Outcome of infants and children with dilated cardiomyopathy

A review of 81 infants and children with dilated, poorly contracting left ventricles without associated structural abnormalities was undertaken to identify risk factors for poor outcome, which could be used in selecting candidates for cardiac transplantation. Significant atrial or ventricular dysrhythmias, or both, were detected on presentation or during follow-up in 24 patients. Arrhythmias were present in only 8 of 51 survivors (16%) but were detected in 16 of 30 patients (53%) who died (p less than 0.05). Patients dying suddenly were even more likely to have had documented dysrhythmias (8 of 11, p less than 0.05). Left ventricular shortening fraction was similar in survivors and nonsurvivors (14.9 +/- 1.0% vs 15.3 +/- 1.7%). Left ventricular end-diastolic pressure in 44 patients who had cardiac catheterization averaged 20.8 +/- 1.6 mm Hg. Left ventricular end-diastolic pressure was significantly higher in patients who died than in those who survived (29.5 +/- 2.2 vs 15.0 +/- 1.6 mm Hg, p less than 0.001). Analysis of actuarial survival revealed that mortality was highest during the first 6 months after presentation (19% mortality). Survival declined more gradually thereafter and was 70% at 2 years, 64% at 5 years and 52% after 11.5 years. Age at initial presentation did not have any significant impact on survival. However, left ventricular end-diastolic pressure greater than 25 torr was associated with a significantly increased mortality rate (p less than 0.05). Early cardiac transplantation should be considered in patients with markedly elevated left ventricular end-diastolic pressure or complex atrial or ventricular arrhythmias.     

Postoperative regression of left ventricular dimensions in aortic insufficiency: a long-term echocardiographic study

The ability of preoperative M-mode echocardiography to predict the clinical course and the decrease in left ventricular size was assessed in 42 patients after uncomplicated valve replacement for isolated aortic insufficiency. During follow-up study, one patient died of chronic heart failure. The New York Heart Association functional class of the 41 survivors improved from 2.4 to 1.2. All patients had a preoperative M-mode echocardiogram. Serial echocardiographic measurements, available in 33 patients, showed a sustained decrease in left ventricular end-diastolic dimension after the first postoperative year from 73 +/- 8 to 57 +/- 9 mm at 6 to 12 months and to 53 +/- 9 mm at 3 years postoperatively (p less than 0.01). Left ventricular cross-sectional area decreased from 31 +/- 8 to 26 +/- 7 cm2 and then to 23 +/- 5 cm2 at the latest follow-up study (p less than 0.01). At 3 years postoperatively, M-mode echocardiograms were available in 37 patients: 24 had a normal left ventricular dimension (group 1), while 13 still had an enlarged left ventricle (group 2). The clinical course in these two groups was similar. The best preoperative predictor of persistent left ventricular enlargement was the end-diastolic dimension (p less than 0.05), whereas fractional shortening and the end-diastolic radius/thickness ratio were not predictive.(ABSTRACT TRUNCATED AT 250 WORDS)     

Correlation of continuous-wave Doppler assessment of chronic aortic regurgitation with hemodynamics and angiography

Fifteen patients with chronic aortic regurgitation (AR) were studied by cardiac catheterization and continuous-wave (CW) Doppler echocardiography. The slope of the AR CW Doppler signal was higher in patients with severe AR (5.7 +/- 2.1 m/s2) than in those with moderate (2.5 +/- 1.3 m/s2) or mild (1.8 +/- 0.7 m/s2) AR (p less than 0.05). The slopes in patients with mild (less than or equal to 18 mm Hg), moderate (19 to 24 mm Hg) and severe (greater than 24 mm Hg) elevation of left ventricular end-diastolic pressure were significantly different (1.9 +/- 0.6, 3.3 +/- 1.2 and 7.1 +/- 0.4 m/s2, respectively, p less than 0.05). Patients with severe AR had shorter pressure half-times than those with mild AR (283 +/- 141 vs 820 +/- 393 ms, p less than 0.05). There was a significant correlation between the slope and left ventricular end-diastolic pressure (r = 0.80, p less than 0.001) and a weaker inverse correlation between pressure half-time and left ventricular end-diastolic pressure (r = -0.59, p less than 0.05). The end-diastolic pressure gradient estimated from CW Doppler using a simplified Bernoulli equation correlated poorly with the catheter measured gradient (r = 0.59, p less than 0.02). The slope of the CW Doppler signal is a better predictor of severity than pressure half-time and is affected by left ventricular end-diastolic pressure in addition to angiographic severity of AR.     

