T Wisenbaugh

Mitral regurgitation following mitral balloon valvotomy. Differing mechanisms for severe versus mild-to-moderate lesions.

BackgroundThis study was designed to evaluate the incidence and mechanisms of mitral regurgitation following mitral balloon valvotomy (MBV) in 40 consecutive patients with symptomatic tight pliable mitral stenosis. Methods and ResultsTransthoracic echocardiography with color flow mapping was performed before and 24 hours after the procedure. Patients who developed significant mitral regurgitation following MBV also underwent transesophageal echocardiography. The relation between increased mitral regurgitation and both valvular morphology and procedure-related factors was examined. Gorlin mitral valve area increased from 0.81 ± 0.3 to 1.95 ± 0.7 cm2 (p < 0.001). No patient had more than 2 + mitral regurgitation by angiography and color Doppler prior to MBV. There was a moderate correlation between Doppler and angiographic increase in mitral regurgitation (r = 0.73, p < 0.0001). By Doppler criteria 33 patients had no (n = 6) or mild (n = 27) increase in mitral regurgitation (group 1), and seven developed significant new mitral regurgitation (group 2). Baseline clinical, echocardiographic, and procedure-related data for the two groups were similar. Multiple regression analysis did not select any individual valve characteristic (valvular thickening, mobility, calcification, and subvalvular disease), total echocardiographic score, balloon diameter, or ratio of balloon to mitral annular diameter as predictors of mitral regurgitation. All seven patients in group 2 had evidence of major leaflet disruption with a torn anterior or posterior mitral leaflet in six and a ruptured papillary muscle in one. Two of these patients have required mitral valve replacement (6 and 9 months following the procedure), whereas the remainder are significantly symptomatic. By contrast, mitral regurgitation in group 1 either occurred at the site of commissural split (n = 20) or was associated with prolapse of the anterior mitral leaflet (n = 6). ConclusionsThus, severe new mitral regurgitation following MBV is due to noncommissural tearing of the mitral leaflet and confers an adverse long-term prognosis. A mild increase in mitral regurgitation following MBV is frequent and occurs at the site of commissural split or is associated with prolapse of the anterior leaflet. Furthermore, in this study, an increase in mitral regurgitation could not be predicted from any valvular or procedure-related factor.

Relationship of contractile state to ejection performance in patients with chronic aortic valve disease.

To assess the relative contributions of afterload mismatch and impaired contractility to pump dysfunction in patients with chronic aortic valve disease, simultaneous left ventricular cineangiography and micromanometry were performed in 56 patients: 21 with severe aortic stenosis, 16 with severe aortic regurgitation, and 19 normal control subjects. Left ventricular mass was increased in patients with aortic stenosis and aortic regurgitation (172 +/- 52 and 224 +/- 63 g/m2, respectively, vs 89 +/- 16 for control subjects; p less than .05) as were end-diastolic volume (101 +/- 39 and 167 +/- 44 vs 77 +/- 16 ml/m2; p less than .05) and end-systolic volume (50 +/- 40 and 84 +/- 43 vs 24 +/- 7 ml/m2; p less than .05). Although ejection fraction was depressed in both abnormal groups (0.56 +/- 0.18 for patients with aortic stenosis and 0.53 +/- 0.13 for those with aortic regurgitation vs 0.69 +/- 0.05 for control subjects; p less than .05), the decrease in ejection fraction was disproportionate to the mild degree of afterload mismatch (end ejection stress 129 +/- 17 in patients with aortic stenosis and 154 +/- 58 in those with aortic regurgitation vs 117 +/- 46 kdyn/cm2 in control subjects; p = NS) with 10 of 21 patients with aortic stenosis and 12 of 16 patients with aortic regurgitation falling below the 95% prediction limit of the linear inverse relationship between ejection fraction and end-systolic stress for controls (EF = 0.78 - 0.00074 X ESS).(ABSTRACT TRUNCATED AT 250 WORDS)

Relation of left ventricular filling dynamics to alterations in load and compliance in patients with and without pressure-overload hypertrophy.

A large atrial contribution to left ventricular (LV) filling (%A) in patients with LV hypertrophy has been assumed by some to indicate abnormal LV compliance. We tested this assumption by examining the influence of short- and long-term changes in load on compliance and filling dynamics using nitroprusside to decrease load in 11 patients with severe aortic stenosis (AS) and ergonovine to increase load in nine normal subjects. LV angiographic volume was analyzed frame-by-frame simultaneous with micromanometer pressure recordings. Operative LV chamber compliance (dV/VdP) and a time constant for isovolumic relaxation rate were computed using three-constant exponential equations fit to the data. Compared with normal subjects, resting left ventricular end-diastolic pressure was increased and dV/VdP was reduced in AS, but %A was not different. %A was inversely related to left ventricular end-diastolic pressure (r = -0.48, p = 0.02) and positively correlated with dV/VdP (r = 0.90, p less than 0.001) within the AS group. Nitroprusside infusion reduced LV peak systolic pressure by 11%, end-diastolic pressure by 38%, and end-diastolic volume by 12% (p less than or equal to 0.004 for each) and tended to increase dV/VdP by 26% (p = 0.23). These alterations in load resulted in a 21% decrease (-16 ml) in the early filling volume (p less than 0.05) and variable increases (mean, +7 ml; p = NS) in the late atrial filling volume and in the percent atrial contribution to ventricular filling (26 +/- 19% to 35 +/- 25% for the AS group, p = NS) that were related to changes in compliance.(ABSTRACT TRUNCATED AT 250 WORDS)

