Propranolol in mitral stenosis during sinus rhythm

Patients with early symptomatic mitral stenosis usually suffer from pulmonary congestion on the basis of left atrial and pulmonary venous hypertension. They are often in sinus rhythm, and cardiac output is usually well maintained. Symptoms occur most often when heart rate, cardiac output, or both are increased. In this study, intravenous propranolol administered to patients with pure mitral stenosis in sinus rhythm resulted in significant reductions in mitral diastolic gradient (-7.1 mm. Hg +/- 1.6 SED), mean pulmonary wedge pressure (--6.9 mm. Hg +/- 1.2) and mean pulmonary artery pressures (--9.0 mm. Hg +/- 1.2). This was due to simultaneous reduction of heart rate (--13.0 beats/minute +/- 2.6 and cardiac output (--0.5 L./minute +/- 0.2). A small associated reduction of left ventricular systolic pressure (--5.1 mm. Hg +/- 2.6) was not accompanied by adverse clinical effects. A potential role for propranolol in medical management of pure mitral stenosis in the presence of sinus rhythm is suggested.     

Congestive heart failure in patients with valvular aortic stenosis. A clinical and echocardiographic Doppler study

The aim of this study was to evaluate echographically anatomic and functional features of the left ventricle in adult patients with valvular aortic stenosis according to the presence or absence of congestive heart failure and the level of ventricular performance. Fifty-six adult patients with moderate-to-severe aortic stenosis underwent echocardiographic Doppler examination in order to evaluate left ventricular mass and dimensions, systolic function and filling dynamics. Twenty-seven patients had no heart failure and were symptomatic for angina (5), syncope (4) or were symptom-free (group I); the other 29 had heart failure (group II): 16 with normal left ventricular systolic performance (fractional shortening > 25%, group IIa) and 13 with systolic dysfunction (fractional shortening < or = 25%, group IIb). Despite a similar left ventricular mass, compared to group IIa, group IIb showed a significant left ventricular dilatation (end-diastolic diameter: 61 +/- 6.5 vs. 45.5 +/- 6.1 mm, p < 0.001) and mild or no increase in wall thickness (11.5 +/- 1.6 vs. 14.9 +/- 2 mm, p < 0.001). Indices of left ventricular filling on Doppler transmitral flow were also significantly different between the two groups, with a higher early-to-late filling ratio and a shorter deceleration time of early filling in group IIb (2.8 +/- 1.9 vs. 1.2 +/- 0.85, p < 0.01, and 122 +/- 66 vs. 190 +/- 87 ms, p < 0.05, respectively), both indirectly indicating higher left atrial pressure. Finally, heart failure was generally more severe in group IIb patients. In some patients with aortic stenosis, symptoms of heart failure may be present despite a normal left ventricular systolic function and seem to depend on abnormalities of diastolic function. The presence of systolic or isolated diastolic dysfunction appears to be related to a different geometric adaptation of the left ventricle to chronic pressure overload.     

Stress-induced left ventricular outflow tract obstruction: a potential cause of dyspnea in the elderly

