Serial assessment of mitral regurgitation by pulsed Doppler echocardiography in patients undergoing balloon aortic valvuloplasty

Mitral regurgitation was serially assessed by pulsed Doppler echocardiography in 144 patients undergoing balloon aortic valvuloplasty for symptomatic aortic stenosis. Regurgitant scores of 0, 1, 2 and 3 were assigned to pulsed Doppler patterns corresponding to no, mild, moderate and severe mitral regurgitation, respectively. Before balloon aortic valvuloplasty, mitral regurgitant score correlated significantly (p less than 0.005) but weakly with aortic valve area (r = -0.24), left ventricular ejection fraction (r = -0.34) and left ventricular systolic pressure (r = 0.23). There was no significant correlation between mitral regurgitation and either mean catheterization or mean Doppler aortic valve gradient. Balloon aortic valvuloplasty produced significant decreases in both catheterization and Doppler mean transvalvular aortic valve gradients (56 +/- 19 to 31 +/- 12 and 60 +/- 19 to 48 +/- 16 mm Hg, respectively; both p less than 0.0001) and a significant increase (p less than 0.0001) in aortic valve area assessed by catheterization (0.6 +/- 0.2 to 0.9 +/- 0.3 cm2). Left ventricular ejection fraction did not change, but cardiac output increased (p less than 0.001) and pulmonary capillary wedge pressure decreased (p less than 0.0001). Pulsed Doppler findings of mitral regurgitation were present in 102 of the 144 patients. Eighty-eight patients had a score compatible with mild or more severe degrees of mitral regurgitation, and 49 had a score indicative of moderate or severe valvular insufficiency. In the entire group of 144 patients, mitral regurgitant score decreased significantly from 1.1 +/- 1.0 to 1.0 +/- 1.0 (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Association between antiphospholipid antibodies and cardiac abnormalities in patients with systemic lupus erythematosus

PURPOSE: Although the antiphospholipid antibodies are well recognized to be associated with thrombosis, recurrent abortion, and thrombocytopenia in patients with systemic lupus erythematosus (SLE), their relationship with cardiac disease is less clear. The purpose of this study was to evaluate the association between anti-phospholipid antibodies and cardiac abnormalities in patients with SLE. PATIENTS AND METHODS: A total of 75 consecutive SLE patients and 60 healthy sex- and age-matched control subjects were evaluated in a case-control study. All participants underwent M-mode, two-dimensional, and Doppler echocardiography. Antiphospholipid antibodies levels were assayed in each patient. The prevalence of antiphospholipid antibodies in patients with and without echocardiographic abnormalities was compared. RESULTS: Compared with the control group, SLE patients had significantly more pericardial abnormalities, left ventricular hypertrophy, left atrial enlargement, left ventricular dysfunction and verrucous valvular thickening, global valvular thickening with dysfunction, and mitral and aortic regurgitation. Among these abnormalities, antiphospholipid antibodies were significantly associated with isolated left ventricular (global or segmental) dysfunction (four of five positive; p less than 0.05), verrucous valvular (mitral or aortic) thickening (seven of nine positive; p less than 0.005), global valvular (mitral or aortic) thickening and dysfunction (five of six positive; p less than 0.02), as well as mitral regurgitation (16 of 19 positive; p less than 0.001) and aortic regurgitation (five of six positive; p less than 0.02). CONCLUSION: Valvular lesions and myocardial dysfunction are associated with elevated antiphospholipid antibodies. This study has important implications for the pathogenic role of anti-phospholipid antibodies in relation to these cardiac abnormalities.     

Impairment of left ventricular diastolic function in systemic lupus erythematosus.

