Myocardial Salvage In Patients Research Articles

Reliability of resolution of ST-segment elevation after coronary reperfusion in predicting myocardial salvage in anterior wall acute myocardial infarction

Resolution of ST-segment elevation (ST resolution) after reperfusion therapy has been shown to correlate with improved left ventricular (LV) function in patients with acute myocardial infarction (AMI). However, not all patients with ST resolution have preserved LV function. We evaluated the clinical significance of ST resolution in 129 patients with anterior wall AMI who underwent successful coronary recanalization within 6 hours after symptom onset by studying the relation to myocardial blush grade, another angiographic marker of myocardial reperfusion. A reduction of ≥50% in ST-segment elevation after recanalization was defined as ST resolution. Ninety-eight patients had ST resolution and 31 patients did not. Patients with ST resolution were subdivided into 2 groups according to myocardial blush grade after recanalization: 67 patients with blush grade 2 or 3, and 31 with blush grade 0 or 1. The QRS score after recanalization was higher (5.9 ± 1.9 vs 3.4 ± 2.0, p <0.01) and predischarge LV ejection fraction was lower (39 ± 8% vs 57 ± 9%, p <0.01) in patients with blush grade 0 or 1 than in those with blush grade 2 or 3. However, the QRS score after recanalization and the predischarge LV ejection fraction were similar in patients who had ST resolution with blush grade 0 or 1 and in those without ST resolution. Our findings suggest that ST resolution after recanalization does not consistently predict myocardial salvage in patients with anterior AMI.

Invited commentary

Invited commentary

Significant myocardial salvage in patients with non-ST elevation myocardial infarction is common: results using serial myocardial perfusion imaging

Significant myocardial salvage in patients with non-ST elevation myocardial infarction is common: results using serial myocardial perfusion imaging

Early peak creatine kinase activity is not always a marker of successful reperfusion with myocardial salvage in patients with reperfused anterior acute myocardial infarction

Background Although early peak creatine kinase activity (peak CK) is considered a reliable marker of coronary reperfusion in patients with acute myocardial infarction (AMI), whether early peak CK indicates good myocardial salvage is unclear. Moreover, some patients have late peak CK despite successful reperfusion, and its clinical implication remains to be elucidated. Methods and Results We examined the association of the time to peak CK with predischarge left ventricular function in 124 patients with a first AMI who had successful reperfusion within 6 hours from symptom onset. Patients were classified according to the time from reperfusion to peak CK: group A, 61 patients with peak CK <6 hours; group B, 42 with peak CK from 6 to 12 hours; and group C, 21 with peak CK >12 hours. There were no differences among the 3 groups in age, sex, method of reperfusion, time from symptom onset to reperfusion, collateral circulation, or the extent of risk area estimated by number of leads with ST-segment elevation. Left ventricular ejection fraction measured by predischarge left ventriculography was lowest in group A, followed by group B, and highest in group C (median values, 43%, 52%, and 60%, P <.01). Left ventricular dysfunction (left ventricular ejection fraction ≤40%) occurred in 26 (43%) patients in group A, 8 (19%) in group B, and none in group C (P <.01). Conclusions We conclude that compared with early peak CK, late peak CK consistently reflects good myocardial salvage in patients with anterior AMI who had successful reperfusion within 6 hours from symptom onset. (Am Heart J 2001;141:759-64.)

Szintigraphically assessed myocardial salvage in patients with acute myocardial infarction undergoing stent supported angioplasty

Szintigraphically assessed myocardial salvage in patients with acute myocardial infarction undergoing stent supported angioplasty

Residual Tc-99m sestamibi uptake predicts myocardial salvage in patients undergoing rescue angioplasty after failed thrombolysis in acute myocardial infarction

Residual Tc-99m sestamibi uptake predicts myocardial salvage in patients undergoing rescue angioplasty after failed thrombolysis in acute myocardial infarction

Determinants of successful myocardial salvage in patients recieving primary PTCA for acute myocaldial infarction

