Echocardiography in chronic alcoholics following prolonged periods of abstinence

Left ventricular function was analyzed using standard echocardiographic techniques in 26 chronic asymptomatic alcoholics without clinical evidence of cardiovascular disease. All were studied following a long period of abstinence (mean 3.1 years; range 3 months to 17 years). Seven asymptomatic children (mean age 14.1 years; range 4 to 19 years) whose mothers had been actively drinking throughout their pregnancies were also studied. The calculated fractional shortening of the left ventricle (per cent ΔS), ejection fraction, mean velocity of circumferential fiber shortening (mean V_CF), excursions and maximal systolic velocites of the ventricular septum and left ventricular posterior wall, preejection period/left ventricular ejection time ratios, mitral valve EF slopes, and thicknesses of the left ventricular posterior wall and ventricular septum were obtained in all. Normal left ventricular function was found in all but one adult alcoholic. In this patient, the per cent ΔS, ejection fraction, and mean V_CF were reduced. One additional adult alcoholic had a minimally thickened ventricular septum. Our results differ from other studies which have shown significant left ventricular dysfunction in asymptomatic chronic alcoholics. A possible explanation is the much longer period of abstinence of our chronic alcoholics at the time of their examinations. It also appears that left ventricular function in children born of alcoholic mothers is not affected when assessed after the long interval following prolonged exposure to alcohol in utero.     

Serial noninvasive assessment of left ventricular hypertrophy and function after surgical correction of aortic regurgitation.

Serial echocardiographic analyses of left ventricular hypertrophy and function, with validation of extent of shortening by first pass radionuclide angiography, was performed in 16 patients before and after surgical correction of severe aortic valve regurgitation. All patients were symptomatic (predominantly in New York Heart Association functional class III or IV) before operation but were in class I or II after operation. The preoperative pattern of eccentric hypertrophy (increased mass with normal ratio of left ventricular cross-sectional wall area to cavity area) changed immediately after operation to a pattern of concentric hypertrophy (increased mass with increased ratio of left ventricular cross-sectional wall area to cavity area) because of a significant reduction in chamber size and increase in wall thickness. On late follow-up (9 to 35 months, average 15 months after operation), the hypertrophy lessened significantly, the cross-sectional area of the ventricular wall decreasing to 21.1 ± 5.4 (mean ± standard deviation) cm² from a preoperative average of 31.6 ± 4.8 cm² (P < 0.01), and the ratio of wall area to cavity area was once again normal. In the same period, left ventricular enddiastolic diameter decreased from 6.52 ± 0.68 to 4.64 ± 0.52 cm (P < 0.01). Preoperatively, ejection phase indexes were normal or only marginally depressed in 12 of 16 patients but were moderately depressed in the remaining 4. At early follow-up (average 4 months) ventricular shortening tended to increase; and at late follow-up the fractional shortening of the minor axis, the ejection fraction and the mean velocity of circumferential fiber shortening increased to 0.39 ± 0.07, 0.68 ± 0.10 and 1.26 ± 0.22 circumference/sec, respectively, from preoperative values of 0.33 ± 0.09, 0.60 ± 0.14 and 1.05 ± 0.31 circumferences/sec (P < 0.05 for each index). In the four subjects with preoperative depression of left ventricular function, the extent and speed of myocardial shortening at late follow-up became normal in three subjects and remained moderately depressed in one patient. Paradoxical septal motion was observed immediately postoperatively and in the early follow-up studies, but it was noted in only 3 of 16 cases by the late follow-up period. Provided septal dyskinesia was not present, echocardiographic and first pass radionuclide determinations of ejection fraction correlated highly (r = 0.92).It is concluded that when aortic valve replacement for symptomatic aortic regurgitation is undertaken prior to severe myocardial decompensation, improvement in clinical status is associated with significant regression of myocardial hypertrophy, reduction in left ventricular size, evolution of a normal $\text{mass}\text{volume}$ ratio, recovery of septal dyskinesia as revealed on echocardiography, and improvement in left ventricular function. These data do not define the type and degree of left ventricular dysfunction which is irreversible.     

