Intracoronary artery thrombus formation in unstable angina: a clinical, biochemical and angiographic correlation.

OBJECTIVES: We examined the relation between the level of urinary fibrinopeptide A and the presence of angiographic intracoronary thrombus in patients with unstable angina to determine whether this marker predicts active thrombus formation. BACKGROUND: Although it is known that thrombus plays a role in acute ischemic syndromes, a noninvasive method to predict its presence in individual patients with unstable angina has not been determined. Fibrinopeptide A is a polypeptide cleaved from fibrinogen by thrombin and thus is a sensitive marker of thrombin activity and fibrin generation. METHODS: Angiographic thrombus, graded 0 to 4, and the presence of ST segment depression or T wave inversions, or both, on the electrocardiogram (ECG) were related to fibrinopeptide A levels in 24 patients with rest angina of new onset, 18 with crescendo angina, 19 with stable angina and 9 with chest pain but without coronary artery disease. All patients had chest pain within the 24 h of sample acquisition. RESULTS: The angiographic incidence of thrombus was significantly higher in patients with new onset of rest angina (67%, p < 0.001) and crescendo angina (50%, p < 0.001) as were fibrinopeptide A levels (p = 0.002). Fibrinopeptide A levels correlated significantly (p < 0.001) with the presence of a filling defect (grade 4 intracoronary thrombus) or contrast staining (grade 3). All patients with fibrinopeptide A > or = 8 ng/mg creatinine showed grade 3 to 4 thrombus and 15 of 16 patients with levels > or = 6.0 ng/mg creatinine exhibited angiographic evidence of thrombus (13 with grades 3 to 4). Patients with reversible ST changes on the ECG had significantly higher levels of fibrinopeptide A (p < 0.001), and ST changes correlated significantly with the presence of angiographic thrombus (p < 0.001). Nonetheless, a significant minority of patients with unstable angina had neither angiographic nor biochemical evidence of thrombus. CONCLUSIONS: Elevated fibrinopeptide A levels in unstable angina reflected active intracoronary thrombus formation and were present in patients with angina of new onset as well as crescendo angina. Reversible ST changes are accompanied by thrombin activity and angiographic thrombus formation. However, a sizable percentage of patients with unstable angina had no evidence of thrombus and these patients may have had transient platelet aggregation without fibrin thrombus formation.

Effects of a new nonionic and a conventional ionic contrast agent on coronary sinus ionized calcium and left ventricular hemodynamics in dogs.

Transient myocardial depression associated with intracoronary injections of contrast medium has been attributed to hypertonicity and to calcium binding. To further assess the importance of calcium binding, a new technique for continuous monitoring of coronary sinus ionized calcium with an intravascular calcium-selective electrode was used. With this calcium-selective electrode the effects of intracoronary injection in dogs of a conventional ionic contrast agent, sodium meglumine diatrizoate (Renografin-76), and a new nonionic agent, iohexol, were assessed and compared. Left ventricular pressure was measured with a micromanometer catheter. After bolus injection of 0.2 ml/kg body weight of Renografin-76 (n = 10), coronary sinus pCa increased by 0.27 from 2.98 +/- 0.02 to 3.25 +/- 0.03, indicating a decrease in ionized calcium from 2.0 to 1.1 mEq/liter. With iohexol (n = 9), pCa increased by only 0.05 +/- 0.01 (p less than 0.001), indicating a decrease in ionized calcium from 2.0 to 1.8 mEq/liter. Peak changes occurred approximately 6 seconds after injection. Renografin-76 caused a marked decrease in left ventricular systolic pressure (140 +/- 7 to 106 +/- 8 mm Hg) and in heart rate (122 +/- 7 to 101 +/- 5 beats/min) with an increase in end-diastolic pressure (5 +/- 1 to 12 +/- 1 mm Hg), whereas iohexol did not significantly alter these variables. Using Renografin-76 with calcium added to achieve an ionized calcium level of 2 (n = 4), 4 (n = 4) or 6 (n = 4) mEq/liter, the changes in coronary sinus pCa were abolished and the hemodynamic changes attenuated. These findings indicate that Renografin-76 results in greater myocardial depression than the new nonionic agent iohexol.(ABSTRACT TRUNCATED AT 250 WORDS)

Improvement in rest and exercise-induced wall motion abnormalities after coronary angioplasty: an exercise echocardiographic study.

