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Using an experimental canine model, we have employed echocardiography to study segmental dyskinesis produced by acute coronary occlusion. Characteristic alterations in posterior wall and septal motion occur after acute coronary ligation; these resemble clinical abnormalities described in acute and old myocardial infarction. The degree of dyskinesis produced is directly related to the severity of the perfusion deficit. Coronary reperfusion had variable effects on dyskinesis; most animals showed improvement but in some the myocardial contraction abnormalities became more severe. A vaviety of interventions were undertaken during ischemia. The elevated level of arterial pressure induced by the administration of methoxamine increased ventricular diameter and presumably oxygen requirements, and was deleterious to ischemic wall motion whereas the administration of norpinephrine reduced ventricular diameter and improved function. Intra-aortic balloon counterpulsation had little effect on either ischemic motion or perfusion. These experimental studies generally support conclusions drawn from clinical echocardiograms about the relationship of abnormalities of wall motion to coronary artery lesions and myocardial ischemia, and suggest further clinical uses for echocardiography in coronary disease.

Protocols used to prepare patients with leukemia for bone marrow transplantation have the potential for cardiac toxicity due to high-dose cyclophosphamide and total-body irradiation. We have reported one regimen, combining cytarabine (5 mg/kg), cyclophosphamide (90 mg/kg), and total-body irradiation (900 cGy), which is relatively effective in the treatment of leukemia. To assess cardiac effects of this treatment regimen, we performed serial echocardiography and radionuclide ventriculography in 28 patients with leukemia (age range, 18-48 years; mean, 31; 21 males) undergoing allogeneic bone marrow transplantation. No significant change in left ventricular fractional minor axis shortening or increase in left ventricular diastolic dimension was seen with weekly echocardiography. At an average of 77 days (range, 28-358) after transplant, repeat radionuclide ventriculography in 17 patients revealed no significant change in resting left ventricular ejection fraction compared to that on admission to the hospital (58% +/- 6.8% vs 56% +/- 8.0% SD; P = not significant). In seven of these 17 patients (41%), resting ejection fraction fell between baseline and discharge (from mean of 60% to 50%). Resting ejection fraction in four of these patients (23% of the entire group) fell into the abnormal range (from mean of 56% to 44%; lowest, 41%). Ten patients also had exercise radionuclide ventriculography and all had normal responses (greater than 5% increase with exercise) pre- and post-transplant. We conclude that this effective bone marrow transplantation regimen has little apparent short-term cardiac toxicity in the majority of patients; since a few patients do exhibit a deterioration in left ventricular function, continued cardiac surveillance is probably indicated in posttransplant patients.

The purpose of this study was to determine the effect of the antiarrhythmic drugs lidocaine and bretylium on the minimal energy requirement for transthoracic defibrillation--the defibrillation threshold. Closed chest dogs were anesthetized with chloralose or pentobarbital; lidocaine was administered at varying rates for 2 hours and defibrillation threshold periodically redetermined. Similar protocols were followed for bretylium. Serum lidocaine levels from therapeutic to toxic ranges were obtained, and up to a 60% (p less than 0.05) increase in defibrillation threshold in the pentobarbital-anesthetized dogs was demonstrated. In chloralose-anesthetized dogs the lidocaine effect was modest, with only a 10 to 20% rise in defibrillation threshold (p = NS) despite similar increases in serum lidocaine levels. Thus, lidocaine increases the minimal energy requirements for transthoracic defibrillation, but this effect is in part anesthesia-related, indicating a lidocaine-pentobarbital interaction. When phentolamine was administered to chloralose-anesthetized dogs receiving lidocaine, defibrillation threshold rose 13% (p less than 0.05); this suggests that alpha-adrenergic receptor blockade is at least in part the mechanism of the pentobarbital-lidocaine interaction on defibrillation threshold. Bretylium with either anesthetic had no significant effect on defibrillation threshold.

