Determination of left ventricular filling parameters by pulsed Doppler echocardiography: a noninvasive method to predict high filling pressures in patients with coronary artery disease

This study investigated the influence of left ventricular end-diastolic filling pressure (LVEDP) on instantaneous transmitral inflow velocities as assessed by pulsed Doppler echocardiography. The study was performed in 87 consecutive patients with coronary artery disease (12 women, 65 men, mean age 58 +/- 8 years, range 37 to 78 years) in whom Doppler tracings of mitral inflow velocities were recorded 24 hours before diagnostic cardiac catheterization. The ratio of early-to-late diastolic velocity integrals was significantly correlated with LVEDP (r = 0.35, SD = 0.77, p less than 0.001). In addition, in a comparison patients with LVEDP greater than or equal to 20 mm Hg to those with LVEDP less than 20 mm Hg, peak early filling velocity (R) was significantly higher, peak late filling velocity (A) was lower, and hence R/A and area under the early filling curve/area under the late diastolic filling curve (E/L) ratios were significantly higher in patients with markedly elevated filling pressures (LVEDP 20 mm Hg: R = 41 +/- 12, A = 56 +/- 16, R/A = 0.75 +/- 0.23, E/L = 1.0 +/- 0.4, n = 54, and LVEDP greater than or equal to 20 mm Hg: R = 49 +/- 18, A = 46 +/- 12, R/A = 1.23 +/- 0.9, E/L = 1.94 +/- 1.2, n = 34. An E/L ratio greater than or equal to 1.4 showed a sensitivity of 59%, a specificity of 83%, a positive predictive accuracy of 69%, and a negative predicting accuracy of 76% in detecting patients with markedly elevated LVEDP.(ABSTRACT TRUNCATED AT 250 WORDS)     

Influence of right ventricular pressure overload on left and right ventricular filling in cor pulmonale assessed with Doppler echocardiography

We evaluated the influence of right ventricular (RV) pressure overload on RV and left ventricular (LV) filling using Doppler echocardiography in cor pulmonale. The LV and RV inflow signals were recorded by Doppler flowmetry. The end-diastolic (ED) and end-systolic (ES) LV short axis images were detected by 2-dimensional echocardiography in 20 healthy subjects and in 36 cases of chronic pulmonary disease (CPD) with pulmonary hypertension. We measured (1) the ratio of the peak velocity of inflow due to atrial contraction to the peak velocity of rapid inflow (A/R), (2) the deceleration half-time of rapid inflow (delta TD), (3) the corrected radius of curvature (cRC) of the interventricular septum (IVS) at ES and ED, and (4) the percent change of length of 16 radial grids (%CL) using the fixed method on the ED and ES short axis images. In 17 of 36 patients with CPD, we measured the systolic pulmonary artery pressure (sPAP), the cardiac index (CI), the mean pulmonary capillary wedge pressure (mPCWP), the end-diastolic right ventricular pressure and the partial oxygen pressure of arterial blood (PaO2). The results were as follows: in CPD, (1) both the RV and the LV diastolic behavior were impaired as shown by increased A/R (1.04 +/- 0.20, 0.98 +/- 0.17, respectively) and prolonged delta TD (115 +/- 20, 100 +/- 17 msec, respectively), (2) the IVS was flattened at ED (cRC of IVS = 0.67 +/- 0.12), (3) the IVS wall motion was impaired (%CL of IVS = 133 +/- 13), (4) the sPAP had an adequate correlation with RV A/R (r = 0.80, p less than 0.01), RV delta TD (r = 0.59, p less than 0.05), LV A/R (r = 0.82, p less than 0.01), LV delta TD (r = 0.61, p less than 0.05), cRC of IVS (r = 0.67, p less than 0.01), %CL of IVS (r = -0.59, p less than 0.05). There was no significant correlation between the LV diastolic behavior and the CI, the mPCWP, the PaO2. It is concluded that the impairment of RV diastolic behavior was caused by the decreased RV compliance due to RV free wall hypertrophy. Moreover, the RV pressure overload interfered with the IVS motion during diastole, this regional impairment of diastolic behavior of the IVS subsequently causing impairment of LV diastolic filling.     

