Midterm outcomes and risk stratification after endovascular therapy for patients with critical limb ischaemia due to isolated below-the-knee lesions.

OBJECTIVES: To assess and risk stratify midterm clinical outcomes after endovascular therapy (EVT) by angioplasty only of patients with critical limb ischaemia (CLI) due to isolated below-the-knee (BTK) lesions. DESIGN: Retrospective multicenter study. MATERIALS AND METHODS: Between March 2004 and October 2010, 465 limbs (Rutherford 5 and 6: 79%) from 406 patients were studied. Overall survival, limb salvage, and re-intervention were examined out to 3 years by the Kaplan-Meier method and the log-rank test. Their independent predictors and risk stratification were analysed. RESULTS: Patient age was 71 ± 11 yrs, with 69% diabetics and 60% on dialysis. Mean follow-up was 18 ± 15 months. Overall survival was 76 ± 2 and 57 ± 4% at 1 and 3, years, respectively. Survival predictors were body mass index <18, non-ambulatory status and ejection fraction <45%. Two-year limb salvage rate was 80 ± 2%. Factors associated with major amputation were ulcers (Rutherford 6), diabetes mellitus, C-reactive protein>5 mg/dL, and age < 60 years. Two-year freedom from re-intervention was 66 ± 3%; age and below-the-ankle runoff number after angioplasty was negatively associated with re-intervention. CONCLUSIONS: Despite relatively high mortality and re-intervention rates, limb salvage rate was acceptable after EVT for CLI patients with isolated BTK lesions. Risk stratification allows occurrence estimation for each end point.

Neointimal coverage of stents in human coronary arteries observed by angioscopy.

OBJECTIVES: The aim of this study was to reveal the time course of the neointimal coverage of stents placed in the human coronary arteries. BACKGROUND: In deciding the protocol of anticoagulant and antiplatelet therapy for patients who undergo stent implantation, the condition of the neointimal coverage of stents should be taken into consideration. However, the time course of the neointimal coverage of stents has not been elucidated in human coronary arteries. METHODS: Serial angioscopic observations were performed immediately after stenting, at 8 to 45 days (short-term follow-up) and at 65 to 142 days (long-term follow-up) in patients who underwent implantation of the Wiktor coronary stent in the restenotic lesion or in the lesion of acute or threatened closure after balloon angioplasty. RESULTS: Angioscopic observations were successfully performed in 14 cases immediately after stenting, in 11 cases at short-term follow-up and in 13 cases at long-term follow-up. Immediately after stenting and even at 8 to 18 days after stenting, the stent was not covered by the neointimal layer in any case. However, at 65 to 142 days after stenting, the stent was covered by the neointimal layer in all cases. Angioscopically, three types of neointimal layer were recognized: a white layer with a cottonlike surface in three cases, a white layer with a smooth surface in eight cases and a transparent layer with a smooth surface in two cases. CONCLUSIONS: Although some experimental results in animals have shown completion of neointimal coverage of stents in a few weeks, in this serial angioscopic follow-up study, the completion of neointimal coverage of stents in human coronary arteries required approximately 3 months.

Effects of changes in coronary stenosis on left ventricular diastolic filling assessed with pulsed Doppler echocardiography.

To determine the effects of changes in coronary stenosis on left ventricular diastolic filling, diastolic filling was serially examined before and after percutaneous transluminal coronary angioplasty using pulsed Doppler echocardiography in 50 patients with stable exertional angina pectoris. Peak rapid filling velocity and the ratio of peak atrial filling to peak rapid filling velocities were measured from the transmitral flow velocity pattern before and 2 and 9 days after coronary angioplasty. Peak rapid filling velocity increased and the ratio of peak atrial filling to peak rapid filling velocities decreased gradually after coronary angioplasty. The improvement in left ventricular diastolic filling was greater in patients with severe (greater than 90%) coronary stenosis than in patients with mild (less than or equal to 90%) coronary stenosis. In the long-term follow-up period, the improved left ventricular diastolic filling worsened in only 11 patients with marked progression to greater than 90% coronary stenosis. Thus, left ventricular diastolic filling improved gradually after coronary angioplasty, possibly reflecting post-ischemic "stunned" myocardium. Serial examinations of left ventricular diastolic filling with pulsed Doppler echocardiography may be a means of noninvasively assessing the temporal changes in the coronary stenosis and predicting the occurrence of coronary restenosis after coronary angioplasty.

