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 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have previously described a new surgical technique for control of arrhythmogenic foci in patients with recurrent ventricular tachycardia that we call balloon electric shock ablation. With this method sequential shocks are delivered to a grid of electrodes on a balloon that can be introduced across the mitral valve into the intact ventricle. A series of experiments was undertaken to investigate possible deleterious effects of balloon electric shock ablation when shocks are delivered directly to the mitral valve apparatus. In six animals shocks totaling 1200 joules were given through a closely spaced electrode grid applied to the area of the mitral valve. Nine to 12 weeks later, left ventricular and mitral valve function were assessed. Balloon electric shock ablation in the basilar portion of the ventricle was associated with decreased myocardial performance, as evidenced by ejection phase indices. In five of six animals balloon ablation led to minor thickening of the valve leaflets and chordal attachments plus necrosis of adjacent myocardium, including papillary muscles. In these animals there was no significant dysfunction of the valve observed. In the remaining animal, however, ablation was centered on the posterior papillary muscle and resulted not only in necrosis of the base of the papillary muscle but also in full-thickness scarring and thinning of the adjacent left ventricular wall. In this dog, mitral regurgitation was seen on long-term follow-up. We conclude that when balloon electric shock ablation is used to destroy a localized area of myocardium in the basilar portion of the intact ventricle, the procedure results in decreased myocardial performance. When shocks were directly applied to the mitral valve apparatus in five of six animals, ablation did not result in significant negative effects on the structure and function of the valve. In the sixth dog, however, shock delivery resulted in transmural necrosis and thinning at the site of papillary muscle insertion and was associated with severe mitral regurgitation with volume loading. Therefore caution should be used when considering clinical application of this technique if the area to be ablated is in the basal portion of the heart.
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PMID:Surgical treatment of ventricular tachycardia by balloon electric shock ablation. Potential effects on the mitral valve apparatus. 154 4

To better understand the pathophysiology of obstruction of left ventricular outflow in hypertrophic cardiomyopathy and to determine the value of intraoperative transesophageal Doppler echocardiography in decision making, 32 consecutive patients undergoing ventriculomyectomy were assessed. The mean preoperative left ventricular outflow gradient was 83 +/- 39 mm Hg and the mean basal septal width was 24 +/- 6 mm. Compared with transesophageal findings in 10 normal control subjects, the mitral leaflets were longer and the coaptation point was abnormal in the patients with obstructive hypertrophic cardiomyopathy (anterior and posterior leaflet lengths in the patients were 31 +/- 4 vs. 22 +/- 3 mm in the control group [p less than 0.00001] and 20 +/- 2 vs. 15 +/- 3 mm in the control group [p less than 0.00001]). The coaptation point in the patient group was in the body of the leaflets at a mean of 9 +/- 2 mm from the anterior leaflet tip, whereas it was at or within 3 mm of the leaflet tip in the normal group. During early systole, the distal third to half of the anterior mitral leaflet angled sharply anteriorly and superiorly (systolic anterior motion), resulting in leaflet-septal contact and incomplete mitral leaflet coaptation in mid-systole. This caused the formation of a funnel, composed of the distal parts of both leaflets, that allowed a jet of posteriorly directed mitral regurgitation to occur in mid- and late systole. The sequence of events in systole was eject/obstruct/leak. Transesophageal echocardiography was also helpful in planning the extent of the resection, assessing the immediate result and excluding important complications. In successful cases, the post-myectomy study showed 1) a dramatic thinning of the septum, with widening of the left ventricular outflow tract to a width similar to that in the normal subjects, 2) resolution of systolic anterior motion and the left ventricular outflow tract color mosaic, and marked reduction or abolition of mitral regurgitation despite persistence of abnormal mitral leaflet length and an abnormal mitral leaflet coaptation point. The routine use of transesophageal echocardiography in patients undergoing surgical myectomy for the treatment of obstructive hypertrophic cardiomyopathy is recommended.
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PMID:Transesophageal Doppler echocardiography in obstructive hypertrophic cardiomyopathy: clarification of pathophysiology and importance in intraoperative decision making. 160 38