Determination of left ventricular ejection fraction by computer densitometric analysis of digital subtraction angiography: Experimental validation and correlation with area-length methods

Conventional methods for calculating left ventricular (LV) ejection fraction (EF) require accurate edge definition and geometric assumptions, which may be compromised in the presence of dyssynergy. Computer densitometric analysis (CDA) of digital subtraction angiography offers the potential for calculation of EF, independent of LV shape, by comparing summated brightness for regions of interest at end diastole and end systole. Therefore, the accuracy of CDA was validated for 2 mechanical heart models of differing geometry, spherical and rectangular. Both models confirmed the close correlation between calculated and measured EF (r = 0.98 and r = 0.99, respectively). Subsequently, the CDA was compared with single and biplane area-length EF calculations in 72 patients, half with a previous myocardial infarction. In patients without previous myocardial infarction, CDA correlated closely with both single-plane and biplane EF (r = 0.91 and 0.93, respectively). The close correlation was maintained regardless of whether CDA was applied to direct LV injection or intravenous digital subtraction angiography. However, in 36 patients with previous myocardial infarction, CDA correlated less closely with single-plane (r = 0.74) than with biplane (r = 0.86) area-length EF. Thus, CDA permits calculation of EF without geometric assumptions, and may be superior to the area-length method in patients with LV dyssynergy after myocardial infarction.

Mechanics of postextrasystolic potentiation in normal subjects and patients with valvular heart disease.

To determine the relative influence of preload, afterload, and inotropic state on postextrasystolic potentiation (PESP) of ventricular performance in man, we computed angiographic left ventricular volume and wall stress frame by frame for a control and potentiated beat in each of 31 patients. In 10 normal subjects, PESP increased ejection fraction by 14%, while left ventricular end-diastolic volume increased by 8% (p less than .001) and end-systolic stress fell by 21% (p less than .005). Enhanced diastolic filling (+6%, p less than .005) with a small decline in end-systolic stress (-8%, p = NS) likewise contributed to potentiation of ejection fraction (+14%, p less than .001) in seven patients with aortic stenosis. Diastolic filling was not significantly augmented during the compensatory pause in six patients with isolated mitral regurgitation, nor in eight patients with aortic regurgitation (+2%, p = NS for both). Although afterload tended to fall for potentiated beats in patients with aortic (-11%, p = NS) and mitral regurgitation (-23%, p = NS), analysis of ejection fraction-end-systolic stress relationships demonstrated an independent effect of inotropic state on potentiated ejection performance. Thus, utilization of preload reserve contributed to PESP in normal subjects and patients with aortic stenosis, but not in those with volume overload imposed by chronic valvular regurgitation. Enhanced inotropic state independent of small changes in afterload was demonstrated in all subgroups.

Effect of mitral regurgitation and volume loading on pressure half-time before and after balloon valvotomy in mitral stenosis

Doppler pressure half-time (PHT) is frequently used to assess mitral valve area (MVA), but the reliability of PHT has recently been challenged, specifically in the setting of balloon mitral valvotomy when hemodynamics have been abruptly altered. The effect of volume loading both before and after balloon mitral valvotomy on computation of MVA by Gorlin and by PHT in 18 patients with high-fidelity micromanometer measurements of left atrial and left ventricular pressure was therefore examined. Echocardiographic MVA increased from 0.91 +/- 0.15 to 1.97 +/- 0.42 cm2 after valvotomy. Volume loading produced significant increases in left atrial pressure (16 to 23 before and 12 to 20 mm Hg after valvotomy), in cardiac output (3.7 to 4.1 before and 3.9 to 4.6 liters/min after valvotomy), and in mitral valve gradient (11 to 14 before and 5 to 7 mm Hg after valvotomy). These hemodynamic changes were associated with modest but significant decreases in PHT and increases in MVA estimated by 220/PHT (0.66 to 0.81 before and 1.64 to 1.96 cm2 after valvotomy), whereas the MVA by Gorlin was not affected in a consistent fashion by volume loading (0.85 to 0.89 before and 1.66 to 1.69 cm2 after valvotomy). The correlation between Gorlin MVA and 220/PHT was only fair (r = 0.73, p less than 0.001) and was significantly poorer among patients with greater than 1+ mitral regurgitation (r = 0.72) than among those with less or no regurgitation (r = 0.79) (p = 0.001 by analysis of covariance for mitral regurgitation effect).(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of aortic valve disease on systolic stiffness of the human left ventricular myocardium.

