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Objectives: To evaluate the short-term and long-term prognostic impacts of acute phase coronary collaterals to occluded infarct-related arteries (IRA) after ST-elevation myocardial infarction (STEMI) in the percutaneous coronary intervention (PCI) era., Design: A prospective observational study., Setting: Osaka Acute Coronary Insufficiency Study (OACIS) in Japan., Participants: 3340 patients with STEMI from the OACIS database who were admitted to hospitals within 24 hours from the onset and who had a completely occluded IRA., Interventions: Patients were divided into 4 groups according to the Rentrop collateral score (RCS) by angiography on admission (RCS-0, no visible collaterals; RCS-1, collaterals without IRA filling; RCS-2, collaterals with partial IRA filling; and RCS-3, collaterals with complete IRA filling)., Primary Outcome Measures: In-hospital and 5-year mortality., Results: Patients with RCS-0/3 were older than patients with RCS-1/2, and the prevalence of previous myocardial infarction was highest in patients with RCS-3. Median peak creatinine phosphokinase levels decreased as RCS increases (p<0.001), suggesting the acute cardioprotective effects of collaterals. Although RCS-1 and RCS-2 collaterals were associated with better in-hospital mortality (adjusted OR 0.48, p=0.046 and 0.38, p=0.010 for RCS-1 and RCS-2, respectively) and 5-year mortality (adjusted HR 0.53, p=0.004 and 0.46, p<0.001 for RCS-1 and RCS-2, respectively) as compared with R-0, presence of RCS-3 collaterals was not associated with improved in-hospital (adjusted OR 1.35, p=0.331) and 5-year mortality (adjusted HR 0.98, p=0.920), possibly because worse clinical profiles in patients with RCS-3 may mask mortality benefit of coronary collaterals., Conclusions: Presence of acute phase coronary collaterals such as RCS-1 and RCS-2 were associated with better in-hospital and 5-year mortality after STEMI in the contemporary PCI era., (Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/)

Background: The addition of a mitral isthmus (MI) block line after pulmonary vein isolation could lead to a favorable outcome of catheter ablation in patients with atrial fibrillation (AF). However, it is sometimes tough to create a complete MI block line, and the cooling effect because of the local coronary flow may prevent the creation of a successful MI block line., Methods and Results: This study enrolled 81 AF patients in whom the creation of an MI block line was attempted in those with persistent or pacing-inducible AF after pulmonary vein isolation. A local coronary artery (LCA) across the MI block line was observed in 43 (53%) of 81 patients, and a bidirectional MI block was successfully accomplished in 53 (65%) of 81 patients, at the estimated MI line. The ratio of a successful MI block line was significantly lower in the patients with an LCA than in those without an LCA (42% versus 92%; P<0.001). The mean diameter of the coronary sinus (0.59 ± 0.18 versus 0.82 ± 0.22 cm; P<0.001) and length of the estimated MI line (33.4 ± 9.9 versus 29.4 ± 7.1 mm; P=0.032) were significantly shorter in the patients with a successful MI block line than in those without a successful MI block line. In the multivariable analysis, an LCA at the MI and a larger coronary sinus diameter were independent risk factors for an unsuccessful MI block line., Conclusions: Local coronary flow at the MI is associated with an increased incidence of an unsuccessful MI block line.

Background: The objective of this study was to investigate whether a distal protection (DP) device can preserve the index of microcirculatory resistance (IMR) after primary percutaneous coronary intervention (PCI) in patients with anterior ST-segment elevation myocardial infarction (STEMI)., Methods and Results: The study group of 36 consecutive patients with anterior STEMI were randomized into 2 groups of primary PCI with or without DP: stenting without DP (non-DP group, n = 17) and with DP (DP group, n = 19). The DP in all cases was Filtrap (Nipro, Japan). Following final coronary angiography after successful PCI, IMR was measured using PressureWire™ Certus (St Jude Medical, USA) at maximal hyperemia. The averaged IMR of the 36 patients with STEMI after primary PCI was 31.6U. The IMR in the DP group was significantly lower than that in the non-DP group (26.6 ± 25.8U vs. 37.2 ± 23.2U, P = 0.03242)., Conclusions: DP as an adjunctive therapy of PCI for acute anterior STEMI may have beneficial effects on myocardial microcirculation because of preservation of IMR.

