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In this study the effects of excimer laser (308 nm) angioplasty on arteries have been studied. We report histology and vasoreactivity properties of human atherosclerotic and normal coronary arteries and bovine coronary arteries after exposure to pulsed excimer laser irradiation. Segments of isolated and pharmacologically active human coronary arteries were obtained within 5-8 hr postmortem. Segments of bovine arteries were obtained from fresh hearts. Side branches were ligated and vessels perfused with Krebs-Ringer's-bicarbonate solution in a perfusion apparatus to maintain their viability. Excimer laser irradiation was performed using a fused silica fiber advanced through the artery within a polyethylene cannula to assist with steerability and to protect against perforation. The fiber delivered a total of 40-60 J at its tip at 100 mJ/pulse at 15 pulses/sec. A total of 5 human atherosclerotic, 2 human normal, and 8 bovine arteries were used. Ablation of plaque was accomplished with remarkable ease and little resistance. Histologic studies showed clear-cut wedges inscribed by the catheter along the arterial wall without charring or thermal effects of coagulation necrosis. Vasoreactivity was assessed by measuring flow changes during perfusion before and after excimer angioplasty using a transient challenge with the vasoconstrictor serotonin. All excimer-irradiated arteries showed no increase in vasoreactivity during the challenge and showed preservation of relaxation properties following the challenge. In conclusion, coronary artery angioplasty by excimer laser appears to allow for effective plaque ablation with simultaneous preservation of structure and pharmacological properties of arteries.

Objectives. The goal of this study was to develop an accurate, simplified proximal isovelocity surface area (PISA) method for calculating volume flow rate using lower blue-red interface velocity produced by a color Doppler zero baseline shift technique. Background. The Doppler color proximal isovelocity surface area method has been shown to be accurate for calculating the volume flow rate (Q) across a narrowed orifice by the formula Q = PISA × Blue-red interface velocity. A hemispheric model is generally used to calculate proximal isovelocity surface area (PISA = 2πa2, where a = the radius corresponding to the blue-red interface velocity). Although a hemispheric model is simple, requiring measurement of one radius, it may underestimate the actual volume flow rate because, in the general case, the shape of a proximal isovelocity surface area is hemielliptic. Although a hemielliptic model is generally more accurate for calculating proximal isovelocity surface area, it is more complex, requiring measurement of two orthogonal radii. Methods. Sixteen in vitro constant flow model studies were performed using planar circular orifices (diameter range 6 to 16 mm). The blue-red interface velocity was changed from 3 to 54 cm/s using color Doppler zero baseline shift. Results. 1) With decreasing blue-red interface velocity, the size of the proximal isovelocity surface area was increased, and its shape changed from hemielliptic to hemispheric. 2) With the blue-red interface velocity in the range 11 to 15 cm/s, the proximal isovelocity surface area became nearly hemispheric; however, it was difficult to determine the blue-red interface radius at a blue-red interface velocity

Normal aging in man is known to be associated with a reduction in left-ventricular diastolic function, including the rates of relaxation and filling. Calcium channel blockers have been reported to improve left-ventricular diastolic function in patients with various forms of heart disease. Clinically, the action of calcium channel blockers may be related to either a direct myocardial effect or may be secondary to the peripheral or coronary vasodilation effects. The purpose of this study is to investigate a possible direct effect of calcium channel blockers on modulation of the reported age-related reduction in myocardial relaxation. The direct effects on myocardial relaxation of the dihydropyridine calcium channel blocker, nifedipine, were studied in isolated, perfused interventricular septa and left-ventricular wall from eight young (ages 9 to 18 months) and 14 old (ages 3 to 5 years) rabbits. Septa were perfused with oxygenated Ringer's solution and paced at 48 beats/min. Maximum relaxation velocity per unit of developed tension [-dT/dt]/T, and relaxation time per unit of developed tension tR/T were continuously measured before and after infusion of calcium channel blockers. In absence of drugs, the older rabbits demonstrated a mean [-dT/dt]/T which was 32% lower (p0.003) and a mean tR/T which was 45% higher (p0.005) than the younger rabbits. When nifedipine was introduced at concentrations10(-8) M equivalent to doses above the therapeutic free-plasma concentration in humans, all contraction and relaxation parameters were depressed. However, at lower doses, equivalent to doses in the clinical therapeutic range, [-dT/dt]/T was increased in the older rabbit septa by 18% in the presence of nifedipine. tR/T was shortened in the older rabbit septa by 17% in the presence of nifedipine. Myocardial relaxation in older rabbits after drug infusion approximated these parameters in the younger rabbits prior to drug infusion (P = NS). Calcium channel blockers had similar beneficial effects on the relaxation properties of the myocardium in younger rabbits. All beneficial effects were observed at concentrations of calcium channel blockers which were within and below the clinically therapeutic range of plasma free drug concentration, i.e., 5 x 10(-9) to 4 x 10(-8) M. Potential differences in relaxation effects related to different segments of the myocardium and different mechanical recording vectors were evaluated. Isolated left ventricle preparations from aging rabbits demonstrated improvements in tR/T and [-dT/dt]/T similar to those observed in the septum. Furthermore, improvement in mechanical function along the y-axis and x-axis vectors of the septum was similar.(ABSTRACT TRUNCATED AT 400 WORDS)

Chronic pulmonary hypertension in humans is characterized by shortening of the pulmonary artery acceleration time as measured by Doppler echocardiography, such that the higher the pulmonary artery pressure, the shorter the pulmonary acceleration time. Increases in heart rate are also known to produce decreases in the pulmonary artery acceleration time. To explore the relationship between mean pulmonary artery pressure, heart rate, and Doppler pulmonary artery acceleration time, experimental acute pulmonary hypertension was created in nine Duroc swine, either by infusion of Sephadex beads with embolization of the pulmonary arterial circulation or by partially occluding the main pulmonary artery 8 to 10 cm distal to the pulmonic valve. Pulmonary artery Doppler flow velocity recordings and invasive pressure measurements were made at baseline and at paced atrial rates ranging from 60 to 160 beats per minute, in 20-beat increments. The results in this acute animal model reveal that increases in heart rate produced significant decreases in Doppler pulmonary artery acceleration time at mean pressures below 25 mm Hg. However, with mean pulmonary artery pressures greater than 25 mm Hg, both heart rate and increases in pulmonary artery pressure had no significant effect on acceleration time. (Chest 1991; 100:470-73)

To determine which factors may affect the image quality when an intravascular ultrasound catheter is used in vivo, the influence of blood, temperature change, and contrast media were evaluated. In addition, to confirm the reproducibility of intravascular ultrasound imaging to measure cross-sectional lumen area, intraobserver and interobserver variability were determined. The findings indicated that ultrasound images in blood are mildly attenuated, that changes from room temperature to body temperature do not have a significant impact on the image quality, that contrast media attenuates the image intensity in a dose-dependent manner, and that the intravascular ultrasound imaging catheter provides a reproducible method for measuring arterial lumen area with excellent intraobserver and interobserver correlation. © 1990, American Society of Echocardiography. All rights reserved.