Right coronary artery occlusion: its role in the mechanism of precordial ST segment depression.

To investigate the mechanism of precordial ST segment depression during right coronary artery occlusion, precordial ST segment shifts and myocardial lactate metabolism were evaluated during coronary angioplasty in 10 patients with (group A) and 7 patients without (group B) precordial ST segment depression during balloon occlusion of the right coronary artery, and in 17 patients with precordial ST segment depression during balloon occlusion of the left anterior descending artery (group C). A 12 lead electrocardiogram was continuously recorded in each patient. Blood lactate in the aorta and great cardiac vein was measured during the procedure, and the lactate extraction ratio in the anterior wall was determined both before and during balloon occlusion. Eight of the 10 patients in group A and 1 of the 7 patients in group B had a dominant large right coronary artery. There were no significant differences in summed ST segment elevation in leads II, III and a VF between group A (0.56 +/- 0.26 mV) and group B (0.46 +/- 0.19 mV) during balloon occlusion of the right coronary artery, and no significant differences in summed ST segment depression in leads V1 to V6 during balloon occlusion between group A (0.44 +/- 0.26 mV) and group C (0.38 +/- 0.14 mV). Lactate extraction ratio before balloon occlusion was similar among the three groups. Patients in group A had a higher lactate extraction ratio during (38 +/- 11%) compared with before (30 +/- 11%) (p less than 0.05) balloon occlusion despite precordial ST segment depression.(ABSTRACT TRUNCATED AT 250 WORDS)

Progressive decreases in coronary vein flow during reperfusion in acute myocardial infarction: clinical documentation of the no reflow phenomenon after successful thrombolysis.

OBJECTIVES: This study was undertaken to examine the effects of coronary flow dynamics after thrombolysis on infarct size limitation. BACKGROUND: It has been commonly accepted that early thrombolysis does not necessarily salvage infarcted myocardium. Plausible causes for myocardial necrosis include such factors as elapsed time to reperfusion, residual stenosis, collateral vessels, hemodynamic loads, preconditioning and reperfusion injury. Recently, the no reflow phenomenon has been elucidated to be associated with infarct extension in clinical studies employing contrast echocardiography or thallium scintigraphy. METHODS: Nineteen patients with early reperfusion in acute anterior myocardial infarction and comparable clinical background were studied. The patients were classified into two groups on the basis of pattern of thermodilution measurements of great cardiac vein flow after reperfusion: group A, 9 patients with a progressive decrease in great cardiac vein flow during the 1st 24 h of the onset of infarction; and group B, 10 patients without this observation. Left ventricular ejection fraction and thallium perfusion defect were compared between the two groups at follow-up. RESULTS: There were no significant differences in systemic hemodynamic variables between groups A and B, and neither group had recurrent ischemic events suggesting reocclusion or restenosis during the study. In group A, both great cardiac vein flow (mean +/- SD 44 +/- 17% reduction) and oxygen extraction (38 +/- 15% reduction) were progressively decreased after the onset of reperfusion. Compared with group B, this group showed a lower left ventricular ejection fraction (36 +/- 7% vs. 63 +/- 15%, p < 0.01) and a larger thallium-201 defect severity index (1,091 +/- 366 U vs. 247 +/- 261 U, p < 0.01) at follow-up. Although other patient characteristics were comparable between the two groups, antecedent angina occurred in 90% of group B patients in contrast to only 33% of group A patients. CONCLUSIONS: Salvage of myocardium from infarction by successful thrombolysis was not observed in the patients demonstrating progressive decreases in great cardiac vein flow (group A). In those patients, inadequate myocardial reperfusion on a microvascular basis might be associated with a much larger myocardial infarction. Antecedent angina may protect against a progressive decrease in coronary flow and may have beneficial effects on infarct size limitation.

A case of hypertensive-diabetic cardiomyopathy demonstrating left ventricular wall motion abnormality.