Exercise echocardiography was performed in 36 patients to evaluate functional improvement after coronary angioplasty. Thirty-one patients (86%) had provokable ischemia before angioplasty including 22 with an abnormal exercise electrocardiographic test (angina or ST depression), 25 with an abnormal exercise echocardiogram (exercise-induced wall motion abnormalities) and 16 with both tests abnormal. Nineteen patients had no induced ischemia after angioplasty. Seventeen (47%) continued to have ischemia that was limited in 12 to exercise-induced wall motion abnormalities, which were less severe compared with those of preangioplasty studies. Fifteen (65%) of 23 patients had improvement in rest wall motion abnormalities after angioplasty. The rest to immediate postexercise change in global wall motion score was significantly improved after angioplasty. The change in regional wall motion score was significantly improved after angioplasty in patients with single vessel right or left circumflex coronary artery disease and approached significant improvement (p = 0.06) in those with single vessel disease of the left anterior descending coronary artery. Exercise echocardiography improves the sensitivity of functional testing for ischemia, aids in localizing the ischemic zone and documents improvement in regional function after coronary angioplasty.

Prevention of subsequent exercise-induced periinfarct ischemia by emergency coronary angioplasty in acute myocardial infarction: comparison with intracoronary streptokinase.

To compare the efficacy of emergency percutaneous transluminal coronary angioplasty and intracoronary streptokinase in preventing exercise-induced periinfarct ischemia, 28 patients presenting within 12 hours of the onset of symptoms of acute myocardial infarction were prospectively randomized. Of these, 14 patients were treated with emergency angioplasty and 14 patients received intracoronary streptokinase. Recatheterization and submaximal exercise thallium-201 single photon emission computed tomography were performed before hospital discharge. Periinfarct ischemia was defined as a reversible thallium defect adjacent to a fixed defect assessed qualitatively. Successful reperfusion was achieved in 86% of patients treated with emergency angioplasty and 86% of patients treated with intracoronary streptokinase (p = NS). Residual stenosis of the infarct-related coronary artery shown at predischarge angiography was 43.8 +/- 31.4% for the angioplasty group and 75.0 +/- 15.6% for the streptokinase group (p less than 0.05). Of the angioplasty group, 9% developed exercise-induced periinfarct ischemia compared with 60% of the streptokinase group (p less than 0.05). Thus, patients with acute myocardial infarction treated with emergency angioplasty had significantly less severe residual coronary stenosis and exercise-induced periinfarct ischemia than did those treated with intracoronary streptokinase. These results suggest further application of coronary angioplasty in the management of acute myocardial infarction.

Quantitative measurement of coronary flow during medical revascularization (thrombolysis or angioplasty) in patients with acute infarction.

This study quantitatively evaluated the change in myocardial blood flow resulting from medical revascularization in patients with acute anterior myocardial infarction. Changes in great cardiac vein flow were measured using a thermodilution technique in 13 patients with acute infarction; 3 received intracoronary streptokinase and 10 percutaneous transluminal angioplasty. Average great cardiac vein flow during left anterior descending coronary artery occlusion was 62 +/- 6 ml/min and increased to 70 +/- 7 ml/min (p = 0.039) after arterial recanalization. There was significant individual variability in the great cardiac vein flow increments that was highly predictive of functional recovery as expressed by the change in ejection fraction at 7 to 10 days (r = 0.93, p = 0.0008). Incremental great cardiac vein flow was inversely correlated with the degree of residual stenosis and the duration of ischemia (r = 0.88, p = 0.0007). Patients with residual stenosis less than or equal to 50% had a significantly larger increase in great cardiac vein flow (14 +/- 5 ml/min) than did those with residual stenosis greater than 50% (0 +/- 2 ml/min, p = 0.026). Neither preinterventional left ventricular ejection fraction, hemodynamics nor age predicted incremental great cardiac vein flow. Therefore, quantitative measurements of great cardiac vein flow during medical revascularization in patients with an acute anterior myocardial infarction demonstrate variable reflow that is physiologically significant. A high grade residual stenosis and prolonged period of ischemia limit large increases in flow and prevent functional recovery. This study emphasizes the fact that recanalization in itself cannot be used as an indicator of the success of interventions designed to produce myocardial reperfusion.