Balloon valvuloplasty for recurrent aortic stenosis after surgical valvotomy in childhood: immediate and follow-up studies

The immediate and intermediate-term effects of balloon valvuloplasty were assessed at cardiac catheterization in nine children with recurrent stenosis after a previous surgical aortic valvotomy. At valvuloplasty the patients ranged in age from 0.35 to 16 years and had undergone surgical valvotomy 0.3 to 12.5 years previously. Balloon valvuloplasty immediately reduced the peak systolic aortic stenosis gradient by 53%, from 88 +/- 9 (mean +/- SEM) to 41 +/- 6 mm Hg (p = 0.004). The left ventricular systolic pressure was reduced from 189 +/- 8 to 157 +/- 8 mm Hg (p = 0.001) and the left ventricular end-diastolic pressure from 17 +/- 1 to 14 +/- 2 mm Hg (p = 0.025). The heart rate and cardiac index remained unchanged. Before valvuloplasty, one patient had 1 + and two patients had 2+ aortic insufficiency. In six of nine patients, balloon valvuloplasty caused no change in the degree of valvular insufficiency. Two patients had a 1 + increase (from 0 to 1 + insufficiency in both), and one patient with no insufficiency developed 2+ aortic insufficiency. Elective follow-up catheterization was performed 0.8 to 2.5 years (mean 1.5 +/- 0.2) after valvuloplasty. At follow-up, the peak aortic stenosis gradient remained significantly reduced from the gradient before valvuloplasty (37 +/- 5 versus 85 +/- 10 mm Hg, p = 0.002). The gradient had not changed significantly from that measured immediately after valvuloplasty (37 +/- 5 versus 38 +/- 5 mm Hg, p = 0.75). At follow-up, aortic insufficiency had decreased from that immediately after valvuloplasty in three patients and had increased in two.(ABSTRACT TRUNCATED AT 250 WORDS)     

Postinfarction ventricular septal rupture: the importance of location of infarction and right ventricular function in determining survival

Over a 5.5 year period, 1264 consecutive patients with acute myocardial infarction as confirmed by enzyme levels were prospectively identified. Of these, 25 (2%) suffered ventricular septal rupture (pulmonary/systemic flow range 1.5 to 6) 7 +/- 7 days after onset of myocardial infarction. Death occurred in 14 patients (56%) and was more common after inferior than anterior myocardial infarction (11 of 15 [73%] vs three of 10 [30%], p less than .05). Among 133 variables analyzed, survivors and nonsurvivors were similar with respect to all premorbid clinical characteristics, infarct size as assessed by peak creatine kinase values, shunt size, two-dimensional echocardiographic and hemodynamic indexes of left ventricular function, and extent of coronary disease. Compared with survivors, the nonsurvivors had greater impairment of right ventricular function as determined by a higher two-dimensional echocardiographically derived right ventricular wall motion index (RVWMI) (0.55 +/- 0.87 vs 1.70 +/- 0.45, p less than .001), greater elevation of right ventricular end-diastolic pressure (11 +/- 6 vs 17 +/- 6, p less than .02), and greater mean right atrial pressure (10 +/- 6 vs 16 +/- 3, p less than .01). Of interest, two of the three patients who presented with anterior myocardial infarction and who died had inferiorly extended infarcts and all had abnormal RVWMIs (greater than or equal to 1.0). As expected, cardiogenic shock shortly after onset of ventricular septal rupture was associated with a 91% mortality, but was more common after inferior than anterior myocardial infarction (60% vs 20%, p less than .05). The mean effective cardiac index was also higher in survivors than nonsurvivors (2.1 +/- 0.5 vs 1.2 +/- 0.5, p less than .001). Finally, multivariate analysis indicated that all nonsurvivors could be identified based on: an effective cardiac index of 1.75 liters/min/m2 or less, the presence of extensive right ventricular and septal dysfunction on the two-dimensional echocardiogram, a mean right atrial pressure of 12 mm Hg or more, and early onset of ventricular septal rupture. Thus, our data demonstrate that: mortality is higher when ventricular septal rupture complicates inferior than when it complicates anterior myocardial infarction, survivors can be distinguished from nonsurvivors and the prediction of outcome is highly accurate, and combined right ventricular and septal dysfunction has a substantial impact on prognosis.     