A method to assess the degree to which an atheroma plaque has been disrupted by percutaneous interventional methods could be of considerable benefit. An intravascular ultrasound catheter could provide quantitative information about the distribution and quality of the atheroma prior to and following a balloon dilatation, laser, or atherectomy procedure. Additionally, the ultrasound transducer could be configured within an angioplasty balloon to visualize the arterial wall in cross section during the dilatation. Visualization of the atheroma and arterial wall also might be of benefit to help characterize the type of tissue within the plaque, which may potentially help suggest which of several alternative therapies may be most effective. The intravascular imaging catheter would provide a feasible method of identifying normal and diseased arterial wall structures during diagnostic and interventional angiographic procedures. This distinction is critical during laser therapy of eccentric plaques to prevent exposure of the uninvolved wall (Fig. 7). These high quality ultrasound images may allow quantitative assessment of the extent of atheromatous involvement of artery walls as well as the character of the atheroma tissue. Such an approach, performed percutaneously in the catheterization lab, could represent a fundamental departure from traditional angiographic methods for assessing the severity of coronary, carotid, or peripheral arterial disease.

A prototype intravascular ultrasound imaging catheter with a 20 MHz transducer was used to obtain 59 cross-sectional images in 14 segments of human atherosclerotic arteries. Three distinct components of the arterial wall were visualized on the ultrasound images: a highly reflective intima, an echolucent media, and a moderately reflective adventitia. Images were obtained at 1 mm increments in vitro and were compared with histologic sections at the same levels. Measurements of the arterial layers showed a close correlation between ultrasound images and histologic sections for the thickness of the intimal plaque (r = 0.91), the media (r = 0.83), and the total wall thickness (r = 0.85). The ultrasound images overestimated the mean intimal and total wall thickness by 0.3 mm and 0.7 mm compared to measurements in histologic sections (p less than 0.001). Intravascular imaging with high-frequency ultrasound is an accurate method for measuring microanatomic arterial dimensions and the extent of atheromatous involvement of the arterial wall. This method could represent an important adjunct to traditional angiographic techniques for assessing the severity of atherosclerosis.

This manuscript describes a new method, validated in in vitro models, for quantitating volume flow rate across an orifice with Doppler color flow mapping. Flow through a narrowed orifice is characterized by the convergence of radial streamlines proximal to the orifice. In this color Doppler method, one or more isovelocity surface areas (PISA), delineated by blue and red aliasing velocity interfaces, can be identified proximal to the narrowed orifice. Volume flow rate (in milliliters per second) can then be calculated as PISA (in square centimeters) multiplied by the isovelocity of the PISA (in centimeters per second). Doppler color flow mapping was performed in in vitro models of constant and pulsatile flow through an orifice in a wall. The first proximal isovelocity surface area, with an isovelocity corresponding to the aliasing velocity, that is, one half the Nyquist sampling limit, could be identified as a blue and red color interface proximal to the orifice. Over a range of circular orifice diameters from 3 mm to 16 mm and flow rates from 0.5 to 18.7 L/min, the proximal isovelocity surface area could be imaged in two planes. This PISA was best described by a hemielliptic mathematical model with two different radii measured from long-axis and short-axis views. In the constant flow model, volume flow rate calculated from the Doppler PISA correlated well with actual volume flow rate measured simultaneously with a cylinder and stopwatch (r = 0.98, p less than 0.001, standard error of the estimate [SEE] = 0.36 L/min). In the pulsatile flow model, with jet velocities ranging from 2.6 to 7.7 m/sec and flow volume ranging from 1.0 to 10.3 L/min, calculated volume flow rate also demonstrated an excellent correlation with actual volume flow rate (r = 0.99, p less than 0.001, SEE = 0.53 L/min). Findings from these in vitro models suggest that quantification of the proximal isovelocity surface area by Doppler color flow mapping appears to be a promising technique for estimating volume flow rate across a narrowed orifice. This new color Doppler flow method may have advantages over previous Doppler methods in estimating volume flow rate in various clinical situations, for example, valvular regurgitation and shunt lesions.

To evaluate the mechanism of excimer laser recanalization and compare the results with those of laser-assisted thermal probe recanalization and mechanical recanalization, a total of 42 human atherosclerotic totally occluded arterial segments (2–15 cm long) were recanalized by excimer laser with a 400–800 micron quartz fiber pulsed at 20 Hz with 50 mJ/mm2of energy (n = 21), an Argon heated thermal probe at 10–12 watts (n = 11), a guidewire directed through a 6 Fr multipurpose catheter, or an angioplasty balloon catheter (n = 10). On histologic examination, the excimer laster created a single round lumen or multiple lumens (“Swiss-cheese” like appearance) with no evidence of thermal injury at the perimeter of the lumen. The incidence of perforation in vitro was less with an excimer laser catherter (8/21 or 38%) than with the thermal prove (10/11 or 91%) (p

In color Doppler flow studies, "variance" is an important display modality for diagnosing stenotic, regurgitant, and shunt lesions. Variance, a mathematical calculation based on the variation in the Doppler signal frequencies, has been reported to reflect the degree of flow disturbance. A wide-band pulsed Doppler spectrum results in a larger degree of variance. It has been suggested that variance area (green color or mosaic area) might provide useful quantitative information regarding the severity of stenotic, regurgitant, and shunt lesions. Since ultrasound machine settings may affect the color Doppler variance image, we evaluated in 101 free jet experiments the effect of packet size (eight versus four samples per line), pulse repetition frequency (3.9 versus 5.2 kHz), frame rate (11 versus 22 frames per second), system gain (+15 dB versus -15 dB), transmit power (high versus low), and moving target indicator (MTI) filter setting (high versus low) on variance display. The variance area was planimetered using an image analysis computer. The following machine parameters were inversely correlated with variance area: (1) packet size (p less than 0.01), (2) pulse repetition frequency (p less than 0.001), and (3) frame rate (p less than 0.05). Both system gain (p less than 0.001) and wall filter setting (p less than 0.01) showed a direct correlation with variance area. We conclude that machine factors must be standardized in evaluating stenotic, regurgitant, and shunt lesions by color Doppler variance display imaging.

