Intracardiac versus transthoracic echocardiographic imaging of translation and rotation of left ventricular center of cavity area in dogs.

Motion of the left ventricular cavity center during the cardiac cycle was compared using transthoracic and intracardiac echocardiography. Rotation was comparable for the 2 methods, however, translation of the left ventricular cavity area center was greater with intracardiac echocardiography.

Current-based transthoracic defibrillation.

This study examines in a prospective, multicenter trial the feasibility and advantage of current-based, transthoracic defibrillation. Current-based, damped, sinusoidal waveform shocks of 18, 25, 30, 35, or 40 amperes (A) were administered beginning with 25 A for polymorphic ventricular tachycardia (VT) and ventricular fibrillation (VF) or 18 A for monomorphic VT; success rates were compared with those of energy-based shocks beginning at 200 J for VF/polymorphic VT and 100 J for VT. The current-based shocks were delivered from custom-modified defibrillators that determined impedance in advance of any shock using a "test-pulse" technique; the capacitor then charged to the exact energy necessary to deliver the operator-selected current against the impedance determined by the defibrillator. Three hundred sixty-two patients received > 1 shock for VF, polymorphic VT, or monomorphic VT: 569 current- based shocks and 420 energy-based shocks. Current-based shocks of 35/40 A achieved success rates of up to 74% for VF/polymorphic VT; 30 A shocks terminated 88% of monomorphic VT episodes. Energy-based shocks of 300 J terminated 72% of VF/polymorphic VT; 200-J shocks terminated 89% of monomorphic VT. We could not demonstrate a significant increase in the success rate of current-based shocks over energy-based shocks for patients with high transthoracic impedance; this may be due to inadequate sample size. Thus, current-based defibrillation is clinically feasible and effective. A larger study will be needed to test whether current-based defibrillation is superior to energy-based defibrillation.

Overlapping sequential pulses. A new waveform for transthoracic defibrillation.

BACKGROUND: A directionally changing shock electrical vector could facilitate defibrillation by depolarizing myocytes with different orientations vis-à-vis the shock field. Such a changing vector can be achieved by a new waveform for transthoracic defibrillation: overlapping sequential pulses. Our purpose was to evaluate this waveform. METHODS AND RESULTS: Ventricular fibrillation was induced in closed-chest dogs. Single and overlapping truncated exponential waveform pulse shocks were then administered from self-adhesive chest electrodes. Single pulse (control) shocks were 7.5-millisecond duration, while the sequential overlapping pulse shocks, using two different pathways, consisted of two pulses, each 5.0-millisecond duration; the second pulse began 2.5 milliseconds after the start of the first pulse and ended 2.5 milliseconds after the end of the first pulse. Thus, the total duration of the sequential overlapping shock was 7.5 milliseconds. During the overlap phase (2.5 milliseconds), the electrical vector orientation is the summation of the individual vectors. Two different electrode placements and corresponding electrical vector orientations were studied: group 1 (n = 14), left lower chest to right upper chest (pulse 1), overlapped by right lower chest to left upper chest (pulse 2), with the sequence then reversed; and group 2 (n = 11), left chest to right chest (pulse 1) overlapped by dorsal (vertebral column) to ventral (sternum) (pulse 2) with the sequence then reversed. At voltages equivalent to energies of 50, 100, and 150 J, the sequential overlapping pulse shocks achieve higher success rates than the single pulse shocks: At the low energy, 50 J, single pulse shock success rates were 0% (group 2) and 14% (group 1), while the overlapping pulse shocks achieved success rates of 39% (group 2) and 55% (group 1) (P < .05). Similarly, at the highest energy tested, 150 J, single pulse shock success rates were 45% (group 2) and 61% (group 1), while the overlapping pulse shock success was 91% (group 2) and 95% (group 1) (P < .05). In a third group of dogs (n = 3), intracardiac plunge electrodes placed orthogonally in the septum showed that the orthogonal components of intracardiac voltage gradient change varied markedly during the three phases of the sequential overlapping shocks, demonstrating the changing direction of the net electrical vector as the shock proceeded. In a fourth group of dogs (n = 5), short-duration (2.5-millisecond) single pulse shocks were compared with longer 7.5-millisecond single pulse shocks and with the sequential overlapping pulse shocks, all at equivalent energies. Despite substantially higher current flow, the 2.5-millisecond-duration single pulse shocks were not more effective than 7.5-millisecond single pulse shocks, and both 2.5- and 7.5-millisecond duration single pulse shocks had markedly inferior success rates compared with the sequential overlapping pulse shocks. CONCLUSIONS: Sequential overlapping pulse shock waveforms facilitate defibrillation compared with single pulse shocks of the same total energy. This is due at least in part to the changing orientation of the electrical vector during the multiple pulse shock.