Left ventricular (LV) diastolic performance was evaluated with pulsed-wave Doppler echocardiography in a cross-sectional population of patients with systemic lupus erythematosus (SLE) in search of subclinical myocardial involvement. Such involvement is reported to occur infrequently, despite pathohistologic evidence of myocarditis in up to 70% of patients with SLE. Thirty-five consecutive patients with SLE were evaluated, 14 with active and 21 with inactive disease, and were compared with 30 age-matched healthy control subjects. Twenty-six patients were restudied at 7 months. All had normal LV systolic function, normal pericardial and valvular structures, and no significant valvular regurgitation on Doppler echocardiography. In SLE patients with active disease, indexes of LV diastolic function differed significantly from the inactive group and from control subjects, with marked prolongation of isovolumic relaxation time (104 +/- 18 vs 74 +/- 13 ms, p = 0.0001), as well as reduced peak early diastolic filling velocity (E) (0.69 +/- 0.19 vs 0.83 +/- 0.17 ms, p = 0.01), reduced ratio of early to late diastolic flow velocity (E/A) (1.15 +/- 0.53 vs 1.47 +/- 0.35, p = 0.02), and prolonged mitral pressure halftime (74 +/- 14 vs 65 +/- 8 ms p = 0.01). Similar significant differences were found between the active and inactive SLE patient groups. SLE patients with inactive disease differed from control subjects in only mild prolongation of mitral pressure halftime. Abnormal prolongation of isovolumic relaxation (greater than 100 ms) was found to be the most useful marker of diastolic impairment, being present in 64% of SLE patients with active disease and in 14% of patients with inactive disease.(ABSTRACT TRUNCATED AT 250 WORDS)     

Improvement in forward cardiac output without a change in ejection fraction during nitroglycerin therapy in patients with functional mitral regurgitation

Left ventricular volumes and forward aortic flow were measured using combined two-dimensional echocardiography and doppler cardiography in seven patients with decompensated congestive heart failure and functional mitral regurgitation prior to and during intravenous administration of nitroglycerin. Total stroke volume was calculated from the difference between end-diastolic and end-systolic volumes, and regurgitant mitral volume from the difference between total stroke volume and forward aortic flow. Regurgitant mitral volume fell from 19 +/- 9 to 3 +/- 3 mL/beat (p less than 0.001), while forward stroke volume increased from 35 +/- 8 to 45 +/- 9 mL/beat (p less than 0.001). The changes were well correlated (r = 0.8, p less than 0.001). Total stroke volume decreased from 54 +/- 12 to 48 +/- 6 mL/beat (p less than 0.05), and ventricular end-diastolic volume from 173 +/- 66 to 158 +/- 66 mL (p less than 0.05). Left ventricular ejection fraction did not change significantly: 33 +/- 9% vs 32 +/- 9% (NS). Thus, in patients with severe congestive heart failure and functional mitral regurgitation, intravenous nitroglycerin redistributes blood flow within the heart by decreasing mitral regurgitation and increasing forward aortic flow, without affecting left ventricular ejection fraction.     

Dissociation of end systole from end ejection in patients with long-term mitral regurgitation

To determine whether left ventricular (LV) end systole and end ejection uncouple in patients with long-term mitral regurgitation, 59 patients (22 control patients with atypical chest pain, 21 patients with aortic regurgitation, and 16 patients with mitral regurgitation) were studied with micromanometer LV catheters and radionuclide angiograms. End systole was defined as the time of occurrence (Tmax) of the maximum time-varying elastance (Emax), and end ejection was defined as the time of occurrence of minimum ventricular volume (minV) and zero systolic flow as approximated by the aortic dicrotic notch (Aodi). The temporal relation between end systole and end ejection in the control patients was Tmax (331 +/- 42 [SD] msec), minV (336 +/- 36 msec), and then, zero systolic flow (355 +/- 23 msec). This temporal relation was maintained in the patients with aortic regurgitation. In contrast, in the patients with mitral regurgitation, the temporal relation was Tmax (266 +/- 49 msec), zero systolic flow (310 +/- 37 msec, p less than 0.01 vs. Tmax), and then, minV (355 +/- 37 msec, p less than 0.001 vs. Tmax and p less than 0.01 vs. Aodi). Additionally, the average Tmax occurred earlier in the patients with mitral regurgitation than in the control patients and patients with aortic regurgitation (p less than 0.01, for both), whereas the average time to minimum ventricular volume was similar in all three patient groups. Moreover, the average time to zero systolic flow also occurred earlier in the patients with mitral regurgitation than in the control patients (p less than 0.01) and patients with aortic regurgitation (p less than 0.05). Because of the dissociation of end systole from minimum ventricular volume in the patients with mitral regurgitation, the end-ejection pressure-volume relations calculated at minimum ventricular volume did not correlate (r = -0.09), whereas those calculated at zero systolic flow did correlate (r = 0.88) with the Emax slope values. We conclude that end ejection, defined as minimum ventricular volume, dissociates from end systole in patients with mitral regurgitation because of the shortened time to LV end systole in association with preservation of the time to LV end ejection due to the low impedance to ejection presented by the left atrium. Therefore, pressure-volume relations calculated at minimum ventricular volume might not be useful for assessing LV chamber performance in some patients with mitral regurgitation.     

