Visual estimates of percent diameter coronary stenosis: "a battered gold standard".
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Biomedical subjects
Publications and source records attributed to R E Kerber.
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A library of arrhythmias obtained from patients with cardiac arrest was developed. Such a data base will permit both in vitro testing of the rhythm analysis system of automatic external defibrillators before clinical field trials are conducted and comparison of devices. Defibrillators equipped with voice/electrocardiographic tape recorders and used in the prehospital defibrillation programs in Iowa and King County, Washington provided the rhythm source. From these recordings, segments of ventricular fibrillation with minimal artifact and a duration of greater than or equal to 6 s were selected. Segments of ventricular fibrillation (n = 102) were categorized by average peak amplitude as fine (1 to less than 3 mm), medium (3 to less than 7 mm), coarse (7 to less than 12 mm) and extra coarse (greater than or equal to 12 mm), and transcribed onto high fidelity videocassette tapes. Nonventricular fibrillation cardiac arrest rhythms (n = 144), which included wide complex idioventricular rhythms, ventricular and supraventricular tachycardias, asystole and artifact, were also transcribed. Automatic external defibrillators developed by three manufacturers reached a treat (shock) decision on 88 to 93% of the ventricular fibrillation rhythms and on 5 to 10% of the nonventricular fibrillation rhythms. The latter decisions were defined as false positive, though for many rapid nonventricular fibrillation rhythms, countershock may be the appropriate treatment response. There were no statistically significant differences among the three devices in the shock/no shock decisions. A variety of ventricular fibrillation arrhythmias and terminology to express the preclinical performance of automatic external defibrillators are defined. Three commercially available automatic external defibrillators appear to successfully identify ventricular fibrillation and nonventricular fibrillation rhythms.(ABSTRACT TRUNCATED AT 250 WORDS)
Videodensitometry is a nongeometric method of coronary angiographic analysis that can be used to provide an index of coronary luminal area. However, there are few direct studies in vivo of the relationship of videodensitometric data to independent measures of luminal area in humans. Although videodensitometry is theoretically independent of angiographic projection and luminal shape, validation of these assumptions in vivo is also limited. We therefore used intraoperative high-frequency epicardial echocardiography, a technique that can directly determine human coronary luminal area and shape in vivo, to further validate videodensitometry. A total of 36 arterial segments in the left anterior descending and right coronary arteries were studied by videodensitometry and high-frequency echocardiography. Videodensitometry was performed on angiograms in which the arterial segment of interest was not markedly foreshortened and was uniformly filled with contrast. In 22 discrete lesions (13 with circular lumens and nine with oval or complex lumens), videodensitometric and echocardiographic measures of luminal area correlated well (r = .86). In 33 coronary arterial segments, the effect of angiographic projection on videodensitometry was determined by comparison of the results of videodensitometry performed on left anterior oblique vs right anterior oblique angiograms of the segments. Here too, the correlation was good (r = .94, y = 1.04x + 0.002). The good correlation of left anterior oblique with right anterior oblique videodensitometric results held true for lesions with circular and oval or complex lumens. This study further validates the ability of videodensitometry to provide an index of coronary luminal area and confirms in vivo previous assumptions that the results of videodensitometric analysis are independent of angiographic projection and luminal shape.
The purposes of this study were two. First, we wanted to evaluate in patients a technique for automated adjustment of selected energy for defibrillation or cardioversion based on transthoracic impedance. Second, we wanted to define the relationship of peak current and shock success in various arrhythmias. Applying a previously validated method of predicting transthoracic impedance in advance of any shock, we modified defibrillators to automatically double the operator-selected energy if the predicted impedance exceeded 70 omega. Success rates of shocks given for ventricular and atrial arrhythmias from these modified energy-adjusting defibrillators were compared with success rates for shocks given from standard defibrillators. We prospectively collected data on 347 patients who received a total of 1009 shocks. Low-energy (100 J) shocks given to high-impedance (greater than or equal to 70 omega) patients had a poor success rate; in such high-impedance patients significant improvement in shock success rate was achieved by the energy-adjusting defibrillators. For example, when 100 J shocks were selected for high-impedance patients in ventricular fibrillation the energy-adjusting defibrillators achieved a shock success rate of 75%, whereas standard defibrillators achieved a shock success rate of only 36% (p less than .01). Similar improvements were seen for ventricular tachycardia and atrial fibrillation. Thus, automated energy adjustment based on transthoracic impedance is a beneficial approach to defibrillation and cardioversion. For ventricular fibrillation, atrial fibrillation, and atrial flutter there was a clear relationship between peak current and shock success.(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 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.