OBJECTIVES: We sought to identify the pattern of disturbed left ventricular physiology associated with symptom development in elderly patients with effort-induced breathlessness. BACKGROUND: Limitation of exercise tolerance by dyspnea is common in the elderly and has been ascribed to diastolic dysfunction when left ventricular cavity size and systolic function appear normal. METHODS: Dobutamine stress echocardiography was used in 30 patients (mean [+/-SD] age 70 +/- 12 years; 21 women, 9 men) with exertional dyspnea and negative exercise test results, and the values were compared with those in 15 control subjects. RESULTS: Before stress, left ventricular end-diastolic and end-systolic dimensions were reduced, fractional shortening was increased, and the basal septum was thickened (2.3 +/- 0.5 vs. 1.4 +/- 0.2 cm, p < 0.001, vs. control subjects) in the patients, but posterior wall thickness did not differ from that in control subjects. Left ventricular outflow tract diameter, measured as systolic mitral leaflet septal distance, was significantly reduced (13 +/- 4.5 vs. 18 +/- 2 mm, p < 0.001). Isovolumetric relaxation time was prolonged, and peak left ventricular minor axis lengthening rate was reduced (8.1 +/- 3.5 vs. 10.4 +/- 2.6 cm/s, p < 0.05), suggesting diastolic dysfunction. Transmitral velocities and the E/A ratio did not differ significantly. At peak stress, heart rate increased from 66 +/- 8 to 115 +/- 20 beats/min in the control subjects, but blood pressure did not change. Transmitral A wave velocity increased, but the E/A ratio did not change. Left ventricular outflow tract velocity increased from 0.8 +/- 0.1 to 2.0 +/- 0.2 m/s, and mitral leaflet septal distance decreased from 18 +/- 2 to 14 +/- 3 mm, p < 0.001. In the patients, heart rate rose from 80 +/- 12 to 132 +/- 26 beats/min and systolic blood pressure from 143 +/- 22 to 170 +/- 14 mm Hg (p < 0.001 for each), but left ventricular dimensions did not change. Peak left ventricular outflow tract velocity increased from 1.5 +/- 0.5 m/s (at rest) to 4.2 +/- 1.2 m/s; mitral leaflet septal distance fell from 13 +/- 4.5 to 2.2 +/- 1.9 mm (p < 0.001); and systolic anterior motion of mitral valve appeared in 24 patients (80%) but in none of the control subjects (p < 0.001). Measurements of diastolic function did not change. All patients developed dyspnea at peak stress, but none developed a new wall motion abnormality or mitral regurgitation. CONCLUSIONS: Although our patients fulfilled the criteria for "diastolic heart failure," diastolic dysfunction was not aggravated by pharmacologic stress. Instead, high velocities appeared in the left ventricular outflow tract and were associated with basal septal hypertrophy and systolic anterior motion of the mitral valve. Their appearance correlated closely with the development of symptoms, suggesting a potential causative link.     

The effect of the ingestion of ethanol on obstruction of the left ventricular outflow tract in hypertrophic cardiomyopathy

BACKGROUND: Ethanol causes vasodilation, which might have an adverse effect, due to increased obstruction of the left ventricular outflow tract, in patients with hypertrophic obstructive cardiomyopathy. We assessed the hemodynamic effects of the ingestion of ethanol, in an amount commonly consumed socially, in patients with hypertrophic cardiomyopathy. METHODS: We performed echocardiography in 36 patients before and several times after the ingestion of either 50 ml of 40 percent ethanol or an isocaloric placebo with the aroma of rum. Each patient received both ethanol and placebo, on different days. The patients, but not the physicians, were blinded to the content of the drink. We measured the sizes of the left atrium and left ventricle, the left-ventricular-wall thickness, blood pressure, heart rate, the degree of systolic anterior motion of the mitral valve, and the pressure gradient across the left ventricular outflow tract. RESULTS: The ingestion of ethanol regulated in a significant drop in the mean (+/- SD) systolic blood pressure (from 130.5 +/- 18.6 to 122.5 +/- 20.3 mm Hg, P<0.001), a significant increase in systolic anterior motion of the mitral valve (from a grade of 2.1 to a grade of 2.5, P<0.001), and a 63 percent increase in the mean gradient across the left ventricular outflow tract (from 38.1 +/- 26.5 to 62.2 +/- 42.4 mm Hg, P<0.001). These changes, which were not associated with symptoms, did not occur after the ingestion of placebo. CONCLUSION: The ingestion of a small amount of ethanol caused an increase in the gradient across the left ventricular outflow tract in patients with hypertrophic obstructive cardiomyopathy, which could have and adverse clinical effect.     

Magnesium transport across the basolateral plasma membrane of the fish enterocyte

The aim of the study was to assess the influence of aortic valve replacement on left ventricular size and muscle hypertrophy according to the type of preexisting valve disease (aortic stenosis, insufficiency or combined disease). The study group consisted of 143 consecutive patients (pts) after aortic valve replacement (109 men, 34 women, mean age 48.1 +/- 10.9 years). Reason for the operation was aortic stenosis in 35 pts, aortic insufficiency in 64 pts and combined disease in 44 pts. Echocardiography was performed before surgery, 1 month and 1 year after operation, and yearly during 5-year follow-up. Transvalvular aortic pressure gradients decreased significantly after valve replacement in all subsets without further changes during follow-up (Pmax (mmHg): from 54.2 +/- 20.7 to 17.9 +/- 9.6 in combined disease pts, from 72.3 +/- 19.9 to 21.6 +/- 14.6 in aortic stenosis and from 34.5 +/- 24.2 to 15.6 +/- 11.3 in aortic insufficiency pts, respectively, P < 0.0005). One year after surgery the diastolic dimension of the left ventricle decreased significantly in all subjects, whereas the systolic dimension only in aortic insufficiency and combined disease pts (from 44 +/- 11.8 to 31.6 +/- 5.4 mm, P < 0.001 and from 41.9 +/- 11.5 to 33 +/- 6.7 mm, P < 0.05, respectively). Further decrease of both diastolic and systolic dimensions was observed only in the aortic insufficiency group. Ejection fraction of left ventricle increased only in combined disease pts (from 51.6 +/- 10% to 56.8 +/- 8.2%, P < 0.05). Wall thickness of the left ventricle decreased 1 year after valve replacement only in the aortic stenosis group and in further follow-up in the aortic stenosis and combined disease group. Normalization of left ventricular size is observed in more than 90% of patients during 5-year follow-up as opposed to left ventricular muscle hypertrophy, regressed only in less than a half of the study population. In patients with aortic valve disease the greatest hemodynamic improvement is observed 1 year after valve replacement. This is expressed by marked reduction of the left ventricular dimensions and wall thickness, without significant improvement of the ejection fraction. Further regression of left ventricle dimensions occurs in patients operated on due to predominant valve insufficiency, whereas regression of left ventricular hypertrophy is observed in patients with preexisting valvular stenosis.     