Downloaded from www.ajronline.org by Univ of California Irvine on 10/07/15 from IP address 128.200.102.37. Copyright ARRS. For personal use only; all rights reserved Case The Mechanism Assisted of Peripheral Thermal Intravascular Recanalization Angioplasty: Cres P. Miranda,1 Larry Deutsch,2 The mechanism of recanalization during laser-assisted an- gioplasty in the treatment of obstructive atherosclerotic vas- cular disease has been controversial. Initial reports claimed that the laser-heated metal-tipped probe ablated atheroma as the hot tip “sought the lumen” and progressed down the artery as it created a new lumen in the central portion of the plaque [1 -3]. In distinction to the initial animal and clinical studies, an in vitro study of the mechanism of recanalization with laser-assisted thermal angioplasty found it to be a pre- dominantly mechanical process in which the laser probe was deflected by the hard, fibrocalcific plaque away from the true lumen and followed a dissection plane between the intimal plaque and the arterial media [4]. However, in human clinical trials, it is difficult to prove the exact pathway of the laser probe by using angiography or angioscopy. Recent work has documented the feasibility of imaging arteries in cross-section with a miniaturized catheter-mounted transducer that generates arterial images from inside the artery lumen [5, 6]. This report documents that the information obtained from the intravascular sonographic de- vice in vivo is consistent with the hypothesis derived from our in vitro study for the mechanism of recanalization by the laser probe. Received 1 Division 2 Division Confirmation Jim Griffith,3 Case 4 The Beckman AJR 155:1100-1102, Inc., Santa Laser by Jim Gessert,3 (SFA) man with claudication occlusions Institute, Irvine, the 100 © American Berns,4 at the had bilateral superficial bifurcation with the common femoral femoral right SFA was 20 cm, and the left SFA was occluded 23 cm. The right femoral artery was recanalized in a retrograde fashion from a puncture in the popliteal fossa. A 1 .5-mm-diameter laser probe (Model PLA-plus, advanced under and an 8-French Trimedyne fluoroscopic angioplasty Inc., Santa Ana, CA) was inserted control guiding through catheter. and an introducing sheath The laser probe was used as a cold mechanical device without turning on the argon laser. The laser probe was advanced by using intermittent forward pressure to puncture the occlusive atheroma. The course of the laser probe was followed under fluoroscopic control until it advanced to the proximal end of the SFA and reentered the lumen of the common femoral artery. The laser probe was then removed, and a guidewire was inserted through a 7-French diagnostic catheter, which was used in a rotary maneuver to enlarge the communication between the SFA and the common femoral artery. The 20-MHz sonographic catheter (Interlherapy, Inc. , Costa Mesa, CA) was advanced in the new channel to the level of the common Figure 1 A shows the level of the distal Roentgen the intravascular SFA before femoral artery. sonogram the sonographic that was obtained catheter , Orange, CA 92668. Address reprint requests to J. M. Tobis. CA 92668. CA 92717. 1990 0361-803X/90/1 Michael artery. Both popliteal arteries were reconstituted, and distal runoff was good. The patient refused surgical intervention but was willing to undergo percutaneous angioplasty. The length of the occlusion of Ana, CA 92705. November Avi Bergman,3 Report A 73-year-old artery February 1 2, 1 990; accepted after revision April 27, 1990. of Cardiology, University of Califomia, Irvine, Medical Center, P.O. Box 14091 of Radiologic Sciences, University of Califomia, Irvine, Medical Center, Orange, InterTherapy by Laser- Sonography Jonathan M. Tobis,1 and Walter Henry1 sonographic Report Ray Society entered at

The Doppler color jet area depicting a regurgitant or shunt lesion may be useful in estimating its severity. However, color jet area may be affected by technical factors. We studied the combined effects of Doppler angle, frame rate, and scanning direction on the Doppler color jet area of a free jet with 10-mL injection. Results: (1) Angle effects: color flow area was 11.7 ± 2.0 cm2 at a Doppler angle of 20°, and 2.3 ± 1.2 cm2 at an angle of 60°, when other parameters were kept constant (frame rate=12 frames/sec, reverse scanning direction). (2) Frame rate effects: with other parameters kept constant (Doppler angle = 20°, reverse scanning direction), color flow area was 11.7 ± 2.0 cm2 at a rate of 12 frames/sec and 6.5 ± 1.8 cm2 at 6 frames/sec. (3) Scanning direction effects: with other parameters kept constant (Doppler angle=20°, frame rate = 9 frames/sec), color flow area was 7.3 ± 1.1 cm2 with scanning in the reverse direction, and 20.5 ± 1.6 cm2 with scanning in the forward direction. (4) Combined effects: In our in vitro studies, the maximum color flow area was 20.5 ± 1.6 cm2, and the minimum area was 1.5 ± 0.2 cm2 (nearly twelve-fold). Conclusions: Doppler color jet area correlated inversely with Doppler angle (P

An array of miniature ultrasound crystals mounted on preassembled subassembly which is, in turn, mounted on a small lumen catheter provides dimensional and other quantitative information relating to arterial wall geometry and character at disease or obstruction sites. Balloons also mounted to the catheter make it possible to use the catheter for the angioplasty (PCTA) procedure while actually imaging, in real time, the artery being dilatated and unblocked by the procedure. Efficient, highly miniature transducers are presented along with several different configurations for catheter structure containing fluid lumen, through-lumen, and electrical microcable assemblies for conducting electrical signals to and from the transducers.

Using a mechanical sector-scanner, two-dimensional echocardiograms were obtained from 28 normal subjects, 15 patients with tetralogy of Fallot, 11 patients with complete transposition of the great arteries and six patients with double outlet right ventricle. The image obtained perpendicular to the long axis of the left ventricle at the base of the venticular septum was superimposed on the image obtained perpendicular to the long axis at the origin of the great arteries. In normal subjects, these superimposed images demonstrated that the aorta originated posterior and to the left of the ventricular septum. In patients with tetralogy of Fallot, the aorta was displaced anterior and to the right resulting in the aorta over-riding the ventricular septum. In patients with double outlet right ventricle both great arteries originated anterior to the ventricular septum (i.e., from the right ventricle). In patients with complete transposition, the aorta originated anterior and the pulmonary artery posterior to the ventricular septum. Thus, cross-sectional echocardiography permits noninvasive identification of the relation of the ventricles and great arteries and, therefore, provides important information for the diagnosis of patients with congenital heart disease.

Peak early diastolic left ventricular (LV) filling rate has been used as an index of LV diastolic function. However, it is known to be affected by LV size. Peak early diastolic transmitral flow velocity measured by pulsed Doppler echocardiography has also been proposed as a noninvasive method of assessing LV diastolic function. To determine if peak early diastolic mitral flow velocity also is influenced by LV size, 20 normal neonates (age 2 days) and 21 normal adults (mean age 38 years) were studied using pulsed Doppler echocardiography to measure mitral flow velocity and M-mode echocardiography to estimate LV end-diastolic volume and mitral valvular area. Peak early diastolic LV filling rate was calculated by multiplying peak early diastolic mitral flow velocity by mitral valvular area. Adults had significantly larger LV end-diastolic volumes (mean +/- standard deviation 108 +/- 25 vs 7 +/- 3 ml) and higher peak early diastolic LV filling rates (305 +/- 75 vs 29 +/- 10 ml/s) than neonates (both p less than 0.001). However, no significant difference was found in peak early diastolic mitral flow velocity between adults and neonates (61 +/- 10 vs 58 +/- 11 cm/s). These data suggest that peak early diastolic mitral flow velocity is independent of LV size. Since peak LV filling rate is equal to the product of peak mitral flow velocity and mitral valvular area, the correlation between peak early diastolic LV filling rate and LV size is probably due to differences in mitral valvular area rather than differences in peak mitral flow velocity.

The heart was evaluated by echocardiography in 56 patients at risk for myocardial iron deposition. Fifty-four had congenital anemia for which they required repeated transfusions, and two had primary hemochromatosis. The data, plotted according to one of three functions of the body surface area, were compared to values obtained in 105 normal subjects whose age spanned a similar range. Left ventricular wall thickness, transverse dimension and mass, as well as left atrial transverse dimension, were increased in the majority of patients with chronic iron overload despite the infrequent occurrence of cardiac enlargement on routine chest films (32 per cent) or electrocardiographic abnormality (16 per cent). Left ventricular ejection fraction was normal in all but four patients. These four patients died within a six month follow-up period suggesting that deterioration in systolic function is an indicator of poor prognosis. Our findings indicate that echocardiography provides a simple noninvasive means for assessing changes in cardiac structure and function that should prove useful in the serial evaluation of patients who are at risk for the development of myocardial iron deposition.