Noninvasive evaluation of left ventricular performance by the shortest distance between mitral leaflets coaptation and interventricular septum at end-systole.

We attempted to evaluate left ventricular performance from the shortest distance between the mitral leaflets coaptation and the interventricular septum at end-systole (MVC-IVS distance). The subjects were 37 patients with coronary artery disease (CAD) with prior myocardial infarction (MI), 8 with CAD without prior MI, 22 with atypical chest pain, and 4 with aortic regurgitation. The MVC-IVS distance was measured on a two-dimensional echocardiogram obtained from the parasternal or apical long-axis view and frozen at end-systole. Left ventricular end-systolic volume and end-diastolic volume were obtained by left ventriculography, and the left ventricular ejection fraction was calculated. A significant positive correlation was observed between the MVC-IVS distance and the end-systolic volume (r = 0.83, p less than 0.001); a close correlation was observed between the MVC-IVS distance end-systolic volume and ejection fraction by monoexponential fitting (r = -0.91, p less than 0.001). Thus, a significant negative correlation was observed between the MVC-IVS distance and the left ventricular ejection fraction (LVEF) (r = -0.83, p less than 0.001). An MVC-IVS distance of greater than or equal to 30 mm suggests diagnosis of left ventricular dysfunction (LVEF less than 50%) with high sensitivity (94.4%) and specificity (90.6%), while a value less than 30 mm suggests that the left ventricular performance is likely to be normal. Thus one can easily evaluate the left ventricular performance noninvasively using this new index.     

Left ventricular shape, afterload and survival in idiopathic dilated cardiomyopathy

Because idiopathic dilated cardiomyopathy is characterized by elevated wall stress and a more spherical left ventricle, the relations among shape, afterload and survival were examined. Thirty-six patients with cardiomyopathy were prospectively studied by two-dimensional echocardiography. Data included echocardiographic short- and long-axis cavity dimensions, their ratio and, with cuff systolic blood pressure, meridional and circumferential end-systolic stress and their ratios. Survivors (n = 16) were followed up for 52 months (range 40 to 76); nonsurvivors (n = 20) died an average of 11 months after study. Survivors had a smaller left ventricular end-diastolic short-axis dimension (6.4 versus 7.1 cm, p less than 0.03) but a similar long-axis length (8.6 versus 8.3 cm). However, overall cavity shape or the ratio of short- to long-axis end-diastolic dimensions was more spherical in those with poorer survival (ratio 0.76 versus 0.68, p less than 0.02). Meridional and circumferential end-systolic stresses were similar in the two groups, but stress was more evenly distributed in the long- and short-axis planes in nonsurvivors (meridional/circumferential stress ratio 0.57 versus 0.52 in survivors, p less than 0.05). Improved survival was associated with an end-diastolic short-axis dimension less than 7.63 cm, a short- to long-axis ratio less than 0.76 and a meridional to circumferential stress ratio less than 0.54. Life table analysis revealed a 28% mortality rate in patients with all three of these characteristics compared with 100% in patients with none. Survivors and nonsurvivors did not differ in systolic cavity dimension, wall thickness, relative wall thickness, cavity volume, percent posterior wall thickening or fractional shortening.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of nifedipine on left ventricular diastolic function in patients with asymptomatic or minimally symptomatic hypertrophic cardiomyopathy

