiography.

We aimed to visualize the coronary flow velocities (CFV) of patients with hypertrophic obstructive cardiomyopathy by using transthoracic Doppler echocardiography, and to determine the relationship between abnormal CFV patterns and conventional echocardiography indices. Guided by 2-dimensional echocardiography and Doppler color flow mapping, CFV in the distal left anterior descending coronary artery were measured in 21 patients with hypertrophic obstructive cardiomyopathy using a 3.5-MHz transducer. The results were compared with those of 18 control subjects. Abnormal systolic flow patterns were observed in 15 (71%) patients (11 systolic-reversal flow and 4 no systolic flow). For patients and control subjects, peak diastolic velocity and velocity-time integral obtained from distal left anterior descending coronary artery were higher (63 +/- 21 cm/s and 18.5 +/- 4 cm vs 41 +/- 11 cm/s and 14.2 +/- 5 cm, respectively; P <.01 for both) whereas peak systolic velocity and velocity-time integral were significantly lower (-17 +/- 10 cm/s and 4.5 +/- 6 cm vs 24 +/- 9 cm/s and 9.5 +/- 4 cm, respectively; P <.001 for both). Significant positive and negative correlations between diastolic CFV and septal thickness index (r = 0.79, P <.0001), and between systolic CFV and septal thickness index (r = -0.65, P <.005), have been observed. CFV abnormalities that could easily be recorded by a standard Doppler echocardiographic study seem to be related to septal thickness rather than the degree of obstruction in hypertrophic obstructive cardiomyopathy.