To assess the type and prevalence of cardiac abnormalities in heavy drinkers with and without overt congestive heart failure, M mode echocardiography was performed in 11 symptomatic chronic alcoholics with dilated (congestive) cardiomyopathy and in 22 asymptomatic chronic alcoholics. Echocardiographic data in both groups were adjusted for age and body surface area using previously derived regression equations. All 11 symptomatic patients had a significantly decreased left ventricular percent fractional shortening (mean 14 percent, normal range 28 to 44) along with significant increases in left ventricular systolic and diastolic dimensions (mean increases of 105 and 48 percent above normal, respectively), left atrial dimension (mean increase 21 percent) and estimated left ventricular mass (mean increase 105 percent). Among the 22 asymptomatic patients, 15 (68 percent) demonstrated significant increases in at least one of the following echocardiographic variables: left ventricular mass, left ventricular dimensions, septal and left ventricular wall thicknesses, and left atrial dimension. Asymptomatic patients could be classified into two subgroups: (1) those with a left ventricular diastolic dimension less than 10 percent above the normal predicted value and an increased left ventricular wall thickness to radius ratio (mean increase 16 percent above normal) and upper normal percent fractional shortening, and (2) those with a left ventricular diastolic dimension 10 to 24 percent above normal and a slightly subnormal thickness to radius ratio and lower normal percent fractional shortening. Echocardiographic abnormalities in asymptomatic chronic alcoholics did not correlate with the presence or absence of auscultatory abnormalities on physical examination and appear to reflect an earlier stage in the spectrum of alcoholic disease before the development of dilated cardiomyopathy.

Pulsed Doppler echocardiography was used to examine the relation between pulmonary valve motion and pulmonary artery (PA) flow velocity patterns in 39 adults. In 16 patients with normal PA pressure (mean pressure less than 20 mm Hg), PA flow velocity accelerated slowly to a peak flow velocity at midsystole (time to peak flow velocity, or acceleration time = 134 +/- 20 ms [mean +/- standard deviation]), followed by a slow deceleration to the end of ejection, producing a "dome-like" appearance. In contrast, in 23 patients with elevated PA pressure (mean pressure 20 mm Hg or more), flow velocity accelerated rapidly to a peak flow velocity in early systole (acceleration time = 88 +/- 25 ms, p less than 0.01), followed by rapid flow velocity deceleration to a nadir in midsystole. In 13 of these patients, a transient increase in flow velocity occurred in late systole, producing a "spike and dome" appearance. In patients with an acceleration time of 120 ms or less, there was a negative linear correlation with mean PA pressure, expressed by the equation: mean PA pressure = 90 - (0.62 X acceleration time). The standard error of the estimate was 8.3 mm Hg. A similar negative linear correlation was found between PA acceleration time and total pulmonary resistance. Using a PA acceleration time of 100 ms or less resulted in a 78% sensitivity and a 100% specificity for detection of elevated PA pressure. Although this Doppler method cannot precisely estimate PA pressure, it can be helpful in separating patients with normal pressure from those with elevated PA pressure.

Clinical and pathologic observations were made in four infants who died with asymmetric septal hypertrophy in the first five months of life. One of these infants was stillborn and the other three were aged 1½ months, 4½ months, and 5 months at the time of their deaths. The three live-born infants demonstrated severe congestive heart failure and cardiac enlargement. The clinical features present in these three infants during life suggested a variety of other congenital cardiac malformations, including congenital mitral regurgitation, pulmonary stenosis, and endocardial fibroelastosis. In each of the four infants the ventricular septum was markedly hypertrophied and was thicker than the postero-basal left ventricular wall; septal to postero-basal free wall thickness ratios ranged from 1.8 to 2.6. Moreover, the septum of each infant contained a disordered arrangement of hypertrophied cardiac muscle cells. In three of the infants the myocardial cellular abnormalities were less marked in the left ventricular free walls than in the ventricular septum. In the fourth infant disorganized cardiac muscle cells were distributed widely in both the ventricular septum and left ventricular free wall; the clinical findings suggested the absence of left ventricular outflow obstruction in this infant. Asymmetric septal hypertrophy was documented in one first degree relative of each infant. It is concluded that asymmetric septal hypertrophy is a genetically transmitted disease that may present clinically in infancy and lead to infant death. Furthermore, the characteristic pathologic feature of asymmetric septal hypertrophy in adults, a disproportionately thickened ventricular septum containing numerous hypertrophied and disorganized cardiac muscle cells, can be present at birth.

To test for an association between the results of ambulatory electrocardiographic monitoring (AEM) and programmed electrical stimulation (PES), or whether other factors better predict the results of PES, 57 patients (36 male and 21 female patients) presenting with either ventricular fibrillation (49 percent; 28/57) or sustained ventricular tachycardia (51 percent; 29/57) were studied. Each patient underwent AEM and PES using up to three ventricular extrastimuli. Sixty-three percent (36/57) had coronary disease; and of these, ventricular tachycardia was present during AEM in 64 percent (23/36) and induced by PES in 78 percent (28/36). With the addition of patients with other cardiac diagnoses, the results were 58 percent (33/57) and 60 percent (34/57), respectively. No AEM variable was positively associated with inducible ventricular tachycardia, including frequency of ventricular premature depolarizations, multiformity, couplets, or ventricular tachycardia. Clinical variables positively associated with inducible ventricular tachycardia were coronary disease, previous myocardial infarction, left ventricular dysfunction, male sex, and a history of recurrent arrhythmia. Therefore, clinical characteristics are more useful for predicting the results of PES than information derived from AEM.

Attempts to measure left ventricular stroke volume utilizing the Doppler aortic flow method have found varying correlations between invasive thermodilution and noninvasive Doppler methods. Because stroke volume is the product of the Doppler flow velocity integral (that is, the area under the flow velocity curve) and the cross-sectional area of the vessel through which blood flows, both variables are potential sources of error. Previous studies have shown that the Doppler flow velocity integral can be measured with acceptable reproducibility in the ascending aorta. Consequently, in this study an attempt was made to determine empirically the optimal method for measuring aortic diameter and area. The diameter of the ascending aorta was measured utilizing four Mmode and seven two-dimensional echocardiographic conventions. Doppler aortic flow velocity patterns were recorded with a 2.25 MHz M-mode echocardiographic transducer from the suprasternal notch by mapping the ascending aorta until aortic peak flow velocity was recorded. In 19 adult patients undergoing cardiac catheterization for clinical indications, Doppler stroke volume estimates utilizing the various echocardiographic conventions for measuring aortic root diameter and area were compared with simultaneous measurements of stroke volume by the thermodilution technique. The best correlation (r = 0.87) with thermodilution stroke volume was obtained by estimating aortic area from the two-dimensional parasternal long-axis images with the aortic dimension measured distal to the aortic sinuses from the inner to inner wall. The data were related by the equation: Thermodilution stroke volume=(0.73)×(two-dimensional Doppler stroke volume)+17cc. M-mode echographic measurements of aortic diameter resulted in Doppler estimates of left ventricular stroke volume that correlated poorly (r < 0.3) with thermodilution estimates. © 1985, American College of Cardiology Foundation. All rights reserved.