To assess the possible role of restoring forces underlying left ventricular wall motion during rapid filling, the time relations between left ventricular dimensions and filling velocity were studied by digitised M-mode and Doppler echocardiography in 23 normal children and 43 patients: 11 with mild and 17 with severe mitral regurgitation, and 15 with left ventricular hypertrophy due to aortic stenosis. In normal children, peak mitral flow velocity characteristically lagged peak rate of dimension increase by 50 +/- 15 msec, and peak rate of posterior wall thinning by 35 +/- 15 msec, (P less than 0.01 for both). Towards the apex, and along the long axis of the ventricle, these phase differences between dimension and flow velocity were not apparent. The characteristic time relations between flow velocity and transverse dimension were also present in patients with left ventricular hypertrophy or mild mitral regurgitation, but when mitral regurgitation was severe they were lost and there was no significant difference in timing between peak flow velocity and peak rate of dimension change (-2 +/- 30 msec) or wall thinning (-4 +/- 25 msec). We conclude that phase differences between left ventricular wall motion and mitral inflow velocity are present in the normal ventricles of children. They cannot be explained on the basis of simple shape changes or passive filling of the relaxing ventricle, but strongly suggest the additional presence of ventricular restoring forces. They persist in patients with left ventricular hypertrophy or mild mitral regurgitation, but are lost when the regurgitation is severe, the filling pattern reverting to that predicted for passive distension of the ventricular cavity by a high left atrial pressure.
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PMID:Phase differences between left ventricular wall motion and transmitral flow in man: evidence for involvement of ventricular restoring forces in normal rapid filling. 252 30

A dilated left ventricle with reduced ejection fraction is usually attributed to impaired systolic function. To investigate the possibility that ventricular filling might also be disturbed, M mode echocardiograms, phonocardiograms, and Doppler cardiograms were recorded in 30 patients with ventricular disease of varying cause. All but four had functional mitral regurgitation. The size of the left ventricular cavity was increased in all and peak velocity of circumferential fibre shortening was reduced. Diastolic abnormalities included a short isovolumic relaxation time, and, on digitised M mode, a reduced rate of dimension increase and of posterior wall thinning. Although the timing of aortic valve closure was normal, mitral regurgitation persisted beyond it by 95 (35) ms and beyond mitral valve opening by 60 (40) ms. This reduced the effective filling time (the interval when the mitral valve was open and mitral regurgitation was absent) to less than 200 ms in seven patients. The effective filling time correlated closely with the RR interval, the regression equation indicating a reduction of 80 ms for each 100 ms fall in RR interval. It was also independently shortened by 2 ms a year with increasing age. The effective left ventricular filling time may thus be very short in patients with left ventricular cavity dilatation and functional mitral regurgitation. It is suggested that when diastolic function is also abnormal, this short filling time may physically limit ventricular inflow. Its close relation to heart rate might contribute to the therapeutic effect of beta blockade in such patients.
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PMID:Impairment of diastolic function by shortened filling period in severe left ventricular disease. 280 69

To assess the time-course of adaptive responses of the left ventricle to chronic volume overload, dogs were instrumented with a left ventricular (LV) micromanometer and pairs of ultrasonic crystals for the measurement of LV wall thickness (WTh), LV chamber diameter (D), and longitudinal segment length (L). Following a control study, mitral regurgitation (MR) was created by a transventricular section of the chordae tendineae. Heart rate was controlled during each study by atrial pacing. Plasma norepinephrine levels at rest were determined by high-performance liquid chromatography. Eight days (mean) after the onset of MR, enddiastolic (ED) D had increased by 9% from 34.2 +/- 2.4 mm (SEM) (P less than 0.001), with significant thinning of the wall thickness (from 8.2 to 7.7 mm, P less than 0.001). Consequently the calculated cross-sectional area (CSA) of the left ventricular wall remained the same. Peak wall stress (WSt) and EDWSt increased by 20% and 152%, respectively. During the subsequent 4 weeks, EDD progressively increased, averaging 11% above the control at 4 weeks, while EDWTh returned to the control level. Thus, the development of hypertrophy was clearly evidenced by an increase in CSA (by 8% over the control, P less than 0.001). These changes were accompanied by a consistent reduction in both peak WSt and EDWSt. Mean velocity of circumferential fiber shortening (meanVcf) and percentage shortening were significantly augmented following the onset of MR and remained at the same level thereafter, indicating no further use of the Frank-Starling mechanisms during chronic ventricular dilation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adaptations of the left ventricle to chronic volume overload induced by mitral regurgitation in conscious dogs. 293 15