Influence of left ventricular mass on coronary artery cross-sectional area

Observations from cardiac catheterization suggest that coronary artery cross-sectional area (CSA) is increased in patients with left ventricular (LV) hypertrophy and is proportional to LV mass. This hypothesis was tested using computer-based quantitative analysis of LV mass and CSA from angiographic images of the left ventricle and proximal coronary arteries from 19 men and 21 women, aged 23 to 78 years (mean 56). Twenty-seven patients had valvular heart disease, 16 of whom had multivalvular involvement; diagnoses included aortic stenosis in 19, aortic regurgitation in 13 and mitral regurgitation in 12. Thirteen patients had normal valvular and ventricular function. All patients had normal coronary arteries. Significant differences between normal patients and those with valvular disease were noted in LV mass (88 +/- 7 vs 165 +/- 12 g/m2, p less than 0.001) and coronary CSA (26 +/- 2 vs 46 +/- 3 mm2, p less than 0.001). Furthermore, a linear relation between LV mass and coronary CSA was noted (r = 0.788, p less than 0.001). Thus, proximal coronary artery CSA is significantly larger in valvular heart disease patients with LV hypertrophy than in those with normal ventricles, and proximal coronary artery area increases in proportion to LV mass in hypertrophied ventricles.     

Pulsed and continuous wave Doppler echocardiographic assessment of valvular regurgitation in normal subjects

To assess the prevalence and flow characteristics of valvular regurgitation detected by Doppler echocardiography in normal subjects, pulsed and continuous wave Doppler studies were performed in 100 adult volunteers without evidence of heart disease. Evidence of valvular regurgitation was present in 73% of subjects. There were 46 subjects with regurgitation of one valve, 24 with regurgitation of two valves and 3 with regurgitation of three valves. Right-sided regurgitation was significantly more common than was left-sided regurgitation (81 versus 22 valves, p less than 0.01). Regurgitant flow was never detected farther than 1 cm from the valve by pulsed Doppler study. Tricuspid regurgitation was detected in 50 subjects and was characterized by a holosystolic velocity signal; a complete spectral envelope was recorded in 32 subjects. The peak velocity of the regurgitant jet for this group was 1.7 to 2.3 m/s (mean 2.0 +/- 0.2). Thirty-one subjects were found to have pulmonary regurgitation with a peak velocity of 1.2 to 1.9 m/s (mean 1.5 +/- 0.2); no subject demonstrated regurgitant flow in early diastole. There were 21 subjects with mitral regurgitation; continuous wave Doppler signals were always of low intensity with a poorly defined spectral envelope and an absence of high velocities. Peak velocities ranged from 1.1 to 4.4 m/s (mean 2.3 +/- 0.9) and in 19 subjects were less than 3.5 m/s. The mean age of subjects with mitral regurgitation was significantly higher than that of subjects without mitral regurgitation (p = 0.01). Aortic regurgitation was detected in only one subject. This study provides further evidence that valvular regurgitation is frequently detected by Doppler echocardiography in normal subjects.(ABSTRACT TRUNCATED AT 250 WORDS)     

