Motion Of Mitral Valve Research Articles

Comparison of mitral valve dimensions and motion in mitral valve prolapse with severe mitral regurgitation to uncomplicated mitral valve prolapse and to mitral regurgitation without mitral valve prolapse

To determine the mitral valve abnormalities associated with hemodynamically important mitral regurgitation (MR) among patients with mitral valve prolapse (MVP), computerized 2-dimensional echocardiographic measurements of mitral leaflet and anular dimensions and motion in 26 patients with MVP and MR were compared to those in 48 subjects with uncomplicated MVP, 16 patients with MR due to etiologies other than MVP (rheumatic in 8) and 35 normal adults. Compared to both uncomplicated MVP and normal subjects, patients with MVP plus MR were older (p <0.05), had strikingly large mitral leaflets and anulus (p <0.0005) and were more likely to have systolic billowing of mitral leaflets in the parasternal long-axis view (24 of 26 [92%] vs 24 of 48 subjects with uncomplicated MVP [50%], p <0.001). Overlap in anular and posterior leaflet dimensions in normal and uncomplicated MVP subjects occurred in the 20 MVP plus MR patients who continue to be followed medically but not in the 6 MVP plus MR patients who underwent mitral valve surgery during 22 ± 14 months follow-up. Patients with MR due to rheumatic or other non-MVP etiologies had enlargement of mitral leaflets and anulus virtually identical to that in MVP plus MR patients. In conclusion, patients with severe MR due to MVP are older, have striking mitral valve enlargement and more frequently exhibit leaflet billowing compared with subjects with uncomplicated MVP. Similar mitral leaflet enlargement was found in patients with non-MVP etiologies of MR, suggesting that mitral anular and leaflet enlargement may play a more general role in the pathogenesis of MR than is currently appreciated.

Sequence of mitral valve motion and transmitral blood flow during manual cardiopulmonary resuscitation in dogs

Sequence of mitral valve motion and transmitral blood flow during manual cardiopulmonary resuscitation in dogs

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 < 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/s 2, p < 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 < 0.02), which was not observed in patients with AR who did not have anterior mitral leaflet fluttering. Thus, in patients with moderate to severe AR, fluttering of the anterior mitral leaflet occurs in a subset of patients in whom the flow-velocity disturbance is directed onto the anterior mitral leaflet, resulting in alterations of early diasolic mitral flow velocities compatible with relative obstruction to mitral inflow.

Sequence of Mitral Valve Motion and Transmitral Blood Flow During Manual Cardiopulmonary Resuscitation in Dogs

Sequence of Mitral Valve Motion and Transmitral Blood Flow During Manual Cardiopulmonary Resuscitation in Dogs

Variable responses of mitral valve motion and flow in systemic hypertension and in idiopathic dilated cardiomyopathy

The relation between transmitral flow and diastolic mitral valve motion were examined in 17 normal persons, 14 patients with hypertension and 12 patients with idiopathic dilated cardiomyopathy. M-mode echograms were analyzed for early and late diastolic mitral leaflet separations, their ratio and E-F slope. Pulsed Doppler transmitral flow was analyzed for early and late velocities, their ratio and early flow deceleration. Early diastolic mitral valve leaflet separation was reduced in patients with hypertension (at 28 ± 5 mm [p < 0.05]) and in patients with cardiomyopathy (at 22 ± 3 mm [p <0.01]). Flow velocity was also reduced in patients with hypertension (at 52 ± 11 cm/s [p <0.05]) and in patients with cardiomyopathy (at 48 ± 15 cm/s [p < 0.01]). However, early leaflet separation and flow velocity were not related (r = 0.26). Late diastolic leaflet separation was similar (at 25 ± 5 mm) in normal subjects and in those with hypertension (at 23 ± 6 mm), but was reduced in patients with cardiomyopathy (at 18 ± 3 mm [p <0.01]). In contrast, late flow velocity was increased in patients with hypertension (at 52 ± 12 cm/s [p < 0.05]) but unchanged in patients with cardiomyopathy (at 42 ± 16 cm/s). The ratio of early to late leaflet separation was similar in all groups, whereas the ratio of flow velocities was reduced in hypertensive patients. Neither the E-F slope nor early flow deceleration was altered in either pathologic group. Thus, hypertension and cardiomyopathy had similar effects in early rather than late diastole. Mitral valve separation did not reflect the increased dependence on atrial systole seen in hypertension readily demonstrable by Doppler analysis.

Sequence of mitral valve motion and transmitral blood flow during manual cardiopulmonary resuscitation in dogs.