Factors that determine the direction and magnitude of precordial ST-segment deviations during inferior wall acute myocardial infarction

Sixty-one patients with inferior acute myocardial infarction (AMI) and no evidence of prior AMI were studied to determine which factors influence the magnitude of precordial ST-segment depression. In the total study group, there was a significant but weak correlation between the magnitude of precordial ST-segment depression and the magnitude of inferior ST-segment elevation (r = -0.46, p less than 0.001). In the 29 patients with evidence of concomitant right ventricular (RV) involvement, precordial ST-segment depression was significantly smaller both in absolute terms (-1.3 +/- 1.8 vs -2.8 +/- 1.9 mm, p less than 0.01) and relative to the magnitude of inferior ST-segment elevation (ratio of -0.2 +/- 1.0 vs -1.1 +/- 0.5, p less than 0.01), whereas in the 15 patients with lateral ST-segment elevation (greater than or equal to 1 mm in lead V6), precordial ST-segment depression was significantly greater both in absolute terms (-3.5 +/- 2.3 vs -1.6 +/- 1.7 mm, p less than 0.01) and relative to the magnitude of inferior ST-segment elevation (ratio of -1.1 +/- 0.8 vs -0.5 +/- 0.9, p less than 0.02). Consistent with these findings, the correlation between the magnitudes of precordial and inferior ST-segment deviations was considerably improved when only the 24 patients with neither evidence of RV involvement nor lateral ST-segment elevation were analyzed (r = 0.89, p less than 0.001, n = 24). These data suggest that in patients with inferior AMI, there is a reciprocal relation between precordial and inferior ST-segment deviations, which is distorted by concomitant RV involvement and by concomitant lateral left ventricular wall involvement.     

Origin and significance of diastolic Doppler flow signals in the left ventricular outflow tract

Diastolic Doppler flow signals (greater than or equal to 0.2 m/s) in the left ventricular outflow tract have not been well characterized, and their origin and significance remain controversial. Fifty-nine patients (55 +/- 16 years of age) with technically good Doppler echocardiographic studies were studied prospectively. There were 14 normal subjects, 21 patients with left ventricular hypertrophy, 10 with dilated cardiomyopathy and 14 with other cardiac disease. The rhythm was sinus in 55 and atrial fibrillation in 4. Two distinct Doppler flow signals were detected in the left ventricular outflow tract during diastole. These were termed E' (early) and A' (active) because they occurred 40 to 100 ms after higher velocity mitral inflow E (passive filling) and A (atrial contraction) signals. Among 59 patients, E' signals were present in 48 (81%) and had a mean velocity of 0.41 +/- 0.23 m/s. In 55 patients with normal sinus rhythm, A' signals were present in 52 (95%) and had a mean velocity of 0.52 +/- 0.24 m/s. No A' signals were present in the four patients with atrial fibrillation. The E' and A' velocities by pulsed wave Doppler ultrasound were low at the left ventricular apex and increased along the basal septum in the left ventricular outflow tract. Prominent A' velocities (greater than or equal to 0.45 m/s) were seen in 62% of patients with left ventricular hypertrophy, 50% of normal subjects and 10% of patients with dilated cardiomyopathy. The A' velocity was higher in patients with left ventricular hypertrophy (0.63 +/- 0.26 m/s) than in those with a normal heart (0.45 +/- 0.16 m/s; p less than 0.05) or dilated cardiomyopathy (0.25 +/- 0.13 m/s; p less than 0.01). The major determinants of diastolic outflow tract velocity were the mitral inflow E and A velocities and left end-diastolic dimension, particularly when combined (r = 0.64, p less than 0.0001 for E'; r = 0.72, p less than 0.0001 for A'). Distinctive E' and A' Doppler outflow tract signals result from mitral inflow and may be detected in most patients with normal heart size. These E' and A' velocities increase from apex to base and are more prominent in patients with a small, normally contracting heart or left ventricular hypertrophy.     

Left ventricular diastolic function and endothelial function in patients with erectile dysfunction