Effects of intravenously administered propranolol on wall motion abnormalities

Although propranolol is frequently utilized as therapy for angina pectoris in patients with previous myocardial infarction, its effects on wall motion abnormalities in such patients have not been adequately defined. Accordingly, using external wall motion video tracking, we studied 18 patients with previous myocardial infarction and wall motion disorders and 5 normal subjects before and after administration of propranolol, 5 mg intravenously. Systolic time intervals, heart rate and left heart size (measured by the distance between the mid-line and left heart border in an X-ray film triggered at end-diastole after a standard inspiration) were also measured before and after administration of propranolol. In each instance propranolol produced a reduction in the amplitude and velocity of wall motion in areas of normal movement, hypokinesis and paradox, resulting in decreased outward bulging. In the normal subjects, the amplitude and velocity of wall motion also decreased. In the patients with previous myocardial infarction, propranolol increased the ratio of the preejection period to the left ventricular ejection time from a mean of 0.377 ± 0.03 (standard error of the mean) to 0.409 ± 0.03 (P <0.001); decreased heart rate by an average of 7.5 beats/min (P <0.001); and increased the distance from the mid-line to the left heart border from 94.3 ± 2.6 to 97.3 ± 2.6 mm (P <0.001). Similar changes occurred in the 5 normal subjects. We conclude that doses of propranolol sufficient to increase the ratio of the preejection period to left ventricular ejection time, decrease heart rate and increase heart size do not exaggerate preexisting paradoxical wall motion or accentuate latent areas of paradox in patients with previous myocardial infarction.     

Echocardiographic evaluation of left ventricular function in children with congestive cardiomyopathy

Echocardiography was used to study left ventricular function in 37 children with congestive cardiomyopathy. Left atrial and left ventricular diameters were approximately 1.5 times that predicted by body weight, whereas systolic decrease in left ventricular diameter (shortening fraction) and increase in posterior wall thickness were half that of normal children. The ratio of left ventricular preejection period to ejection time was increased in 25 patients and normal in 10. The mean velocity of circumferential fiber shortening was decreased in 30 of 34 patients and averaged 52 percent of that predicted by heart rate.

The shortening fraction was higher in the 12 patients who were asymptomatic at the time of study than in the 25 who had symptoms of congestive heart failure (19.6 ± 2.4 standard error of the mean versus 14.6 ± 1.2) (P < 0.05). In 11 patients whose condition improved after therapy with digoxin and diuretic drugs, serial echocardiograms showed significant increases in shortening fraction and posterior wall thickening and decreases in left atrial diameter and the ratio of preejection period to ejection time. However, one or more indexes of left ventricular function remained abnormal, despite the resolution of symptoms and a return of heart size to normal as judged from the chest roentgenogram.     

Echocardiographic evaluation of right ventricular function in complete transposition of the great arteries: angiographic correlates.

Right ventricular function of patients with complete transposition of the great arteries may be impaired. To assess whether the M mode echocardiogram could predict right ventricular function 64 echocardiograms and ventricular angiograms of 62 patients were studied, 33 obtained before repair of the defect (group I) and 31 (including 2 from patients in group I) obtained after the Mustard procedure (group II). Each group was subdivided according to whether a ventricular septal defect or patent ductus arterposus was or had been present preoperatively.The right ventricular preejection period was expressed as the ratio of the observed to the predicted value for a systemic left ventricle. This value was above normal In all groups and was not significantly different in the 13 patients with right bundle branch block. The observed ejection time expressed as a percent of that predicted for a systemic left ventricle correlated with right ventricular ejection fraction (r = 0.47). The ratio of the observed preejection period/ejection time had a higher correlation with right ventricular ejection fraction (r = ? 0.70). Nine patients had a low right ventricular ejection fraction (an ejection fraction of 0.55 or less was considered indicative of poor right ventricular function). These nine patients were all in group II and all had right bundle branch block.Most patients with poor right ventricular function had had a ventricular septal defect or patent ductus arteriosus before repair of the transposition, and postoperatively had angiographic tricuspld regurgitation, right bundle branch block, a preejection period/ejection time ratio greater than 0.55 and a percent predicted ejection time of 96 percent or less. Most patients who had good right ventricular function (ejection fraction greater than 0.55) had none of these findings. Systolic time intervals obtained with M mode echocardiography can be used for the assessment and longitudinal follow-up of right ventricular function in patients with transposition.     