Background: Although the elevation of circulating plasma matrix metalloproteinase (MMP)-9 levels in patients with acute myocardial infarction (AMI) has been documented, the origin of MMP-9 remains unclear., Methods and Results: Plasma MMP-9 levels in both the peripheral circulation and coronary arteries were measured in patients with AMI (n=23) and with stable angina pectoris (SAP, n=10) during percutaneous coronary intervention (PCI) with a distal protection device. Blood samples were collected from the femoral artery (FA) and the coronary artery before (Initial) and after (Second) dilation of the culprit lesion. Coronary sinus blood samples were obtained immediately after PCI (n=7). Coronary artery plaque fragments were aspirated in patients with AMI (n=20) and compared with those from patients with SAP who underwent directional atherectomy (n=10). MMP-9 levels in Initial and Second were significantly higher in patients with AMI than in patients with SAP (p<0.01). In AMI patients MMP-9 levels were significantly higher in Initial than in the FA (p<0.05), and were further increased in Second (p<0.0001), whereas those in the coronary sinus were similar to the FA. Immunohistochemistry revealed augmented MMP-9 expression in the coronary artery plaque fragments from AMI patients., Conclusions: MMP-9 is mainly released into the coronary circulation from the coronary artery plaque in patients with AMI.

Plaque characterization by intravascular ultrasound (IVUS) before percutaneous coronary intervention (PCI) was evaluated in 81 consecutive patients with acute myocardial infarction (AMI) to establish if IVUS can predict the occurrence of the 'no-reflow' phenomenon. Angiographic no-reflow was defined as TIMI flow grade 1 or 2 without any mechanical obstruction in the epicardial artery. Patients were divided into 2 groups according to the post-PCI angiograms: normal flow (group R, n=60) and no-reflow (group NR, n=21). Although the incidence of either soft or noncalcified plaque was not statistically different between the groups, positive vessel remodeling was more frequent in group NR than in group R (57.1% vs 31.6%, p<0.05). Lipid core was also more frequently found in group NR than in group R (61.9% vs 25.0%, p<0.01). Positively remodeled vessels with lipid-rich plaques as characterized by IVUS before PCI predicted the occurrence of angiographic no reflow with a sensitivity of 43% and a specificity of 60%.

Background: No-reflow associated with direct angioplasty (PCI) of patients with acute coronary syndromes (ACS) is associated with unfavorable results., Methods and Results: We used a new thrombectomy device to treat 51 lesions in 48 consecutive ACS patients (40 male and 8 female; mean age 63 years) and conducted a microscopic analysis of aspirates and blood samples retrieved from the culprit coronary artery. The first aspirate was collected before PCI and the second was collected separately after percutaneous transluminal coronary angioplasty or stenting, including samples from the no-reflow lumen. Light microscopy showed that the materials obtained from the pre-PCI aspiration consisted of thrombus in 37.5%, thrombus and atheroma in 35.0%, and atheromatous plaque in 27.5%. The materials collected from the post-PCI aspiration were thrombus in 8.3%, thrombus and atheroma in 41.7%, and atheromatous plaque in 50.0%. We then compared the 9 lesions (19.1%) with no-reflow to those without no-reflow. There was no difference in the pre-PCI aspirates. However, after PCI, there was more atheromatous plaque retrieved from patients with no-reflow (P<0.001) as well as significantly more platelet and fibrin complex, macrophages, and cholesterol crystals in the blood aspirated from no-reflow cases. Aspiration of these elements improved the no-reflow in 7 of 9 lesions to TIMI-3 flow., Conclusions: No-reflow after angioplasty may be caused by gruel that formed from an atheroma attributable to mechanical plaque disruption during intervention.

The present study seeks to estimate the difference between coronary zero flow pressure (Pzf) by analysis of the baseline pressure-flow relationship and the Pzf calculated during a long diastole in humans. Although Pzf is likely to provide meaningful information about the characteristics of coronary circulation, there are no available data on Pzf in humans because Pzf is overestimated when it is calculated during normal cardiac cycles. Actual Pzf was determined in 15 subjects by analyzing the coronary pressure-flow relationship during a long cardiac cycle induced by an intracoronary adenosine triphosphate (ATP) infusion, and it was compared with the Pzf calculated during a normal cardiac cycle in order to estimate the difference. Pzf calculated during a normal cardiac cycle was 47 +/- 15 mmHg, which decreased to 36 +/- 9mmHg after intracoronary administration of ATP (0.05 mg) whereas actual Pzf was 21 +/- 7 mmHg. Pzf calculated in a pressure-flow relationship during a normal cardiac cycle under vasodilation correlated well with that during a long diastole (r = 0.75, p < 0.01), although it was 15 +/- 6 mmHg greater than the actual Pzf. It was concluded that Pzf during a normal cardiac cycle could be used to anticipate Pzf.