Evaluation of patterns of perfusion and metabolism in dobutamine-responsive myocardium.

OBJECTIVES: We investigated the patterns of perfusion and metabolism in dysfunctional myocardium whose contractility improved with dobutamine. BACKGROUND: Clinical studies have suggested that dobutamine echocardiography can identify hibernating myocardium, but laboratory studies suggest that reduced perfusion limits the response to dobutamine. METHODS: Twenty-five patients with coronary disease and ventricular dysfunction underwent low (5 and 10 micrograms/kg body weight per min) and high dose (maximum of 50 micrograms/kg per min) dobutamine echocardiography and positron emission tomography (PET) using nitrogen-13 (N-13) ammonia and fluorine-18 fluorodeoxyglucose (FDG) for imaging of perfusion and metabolism. Wall motion and tracer uptake were scored in 16 left ventricular segments. RESULTS: Perfusion and metabolism were normal in 56.4%, mildly reduced in 29.1% and mismatched (reduced perfusion, preserved FDG uptake) in 14.5% of dysfunctional segments viable on PET. Wall motion improved with dobutamine in 89 dysfunctional segments (62 at low dose, 27 only at peak dose), and 86 of these (97%) were viable on PET. Improvement in wall motion with dobutamine was more common in segments with normal perfusion and metabolism (56.5%) than in those with mildly reduced tracer uptake (28.5%, p < 0.001) and those with mismatch (32%, p = 0.03). All the segments with a biphasic response were supplied by vessels with > or = 70% stenosis, and 88% had normal perfusion and metabolism. CONCLUSIONS: The majority of viable segments with rest dysfunction had normal perfusion and metabolism, suggesting that myocardial stunning was common. Improvement of wall motion at low and high doses of dobutamine was highly correlated with myocardial viability on PET and was more common in myocardium with normal perfusion. A biphasic response to dobutamine identified segments with normal perfusion and metabolism supplied by severely diseased vessels.

Effects of ischaemia and reperfusion on calcium exchange and mechanical function in isolated rabbit myocardium.

We have studied calcium exchanges and mechanical function in heart muscle during and after a period of ischaemia. The experimental preparation was the isolated but arterially perfused interventricular septum of the rabbit. Uptake of calcium was measured with 47Ca2+ and efflux with 45Ca2+. 51Cr-EDTA was used as a marker of the extracellular space. Ischaemia caused a rapid decline of developed tension followed by a rise in resting tension. Tissue counts of 47Ca2+ decreased due to a reduction in the extracellular space. On reperfusion after ischaemia developed tension partially recovered and resting tension increased further before returning towards control values. A large and prolonged uptake of 47Ca2+ occurred immediately on reperfusion while 45Ca2+ efflux rose transiently. The uptake of calcium was related to the severity and duration of ischaemia and to the degree of mechanical recovery. Calcium accumulation on reperfusion is due to an increased influx which is not related to gross disruption of the cell membrane but more probably to a specific abnormality of ionic channels.

Comparison of contrast angiography and two-dimensional echocardiography for the evaluation of left ventricular regional wall motion abnormalities after acute myocardial infarction.