We investigated the effects of nifedipine on left ventricular diastolic function in 17 asymptomatic or minimally symptomatic patients with hypertrophic cardiomyopathy by simultaneously measuring left ventricular pressure and volume with a catheter-tipped manometer and biplane cineangiography. Studies were performed before and 20 minutes after sublingual administration of nifedipine (20 mg). Heart rates were held constant (79 +/- 12 beats/min, mean +/- SD) by right atrial pacing. Left ventricular volumes and instantaneous rates of left ventricular volume were derived from frame-by-frame (20-msec) analyses of left ventricular biplane angiograms. Left ventricular peak systolic pressure (from 122 +/- 21 to 108 +/- 13 mm Hg, p less than 0.01 vs. control) and mean aortic pressure (from 96 +/- 15 to 87 +/- 11 mm Hg, p less than 0.01) decreased significantly with nifedipine. With afterload reduction, left ventricular ejection fraction (from 0.69 +/- 0.12 to 0.74 +/- 0.08, p less than 0.01) and cardiac output (from 6.4 +/- 2.0 to 7.2 +/- 2.2 l/mm, p less than 0.05) increased significantly. However, there was a slight but significant increase in left ventricular end-diastolic pressure (from 15 +/- 8 to 18 +/- 8 mm Hg, p less than 0.05). Nifedipine did not improve left ventricular relaxation as assessed by the time constants of isovolumic pressure decay (t1/2, from 39.8 +/- 6.6 to 39.4 +/- 7.7 msec, NS; t1/e, from 53.8 +/- 9.0 to 54.4 +/- 10.7 msec, NS).(ABSTRACT TRUNCATED AT 250 WORDS)     

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)     

Effects of sublingual nitrate in patients receiving sustained therapy of isosorbide dinitrate for coronary artery disease

To examine the effects of sublingual isosorbide dinitrate (ISDN) in patients receiving sustained ISDN therapy, 24 patients with coronary artery disease were divided into 2 groups. Group C comprised 12 patients without sustained ISDN therapy and group N included 12 patients with sustained ISDN therapy. Before and during administration of sublingual ISDN in both groups, aortic systolic pressure, left ventricular end-diastolic pressure and coronary artery diameter were examined at cardiac catheterization. During sublingual ISDN, the aortic systolic pressure decreased by 20 +/- 6% (138 +/- 26 to 112 +/- 27 mm Hg, p less than 0.01) in group C and 10 +/- 6% (127 +/- 26 to 113 +/- 23 mm Hg, p less than 0.01) in group N (p less than 0.01, group C vs group N). The left ventricular end-diastolic pressure decreased by 65 +/- 16% (11 +/- 5 to 4 +/- 3 mm Hg, p less than 0.01) in group C and 43 +/- 14% (12 +/- 5 to 7 +/- 3 mm Hg, p less than 0.01) in group N (p less than 0.01, group C vs group N). During sublingual ISDN, the diameters of the proximal and distal segments of the left anterior descending and circumflex coronary arteries increased more significantly in group C than in group N (p less than 0.01, group C vs group N). Thus, sublingual ISDN produced less reduction of aortic systolic pressure and left ventricular end-diastolic pressure, and less dilation of coronary artery diameter in patients receiving sustained therapy with ISDN than in those without sustained therapy.(ABSTRACT TRUNCATED AT 250 WORDS)     

Clinical and hemodynamic characteristics of patients with inducible pulsus alternans

Pulsus alternans can be found in some patients with abnormal left ventricular function and also can develop after spontaneous premature beats. The purposes of this study were to: (1) determine the inducibility of pulsus alternans in a series of patients referred for routine cardiac catheterization and (2) define the clinical and hemodynamic characteristics of those who develop pulsus alternans. In 104 patients referred for right and left heart catheterization, atrial premature beats and rapid atrial pacing were used to try to provoke pulsus alternans. The 29 patients who developed pulsus alternans in response to these maneuvers were older (63 +/- 6 vs 59 +/- 10 years, p less than 0.01) and had a greater incidence of valvular heart disease (45% vs 23%, p less than 0.01) and congestive heart failure (38% vs 17%, p less than 0.05). Aortic stenosis was the most prevalent valve lesion found. Those who developed pulsus alternans in response to pacing were further characterized by higher left ventricular systolic (143 +/- 42 vs 121 +/- 23 mm Hg, p less than 0.02) and end-diastolic pressures (17 +/- 9 vs 13 +/- 6 mm Hg, p less than 0.05), higher pulmonary artery systolic pressure (35 +/- 14 vs 29 +/- 11 mm Hg, p less than 0.04), and lower left ventricular ejection fractions (0.42 +/- 0.13 vs 0.53 +/- 0.14, p less than 0.001). Eight patients (28%) with inducible pulsus alternans had a normal left ventricular ejection fraction (greater than 0.50) and left ventricular end-diastolic pressure (less than 13 mm Hg).(ABSTRACT TRUNCATED AT 250 WORDS)     