Adenosine triphosphate (ATP) is reported to be released mainly from presynaptic vesicles and cardiomyocytes. The released ATP, which can be degraded to adenosine, may cause coronary vasodilation. However, there is no clear evidence that ATP is degraded to adenosine and causes coronary vasodilation in humans. The present study was undertaken to test whether intracoronary administration of ATP increases myocardial adenosine levels and coronary blood flow. In 11 patients, 3 doses of ATP (0.1, 0.2, and 0.4 mg) were injected into the left anterior descending coronary artery. The velocity of coronary blood flow was measured by Doppler flow probe, and the adenosine concentration in the coronary sinus blood was measured. We also continuously infused ATP (0.2 mg/min) for 1 min in another 10 patients. Coronary blood flow increased dose dependently soon after injection of ATP. Coronary arteriovenous differences in adenosine concentration increased [from 21 +/- 15 to 178 +/- 15 pmol/ml (p < 0.05) 10 sec after the injection of ATP (0.4 mg)] and there were marked reductions in both aortic blood pressure and heart rate. The adenosine levels returned to baseline 20 sec after the injection of ATP, and aortic blood pressure and heart rate also recovered, although coronary blood flow remained increased. Furthermore, continuous infusion of ATP for 1 min increased coronary blood flow velocity and coronary arteriovenous differences in adenosine concentration from 25 +/- 14 to 71 +/- 13 pmol/ml (p < 0.05) in 10 patients. These results indicate that intracoronary administration of ATP immediately increases coronary blood flow and the adenosine concentration of coronary venous blood, which returns to the baseline level thereafter. The differences in the time courses of increases in coronary venous adenosine levels and coronary blood flow after ATP injections suggest that vasodilatory mechanisms other than adenosine, eg, nitric oxide and prostaglandins, may also be involved in the ATP-induced coronary vasodilation. ATP may be used as a cardioprotective agent as well as adenosine.

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.

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.

Background: Although the presence of a functional border zone (FBZ), defined as the nonischemic but asynergic myocardium adjacent to the ischemic area, has been demonstrated in animal hearts, it is not known whether this zone exists in humans., Methods and Results: Myocardial contrast echocardiography (MCE) was performed before and during balloon inflation in the area of coronary stenosis by injecting contrast medium through the guiding catheter in 13 patients with effort angina who underwent successful coronary angioplasty. The area showing MCE defect during balloon inflation was determined with reference to the preangioplasty MCE and was regarded as an ischemic area. The size of the FBZ was assessed by measuring the length of the endocardium that showed asynergy in the echo-enhanced (nonischemic) area. The FBZ measured was 13 +/- 4 mm in the short-axis view (n = 5) and 16 +/- 9 mm in the long-axis view (n = 8)., Conclusions: Nonischemic contractile dysfunction exists even in human hearts. The presence of an FBZ may limit the use of wall motion analysis in assessing the risk or ischemic area in patients with myocardial infarction. MCE appears to be a unique technique for assessing the risk or ischemic area.

Impaired coronary flow reserve immediately after coronary angioplasty may be attributed to an increase in resting coronary blood flow. To test this hypothesis we measured great cardiac venous flow (GCVF) at rest and during rapid atrial pacing before and immediately after angioplasty in 22 patients with significant narrowing of the left anterior descending artery and 12 patients (control group) with minimal narrowing. A follow-up (6 months) study was also done in seven patients. Immediately after angioplasty the coronary flow reserve (peak GCVF during pacing/resting GCVF) was not fully restored (1.5 +/- 0.36 before angioplasty, 1.76 +/- 0.42 after angioplasty, and 2.13 +/- 0.33 in the control group). Resting coronary vascular resistance (2.4 +/- 0.9 mm Hg/ml/min) was significantly decreased after angioplasty (2.0 +/- 0.8 mm Hg/ml/min), whereas coronary vascular resistance during rapid pacing was fully restored to normal. Resting hyperemia was restored 6 months later, whereas coronary vascular resistance during pacing was unaltered. In five patients, however, slight ischemic ST-T changes were observed during rapid pacing, even after successful angioplasty associated with a decrease in the lactate extraction ratio. These results indicate that the impaired coronary flow reserve immediately after angioplasty may be attributed mainly to the temporal but significant increase in resting coronary flow, although impaired coronary vascular response to augmented myocardial oxygen demand may also be partially involved.