We report a case of hypertensive-diabetic cardiomyopathy demonstrating left ventricular regional wall motion abnormality, with a normal coronary artery documented on coronary arteriography. Dipyridamole-infusion 201Tl scintigraphy demonstrated transient perfusion defects in the infero-posterior wall of the left ventricle, where reduced wall motion was demonstrated on contrast left ventriculography. Myocardial SPECT (single photon emission tomography) imaging with [123I] beta-methyliodophenylpentadecanoic acid (BMIPP) and 201Tl demonstrated reduced [123I]BMIPP uptake compared with 201Tl uptake in the infero-posterior wall of left ventricle. These results suggest that the impairment of myocardial free fatty acid metabolism is an etiologic or contributory factor for regional wall motion abnormality, together with small-vessel coronary artery disease, in this patient.

Mechanism of impaired left ventricular wall motion in the diabetic heart without coronary artery disease.

OBJECTIVE: To elucidate whether impairment of the myocardial free fatty acid (FFA) metabolism and small vessel abnormalities in the myocardium are etiologic or contributory factors of myocardial dysfunction in patients with NIDDM without any significant coronary artery disease. RESEARCH DESIGN AND METHODS: We performed myocardial imaging with 123I-labeled beta-methyl-p-iodophenyl pentadecanoic acid (BMIPP), a branched analog of FFA, and dipyridamole-infusion 201thallium scintigraphy (Dip) in nine patients who demonstrated left ventricular wall motion abnormalities without any significant coronary artery disease and in fifteen control cases. As an index of myocardial FFA metabolism, the heart-to-mediastinum count ratio (H/M) of BMIPP was calculated from the mean count in the regions of interest at the heart and the upper mediastinum. RESULTS: Nine patients with reduced wall motion documented by left ventriculography (LVG), (hypokinetic group) demonstrated significantly lower BMIPP uptake (2.1 +/- 0.2, mean +/- SD) than fifteen patients with normal wall motion (normokinetic group) (2.3 +/- 0.2, P < 0.05). Regional ventricular wall motion observed by LVG, regional BMIPP uptake, and regional redistribution phenomenon (RD) were evaluated for five regions of the left ventricle: anterior, septal, apical, lateral, and inferoposterior regions. Wall motion was abnormal in 24 out of 120 regions. Regional BMIPP uptake was reduced in 47 regions. RD in Dip was observed in 23 regions. In regional analysis, the existence of defect in the BMIPP image showed significant correlation with wall motion abnormality (P < 0.01), but there was no significant relationship between the RD in Dip and regional wall motion abnormality (P = 0.16). Myocardial biopsy specimens obtained from the right ventricle of 20 patients showed no pathologic changes, with the exception of two patients. CONCLUSIONS: Our findings suggest that impairment of myocardial FFA metabolism rather than small vessel abnormalities in the myocardium is responsible for modest left ventricular dysfunction in patients with diabetes.

Functional significance of transient collaterals during coronary artery spasm.

Coronary collateral vessels appear transiently during vasospasm. To examine the functional role of such collaterals in acute myocardial ischemia, regional coronary flow was determined in patients who showed isolated total spasm in the proximal left anterior descending coronary artery associated with (n = 7, group I) and without (n = 9, group II) collaterals, which were donated by the nonspastic right coronary artery during ergonovine provocative test. Aortic pressure and heart rate were not significantly different in the 2 groups before and during spasm. During vasospasm, the levels of pulmonary artery end-diastolic pressure were significantly higher in group II (19 +/- 2 mm Hg, mean +/- standard error) than in group I (15 +/- 1 mm Hg, p less than 0.05). Under these conditions, great cardiac vein flow (GCVF) measured by thermodilution was markedly reduced in group II (from 60 +/- 4 ml/min to 37 +/- 4 ml/min, p less than 0.01), whereas GCVF was slightly reduced in group I (from 56 +/- 4 ml/min to 51 +/- 4 ml/min), indicating that residual GCVF was greater in patients with than in those without collaterals (p less than 0.05). The calculated coronary collateral resistance index during vasospasm was significantly lower in group I (2.06 +/- 0.18 mm Hg min/ml) than in group II (2.91 +/- 0.30 mm Hg min/ml, p less than 0.05). Total left anterior descending coronary artery spasm with collaterals was less frequently associated with ST elevation in the precordial electrocardiogram recorded during spasm.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary collaterals assessed with myocardial contrast echocardiography in healed myocardial infarction.