The major cause of morbidity and mortality in patients with the hypereosinophilic syndrome is cardiac dysfunction. A review of 65 cases from the literature (historic series) revealed the following cardiovascular manifestations to be most common: dyspnea (60 per cent), signs of congestive heart failure (75 per cent), murmur of mitral regurgitation (49 per cent), cardiomegaly (37 per cent), T wave inversions on electrocardiogram (37 per cent) and pathologic findings of endocardial fibrosis, myocardial inflammation and mural thrombus formation (57 per cent). We have prospectively followed 26 patients with the hypereosinophilic syndrome for up to nine years (average follow-up prospectively was 3.3 years, retrospectively 5.7 years). Common cardiac findings in our 26 patients were dyspnea (42 per cent), chest pain (27 per cent), signs of congestive heart failure (38 per cent), murmur of mitral regurgitation (42 per cent), cardiomegaly (35 per cent) and T wave inversions (35 per cent). Thus, these patients demonstrated cardiovascular manifestations similar to those in the historic series, although the literature review showed a higher incidence of overt congestive heart failure. Of 22 patients having echocardiograms, 55 per cent demonstrated some clinical, roentgenographic or electrocardiographic evidence of cardiac involvement, but 82 per cent had echocardiographic abnormalities. This suggests that the echocardiogram is a sensitive and perhaps early indicator of cardiac involvement in this disease. Common echocardiographic findings included increased left ventricular wall thickness (68 per cent), left ventricular mass (73 per cent) and left atrial size (37 per cent). Prospective echocardiographic follow-up of 18 patients (for up to four and a half years) revealed that seven of eight untreated or inadequately treated patients had increases in left ventricular wall thickness, whereas all 10 adequately treated patients had decreases (eight of 10) or no change (two of 10) in left ventricular wall thickness. This suggests that adequate antihypereosinophilic therapy (with prednisone and/or hydroxyurea) may stabilize and, in some cases, reverse the cardiac manifestations of the hypereosinophilic syndrome. In previous studies, congestive heart failure due to eosinophilic cardiomyopathy has been reported to be very resistant to therapy. In our patients with congestive heart failure, treatment has been almost invariably effective when digitalis and diuretics were combined with adequate antihypereosinophilic therapy.

Cardiovascular complications are a major source of morbidity and mortality in hypertensive patients. To assess the prevalence of anatomic and functional abnormalities of the heart in such patients, we studied 234 asymptomatic subjects with mild-to-moderate systemic hypertension by echocardiography. After adjusting the echocardiographic values for age and body surface area, we found abnormally increased ventricular septal and/or posterobasal free-wall thickness in 61% of the hypertensive subjects. We found increased left atrial, aortic root, and left ventricular internal dimension (at end-diastole) in 5-7%, and decreased mitral valve closing velocity (E-F slope) and left ventricular ejection fraction were noted in six and 15% of the subjects, respectively. Four percent of the patients had disproportionate septal thickening (i.e., ventricular septal-to-left ventricular free-wall thickness ratio greater than or equal to 1.3). In contrast to the high prevalence of cardiac abnormalities detected by echocardiography, less than 10% of the hypertensive subjects had abnormal 12-lead ECGs or abnormal chest x-rays. These findings demonstrate a high prevalence of cardiac abnormalities in a population of asymptomatic hypertensive subjects. These abnormalities can be detected by echocardiography before they are otherwise apparent.

We compared determinations of cardiac output using various combinations of injectate volumes and temperatures to results obtained with 10 ml of iced (0°C) injectate (standard technique) in 33 critically ill patients. The use of a 10-ml injectate at room temperature resulted in comparable reproducibility (12.7 vs 10.8 percent; not significant) and a small and nonsignificant error (–0.013 ± 0.543 L/min). Five milliliters at room temperature resulted in markedly decreased reproducibility (17.9 vs 8.9 percent; p

Fifty consecutive patients undergoing aortic valve replacement for isolated aortic regurgitation were studied prospectively by echocardiography, electrocardiography and cardiac catheterization. Good quality echocardiograms were obtained in 49 of the 50 patients. Left ventricular (LV) dilatation was present in all 49 patients. LV systolic function, as assessed by echocardiographic percent fractional shortening, was normal in many patients but was moderately to severely reduced (less than 25%) in 14 patients (29%). Echocardiographic studies 6 months postoperatively revealed significant reductions in LV end-diastolic dimension (73.8 mm vs 58.7 mm; p less than 0.01), and serial echocardiographic studies early and late after operation revealed that the decrease in LV size had occurred by the time of the early study (8-22 days postoperatively), with little additional change thereafter. Operative deaths occurred in three of the 49 patients (6%). Eight of the 49 patients (16%) died of congestive heart failure (CHF) after hospital discharge at times ranging from 5-43 months after operation. Preoperative echocardiographic measurements of the LV end-systolic dimension and percent fractional shortening were strongly associated (p less than 0.01) with these late CHF deaths. Preoperative LV end-systolic dimension greater than 55 mm and fractional shortening less than 25% identified the high-risk group: nine of 13 patients (69%) in this group died either at operation or subsequently from CHF. In contrast, of 32 patients with LV end-systolic dimension less than 55 mm, only one died at operation and one died late from CHF. Thus, the population at high risk of late death from CHF was identified before operation by echocardiography.

Left ventricular ejection fraction (LVEF) was calculated from 25 first-pass digital subtraction angiograms using a densitometric analysis. Digital subtraction angiograms are obtained in a computerized format; therefore, they can be readily analyzed with computer software to measure the density of the iodine signal within the image. The video signals from the image intensifier were logarithmically amplified so that there was a linear correlation between the video signal intensity and the depth of the iodine contrast material represented by that video signal. LVEF was also calculated by the area-length method from the same digital subtraction angiograms. There was close correlation between these two techniques (r = 0.94, standard error of the estimate = 5.04%). The videodensitometric EF technique is simple to perform, it correlates well with the standard area-length method, and is not dependent on geometric assumptions of LV geometry. © 1983.

In an attempt to define quantitatively the relation between left atrial size and atrial fibrillation, echocardiography was used to study 85 patients with isolated mitral valve disease, 50 patients with isolated aortic valve disease, and 130 patients with asymmetric septal hypertrophy. In all three groups of patients, atrial fibrillation was rare when left atrial dimension was below 44 mm (3 of 117 or 3%) but common when this dimension exceeded 40 mm (80 of 148 or 54%). In addition, when left atrial dimension exceeds 45 mm, cardioversion, while initially successful, is unlikely to produce sinus rhythm that can be maintained at least six months. These data suggest that left atrial size is an important factor in the development of atrial fibrillation and in determining the long term result of cardioversion. The pathophysiologic mechansim most consistent with this is that a chronic hemodynamic burden initially produces left atrial enlargement which in turn predisposes to atrial fibrillation. Only prospective studies will determine definitively whether these observations will be useful in decisions concerning prophylactic anticoagulation and elective cardioversion.