Regional left ventricular wall motion abnormalities were assessed using 2-dimensional echocardiography and contrast ventriculography within 12 hours of the onset of chest pain in 20 patients with acute myocardial infarction (AMI); 10 patients had anterior infarctions and 10 had inferior. End-diastolic and end-systolic sinus beats from right anterior oblique contrast ventriculograms were analyzed using the center-line chord technique with both a standard overlap method of chord assignment and a nonoverlap method. Echocardiograms were obtained in parasternal long- and short-axis and apical 2- and 4-chamber views and analyzed using a 16-segment scoring system to derive anterior and infero-posterolateral wall motion indexes using both overlap (10 segments for anterior, 8 inferior) as well as nonoverlap (9 segments anterior, 7 inferior) methods of segment assignment. There was a significant inverse correlation between the standard (nonoverlap) echocardiographic analysis and the standard (overlap) angiographic analysis for infarct regions (y = -0.43 X +1.11, r = -0.59, p less than 0.05). Fifteen of 18 patients with angiographic infarct regional score less than or equal to -1 standard deviation/chord had an echocardiographic index greater than or equal to 1.5, while 15 of 16 patients with echocardiographic regional infarct index greater than or equal to 1.5 had an angiographic score less than or equal to -1 standard deviation/chord. Correlation between the 2 methods for noninfarct territories was poor (r = -0.34) because the angiographic method assesses hyperkinesis while the echocardiographic method does not.(ABSTRACT TRUNCATED AT 250 WORDS)

Hemodynamic effects of intravenous metoprolol.

The hemodynamic effects of the cardioselective beta adrenergic blocking agent metoprolol, at a dose of 0.1 mg/kg body weight administered intravenously, were studied in 10 patients undergoing routine cardiac catheterization. The beta adrenergic blocking effect of the drug was confirmed by a highly significant reduction (53 percent, P less than 0.001) in the mean heart rate response to a challenge with isoproterenol, and by a mean heart rate rssponse to a challenge with isoproterenol, and by a highly significant reduction (73 percent, P less than 0.001) in the isoproterenol-induced increase in the first derivative of left ventricular pressure (dP/dt). An intrinsic negative inotropic effect was shown by a 43 percent reduction (P less than 0.05) in the response of mean left ventricular dP/dt when the heart rate was fixed by atrial pacing alone. With the combination of atrial pacing and isoproterenol, metoprolol produced a 48 percent reduction (P less than 0.01) in the response of mean left ventricular dP/dt, resulting from both the intrinsic depressor effect and the beta adrenergic blocking effect on the rate-independent beta agonist activity of isoproterenol. There was no significant change in right atrial, femoral arterial or left ventricular end-diastolic pressure; analysis of left ventricular angiograms performed during atrial pacing before and after metoprolol revealed no significant effect on angiographic ejection fraction, pressure-volume loops or diastolic compliance. In two patients improvement in segmental wall motion was noted, and no deterioration was seen in any patient. Metoprolol is an effective cardioselective beta adrenergic blocking agent that, under these conditions, reduces catecholamine-induced increases in heart rate and left ventricular dP/dt without significant alteration in ejection fraction, preload or afterload.

Direct cardiac and peripheral vascular effects of intracoronary and intravenous nifedipine.

The hemodynamic effects of a new parenteral formulation of nifedipine administered by the intravenous (1 mg) and intracoronary (IC) (0.1 and 0.2 mg) routes were studied in 10 patients with symptomatic coronary artery disease undergoing diagnostic right- and left-sided cardiac catheterization. Intravenous nifedipine (1 mg) reduced systemic vascular resistance by 34% (p less than 0.01), increased cardiac output by 28% (p less than 0.01) and decreased mean arterial pressure by 10% (p less than 0.01). It had less effect on peak positive dP/dt (-8% p less than 0.025) and on peak negative dP/dt (-15% p less than 0.01). Coronary blood flow increased 20% (p less than 0.025). In contrast, IC nifedipine (0.2 mg) increased coronary blood flow 46% (p less than 0.025), depressed contractility as assessed by peak positive dP/dt (-26% p less than 0.01) and prolonged diastolic relaxation time. The effect of 0.1 mg was similar but less pronounced. These data suggest that the primary therapeutic effect of nifedipine administered systemically to patients at rest results from an increase in coronary blood flow and, to a lesser extent, from afterload reduction; its myocardial depressant effects are small, transient and masked by reflex catecholamine release. IC nifedipine increases coronary blood flow, has a transient negative inotropic effect and prolongs relaxation. The relative importance of these myocardial effects in preventing myocardial ischemia is not known.