According to the thoracic pump model of cardiopulmonary resuscitation (CPR), the heart serves as a passive conduit for blood flow from the pulmonary to the systemic vasculature, necessitating an open mitral valve and anterograde transmitral blood flow during chest compression. To assess the applicability of this model to manual CPR techniques, two-dimensional echocardiograms were recorded from the right chest wall and/or the esophagus in nine dogs (18 to 26 kg) during manual CPR. The aortic valve opened with chest compression and closed with release, while the pulmonary and tricuspid valve leaflets closed with compression and opened during release. The mitral valve remained open during ventilation alone and during abdominal compressions. With the onset of brief, high-velocity (high-impulse) chest compressions, the mitral valve closed rapidly and the left ventricle was deformed, whether compressions were applied to the sternum or the left mid-chest wall. The mitral valve reopened with release of each compression. Left atrial echocardiographic contrast injections confirmed the absence of anterograde transmitral blood flow during high-impulse compression and its presence during release. Failure of mitral leaflet approximation during chest compression was observed only when a very low-velocity, prolonged (low-impulse) compression technique was used, or when regions that did not directly overlie the heart were compressed. Consistent with these observations, simultaneous recordings of the left ventricular and left atrial pressures during high-impulse sternal compressions in five dogs (19 to 25 kg) demonstrated peak and mean left ventriculoatrial pressure gradients of 38.5 +/- 4.0 and 13.5 +/- 2.9 mm Hg, respectively, and these pressure gradients declined with less impulsive compressions. The observations made during all but low-impulse chest compressions are inconsistent with the thoracic pump model, and support direct cardiac compression as the primary mechanism of forward blood flow with more impulsive manual chest compression techniques.

Prevalence and clinical features of mitral valve prolapse

As a consequence of advances in cardiac imaging, mitral valve prolapse (MVP) has become a commonly recognized finding, occurring in 2.5 % to 5 % of the general population. Original concepts of MVP were based on limited experience with highly select groups of subjects with nonejection clicks and mid to late systolic murmurs. Such subjects were typically found to have systolic billowing of the mitral valve leaflets into the left atrium on angiographic evaluation.lv2 Pathologic examination of affected valves often demonstrated myxomatous changes with disruption of collagen.3 Furthermore, follow-up of highly selected patients with MVP4s5 suggested increased risk for infective endocarditis, progressive mitral regurgitation, ruptured chordas, and sudden cardiac death. The advent of M-mode echocardiography permitted noninvasive detection of mitral leaflet displacement (prolapse) into the left atrium. This finding has been found to be associated with angiographic evidence of billowing mitral leaflets in subjects with the click-murmur syndrome.6s7 Two-dimensional echocardiography has been proposed, in advance of adequate validation studies, as the best available standard for the diagnosis of MVP.8 The ease with which mitral valve motion is depicted by echocardiography has resulted in widespread use of this tool for the definition of MVP. Owing to ease of detection and expanding interest in MVP, the medical literature swells with case reports of associations between MVP and an evergrowing list of clinical features and sequelae. It is no surprise that MVP was described in the 1970s as the “cardiac disease, of the decade.“g Recent studies, however, have underscored the benign clinical course of MVP, raising questions about the very existence of a “mitral valve prolapse syndrome.”

Computer simulation of human mitral valve mechanics and motion

The human mitral valve is the left atrio-ventricular valve which is composed of several components including leaflets, chordae tendineae, papillary muscles, and the valve annulus. Any or all of these components may fail and contribute to various valvular diseases including mitral regurgitation and mitral valve prolapse. A computer simulation of mitral valve mechanics and motion was written in BASIC for micro-computers. This program allows valvular geometry and biomechanical parameters to be varied and records time varying motion of the valve and all components during systole including a graphic display of the valve leaflets.

The equilibrium position of the mitral valve: An accurate model of mitral valve motion in humans

A "semiopen" diastolic equilibrium position of the mitral valve that is assumed in the absence of transmitral flow has been demonstrated in instrumented dogs. It has been suggested that the papillary muscles and chordae tendineae play an integral role in returning the valve to this position after initial diastolic opening. To determine whether such a model of mitral valve motion is valid in noninstrumented humans without underlying valvular disease, M-mode and Doppler ultrasound studies were performed in 6 subjects who underwent prolonged periods of ventricular diastole and atrial inactivity. After maximal opening, the mitral valve assumed a stable open position in which mean separation of the anterior and posterior mitral leaflets was 52% of maximal separation. This position was maintained for a mean duration of 585 ms, during which time transmitral flow fell to 0 m/s. Peak mitral valve opening preceded the early transmitral flow peak by an average of 42 ms, suggesting an active closure of the mitral valve as flow continued to accelerate. It is concluded that a semiopen equilibrium position of the mitral valve is assumed during prolonged diastolic periods in the absence of transmitral flow and is an accurate model describing diastolic mitral valve motion in noninstrumented humans. The chordae tendineae and papillary muscles may actively participate in the genesis and maintenance of the equilibrium position.