Effects of cardiomyoplasty on right ventricular filling during volume loading

BACKGROUND: Although cardiomyoplasty (CMP) is thought to improve ventricular systolic function, its effects on ventricular diastolic function are not clear. Especially the effects on right ventricular diastolic filling have not been fully investigated. Because pericardial influences are more pronounced in the right ventricle than in the left ventricle, CMP with its external constraint may substantially impair right ventricular diastolic filling. METHODS: Fourteen purebred adult beagles were used in this study. Seven underwent left posterior CMP, and 7 underwent a sham operation with a pericardiotomy and served as controls. Four weeks later, the hemodynamic effects of CMP were evaluated by heart catheterization before and after volume loading (central venous infusion of 10 mg/kg of 4.5% albumin solution for 5 minutes). RESULTS: In the CMP group, mean right atrial pressure and right ventricular end-diastolic pressure increased significantly from 3.1 +/- 1.2 mm Hg to 6.1 +/- 2.0 mm Hg (p < 0.001) and from 4.0 +/- 1.8 mm Hg to 9.6 +/- 2.5 mm Hg (p < 0.001), respectively. Volume loading in the control group did not significantly increase either variable. Right ventricular end-diastolic volume and stroke volume did not change significantly (from 53 +/- 9.3 mL to 60 +/- 9.0 mL and from 20 +/- 2.3 mL to 21 +/- 3.2 mL, respectively) in the CMP group. In the control group, however, right ventricular end-diastolic volume and stroke volume increased significantly from 45 +/- 7.7 mL to 63 +/- 14 mL (p < 0.05) and from 18 +/- 4.3 mL to 22 +/- 4.2 mL (p < 0.05), respectively. CONCLUSIONS: These results suggest that CMP may reduce right ventricular compliance and restrict right ventricular diastolic filling in response to rapid volume loading because of its external constraint.     

Evaluation of left atrial contribution to left ventricular filling in aortic stenosis by velocity-encoded cine MRI

Velocity-encoded cine MRI (VEC-MRI) can measure volume flow at specified site in the heart. This study used VEC-MRI to measure flow across the mitral valve to compare the contribution of atrial systole to left atrial filling in normal subjects and patients with left ventricular hypertrophy. The study population consisted of 12 normal subjects (mean age 34.5 years) and nine patients with various degrees of left ventricular hypertrophy resulting from aortic stenosis (mean age 70 years). VEC-MRI was performed in double-oblique planes through the heart to measure both the mitral inflow velocity pattern (E/A ratio) and the volumetric flow across the mitral valve. The left atrial contribution to left ventricular filling (AC%) was calculated. The results were compared with Doppler echocardiographic parameters. The VEC-MRI-derived mitral E/A ratios showed a significant linear correlation with E/A ratios calculated from Doppler echocardiography (r = 0.94), and the VEC-MRI-derived E/A ratios (2.1 +/- 0.5 vs 1.0 +/- 0.4) and AC% values (24.9 +/- 7.2 vs 45.7 +/- 16.4) were significantly different between normal subjects and patients with aortic stenosis (p < 0.01 in both groups). The same differences were seen in the Doppler echocardiographic parameters. The VEC-MRI-derived E/A ratio and AC% showed significant hyperbolic and linear correlations with left ventricular mass indexes (r = 0.95 and 0.86). In addition, the VEC-MRI-determined E/A ratio and the volumetric AC% displayed a highly significant hyperbolic correlation (r = 0.95). Thus VEC-MRI can be used to evaluate left ventricular diastolic filling characteristics in normal subjects and patients with abnormalities of diastolic filling.     