Determinants of successful myocardial salvage in patients recieving primary PTCA for acute myocaldial infarction

Prevalence of spontaneous reperfusion and associated myocardial salvage in patients with acute myocardial infarction

This study sought to determine the prevalence of spontaneous reperfusion of an infarct-related artery (IRA) and associated myocardial salvage in the absence of thrombolysis or angioplasty. Twenty-one patients with acute myocardial infarction received only heparin and aspirin. At a median of 18 hours after presentation, 12 patients (57%) had angiographic patency of the IRA. Technetium-99m sestamibi was injected acutely on presentation and again at hospital discharge. Acute and final perfusion defect sizes were measured. Their difference, myocardial salvage, was calculated along with salvage index (myocardial salvage/acute defect). Comparing patients with a patent versus occluded IRA, myocardium at risk was similar (16% ± 12% vs 12% ± 9% left ventricle, p = NS); however, myocardial salvage (9% ± 9% vs –2% ± 7% left ventricle, p = 0.01), and salvage index (0.62 ± 0.37 vs 0.19 ± 0.33, p = 0.01) were greater in patients with spontaneous reperfusion. Resolution of chest pain was greater in patients with a patent IRA (100% vs 55%, p = 0.003). Spontaneous reperfusion of the IRA occurs frequently in patients with acute myocardial infarction and is associated with significant myocardial salvage. (Am Heart J 1998;135:421-7.)

Beneficial Effect of Intracoronary Verapamil on Microvascular and Myocardial Salvage in Patients With Acute Myocardial Infarction

Objectives. We assessed the acute effect of intracoronary injection of verapamil on microvascular function after primary percutaneous translumanal coronary angioplasty (PTCA) for acute myocardial infarction (AMI) with myocardial contrast echocardiography (MCE) in relation to functional outcomes.Background. Recent clinical studies have documented the potential of verapamil for possible increase in coronary blood flow after primary PTCA.Methods. Forty patients with a first AMI were randomly assigned to the verapamil group (n = 20) or the control group (n = 20). In the verapamil group, verapamil (0.5 mg) was injected into the infarct-related artery shortly after PTCA, followed by the oral administration. We performed MCE with an intracoronary injection of sonicated microbubbles before and after verapamil. To assess microvascular integrity, we determined the baseline-subtracted peak intensity in the risk area and the ratio of the no reflow zone plus the low reflow zone to the risk area (low reflow ratio). We determined the average wall motion score (dyskinesia/akinesia = 3; normal = 0) in the risk area on the day of AMI and a mean of 24 days later.Results. The low reflow zone was observed shortly after PTCA in 14 verapamil group patients, and the low reflow ratio decreased after verapamil (0.39 ± 0.23 vs. 0.29 ± 0.17 [mean ± SD], p < 0.05). Peak intensity significantly (p < 0.05) increased from 6 ± 5 to 12 ± 6 after verapamil. The reduction in wall motion score from the acute (day −1) to the late stage (day −24) was significantly greater in the verapamil group than in the control group (0.7 ± 0.8 vs. 0.2 ± 1.3, respectively, p < 0.05).Conclusions. Intracoronary administration of verapamil after primary PTCA can attenuate microvascular dysfunction and thereby augment myocardial blood flow in patients with AMI, leading to better functional outcome than with PTCA alone.

Reduction of myocardial infarct size in rabbits and inhibition of activation of rabbit and human neutrophils by lidocaine