Ultrafast Computed Tomography: A New Method for the Evaluation of Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy (HCM) presents with a wide spectrum of heterogeneous morphology. Modalities used to assess HCM include echocardiography, cardiac catheterization, radionuclide angiography, conventional computed tomography (CT), and magnetic resonance imaging. This investigation was performed to assess the feasibility of using ultrafast CT with 50 ms/scan acquisition time in the cine mode to compare 11 patients with HCM to 11 patients with normal studies. A specific advantage of this technique includes tomographic representation of ventricular anatomy coupled with the ability to evaluate multiple parameters of dynamic function. Global and tomographic ejection fraction, left ventricular mass, wall thickness, left atrial size, and diastolic filling rates are among the parameters that can be measured. Mitral valve motion can also be assessed. Comparisons were made between the HCM and normal groups using a sample t test. There was a significant difference in left ventricular mass (p < 0.05) between the groups. Specific wall thickness parameters were also measured. Comparisons of the septal basal, septal mid-left ventricular, anterior basal, anterior mid-left ventricular, lateral, and posterior walls revealed a significant difference (p < 0.05). The left atrial dimensions also demonstrated a significant difference (p < 0.05). Quantitative assessment of HCM can be performed by ultrafast CT. The combination of excellent spatial and temporal resolution makes it competitive and potentially superior to other techniques. Ultrafast CT should be considered when confronted with the need for diagnostic evaluation and subsequent follow-up in HCM.

Hypertrophic Cardiomyopathy: Noninvasive Identification of Patients with Significant Pressure Gradient

In 49 patients with hypertrophic cardiomyopathy, systolic time interval measurements, echocardiograms, and catheterization were performed within 48 h. Eighteen patients were without left ventricular outflow tract pressure gradient (LV-PG), 16 had mild to moderate LV-PG (l-< 50 mm Hg), and 15 had significant LV-PG (> 50 mm Hg). A high degree of correlation was found between heart rate corrected left ventricular ejection time (LVETI) and LV-PG (r = 0.87). LVETI in patients with hypertrophic cardiomyopathy, but no LV-PG, was shorter than normal (389 ± 17 vs. 413 ± 13 ms; p < 0.01). All patients with significant LV-PG (> 50 mm Hg) had LVETI > 423 ms, and only 1 patient without significant LV-PG had LVETI >423 ms (100% sensitivity, 97% specificity). In 4 patients in whom LVETI and LV-PG were measured before and during isoproterenol infusion, changes in both parameters were parallel. No other échocardiographie (including systolic anterior motion of mitral valve) or systolic time interval measurements reliably identified patients with significant LV-PG. Thus, in patients with hypertrophic cardiomyopathy (1) LVETI is shorter than normal in the absence of LV-PG, and (2) the measurement of LVETI reliably identifies patients with significant LV-PG at rest and during adrenergic stimulation.

Demonstration of mitral valve function by cine computed tomography using a new long axis view.

Comparison was made between contrast enhanced cine computed tomography (Cine/CT) and echocardiography in the imaging of the mitral valve in 14 patients. The mitral valve was seen in all 14 patients by Cine/CT using a new long axis view. There was agreement with echocardiography in 12 patients. Abnormalities in mitral valve movement were detected by Cine/CT. Left atrial size and contraction was measured by Cine/CT with a difference in left atrial ejection fraction observed between 13 patients with no evidence of mitral disease and 3 patients with mitral disease.

軽度対称性左室肥大例における僧帽弁輪の石灰化による左室流出路狭窄

The combination of the systolic anterior motion of the anterior leaflet of the mitral valve and/or the mitral annular calcification in the case of asymmetrical septal hypertrophy has been fully recognized. However, in concentric left ventricular hypertrophy the systolic anterior motion of the anterior mitral valve and the massive posterior submitral calcification have not been commonly reported. We present a case with mild concentric left ventricular hypertrophy and massive posterior submitral calcification which displace the entire mitral ring anteriorly, namely, toward the left ventricular outflow tract. In this case, typical left ventricular outflow obstruction with systolic anterior motion of the anterior mitral valve was seen. Thus, we considered that this rare condition may have contributed to the formation of the systolic anterior motion of the anterior mitral leaflet in this case. We have provided additional information regarding the possible causes of systolic outflow obstruction in hypertrophic obstructive cardiomyopathy.