Decreased systolic wall thickening in myocardium adjacent to ischemic zones in conscious swine during brief coronary artery occlusion

The purpose of this study was to examine wall thickening in normally perfused myocardium adjacent to acutely ischemic zones. Regional wall thickening (%WT), internal minor axis diameter, and hemodynamics were monitored in nine conscious swine during temporary occlusion of the left circumflex coronary artery (LCCA). Animals were chronically instrumented with ultrasonic dimension gauges for measuring left ventricular (LV) wall thickness and minor axis, catheters in the left atrium and aorta, and a pneumatic occluder around the proximal LCCA. During a 2-minute occlusion of the LCCA, radiolabeled tracer microspheres (10 μm) were injected into the left atrium to determine regional myocardial blood flow (RMBF). Within the ischemic zone, reduction of %WT was related linearly (Y = 24.9 X ?4.1, p < 0.001) to reduced RMBF and endocardial/epicardial blood flow ratio was reduced from 1.30 ± 0.12 (mean ± SE) to 0.87 ± 0.11 (p < 0.01). In zones adjacent to the ischemic zones RMBF was unchanged by LCCA occlusion. RMBF and %WT were poorly correlated (r = 0.38) and endocardial/epicardial blood flow ratio was unchanged from preocclusion values. Therefore, myocardium adjacent to ischemic zones may have reduced thickening despite no apparent blood flow changes. We conclude that such dysfunction may be due to either mechanical tethering effects or a reduction of global LV function due to the presence of an acutely ischemic zone.     

Depressed inotropic state and reduced myocardial oxygen consumption in the human heart

The relation between myocardial oxygen uptake (MVO₂) and the mechanical properties of left ventricular contraction were studied in 14 patients with and without left ventricular dysfunction. Coronary blood flow was estimated by helium washout, and left ventricular inotropic state was characterized from the mean left ventricular circumferential fiber shortening velocity in the minor equator (mean V_CF) and the value at peak tension (V_CF at max T). Ten patients with left ventricular dysfunction whose mean V_CF values were less than 1 circumference/sec were compared with patients whose mean V_CF values fell within the normal range. Patients with depressed shortening velocity had lower than normal average coronary blood tlow values (53 ± 3 vs. 70 ± 3 ml/100 g per min, respectively, P < 0.005) and reduced MVO₂ (75 ± 5 vs. 120 ± 6 μl/100 g per beat, P < 0.001). Coronary venous washout curves were well fitted by mono-exponential functions in normal patients but deviated appreciably from a single exponential in patients with left ventricular dysfunction, thereby indicating nonuniform distribution of coronary blood flow in the latter group. Peak and mean developed tension at the minor circumference, tension-time index, stroke work and fiber-shortening work per myocardial volume correlated poorly with MVO₂. However, mean V_CF and V_CF at max T correlated significantly with MVO₂ (r = 0.63, P < 0.02). These findings are in agreement with previous experimental findings demonstrating the importance of the contractile state as a determinant of myocardial oxygen consumption.     

Effects of changes in preload,afterload and inotropic state on ejection and isovolumic phase measures of contractility in the conscious dog