Effects of CI-914 in congestive heart failure due to coronary artery disease or idiopathic cardiomyopathy.

The hemodynamic effects of CI-914, a phosphodiesterase inhibitor, were studied in 12 patients with left ventricular (LV) dysfunction who were undergoing diagnostic cardiac catheterization. CI-914 was infused intravenously at a rate of 0.8 to 7.0 micrograms/kg/min for 30 to 60 minutes; hemodynamic values were measured every 10 minutes. No effect was seen in the patient receiving 0.8 microgram/kg/min. At infusion rates of 1.2 to 2.4 micrograms/kg/min, cardiac index increased by 14% (p less than 0.025). At infusion rates of 4.5 to 7.0 micrograms/kg/min, cardiac index increased by 21% (n = 8, difference not significant [NS]). Among 4 patients (group B) with an initial pulmonary artery wedge pressure greater than 20 mm Hg and cardiac index less than 2.5 liters/min/m2, cardiac index increased by 50% (p less than 0.001); it did not change among the 4 patients with an initial pulmonary artery wedge pressure of less than 20 mm Hg and cardiac index of more than 2.5 liters/min/m2 (group A). Although systemic vascular resistance decreased in all 8 patients by 26% (p less than 0.01), the reduction was greater in group B (33%, p less than 0.01) than in group A (16%, NS). Peak +dP/dt increased in all 8 patients by 13% (p less than 0.01). Mean stroke work index increased from 29 +/- 15 to 34 +/- 13 g-m/m2; the double product fell from 101 +/- 31 to 91 +/- 23 (NS). In all 12 patients, a linear correlation between peak venous blood concentration and peak effect on cardiac index, systemic vascular resistance and pulmonary artery wedge pressure was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Assessment of potentially salvageable myocardium during acute myocardial infarction: use of postextrasystolic potentiation.

Twenty-three patients with evolving acute myocardial infarction (AMI) undergoing catheterization for thrombolytic therapy had interventional contrast ventriculography using programmed atrial stimulation. Postextrasystolic (PES) potentiation was present in 67% of infarct-related segments up to 9 hours after the onset of AMI. The presence of segmental potentiation was not related to time from onset of pain to ventriculography, initial ejection fraction, presence of collaterals, left ventricular end-diastolic pressure or the PES delay. In 18 patients reperfusion was successful using intracoronary streptokinase an average of 6.2 hours after the onset of AMI; in these patients repeat contrast ventriculography was performed an average of 11 days after AMI. Improved chronic segmental ventricular function was predicted by the presence of collaterals to the infarct-related artery at the time of acute catheterization (p = 0.02), but was best predicted by analysis of acute PES potentiation (p less than 0.0001). The predictive value of PES analysis was highest in segments without collaterals. Thus, atrial stimulation is safe during AMI and analysis of segmental ventricular function shows potentially viable myocardium up to 9 hours after the onset of AMI. In addition, analysis of PES segmental function can predict chronic function if reperfusion is successful, especially in segments without collaterals. PES ventriculographic analysis may allow prospective determination of which patients during AMI are most likely to benefit from acute thrombolytic therapy.

Early recovery of regional left ventricular function after reperfusion in acute myocardial infarction assessed by serial two-dimensional echocardiography.