The epicardial coronary collateral vessels are visualized with coronary angiography, but this method does not provide significant information about the myocardial perfusion supplied with the collaterals. In this study, myocardial contrast echocardiography (MCE) was performed to assess the coronary collaterals in 29 patients with old myocardial infarction. MCE was performed by intracoronary injection of 2 ml agitated amidotrizoate sodium meglumine. The peak background-subtracted gray level (PGL) in the infarct area was determined from the digitized echocardiographic images obtained before and after injection into the noninfarct and donor artery. PGL was compared with the 3-point coronary angiographic grades of collaterals. PGL in the infarct area was significantly lower in patients with poor collaterals than in patients with moderate to good collaterals (5 +/- 4 vs 18 +/- 8 U mean +/- standard deviation, p less than 0.01). PGL in the infarct area was less than 10 U in the 3 patients with severe asynergy despite the moderate to good collateral supply, suggesting that activity of the collaterals was not good enough to preserve the wall motion effectively. It is concluded that (1) the degree of MCE enhancement in the infarct area generally corresponded to the collateral grades assessed with coronary angiography, and (2) MCE may provide a measure of the collateral perfusion.

Left ventricular papillary muscle perfusion assessed with myocardial contrast echocardiography.

This myocardial contrast echocardiographic study shows that left ventricular posteromedial papillary muscle is supplied by either the right or left coronary artery in most subjects, but may be supplied by both coronary arteries. The posteromedial papillary muscle and its adjacent area may be supplied by a different coronary artery.

Elevation of the plasma histamine concentration in the coronary circulation in patients with variant angina.

In the present study plasma histamine was found to be elevated in the great cardiac vein in 8 of 11 patients with variant angina but in none of 8 control patients. Although further investigation is required to determine the exact cause-and-effect relation between histamine release and provocation of spontaneous variant anginal attacks, the present study presents clinical evidence that histamine may well be related to episodes of variant angina as suggested in animal studies.

Metabolic changes in hibernating myocardium after percutaneous transluminal coronary angioplasty and the relation between recovery in left ventricular function and free fatty acid metabolism.

To elucidate the changes in oxidative metabolism in hibernating myocardium after coronary revascularization, we performed myocardial single-photon emission computed tomography with a free fatty acid analog, I-123 beta-methyliodophenylpentadecanoic acid (BMIPP), and thallium-201 before and 1 month after percutaneous transluminal coronary angioplasty (PTCA) in 11 patients with angina pectoris caused by single artery stenosis. All patients had improvement in wall motion after PTCA at the region with coronary stenosis; the wall motion abnormality score evaluated by left ventriculography decreased from 5.5+/-0.8 (mean +/- SE) to 2.1+/-0.9, p <0.01) after PTCA. The defect score of I-123 BMIPP images was significantly larger than that of thallium-201 images either before (14+/-1.3 vs 8.9+/-1.1, p <0.01) or 1 month after (7.4+/-1.5 vs 3.7+/-0.8, p <0.01) PTCA. The decrease in the defect score of both images was significant (p <0.01). Changes in the wall motion abnormality score showed a significant correlation with both the change in the defect score of thallium-201 images (r = 0.58, p < 0.01) and that of I-123 BMIPP images (r = 0.75, p <0.01). These results indicate that the metabolism of free fatty acid is impaired in hibernating myocardium, and that improvement in left ventricular function after successful PTCA is strongly associated with the recovery of oxidative metabolism.

Spontaneous near disappearance of bilateral coronary artery-pulmonary artery fistulas.

Although coronary artery fistula is a relatively rare anomaly, it sometimes develops with advancing age, requiring surgical removal. We report a unique case of a patient whose bilateral coronary artery-pulmonary artery fistulas nearly disappeared in the course of four years. This case is interesting in view of recognizing one of the natural courses of this entity.

Diagnostic performance of myocardial contrast echocardiography for detection of stunned myocardium.