Changes in left ventricular diastolic function 6 months after nonsurgical septal reduction therapy for hypertrophic obstructive cardiomyopathy

BACKGROUND: Nonsurgical septal reduction therapy (NSRT) decreases left ventricular outflow tract (LVOT) gradient and improves symptoms in patients with hypertrophic obstructive cardiomyopathy (HOCM). NSRT effects on LV/left ventricular diastolic function are currently unknown. METHODS AND RESULTS: HOCM patients (n=29) had Doppler echocardiography at baseline and 6 months after NSRT to evaluate changes in LV volume, pre-A-wave pressure, early diastolic mitral annulus velocity (Ea) by tissue Doppler, and tau. At 6 months, a significant reduction in LVOT gradient (from 53.6+/-15 to 6+/-5 mm Hg; P<0.001) was accompanied by improvement in exercise duration (from 284+/-147 to 408+/-178 seconds; P=0.04) and New York Health Association class (from III to I; P<0.001). Pre-A pressure (18+/-6 to 14+/-5 mm Hg; P<0.01) and tau (62+/-8 to 51+/-8 ms; P<0.01) decreased, whereas Ea (5.8+/-1.8 to 8+/-1.8 cml/s; P<0.01) and LV end-diastolic volume (117+/-16 to 130+/-22 mL; P<0.01) increased. CONCLUSIONS: NSRT improves LV relaxation and compliance, which contributes to the symptomatic relief seen at 6 months.     

Partial left ventriculectomy with mitral valve preservation in the treatment of patients with dilated cardiomyopathy

OBJECTIVE: This study reports initial results of partial left ventriculectomy performed with preservation of the mitral valve in the treatment of 27 patients with idiopathic dilated cardiomyopathy. METHODS: Patients were in New York Heart Association class III or IV. Partial ventriculectomy was performed as an isolated procedure in four patients and associated with mitral annuloplasty in 23 patients. There were four hospital deaths (14.8%) and the remaining patients were followed for 11.2 +/- 6 months. RESULTS: Decrease of left ventricular diastolic diameter (81.8 +/- 8.7 to 68.5 +/- 7.6 mm, p < 0.001) and improvement of left ventricular wall shortening (12% +/- 3.1% to 18.1% +/- 3.9%, p < 0.001) were demonstrated by echocardiography after the operation. Left ventricular radioisotopic angiography showed reduction of diastolic volume (495 +/- 124 ml to 352 +/- 108 ml, p < 0.001) and increase of ejection fraction (17.7% +/- 4.6% to 23.7% +/- 8.8%, p < 0.001). Right-sided heart catheterization demonstrated improvement of stroke index (24.3 +/- 7.7 ml/m2 to 28.3 +/- 7.6 ml/m2, p < 0.01) and decrease of pulmonary wedge pressure (23.2 +/- 8.8 mm Hg to 17 +/- 7 mm Hg, p < 0.01). Similar results were documented at 6 and 12 months of follow-up. Functional class improved from 3.6 +/- 0.5 to 1.4 +/- 0.6 (p < 0.001). However, seven patients died at midterm follow-up because of heart failure progression or arrhythmia-related events, and survival rate was 59.2% +/- 9.4% from 6 to 24 months of follow-up. CONCLUSIONS: Partial left ventriculectomy performed with preservation of the mitral valve improves left ventricular function and congestive heart failure in patients with dilated cardiomyopathy. Nevertheless, the high incidences of heart failure progression and arrhythmia-related deaths observed after this procedure preclude its wide clinical application.     

Comparison of immediate hemodynamic response to closed mitral commissurotomy, single-balloon, and double-balloon mitral valvuloplasty in rheumatic mitral stenosis