111In-labeled platelet scintigraphy and two-dimensional echocardiography were performed in 40 dogs to determine the ability of the two techniques to detect left atrial appendage thrombi. Thrombi were induced in 33 dogs that were classified into two groups, "acute" or "chronic," according to the time of labeled-platelet injection after thrombus induction. In the acute group (17 dogs), platelets were injected 24 hours after thrombus induction. In the chronic group (16 dogs), platelets were injected 4-8 days after thrombus induction. "Sham" thoracotomies were performed on seven additional control dogs who did not receive thrombin injections. Analog and blood pool-corrected 111In-labeled platelet scintigraphy images were obtained 4-72 hours later. Closed-chest two-dimensional echocardiography was performed before thoracotomy and repeated at the time of scintigraphy. The location and size of each thrombus were verified at autopsy. Two-dimensional echocardiography detected three of 17 acute (mean volume, 1.2 +/- 1.0 cc) and three of 10 chronic (mean volume, 0.4 +/- 0.3 cc; p less than 0.025) left atrial appendage thrombi. 111In-labeled platelet scintigraphy detected all 17 acute thrombi but only two of 10 chronic thrombi. The measured radioactivity levels of the excised thrombi were 1,949 +/- 1,665 cpm/clot/dose in group 1 and 228 +/- 213 cpm/clot/dose in group 2 (p less than 0.005). In this model, 111In-labeled platelet scintigraphy was able to detect acute left atrial appendage thrombi that could not be identified by two-dimensional echocardiography. Both techniques showed poor sensitivity for detection of chronic thrombi. The decline in sensitivity of 111In-labeled platelet scintigraphy for detection of older thrombi is probably due to diminished labeled-platelet incorporation.
Transthoracic impedance is a major determinant of successful defibrillation or cardioversion, but no data are available concerning the range and determinants of transthoracic impedance in children. Transthoracic impedance was measured in ten ambulatory infants, 6 weeks to 9 months of age, and 37 children, 1.5 to 15 years of age, using a previously validated "test pulse" technique that measures transthoracic impedance without actually delivering a shock. We used hand-held "pediatric" (21 cm2) and "adult" (83 cm2) electrode paddles coated with either Redux paste or Redux creme. Transthoracic impedance in children was 108 +/- 24 omega (range 61 to 212 omega) using pediatric paddles. Using adult paddles lowered the transthoracic resistance by 47% to 57 +/- 11 omega (range 29 to 101 omega), P less than .05. In infants, transthoracic impedance (measured only with pediatric paddles) was 94 +/- 17 omega (range 74 to 124 omega). Using Redux paste as the coupling agent reduced transthoracic impedance by 13% (P less than .05). Transthoracic impedance was significantly but poorly related to body weight and body surface areas, but the correlations were not sufficiently high to be clinically useful. These data indicate that the larger adult electrode paddles will minimize transthoracic impedance and should be used when the child's thorax is large enough to permit electrode to chest contact over the entire paddle surface. This transition occurred at an approximate weight of 10 kg.
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Postmortem studies suggest that coronary angiography does not always accurately delineate the extent of coronary-artery disease. We examined this problem in living human hearts by performing high-frequency epicardial echocardiography at the time of cardiac surgery. The ratio of the diameter of the lumen of the coronary artery to the thickness of its wall was used to quantify the severity of coronary lesions. In 11 patients with no angiographic evidence of coronary disease anywhere in the coronary tree, the mean (+/- SEM) ratio was 5.9 +/- 0.3. In 21 patients with angiographic disease at the site evaluated by echocardiography, the mean ratio was lower (2.3 +/- 0.2, P less than 0.05), reflecting encroachment into the arterial lumen by atherosclerotic plaque. In 15 patients with arterial segments that were angiographically normal but with arterial stenoses elsewhere in the coronary tree, the mean ratio was 4.1 +/- 0.3, with marked overlap with the values in the patients who had angiographic disease at the site of the echocardiographic evaluation. These results demonstrate, in living human hearts, that diffuse coronary atherosclerosis is often present when coronary angiography reveals only discrete stenoses. This finding suggests that coronary angiography may underestimate the severity and extent of coronary disease.
Between October 1983 and November 1986, 20 patients suspected of having a paradoxical cerebral or retinal embolism were identified. Cerebral infarction was the most common presentation. Six patients had a patent foramen ovale demonstrated by cardiac catheterization or surgery. Three patients had a newly discovered atrial septal defect, and one had an atrial septal defect that had previously been treated surgically. Results of the cardiac physical examination, chest roentgenography, and electrocardiography were unremarkable in 12 patients. Eighteen patients had a right-to-left shunt demonstrated by contrast echocardiography. Nine of these patients underwent cardiac catheterization; seven had abnormal catheterization study results: four had a patent foramen ovale and three had an atrial septal defect. Sixteen patients received medical therapy only while four underwent surgery. All patients survived the initial insult. There were no deaths or ischemic recurrences on follow-up ranging from one month to three years. We believe that contrast echocardiography can provide important diagnostic information, even in situations in which cardiac involvement is not suspected. Additional studies are needed before the optimal treatment of presumptive paradoxical cerebral embolism can be determined.