Despite much investigation, the usefulness of various indexes employed clinically for detecting alterations in ventricular contractility in the intact circulation remains controversial. The effects of acute preload, afterload and contractility changes on both ejection and isovolumic phase measures of left ventricular function were analyzed in normal, trained conscious dogs instrumented with micromanometers and endocardial ultrasonic diameter gauges. Rapid volume overload increased the excursion of the left ventricular diameter (Δ LVD) by 7 percent above the control level, but mean velocity of circumferential shortening (V_CF) did not change significantly; peak rate of left ventricular pressure rise (dP/dt) increased by 11 percent and (dP/dt)/DP40 (DP = developed pressure) was augmented by 10 percent, but maximal [(dP/dt)/LVP], or “V_pm” decreased by 20 percent. Pressure overload by phenylephrine infusion decreased Δ LVD by 15 percent and mean V_CF fell by 26 percent; peak dP/dt and (dP/dt)/DP40 remained unaltered, but V_pm was reduced by 37 percent. Isoproterenol augmented peak dP/dt by 55 percent, and (dP/dt)/DP40, V_pm and mean V_CF were increased comparably. Propranolol decreased these measures equally by about 16 percent. Therefore, in the conscious animal in the steady state, isovolumic phase indexes were mildly influenced by acute volume loading, whereas ejection phase indexes were not. Acute increases in aortic pressure markedly reduced ejection phase measures, whereas the isovolumic indexes were unaffected. All of the indexes studied were comparably sensitive to acute alterations in contractility, but we conclude that no single measure can always be used for defining an acute contractility change in the intact circulation.     

Serial measurements of left ventricular ejection fraction by radionuclide angiography early and late after myocardial infarction

The left ventricular ejection fraction was determined serially with radioisotope angiography in 63 patients with acute myocardial infarction. After the peripheral injection of a bolus of technetium-99m, precordial radioactivity was recorded with a gamma scintillation camera and the ejection fraction calculated from the high frequency left ventricular time-activity curve. Since this technique requires no assumptions with respect to left ventricular geometry, it is particularly useful in patients with segmental left ventricular dysfunction. Serial measurements during the first 5 days after hospital admission were made in 50 patients, 30 of whom were studied during the subsequent 2 to 39 months (mean 19.9 months). Late follow-up serial studies were also performed in an additional 13 patients who had only one measurement of the left ventricular ejection fraction during the early postinfarction period.Early after infarction, the left ventricular ejection fraction was normal (more than 0.52) in only 15 of the 63 patients, and averaged 0.52 ± 0.05 (standard deviation) in the 27 patients with an uncomplicated infarct. The ejection fraction was reduced in 24 patients with mild to moderate left ventricular failure (0.40 ± 0.05, P < 0.0001) and in the 12 patients with overt pulmonary edema (0.33 ± 0.07, P < 0.0001). In 35 patients the ejection fraction correlated with the mean pulmonary arterial wedge pressure (r = 0.72). In 15 patients with normal left ventricular wall motion by heart motion videotracking, the ejection fraction was significantly higher (0.53 ± 0.08) than in the 26 patients with regional left ventricular dysfunction (0.41 ± 0.10, P < 0.0001). During the early postinfarction period, the left ventricular ejection fraction improved in 55 percent of patients and remained unchanged or decreased in 45 percent. A further increase in the ejection fraction was noted in 61 percent of patients during the late follow-up period. Patients with an initially low or decreasing ejection fraction had a significantly greater incidence of early mortality and left ventricular dysfunction (P < 0.02) than those whose ejection fraction was normal or improved to normal early after infarction. These data indicate that the ejection fraction is a sensitive indicator of left ventricular function after acute myocardial infarction and that serial measurements are helpful in predicting early mortality and morbidity.     

Noninvasive assessment of clinical response to oral propranolol therapy

Nineteen patients with severe but stable angina pectoris entered a double blind controlled study to evaluate the effect of orally administered propranolol on exercise tolerance measured with a bicycle ergometer, and left ventricular function measured by echocardiography and systolic time intervals. In the group treated with propranolol the dose was increased from 80 to 320 mg/day. Studies including determination of propranolol blood levels were obtained before treatment and for each dose of propranolol. With propranolol, 80 mg/day, total work performance increased by 128 percent from 765 ± 125 before treatment to 1,792 ± 285 kilopond-meters (mean ± standard error) (P < 0.01). With 160 mg of propranolol daily, total work performance decreased, but remained higher than at control levels. In the group given propranolol, left ventricular function decreased progressively with increasing doses of the drug. As measured from the echocardiogram, maximal endocardial posterior wall velocity decreased 42 percent, from 72 ± 7 to 41 ± 4 mm/sec (P < 0.02); ejection fraction decreased 13 percent, from 0.68 ± 0.01 to 0.59 ± 0.01; and end-diastolic volume increased 28 percent, from 79 ± 11 to 102 ± 9 ml/m² (P < 0.05). The preejection period and the ratio between preejection period and left ventricular ejection time significantly increased with progressive dose increments. There was no correlation between blood level of propranolol and improved work performance. Exercise tolerance was maximally improved with doses of 80 to 160 mg/day. At higher dose levels left ventricular function deteriorated and exercise work decreased. Noninvasive assessment of left ventricular function proved more valuable than determination of drug blood levels in managing patients with angina pectoris and provided a guide to optimal adjustment of dosage.     