Color-coded Doppler imaging of systolic flow patterns in hypertrophic cardiomyopathy

We studied 11 patients with hypertrophic cardiomyopathy by color Doppler echocardiography (Group I: 6 patients with outflow obstruction, and Group II: 5 patients without outflow obstruction) to assess systolic structure and function as observed by cross-sectional echocardiography in relation to the flow dynamics. The structure and function included systolic anterior motion of mitral valve (SAM), midsystolic aortic valve closure (AoC), systolic cavity obliteration and the presence and timing of mitral incompetence. Their occurrence and timing was related to presence of aortic systolic flow and presence of turbulence. While all patients in Group I had SAM and turbulence, none of the patients in Group II had SAM nor turbulence. Early mitral incompetence appearing before SAM and turbulence, occurred in all patients of Group I and in none of Group II. Midsystolic aortic valve closure was only present in Group I and blood flow was unilaterally directed so that only 60% of aortic cross-sectional area showed blood flow. We conclude that mitral incompetence in hypertrophic cardiomyopathy in early systole is common when outflow gradient is present and is independent of mitral incompetence of mid- and late systole. During SAM, turbulence in the subaortic area and mid and late mitral incompetence occurred simultaneously. The midsystolic aortic valve closure was related to the unilaterally directed blood flow through the aortic cross-sectional area.

Echocardiographic Analysis of Systolic Mitral Valve Motion in Healthy Young Males - With Particular Reference to Mitral Valve Prolapse -

Echocardiographic Analysis of Systolic Mitral Valve Motion in Healthy Young Males - With Particular Reference to Mitral Valve Prolapse -

Reverse doming of the anterior mitral leaflet with severe aortic regurgitation

The normal anatomic relation of the anterior mitral leaflet to the left ventricular outflow tract suggests that significant aortic regurgitation should have a predictable hemodynamic effect on the motion and configuration of the leaflet, an effect that should be seen by two-dimensional echocardiography. Previous reports have identified an abnormality of mitral opening in the short-axis view that was quite specific but not sensitive. This study was undertaken to evaluate mitral valve motion and configuration in aortic insufficiency using two-dimensional echocardiography. A characteristic pattern of anterior leaflet motion was found in patients with moderately severe and severe aortic regurgitation. This pattern, termed "reverse doming," was seen in the apical and long-axis views in 19 of 22 such patients. The previously described "diastolic indentation" in the short-axis view was found in 16 of these 22 patients. Only 2 of 16 patients with lesser degrees of insufficiency had reverse doming. The sign was not seen in normal subjects nor in 16 patients with cardiomyopathy. For each of the few false positive and false negative findings, there is a seemingly logical hemodynamic explanation. It is concluded that reverse doming of the anterior mitral leaflet appears to be a sensitive and specific sign for moderately severe and severe aortic regurgitation.

Systolic anterior motion of the posterior mitral leaflet: a previously unrecognized cause of dynamic subaortic obstruction in patients with hypertrophic cardiomyopathy.

Dynamic obstruction to left ventricular outflow in patients with hypertrophic cardiomyopathy usually occurs when the anterior mitral leaflet moves forward in systole and approaches or contacts the ventricular septum. However, we have recently identified, by M mode and two-dimensional echocardiography, 21 patients with hypertrophic cardiomyopathy who had a unique pattern of mitral valve motion characterized by abnormal mitral valve coaptation and systolic anterior motion of the posterior mitral leaflet. This abnormality of mitral valve motion was most reliably identified with two-dimensional echocardiography in views of the left ventricle obtained from the apex. At end-diastole the anterior and posterior mitral leaflets did not appear to coapt at their distal free margins. Rather, at mitral valve closure, the anterior mitral leaflet contacted the basal portion of posterior mitral leaflet. Subsequently, during systole the "residual" distal portion of posterior mitral leaflet approached or contacted the ventricular septum. Morphologic observations in nine other patients with hypertrophic cardiomyopathy suggested that systolic anterior motion of the posterior mitral leaflet is due to elongation of the middle scallop of the posterior leaflet, which probably comes into apposition with the ventricular septum during systole by passing through the space created by the normal pattern of chordal attachments onto the anterior mitral leaflet. Of the 16 patients who underwent cardiac catheterization, nine had basal subaortic gradients of 20 to 85 mm Hg, which were apparently due to moderate or marked systolic anterior motion of the posterior mitral leaflet. Ventricular septal myotomy-myectomies were performed in two patients and resulted in markedly diminished systolic anterior motion of the posterior mitral leaflet in each and abolition of subaortic gradient in the one patient who underwent postoperative cardiac catheterization. Hence, in patients with hypertrophic cardiomyopathy, systolic anterior motion of the posterior mitral leaflet (1) is not uncommon (identifiable in about 10% of a consecutively studied series of patients), (2) constitutes a previously undescribed mechanism for dynamic subaortic obstruction, and (3) is due to a malformation of the posterior mitral leaflet.