Myocardial reperfusion is associated with increased influx of activated neutrophils and intracellular accumulation of sodium in the ischemic zone. Lidocaine is a sodium channel blocker that also inhibits several neutrophil functions. We investigated the effect of lidocaine on infarct size in rabbits undergoing 30 minutes of ischemia and 48 hours of reperfusion. Animals randomly received lidocaine (10 mg/kg, n = 11) or saline ( n = 11) during occlusion. The area of necrosis (AN) was measured histologically and expressed as a percentage of the area at risk (AR). Myocardial oxygen consumption and the perfusion bed at risk were similar in the two groups. Lidocaine reduced infarct size compared with control (AN/AR = 30% ± 4% vs 61% ± 5%, respectively; p = 0.0001). This reduction was associated with a significant decrease in neutrophil infiltration and in the degree of hemorrhage in the reperfused myocardium. Lidocaine also significantly inhibited superoxide anion production by rabbit and human neutrophils in whole blood. Therefore, lidocaine treatment results in a significant reduction in infarct size in the rabbit model, partly through reduction of neutrophil-mediated injury to viable cells, suggesting that lidocaine may be useful to enhance myocardial salvage in patients undergoing pharmacologic or mechanical reperfusion. (Am Heart J 1997;133:315-22.)

Myocardial salvage: Its assessment and prediction by the analysis of serial myocardial contrast echocardiograms in patients with acute myocardial infarction

It has been difficult to assess myocardial salvage in patients with coronary reflow because of the lack of appropriate methods of determining the risk area and assessing myocardial perfusion in the risk area. To clarify the value of serial myocardial contrast echocardiography in assessing effects of coronary reflow in patients, myocardial contrast echocardiography was performed in 28 patients with acute myocardial infarction before reperfusion, immediately after reperfusion, and in the chronic stage with the right and left coronary arterial injection of sonicated ioxaglate. Contrast-deficit and contrast-filled areas before reperfusion were defined as the risk area and noninfarct area, respectively. If the ratio of peak subtracted gray level in the risk area to that in the noninfarct area was <0.4, the risk area was taken as a contrast defect. Contrast defect was observed even after reperfusion in 8 (29%) patients, and the defect was consistently observed in the chronic stage in all of them. Contrast defect disappeared after reperfusion in the other 20 patients but reappeared in 4 (20%) of them in the chronic stage despite the patent infarct-related vessel. Left ventricular function recovery of the risk area in the chronic stage as assessed with regional wall motion and wall thickness was better in the patients without contrast defect after reperfusion than in patients with persistent or reappeared contrast defect. In conclusion, (1) myocardial salvage is improbable in patients with contrast defect immediately after reperfusion, (2) contrast enhancement immediately after reperfusion does not necessarily imply myocardial salvage in the chronic stage, and (3) myocardial contrast echocardiography in the chronic stage may provide clinically useful information about myocardial salvage in patients with myocardial infarction.

Residual flow to the infarct zone as a determinant of infarct size after direct angioplasty.

In acute myocardial infarction, residual flow to the infarct zone either through antegrade flow in the infarct-related coronary artery or collateral flow from the non-infarct-related arteries is often present before reperfusion therapy. The purpose of this study was to assess the influence of antegrade flow in the infarct-related artery and/or collateral flow to the infarct zone before successful direct angioplasty on infarct size and myocardial salvage in patients with acute evolving myocardial infarction. Sixty patients with acute evolving myocardial infarction underwent direct successful angioplasty without prior thrombolytic therapy. The myocardium at risk of infarction, the final infarct size, and myocardial salvage were measured by tomographic perfusion imaging with 99mTc sestamibi. Antegrade flow in the infarct-related artery before intervention was graded according to the Thrombolysis in Myocardial Infarction (TIMI) study group classification. Collateral flow to the infarct zone before angioplasty was also graded (0 through 3, 0 being no collateral flow). The presence of even minimal antegrade flow before angioplasty (TIMI grade 1) in the infarct-related artery compared with absent flow was associated with a significant reduction in final infarct size (9 +/- 17% versus 23 +/- 19% of left ventricle, P = .02) and a significant increase in myocardial salvage (23 +/- 16% versus 14 +/- 13% of left ventricle, P = .05) after angioplasty. When antegrade flow in the infarct-related artery was absent before angioplasty, the presence of collateral flow before angioplasty resulted in a significantly smaller final infarct size (P = .01) and more myocardial salvage (P = .05) after angioplasty. Both antegrade infarct-related artery flow and collateral flow to the infarct zone had significant independent ability to predict infarct size after angioplasty. When collateral grade and TIMI grade were added to provide an estimate of residual flow, a model including residual flow, myocardium at risk, and the interaction of residual flow and infarct site explained 83% of the variability in infarct size after angioplasty. The presence of antegrade flow in the infarct-related artery and/or collateral flow to the infarct zone before direct angioplasty in acute evolving infarction results in a smaller infarct size after direct successful angioplasty.