Color Doppler evaluation of valvular regurgitation in normal subjects

To determine prospectively the prevalence of mitral, aortic, tricuspid, and pulmonary regurgitation in normal persons, 211 consecutive, apparently healthy volunteers were examined with a color Doppler flow imaging system. The subjects were divided into five age groups (group 1, 6-9 years old; group 2, 10-19 years old, group 3, 20-29 years old, group 4, 30-39 years old, and group 5, 40-49 years old). The prevalence rate of mitral regurgitation in the normal subjects was 38-45% in each group. The mitral regurgitant jets came from the posteromedial commissure in all but two subjects. No aortic regurgitant flow signals were detected in the normal subjects. Tricuspid regurgitation was detected in 15-77% in each group, and pulmonary regurgitation was detected in 28-88%. Regarding the tricuspid and pulmonic valves, the prevalence rate of regurgitation is age dependent (p less than 0.01) and tends toward the lower rate in groups over the age of 30 years. The tricuspid and pulmonary regurgitant jets came from the center of the coaptation of each valve. The area of the regurgitant jet signals in normal persons was significantly smaller (p less than 0.001) than that obtained from patients with organic valve disease. Our study shows that in a large proportion of normal persons under the age of 50 years color Doppler echocardiography permits recording of regurgitant signals behind all valves except the aortic. In conclusion, one should be aware of the existence and characteristics of regurgitation in normal persons when evaluating valvular regurgitation by Doppler techniques.     

Dynamics of mitral regurgitation during nitroglycerin therapy: a Doppler echocardiographic study

Seven patients with decompensated chronic heart failure and functional mitral regurgitation were studied before and during administration of nitroglycerin at a mean dose of 42 micrograms/min (range 20 to 90 micrograms/min). Forward aortic flow obtained by pulsed Doppler increased significantly from 35 +/- 8 to 45 +/- 9 ml/beat (p less than 0.001) and correlated well with the cardiac output measured by thermodilution technique (r = 0.8). Whereas regurgitant mitral volume calculated from the difference between echocardiographic total stroke volume and forward aortic flow decreased significantly from 19 +/- 9 to 3 +/- 3 ml/beat (p less than 0.001), peak velocity of mitral regurgitant flow increased from 4.1 +/- 0.9 to 4.4 +/- 1.0 m/sec (p less than 0.05). The decrease in effective mitral regurgitation area derived from a modified Gorlin formula average 80%. Accordingly, in patients with decompensated chronic heart failure and functional mitral regurgitation, nitroglycerin decreases mitral regurgitant area substantially, and thus almost abolishes mitral regurgitation despite an increase in systolic pressure gradient between left ventricle and atrium. Moreover, the increase in forward flow can be entirely accounted for by the reduction in mitral regurgitant flow.     

Aortic regurgitation: evaluation by pulsed Doppler echocardiography

Ninety-one consecutive patients with aortic regurgitation, either isolated (23 subjects) or associated with other valvular diseases (68 subjects), were studied with pulsed Doppler echocardiography and subsequent aortography, and the results were compared in order to assess the value of the noninvasive technique for a semiquantitative evaluation of the degree of the aortic regurgitation. Both the noninvasive and invasive estimations were graded on a four-point scale. In the long-axis parasternal view, the outflow tract of the left ventricle was divided in four areas going from the aortic valve to the apex. Echo-Doppler grading (from + 1 to +4) was obtained by assessing the area where the abnormal diastolic flow could still be recorded. In the group as a whole, concordant degrees of the aortic insufficiency were obtained in 73 of 91 patients (r = .93; p less than .001); the degree of the aortic regurgitation was overestimated in 8 cases (9%) and underestimated in 10 cases (11%). Most of the discrepancies between the Doppler and the aortographic evaluation were found in patients with intermediate degree (+2, +3) of aortic regurgitation; the degree of discordance was never more than +1 or -1. Correlation between Doppler and aortography was higher in the subjects with pure aortic regurgitation (r = .94, p less than .001) and lower in the subgroup of the subjects with associated mitral stenosis (r = .87, p less than .001). Two-dimensional pulsed Doppler echocardiography is a simple and little time consuming technique that in selected groups of patients can be relied upon for the semiquantitated evaluation of the degree of aortic regurgitation.     