Is transthoracic impedance arrhythmia specific? Experimental studies.

Transthoracic impedance (TTI) is a major determinant of current flow in defibrillation, and it is therefore important to understand the factors that determine TTI. Our purpose was to evaluate the effect of atrial and ventricular arrhythmias on TTI. In anesthetized, closed-chest dogs we measured TTI by means of a technique previously validated by us, which did not require administration of actual shocks. Measurements were made at baseline (sinus rhythm) and during rapid atrial pacing (atrial fibrillation), rapid ventricular pacing, and electrically induced ventricular fibrillation (VF) with respiration discontinued. TTI was unchanged by rapid atrial or ventricular pacing. When VF was induced and respiration was discontinued, TTI fell immediately from 51.6 +/- 4.3 ohms to 45.6 +/- 4.7 ohms (p < 0.01) and did not change thereafter. The drop in TTI was probably due to respiratory arrest and decreased chest size with full exhalation; when VF was induced but respiration was continued TTI did not change, whereas discontinuing respiration caused TTI to fall even if VF was not induced. We conclude that TTI is not altered by arrhythmias.

Lidocaine and dextran sulfate inhibit leukocyte accumulation but not postischemic contractile dysfunction in a canine model.

Leukocytes have been implicated as a possible factor in the pathogenesis of postischemic contractile dysfunction, probably through the release of oxygen free radicals. Lidocaine and dextran sulfate are known to inhibit leukocyte adherence to endothelial cells in vitro and in vivo. In an acute open-chest canine model both agents were found to inhibit the augmented accumulation of indium-111-labeled leukocytes in briefly ischemic and subsequently reperfused myocardium. Pharmacologic inhibition of leukocyte accumulation by lidocaine and dextran sulfate, however, was not associated with improvement in postischemic contractile dysfunction.

Cardiac geometry and mass changes associated with pacing-induced cardiomyopathy in the dog.

We evaluated the effects of chronic rapid pacing (240 beats/min) on ventricular geometry and function and on cardiac mass in a canine model. Forty dogs were studied by two-dimensional echocardiography before and after 45 days of pacing. Compared with sham-operated control animals, the paced animals had significant increases in end-diastolic and end-systolic volume and a decrease in ejection fraction. The increase in ventricular volume was primarily the result of dilation of the short axis of the ventricular lumen, without significant changes in the long-axis dimension. Paced animals had biatrial hypertrophy but no change in ventricular or total cardiac mass.

Validation by high-frequency epicardial echocardiography of a new method of analyzing coronary angiography quantitatively in coronary artery disease.

In coronary atherosclerosis, the arterial lumen size and shape can be markedly irregular, eccentric and variable. Traditional angiographic interpretation, emphasizing percent diameter stenosis, has been criticized as an inadequate descriptor of such diseased arteries. Computerized quantitative angiographic technologies, yielding a true lumen area measurement, may be superior. High-frequency epicardial echocardiography (HFEE) is a technique that allows on-line evaluation of coronary arterial wall and lumen at the time of cardiac surgery. It has been extensively validated and yields accurate measurements of normal and diseased coronary lumen areas. This study compares quantitative coronary angiography (QCA) estimates of lumen area to those obtained by HFEE to determine if the computerized angiographic method more accurately predicts residual luminal area than traditional angiographic percent diameter stenosis measurements. Although actual luminal morphology was quite variable, there was a good correlation between lumen areas determined by HFEE versus QCA: r = 0.85, n = 67, HFEE = 0.8 QCA - 0.1 (HFEE 4.0 +/- 0.30 mm2, mean +/- SEM range 0.3 to 14.0; QCA 5.1 +/- 0.40 mm2, range 0.7 to 11.8). Percent diameter stenosis determined from the angiograms did not correlate well with HFEE or QCA measurements of residual luminal area. Separation of "normal" arterial segments (defined as < 25% diameter stenosis) from "abnormal" segments (> 50% diameter stenosis) by angiography did not agree with lumen areas as defined by either HFEE or QCA. Better separation occurred when QCA-determined luminal areas were used to separate normal from abnormal arterial segments.(ABSTRACT TRUNCATED AT 250 WORDS)

Transthoracic defibrillation: effect of dual-pathway sequential pulse shocks and single-pathway biphasic pulse shocks in a canine model.