Hypertrophic cardiomyopathy is a diverse clinical and pathophysiologic disorder of unknown cause that principally involves the left ventricle and is manifested as asymmetric or concentric hypertrophy. If asymmetric, the hypertrophy is usually greatest in the ventricular septum, but variations occur in which the hypertrophy may be maximal at the mid-ventricular level, at the apex, or rarely, in the free wall of the left ventricle. Right ventricular involvement is usually less evident. The principal abnormality in systole is the obstruction to left ventricular outflow caused by systolic anterior motion (SAM) of the anterior or posterior mitral leaflet(s) with mitral leaflet-septal contact. SAM occurs as the result of the Venturi forces created by the rapid ejection of blood through an outflow tract that is narrowed by upper septal hypertrophy, drawing the mitral leaflet(s) anteriorly. The time of onset and duration of mitral leaflet-septal contact determine the magnitude of the pressure gradient. Mitral regurgitation invariably accompanies the obstruction to outflow. Ventriculomyectomy surgery, by thinning the septum and widening the outflow tract, abolishes the abnormal mitral leaflet motion and, consequently, the obstruction to outflow and the mitral regurgitation. In symptomatic patients with resting obstruction this form of surgery more dramatically relieves the systolic abnormalities and the accompanying symptoms than any form of medical therapy currently available. The extent of hypertrophy is believed to be the principal determinant of impaired left ventricular relaxation and increased chamber stiffness that characterize diastole in hypertrophic cardiomyopathy. Diastolic dysfunction is common to most such patients irrespective of the presence or absence of outflow obstruction. Calcium entry blockers may improve the left ventricular relaxation process and relieve symptoms in patients with hypertrophic cardiomyopathy, particularly the subgroup with no obstruction to outflow. Atrial and ventricular arrhythmias are responsible for a significant proportion of the morbidity and mortality, and their prevalence appears to depend on the presence of obstruction and the extent of hypertrophy. Thus, the major manifestations of hypertrophic cardiomyopathy in systole and diastole, as well as the disturbances in rhythm, appear to be related to the site and/or extent of the hypertrophic process. We have learned much about hypertrophic cardiomyopathy in the 30 years since its modern description. The vast majority of symptomatic patients can now be improved with specific medical or surgical therapy.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Hypertrophic cardiomyopathy. 306 84

Hypertrophic cardiomyopathy is a diverse clinical and pathophysiologic entity that involves principally the left ventricle and is caused by asymmetric or concentric hypertrophy of unknown cause. If asymmetric, the hypertrophy is usually greatest in the ventricular septum, but variations occur in which the hypertrophy may be maximal at the apex, at the midventricular level, or, rarely, in the free wall of the left ventricle. Right ventricular involvement is usually less evident. The principal abnormality in systole is the obstruction to left ventricular outflow caused by upper septal hypertrophy narrowing the outflow tract and setting the stage for Venturi forces to cause systolic anterior motion of the anterior or posterior mitral leaflets. The time of onset and duration of mitral leaflet-septal contact determine the magnitude of the pressure gradient. Mitral regurgitation invariably accompanies the obstruction to outflow. Ventriculomyotomy-myectomy surgery, by thinning the septum and widening the outflow tract, abolishes the abnormal mitral leaflet motion and, consequently, the obstruction to outflow and the mitral regurgitation. This form of surgery more dramatically relieves the systolic abnormalities and the accompanying symptoms than any form of medical therapy available today. The extent of hypertrophy is believed to be the principal determinant of the impaired left ventricular relaxation and increased chambers stiffness (decreased compliance) that characterize diastole in hypertrophic cardiomyopathy. Relaxation is impaired by the contraction load (the obstruction), by a decrease in the principal relaxation loads, by a pathologic degree of nonuniformity of contraction and relaxation, and in all likelihood, by impaired inactivation of the biochemical processes responsible for contraction (? due to primary or ischemia-induced calcium overload). Calcium channel-blocking agents may dramatically improve left ventricular relaxation by speeding up the inactivation process, by decreasing the degree of nonuniformity, or by altering the contraction and relaxation loads in a favorable manner. Atrial and ventricular arrhythmias are responsible for a significant proportion of the morbidity and mortality, and their occurrence also appears to depend on the extent of hypertrophy. Thus, the major manifestations of hypertrophic cardiomyopathy in systole and diastole as well as the disturbances of rhythm appear to be related to the site and/or extent of the hypertrophic process.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Hypertrophic cardiomyopathy. The importance of the site and the extent of hypertrophy. A review. 316 67