Noninvasive quantification of mitral regurgitation in dilated cardiomyopathy: correlation of two Doppler echocardiographic methods

The presence and severity of functional mitral regurgitation were quantified by Doppler echocardiography in 17 patients with dilated cardiomyopathy and no evidence of primary valvular disease. Mitral regurgitant fraction was greater than 20% in 11 of the 17 patients, and exceeded 40% in four patients. Total stroke volume, calculated from the difference between end-diastolic and end-systolic volumes obtained by two-dimensional echocardiography, correlated well with mitral valve inflow determined by Doppler echocardiography (r = 0.90, p less than 0.001). Similarly, mitral regurgitant volume, calculated as the difference between echocardiographic total stroke volume and forward aortic volume obtained by Doppler echocardiography, correlated well with regurgitant volume calculated as the difference between mitral valve inflow and forward aortic flow, both determined by Doppler echocardiography (r = 0.90, p less than 0.001). Accordingly, functional mitral regurgitation can be conveniently demonstrated in patients with dilated cardiomyopathy by two different Doppler echocardiography methods, whose results are closely correlated. Mitral regurgitant fraction is greater than 20% in two thirds of the patients with a dilated cardiomyopathy.     

Left ventricular systolic and diastolic flow abnormalities determined by Doppler echocardiography in obstructive hypertrophic cardiomyopathy

To analyze the relation of systolic anterior motion (SAM) of the mitral valve, peak left ventricular (LV) outflow tract velocity, aortic flow and mitral flow, 17 patients with obstructive hypertrophic cardiomyopathy (HC) (8 men, 9 women), aged 19 to 88 years (mean 45), were studied using M-mode and 2-dimensional echocardiography and pulsed and continuous-wave Doppler echocardiography and results were compared with those from 18 age-matched normal subjects. SAM was present in all patients with HC and absent in normal subjects. Time to peak outflow velocity as a percentage of LV ejection time was 63% in patients with HC and 29% in normal subjects (p less than 0.001). In 13 patients, time from the R-wave peak to the closest approximation of the mitral valve to the ventricular septum or initial contact during SAM was determined and was 242 +/- 66 ms and time from the R-wave peak to the peak LV outflow tract velocity was 242 +/- 73 ms (r = 0.90). In 11 patients time from the R-wave peak to cessation of flow in the ascending aorta was measured and was 286 +/- 80 ms; time from the R-wave peak to the peak LV outflow tract velocity was 246 +/- 75 ms. The ratio of early to late diastolic filling velocities of the left ventricle was 1.47 +/- 0.40 in the normal subjects and 1.26 +/- 0.84 in patients with HC (difference not significant). The early to late ratio of the 12 patients without mitral regurgitation was 0.99 +/- 0.52 (p less than 0.01 vs normal subjects).(ABSTRACT TRUNCATED AT 250 WORDS)     

Noninvasive evaluation of the magnitude of aortic and mitral regurgitation by means of Doppler two-dimensional echocardiography

Using transmitral flow velocity and left ventricular ejection flow velocity, we measured left ventricular inflow volume (LVIV) and left ventricular outflow volume (LVOV) by pulsed Doppler echocardiography in 73 patients who had mitral valve regurgitation (MR), aortic valve regurgitation (AR), or no valvular regurgitation. Doppler-determined regurgitant volume (DOPRV), Doppler-determined regurgitant fraction (DOPRF), total stoke volume, and forward stroke volume were calculated to compare the severity assessed by angiographic scoring and the regurgitant fraction determined by radionuclide angiography (RIRF). In 17 patients with MR, LVIV (84.4 +/- 20.4 ml) was significantly greater (p less than 0.01) than LVOV (52.5 +/- 15.7 ml). LVOV, which is equivalent to forward stroke volume, was lower in patients with MR (52.2 +/- 15.7 ml) than in normal subjects (67.0 +/- 15.7 ml). In 15 patients with AR, LVOV (121.7 +/- 61.1 ml) was significantly greater (p less than 0.01) than LVIV (75.1 +/- 28.1 ml) and LVOV, which is equivalent to total stroke volume, was greater in patients with AR (121.7 +/- 61.1 ml) than in normal subjects (64.0 +/- 14.4 ml). DOPRF correlated with RIRF (r = 0.79, p less than 0.01, n = 11). DOPRV (mild: 10.5 +/- 8.5 ml; moderate: 28.8 +/- 13.6 ml; severe: 74.5 +/- 36.7 ml) and DOPRF (mild: 13.7% +/- 11.5%; moderate: 33.1% +/- 14.2%; severe: 52.6% +/- 15.3%) increased markedly with the severity of regurgitation as assessed by cineangiography. In AR, total stroke volume influenced both forward stroke volume and regurgitant volume, and in MR, regurgitant volume influenced both total stroke volume and forward stroke volume. Total stroke volume in AR and regurgitant volume in MR may play a key role in valvular regurgitation.     