Assessment of mitral valve E point-septal separation as an index of left ventricular performance in patients with acute and previous myocardial infarction

A new echocardiographic index of left ventricular function, mitral valve E point-septal separation, was compared with the radionuclide ejection fraction determined using the first pass method in 60 patients (73 studies) with ischemic heart disease. Thirty-eight patients had acute myocardial infarction and 22 patients were studied an average of 24 months after acute infarction. In 30 normal subjects, E point-septal separation ranged from 0 to 5.4 mm (average 1.3 mm). In 57 studies (78 percent) E point-septal separation correctly identified patients with a normal or reduced ejection fraction (less than 0.52), but in 13 studies (18 percent) E point-septal separation was normal and ejection fraction depressed. In only three studies (4 percent) was there a normal ejection fraction and an abnormal E point-septal separation. Results did not differ between patients with acute infarction and those studied late after infarction. An E point-septal separation of more than 5.5 mm was highly specific (92 percent) for a reduced ejection fraction, but the sensitivity rate was only 65 percent. Abnormal wall motion as assessed with echocardiography or videotracking, or both, occurred equally among patients with normal and increased E point-septal separation, but this measure was less accurate in patients with more severe wall motion abnormalities. E point-septal separation was unrelated to heart rate; an abnormal value was equally distributed among patients with a normal and those with an enlarged left ventricular end-diastolic dimension on echocardiography. E point-septal separation was superior to other echocardiographic indexes of left ventricular function (percent of fractional shortening, mean rate of diameter shortening and ejection fraction). Thus, E point-septal separation is a simple noninvasive measure of left ventricular function. We conclude that an abnormal E point-septal separation is useful for identifying depressed left ventricular function in patients with acute myocardial infarction and chronic ischemic heart disease. However, 28 percent of our patients with a normal E point-septal separation had a depressed radionuclide ejection fraction. Therefore a normal value for E point-septal separation does not exclude the presence of abnormal left ventricular function in such patients.     

Echocardiographic study of cardiac dimensions and function in the endurance-trained athlete

Adaptive cardiac responses to isotonic training were studied with echocardiographic measurement of cardiac dimensions and function in 20 endurance runners whose maximal aerobic capacity on the treadmill was 4.88 ± 0.13 (mean standard error of mean) liters of oxygen/min. They were compared with 26 young sedentary control subjects whose capacity was 3.34 ± 0.11 liters of oxygen/min (P < 0.001). A modest degree of right and left ventricular chamber enlargement and left ventricular hypertrophy was observed in endurance runners (left ventricular mass index 140 ± 6 g/m² compared with 107 ± 4 g/m² in sedentary control subjects, (P < 0.001). Resting heart rate was slower in endurance runners (51 ±2 versus 62 ±2 beats/min, P < 0.001) and resting left ventricular function as evaluated with ejection fraction and maximal posterior wall shortening velocity and mean circumferential shortening velocity (V_CF) was comparable or slightly depressed in endurance runners (0.98 ± 0.03 versus 1.02 ± 0.05 circumferences/sec [difference not significant]). This study suggests that isotonic training results in adaptive changes in ventricular volume and mass, slower heart rates that may be associated with more efficient pumping function (that is, increasing stroke volume) and insignificant alterations in resting ejection phase indexes of left ventricular function.     