Improvement in regional wall motion after acute myocardial infarction has been described up to 2 to 3 weeks after the acute event despite restoration of blood flow by early successful reperfusion therapy. The prospective identification of potentially reversible ventricular dysfunction caused by stunned myocardium has significant clinical implications. Twenty-seven patients with acute myocardial infarction underwent myocardial contrast echocardiography (MCE) before, immediately after, and 4 weeks after successful reperfusion therapy. MCE was performed by imaging a parasternal short-axis view during intracoronary arterial injection of 2 ml sonicated ioxaglate (Hexabrix-320). The contrast defect area and contrast-filled area before reperfusion were defined as the risk area and noninfarct area, respectively. The normalized gray level was defined as the ratio of the gray level in the risk area/gray level in the noninfarct area. In 21 patients, wall motion was akinetic or dyskinetic immediately after reperfusion, and 10 of 21 patients in whom wall motion recovered during the chronic stage were defined as patients with stunned myocardium. In patients who showed asynergic wall motion immediately after reperfusion, MCE predicted the recovery of left ventricular wall motion (stunned myocardium) during the chronic stage with a sensitivity of 77%, specificity of 100%, and predictive accuracy of 86%, when a normalized gray level of more than 0.4 was presumed to predict stunned myocardium. We conclude that MCE provided the prospective identification of potentially reversible ventricular dysfunction caused by stunned myocardium, and wall motion in the area of nonenhanced myocardium on MCE immediately after reperfusion is not expected to show reversible dysfunction.

Clinical assessment of elastic properties of large coronary arteries: pressure-diameter relationship and dynamic incremental elastic modulus.

Vascular elastic properties in vivo (dynamic incremental elastic modulus [Ep(dyn)]) of large coronary arteries were assessed from the pressure-diameter relationships of the large coronary arteries in 46 patients with suspected ischemic heart disease. Ep(dyn) represents the vascular stiffness primarily determined by the organic sclerotic changes of the vascular wall and the vascular smooth muscle tone. Coronary arterial diameter was obtained from the magnified cine coronary arteriograms by using a computerized caliber measurement technique. The mean Ep(dyn) of the left main coronary artery and the proximal portions of the left anterior descending and circumflex coronary arteries with apparently normal angiograms were significantly (P less than 0.01) increased as the number of involved coronary vessels was increased. Mean Ep(dyn) values in multi-vessel disease were comparable with those of dilated segment by the percutaneous transluminal coronary angioplasty, indicating that the vascular sclerotic changes are not localized to the narrowed segments but diffusely distributed to the angiographically normal vascular wall. In 4 patients who had successful percutaneous transluminal coronary angioplasty, Ep(dyn) of the dilated coronary segment showed markedly higher values (0.21-0.30 X 10(6) Nm-2) than the normal values (0.16 +/- 0.06 X 10(6) Nm-2 in left anterior descending coronary artery). In contrast, there was no significant difference in Ep(dyn) values of the angiographically normal left main coronary trunk, proximal portions of left anterior descending and circumflex arteries between patients with and without vasospastic angina. During myocardial ischemia induced by ergonovine maleate, vasospastic response of the non-diseased segment was comparable with that in patients who did not have an anginal attack during the ergonovine test. Thus, in contrast to the sclerotic change, abnormal vasoconstrictive property of the coronary artery may be localized to the diseased segment.

Adverse effects of epinephrine in patients with advanced left ventricular dysfunction: analysis of ventriculo-arterial coupling.

We examined the response of ventriculo-arterial coupling to epinephrine in 19 patients with normal left ventricular function and with left ventricular dysfunction of various degrees using a conductance catheter. They were divided into three groups: group I, seven patients without left ventricular wall motion abnormality; group II, six patients with ejection fraction of 45-60%; group III, six patients with ejection fraction of 28-40%. Changes in the slope of the end-systolic pressure-volume relationship (end-systolic elastance), the effective arterial elastance, the ratio of effective arterial elastance to end-systolic elastance and the ventricular work efficiency during administration of two different doses of epinephrine (0.05 and 0.1 micrograms/kg/min) were compared among the three groups. At baseline there were no significant differences among the three groups in the ratio of effective arterial elastance to end-systolic elastance, or ventricular work efficiency. At the lower dose of epinephrine, the mean ratio of effective arterial elastance to end-systolic elastance decreased and the mean ventricular work efficiency increased in any groups. At the higher dose of epinephrine the mean ratio of effective arterial elastance to end-systolic elastance further decreased and the mean ventricular work efficiency further increased in groups I and II. However, the mean ratio of effective arterial elastance to end-systolic elastance did not decrease but the mean ventricular work efficiency even decreased in group III. Thus, in patients with advanced left ventricular dysfunction, even a high dose of epinephrine does not modulate the ventriculo-arterial coupling to increase ventricular work efficiency.

Effect of successful angioplasty following thrombolysis on infarct size and left ventricular function.