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.

In this study ECG changes were analyzed to assess the acute effects of antegrade blood flow on the ECG in patients with AMI. The study population consisted of 22 patients with MI in whom the totally occluded left anterior descending artery (LAD) or right coronary artery (RCA) was recanalized by intracoronary urokinase infusion (recanalized group) and 14 patients in whom the occluded coronary artery was not successfully recanalized (control group). No significant difference was found in the sum of ST segment elevation (V2-V4 leads for the LAD-occluded group, II, III and aVF leads for the RCA-occluded group) before urokinase infusion. In the recanalized group sigma ST abruptly increased in 5 min after recanalization in 13 of 16 LAD-occluded patients from 1.49 +/- 0.89 mV to 2.44 +/- 1.67 mV (p less than 0.005), and in 4 of 6 RCA-occluded patients from 0.66 +/- 0.12 mV to 1.42 +/- 0.52 mV (p less than 0.01). However increased sigma ST in the recanalized group was reduced to the control value existing before recanalization within 30 min after recanalization and continued to decline more rapidly than in the control group. These transient ST segment elevations were not correlated with long-term angiographic determinants of left ventricular function. We conclude that ST segment shows abrupt augmentation after successful thrombolysis and that continuous ST segment monitoring is useful for assessing thrombolysis in AMI.

Regional myocardial perfusions obtained by myocardial contrast echocardiography were compared with wall motion abnormalities evaluated by two-dimensional echocardiography in 26 patients with old myocardial infarction (12 with a QS pattern and 14 with a non-QS pattern on electrocardiograms). Myocardial contrast echocardiography was performed by the intracoronary injection of 2 ml of hand-agitated Urografin-76, and short-axis views of the left ventricle were recorded on VTR. Regional myocardial perfusion was categorized using a three-point scale based on the gray levels, and was compared with wall motion abnormalities of the corresponding region as assessed by two-dimensional echocardiography.

The dose-response relation of contrast medium-induced hyperemic response in coronary blood flow (contrast hyperemia) was investigated to determine the optimal dose of contrast medium (CM, Urografin-76) for the assessment of coronary flow reserve in man. The great cardiac venous flow (GCVF) was determined with the continuous thermodilution method during the contrast hyperemia induced by the intracoronary injection of CM of three different doses, ie, 2, 4, and 6 ml/60 kg of body weight, into left coronary artery. Submaximal coronary vasodilation could be obtained by intracoronary injection of 4 ml of CM with minimal changes in systemic hemodynamics. The contrast hyperemia with this dose of CM was reproducible and also closely correlated with that obtained during pacing-induced angina. Thus, we conclude that the contrast hyperemic technique with intracoronary injection of 4 ml of Urografin-76 could be a reliable method to assess the coronary flow reserve.

The pathophysiological significance of coronary collateral vessels remains controversial, despite previous intensive studies. We performed the multistage supine ergometer stress test for 26 patients with effort angina and collaterals. The changes in the collaterals were observed during each anginal attack by coronary angiography before and after intravenous nitroglycerin. The collaterals of 21 patients disappeared or diminished during exercise-induced angina before nitroglycerin administration, and were unchanged in the remaining five cases. However, the collaterals of all patients after nitroglycerin administration were unchanged or increased during exercise-induced angina. Considering there were no significant changes in pulmonary arterial end-diastolic pressures during angina before and after nitroglycerin administration, a pressure gradient between the donor and recipient coronary arteries was suggested as being related to the patency of the collaterals. These results suggested the following: 1. It is not appropriate to postulate that the collaterals visualized at rest may remain unchanged during exercise-induced angina. 2. It is not reasonable to conclude that exercise accelerates the development of collateral circulation. 3. One favorable effect of nitroglycerin administration is the prevention of exercise-induced ischemia via collateral circulation.