The aim of this study was to assess left ventricular diastolic function and forearm endothelial function in patients with erectile dysfunction (ED) without overt cardiovascular disease. Forearm endothelial function and diastolic Doppler parameters, including tissue Doppler imaging, were studied in 32 men with ED and 27 age-matched, healthy, male control subjects. Left ventricular diastolic function in patients with ED and the relation between endothelium-dependent vasodilation and the Doppler parameters of left ventricular diastolic function, including tissue Doppler imaging, were assessed. Endothelium-dependent vasodilation (4.1+/-3.3% vs 9.7+/-4.2%, p<0.001) as well as the mitral inflow E velocity (0.66+/-0.17 vs 0.80+/-0.16 m/s, p=0.01), the E/A ratio (the ratio of mitral inflow E velocity to mitral inflow A velocity; 0.91+/-0.3% vs 1.22+/-0.26%, p<0.001), and the E/Em ratio (the ratio of mitral A-wave velocity to early diastolic velocity in the annulus derived by tissue Doppler imaging; 7.4+/-2.7% vs 6.6+/-1.6%, p=0.03) were smaller in the ED group than in the control group. Deceleration time (228.6+/-61.6 vs 192.9+/-44.6 ms, p=0.03) and isovolumetric relaxation time (112.8+/-18 vs 94+/-15.9 ms, p<0.001) were also prolonged in the ED group compared with the control group. The mitral E-wave velocity (r=0.40, p=0.022), the E/A ratio (r=0.40, p=0.027), and the E/Em ratio (r=-0.52, p= 0.003) were related to endothelium-dependent vasodilation by nivariate analysis. Only the E/Em ratio was correlated with endothelium-dependent vasodilation by multivariate analysis. In conclusion, this study indicates that endothelial function and left ventricular diastolic function are impaired in patients with ED without overt cardiovascular disease.     

Left ventricular diastolic filling in children with hypertrophic cardiomyopathy: assessment with pulsed Doppler echocardiography

Altered left ventricular filling patterns in hypertrophic cardiomyopathy have been demonstrated by M-mode echocardiographic and radionuclide techniques. Because pulsed Doppler ultrasound provides the capability to directly measure blood flow velocity across the mitral valve, it was hypothesized that this technique would be useful for demonstrating left ventricular filling abnormalities. Simultaneous Doppler ultrasound examination of the left ventricular inflow, M-mode echocardiograms and phonocardiograms were performed in 17 children and young adults: 10 with hypertrophic cardiomyopathy (aged 6 to 20 years) and 7 with a normal heart (aged 10 to 18 years). From the Doppler studies, measurements of various diastolic time intervals, peak flow velocity during rapid filling (E velocity) and peak flow velocity during atrial contraction (A velocity) were made. Several areas within the Doppler flow envelope were calculated: first 33% of diastole (0.33 area), first 50% of diastole, triangle under the E velocity (E area) and triangle under the A velocity (A area). These were expressed as a percent of area under the total flow envelope. From the M-mode studies, left ventricular endocardial echoes were digitized and peak rates of increase in left ventricular dimension were determined and normalized for end-diastolic dimension. Diastolic time intervals, including isovolumic relaxation time, were calculated using the phonocardiogram to determine end-systole. The E velocity was lower (0.71 +/- 0.23 versus 0.91 +/- 0.11 m/s, p less than 0.05), 0.33 area/total area was less (0.46 +/- 0.11 versus 0.58 +/- 0.08, p less than 0.05) and the isovolumic relaxation time was prolonged (56 +/- 2 versus 31 +/- 1 ms, p less than 0.05) in patients with hypertrophic cardiomyopathy.(ABSTRACT TRUNCATED AT 250 WORDS)     

Long-term assessment of right ventricular diastolic filling in patients with pulmonic valve stenosis successfully treated in childhood

Patients with severe pulmonic stenosis (PS) have right ventricular (RV) diastolic filling abnormalities detectable by tricuspid valve pulsed Doppler examination. To determine if these abnormalities persist long term after successful therapy of PS, 19 patients were examined 8 +/- 3 years after PS therapy. At the time of follow-up Doppler examination, the PS gradient was 15 +/- 8 mm Hg. From the tricuspid valve inflow Doppler study, the following measurements were obtained at peak inspiration: peak velocities at rapid filling (peak E) and during atrial contraction (peak A), ratio of peak E to peak A velocities, RV peak filling rate normalized for stroke volume, deceleration time, the fraction of filling in the first 0.33 of diastole as well as under the E and A waves, and the ratio of E to A area. Data from PS follow-up patients were compared with our previously reported data from 12 age-related control subjects and 14 untreated patients with PS. Patients with PS who were followed up had higher peak E velocity (0.75 +/- 0.14 vs 0.59 +/- 0.21 m/s), lower peak A velocity (0.47 +/- 0.09 vs 0.64 +/- 0.28 m/s), higher E/A velocity ratio (1.65 +/- 0.33 vs 1.11 +/- 0.52), higher 0.33 area fraction (0.52 +/- 0.08 vs 0.34 +/- 0.14), lower A area fraction (0.29 +/- 0.06 vs 0.45 +/- 0.21) and higher E/A area ratio (2.48 +/- 0.82 vs 1.73 +/- 1.05) than PS patients without treatment (p less than 0.03). All Doppler indexes of the patients with PS who were followed up were the same as those of the control subjects except for the peak E velocity that was slightly higher (0.75 +/- 0.14 vs 0.63 +/- 0.11 m/s), the peak A velocity that was slightly higher (0.47 +/- 0.09 vs 0.38 +/- 0.09 m/s) and the E/A area ratio that was slightly lower (2.48 +/- 0.82 vs 3.50 +/- 1.25) (p less than 0.03). Thus, at long-term follow-up, all RV diastolic filling indexes in successfully treated patients with PS improved compared with the untreated patients and approached values found in normal subjects.(ABSTRACT TRUNCATED AT 250 WORDS)     