Successful therapy of atrial fibrillation (AF) has been reportedly influenced by a variety of factors including patient age, type of underlying heart disease, duration of arrhythmia, left ventricular function and left atrial (LA) size. To determine which of these factors are associated with maintenance of sinus rhythm after conversion, 43 patients with symptomatic chronic AF in the setting of a dilated left atrium (greater than or equal to 45 mm, range 45 to 78) were followed for at least 6 months after the return of sinus rhythm. Class IA drugs, IC drugs or amiodarone were used for therapy. Life table analysis showed sinus rhythm to be maintained in 81% for 6 months, 79% for 12 months and 60% for 24 months. Factors positively associated with success were conversion with drug therapy alone, duration of chronic AF less than or equal to 1 year, absence of mitral valve disease and LA dimension less than or equal to 60 mm (all p less than 0.05). Patient age, left ventricular function and presence of coronary disease were not associated with outcome. Thus, patients with moderate LA dilatation (45 to 60 mm) and a short duration of chronic AF can often be maintained in sinus rhythm, especially if they convert with pharmacologic intervention alone.

The results of operative treatment in 83 patients with idiopathic hypertrophic subaortic stenosis (IHSS) are described. Most patients with the disease are asymptomatic, or derive satisfactory symptomatic improvement from nonoperative therapy: administration of propranolol, exerice limitation, control of arrhythmia, etc. Operation is required, however, in 10-15% of patients, those who remain severely symptomatic after nonoperative treatment or who become refractory to it. Operation relieves symptoms in IHSS by relieving obstruction to left ventricular outflow, and for a patient to be considered an operative candidate severe obstruction must be documented at left heart catheterization either under resting conditions or after provocative interventions. All 83 patients were severely incapacitated--58 in Class III and 24 in Class IV. Seventy had obstruction at rest (average gradient 96 mm Hg), and 13 had only provocable obstruction. At operation the hypertrophic interventricular septum was exposed via an aortotomy, and a vertical bar of muscle was resected between parallel myotomy incisions. There were six operative deaths (7%); no patient has died since 1970. Seven patients have died late after operation, five of them from causes unrelated to their heart disease or the operation. All surviving patients describe symptomatic improvement. Fifty-two patients with obstruction at rest preoperatively (average gradient 95 mm Hg) have been studied postoperatively: no resting gradient was evident in 47, while in the remaining five the gradient was less than 25 mm Hg. Recurrence of obstruction has never been observed at late catheterization (21 pts) or late echocardiographic examination (37 pts). Obstruction could not be provoked postoperatively in ten of the 11 patients who had large gradients only with the Valsalva maneuver or isoproterenol administration preoperatively. Obstructed and provocable obstructed patients had similar symptomatic improvement after operation. A variety of rhythm and conduction abnormalities were observed both pre and postoperatively, and these are described in detail. The results of operation in these 83 patients with IHSS demonstrate that gratifying symptomatic and hemodynamic improvement uniformly follows left ventriculomyotomy and myectomy. Relief of obstruction and amelioration of symptoms have proved to be long-lasting during postoperative observation periods extending to 14 years. Continued application of the operative procedure in properly selected patients appears to be indicated.

To determine the clinical characteristics of patients with life-threatening ventricular tachyarrhythmias with no identifiable heart disease, we analyzed six patients who presented with either cardiac arrest or syncope associated with documented ventricular tachycardia or fibrillation. Electrocardiographic and echocardiographic examination and cardiac catheterization results were normal in all patients. Electrocardiographic monitoring revealed ventricular tachycardia in all patients. Exercise testing did not provoke sustained ventricular tachycardia in any patient. Programmed extrastimulation did not induce ventricular tachycardia in any patient. Isoproterenol infusion facilitated provocation of sustained ventricular tachycardia in only one patient. All six patients were treated with solitary beta-blocker therapy. Following treatment, there was a significant reduction in the incidence of ventricular tachycardia, couplets and total ventricular ectopic beats. During a follow-up period ranging from 16 to 36 (mean 22) months, all patients remain alive without clinically significant recurrence. Therefore, patients with life-threatening ventricular tachyarrhythmias without identifiable heart disease may respond to solitary beta-blocker therapy.

Echocardiography was used to evaluate the heart in 19 patients with one of various systemic diseases known to be associated with infiltrative cardiomyopathy. Four patients had systemic amyloidosis, 10 had idiopathic hypereosinophilia and 5 had iron overload caused by multiple blood transfusions. Although 10 patients (53 percent) had no clinical evidence of cardiac disease, all 19 had echocardiographic abnormalities; the left ventricle was symmetrically thickened (more than 11 mm) and left ventricular mass was increased (more than 275 g) in all; the left ventricular transverse dimension was modestly increased (more than 52 mm) in 5 patients (26 percent) and the velocity of mitral valve closure in early diastole was reduced (less that 60 mm/sec) in 5 patients. Systolic function, as evidenced by ejection fraction, was well maintained (greater than 60 percent) in 18 of 19 patients. Thus, it appears that echocardiographic abnormalities can be detected in many patients with a systemic disease associated with infiltrative cardiomyopathy even before clinically evident heart disease develops.

Idiopathic left ventricular hypertrophy is diagnosed when hypertrophy without dilatation appears to be present without apparent cause. Since asymmetric septal hypertrophy occurs commonly, and since it may present nonspecifically as left ventricular hypertrophy, we hypothesized that many patients with idiopathic left ventricular hypertrophy might in fact have asymmetric septal hypertrophy. We therefore evaluated echocardiographically 39 patients with idiopathic left ventricular hypertrophy diagnosed by physical findings or electrocardiographic criteria or both. All family members of patients with known asymmetric septal hypertrophy were excluded. Of the 39, 33 had asymmetric septal hypertrophy, six were normal, and none had evidence of idiopathic left ventricular hypertrophy. All six of those with normal echocardiograms had left ventricular hypertrophy solely by electrocardiographic criteria and were without cardiac symptoms, suggesting a false-positive diagnosis. If idiopathic left ventricular hy...

Previous reports have suggested that patients with heart failure and coexistent ventricular tachyarrhythmias have a 1-year mortality of 40% to 60%. To assess whether an antiarrhythmic management program could reduce mortality, we studied 20 consecutive patients with ventricular fibrillation (12) or ventricular tachycardia (eight) and heart failure. Coronary disease was the most common underlying cardiac disorder (85%). Heart failure was managed with digoxin (16), diuretics (16), and vasodilators (seven). All patients received antiarrhythmic drug therapy guided by both noninvasive and invasive studies. This included single (10) or combination drug therapy (10). Beta blockers were used alone or in combination for arrhythmia control in 11 patients. One-year survival was 89%. We conclude that an effective program can be developed for patients with life-threatening ventricular tachyarrhythmias and heart failure. Combination antiarrhythmic drug therapy is often required. Despite impaired left ventricular function, beta-blocking drugs can be used, and may be important.