Spiral artery morphology in pregnancies complicated by chronic hypertension: The effect of antihypertensive therapy and the relation to superimposed pre-eclampsia

The ability of primary percutaneous coronary intervention (PCI) to salvage myocardium in patients with acute ST-segment elevation myocardial infarction (STEMI) presenting >12 hours after symptom onset is questionable. The aim of this study was to assess the ability of primary PCI to salvage myocardium in patients with STEMI presenting between 12 and 48 hours after the symptom onset.In the BRAVE-2 trial, 365 patients with acute STEMI presenting between 12 and 48 hours from the symptom onset were randomized to an invasive (PCI) or a conservative treatment strategy. Two-hundred sixty-one patients enrolled in 2 centers had scintigraphy before randomization and 5 to 10 days later and constitute the cohort of the present study. Salvage index (proportion of initial perfusion defect salvaged) was the primary end point of this study.There were 131 patients randomly assigned to the invasive treatment and 130 patients assigned to the conservative treatment. Initial perfusion defect (median [25th-75th percentiles]) did not differ between groups (17.0% [9.0-28.5] vs 16.0% [9.0-37.5] of the left ventricle; P = .99). The final infarct size, measured in the follow-up scintigraphy, was significantly smaller in patients assigned to the invasive treatment than in those assigned to the conservative treatment (8.0% [2.0-16.0] vs 12.0% [3.2-25.0] of the left ventricle; P = .004). Salvage index was 0.44 (0.13-0.80) in the invasive group versus 0.23 (0.0-0.50) in the conservative group (P < .001).Primary PCI leads to significant myocardial salvage in patients with STEMI presenting between 12 and 48 hours after symptom onset.

Role of perfluorochemical emulsions in the treatment of myocardial reperfusion injury

Perfluorochemicals are substances with small particle size, low viscosity, and high oxygen-carrying capacity. The role of one perfluorochemical preparation, Fluosol, and emulsion of two perfluorocarbons, a detergent Pluronic F-68 (poloxamer 188), and phospholipids on myocardial reperfusion injury was investigated in a closed-chest canine model of regional ischemia. Intracoronary and intravenous infusions of Fluosol in the perireperfusion period significantly reduced infarct size and improved ventricular function in animals that were examined for up to 2 weeks after reperfusion. Fluosol preserved endothelial structure and endothelium-dependent relaxation of large and small vessels. Fluosol reduced neutrophil plugging of capillaries and attenuated neutrophil infiltration into the reperfused bed. Ex vivo studies of neutrophil function demonstrated apparent suppression of chemotaxis and lysozyme degranulation in cells from animals that were treated with Fluosol. However, treatment of cells in vitro manifested enhanced superoxide anion production within 5 minutes of incubation even with low concentrations of Fluosol. This effect was found to be almost entirely attributable to the detergent, Pluronic F-68. The stimulation of neutrophils by Fluosol was found to result directly from phagocytosis and indirectly from activation of the complement cascade. These findings suggest that perfluorochemicals may provide a novel form of therapy to enhance myocardial salvage after successful reperfusion. The mechanism appears to be due to stimulation and subsequent “deactivation” of neutrophils peripherally, which thereby reduces their cytotoxic potential in the reperfused myocardium. The role of the oxygen-carrying ability of the perfluorocarbons in the reduction of reperfusion injury remains to be determined. In a pilot study in human beings, Fluosol that was used as adjunctive therapy with angioplasty has also been shown to improve regional ventricular function. Clinical trials with perfluorochemical emulsions appear warranted to determine the role of reperfusion injury in limiting myocardial salvage in patients who are undergoing pharmacologic or mechanical reperfusion.