Pattern of left ventricular diastolic filling associated with right ventricular enlargement

Right ventricular (RV) dilatation associated with pressure overload may alter left ventricular (LV) geometry resulting in abnormal diastolic function as demonstrated by a smaller LV diastolic volume for a given LV diastolic pressure. To determine whether abnormalities in LV geometry due to RV dilatation result in abnormalities in the LV diastolic filling pattern, we obtained pulsed Doppler transmitral recordings from 23 patients with RV dilatation with RV systolic pressure estimated to be less than 40 mm Hg (group 1), 18 patients with RV dilatation and RV systolic pressures greater than or equal to 40 mm Hg (group 2) and 33 normal patients. RV systolic pressures were estimated from continuous wave Doppler peak tricuspid regurgitation velocities using the modified Bernoulli equation. Diastolic filling parameters in group 1 patients were similar to normals. In group 2 patient, increased peak atrial filling velocity (76 +/- 14 vs 57 +/- 12 cm/s, p less than 0.001), decreased peak rapid filling velocity/peak atrial filling velocity (1.1 +/- 0.4 vs 1.5 +/- 0.4, p less than 0.01), increased atrial filling fraction (41 +/- 14 vs 30 +/- 10%, p less than 0.01) and prolongation of the atrial filling period (171 +/- 47 vs 152 +/- 39 ms, p less than 0.05) were noted compared with the normal group. RV end-diastolic size and LV end-systolic shape were significantly correlated with the atrial filling fraction in group 2 patients. In patients with RV dilatation and RV systolic pressures greater than or equal to 40 mm Hg, there is increased reliance on atrial systolic contribution to the LV filling volume.     

Doppler left ventricular diastolic filling abnormalities in aortic stenosis and their relation to hemodynamic parameters

Doppler mitral flow indexes and their relation to invasively measured hemodynamic diastolic indexes were assessed in 13 patients with isolated aortic stenosis (AS), and compared to Doppler indexes in 10 normal subjects matched for age, heart rate, left ventricular (LV) ejection fraction and LV load. Patients with AS showed no difference in Doppler early filling (E) indexes, but demonstrated greater Doppler atrial filling (A) indexes in comparison to normal subjects: atrial velocity (89 +/- 31 vs 56 +/- 7 cm/s), atrial integral (11.4 +/- 4.8 vs 5.7 +/- 1.6 cm), A/E velocity (1.69 +/- 0.89 vs 1.06 +/- 0.26) and A/E integral (3.53 +/- 6.64 vs 0.81 +/- 0.27) (all p less than 0.05). Doppler indexes in patients with AS did not correlate with hemodynamic indexes of LV relaxation or chamber stiffness. Significant correlations were observed between Doppler and angiographic peak filling rates (r = 0.70) and between Doppler atrial filling velocity and LV end-diastolic volume (r = -0.66), LV end-diastolic pressure (r = -0.48) and LV ejection fraction (r = 0.53) (all p less than 0.05). These data indicate that, compared to matched normal subjects, most patients with AS have an increased atrial contribution to LV filling. However, in patients with decreased LV function, atrial function may also be depressed, as indicated by a decreased atrial contribution to LV filling, resulting in "normalization" of the Doppler mitral flow pattern.     

Role of transmitral blood flow velocity by Doppler echocardiography in the evaluation of coronary artery disease