Predictors of long-term survival after percutaneous aortic valvuloplasty: report of the Mansfield Scientific Balloon Aortic Valvuloplasty Registry

Percutaneous balloon aortic valvuloplasty was used to prospectively treat 492 elderly, symptomatic, nonsurgical patients suffering from severe aortic stenosis in 27 centers in North America and Europe. At 1 year the overall survival rate was 64% and the event-free survival rate (survival free of valve replacement or repeat valvuloplasty) was 43%. Clinical, catheterization and procedural variables were assessed to define prognostic variables. Univariate analysis revealed that patients who survived had a lesser frequency of previous myocardial infarction (2% versus 6%, p less than 0.005), lower incidence of severe ventricular dysfunction (22% versus 48%, p less than 0.001) and lower incidence of symptoms of heart failure (60% versus 75%, p less than 0.02). History of angina (56% versus 45%, p = NS) and syncope (23% versus 16%, p = NS) were similar for both groups. Values obtained at cardiac catheterization that differed in survivors and nonsurvivors included lower pulmonary artery systolic pressure (43 +/- 1 versus 54 +/- 2 mm Hg, p less than 0.001), lower mean pulmonary artery pressure (28 +/- 1.0 versus 36 +/- 1.0 mm Hg, p less than 0.001) and larger initial valve area (0.52 +/- 0.01 versus 0.47 +/- 0.02 cm2, p = 0.006). Discriminate function analysis was performed to identify variables that independently predicted improved probability of survival. Eight variables were significantly and independently predictive. These included age, initial cardiac output, initial left ventricular systolic pressures, initial left ventricular end-diastolic pressures, presence of coronary artery disease, New York Heart Association dyspnea classification, number of balloon inflations and final valve area.(ABSTRACT TRUNCATED AT 250 WORDS)     

Change of left atrial systolic pressure waveform in relation to left ventricular end-diastolic pressure

The relation between the left atrial systolic pressure waveform and left ventricular end-diastolic pressure was observed in 17 patients who underwent diagnostic cardiac catheterization. Left atrial pressure and left ventricular pressure were simultaneously recorded from a multisensor catheter before and during angiotensin infusion. Left ventricular systolic pressure and left ventricular end-diastolic pressure were 133 +/- 17 and 12.3 +/- 3.2 mm Hg, respectively, before angiotensin infusion and increased to 168 +/- 18 (p less than 0.01) and 19.4 +/- 4.5 mm Hg (p less than 0.01), respectively, during infusion. The left atrial systolic pressure curve consisted of two positive waves--a first wave (A) and a second wave (A'). The A and A' wave pressures were 11.6 +/- 2.3 and 10.2 +/- 3.9 mm Hg, respectively, before angiotensin infusion and 16.5 +/- 2.9 (p less than 0.01) and 18.1 +/- 4.7 mm Hg (p less than 0.01), respectively, during infusion. The ratio of A'/A of left atrial systolic pressure was 0.81 +/- 0.27 before angiotensin infusion and 1.08 +/- 0.14 (p less than 0.01) during infusion. The ratio of A' to A of left atrial systolic pressure was linearly related to left ventricular end-diastolic pressure before and during (p less than 0.01) angiotensin infusion. The amplitude of the A wave exceeded that of the A' wave at normal left ventricular end-diastolic pressures. However, as the left ventricular end-diastolic pressure increased either at rest or during angiotensin infusion, the amplitude of the A' wave increased and often exceeded that of the A wave. These results suggest that the second (A') wave might be attributed to the increased reflection associated with increased left ventricular end-diastolic pressure.     

Left ventricular end-systolic wall stress--dimension relationship in unanesthetized dogs with perinephritic hypertension