Impact of atrial fibrillation on tricuspid and mitral annular dilatation and valvular regurgitation.

To investigate the effects of atrial fibrillation (AF) on the mitral and tricuspid valves, the corresponding annular dilatation and valvular regurgitation were compared with 2-dimensional and Doppler echocardiography in 31 consecutive patients with lone AF and 28 normal controls. Mid-systolic mitral and tricuspid annular areas were measured from 2 diameters in 2 orthogonal apical echocardiograms. Percent (%) mitral regurgitant (MR) or tricuspid regurgitant (TR) jet area to the left or right atrial area was evaluated and % MR or TR jet area >20% was considered moderate or significant. Both the mitral and tricuspid annular areas in patients with lone AF were significantly larger compared with the controls (mitral: 9.5 +/- 1.2 vs 6.6 +/- 0.9 cm2, lone AF vs control, p < 0.01) (tricuspid: 12.0 +/- 2.0 vs 7.5 +/- 0.9 cm2, p < 0.01). The % increase in the annular area relative to the mean normal value was significantly greater in the tricuspid valve (44 +/- 18 vs 60 +/- 28%, p < 0.01). Moderate or severe MR was not observed and the incidence of moderate or severe valve regurgitation (% jet area >20%) was significantly higher in the tricuspid valve (0/31 vs 11/31, MR vs TR, p < 0.01) in patients with lone AF. The % TR jet area showed significant correlation with tricuspid annular area (r2 = 0.65, p < 0.001). Lone AF is associated with annular dilatation of both mitral and tricuspid valves, but the annular dilatation and valvular regurgitation are significantly greater in the tricuspid valve.     

Effect of isometric exercise on mitral and aortic regurgitation as assessed by color Doppler flow imaging

Isometric exercise produces well-defined hemodynamic changes in normal and diseased states. However, the effect of isometrics on the degree of valvular regurgitation recorded by color Doppler flow imaging (CDFI) has not been reported. CDFI was therefore used to evaluate changes in valvular regurgitation in 34 patients, mean age 53 +/- 16 years. Data were collected for 43 regurgitant lesions including 20 cases of aortic regurgitation and 23 cases of mitral regurgitation. Isometrics produced a significant increase in heart rate (71 to 83 beats/min) and blood pressure (132/64 to 153/70 mm Hg) in all patients (p less than 0.0001). Regurgitant jet area by CDFI increased significantly in both aortic regurgitation (4.5 to 6.2 cm2, p less than 0.0001) and mitral regurgitation (6.2 to 8.2 cm2, p less than 0.001). Patients taking concurrent vasodilator or angiotensin-converting enzyme inhibitor therapy had similar responses to those not receiving long-term therapy. Thus, CDFI detects an increase in aortic and mitral regurgitant jet area induced by isometric exertion. The change in CDFI jet area with handgrip demonstrates the influence of loading conditions on the size of a regurgitant jet area, and suggests that isometric exertion may increase the magnitude of mitral and aortic regurgitation.     

A Doppler echocardiographic study of normal and dysfunctioning Carpentier-Edwards bioprostheses