The hemodynamic response to closed mitral commissurotomy, single-balloon, and double-balloon mitral valvuloplasty was compared using 20 patients in each group. All patients had symptomatic rheumatic mitral stenosis with a mitral valve area < 1 cm2, without any left atrial clot, mitral valve calcification, or mitral regurgitation. There was a significant improvement in hemodynamics following intervention in all three groups. The mean pulmonary artery pressure decreased from 49.1 +/- 17.5 to 28.6 +/- 8.3 mm Hg (p < 0.001), 48.8 +/- 12.3 to 34.0 +/- 13.9 mm Hg (p < 0.001), and 46.7 +/- 18.0 to 26.3 +/- 13.7 mm Hg (p < 0.001) in the closed mitral commissurotomy, single-balloon, and double-balloon mitral valvuloplasty groups, respectively. The mitral valve area increased from 0.62 +/- 0.27 to 1.5 +/- 0.5 cm2 (p < 0.001), 0.68 +/- 0.24 to 1.5 +/- 0.4 cm2 (p < 0.001), and 0.68 +/- 0.25 to 1.9 +/- 0.8 cm2 (p < 0.001) in the closed mitral commissurotomy, single-balloon, and double-balloon mitral valvuloplasty groups, respectively. The increase in the mitral valve area was maximum in the group with double-balloon mitral valvuloplasty. In the closed mitral commissurotomy group there was a significant rise in left ventricular end-diastolic pressure, from 6.8 +/- 3.9 to 9.3 +/- 3.1 mm Hg (p < 0.001), but this remained unchanged in the single-balloon and double-balloon mitral valvuloplasty groups. Our study shows that single-balloon and double-balloon mitral valvuloplasty are comparable to closed mitral commissurotomy in the immediate hemodynamic response, with a larger valve area in the double-balloon mitral valvuloplasty group.     

Managing complex orthodontic problems: the use of implants for anchorage

In congestive heart failure captopril modifies the left ventricular filling pattern mainly by unloading the heart. We investigated whether the structural characteristics of the left ventricle may influence the acute effects of captopril on this pattern in patients with untreated hypertensive (H group, 6 patients) or idiopathic (I group, 14 patients) cardiomyopathy. We evaluated changes of pulsed Doppler mitral flow, of systemic arterial and wedge pulmonary pressures 40 min after 25 mg captopril administered sublingually, and correlated these changes with the M-mode echocardiographic relative wall thickness index (h/r). Baseline mean arterial pressure (H = 137 +/- 20 mm Hg, mean +/- SD, I = 95 +/- 19 mm Hg; p < 0.001), and h/r (H = 0.38 +/- 0.03, I = 0.28 +/- 0.09; p < 0.05) were greater in the high blood pressure group; wedge pressure, echocardiographic biplane ejection fraction, and Doppler indexes of the left ventricular filling were similar in the two populations. After captopril, ejection fraction did not change significantly, mean arterial pressure decreased significantly in hypertensive patients (H group, baseline = 137 +/- 20, captopril = 119 +/- 10, p = 0.02; I group, baseline = 95 +/- 19, captopril = 90 +/- 24, p = nonsignificant), and the wedge pressure was reduced by the same extent in both groups (H group, baseline = 27.7 +/- 3, captopril = 21 +/- 7, p < 0.05; I group, baseline = 20 +/- 12, captopril = 15 +/- 8, p < 0.05). In the H group early mitral flow increased [(E wave integral) x (mitral annulus area)] by 38 +/- 15%, and was almost steady in the I group (-1.3 +/- 30%; group H vs. I = p < 0.01); late mitral flow [(A wave integral) x (mitral annulus area)] showed a pattern exactly opposite to this (H = +0.4 +/- 40%, I = +38 +/- 19; p < 0.01). In the whole population there was a significant correlation between the early/late flow ratio variations and baseline h/r (r = 0.6, p < 0.05). In chronic congestive heart failure, changes in left ventricular filling with captopril are related to h/r: a higher index, as recorded in the H group, is associated with "true normalization' of the filling pattern after captopril; a lower index, as recorded in the I group, is associated with "pseudonormalization' despite a similar decrease of left ventricular filling pressure.     

Relation between mitral orifice surface area and extent of hemodynamic disorder of the pulmonary circulation in patients with mitral stenosis