Although global and regional left ventricular (LV) function has been demonstrated to improve after reperfusion in acute myocardial infarction (AMI), the timing of these changes has not been well established. In this study, serial 2-dimensional echocardiography was used to assess regional LV function in 23 patients with AMI in whom reperfusion was accomplished by thrombolysis alone, by coronary angioplasty alone or by both interventions within 6 hours after onset of chest pain. Echocardiograms were performed before or within 6 hours after reperfusion (n = 23) and at 1 (n = 19), 3 (n = 21) and 7 (n = 20) days after reperfusion. Wall motion index and percentage of normally functioning muscle were calculated using a 16-segment scoring system analyzed in blinded fashion without knowledge of patient identity, therapy or time of study. The mean wall motion index improved from 1.78 +/- 0.48 to 1.56 +/- 0.38 at 1 day (n = 19, p less than 0.01), and to 1.48 +/- 0.37 at 3-7 days (p less than 0.01), with no significant difference between 3 days (1.49 +/- 0.39) and 7 days (1.42 +/- 0.30). There was a corresponding improvement in the percentage of normally functioning muscle, from 53 +/- 24% at 6 hours to 62 +/- 20% at 1 day (p less than 0.05) and to 67 +/- 18% at 3-7 days (p less than 0.01), again with no significant difference between 3 days (67 +/- 21) and 7 days (70 +/- 20).(ABSTRACT TRUNCATED AT 250 WORDS)

Exercise echocardiography, angiography, and intracoronary ultrasound after cardiac transplantation.

Fifty-one consecutive patients underwent exercise echocardiography, angiography, and intracoronary ultrasound (ICUS) 2.5 years (range from 1 to 6) after cardiac transplantation. The average age of the donor was 29 years (range 13 to 50), and the average age of the recipient was 49 +/- 12 years. In total, 78 studies were performed, as 25 patients had >1 annual evaluation and 2 patients had 3 consecutive annual evaluations. Of the 78 angiographic studies, 40 (26 patients) had evidence of coronary artery disease, defined as a focal stenosis (>20%, n=4) or luminal irregularities (n=36). However, by ICUS all 51 patients had intimal thickening at some point, with 34 patients possessing diffuse disease and 17 focal intimal thickening only. Of the 25 serial studies, 12 progressed by at least 1 Stanford class. The sensitivity of angiography for determination of class III to IV intimal thickening was 64% and the specificity was 76%. On exercise echocardiography, 6 examinations revealed resting wall motions abnormalities, whereas 6 had inducible wall motion abnormalities with exercise. The sensitivity of exercise echocardiography to determine class III to IV intimal thickening was 15%, and the specificity was 85%. In conclusion, exercise echocardiography is an insensitive method for predicting transplant-mediated coronary artery disease, whereas luminal irregularities on angiography may predict the presence of Stanford grade III to IV intimal thickening.

Value of percutaneous transluminal coronary angioplasty after unsuccessful intravenous streptokinase therapy in acute myocardial infarction.

The effect of sequential high-dose intravenous streptokinase (SK) (1.5 million units) followed by emergency percutaneous transluminal coronary angioplasty (PTCA) on preserving left ventricular function was assessed prospectively in 34 patients with acute myocardial infarction (AMI). Intravenous SK therapy was initiated 2.6 +/- 1.3 hours (mean +/- standard deviation) after the onset of chest pain. Urgent coronary angiography showed persistent total occlusion in 13 patients, significant diameter stenosis (70 to 99%) in 18 patients and a widely patent artery (less than 50% stenosis) in 3 patients. Emergency PTCA was performed in 29 patients 5.0 +/- 2.1 hours after symptom onset. Successful recanalization was achieved in 33 of the 34 patients (97%) treated with sequential therapy. Repeat contrast ventriculograms recorded 7 to 10 days after intervention in 23 patients showed that the left ventricular ejection fraction increased from 53 +/- 12% to 59 +/- 13% (area-length method, p less than 0.002). Regional wall motion of the infarcted segments improved from -2.7 +/- 1.1 to -1.5 +/- 1.7 SD/chord (centerline method, p less than 0.003). In the subgroup of patients with an occluded artery on initial angiography (group A, n = 10), both global left ventricular ejection fraction (49 +/- 12% vs 59 +/- 12%, p less than 0.002) and regional wall motion (-3.2 +/- 1.0 vs -1.9 +/- 1.7 SD/chord, p less than 0.002) improved significantly. In contrast, no significant improvement was seen in patients with a patent artery on initial angiography (n = 13). Thus, sequential intravenous SK and emergency PTCA is efficacious in achieving coronary reperfusion and in improving both global and regional left ventricular function.(ABSTRACT TRUNCATED AT 250 WORDS)

Comparison of regional and global left ventricular function by serial echocardiograms after reperfusion in acute myocardial infarction.