Doppler measurements of pulmonary artery (PA) acceleration time (AT) have been used clinically to estimate PA pressure. However, these studies have been performed primarily in patients without tachycardia. To determine the effect of acute changes in heart rate on PA AT, atrial pacing studies were performed in seven closed-chest pigs. Pulsed Doppler PA flow velocity recordings were obtained from a parasternal position at pacing rates from 100 to 140 beats/min. PA pressure remained constant (mean +/- SD = 14 +/- 5 mm Hg) over the entire range of paced rates. When PA Doppler measurements were compared at heart rates of 100 and 140 beats/min, there were decreases at the higher heart rate in both acceleration time (110 +/- 12 vs 83 +/- 11 ms, p less than 0.01) and ejection time (ET) (315 +/- 23 vs 237 +/- 21 ms, p less than 0.01). In contrast, there was no change in either PA peak flow velocity (69 +/- 15 vs 62 +/- 18 cm/s) or the ratio of AT/ET (0.35 +/- .02 vs. .36 +/- .03). Consequently, when estimating PA pressure in states of tachycardia, the PA AT/ET ratio may be a more useful measurement than PA acceleration time.

Patients with dilated cardiomyopathy (DC) have been reported to have abnormal left ventricular (LV) diastolic properties. To evaluate LV diastolic filling characteristics in patients with DC, pulsed Doppler echocardiography was used to study mitral flow velocity in 21 patients with DC and mitral regurgitation (MR), 12 patients with DC but no MR and 19 age-matched normal subjects. Diagnosis of MR was based on the Doppler echocardiographic finding of holosystolic turbulent flow in the left atrium. Peak mitral flow velocity in early diastole (PFVE) and during atrial systole (PFVA), PFVA/PFVE and deceleration half-time of early diastolic flow were measured from Doppler mitral flow velocity recordings. In 21 patients with DC and MR, PFVE (61 +/- 13 cm/s), PFVA (37 +/- 19 cm/s) and PFVA/PFVE (0.6 +/- 0.4) were not significantly different from PFVE (53 +/- 10 cm/s), PFVA (47 +/- 12 cm/s) and PFVA/PFVE (1.0 +/- 0.4) in normal subjects (p greater than 0.05). Deceleration half-time in DC patients with MR (62 +/- 32 ms) was shorter than normal (87 +/- 25 ms) (p less than 0.05). In contrast, PFVE (31 +/- 11 cm/s) was lower and PFVA/PFVE (1.7 +/- 0.8) was higher in the 12 DC patients without MR than in normal subjects and DC patients with MR (p less than 0.005). PFVA (46 +/- 8 cm/s) and deceleration half-time (88 +/- 33 ms) in patients without MR were not significantly different from normal mean values. Thus, abnormalities of peak diastolic mitral flow velocity were detected in DC patients without MR but not in DC patients with MR, suggesting that MR masks LV filling abnormalities in patients with DC.

One hundred and thiry-four patients with hypertrophic cardiomyopathy were evaluated by standard 12-lead electrocardiography. Normal electrocardiograms were extremely uncommon, occurring in less than 7% of each subgroup of patients (i.e., those with or without either symptoms or obstruction to left ventricular outflow), with the exception of those who were both asymptomatic and had no left ventricular outflow obstruction. Even in this subgroup, however, normal electrocardiograms occurred in only 27% of patients. Repolarization abnormalities and left ventricular hypertrophy were the most common abnormalities, occurring in 81% and 62%, respectively, of the total population. A broad spectrum of other electrocardiographic abnormalities was found, but none was unique to hypertrophic cardiomyopathy. Patients with vs those without electrocardiographic left ventricular hypertrophy or left atrial abnormality had significantly (P less than 0.005) greater mean ventricular septal thickness (22 +/- 0.6 vs 19 +/- 0.6 mm) and left atrial dimension (48 +/- 1 vs 40 +/- 1 mm) measured by echocardiography, and signficantly (P less than 0.01) higher mean pulmonary capillary wedge pressure (16 +/- 1 vs 10 +/- 1 mm Hg) and left ventricular end-diastolic pressure (20 +/- 1 vs 15 +/- 1 mm Hg). The high prevalence and diverse nature of electrocardiographic abnormalities suggest that any patient with an unusual and unexplained electrocardiogram should be suspected of having hypertrophic cardiomyopathy even if the physical examination is normal, as is often the case in patients without obstruction.

In an attempt to improve visualization of the position of the guidewire and dilatation balloon during coronary angioplasty, a method was developed called digital coronary roadmapping. With this method a digitally acquired coronary angiogram is interlaced with the live fluoroscopic image of the guidewire and balloon catheter. The digital coronary angiogram is superimposed at the same magnification and radiologic projection as the live fluoroscopic image onto the video monitor above the catheterization table. The digital roadmap image thus provides immediate feedback to the angiographer to assist in directing the guidewire into the appropriate coronary artery branch and to help in placement of the balloon so that it straddles the site of stenosis. © 1985.

Patients with typical idiopathic hypertrophic subaortic stenosis (IHSS) represent only one subgroup of a cardiac disease in which the characteristic anatomic abnormality is asymmetric septal hypertrophy (ASH). In most patients with ASH, left ventricular outflow obstruction is absent and cardiac dysfunction presumably is due to widespread involvement of the left ventricle by an underlying myocardial abnormality. In other patients with ASH, left ventricular outflow obstruction is present (typical IHSS) and constitutes a major feature of the hemodynamic and physical findings. To determine whether patients with outflow obstruction also have the underlying myocardial abnormality diffusely involving the left ventricle, the gross morphology of hearts from patients with and without outflow obstruction were studied both by necropsy and by echocardiography. Echocardiographic studies revealed that the ventricular septum was thicker in obstructive ASH, a finding confirmed by the postmortem studies. The necropsy studies also indicated that although the left ventricular free wall was thickened in both obstructive and nonobstructive ASH, the configuration of the left ventricular free wall was distinctly different in the two groups. In obstructive ASH, the free wall was hypertrophied and identical in appearance to that seen in valvular aortic stenosis. Moreover, echocardiographic studies indicated that the thickening of the free wall behind posterior mitral leaflet appeared to regress after operative relief of the outflow obstruction. In contrast, the left ventricular free wall of severely symptomatic patients without outflow obstruction had a markedly different and unique appearance; the free wall of left ventricle directly behind the posterior mitral leaflet was of normal or less than normal thickness, whereas the remaining free wall was nonuniformly thickened. On the basis of these findings and the microscopic data presented in the companion paper, we conclude that the myocardial abnormality in obstructive ASH (typical IHSS) is localized largely to the ventricular septum, with left ventricular free wall thickening occurring as a consequence of outflow obstruction. In symptomatic patients with nonobstructive ASH, however, the data suggest that the left ventricle, including free wall, is extensively involved with a primary myocardial abnormality.

The application of noninvasive techniques to the evaluation of cardiac function in iron overload has identified a high incidence of abnormalities in asymptomatic patients prior to the onset of overt cardiac deterioration. Of the tests we have used, radionuclide cineangiography appears to be the most sensitive because it can be conveniently applied during the physiological stress of exercise. Other tests of cardiac function that include stress are also likely to be more sensitive than resting measurements of cardiac function. Systematic application of these techniques to the study of patients on iron chelation therapy should results in an early determination of the efficacy of such treatment.