In order to evaluate the relationship between regional myocardial perfusion and segmental dyskinesis, 22 open chest dogs were studied using ultrasound to register cardiac wall motion and radioactive labeled microspheres to determine myocardial perfusion. In six dogs, motion and perfusion were correlated at two levels of partial circumflex coronary artery occlusion followed by complete occlusion. A good correlation between declining myocardial perfusion of all the ischemic segments and development of aneurysmal bulging (during isometric contraction) was seen: r = minus 0.80. A similar correlation between myocardial perfusion and endocardial wall velocity (during systolic ejection) was observed: r = 0.92. In nine dogs, the effect of 45 minutes of complete coronary occlusion followed by 30 minutes of reperfusion was evaluated with respect to perfusion and motion. After coronary reperfusion myocardial perfusion of the ischemic area returned to control levels (from 32.6 +/- 3.5 to 130.3 +/- 13.3 ml/100 g/min), but aneurysmal bulging during isometric contraction persisted. Endocardial wall velocity during systolic ejection showed a variable response to reperfusion, achieving values ranging from 32% to 162% of the preocclusion levels. In seven dogs the ultrasound beam was reflected off nonischemic myocardium adjacent to areas of ischemia resulting from coronary occlusion. Despite preservation of normal myocardial perfusion in these nonischemic areas wall motion abnormalities were evident: endocardial wall velocity declined from 25.8 +/- 5.8 to 14.0 +/- 4.9 mm/sec (P less than 0.01), and aneurysmal bulging in three animals. These changes may be due to transient undetected ischemia in the segments struck by the ultrasound beam, or to passive alteration of the motion of the normally perfused areas by the severe dyskinesis of the adjacent ischemic myocardium.

The intraoperative evaluation of the technical adequacy of coronary artery bypass graft anastomoses has been limited by a lack of suitable tools. To evaluate the role of intraoperative high-frequency epicardial echocardiography we examined 82 coronary artery bypass graft anastomoses in 29 patients shortly before or just after weaning from cardiopulmonary bypass. Minor defects that did not compromise the lumen of the anastomoses were seen in two patients. One major technical error, a near total occlusion of an internal mammary-to-coronary artery anastomosis, was not apparent on external inspection, but was clearly identified with high-frequency epicardial echocardiography. This was revised immediately. Thus, high-frequency epicardial echocardiography permits the intraoperative evaluation of coronary artery bypass graft anastomoses so that technical errors can be quickly identified and corrected.

We have used a high frequency epicardial echocardiographic technique to visualize and measure coronary artery lumens and walls in patients undergoing cardiac surgery. A 12 MHz probe (Surgiscan, Biosound Corp.) is sterilized and placed on the exposed epicardial coronary arteries. Transverse cross-sectional views are obtained from the arteries on the anterior surface of the heart: the right coronary artery to the cardiac margin and the left anterior descending coronary artery to the cardiac apex. Numerous echocardiographic-angiographic-pathological correlations have been obtained from this work. We have validated the echocardiographic lumen and wall measurements by comparing the echo measurements to histological material from pressure-distended coronary arterial segments (from animals and fresh human autopsy specimens). We have shown by comparison with angiography that coronary arteries which appear normal or only minimally diseased by angiograms are often diffusely and severely atherosclerotic. We have also evaluated the shape of atherosclerotic lesions and demonstrated a wide range of lumen shapes (oval, circular, complex) and location within the residual coronary lumen (eccentric vs. concentric). Highly eccentric lesions are characterized by relative preservation of portions of the arterial wall, and this may preserve vasoreactivity of the atherosclerotic vessel. We have also demonstrated remodeling of atherosclerotic lesions: enlargement of the total arterial area (wall plus lumen) as a compensatory mechanism to preserve the arterial lumen in the face of encroaching atherosclerosis. High frequency epicardial echocardiography offers an accurate, real-time, in-vivo method for the anatomic and functional evaluation of coronary atherosclerosis. This dynamic, in-vivo technique supports and extends information previously obtainable only from pathologic studies.(ABSTRACT TRUNCATED AT 250 WORDS)

The usefulness of two-dimensional color-Doppler flow-imaging (2D Doppler) in the detection, localization, and quantitation of bioprosthetic mitral valve regurgitation is uncertain. Mitral bioprostheses, before and after the creation of transvalvular (n = 33), paravalvular (n = 17), or combined (n = 23) defects, were mounted in a pulsed duplication system (flow rates, 2.5-6.5 l/min; pulse rate, 70 beats/min). An Aloka 880 2D Doppler system (Japan) was used to image the regurgitant jets in the simulated left atrial chamber, analogous to images obtained with transesophageal echocardiography. Jet area was corrected to an estimate of stroke volume: 2D Doppler measurements were divided by [(valve effective orifice area) X (continuous-wave Doppler-determined mean diastolic filling velocity)]/pulse rate. Regurgitant fraction and regurgitant volume were measured by an electromagnetic flow probe. 2D Doppler correctly identified the presence and location of paravalvular regurgitation. In transvalvular and combined transvalvular-paravalvular defects, there were six incorrect interpretations, all having transvalvular regurgitant volumes less than 4 ml/beat. In the presence of transvalvular regurgitation, jet area, length, and width correlated linearly with regurgitant volume (r = 0.82, 0.80, and 0.68, respectively; p less than 0.0001) and regurgitant fraction (r = 0.62, 0.61, and 0.45, respectively; p less than 0.001). Correlations with regurgitant fraction were improved when 2D Doppler measurements were corrected for stroke volume (r = 0.78, 0.79, and 0.67, respectively; p less than 0.0001). Mitral bioprostheses with transvalvular defects were also studied at varying flow rates (3.2-7.5 l/min) and pulse rates (70, 90, and 110 beats/min). The correlation between jet area and regurgitant volume was improved with a second-order polynomial regression (r = 0.93, p less than 0.0001). Our conclusions are that 1) in this in vitro model analogous to transesophageal imaging, 2D Doppler accurately detects and localizes bioprosthetic mitral valve regurgitation; 2) in transvalvular bioprosthetic mitral valve regurgitation, 2D Doppler measurement of jet area has a curvilinear relation with regurgitant volume, and correlation with regurgitant fraction is improved with correction for stroke volume; and 3) in paravalvular bioprosthetic mitral valve regurgitation, correlations between 2D Doppler measurements and regurgitant volumes are weaker, possibly because of jet eccentricity.