To determine whether dual-pathway sequential shocks and single-pathway biphasic shocks improved the efficacy of transthoracic defibrillation, we delivered single or sequential truncated waveform shocks of variable duration, voltage, and direction (polarity) to three groups of closed-chest dogs. Dual-pathway sequential shocks were assessed in group 1 (eight animals), biphasic shocks with a single pathway were compared in 11 dogs (group 2), and the effect of varying the duration of the biphasic shocks was assessed in group 3 (four animals). There was no improvement in success rates of the intervention shocks compared with a standard single "control" shock at any energy level. In this experimental model unidirectional or biphasic sequential shocks given over single or dual pathways were not superior to standard single-pulse transthoracic defibrillation.

Variable morphology of coronary atherosclerosis: characterization of atherosclerotic plaque and residual arterial lumen size and shape by epicardial echocardiography.

The purpose of this study was to evaluate the in vivo characteristics of coronary atherosclerosis by using high frequency epicardial echocardiography. High frequency epicardial echocardiography was used to evaluate residual lumen and wall morphology at the sites of maximal coronary atherosclerosis in 26 patients undergoing coronary artery bypass grafting. The maximal/minimal wall thickness ratio was 3.1 +/- 0.2 (mean +/- SEM) with a large range (1.3 to 7.5). Portions of the wall were normal in 16 of 31 lesions; the percent normal circumference ranged from 9% to 85%. Maximal/minimal lumen diameter ratio was 1.5 +/- 0.1 (range 1.1 to 2.9). The shape of the residual coronary lumen was noncircular in 16 lesions: oval in 13 and complex in 3. The residual coronary lumen was eccentrically placed within six arteries. These data emphasize the variability of residual lumen and wall geometry in atherosclerosis.

Effect of nisoldipine on hemodynamic responses to defibrillation.

Sequences of ventricular fibrillation-defibrillation cause transient hypertension; we hypothesized that this "adrenergic overshoot" might be blunted by the functional antiadrenergic effect of the calcium channel blocking drug nisoldipine, with a potentially beneficial reduction in myocardial oxygen requirements. However, other calcium channel blocking drugs have been shown to reduce shock success for defibrillation, a deleterious effect. Thus the purposes of this study were to assess the effect of nisoldipine on the hemodynamic responses to the sequences of ventricular fibrillation-defibrillation, and its effect on the energy requirements for defibrillation. In 16 dogs we administered intravenous nisoldipine (1 microgram/kg bolus followed by an infusion of 0.075 to 0.50 microgram/kg/min) to lower mean blood pressure 10% and 20% below baseline. Ventricular fibrillation was induced electrically, and shocks of varying energy levels (30, 50, and 100 joules) were administered to determine defibrillation energy requirements. Heart rates and blood pressures were recorded up to 3 minutes after each shock to determine hemodynamic responses. Measurements were made before nisoldipine administration and again at the two levels of drug-induced blood pressure decline. We found that the usual systolic blood pressure "overshoot" after defibrillation (typically maximum at 15 to 30 seconds after shocks) was significantly blunted after nisoldipine administration (p less than 0.05). Heart rate slowing after defibrillation (a cholinergic response) was not affected. Nisoldipine did not alter shock success rates, which varied from 12 +/- 7%SE at 30 joules to 68 +/- 12% at 100 joules. Thus nisoldipine blunted the "adrenergic overshoot" of systolic blood pressure following defibrillation, a potentially beneficial effect, without altering the energy requirements for transthoracic defibrillation.

Effect of age on diastolic left ventricular filling at rest and during inotropic stimulation and acute systemic hypertension: experimental studies in conscious beagles.