To determine the relation between presence and severity of coronary artery disease and diastolic filling abnormalities by Doppler echocardiography, recordings of transmitral inflow velocity were made at rest in 90 patients with coronary artery disease and 28 normals. At the time of the Doppler examination, 81 patients with coronary artery disease (90%) and 10 normals (36%) were treated with antianginal medications. No difference was found in the ratio between early (E) and late (A) diastolic filling velocity (E/A ratio) when comparing patients with greater than 70% obstruction of at least one coronary artery to age-matched normals, regardless of the presence or absence of wall motion abnormalities. The E/A ratio was 1.3 +/- 0.46 in coronary patients with normal wall motion, 1.2 +/- 0.47 in coronary patients with abnormal wall motion, and 1.3 +/- 0.53 in both samples of age-matched normals. Multivariate analysis of the relation between E/A ratio and other variables showed that heart rate (F = 24.46, p less than 0.00001) and age (F = 19.51, p less than 0.00001) were significant independent determinants of the E/A ratio, while the presence or severity of coronary artery disease, the presence of hypertension, the magnitude of wall motion abnormalities, and end-diastolic dimension by echocardiography were not. These data suggest that transmitral inflow velocity recordings by Doppler have limited value for the recognition of coronary artery disease, since the E/A ratio is profoundly influenced by other factors, such as heart rate and age.     

Pulsed Doppler evaluation of right ventricular diastolic filling in children with pulmonary valve stenosis before and after balloon valvuloplasty

To assess right ventricular (RV) diastolic filling in children with pulmonary stenosis (PS), 14 patients (mean age 5.1 years) were examined immediately before and after pulmonary balloon valvuloplasty. Fourteen normal children (mean age 4.8 years) were also studied. From the tricuspid valve inflow Doppler study, the following measurements were made at peak inspiration: peak velocities at rapid filling (peak E) and during atrial contraction (peak A), ratio of peak E to peak A velocities, RV peak filling rate normalized for stroke volume, total area under the Doppler curve, percent of the total Doppler area occurring in the first third of diastole (0.33 area fraction), percent of the total area occurring under the E wave (E area fraction), percent of the total area occurring under the A wave (A area fraction) and the ratio of E area to A area. Before balloon valvuloplasty, the patients with PS had higher peak A velocity (0.64 +/- 0.28 vs 0.39 +/- 0.08 m/s), lower E/A velocity ratio (1.11 +/- 0.52 vs 1.76 +/- 0.45), lower 0.33 area fraction (0.34 +/- 0.14 vs 0.49 +/- 0.08), higher A area fraction (0.45 +/- 0.21 vs 0.27 +/- 0.09) and lower E/A area ratio (1.73 +/- 1.05 vs 2.96 +/- 1.14) than the normal subjects (p less than 0.01). In patients before and after balloon valvuloplasty, there was a significant difference in RV outflow gradient (71 +/- 35 vs 28 +/- 15 mm Hg), but there was no change in any Doppler index. Thus, patients with PS have abnormal diastolic filling with decreased filling in early diastole and increased filling during atrial contraction.(ABSTRACT TRUNCATED AT 250 WORDS)     

Ratio of ST-segment depression in lead V2 to ST-segment elevation in lead aVF in evolving inferior acute myocardial infarction: an aid to the early recognition of right ventricular ischemia

The potential value of the ratio of precordial ST-segment depression to inferior ST-segment elevation as a sign of concomitant right ventricular (RV) ischemia was examined. The study group consisted of 68 patients, admitted within 3 hours of the onset of inferior acute myocardial infarction (AMI), in whom there was no evidence of prior AMI. In 27 of the 34 patients in whom inferior AMI was the result of right coronary artery occlusion proximal to the RV branch, the magnitude of ST-segment depression in lead V2 was 50% or less of the magnitude of ST-segment elevation in lead aVF, whereas in only 3 of the 34 patients in whom the site of occlusion was either distal to the RV branch (n = 23) or in the left circumflex artery (n = 11) was this ratio 50%; in no patient was it less than 50% (p less than 0.001). All 34 patients with occlusion of the right coronary artery proximal to the RV branch also had regional or global ischemic RV dysfunction by radionuclide ventriculography, with a mean RV ejection fraction of 30 +/- 10% compared with 42 +/- 6% in patients with occlusion distal to the RV branch or in the left circumflex artery (p less than 0.001). In conclusion, in patients with evolving inferior AMI, ST-segment depression in lead V2 of 50% or less of the magnitude of ST-segment elevation in lead aVF may be a useful sign (sensitivity 79%, specificity 91%, positive predictive value 90% and negative predictive value 82%) for identifying patients with concomitant RV ischemia.     