The hemodynamic response to sequences of ventricular fibrillation and defibrillation includes an adrenergic component that is important for the maintenance of blood pressure after successful defibrillation. Because calcium channel blocking drugs have antiadrenergic effects, we hypothesized that they might blunt the adrenergic response to defibrillation. Ventricular fibrillation was induced in 35 closed-chest dogs. Each received 4 to 7 direct current transthoracic shocks at three energy levels to determine defibrillation energy requirements. Heart rate and blood pressure were recorded. Energy sequences were repeated after 45 minutes of no intervention (control, n = 5) or after 45-minute infusions of diltiazem (0.1 mg/kg/min, n = 10), verapamil (0.1 mg/kg bolus plus 0.01 mg/kg/min, n = 10), or nifedipine (40 micrograms/min for 3 minutes plus 2 to 20 micrograms/min adjusted to maintain a 10 mm Hg drop in mean arterial pressure, n = 10). Our results show that the normal post-shock rise in mean arterial pressure was blunted by the calcium channel blockers diltiazem (systolic arterial pressure at 15 and 60 seconds post-shock, pre-drug versus post-drug: 102 +/- 9 versus 64 +/- 9 mm Hg and 113 +/- 10 versus 87 +/- 6 mm Hg; p less than 0.05) and verapamil (108 +/- 9 versus 78 +/- 12 mm Hg and 113 +/- 7 versus 90 +/- 10 mm Hg, p less than 0.05). There were no differences in blood pressure responses after nifedipine treatment or no drug. Heart rate responses were not altered by diltiazem or verapamil; after nifedipine administration, post-shock heart rates were slower.(ABSTRACT TRUNCATED AT 250 WORDS)

Pericardial effusion is a recognized consequences of myxedema. Its incidence is unknown, primarily because of past difficulties in establishing the diagnosis. We studied 33 hypothyroid patients by echocardiography. Ten of the 33 patients (30%) had positive echoes for pericardial effusion. Seven of these ten patients had enlarged hearts on chest X-ray. Five patients had cardiac enlargement but no echo evidence of pericardial effusion. Serum concentrations of thyroxine, 1.8+/-0.3 vs 1.5+/-0.1 mcg/dl and of thyroid stimulating hormone, 34+/-4 vs 38+/-5 muU/ml did not differ in the groups with and without pericardial effusion, respectively. However, the pericardial effusion group had significantly slower heart rates on ECG than those without pericardial effusion: 53+/-8 vs 68+/-2 beats/min, P less than 0.05. Low voltage was present in five of the ten patients with pericardial effusion and five of the 23 nonpericardial effusion patients. None of the patients with pericardial effusion developed tamponade. Seven patients with pericardial effusion were restudied after periods of thyroxine replacement therapy ranging from six months to two years. All were euthyroid and had negative echoes on follow-up, but two still showed cardiomegaly on chest X-ray (both had associated coronary artery disease). We conclude that pericardial effusion occurs frequently in patients with myxedema. Tamponade is uncommon and the effusions disappear with thyroid replacement therapy. Cardiomegaly on chest X-ray and low voltage on ECG are not reliable indicators of pericardial effusion.