The aim of this study was to delineate the Doppler echocardiographic characteristics of normal and dysfunctioning Carpentier-Edwards bioprostheses. Echocardiographic and Doppler studies were performed on 61 mitral and 41 aortic valves; by means of on clinical evaluation, 15 mitral and 12 aortic valves were considered to be abnormally functioning. The maximum velocity (Vmax) of diastolic left ventricular inflow, pressure half-time and valve orifice area were assessed for prostheses in mitral position, while the maximum velocity (Vmax) of transaortic flow was calculated for prostheses in aortic position. Moreover, the quantitative assessment of mitral and/or aortic regurgitation was performed using the mapping technique with pulsed Doppler wave mode. Normally functioning mitral prostheses were characterized by Vmax less than 2.20 m/s and pressure half-time less than 164 ms; furthermore, mean values of Vmax and pressure half-time were significantly lower in normal than in dysfunctioning prostheses (1.70 +/- 0.33 vs 2.09 +/- 0.52 m/s; p less than 0.01 and 96.14 +/- 29.76 vs 147.87 +/- 57.41 ms; p less than 0.01 respectively). All dysfunctioning mitral valves were characterized by regurgitation graded as severe in 8 cases and moderate in 7 but only 40 and 20% of these presented respectively Vmax and pressure half-time values which were higher than those of normally functioning valves (2.20 m/s and 164 ms respectively); no pure stenosis was found. In the aortic position, normally functioning prostheses were characterized by Vmax less than 3.10 m/s. Furthermore, mean Vmax values were lower in normal than in dysfunctioning prostheses (2.55 +/- 0.53 vs 3.18 +/- 0.80; p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Doppler echocardiographic study of the frequency and severity of aortic regurgitation in hypertrophic cardiomyopathy

Aortic regurgitation (AR) has been reported sporadically in hypertrophic cardiomyopathy (HC) but neither its frequency nor severity has been determined. Thirty-one consecutive patients with HC were evaluated by Doppler echocardiography over a 2-year period. Twenty-nine had echocardiographically normal aortic cusps and participated in the study; 2 had calcified aortic valves and were excluded. AR of grade I to grade II severity was demonstrated in 9 of 29 (31%) patients. Patients were divided into 2 groups: group 1 (n = 9) with AR and group 2 (n = 20) without AR. Group 1 patients were significantly older than group 2 patients (73 +/- 7 vs 60 +/- 17 years, p less than 0.05) and had larger end-diastolic (4.5 +/- 0.5 vs 4.0 +/- 0.7 cm, p less than 0.01) and end-systolic (2.7 +/- 0.4 vs 2.3 +/- 0.4, p less than 0.02) left ventricular dimensions. Left ventricular wall thickness, degree of asymmetric septal hypertrophy and left ventricular fractional shortening were similar in the 2 groups. Mitral regurgitation was more common in group 1 (100% vs 35%, p less than 0.005), although there were no differences in left atrial size between the 2 groups. The HC patients were compared with a control group of 23 normal subjects of similar age. There was no mitral regurgitation or AR in the normal subjects. Thus, nearly one-third of patients with HC had mild AR by Doppler. The AR most probably results from high-velocity systolic blood flow causing microscopic damage to the valve cusps.     

Methodologic issues in clinical evaluation of stenosis severity in adults undergoing aortic or mitral balloon valvuloplasty. The NHLBI Balloon Valvuloplasty Registry.

Although both catheterization and Doppler measures of valvular stenosis severity have been validated, each has specific advantages and limitations, particularly in the setting of balloon valvuloplasty. Invasive valve area and mean pressure gradient recorded immediately before and after aortic (n = 589) or mitral (n = 608) catheter balloon valvuloplasty were compared with Doppler valve area and mean pressure gradient recorded less than 30 days before and 24 to 72 hours after the procedure. For aortic stenosis, Doppler valve area ranged from 0.1 to 1.4 cm2 before and 0.2 to 2.3 cm2 after catheter balloon valvuloplasty. Doppler and invasive aortic valve areas differed by less than or equal to 0.5 cm2 in 99% and by less than 0.2 cm2 in 92% of patients. Linear correlation was higher before versus after catheter balloon valvuloplasty, for both valve area (r = 0.49 vs r = 0.35, p = 0.01) and mean pressure gradient (r = 0.64 vs r = 0.50, p = 0.01). Group mean invasive valve area was slightly smaller before (0.50 vs 0.59 cm2, p less than 0.0001) but was not different after (0.80 vs 0.78 cm2, p = 0.16) catheter balloon valvuloplasty. Variables affecting the valve area differences were cardiac output, aortic regurgitation, heart rate and blood pressure. Mean pressure gradient differences were related to echo quality, blood pressure and mitral regurgitation. For mitral stenosis, 2-dimensional echocardiographic valve area ranged from 0.4 to 2.8 cm2 before and 0.7 to 3.8 cm2 after catheter balloon valvuloplasty. Two-dimensional echocardiography and invasive mitral valve areas differed by less than or equal to 0.5 cm2 in 96% and by less than 0.2 cm2 in 81% of cases. Linear correlation was not different before versus after catheter balloon valvuloplasty for two-dimensional echocardiographic valve area (r = 0.40 vs 0.36), pressure halftime valve area (r = 0.31 vs 0.32) or mean pressure gradient (r = 0.55 vs r = 0.46). Group mean 2-dimensional echocardiography and pressure halftime valve areas were larger than invasive valve areas before (1.09 vs 1.02 cm2, p = 0.001) and smaller after (1.71 vs 2.02 cm2, p less than 0.0001) catheter balloon valvuloplasty. Important variables affecting the differences were mitral regurgitation, interatrial shunt, cardiac output and heart rate. Nonsimultaneous studies, differing volume flow measurements, and the underlying accuracy of each technique largely account for discrepancies between these methods. The clinical use of each will depend on its ability to predict long-term patient outcome.     