The acute effects of intravenous trapidil on hemodynamics, coronary circulation and myocardial metabolism were evaluated in 19 patients (Group I: 10 patients of chest pain syndrome; Group II: 9 patients of coronary heart disease). The heart rate increased (p less than 0.05) and aortic pressure decreased (p less than 0.01) during a 6-min study period. Pulmonary arterial end-diastolic pressure decreased slightly in both groups and cardiac output increased prominently in Group II. Myocardial oxygen consumption did not change significantly 3 and 6 min after trapidil injection. Coronary sinus flow increased slightly (statistically not significant) despite a decrease in aortic pressure, and thus, coronary vascular resistance decreased significantly in both groups. Coronary A-V O2 difference decreased 3 min after trapidil injection and no significant change in the lactate extraction ratio was observed. The diameter of the left main coronary artery increased by about 6% after an administration of trapidil. These results suggest that trapidil has the beneficial effect of coronary vasodilation and it increases cardiac output, despite a decrease in the preload, without a significant increase in myocardial oxygen consumption. The latter may be due to an afterload reduction effect of this drug.

To examine the angiographic features of vasospastic angina associated with ST segment depression, we attempted to analyze the coronary arteriograms of 12 patients who exhibited ST segment depression during the ergonovine provocative test. Right and left coronary arteriograms were obtained successively within a short period when the ergonovine administration revealed ST segment depression. Eight out of 12 patients showed non-total spastic obstructions in one of the major coronary arteries. Among them, a collateral augmentation was found only in one patient. Two cases exhibited the well-developed collateral channels during non-anginal periods and in one case a collateral blood supply was reduced by the spasm occurred in the donating artery. In another one, the collateral circulation did not change during anginal period. Three out of 4 patients who showed total spastic obstructions demonstrated transiently augmented collateral circulation which was supplied by the non-spastic artery. These findings may indicate that ST segment depression during coronary artery spasm could attribute to a subendocardial ischemia caused by an incomplete occlusion of large coronary artery and transient reduction or augmentation of collateral blood flow.

Eleven patients with coronary heart disease, in whom at least one of several bypass grafts to the left coronary artery was patent, were selected for the study. The hemodynamics, coronary sinus blood flow, myocardial oxygen consumption, and myocardial lactate metabolism were evaluated at rest and during atrial pacing stress test before and after surgery. There were no significant improvements in the cardiac index, pulmonary arterial end-diastolic pressure, and left ventricular ejection fraction after aortocoronary bypass surgery. However, significant improvement of coronary sinus blood flow, myocardial oxygen consumption, and myocardial lactate extraction and consumption were found during postoperative atrial pacing compared with the preoperative findings. These results suggest that successful bypass grafting may improve myocardial lactate metabolism in ischemic lesions and contribute to the postoperative relief of angina.

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)

The morphology of collateral vessels can be imaged by coronary angiography, but no method has been available for evaluating their function. This is a report of the use of regional myocardial perfusion to visualize collateral flow by means of myocardial contrast echocardiography in 28 patients with old myocardial infarction. Myocardial contrast echocardiography was accomplished by the intracoronary injection of two ml agitated amidotrizoate sodium meglumine. Short-axis images of the left ventricle were recorded on video tape. Those images were digitized off-line into a 512 x 512 pixel matrix. Using coronary angiography, the morphology and function of the collateral vessels were evaluated, then classified as poor, moderate or good. Myocardial perfusion was evaluated using the enhanced gray level after contrast injection, and the level was compared with the morphology and degree of collateral development. The enhanced gray level was evaluated arbitrarily as 3 +/- 2 U (mean +/- S.D.) in the "poor" group; 13 +/- 6 U in the "moderate" group; and 20 +/- 11 U in the "good" group (p less than 0.01 vs the "poor" group; NS vs the "moderate" group). Regional myocardial perfusion via the collateral vessels was generally proportional to the morphology. However, there were a few discrepancies between these two parameters.