Assessment of left ventricular dimensions and function by echocardiography

Left ventricular dimensions and function indexes were measured in 40 patients with cardiac disease by both angiocardiographic and echocardiographic techniques. Good correlation was obtained between echocardiographic and angiographic values in 18 patients with technically excellent studies obtained by both techniques. The left ventricular echogram appears to be an effective technique for the noninvasive determination of left ventricular dimensions and volume. Echocardiographic indexes of ventricular function, including percent shortening of internal diameter, mean shortening velocity of internal diameter, ejection fraction, percent thickening of posterior wall and mean posterior wall velocity, distinguished between groups of patients with normal and abnormal left ventricular function. However, a single echocardiographic or angiographie measurement does not appear to provide selective data for the accurate functional classification of most individual patients.     

Accuracy of left ventricular ejection fraction determined by the nuclear stethoscope

We assessed left ventricular ejection fraction 47 times in 21 patients with sinus rhythm by a portable non-imaging nuclear probe. After ^99mTc blood pool labelling, left ventricular ejection fraction was determined by probe in two different ways: on a beat-to-beat basis, and by the so-called ventricular function mode, based on the gated equilibrium principle, and subsequently compared with left ventricular ejection fraction measured by gated equilibrium radionuclide angiocardiography using a gamma camera.Left ventricular ejection fraction by probe correlated well with left ventricular ejection fraction by gamma camera: beat-to-beat versus gamma camera: r = 0.90, y = 0.75x + 0.12; ventricular function versus gamma camera: r = 0.88, y = 0.87x + 0.08. Also, left ventricular ejection fraction values determined by the two probe methods correlated closely: r = 0.97, y = 0.83x + 0.07. Compared with the gamma camera, the probe overestimated slightly the small values of left ventricular ejection fraction and underestimated high values. Correct determination of left ventricular ejection fraction by a non-imaging probe depends on correct positioning over the left ventricle and selection of a proper background activity level.The main application of this instrument is probably non-invasive bedside determination and monitoring of changes of left ventricular function occurring spontaneously or caused by cardiac arrhythmias or treatment with cardiac drugs.     

Effects of submaximal isometric handgrip on left ventricular size and wall motion

To evaluate the effects of sustained submaximal isometric handgrip exercise on the left ventricle in patients with previous myocardial infarction, we utilized the noninvasive techniques of radarkymographic video tracking, measurement of the left heart dimension and calculation of systolic time intervals to assess alterations in wall motion and left ventricular size and function during handgrip exercise performed at a tension level of 15 percent of maximal voluntary contraction. In 9 of 12 patients with dyskinesis or asynchrony at rest the mean amplitude and velocity of systolic outward movement increased during handgrip exercise (P < 0.05), whereas in 11 patients with initially hypokinetic areas mean amplitude and velocity decreased (P < 0.05); in 3 patients dyskinesis was produced de novo. In all 12 patients both amplitude and velocity decreased in areas of normal wall motion (P < 0.05); similar changes occurred in 5 normal control subjects. Alterations in systolic time intervals during handgrip exercise were variable, and no consistent patterns were observed in either patients or control subjects. In seven patients whose left heart dimension increased during handgrip exercise, wall motion abnormalities were more severe at rest than in the five patients whose left heart dimension decreased. The five control subjects showed a decrease in left heart dimension during handgrip exercise.We conclude that the normal response to submaximal isometric handgrip exercise at 15 percent of maximal voluntary capacity is a decrease in left ventricular size and a reduction in both the amplitude and velocity of left ventricular wall motion. Furthermore, in patients with previous myocardial infarction sustained isometric handgrip exercise is a useful maneuver for the intensification or induction of left ventricular wall motion abnormalities. By contrast, no consistent alterations in systolic time intervals were observed during handgrip exercise either in normal subjects or in patients with previous myocardial infarction. Thus, systolic time intervals do not appear to be useful for evaluating the left ventricular response to submaximal handgrip exercise in individual patients.     