In several patients with asymmetric septal hypertrophy (ASH) diagnosed by echocardiography (septal-free wall thickness ratios greater than or equal to 1.3), we have discovered marked discrepancies between the echocardiographic and necropsy measurements of wall thicknesses that led to uncertainty regarding the actual cardiac diagnosis. To resolve these apparent incongruities, the echocardiograms and hearts of 17 patients with cardiac disease were studied. Six of nine patients with abnormal septal-free wall ratios greater than or equal to 1.3 during life had septal-free wall ratios that were not diagnostic of disproportionate septal thickening at necropsy. Such discrepancies may be explained as follows: 1) echocardiographic measurements during life were made in diastole (as per convention), but measurements at necropsy were made in hearts that appeared to have been in the systolic phase of the cardiac cycle; 2) the left ventricular free wall thickens considerably more than the ventricular septum in systole, as determined by echocardiography. This latter phenomenon resulted in septal-free wall ratios in systole that were consistently smaller than those in diastole. Furthermore, septal-free wall ratios obtained at necropsy corresponded most closely to those obtained by echocardiography in systole.

Eleven apparently normal children whose electrocardiograms demonstrated greatly increased precordial QRS voltages suggestive of left ventricular hypertrophy were studied by echocardiography to determine whether this finding represented an early manifestation of cardiac disease. Echocardiographic measurements of the thickness of the ventricular septum and of the left ventricular posterobasal wall were normal in all 11 subjects when compared with normal values for age. Also within normal limits were left ventricular, left atrial and aortic root internal diameters, left ventricular mass and the motion and structure of the anterior and posterior mitral valve leaflets. We conclude: (1) These children probably have normal hearts; (2) increased precordial QRS voltage in children and adolescents, in the absence of other abnormalities, is an unreliable indicator of left ventricular hypertrophy; and (3) echocardiography is a powerful diagnostic test in determining the significance of abnormal electrocardiograms suggestive of left venticular hypertrophy.

Pericardial tamponade occurring late in the hospitalization of a patient who has undergone a heart operation can be life threatening. Recognition of this insidious, but treatable, complication is difficult. Three patients experienced delayed tamponade while receiving warfarin prophylactically following coronary artery bypass. Two-dimensional echocardiography was useful in recognizing the effusion (and thus aided the diagnosis of tamponade) in each patient. The question of whether prophylactic anticoagulation should be employed for patients undergoing coronary artery bypass procedures is also considered in light of both the present experience and collected reports from the literature.

Doppler echocardiography is established as a useful method for detecting mitral regurgitation (MR). However, studies also show that Doppler echocardiography may be too sensitive for diagnosing pathologic MR. To determine whether the false-positive or clinically insignificant diagnosis of MR can be eliminated by defining more specific diagnostic criteria, pulsed Doppler findings were compared with left ventricular angiographic findings in 81 patients. Using the conventional Doppler criterion of any systolic increased spectral dispersion detected in the left atrium, sensitivity was 100% and specificity was 76%. Using holosystolic increased spectral dispersion as the criterion, sensitivity was 100% and specificity was 92%. Using the combined criteria of holosystolic increased spectral dispersion plus peak regurgitant blood flow velocity of greater than 150 cm/s, sensitivity was 100% and specificity was 97%. Doppler studies in 20 clinically normal persons showed that the combined Doppler criteria were 100% specific. In conclusion, the presence of holosystolic increased spectral dispersion within the left atrium with a peak regurgitant flow velocity greater than 150 cm/s appears to be as sensitive as and more specific than the presence of any systolic Doppler increased spectral dispersion in identifying patients with MR.

Echocardiographic and necropsy studies were performed in 304 patients with various cardiac diseases. The overall prevalence of disproportionate ventricular septal thickening (septal to free wall ratio greater than or equal to 1.3) was 10%. However, it was related to the type of cardiac lesion. Prevalence was high (greater than 20%) in pulmonary stenosis or primary pulmonary hypertension, lower (less than 15%) in Eisenmenger syndrome or aortic or mitral valvular disease and was not present in atrial or ventricular septal defect. In right ventricular overload, prevalence of disproportionate septal thickening correlated with increasing ventricular systolic pressure. None of 16 patients with disproportionate septal thickening studied at necropsy showed marked disorientation of cardiac muscle cells in the ventricular septum, characteristic of genetically transmitted asymmetric septal hypertrophy (ASH). Furthermore, disproportionate septal thickening was demonstrated by echocardiography in only one of 59 first degree relatives of patients with disproportionate septal thickening and associated cardiac diseases. Thus, disproportionate ventricular septal thickening associated with other cardiac diseases usually is due to secondary hypertrophy and is not a manifestation of genetically transmitted ASH.

To determine the optimal time for recording left ventricular angiograms during atrial pacing stress tests, digital subtraction left ventriculograms were obtained using 12 ml of contrast material in 40 patients at rest and at peak pacing. Nineteen of the 40 patients had a third digital left ventriculogram performed between 5 and 10 seconds and 21 patients had a third digital left ventriculogram performed 30 seconds after pacing was stopped. Coronary angiography showed significant coronary artery disease (CAD) in 29 patients and no evidence of significant CAD in 11 patients. Ejection fraction (EF) increased or did not change at peak pacing in 10 of 11 patients without CAD. In the 29 patients with CAD, mean EF decreased an average of 10 percentage points (p < 0.001) and fell 2 or more percentage points in 25 patients (86%) at peak pacing. These changes in EF were accompanied by the development of wall motion abnormalities, which occurred in segments of myocardium that were supplied by coronary arteries with angiographic CAD (more than 50% diameter narrowing). In contrast, the mean EF during the postpacing studies decreased only 2.2 percentage points (difference not significant) over rest values. Moreover, 15 to 29 patients (52%) with CAD had a decrease in EF of 2 or more percentage points. Therefore, the sensitivity of the atrial pacing stress test was diminished when the analysis was performed at 10 or 30 seconds after pacing. It is concluded that EF changes and wall motion abnormalities induced by atrial pacing are of short duration. As a result, the optimal time for performing left ventricular analysis of EF and wall motion during atrial pacing is apparently at the peak heart rate and not 10 to 30 seconds after pacing is stopped. © 1985.

Real-time, two dimensional echocardiography was used to identify great artery relations in 23 infants and small children, including 16 patients with angiography documented transposition of the great arteries, tetralogy of Fallot, or pulmonary aresia. Using this technique, the heart was scanned perpendicular to its long axis at the origin of the great arteries. Great arteries cross-sectioned perpendicular to their long axes appear as circles; when sectioned longitudinally these arteries appeared as elongated sausage-shaped structures. I- patients with normally related great arteries, a curcular structure (aorta) always was positioned posterior to an elongated, sausage-shaped structure (distal right ventricular outflow tract and proximal main pulmonary artery). In transposition of the great arteries, two adjacent circular structures were observed; the anterior circle (aorta) was located to the right, left or directly anterior to the posterior circle (pulmonary artery). In pulmonary atresia or hypoplasis, a large posterior circle (aorta) was associated with an anteriorly positioned structure that was either short and small (atretic right ventricular outflow tract) or elongated with an area of severe narrowing (hypoplastic right ventricular outflow tract). Thus, real-time two-dimensional echocardiography provides a rapid, noninvasive means of accurately identifying congenital malformations of the great arteries in infants and small children and may be a useful adjunct to cardiac catheterization in the diagnosis of cyanotic congenital heart disease.