"Pharmacologic" stress testing with inotropic stimulation is useful in the detection of coronary artery disease when ventricular dysfunction is provoked. However, abnormal diastolic filling may be masked or mimicked because of the influence of aging, heart rate, and loading conditions. We evaluated age effects on left ventricular filling at rest in young (n = 5) and old (n = 6) purebred beagles that were free of occlusive coronary disease and left ventricular hypertrophy, and we also evaluated age-related differences in left ventricular filling velocities in response to dobutamine and phenylephrine. Pulsed Doppler echocardiography of left ventricular filling velocities was performed at baseline and then after the administration of dobutamine (10 to 20 micrograms/kg/min) infusion. Repeat baseline recordings were obtained and then phenylephrine was administered intravenously in doses of 5 to 25 micrograms/kg/min until systolic arterial pressure increased by at least 30 mm Hg above baseline. At baseline, Doppler echocardiography revealed that there were no significant differences in the early (E) velocity or velocity time interval (VTI), and atrial (A) velocity or the A/E velocity ratio between the young and old groups. However, the A VTI and the A/(A + E) VTI ratio were significantly increased in the old group. With dobutamine administration, the E velocity did not significantly increase from baseline in either group. The E VTI, A velocity and A VTI increased significantly in both groups, but the increases were not different between groups. With phenylephrine infusion there was a significant decrease in the E VTI in the old group but neither the A/E velocity or the A/(A + E) VTI ratio significantly changed from baseline.(ABSTRACT TRUNCATED AT 250 WORDS)

Characterization of acute experimental left ventricular thrombi with quantitative backscatter imaging.

Two-dimensional echocardiography is an excellent technique for detecting left ventricular thrombi, however, acute clot is sometimes difficult to differentiate from adjacent myocardium and intracavitary signals. We hypothesized that quantitative assessment of the acoustic properties of acute left ventricular thrombi using a quantitative backscatter imaging system would permit the differentiation of thrombus from adjacent myocardium and intracavitary echoes. Acute, experimental left ventricular thrombi in seven dogs were evaluated with a quantitative backscatter imaging system that allowed the measurement of relative integrated backscatter and cyclic (i.e., diastolic minus systolic) variation in integrated backscatter. Coronary ligation abolished the cyclic variation in relative backscatter that occurred in normal myocardium. The end-diastolic relative backscatter in the thrombus (16.9 +/- 1.3 dB) was significantly higher than in apical myocardium (13.2 +/- 0.6 dB, p less than 0.05). There was no significant difference in the cyclic variation in relative backscatter among thrombus, ischemic myocardium, or intracavitary blood. Thus, the quantitative assessment of the acoustic properties of left ventricular thrombi can be useful in their detection and in the differentiation from myocardium and intracavitary signals.

Transthoracic defibrillation using sequential and simultaneous dual shock pathways: experimental studies.

Dual pathway sequential DC shocks reduce energy requirements for internal defibrillation. Our purpose was to determine if dual pathway shocks similarly reduce energy requirements or improve shock success in transthoracic (external) defibrillation. We studied 39 closed-chest anesthetized mongrel dogs. The dual pathways used were left chest to right chest and left chest to posterior. In eight dogs we also assessed dual shock pathways oriented orthogonally, left lower chest to right upper chest and left upper chest to right lower chest. Four different dual pathway groups were studied: group 1: simultaneous shocks, sinusoidal waveform; group 2: sequential shocks, sinusoidal waveform, 100-msec shock separation, orthogonal shock pathways; group 3: sequential shocks, sinusoidal waveform, 100 msec shock separation; and group 4: sequential shocks, rectangular waveform (sequential shocks: 2 pulses, 2.5 msec each, 0.1-msec separation; single shock: 1 pulse, 5 msec). Shocks were given at 50 (J) joules, 100 J and 150 J and curves of energy versus success compared for dual pathway shocks versus single shocks. We found that the highest mean success rates (96 +/- SD 9%) were achieved by simultaneous sinusoidal waveform dual pathway shocks at 100 J; this was identical to results achieved by the single pathway sinusoidal waveform comparison shocks at 100 J. Sequential dual pathway sinusoidal shocks separated by 100 msec achieved a mean success rate of 79 +/- 31% at 150 J; the comparison single pathway mean success rate was similar: 81 +/- 22% at 150 J. Thus, dual pathway sequential or simultaneous transthoracic shocks did not demonstrate clear superiority over single pathway shocks.