The new concept of systolic myocardial stiffness was applied to the study of ejection mechanics in aortic valve disease. Frame-by-frame analysis of stress (sigma) and volume (V) was performed for two differently loaded beats in 26 patients who underwent simultaneous cineangiography and micromanometry: nine normal subjects, eight with isolated aortic regurgitation (AR), and nine with aortic stenosis (AS). Maximum myocardial stiffness (maxEav) was defined as the slope of the end-systolic (es) stress-strain relationship. End-systole was defined as the frame where stiffness was maximal, and strain was defined as epsilon = loge (Dm/Dom), where Dm is left ventricular midwall diameter and Dom is the theoretical Dm at zero stress. Expressed in terms of cavity volume, epsilon = gamma X loge (V/Vo), where gamma is the geometric factor relating Dm to V during systole. Vo was obtained by extrapolating to sigma es = 0 the function, sigma es = maxEav X gamma X loge (Ves/Vo), which was fit to the end-systolic data. Vo always had a value greater than zero. MaxEav was preserved in the AR group (1575 +/- 565) and increased in the AS group (1877 +/- 544; p = .02) compared with normal (1320 +/- 268), suggesting maintenance of contractile force per unit of myocardium in these two lesions. However, theoretical unloaded shortening fraction (SFo) was depressed in the AS group (0.30 +/- 0.06; p = .01) compared with normal (0.37 +/- 0.04), preserved in the AR group (0.34 +/- 0.07; p = .24), and inversely related to maxEav (r = -.66, p = .01), suggesting a disparity between shortening potential and force potential.(ABSTRACT TRUNCATED AT 250 WORDS)

Short-term vasodilator effect of captopril in patients with severe mitral regurgitation is parasympathetically mediated.

Background Few data exist regarding the effects of angiotensin converting enzyme inhibitors in patients with regurgitant valvular lesions. We postulated an immediate improvement in cardiac performance with captopril in mitral regurgitation, which, in a hemodynamically compensated group of patients, might be mediated through parasympathetic vasodilation rather than through blockade of angiotensin converting enzyme. Methods and Results Hemodynamics were examined before and 90 minutes after oral captopril (25–50 mg) in 18 patients (mean age, 31 years) with chronic, severe mitral regurgitation in New York Heart Association functional class II and III. One group of patients was given captopril alone (group 1, n = 9) and a second group was given captopril plus atropine 0.04 mg/kg i.v. (group 2, n=9). Captopril alone (group 1) produced decreases in heart rate (90- 81 beats/min) Conclusions In patients with chronic, severe mitral regurgitation, captopril reduced systemic arterial and left ventricular filling pressures but did not immediately augment cardiac output as expected. Furthermore, the modest systemic vasodilator effect of captopril was parasympatheti-cally mediated.

Effect of abrupt mitral regurgitation after balloon valvuloplasty on myocardial load and performance

The concept that mitral regurgitation masks myocardial dysfunction by reducing afterload and augmenting ejection performance has not been well established in humans. The effect of abruptly produced mitral regurgitation on left ventricular loading and performance was therefore evaluated in five patients who developed this complication after an otherwise successful percutaneous balloon mitral valvuloplasty. Mitral valve area by Gorlin formula calculated with forward flow increased from 0.92 +/- 0.14 to 2.75 +/- 0.82 cm2. Mean left atrial pressure did not decrease (19 +/- 4 to 19 +/- 6 mm Hg). The size of the left atrial V wave relative to mean left atrial pressure (peak V - mean left atrial pressure) increased from 7 +/- 4 to 19 +/- 6 mm Hg. Angiographic mitral regurgitation increased from 0+ or 1+ to greater than 3+ in each patient and regurgitant fraction increased from 0.23 +/- 0.11 to 0.55 +/- 0.09 (p less than 0.01). End-diastolic volume increased modestly from 148 +/- 15 to 159 +/- 15 ml (p = NS). Heart rate increased from 54 +/- 5 to 71 +/- 8 beats/min (p less than 0.05), which may have prevented further increases in preload by shortening the filling period. End-systolic stress decreased by 32% from 277 +/- 34 to 188 +/- 52 kdyn/cm2 (p less than 0.01) as a result of a 25% decrease in end-systolic pressure from 121 +/- 8 to 91 +/- 7 mm Hg and a 16% decrease in end-systolic volume from 67 +/- 13 to 56 +/- 8 ml (p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)