Sixteen acromegalic patients underwent echocardiography, phonocardiography, stress electrocardiography with Thallium perfusion scanning and gated radioisotope left ventricular angiocardiograms. Abnormalities consisting of increased echo left ventricular mass index, low velocity of circumferential fiber shortening or elevated pre-ejection period to left ventricular ejection time ratio were found in six patients with coexistent hypertension or coronary disease. Concentric left ventricular hypertrophy was also found in three patients with no known etiology other than acromegaly of greater than thirteen years' duration or with fasting growth hormone concentrations greater than 100 ng/ml. One of these three also had left ventricular dysfunction. Neither hypertrophy nor ventricular dysfunction was found in other acromegalics with shorter duration of disease or lower growth hormone concentrations or with normal growth hormone concentrations after therapy. A high prevalence of coronary artery and hypertensive heart disease is associated with acromegaly. A few patients with acromegaly have a specific, potentially reversible cardiomyopathy probably related to prolonged acromegaly or very high growth hormone concentrations.

Four methods of computer-based edge detection were evaluated for identification of endocardial and epicardial borders on 2-dimensional echocardiograms of excised hearts. A method was also evaluated for observer identification of cardiac borders in the same hearts. The accuracy of computer-derived borders and of observer-derived borders were determined by comparison to anatomic borders measured from photographs of slices of the excised hearts. Echocardiographic borders were compared with anatomic borders by calculation of segmental cavity areas and wall thickness. Each of the methods tested (computer and observer) identified endocardial borders accurately, resulting in cavity segment areas that correlated well with the corresponding anatomic data (r = 0.90 to 0.92). Regional wall thicknesses correlated less well with anatomic data (r = 0.74 to 0.80), suggesting that endocardial borders were identified more accurately than were epicardial borders. Thus, the methods of computer-assisted echocardiographic border detection tested identified the endocardium and epicardium as accurately as a trained observer evaluating unprocessed echocardiograms. Computer-based methods of border detection may be useful in the automated analysis of clinical echocardiograms.

This article describes the production, analysis, and reproducibility of forming microbubbles for contrast ultrasound imaging. The sonication method used to generate microbubbles was tested by four independent observers, and a subsequent laser particle counter analysis of microbubble size and concentration determined the reproducibility of the method. The results indicated that the mean bubble size was 3.3 +/- 1.2 microns for the entire group, based on three trials of each of the four participants. The characteristics of the bubble size of the microbubbles between observers were assessed with a Poisson distribution with the reproducibility based on the sample mean for each observer's trials. Standardization and calibration of the laser particle counter was accomplished with commercially available latex spheres, sonicated albumin microspheres, and a Coulter counter analysis. Our results indicate that the sonication technique generates small microbubbles with a reproducible uniform size distribution. The method of microbubble production is reproducible and can be widely applied for use in contrast echocardiographic perfusion imaging of tissue in a variety of research and clinical studies.

Available clinical data indicate that an initial shock energy of 200 J will defibrillate the majority of patients. There is no advantage in starting at a higher energy, and lower energy shocks may be safer. Measurements of transthoracic impedance may permit the use of even lower energy levels for initial shocks. If the initial shock fails to defibrillate it should be repeated immediately, at the same energy level, and then increased if defibrillation is still not achieved. If the initial shock defibrillates but refibrillation occurs later there is no reason to increase the energy; it should be repeated at 200 J. We suggest the following energy selection algorithm for defibrillation (VF = ventricular fibrillation): (Formula: see text).

The purpose of the present study was to evaluate the response of briefly ischemic and reperfused myocardium to subsequent moderate reductions of coronary arterial flow. In mongrel dogs, a carotid to left anterior descending coronary shunt was constricted to produce moderate coronary flow reductions (50-60% of control) and to thereby reduce regional systolic thickening (measured by echocardiography or sonomicrometry). First, we demonstrated an abnormal response of reperfused myocardium to subsequent flow reductions. We performed two episodes of coronary shunt stenosis, with an intervening 5-minute complete coronary shunt occlusion followed by 30 minutes of reperfusion. In a control group, the same two shunt stenoses were done, but no intervening shunt occlusion was performed. In the control dogs, repeated coronary shunt stenosis that produced equivalent perfusion reductions also produced equivalent declines in regional wall thickening. In contrast, in the intervention group (animals undergoing the intervening occlusion-reperfusion sequence between two shunt stenoses), the second coronary shunt stenosis produced an exaggerated decline in regional systolic thickening, even though the decline in myocardial perfusion was similar to the first stenosis. Second, we sought to demonstrate the mechanism of the exaggerated decline of the reperfused myocardium to subsequent moderate flow reductions. Again, two groups of animals were studied. Each group underwent two episodes of coronary shunt stenosis with an intervening sequence of 5 minutes of complete shunt occlusion and 30 minutes of reperfusion. In addition, one of the groups received an infusion of the oxygen free radical scavengers superoxide dismutase and catalase during the occlusion-reperfusion sequence. In the superoxide dismutase and catalase-treated animals, the decline in regional systolic function during the postreperfusion shunt stenosis was similar to the preocclusion stenosis. Thus, oxygen free radical scavengers blocked the exaggerated contraction decline in response to the postreperfusion flow reduction. We conclude that briefly ischemic and reperfused myocardium displays an exaggerated response to subsequent coronary arterial flow reductions and that this response is a subtle manifestation of postischemic ventricular dyskinesis, or "stunning." The mechanism is probably oxygen free radical toxicity.