Mechanisms responsible for decline in transthoracic impedance after DC shocks.

To test the hypothesis that tissue hyperemia and edema in the current pathway cause a decrease in transthoracic impedance (TTI) following direct current (DC) shock, the thoracic-skin and skeletal blood flow and blood volume were measured in anesthetized dogs after three 100-J shocks. TTI declined 11% (P less than 0.01) after DC shocks. Blood flow increased 10-fold in skeletal muscle from 0.9 +/- 0.2 to 11.3 +/- 2.6 (SE) ml.100 g-1.min-1 (P less than 0.05). Blood flow did not change outside the current pathway. Blood volume increased in skin in the current pathway from 7.6 +/- 1.5 ml/100 g preshock to 17.5 +/- 2.0 ml/100 g (P less than 0.01) at 60 min after shock; skeletal muscle blood volume did not change. We also determined postshock tissue weight before and after 72 h of drying at 70 degrees C. The percentage decline from wet weight after drying was 68.4 +/- 3.4% in the current pathway vs. 64 +/- 3.8% outside the pathway (P less than 0.05), indicating the tissue in the current pathway was more edematous. Finally, hindlimb edema was induced by deliberate overperfusion. As hindlimb circumference (edema) increased, impedance declined. We conclude that increases in tissue blood flow or tissue blood volume or tissue edema contribute to the decline in transthoracic impedance after DC shock.

Effect of calcium channel blockers on hemodynamic responses to defibrillation.

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)

Sensitization of reperfused myocardium to subsequent coronary flow reductions. An extension of the concept of myocardial stunning.

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.

Ultrasound characterization of acoustic properties of acute intracardiac thrombi: studies in a new experimental model.

Echocardiographic differentiation among intracavitary thrombus, cavity noise, and adjacent myocardium can be difficult. As an initial step toward quantitative thrombus characterization with ultrasound, 11 dogs were studied with an in vivo intracardiac thrombus model to delineate the acoustic properties of acute thrombi. The apical coronary arteries were ligated, and subsequently injections of 5% sodium rescinoleate and 1000 units of thrombin at the endocardium-blood interface created left ventricular mural thrombi. Echocardiographic images were obtained in long- and short-axis views with a digital acquisition system, and a statistical analysis of echo intensities was performed in regions of interest in the thrombus, surrounding ventricular cavity and adjacent myocardium. Statistical measurements used to evaluate echo intensities in each region of interest included mean gray level, standard deviation, skewness, and kurtosis. The results showed that thrombus could be distinguished from myocardium (by mean gray level and standard deviation) only in short-axis views, where regions of interest could be placed at similar depths of field. Mean gray level, standard deviation, and skewness all distinguished thrombus from intracavitary blood regardless of the region of interest placement. The phase of the cardiac cycle at which data were acquired did not alter the results. We conclude that acute intracardiac thrombi can be distinguished from surrounding blood and myocardium with ultrasound tissue characterization techniques that may have the potential for clinical application.

Myocardial risk area and peak gray level measurement by contrast echocardiography: effect of microbubble size and concentration, injection rate, and coronary vasodilation.

Contrast agents were injected via the intracoronary route in eight dogs during two-dimensional echocardiographic imaging to determine the influence of microbubble size and concentration, injection rate, and coronary vasodilation on risk area and peak gray level measurement. At an injection rate at 13 cc/sec, the average background-subtracted peak gray level intensity of hand-agitated diatrizoate meglumine/diatrizoate sodium was significantly (p less than 0.01) higher than that of hand-agitated diatrizoate meglumine/diatrizoate sodium + 0.9% saline, sonicated diatrizoate meglumine/diatrizoate sodium, and sonicated 70% sorbitol. These differences were abolished by the use of 38 cc/sec injection rates and intracoronary injection of adenosine. Perfusion area determinations as assessed by planimetry were unaffected by the contrast agent used, the injection rate, or by intracoronary administration of adenosine. We conclude that risk area measurement by the ultrasound contrast technique is not affected by varying contrast agents, injection rates, or vasodilation. However, peak gray level intensity is variable among contrast agents and may result in variability of time-activity curve analysis.

Altered response of reperfused myocardium to repeated coronary occlusion in dogs.

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)

Delineation of the extent of coronary atherosclerosis by high-frequency epicardial echocardiography.

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.