Internally recorded systolic time intervals in hypertrophic subaortic stenosis

The cardiac catheterization records of 20 patients with documented hypertrophic subaortic stenosis were analyzed to evaluate the utility of systolic time intervals in quantitating left ventricular outflow tract obstruction in this disease. The preejection period, ejection time and instantaneous peak outflow pressure gradient were measured from simultaneous recordings of the electrocardiogram and left ventricular and central aortic pressure signals, and the preejection period/ejection time (PEP/ET) ratio was computed. Most patients had a significant spontaneous or induced (with isoproterenol or postextrasystolic potentiation) variation in peak outflow gradient (range 0 to 186, average 85 mm Hg) with a high linear correlation between the peak outflow gradient and the systolic time intervals. For the group, peak outflow gradient correlated best with PEP/ET ratio (r = −0.82, no. = 183) and less well with preejection period (r = −0.62), ejection time (r = 0.56) or their rate-corrected values (r = −0.71 and r = 0.60, respectively). The PEP/ET ratio for beats recorded at the time of cardiac output measurement correlated with instantaneous mean outflow pressure gradient (r = −0.88, no. = 28, P < 0.001) and calculated left ventricular outflow orifice size (r = 0.72, no. = 28, P < 0.001), each of which correlated less well with preejection period, ejection time or their rate-corrected values. These findings indicate that the systolic time intervals are importantly affected by the degree of outflow obstruction as best exemplified in the relation between the PEP/ET ratio and mean outflow pressure gradient. In view of the previously documented close correspondence between internally and externally recorded systolic time intervals, the latter may be useful in the noninvasive assessment of outflow obstruction in this disease.     

Left ventricular performance in patients with atrial septal defect: evaluation with noninvasive methods

Eighteen patients with an atrial septal defect (Group I) and 45 patients whose defect had been repaired (Group II) were studied with echocardiography and systolic time Intervals. All patients In Group I had an increased right ventricular diameter (mean 24.5 mm/m²) that showed a direct linear relation to the size of the shunt (Qp/Qs ratio). In Group II the right ventricular diameter was significantly smaller (mean 15.6 mm/m²) (P < 0.001). The left ventricular diameter measured less than the mean normal value in 13 of the 18 patients in Group I (mean 23.2 mm/m²) and was significantly larger in the 45 in Group II (mean 27.7 mm/m²) (P < 0.001).Comparison of systolic time intervals in Groups I and II showed that patients in the former group had shorter mean left ventricular ejection time index (LVETI) (407.9 versus 420.8 msec, P < 0.05), a longer mean preejection period index (PEPI) (140.9 versus 126.7 msec, P < 0.001) and a higher mean ratio of preejection period to ejection time (PEP/LVET) (0.39 versus 0.33, P < 0.001). A direct linear relation existed between both the preejection period index and the PEP/LVET ratio and the size of the shunt (Qp/Qs) in Group I. In three patients the abnormal systolic time intervals were consistent with mildly diminished left ventricular performance preoperatively but promptly returned to normal postoperatively. However, echocardiographic assessment revealed that left ventricular wall contractility was normal or hyperdynamic in all cases.The mildly diminished overall left ventricular performance as shown by systolic time intervals appears to be related to the volume overload of the right ventricle and to the concomitantly diminished volume of the left ventricle rather than to any impairment of myocardial contractility. After closure of the defect the size of the ventricle and its performance return to normal.     

Quantitative left ventricular cineangiography in patients with chronic obstructive pulmonary disease.

Using quantitative measurements from cineangiograms, left ventricular function was evaluated in 19 patients with disabling COPD, 10 without and nine with previous right-sided heart failure. None had clinical evidence of diseases known to affect left ventricular function. Severity of airway obstruction was similar in patients without and with prior right-sided heart failure, but hypoxemia and pulmonary hypertension were significantly more severe in the latter. Mean resting cardiac index, left ventricular filling pressure and end-diastolic volume were normal in both groups. In 16 patients (10 without and six with prior right-sided heart failure), left ventricular function was clearly normal, as indicated by normal left ventricular wall motion, ejection fraction and mean velocity of circumferential fiber shortening (V_CF). The remaining three patients had abnormal left ventricular wall motion, ejection fraction and V_CF; these abnormalities could probably be attributed to coronary artery disease in two of the three patients but could not be explained in the third. Abnormal left ventricular function could not be correlated with the severity of COPD, hypoxemia or pulmonary hypertension. Left ventricular wall thickness and mass were normal in all, except for minimal increases in one patient without and one with prior rightsided heart failure. There are no previous reports of quantitative left ventricular cineangiography in patients with COPD, but our results are similar to those reported recently by investigators who measured ejection indices by other methods. It is concluded that a majority of patients with COPD, with or without right-sided heart failure, have normal left ventricular function in the absence of other heart disease.     