Mitral regurgitation (MR) reportedly develops by ischemia of the papillary muscles, which is called papillary muscle dysfunction. This report deals with the roles of papillary muscles and left ventricular walls on the pathogenesis of MR using graded injuries of these structures in 23 dogs. Implanted ultrasonic microcrystal and occluder with an electromagnetic flowmetry for the left circumflex coronary artery were the main experimental setting. Graded occlusion of the artery was done by the six-step approach regarding coronary blood flow (CBF) reduction (C1-C6). Left ventricular (LV) pressure, systolic thickening (%W: sonomicrometry) of the LV anterior (AW) and posterior walls (PW), and systolic longitudinal shortening (%S: sonomicrometry) of both the anterior and posterior papillary muscles (PPM) were measured. MR was assessed by left ventricular contrast two-dimensional echocardiography. In eight dogs, all the data were adequate for analysis. In category 3 (C3: 55-70% CBF of control), %S in PPM decreased, but %W did not change significantly, and only mild MR developed in three of the eight dogs. MR clearly developed in category 4 (C4: 40-54% CBF as compared with the control stage), where %S was replaced by holosystolic lengthening and %W reduced to 50% of the control state, and total occlusion (C6) accompanied by significant thinning of both the PW and AW. Thus, the asynergy of the LVPW was needed to induce the MR in seven of the eight dogs. It was concluded that the injury of the PPM alone is not sufficient to cause MR, and the associated ischemic changes of the LV free wall as well as LV dilatation are necessary to induce severe MR.
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PMID:[Experimental mitral regurgitation in ischemia-induced papillary muscle dysfunction]. 325 3

The significance of a combined echocardiographic study of patients who survived myocardial infarction for evaluation of ventricular hemodynamic disturbances was shown. According to the ultrasonic B-scanning data the left ventricular end-diastolic and endsystolic volumes in such patients were increased, and ejection fraction values, delta S and VCF were markedly decreased. The most pronounced left ventricular pump and contractility dysfunctions occurred in transmural and anterior myocardial infarctions. During M-mode echocardiography in patients with posterior wall hypokinesia, the prolongation of isovolumic relaxation and contraction followed by the shortening of rapid filling was observed. A significance correlation between the prolongation of isovolumic relaxation and polygraphic T interval was found. The thinning of the left ventricular hypokinetic posterior wall was observed during the ejection period, and that of hypokinetic ventricular septum was seen within the cardiac cycle. The signs of more marked left ventricular dilatation with its decreased contractility were found in patients with systolic murmur recorded soon after myocardial infarction development. Such a murmur phonocardiographically recorded was a sign of mitral valve insufficiency.
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PMID:[Left ventricular function in patients who have had a myocardial infarct, based on echocardiographic study data]. 650 23

We prospectively evaluated 50 patients with mitral stenosis (43 women and 7 men; mean age 45 years) to assess the results of surgical reconstruction of the mitral valve. All patients underwent a complete echocardiographic examination before and after operation. Surgical reconstruction was extensive, and included commissurotomy, thinning of the valvular leaflets, calcification removal, splitting of subvalvular apparatus, and posterior annuloplasty. Surgical reconstruction resulted in increasing mitral functional area from 0.89 +/- 0.23 to 2.07 +/- 0.42 cm2. NYHA functional class decreased from 2.76 +/- 0.55 to 1.52 +/- 0.71. Before discharging, 10% of patients had moderate mitral insufficiency. All patients were followed at 6-month intervals in our clinic. Mean follow-up was 37 +/- 18 months. During follow-up 5 patients (10%) developed severe mitral incompetence, which required mitral valve replacement. Chi-square and Student t-test were used to analyze the correlation between variables and outcome. The occurrence of severe mitral incompetence was correlated with: the degree of enlarged left atrium; chronic atrial fibrillation; postoperative more than mild mitral regurgitation. No correlation was found with anatomical parameters detected by echocardiography, or intraoperative anatomy. In conclusion, surgical reconstruction of mitral stenosis provides satisfactory short-term results. We believe that the low mortality rate and the low incidence of complications justify an effort to save the native mitral valve before considering prosthetic replacement. More attention to the development of residual mitral incompetence with intraoperative control may improve long-term results.
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PMID:[Conservative surgical treatment of rheumatic mitral stenosis]. 755 96


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