Coronary vasospasms are usually indicated by ST elevation or depression in the electrocardiogram (ECG). To test the hypothesis that ST elevation represents more severe myocardial ischemia than does ST depression, we determined the coronary sinus blood flow (CSBF) and the transcardiac lactate extraction ratio (LER) in 19 selected patients who had focal vasospasms in the left anterior descending artery. In 10 patients, ergonovine (0.11 +/- 0.02 mg, mean +/- SEM) provoked severe (total or subtotal) coronary vasospasm with ST elevation. Under these conditions, CSBF significantly decreased (from 97 +/- 8 ml/min to 79 +/- 5 ml/min, p less than 0.01) with a marked reduction in LER (from 29 +/- 5% to -14 +/- 6%, p less than 0.01). In contrast, 10 vasospastic events with ST depression after ergonovine (0.15 +/- 0.04 mg, NS) were recognized as mild spastic narrowing or severe spasms with well developed collateral circulation. Alteration of CSBF was significant in only a few patients and the overall CSBF response was non-significant (from 106 +/- 12 ml/min to 103 +/- 13 ml/min). The reduction in LER in this group was less pronounced than those in patients with ST elevation (p less than 0.05). These results indicate that coronary vasospasm with ST elevation may be related to the more pronounced reduction in coronary blood flow accompanied by more severe myocardial ischemia. Such observations may support the contention that some ischemic events associated with ST elevation or depression can be interpreted as a continuous spectrum of vasospastic disorders.

Myocardial contrast echocardiography is a new cardiovascular imaging technique that can be used to evaluate regional myocardial perfusion. Regional myocardial perfusion was studied in 12 patients with normal coronary arteries, 14 patients with old myocardial infarction, four patients with acute myocardial infarction, and 15 patients with effort angina. Conventional two-dimensional echo imaging was obtained during intracoronary injections of relatively small volumes (2 ml) of agitated Urografin-76. The echo intensities were measured before and after injecting contrast agents and the subtraction images were composed by a high-speed image processor (NEXUS 6400). Clear myocardial images were obtained in 10 of 12 the patients with normal coronary arteries, and they reflected well the epicardial arterial architecture by coronary angiography. In cases of old myocardial infarction, the infarcted areas appeared as contrast defects in seven and as slightly enhanced areas in three of the 10 patients. In cases of acute myocardial infarction, contrast defect areas in the myocardial images were less in two cases of successful early coronary thrombolysis or percutaneous transluminal coronary angioplasty (PTCA). However, contrast defects remained unchanged despite good recanalization in one case of delayed PTCA. In cases of effort angina, anginal attacks were successfully induced by rapid atrial pacing in six of the 15 patients. In four of the six patients, contrast enhancement in myocardial imaging during anginal attack decreased more in the endocardial than in the epicardial myocardium, possibly reflecting subendocardial ischemia. It is concluded that this technique can identify regional myocardial perfusion, which is not revealed by coronary angiography, and it is therefore useful for the clinical analysis of ischemic heart disease.

Previous studies indicate the degree of myocardial echo contrast enhancement may be related to regional myocardial perfusion. In this study, myocardial contrast echocardiography was used to characterize changes in the transmural myocardial blood flow distribution that were provoked by rapid atrial pacing in 11 patients with one-vessel coronary artery disease. Ten patients without coronary artery disease served as controls. Myocardial contrast echocardiography was performed by intracoronary injection of 2 ml hand-agitated amidotrizoate sodium meglumine (Urografin-76) and by imaging a short-axis view of the left ventricle with two-dimensional echocardiography before and during injection of the contrast agent. The two-dimensional echocardiographic images at end diastole, before and after injection of the contrast agent, were digitized off-line into a 512 x 512 pixel matrix with 256 gray levels/pixel to quantify the degree of the enhancement of the peak gray level after injection. Transmural myocardial blood flow distribution was evaluated by measuring the ratio of the enhanced gray level in the endocardial half (endo) to that in the epicardial half (epi) (endo:epi gray level ratio) in the anteroseptal, posterolateral, and inferior segments before and just after rapid atrial pacing in each patient. In patients without coronary artery disease, there were no differences in the endo:epi gray level ratio between any of the three segments both before and after pacing. Mean values of the three segments were 0.95 +/- 0.08 before pacing and 0.90 +/- 0.13 after pacing, respectively. In contrast, in patients with coronary artery disease, the endo:epi gray level ratio for the segment supplied with stenotic coronary artery decreased after pacing (0.40 +/- 0.21 vs. 0.93 +/- 0.18, p less than 0.01), probably reflecting subendocardial myocardial ischemia, whereas that for the segment supplied with nonstenotic coronary artery remained unchanged (0.88 +/- 0.20 vs. 0.99 +/- 0.23, NS). Thus, changes in transmural myocardial blood flow distribution with rapid pacing, which may be due to transient subendocardial ischemia, are visualized with myocardial contrast echocardiography.