Fifty patients undergoing successful reperfusion therapy (percutaneous transluminal coronary angioplasty 20, thrombolysis 10, combined 20) for acute myocardial infarction were evaluated with serial two-dimensional echocardiograms performed early (less than 24 hours, mean 8 hours) and late (greater than 3 days, mean 6 days) after presentation. Treatment occurred within 12 hours of the onset of symptoms with most patients achieving reperfusion in less than 6 hours (mean 4.7 hours) from the onset of pain. Reperfusion was demonstrated short-term by angiography in 42 of 50 patients (84%). Four patients had clinical signs of reperfusion and subsequent angiographic confirmation. An additional four patients with "stuttering" infarct courses were treated late by percutaneous transluminal coronary angioplasty. Echocardiograms were analyzed for global performance by calculation of fractional area change at the papillary muscle level and ejection fraction (biplane Simpson's rule) in 18 patients in whom this analysis could be performed. Measurements of regional function included fractional shortening at the base (n = 37), regional wall motion index (n = 50) and percent of normal functioning myocardium (n = 50). Overall there was a significant improvement in regional wall scores and percent of functioning myocardium (regional wall motion index 1.73 to 1.43, p less than 0.001 and percent of functioning myocardium 0.61 to 0.70, p less than 0.001) but only a trend toward improvement when global function was assessed by ejection fraction (0.42 to 0.48, p less than 0.14).(ABSTRACT TRUNCATED AT 250 WORDS)

Intracardiac echocardiography-guided biopsy of intracardiac masses.

A 69-year-old man diagnosed with lung cancer had a transesophageal echocardiogram performed because of suspicion of intramyocardial tumor. The transesophageal echocardiogram confirmed the presence of both a right and left atrial mass. The lung cancer was believed to be potentially resectable if this mass did not represent tumor; therefore, biopsy of the intracardiac mass was requested. Intracardiac ultrasound was used to guide the biopsy procedure. Using intracardiac ultrasound guidance, a successful biopsy was performed that revealed the presence of tumor cells.

Regional wall motion index for infarct and noninfarct regions after reperfusion in acute myocardial infarction: comparison with global wall motion index.

A regional wall motion index has been derived from two-dimensional echocardiograms by use of a 16-segment model that was subdivided into anterior (nine segments) and infero-postero-lateral (seven segments) regions. This new method is compared with the use of a previously described global wall motion index for the analysis of serial echocardiograms after reperfusion in 23 patients who had acute myocardial infarction. Mean global index improved from 1.84 +/- 0.46 to 1.56 +/- 0.37 at 24 hours (p less than 0.01) and to 1.50 +/- 0.29 after 3 days to 7 days (p less than 0.02), whereas mean regional index for infarct regions improved from 2.28 +/- 0.73 to 1.82 +/- 0.58 at 24 hours (p less than 0.01) and to 1.70 +/- 0.42 after 3 to 7 days (p less than 0.01), with no significant change in the noninfarct index (1.34 +/- 0.32 initially and 1.28 +/- 0.36 after 3 to 7 days). Although both global and regional indexes effectively demonstrate early recovery of left ventricular function, (within 24 hours in many patients), the regional index for infarct regions is higher than the global index and effectively distinguishes between infarct and noninfarct segments. An overlap index in which an additional apical segment is included in the anterior region (10 segments) for anterior infarctions and in the infero-postero-lateral region (eight segments) for inferior infarctions results in a greater differentiation between infarct and noninfarct regions, with the mean initial noninfarct overlap index (1.17 +/- 0.33) significantly less than the nonoverlap index.(ABSTRACT TRUNCATED AT 250 WORDS)