The role of the angioplasty following thrombolysis in acute myocardial infarction has been discussed in several studies, however the effect of successful angioplasty on infarct size and left ventricular function has not been properly evaluated. Successful reperfusion was achieved in 79 out of 104 patients with primary anterior acute myocardial infarction. These patients were classified as follows, according to the type of intervention during the acute phase: 50 patients in which thrombolysis was successful (the thrombolysis group); 12 patients who underwent successful immediate angioplasty following successful thrombolysis (the immediate angioplasty group); and 17 patients in which rescue angioplasty was successful (the rescue angioplasty group). The 25 patients whose infarct-related vessels were not reperfused after intervention were classified as the non-reperfused group. Infarct size, evaluated as defect volume by T1-201 SPECT, 1 month after the onset, was 840 +/- 154 units (mean +/- S.D.) in the immediate angioplasty group and was similar to that in the thrombolysis group (948 +/- 88 units), but significantly smaller than in the non-reperfused group (1759 +/- 108 units). There were no significant differences in left ventricular function in the immediate angioplasty group and the thrombolysis group. Successful rescue angioplasty did not have any beneficial effect on left ventricular functions or infarct size, when compared with the failed thrombolytic group (1105 +/- 169 units vs. 1617 +/- 169 units). End-diastolic volume (52 +/- 3 ml/m2) in the successful rescue angioplasty group, however, was significantly smaller than in the failed thrombolysis group (67 +/- 3 ml/m2).(ABSTRACT TRUNCATED AT 250 WORDS)

Zero flow pressure in human coronary circulation.

UNLABELLED: Coronary pressure flow (P/F) relationship has been investigated mainly from the viewpoint of coronary resistance. However, recent experimental evidence suggests that the zero flow pressure intercept (Pzf) provides important characteristics of coronary circulation. Although Pzf is likely to provide meaningful information about characteristics of coronary circulation, no data are available about Pzf in humans. The authors attempted to determine Pzf in humans by analyzing P/F relationship during long cardiac pause. This relationship, provoked by intracoronary adenosine triphosphate (ATP) infusion, was analyzed in 9 patients (8 men, 1 woman) with coronary heart disease (ages: fifty-six +/- six years). After the diagnostic cardiac catheterization, ATP, 0.6 mg/3 mL, was administrated by bolus intracoronary injection during measurements of coronary blood flow velocity. Coronary blood flow velocity in the left anterior descending artery was measured with a 0.018-inch Doppler angioplasty guide wire (FloWire, Cariometrics, Inc., Mountain View, Calif.). The dynamic P/F relationship was obtained by correlation of the instantaneous aortic pressure and flow velocity with each other at constant intervals. The least square linear regression analysis was applied to the P/F data to yield the extrapolated Pzf axis. Immediately after intracoronary injection of ATP, long pause (5320 +/- 1498 msec) appeared and coronary blood flow velocity decreased to 11 +/- 8 cm/sec. Pzf calculated with P/F relationship was 14 +/- 7 mmHg. CONCLUSIONS: Thus, the results clearly demonstrate that Pzf is higher than right atrial and left ventricular end-diastolic pressure in humans, indicating the complexity of the determinants of the Pzf.

Subendocardial myocardial ischemia as assessed with myocardial contrast echocardiography in patients with ischemic heart diseases.

Myocardial contrast echocardiography was used to characterize changes in the regional and transmural myocardial blood flow distribution that were provoked by rapid atrial pacing stress in patients with coronary artery diseases. In patients with coronary organic stenosis, a decrease in the myocardial contrast-enhancement in the subendocardial half after rapid atrial pacing was associated with stress-induced chest pain and electrocardiographic ST-T changes. The decrease in the myocardial contrast-enhancement in the subendocardial half after rapid atrial pacing was not observed in patients without coronary stenosis or after coronary angioplasty. Thus, the finding was considered to reflect myocardial ischemia. Pacing-induced decreases in myocardial contrast-enhancement were observed in some patients with old myocardial infarction and significant resting coronary collaterals. In these patients, myocardial ischemia was considered to have developed at rapid pacing because collateral function was good enough to perfuse the infarct myocardium at rest, but was not good enough to prevent myocardial ischemia at stress. Thus, myocardial contrast echocardiography seems to be particularly useful in assessing myocardial ischemia at stress due to coronary stenosis in patients with angina pectoris and due to poor dynamic collateral function in patients with old myocardial infarction.