Role of exercise Doppler echocardiography in isolated mitral stenosis

This study reports the role of Doppler ultrasound during exercise for assessment of patients with mitral stenosis. Doppler echocardiography was performed at rest and during symptom-limited supine bicycle exercise in ten patients with isolated mitral stenosis. The mean mitral valvular gradient was calculated using modified Bernoulli's equation, and the mitral valvular area was estimated from the equation, 220/pressure half-time. During exercise the heart rate increased from 74 +/- 14 beats per minute (mean +/- SD) at rest to 110 +/- 8 beats per minute (p less than 0.001) during exercise. The mean mitral gradient increased from 9 +/- 5 mm Hg at rest to 18 +/- 7 mm Hg (p less than 0.01) during exercise. The mitral pressure half-time decreased from 225 +/- 62 msec at rest to 190 +/- 42 msec during peak exercise (p less than 0.005). This corresponded to a reduction of 15 percent. The estimated mitral valvular area increased from 1.0 +/- 0.4 sq cm at rest to 1.2 +/- 0.3 sq cm at peak exercise (p less than 0.005). In conclusion, Doppler echocardiography can be used to evaluate patients with mitral stenosis, with the response of the mitral valvular gradient being the index of obstruction; however, caution should be used in applying the mitral pressure half-time for estimation of the mitral valvular area at high heart rates and flows.     

Determinants of anterior mitral leaflet fluttering in pure aortic regurgitation from pulsed Doppler study of the early diastolic interaction between the regurgitant jet and mitral inflow

Fluttering of the anterior mitral leaflet may be absent in patients with moderate to severe aortic regurgitation (AR), suggesting that the volumetric severity of AR alone does not determine the presence or absence of abnormal diastolic mitral valve motion. Fifteen patients with moderate to severe AR and normal mitral valves, 9 of whom demonstrated anterior mitral leaflet fluttering, were studied to elucidate the determinants of abnormal anterior mitral leaflet motion in these patients. Pulsed Doppler mapping of the flow-velocity disturbance of AR demonstrated its presence in the third of the left ventricular outflow tract adjacent to the anterior mitral leaflet in 8 of 9 patients with anterior mitral leaflet fluttering and none of the 6 patients without anterior mitral leaflet fluttering (p less than 0.02). The impact of this regurgitant jet on early diastolic transmitral inflow was examined with pulsed Doppler in these 2 groups of patients with AR and in age-matched control subjects. Deceleration of early diastolic transmitral filling was slower in patients with AR and anterior mitral leaflet fluttering than in age-matched control subjects (283 +/- 107 vs 457 +/- 176 cm/s2, p less than 0.02), whereas it was not significantly different from controls in AR patients without anterior mitral leaflet fluttering. This resulted in significant prolongation of the duration of early diastolic transmitral filling in patients with AR and anterior mitral leaflet fluttering (297 +/- 93 vs 203 +/- 44 ms for age-matched control subjects, p less than 0.02), which was not observed in patients with AR who did not have anterior mitral leaflet fluttering.(ABSTRACT TRUNCATED AT 250 WORDS)