Mitral annulus and valves form the mitral orifice area with the size between 4.0-6.0 cm2. Every area which is smaller than this, represents mitral stenosis. As a consequence of mitral stenosis hemodynamic gradients occur over the mitral orifice with circulation disturbances below and above the stenotic mitral valve. The size of transmitral gradient is important in the evaluation of functional or/and structural changes in the blood vessels of pulmonary circulation. This investigation included 40 patients with mitral stenosis (or accompanying minimal mitral regurgitation). All patients underwent echocardiographic examination: area of the mitral orifice was determined and hemodynamic procedure with the left and right heart catheterization was performed. The following hemodynamic parameters were measured: mean capillary wedge pressure, left ventricular filling pressure, left ventricular mean diastolic pressure, mean pulmonary artery pressure. According to these parameters resistance in the pulmonary circulation was measured. The size of the mitral orifice was determined according to oximetry blood analyses and hemodynamic parameters. All patients were divided into 4 groups: minimal (2.5-4.0 cm2), mild (1.5-2.5 cm2), moderate (1.0-1.5 cm2) and severe mitral stenosis (1.0 cm2). The comparison of echocardiographic and hemodynamic parameters revealed a high and positive correlation between the area of mitral orifice. There was also a negative and moderate correlation between the values of stenotic mitral orifice area and total pulmonary resistance, i.e. in all patients with severe mitral stenosis there was an increased pulmonary arteriolar resistance. CONCLUSION: Noninvasive echocardiographic method is valid in the evaluation of stenotic mitral valve area. In the evaluation of hemodynamic parameters in the pulmonary circulation the index of arteriolar pulmonary systemic vascular resistance is very important. In all patients with the area of stenotic mitral orifice 1.0 cm2, there are functional or pathomorphologic changes in the pulmonary circulation of the blood vessel wall.     

Left ventricular systolic torsion and early diastolic filling by echocardiography in normal humans

This study describes a novel 2-dimensional echocardiographic technique to measure left ventricular (LV) systolic twist in humans and relates this measure to early ventricular filling. LV twist is the counterclockwise rotation of the left ventricle during systole when viewed from the apex. The effect of ventricular twist has been postulated to store potential energy, which ultimately aids in diastolic recoil, leading to ventricular suction. The generated negative early diastolic pressures may augment early ventricular filling. We measured ventricular twist in 40 patients with normal transthoracic echocardiograms. End-systolic twist was determined by measuring rotation of the anterolateral papillary muscle about the center of the ventricle. LV filling was assessed by analysis of transmitral Doppler flow velocities. The mean value obtained was 9 +/- 7 degrees of rotation. Twist measurements were highly reproducible with an intraobserver correlation coefficient of r = 0.881, p <0.001. The magnitude of ventricular twist was strongly correlated positively with acceleration of the mitral E-wave (r = 0.75; p <0.0001) and negatively with the mitral E-wave acceleration time (r = -0.83; p <0.0001).     

Evaluation of the severity of aortic stenosis using 2-dimensional Doppler echocardiography

Hemodynamic evaluation of aortic ostial stenosis (AOS) was made in 89 patients at Doppler echocardiography. Maximal circulation rate (MCR) through the aortic valve averaged 3.47 +/- 0.073 m/s, maximal transaortic pressure gradient (TPG) made up 49.97 +/- 2.11 mm Hg, the aortic ostium area (AOA) amounted to 0.85 +/- 0.031 sm2. It was established that AOA evaluation is most reasonable, as MCR and TPG vary with cardiac output. Especially desirable this measurement is believed in patients with TPG under 64 mm Hg and small left ventricular ejection. Mitral regurgitation is a frequent finding in AOS patients. Unless calcinosis of the mitral ring, mitral valve affection would be absent. In mitral regurgitation the disease took a more severe course, the patients having reduced AOA and left ventricular ejection, though larger end-diastolic diameter and end-diastolic volume. The emergence of mitral regurgitation in AOS is a result of left ventricular hypertrophy and dilatation suggesting a low compensatory reserve of the myocardium.     

Percutaneous mitral commissurotomy using Inoue's balloon during pregnancy

The authors present three cases of pregnant women with symptomatic severe mitral stenosis with a mean age of 28.6 +/- 2.3 years, and during 27.6 +/- 1.52 weeks of pregnancy. Two patients were in class III and one in class IV of the New York Heart Association (NYHA). All patients had a mitral valvular area equal or less than 1 cm2, with a Wilkins score of 7 to 9 and mitral insufficiency grade I in two cases; two, had severe pulmonary arterial hypertension (mean > 50 mm Hg). After Percutaneous Mitral Valvuloplasty (PMV) the mitral valve measured by 2D echocardiography increased form 0.83 +/- 0.2 cm2 to 1.8 +/- 0.15 cm2; the mean transmitral gradient diminished from 13 +/- 3.4 mm Hg to 3.6 +/- 1.15 mm Hg; the degree of mitral insufficiency was no modified in neither case. Hemodynamic results revealed increasing of the mitral valve from 0.83 +/- 0.18 cm2 to 2.23 +/- 0.3 cm2; the mean mitral gradient decreased from 21.6 +/- 9 to 4.3 +/- 0.5 mm Hg; the mean left atrial pressure from 30 +/- 12 to 12.3 +/- 4 mm Hg; the mean pressure of the pulmonary artery diminished suddenly from 44.3 +/- 16 to 25.6 +/- 11 mm Hg. The average fluoroscopic time was 15.3 +/- 3 minutes. There were no complications. The patients were discharged 48 hours after the procedure and continued their pregnancies in class I NYHA, which resolved in a non complicated vaginal delivery with normal products. We conclude that PMV is a safe and useful therapy in pregnant patient with severe mitral stenosis refractory to medical treatment.     