To study myocardial contractility in hypertensive hearts with normal wall motion, we examined left ventricular end-systolic wall stress-dimension relationships (ESWDR) during a baseline period (CS: control stage) and in the eighth week after induction of systemic hypertension by Page's method (HS: hypertensive stage) in unanesthetized dogs. The mean aortic blood pressure increased from 94 +/- 11 to 142 +/- 26 mmHg (p less than 0.01). The end-diastolic left ventricular posterior wall thickness increased significantly during the HS (9.4 +/- 1.3 vs 7.3 +/- 1.3 mm; HS vs CS), and its dimension was significantly (p less than 0.05) smaller than it was during the CS (37.0 +/- 4.2 vs 39.9 +/- 4.6 mm; HS vs CS). There were no significant differences between the 2 stages in left ventricular fractional shortening (31.9 +/- 5.0 vs 32.6 +/- 2.8; HS vs CS), in end-systolic meridional left ventricular wall stress (75.3 +/- 10.8 vs 68.3 +/- 15.6 10(3) dynes/cm2; HS vs CS), or in the ESWDR slopes (98.6 +/- 17.7 vs 94.0 +/- 19.7; HS vs CS). The ESWDR dimension intercepts significantly decreased from 2.0 +/- 0.3 to 1.8 +/- 0.3 cm during the HS; that is, the relationship shifted to the left with no significant change in the slope. At autopsy, the ratio of left ventricular weight to body weight of the hypertensive dogs was significantly (p less than 0.01) greater than that of sham-operated control dogs (6.0 +/- 0.9 vs 4.3 +/- 0.5 g/kg).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of regional systolic asynchrony on left ventricular global diastolic function in patients with coronary artery disease.

Patients with coronary artery disease often have impaired left ventricular diastolic filling despite normal global systolic function. The influence of regional systolic asynchrony on diastolic function was assessed by radionuclide angiography in 60 patients with coronary artery disease and normal ejection fraction at rest: group 1 (n = 30) with normal wall motion at rest and group 2 (n = 30) with abnormal wall motion. Data were compared with those obtained from 19 normal volunteers. Age, heart rate, ejection fraction and echocardiographic end-diastolic dimension did not differ among the three groups. Peak filling rate in group 1 and group 2 was similar (2.5 +/- 0.5 and 2.3 +/- 0.6 end-diastolic counts/s, respectively) and significantly lower than that in the normal subjects (2.8 +/- 0.7 end-diastolic counts/s; p less than 0.01 vs. group 2, p less than 0.05 vs group 1). Time to peak filling rate was prolonged in group 2 (184 +/- 27 ms) compared with that in normal subjects (162 +/- 19 ms; p less than 0.01) and group 1 (172 +/- 15 ms; p less than 0.05). Left ventricular end-diastolic pressure was significantly higher in group 2 than in group 1 (14 +/- 7 vs. 10 +/- 5 mm Hg, respectively; p less than 0.05). Asynchrony was assessed by sector analysis of the radionuclide left ventricular region of interest. Diastolic asynchrony was similar in the two patient groups (30 +/- 23 ms in group 2, 26 +/- 16 ms in group 1) and was higher in both groups than in the normal subjects (16 +/- 8 ms; p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

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

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

Doppler evaluation of aortic valve area in children with aortic stenosis

To evaluate the usefulness of the Doppler-derived aortic valve area calculated from the continuity equation in assessing the hemodynamic severity of aortic valve stenosis in infants and children, two-dimensional and Doppler echocardiographic examinations were performed on 42 patients (aged 1 day to 24 years) a median of 1 day before or after cardiac catheterization. The left ventricular outflow tract diameter was measured from the parasternal long-axis view at the base of the aortic cusps from inner edge to inner edge in early systole. The flow velocities proximal to the aortic valve were measured from the apical view with use of pulsed Doppler echocardiography; the jet velocities were recorded from the apical, right parasternal and suprasternal views by using continuous wave Doppler echocardiography. The velocity-time integral, mean velocity and peak velocity were measured by tracing the Doppler waveforms along their outermost margins. Seventeen patients (all less than or equal to 6 years old) had a very small left ventricular outflow tract diameter (less than or equal to 1.4 cm) and cross-sectional area (less than or equal to 1.5 cm2). The Doppler aortic valve area calculated with use of velocity-time integrals in the continuity equation (0.57 +/- 0.25 cm2/m2, mean value +/- SD) correlated well with the Doppler aortic valve area calculated by using mean (0.55 +/- 0.25 cm2/m2) and peak (0.54 +/- 0.24 cm2/m2) velocities, with correlations of r = 0.97 and 0.95, respectively. Thirty-four patients had sufficient catheterization data to calculate aortic valve area from the Gorlin formula.(ABSTRACT TRUNCATED AT 250 WORDS)     