Demonstration of myocardial reperfusion injury in humans: Results of a pilot study utilizing acute coronary angioplasty with perfluorochemical in anterior myocardial infarction

Reperfusion may limit the amount of potentially salvageable myocardium through the introduction of cellular elements into previously ischemic but viable myocardium (reperfusion injury). It has been demonstrated that intracoronary infusion of a 20% intravascular perfluorochemical emulsion (Fluosol) significantly reduces infarct size and results in improved left ventricular function in the canine model. This pilot study was performed to explore the existence of myocardial reperfusion injury in humans.Utilizing Fluosol as a probe in conjunction with emergency coronary angioplasty, 26 patients presenting within 4 h with a first anterior myocardial infarction were randomized to emergency angioplasty or angioplasty followed by a 30-min intracoronary infusion of Fluosol at 40 ml/min. Global and regional ventricular function were assessed immediately and a mean of 12 days after successful angioplasty with contrast ventriculography. Infarct size was semiquantitated with thallium-201 single-photon emission computed tomography (SPECT) images before discharge. Twelve patients (six undergoing angioplasty alone, six treated with angioplasty and Fluosol) had an occluded infarct-related vessel (Thrombolysis in Myocardial Infarction [TIMI] grade 0 to 1) at the time of emergency catheterization and were included in the final analysis.At 12 days after successful angioplasty, the improvement in regional ventricular function was greater in patients receiving adjunctive therapy with intracoronary Fluosol versus those undergoing angioplasty alone utilizing both the radial shortening and centerline method, respectively (23 ± 3.1% vs. 8 ± 2.3%, p < 0.02; and −1.6 ± 0.4 vs. −2.9 ± 0.2 SD/chord, p < 0.05). Tomographic infarct size expressed as a percent of the left ventricle was also reduced in Fluosol-treated patients (3.5 ± 2.2% vs. 18.3 ± 4.7%, p < 0.05). No significant differences in collateral blood flow, extent of coronary artery disease or residual stenosis after angioplasty were observed.This preliminary study suggests that myocardial reperfusion injury may be an important factor in limiting myocardial salvage in patients undergoing reperfusion. These findings have important clinical implications because adjunctive therapy may further amplify the beneficial effects of mechanical or pharmacologic reperfusion. Additional prospective randomized trials must be done to confirm and extend these preliminary results.

Time from onset of symptoms to thrombolytic therapy: A major determinant of myocardial salvage in patients with acute transmural infarction

Time from onset of symptoms to thrombolytic therapy: A major determinant of myocardial salvage in patients with acute transmural infarction

Time from onset of symptoms to thrombolytic therapy: A major determinant of myocardial salvage in patients with acute transmural infarction

To determine whether myocardial salvage after successful intracoronary or intravenous thrombolysis is time dependent, the relation between left ventricular wall motion and the time to treatment was studied in 69 patients admitted less than 3 hours after onset of acute transmural myocardial infarction (42 patients with reperfusion by intracoronary streptokinase, 27 by intravenous urokinase). A similar significant relation between the time to treatment and the severity of regional hypokinesia at follow-up was found in the intracoronary and intravenous groups. To better define this relation, particularly during the early phase of infarction, the groups were combined. In patients in whom thrombolytic treatment was initiated within 2 hours after symptom onset, wall motion at follow-up was within 2 standard deviations of the normal mean in 82% (14 of 17 patients). If treatment was started 2 to 5 hours after symptom onset, the probability of improved wall motion decreased to 46% (24 of 52 patients, p less than 0.025). The time/wall motion relation appeared to be independent of infarct location, angiographically visible collateral vessels and the presence of subtotal coronary artery occlusion. The severity of hypokinesia at follow-up study correlated with the magnitude of peak serum creatine kinase (r = -0.71), indicating that thrombolytic therapy initiated within 2 hours after the onset of symptoms improves regional left ventricular function and reduces infarct size more than later therapy does.

Release of adenosine in reactive hyperemia of the dog heart.

Release of adenosine in reactive hyperemia of the dog heart.