Prosthetic mitral valve motion during cardiac dysrhythmias as determined by echocardiography

To assess the changes and physiologic mechanisms of prosthetic valve motion during cardiac dysrhythmias as well as the role of atrial systole in the closure of the mitral valve, M-mode echocardiography was performed in 36 patients with normally functioning prosthetic mitral valves (Björk-Shiley, Starr-Edwards, and Beall valve). Premature closure of the prosthetic mitral valve in diastole with a "sharp" closing motion was seen during first-degree atrioventricular block, atrial fibrillation with ventricular rates less than 60 beats/min, and atrial flutter. A "rounded" premature valve closure due to atrial systole was seen during atrial tachycardia and complete heart block. Atrial systole initiates a closing motion of the prosthetic mitral valve at end-diastole, and ventricular systole completes this closure during normal sinus rhythm. When first-degree atrioventricular block is present, atrial systole alone completes this closure before ventricular contraction. Atrial contraction alone also can effectively close the prosthetic mitral valve during atrial flutter and atrial tachycardia. Other factors (such as left ventricular diastolic volume) may play a role in the effective closure of the prosthetic mitral valve during atrial fibrillation with slow ventricular rates and complete heart block. These findings must be considered in the echocardiographic evaluation of suspected malfunctioning prosthetic mitral valves. A baseline postoperative echocardiogram after prosthesis insertion is important for future evaluation when clinically indicated.

Mechanism of systolic anterior motion of mitral valve and site of intraventricular pressure gradient in hypertrophic obstructive cardiomyopathy.

The mechanism of systolic anterior motion of the mitral valve and the localisation of the intraventricular pressure gradient were determined in 15 cases of hypertrophic obstructive cardiomyopathy by the combined use of real time two dimensional echocardiography and intracardiac manometry. We arrived at the following conclusions. The systolic anterior motion of the mitral echo in the M-mode echocardiogram can be classified into two types, I and II, based on two dimensional echocardiographic findings. In type I, the echo sources of systolic anterior motion are the anteriorly shifted mitral chordae and, in part, the papillary muscles. The intraventricular pressure gradient occurs at the level of the tip of the papillary muscle. The suprapapillary part of the outflow tract and the inflow part show a low pressure, while the apical cavity shows a high pressure. In type II, the echo sources of systolic anterior motion are the anterior and posterior mitral leaflets which are oriented in such a way as to obstruct the outflow tract. The pressure gradient occurs at the level of the anterior and posterior mitral leaflets. The inflow tract and the outflow tract just below the mitral leaflets show a high pressure, in contrast to type I systolic anterior motion. The inappropriate and maloriented papillary muscles play an essential role in causing both types of systolic anterior motion and outflow obstruction. The direction of the axis of the papillary muscle is changed in late systole, moving its tip away from the interventricular septum, resulting in a simultaneous reduction in systolic anterior motion.

M‐MODE ECHOCARDIOGRAPHY AS A DIAGNOSTIC AID FOR FELINE CARDIOMYOPATHY

Normal cats and cats with congestive cardiomyopathy (CCM) and hypertrophic cardiomyopathy (HCM) were examined using M‐mode echocardiography to determine its diagnostic capabilities. Sixteen normal cats were examined to verify previously reported data and to add further echocardiographic inforamtion (left atrial/aortic root ratio, left posterior wall thickness at end systole and end diastole, amplitude of mitral valve excursions, and velocity of valve opening and closure) to aid in differential diagnosis. Significant (p&lt;0.05) changes were detected between the normal cats and those with cardiomyopathy. In each type of cardiomyopathy, alterations in left atrial dimension, left atrial/aortic root ratio, left ventricular dimension, left ventricular wall thickness and percentage of ventricular dimensional change were identified. Altered mitral valve motion was found with HCM. Echocardiography was found to be an accurate technique for definitive diagnosis of feline cardiomyopathy.