It is hypothesized that myocardium subjected to a 5 minute period of coronary occlusion and a 30 minute period of reperfusion has latent abnormalities that become overt when the reperfused myocardium is "challenged" by a subsequent coronary occlusion. This hypothesis is clinically relevant because reperfused myocardium is frequently subjected to recurrent ischemia, as in patients with unstable angina, vasospastic angina or recurrent thrombosis after initial coronary occlusion and thrombolysis. In 19 open chest dogs, the response of regional myocardial function to brief coronary occlusions was studied. Systolic wall thickening and diastolic thinning were measured using a specially developed miniature 5 MHz echocardiographic transducer fixed to the epicardium by suction. All 19 dogs underwent an initial "challenge" coronary occlusion (30 seconds). Thereafter, the control group (n = 8) underwent no intervention for 30 minutes, while the intervention group (n = 11) underwent 5 minutes of coronary occlusion followed by 30 minutes of reperfusion. All dogs were then subjected to a second "challenge" coronary occlusion (30 seconds). In the control group, responses to the second challenge occlusion were the same as to the first occlusion. In the intervention group, regional and global systolic function and myocardial perfusion after the 5 minute coronary occlusion intervention returned to baseline levels, but the response to the second challenge coronary occlusion was significantly different in the intervention group.(ABSTRACT TRUNCATED AT 250 WORDS)

To establish the effect of local and remote myocardial ischemia on interventricular septal motion, 27 open-chest dogs were studied using ultrasound and radioactive microspheres. In 14 dogs the left anterior descending coronary artery was ligated. If the ultrasound beam traversed ischemic septum (proximal LAD occlusion), significant (P less than 0.05) declines in systolic septal velocity (26.4 +/- 2.9 to 6.4 +/- 1.8 mm/sec), and excursion (2.6 +/- 0.3 to 0.7 +/- 0.2 mm) occurred, and systolic thickening was reduced. Similar significant changes were seen when the ultrasound beam traversed nonischemic septum adjacent to the ischemic area (distal LAD occlusion). In 13 additional dogs, circumflex coronary ligation produced posterior ischemia. The mean septal velocity for this group increased significantly (21.8 +/- 2.6 to 26.5 +/- 3.3 mm/sec), as did the septal excursion (2.5 +/- 0.2 to 3.1 +/- 0.4 mm). We conclude that acute LAD occlusion causes a reduction in systolic velocity, excursion, and thickening of both the involved ischemic and the adjacent nonischemic septum. When myocardial ischemia was produced in a part of the ventricle remote from the septum, septal velocity and excursion increased.

A computer simulation of a pulsed HF laser pumped by the H(2) + F(2) chain reaction is presented. A chemical kinetic model encompassing sixty-eight reactions is used to approximate the reacting mixture contained within an optical cavity. For each vibrational level, a Boltzmann distribution for the rotational levels is assumed, with lasing on the vibrational band at line center of the transition having maximum gain. An analysis of cavity and chemical mechanisms yields a simple relationship between the pumping and depletion rates of the vibrational levels. This relationship is used to make a comprehensive study of the effects of cavity and chemical parameters on the laser pulse. The effect of changes in uncertain chemical reaction rate coefficients is assessed. A competition exists between vibrationtranslation deactivation reactions and stimulated emission. Laser performance is most sensitive to the relative rates of the vibrational-translational and pumping reactions. In addition, the effect of the photon flux on the chemical mechanisms is significant.

A rate equation model of a pulsed DF-CO(2) chemical transfer laser is Simplified by investigating the relationship of kinetic mechanisms. The model reduces to one equation which when Solved permits calculation of all pulse characteristics as a function of time. At low levels of initiation, predictions of this laser simulation model are in excellent agreement with those of a more comprehensive model presented in an earlier paper. Model predictions are also found to be consistent with experiment. The simplicity of the present model lends itself to easy physical interpretation and permits efficient and accurate prediction of transfer laser performance characteristics in regimes of practical interest.