Doppler evaluation of left ventricular diastolic filling in children with systemic hypertension

To assess left ventricular (LV) diastolic function in children with systemic hypertension, 11 patients with hypertension (mean blood pressure 99 mm Hg) and 7 normal patients (mean blood pressure 78 mm Hg) underwent M-mode echocardiography and pulsed Doppler examination of the LV inflow. From a digitized trace of the LV endocardium and a simultaneous phonocardiogram, echocardiographic diastolic time intervals, peak rate of increase in LV dimension (dD/dt), and dD/dt normalized for LV end-diastolic dimension (dD/dt/D) were measured. Doppler diastolic time intervals, peak velocities at rapid filling (E velocity) and atrial contraction (A velocity), and the ratio of E and A velocities were measured. The following areas under the Doppler curve and their percent of the total area were determined: first 33% of diastole (0.33 area), first 50% of diastole, triangle under the A velocity (A area), and the triangle under the E velocity (E area). The A velocity (patients with hypertension = 0.68 +/- 0.11 m/s, normal subjects = 0.49 +/- 0.08 m/s), the 0.33 area/total area (patients with hypertension = 0.49 +/- 0.09, normal subjects = 0.58 +/- 0.08), the A area (patients with hypertension = 0.17 +/- 0.05, normal subjects = 0.12 +/- 0.03), and the A area/total area (patients with hypertension = 0.30 +/- 0.11, normal subjects = 0.20 +/- 0.07) were significantly different between groups (p less than 0.05). M-mode and Doppler time intervals, (dD/dt)/D, E velocity, and the remaining Doppler areas were not significantly different between groups.(ABSTRACT TRUNCATED AT 250 WORDS)     

Doppler-echo evaluation of left ventricular diastolic filling in patient with mixed connective tissue disease

Left ventricular diastolic function was assessed in 17 patients (2 males and 15 females; mean age 44 +/- 9 years) with mixed connective tissue disease (MCTD) and 18 sex- and age-matched healthy control subjects (2 males and 16 females; mean age 44 +/- 8 years) by means of M-mode and pulsed Doppler echocardiography. None had clinical evidence of overt myocardial disease or abnormal left ventricular systolic function. Compared with the control group, patients with MCTD had a significantly longer isovolumic relaxation time (IVRT) (59 +/- 7 versus 70 +/- 12 ms; p less than 0.01), a lower peak early diastolic flow velocity (E) (0.79 +/- 0.10 versus 0.70 +/- 0.07 m/s; p less than 0.005), a higher peak late diastolic flow velocity due to atrial contraction (A) (0.47 +/- 0.08 versus 0.54 +/- 0.08 m/s; p less than 0.05) and a reduced E/A ratio (1.72 +/- 0.37 versus 1.33 +/- 0.26; p less than 0.005). Although there was no significant correlation of left ventricular diastolic filling indexes with age, heart rate, left ventricular end-diastolic and end-systolic dimensions, interventricular septal and left ventricular posterior wall thickness, and fractional shortening, the duration of illness was significantly related to IVRT (r = 0.62; p less than 0.01), peak A (r = 0.79; p less than 0.001) and velocity half-time (r = 0.54; p less than 0.05). The results suggest the presence of an abnormal left ventricular diastolic filling pattern in patients with MCTD and may represent myocardial involvement in this disease.     

Cardioprotective effects of magnesium sulfate in patients undergoing primary coronary angioplasty for acute myocardial infarction.

BACKGROUND: Experimental evidence indicates that magnesium sulfate may have potential cardioprotective properties as an adjunct to coronary reperfusion. The present study was designed to examine the hypothesis that magnesium might have beneficial effects on left ventricular (LV) function and coronary microvascular function in patients with acute myocardial infarction (AMI). METHODS AND RESULTS: The study population of 180 consecutive patients with a first AMI (anterior or inferior) underwent successful primary coronary intervention. Patients were randomized to treatment with either intravenous magnesium (magnesium group, n=89) or normal saline (control group, n=91). Pre-discharge left ventriculograms were used to assess LV ejection fraction (LVEF), regional wall motion (RWM) within the infarct-zone and LV end-diastolic volume index. The Doppler guidewire was used to assess coronary flow velocity reserve (CFVR) as an index of coronary microvascular function. Magnesium group subjects showed significantly better LV systolic function (LVEF 63+/-9% vs 55+/-13%, p<0.001; RWM: -1.01+/-1.29 SD/chord vs -1.65+/-1.11 SD/chord, p=0.004), significantly smaller LV end-diastolic volume index (63+/-17 ml/m(2) vs 76+/-20 ml/m(2), p<0.001), and significantly higher CFVR (2.95+/-0.76 vs 2.50+/-0.99, p=0.023) than controls. CONCLUSION: Magnesium sulfate as an adjunct to primary coronary intervention shows favorable functional outcomes in patients with AMI.     