Inotropic effect of post-stimulation potentiation in man: an echocardiographic study.

To determine the magnitude of enhancement of the inotropic state in the intact human left ventricle, echocardiographic studies were performed in 11 subjects during pacing-induced changes in heart rate. Incremental atrial or ventricular pacing (80 to 160 beats/min) was performed for 1 minute at each rate, and echocardiographic variables of left ventricular function and indexes of left ventricular thickening were assessed for the post-stimulation beats and compared with the values obtained during sinus rhythm before pacing. For the first post-stimulation beat at maximal paced rates (146 ± 3 beats/min, mean ± standard error of mean), the ejection fraction (+23 percent P < 0.001), percent fractional shortening (+45 percent, P < 0.001) and mean velocity of circumferential fiber shortening (+45 percent, P < 0.001) increased significantly, whereas the end-systolic dimension (?22.4 percent, P < 0.001) and volume (? 52 percent, P < 0.001) decreased significantly. The end-diastolic dimension (+1.42 percent) and volume (+4.8 percent) did not change significantly. Similarly, septal thickening (+21.89 percent, P < 0.005), posterior wall thickening (+23.4 percent, P < 0.001), left ventricular thickening (+21.91 percent, P < 0.001) and the mean rate of left ventricular thickening (+33 percent, P < 0.001) increased significantly. Similar significant changes, although of a lesser magnitude, occurred at lower paced rates; the magnitude of these changes was proportional to the pacing rate. Decay in potentiation occurred within four to five beats after pacing was stopped at any given rate.Thus, in the intact human heart (1) the positive inotropic effects of stimulation on the left ventricle are reflected as post-stimulation potentiation, (2) potentiation is related to the pacing rate, and (3) decay in potentiation occurs rapidly when pacing is stopped.     

Echocardiographic prediction of left ventricular function after correction of mitral regurgitation: Results and clinical implications

Objectives. This study attempted to determine the incidence, prognosis and predictability of postoperative left ventricular dysfunction in patients undergoing correction of mitral regurgitation.Background. Left ventricular fonction in patients with mitral regurgitation is altered by loading conditions and is difficult to assess. Predictive value of preoperative variables on postoperative left ventricular function and the role of echocardiography are uncertain.Methods. In 266 patients undergoing correction of mitral regurgitation between 1980 and 1989, left ventricular fonction was echocardiographically assessed preoperatively (within 6 months) and postoperatively (within 1 year).Results. After correction of mitral regurgitation, left ventricular ejection fraction decreased significantly ([mean ± SD] 50% ± 14% vs. 58% ± 13%, p < 0.0001). Postoperative left ventricular dysfunction (ejection fraction < 50%) was frequent (41% of patients) and carried a poor prognosis (at 8 years survival, 38% ± 9% vs. 69% ± 8%, p < 0.0001). Four preoperative echocardiographic variables showed good correlation with postoperative ejection fraction: preoperative ejection fraction (r = −0.70), systolic diameter (r = −0.63), diameter/thickness ratio (r = − 0.64) and end-systolic wall stress (r = −0.62) (all p < 0.0001). With multivariate analysis, ejection fraction (p = 0.0001) and systolic diameter (p = 0.0005) were independent predictors of postoperative ejection fraction, and angiographic variables provided no incremental predictive power. In addition to echocardiographic variables, recent regurgitation, functional class and coronary artery disease were also independent predictors of postoperative ejection fraction.Conclusions. After surgical correction of mitral regurgitation, left ventricular dysfunction is frequent and carries a poor prognosis. Postoperative ejection fraction can be predicted by echocardiographic preoperative ejection fraction and systolic diameter. Recent onset of regurgitation, mild or no symptoms, and absence of coronary artery disease are independent and favorable predictors of postoperative ejection fraction. These results should lead to consideration of surgical correction at an earlier stage.