Perindopril in monotherapy of primary hypertension--6 month observation

We evaluated effects of perindopril (Prestarium-SERVIER) in the treatment of the primary hypertension in 41 patients (mean age 41.6) in the I or II degrees WHO using 24 ambulatory blood pressure measurement and echocardiography. Investigation were performed before and after 3 and 6 months of the treatment. Initially 4 mg of perindopril was given and individually was increased after 3 months to 8 mg according to 24 ambulatory blood pressure measurement results. We obtained significant decrease of blood pressure in 3 (134.6/86.6 mm Hg) and in 6 (135/88, 9 mm Hg) months of treatment in comparison to baseline values (141.8/91.1 mm Hg), decrease of left ventricular mass to 244.4 g in 3 and 248.8 g after 6 months (baseline 258.5 g), as well as index of left ventricular mass, wall thickness and left ventricular end diastolic volume. There was no significant differences in: ejection, heart rate, left ventricular inflow on the successive investigations. Good effect of perindopril we observed in 31 patients (75.6%) after 6 months of treatment. We did not observe any serious side effects of perindopril. CONCLUSION: Perindopril in treatment hypertension effectively reduces the level of blood pressure (systolic, diastolic and mean) without any effect on heart rate. Prestarium reduces left ventricular mass, intraseptal wall thickness and left ventricular end diastolic volume. There is no influence on inflow to the left ventricle as well as on ejection fraction.     

Hypertrophic obstructive cardiomyopathy in pediatric patients: results of surgical treatment

Between April 1975 and May 1995, 25 pediatric patients on one hospital service underwent extended left ventricular septal myectomy because of hypertrophic obstructive cardiomyopathy. Ages ranged from 2 months to 20 years (mean, 11.2 years). Seventeen patients had moderate to severe mitral valve insufficiency. Medical therapy had failed in all patients and one patient had undergone dual-chamber pacemaker implantation without improvement. Left ventricular outflow tract gradients ranged from 50 to 154 mm Hg (mean, 99.9 +/- 25.2). Concomitant cardiac procedures included mitral valve repair (n = 2), automatic implantable cardioverter defibrillator implantation (n = 1), and closure of atrial septal defect (n = 1). Intraoperative premyectomy left ventricular outflow tract gradients ranged from 20 to 117 mm Hg (mean, 60.4 + 26.2) and postmyectomy gradients ranged from 0 to 20 mm Hg (mean, 6.6 +/- 5.9). Postmyectomy mitral insufficiency was reduced to a regurgitant fraction of 0% to 12%, and no patient required mitral valve replacement. One patient required a pacemaker because of complete heart block; on subsequent follow-up, normal sinus rhythm had returned. There was no early mortality and no instance of aortic or mitral valve injury or ventricular septal defect. Follow-up ranged from 10 months to 20 years (mean, 6.4 years). There were no late deaths. Left ventricular outflow tract gradients by echocardiography were a mean of 14.2 mm Hg with a median of 5.0 mm Hg. All patients had normal sinus rhythm. Reoperation because of recurrent left ventricular outflow tract obstruction was necessary in two patients at 3.2 years and 12.4 years after initial myectomy, respectively. All patients but one have New York Heart Association class I or II function. We conclude that extended septal myectomy is a safe and effective means of relieving cardiac symptoms and left ventricular outflow tract obstruction in pediatric patients with severe hypertrophic obstructive cardiomyopathy unresponsive to medical management, and late survivorship compares favorably with the natural history of the disease.     