Alterations in left ventricular geometry, wall stress, and ejection performance after correction of congenital aortic stenosis

Children with congenital aortic stenosis have "excessive" left ventricular hypertrophy with reduced resting systolic wall stress that allows for supernormal ejection performance. If aortic stenosis is uncorrected, this pattern persists until adulthood. The effect of removing the aortic pressure gradient on left ventricular hypertrophy and wall stress in children with congenital aortic stenosis is unknown. To test the hypothesis that removal of the stimulus for hypertrophy by aortic valve replacement or repair would normalize left ventricular mass and wall stress, we measured left ventricular ejection performance, wall stress, and contractile function in seven patients at cardiac catheterization before and 36 +/- 7 months after surgical correction of congenital aortic stenosis. After aortic valve replacement or repair, the aortic valve gradient fell from 87 +/- 12 to 7 +/- 4 mm Hg, and peak left ventricular pressure fell from 187 +/- 14 to 128 +/- 8 mm Hg. Left ventricular ejection fraction decreased postoperatively from 86 +/- 4% to 74 +/- 4% (p less than 0.001), whereas velocity of circumferential fiber shortening decreased from 2.15 +/- 0.15 to 1.6 +/- 0.11 (p less than 0.002). Left ventricular mass remained unchanged preoperatively (121 +/- 14 g/m2) and postoperatively (121 +/- 16 g/m2), but wall thickness (h) decreased in relation to ventricular radius (r) (h/r = 0.55 +/- 0.05 preoperatively, 0.36 +/- 0.02 postoperatively; p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Improvement in indexes of diastolic performance in patients with congestive heart failure treated with milrinone

To elucidate the mechanisms by which the new bipyridine inotropic agent milrinone improves cardiac function, we examined multiple indexes of left ventricular diastolic function before and after administration of milrinone to patients with advanced (NYHA class III or IV) congestive heart failure. In 13 patients left ventricular pressure measurements were made with a micromanometer to permit assessment of peak negative dP/dt and the time constant of left ventricular isovolumic relaxation, T, before and after milrinone. In nine patients radionuclide ventriculographic studies were performed during left heart catheterization, allowing calculation of left ventricular peak filling rate, volumes, and the diastolic pressure-volume relationship before and after milrinone. After intravenous administration of milrinone, peak negative dP/dt increased (+ 18%; p less than .01) and T decreased (-30%; p less than .01), while heart rate increased by only 8% (87 +/- 12 to 94 +/- 15 beats/min; p less than .01), left ventricular systolic pressure did not change, and mean aortic pressure fell by 11% (p less than .01). Left ventricular peak filling rate increased (1.2 +/- 0.6 to 1.7 +/- 0.7 end-diastolic volumes/sec; p less than or equal to .02) despite a decrease in left ventricular filling pressure (mean pulmonary wedge pressure 27 +/- 7 to 18 +/- 9 mm Hg; p less than .01). There was a fall in left ventricular end-diastolic pressure (28.6 +/- 6 to 19 +/- 7 mm Hg; p less than or equal to .01), with no significant change in left ventricular end-diastolic volume. This was associated with a downward shift in the left ventricular diastolic pressure-volume relationship in most cases.(ABSTRACT TRUNCATED AT 250 WORDS)     

Assessment of left ventricular aneurysm resectability by two-dimensional echocardiography

Mortality of surgical resection of a left ventricular (LV) aneurysm is largely determined by size and function of nonaneurysmal or residual myocardium. A residual myocardial index was determined using 2-dimensional echocardiography (2-D echo) in 56 consecutive patients scheduled for LV aneurysmectomy, and these results were correlated with surgical outcome. The index was calculated using 3 apical cross sections: the 2- and 4-chamber views and the long-axis view. These views were recorded at mutual angles of 60 degrees. In each view the end-diastolic length of normally moving endocardium of the 2 opposite walls was expressed as a fraction of the end-diastolic LV long axis. The index was assessed by averaging the 6 ratios obtained. In 41 survivors the index ranged from 40 to 71% (mean +/- standard deviation 53 +/- 7.8) and in 15 nonsurvivors from 29 to 67% (mean 38 +/- 8.5, p less than 0.01). With 1 exception, this echocardiographic index sharply separated survivors from nonsurvivors. The lower limit to survive aneurysmectomy was 40%.