Doppler echocardiographic evaluation of left ventricular diastolic filling in isolated valvular aortic stenosis

Doppler echocardiography was used to study left ventricular (LV) diastolic filling in 49 adults with isolated aortic stenosis (AS), selected from 155 consecutive patients with AS by excluding coexisting mitral disease (n = 41) and/or significant aortic regurgitation (n = 80). There were no differences between patients with AS and age-matched normal subjects for early diastolic filling (E) velocity (68 +/- 17 vs 67 +/- 13 cm/s), late diastolic filling (A) velocity (79 +/- 25 vs 67 +/- 21 cm/s), E/A ratio (1.00 +/- 0.78 vs 1.06 +/- 0.32) or early diastolic deceleration slope (264 +/- 151 vs 319 +/- 137 cm/s2, differences not significant for all). There was no correlation between any LV filling parameter and AS severity, but late diastolic filling velocity was higher in patients with AS who had LV hypertrophy (n = 33) vs those who did not (n = 16) (86 +/- 23 vs 65 +/- 26 cm/s, p less than 0.01). In the patients with AS and systolic dysfunction (LV ejection fraction less than 50%) (n = 6), early diastolic filling velocity was higher (88 +/- 20 vs 65 +/- 15 cm/s, p less than 0.01), late diastolic filling velocity lower (53 +/- 23 vs 83 +/- 23 cm/s, p less than 0.01), E/A ratio higher (2.20 +/- 1.80 vs 0.84 +/- 0.28, p less than 0.01), deceleration slope steeper (439 +/- 230 vs 240 +/- 121 cm/s2, p = 0.02) and LV end-diastolic pressure higher (23 +/- 9 vs 10 +/- 6 mm Hg, p less than 0.01) than in patients with AS and normal systolic function.(ABSTRACT TRUNCATED AT 250 WORDS)     

Pericardial influences on right and left ventricular filling dynamics

The influence of the pericardium on right and left ventricular filling was studied using two-dimensional and Doppler echocardiography in 14 open-chest dogs. Doppler echo parameters of filling included early (E) and late (A) velocities and their ratio (E/A) for the mitral and tricuspid valves. Right and left ventricular volumes were calculated from orthogonal two-dimensional echocardiographic images. Data were compared at three levels of left ventricular end-diastolic pressure (6 +/- 2, 13 +/- 3, and 21 +/- 4 mm Hg) at matched heart rates before and after pericardiectomy. The instantaneous diastolic pressure gradient was measured in 12 of the dogs. Pericardiectomy resulted in an increase in early mitral velocity, peak early diastolic pressure gradient, and E/A but not early mitral velocity normalized for end-diastolic volume. In contrast, for the tricuspid valve flow, pericardiectomy did not change E but caused a marked increase in A and a decrease in E/A. Right ventricular end-diastolic volumes at matched left ventricular end-diastolic volumes were similar before and after the pericardium was removed. However, removal of the pericardium caused a significant decrease of the slope for the right (86.0 +/- 27.0 x 10(-4) versus 50.0 +/- 19.5 x 10(-4) mm Hg/ml, p less than 0.01), but not left, ventricular ln end-diastolic pressure-volume relation (21.2 +/- 9.2 x 10(-3) versus 21.4 +/- 5.3 x 10(-3) mm Hg/ml, p = NS), and a decrease of the pressure intercept for the left (3.0 +/- 2.0 versus 1.6 +/- 0.9 mm Hg, p less than 0.05), but not right, ventricular ln end-diastolic pressure-volume relation (2.8 +/- 1.4 versus 1.4 +/- 0.8 mm Hg, p = NS). In conclusion, filling of the two ventricles is affected by the pericardium over a wide range of physiological ventricular volumes and pressures. At matched left ventricular end-diastolic volume, pericardiectomy causes a fundamental alteration in right, but not left, ventricular filling.     

Relation of left ventricular dilation during acute myocardial infarction to systolic performance, diastolic dysfunction, infarct size and location