We compared self-adhesive, dual-function monitor/defibrillation electrode pads to standard chest monitoring leads and hand-held electrode paddles in the management of prehospital ventricular fibrillation in a single urban paramedic service. Shocks were delivered more quickly following paramedic arrival with self-adhesive pads than with hand-held paddles (1.6 vs 2.5 min; P less than .001). Ventricular fibrillation was terminated more frequently when shocks were delivered using the self-adhesive pads (55 of 58 patients, 95%) than when shocks were delivered using hand-held paddles (49 of 69 patients, 71%; P less than .005). Initial shocks delivered with self-adhesive pads were especially effective, converting 40 of 58 (69%) patients to an organized rhythm on the first or second shock; this was true of only 24 of 69 (35%) patients shocked with hand-held paddles (P less than .001). Patient survival to hospital admission improved when self-adhesive pads were used: 30 of the 58 (52%) patients shocked with self-adhesive pads achieved hospital admission, while only 21 of 69 patients (30%; P less than .025) survived to admission when hand-held paddles were used. In addition, electrical artifact that interfered with accurate rhythm interpretation was far more prevalent when standard monitoring electrodes were used, including artifact that resulted in inappropriate shock delivery (23% of patients monitored with standard electrodes vs 3% of patients monitored with self-adhesive pads; P less than .005). Self-adhesive monitor/defibrillation pads are superior to standard monitoring leads and hand-held electrode paddles in the management of prehospital ventricular fibrillation.
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)
The effect of acute myocardial ischemia on the myocardial elastic modulus has been a matter of controversy. To evaluate this question, diastolic elastic modulus was assessed by finite element analysis of left ventricular geometry using three-dimensional echocardiographic reconstructions and right and left ventricular pressure recordings. Elastic properties were estimated before and after coronary occlusion in 6 open-chest dogs. Elastic modulus values were derived by means of a computer program that determined the global elastic modulus that best predicted the diastolic changes in left ventricular geometry. In the finite element analysis after coronary occlusion, two analyses were performed: one utilizing the control elastic modulus for all segments of the left ventricle and one in which ischemic (dyskinetic) segments were assigned a higher elastic modulus. Results showed that the control elastic modulus was a poor predictor of diastolic left ventricular expansion after coronary occlusion. The finite element analysis in which the ischemic segments were assigned a higher elastic modulus better predicted ischemic diastolic wall motion patterns. Error values (difference between predicted and actual left ventricular segmental diastolic motion) were: control, 1.9 +/- 0.3 mm (mean +/- SD), ischemia, 2.9 +/- 0.5 mm, and 2.2 +/- 0.4 mm using the stiffer elastic modulus for ischemic segments. Error values were significantly higher (p less than 0.05) under ischemic conditions when the control elastic modulus was uniformly applied compared with control and ischemia with dyskinetic segments assigned a higher elastic modulus. From these data, it is concluded that the myocardial diastolic elastic modulus is increased by ischemia and that this approach may allow clinical assessment of intrinsic muscle stiffness.
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.
During coronary revascularization, the precise location of major coronary arteries may be obscured by overlying fat, myocardial bridging, or epicardial scarring. High-frequency epicardial echocardiography can be used intraoperatively to quickly image and locate such arteries and eliminate the need for time-consuming epicardial exploration or potentially deleterious retrograde probing of distal coronary artery branches. This technique can be applied using commercially available equipment and the aid of a skilled technician.
The purpose of this study was to determine the accuracy of a new high frequency echocardiographic technique for the quantitative assessment of coronary artery luminal and wall dimensions. In 32 open chest animals, high frequency echocardiographic measurements (echo) of luminal diameter correlated well with in vitro histologic measurements (Histo) (r = 0.86; high frequency echo = 0.89 Histo + 0.79) (range 1.7 to 5.8 mm). Similar results were found in the evaluation of five human autopsy hearts studied in vitro. Coronary artery wall thickness measurements in human autopsy hearts showed a good correlation with high frequency echocardiographic measurements (r = 0.86; high frequency echo = 0.65 Histo + 0.24) (range 0.3 to 0.8 mm). In eight open chest calves, high frequency echocardiographic measurements of total vessel diameter correlated well with sonomicrometer measurements (Sono) (r = 0.94; high frequency echo = 1.03 Sono + 0.4) (range 2.1 to 5.3 mm). Inter- and intraobserver variability measurements of high frequency echocardiographic measurements demonstrated excellent reproducibility (r = 0.95, interobserver variability for wall thickness; r = 0.97, interobserver variability for luminal diameter; n = 10 postmortem human coronary arteries). In conclusion, high frequency echocardiography is an accurate and reproducible method of measuring coronary luminal and wall geometry and may be a potentially useful tool for in vivo coronary artery evaluation in 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.