Interference of mitral valve stenosis with left ventricular diastole and left atrial appendage flow

Atrial fibrillation (AF) has been reported as an independent risk factor of systemic thromboembolism. Almost half of the left atrial thrombi are located in the left atrial appendage (LAA). LAA function, reflected by LAA flow, thus has an influence on the potential of distal embolic complications. To identify factors other than atrial contraction that influence LAA flow during AF, transthoracic and transesophageal echocardiographic studies were performed on 130 patients. Seventy patients with nonrheumatic AF were divided into two groups with higher peak LAA outflow velocity (group 1) and lower peak LAA outflow velocity (group 2) at the ventricular systolic phase. Sixty patients with rheumatic AF were classified as group 3. Group 1 had a higher peak LAA outflow velocity than group 2 at both the ventricular systolic and diastolic phases. Group 2 had a higher peak LAA outflow at the ventricular diastolic phase than group 3 (18.9 +/- 8.0 vs. 11.8 +/- 7.5 cm/s, p < 0.001), whereas there was no significant difference in the peak LAA outflow at the ventricular systolic phase between the two groups (9.6 +/- 4.0 vs. 10.8 +/- 6.8 cm/s, p = NS). Group 3 was subdivided according to mitral valve area. Patients with severe mitral stenosis (mitral valve area < 1 cm2) had a significantly lower diastolic augmentation of LAA outflow velocity (difference of LAA outflow velocity between ventricle systole and diastole) than patients with mild to moderate stenosis (0.5 +/- 3.2 vs. 2.6 +/- 4.9 cm/s, p < 0.05). In conclusion, patients with rheumatic AF, especially those with severe mitral stenosis, have a lower diastolic augmentation of LAA outflow velocity. The lower diastolic augmentation of the LAA outflow velocity at the ventricular diastolic phase might result from interference with the suction effect of the left ventricular diastole by the stenotic mitral valve.     

Left ventricular diastolic filling alterations in subjects with mitral valve prolapse: a Doppler echocardiographic study

To assess left ventricular diastolic filling in mitral valve prolapse (MVP), we studied 22 patients with idiopathic MVP and 22 healthy controls matched for sex, age, body surface area and heart rate. A two-dimensional, M-mode and Doppler echocardiographic examination was performed to exclude any cardiac abnormalities. The two groups had similar diastolic and systolic left ventricular volumes, left ventricle mass and ejection fraction. Doppler measurements of mitral inflow were: E and A areas (the components of the total flow velocity-time integral in the early passive period of ventricular filling, E; and the late active period of atrial emptying, A), the peak E and A velocities (cm.s-1), acceleration and deceleration half-times (ms) of early diastolic rapid inflow, acceleration time of early diastolic flow (AT), total diastolic filling time (DFT) (ms), and the deceleration of early diastolic flow (cm.s-2). From these measurements were calculate: peak A/E ratio (A/E), E area/A area, the early filling fraction, the atrial filling fraction, AT/DFT ratio. All the Doppler measurements reported are the average of three cardiac cycles selected at end expiration. The mean peak A velocity, A/E velocity ratio, deceleration half time and atrial filling fraction were each significantly higher for subjects presenting a MVP (60 +/- 12 cm.s-1 vs 49 +/- 14, P < 0.008; 98 +/- 13% vs 64 +/- 12%, P < 0.0001; 120 +/- 36 ms vs 92 +/- 11, P < 0.002; 0.45 +/- 0.14 vs 0.36 +/- 0.08, P < 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)     

Hemodynamic effects of intravenous prenalterol in severe heart failure

Nine patients with chronic severe low output heart failure (radionuclide left ventricular ejection fraction 17 +/- 5 percent [mean +/- standard deviation], left ventricular filling pressure 26 +/- 6 mm Hg, cardiac index 1.9 +/- 0.4 liters/min per m2, left ventricular stroke work index 18 +/- 6 g-m/m2) from various causes were treated with intravenous prenalterol (a new catecholamine-like inotropic agent) in doses of 1,4 and 8 mg. Significant hemodynamic improvement occurred as measured by increased left ventricular ejection fraction (to 26 +/- 4 percent), decreased left ventricular filling pressure (to 21 +/- 8 mm Hg) and increased cardiac index (to 2.4 +/- 0.6 liters/min per m2) and left ventricular stroke work index (to 25 +/- 8 g-m/m2). Significant increases in heart rate (from 87 +/- 18 to 91 +/- 18 beats/min) and mean systemic arterial pressure (from 87 +/- 8 to 92 +/- 7 mm Hg) also occurred. Peak hemodynamic response occurred at various doses. Significant adverse effects associated with prenalterol consisted of increased ventricular ectopic beats in two patients and asymptomatic ventricular tachycardia in two patients. Thus, intravenous prenalterol produces hemodynamic improvement in patients with a chronic severe low output state but may be associated with increased ventricular ectopic activity.