The quantification of left ventricular (LV) volumes and assessment of their relation to systolic and diastolic dysfunction, infarct size and anatomic location were performed in 54 patients with a first acute myocardial infarction (AMI). Blood pool radionuclide angiography was used to assess LV end-diastolic, end-systolic, and stroke volume indexes, ejection fraction and peak diastolic filling rate. Infarct size was estimated from plasma MB creatine kinase activity. Substantial LV dilation occurred within the initial 24 hours of AMI. The peak diastolic filling rate was low, even in those patients with a normal ejection fraction. In comparison with inferior AMI (n = 25), patients with anterior AMI (n = 29) had a larger end-diastolic volume index (105 +/- 8 vs 81 +/- 4 ml/m2, p less than 0.01) and end-systolic volume index (64 +/- 7 vs 37 +/- 4 ml/m2, p less than 0.001), but similar stroke volume index (41 +/- 3 vs 43 +/- 2 ml/m2, difference not significant). No significant relation was noted between infarct size estimated by MB creatine kinase and any volumetric index. On repeat study (day 10 after AMI), end-diastolic and end-systolic volume indexes increased further (p less than 0.05 vs day 1) but ejection fraction and peak diastolic filling rate were unchanged. It was concluded that: (1) LV dilation occurs within hours of AMI in both inferior and anterior AMI, but is more marked in the latter; (2) significant LV diastolic dysfunction is the rule, even in patients with preserved LV systolic function; and (3) LV dilation is an early compensatory mechanism that maintains normal stroke volume, even in patients with severely reduced LV function.     

Dynamic determinants of left ventricular early diastolic filling in old myocardial infarction.

The determinants of left ventricular early diastolic filling were assessed in 15 patients with old myocardial infarction. The left atrial pressure (LAP) and left ventricular pressure (LVP) were simultaneously measured by a Millar's multisensor micromanometer with the pusled Doppler mitral inflow velocity at baseline and during angiotensin infusion (20 ng/kg/min). Cardiac output was measured by a thermodilution method. LV peak systolic pressure and end-diastolic pressure were significantly (p less than 0.001) increased during angiotensin infusion from 137 +/- 19 to 170 +/- 21 mmHg and from 13.3 +/- 5.9 to 20.4 +/- 6.2 mmHg, respectively. Cardiac index was significantly decreased during angiotensin infusion. Heart rate, diastolic time, and peak positive dP/dt were unchanged. Although the LA-LV peak pressure gradient[(LAP-LVP) max] was unchanged (from 2.8 +/- 1.0 to 3.0 +/- 1.4 mmHg), the pressure gradient interval (the interval between the first and second points of transmitral pressure crossover) was significantly (p less than 0.001) decreased from 154 +/- 38 to 117 +/- 26 msec during angiotensin infusion. Peak early diastolic mitral inflow velocity (peak E) and the time-velocity integral of E wave (Ei) were significantly decreased during angiotensin infusion from 51 +/- 10 to 45 +/- 11 cm/sec (p less than 0.002) and from 7.47 +/- 1.96 to 5.70 +/- 1.66 cm (p less than 0.001), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparison of usefulness of left ventricular diastolic versus systolic function as a predictor of outcome following primary percutaneous coronary angioplasty for acute myocardial infarction

Left ventricular (LV) diastolic function is an important predictor of morbidity and mortality after acute myocardial infarction (AMI). We evaluated the role of diastolic function in predicting in-hospital events and LV ejection fraction (EF) 6 months after a first AMI that was treated with primary percutaneous coronary intervention (PCI). We prospectively enrolled 59 consecutive patients who were 60 +/- 15 years of age (48 men), presented at our institution with their first AMI, and were treated with primary PCI. Patients underwent 2-dimensional and Doppler echocardiography, including tissue Doppler imaging of 6 basal mitral annular regions within 24 hours after primary PCI and were followed until discharge. Clinical and echocardiographic variables at index AMI were compared with a combined end point of cardiac death, ventricular tachycardia, congestive heart failure, or emergency in-hospital surgical revascularization. Follow-up echocardiographic assessment was performed at 6 months in 24 patients. During hospitalization, 3 patients died, 7 developed congestive heart failure, 4 had ventricular tachycardia, and 1 required emergency surgical revascularization. Stepwise logistic regression analysis showed the ratio of early mitral inflow diastolic filling wave (E) to peak early diastolic velocity of non-infarct-related mitral annulus (p < 0.01) (E') and mitral inflow E-wave deceleration time (p < 0.02) to be independent predictors of in-hospital cardiac events (generalized R2 = 0.66). In a stepwise multiple linear regression model, independent predictors of follow-up LVEF were mitral inflow deceleration time (R2 = 0.39, p = 0.002), baseline LVEF (R2 = 0.54, p < 0.02), and mitral inflow peak early velocity/mitral annular peak early velocity (or E/E') of infarct annulus (R2 = 0.66, p = 0.02). In conclusion, in patients who are treated with primary PCI for a first AMI, E/E' velocity ratio and mitral inflow E-wave deceleration time are strong predictors of in-hospital cardiac events and of LVEF at 6-month follow-up.