Citations

BACKGROUND 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. METHODS AND RESULTS 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. CONCLUSIONS 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.

BACKGROUND Experimental animal studies have demonstrated that myocardium at risk, residual collateral flow, and duration of coronary artery occlusion are important determinants of final infarct size. The present study examined these variables in patients with acute myocardial infarction in relation to final infarct size. METHODS AND RESULTS Myocardium at risk was assessed with hexakis(2-methoxyisobutyl isonitrile) technetium (I) (99mTc sestamibi) in 89 patients with first-time myocardial infarction (anterior, 48 patients; inferior, 41 patients). All patients had successful reperfusion therapy with either intravenous thrombolysis (32 patients) or primary coronary angioplasty (57 patients) within 24 hours of the onset of chest pain (4.7 +/- 3.9 hours; range, 0.5-21.5 hours) documented by coronary angiography. 99mTc sestamibi was injected intravenously before reperfusion therapy, and tomographic imaging was performed 1-6 hours later. Myocardium at risk was quantitated for each patient and expressed as a percentage of the left ventricle: 35 +/- 19%; range, 2-73%. Collateral flow was estimated by both invasive and noninvasive methods. Fifty-three patients with TIMI grade 0 or I flow who underwent primary coronary angioplasty had collateral flow graded angiographically (0-3) before the first balloon inflation. All patients had collateral flow estimated noninvasively from the acute sestamibi short-axis profile curve by three methods that assess the severity of the perfusion defect. Each of these three methods was significantly associated with angiographic collateral grade. Final infarct size was determined at hospital discharge by a second sestamibi study (17 +/- 17%; range, 0-59%). Myocardium at risk (r = 0.61, p less than 0.0001), angiographic collateral grade (p = 0.0003), and radionuclide estimates of collateral flow (r = 0.69-0.70, all p less than 0.0001) were all significantly associated with final infarct size. The time to reperfusion therapy was not significantly associated with final infarct size by univariate analysis (r = 0.18, p = 0.10). Two multivariate models were constructed to determine which variables were independently associated with final infarct size. In the invasive model, myocardium at risk, angiographic collateral grade with an interaction term for infarct location, and time to reperfusion were all independently significant and accounted for 70% of the variability in final infarct size. The noninvasive model, which substituted a radionuclide estimate of collateral flow for angiographic collateral grade, showed nearly identical results, accounting for 68% of the variability in infarct size in patients where the infarct artery was known to be occluded. When all patients were included (patients with and without acute angiography), the noninvasive model accounted for 59% of the variability in infarct size. CONCLUSIONS Myocardium at risk, collateral flow, and duration of coronary occlusion are each independently associated with final infarct size and account for most of its variability. Ideally, all three parameters should be examined in evaluation of the efficacy of new treatment strategies for acute myocardial infarction.

BACKGROUND Patients who have chest pain without electrocardiographic ST elevation are not candidates for thrombolytic therapy in most clinical trials. This study examined the value of technetium-99m-Sestamibi tomographic imaging to assess myocardial perfusion in patients during chest pain without ST elevation. METHODS AND RESULTS Tc-99m-Sestamibi was injected in 14 patients who had chest pain without ST elevation, who subsequently developed enzymatic evidence of myocardial infarction within 24 hours. Tomographic imaging was performed 1-6 hours after injection. Thirteen of 14 patients showed significant perfusion defects indicative of acute myocardial infarction consistent with absent perfusion (20 +/- 15% of the left ventricle; range, 2-53%); one patient had normal images. Because of the absence of definitive electrocardiographic changes, only five patients received reperfusion therapy within 6 hours of the onset of chest pain. Regional wall motion abnormalities were present in nine of nine patients undergoing contrast ventriculography and correlated with the location of the Tc-99m-Sestamibi perfusion defect. At the time of subsequent coronary angiography, total arterial occlusion was present in 11 of the 14 patients. The infarct-related artery could be identified in 13 of the 14 patients. In six of these 13 patients, the left circumflex was the infarct-related artery. CONCLUSIONS Patients who have chest pain without electrocardiographic ST elevation may have arterial occlusion and significant myocardium at risk. Tc-99m-Sestamibi imaging may be of benefit in identifying these patients early so that they can be considered for acute reperfusion therapy.

A simple classification of atrioventricular block, criteria for diagnosis, and suggested therapy are discussed. The differences between Mobitz I and II second-degree A-V block are reviewed. Good management of patients who have bundle-branch or other forms of intraventricular block depends on informed judgment which includes consideration of (1) the effect of intraventricular conduction disturbances on the pumping action of the heart, and (2) the likelihood that a specific intraventricular conduction disturbance will be complicated by complete heart block. Evidence suggests that common forms of intraventricular disturbance, unlike ventricular fibrillation, do not alter significantly the pumping action of the heart. The role of intraventricular conduction disturbances in the genesis of ventricular fibrillation is assessed. We concluded that only when right bundle-branch block is combined with block of the anterior or posterior fascicle of the left bundle branch is complete heart block sufficiently imminent to warrant special concern. If bilateral block is associated with symptoms of episodic severe bradycardia, pacemaker therapy is indicated.

The spread of the excitatory process in the ventricular septum of the dog's heart has been studied in the isolated organ perfused by the Langendorff technic. It has been possible to remove large portions of the free wall of the right and left ventricles and explore the septal surfaces under direct vision. The mean excitatory pathway in the muscular mass of the dog's ventricular septum has been demonstrated to be from apex to base. The left side of the septum is activated before the right side, and the apical part of the right side is activated before its base.

On isolated perfused canine hearts, studies were made of the electrocardiographic changes which attend injury to the endocardium of the free wall of the left ventricle and of changes which develop following extension of the injury onto the left ventricular aspect of the septal endocardium. In an epicardial lead, the depression of RS-T segment produced by a subendocardial injury of the free wall of the left ventricle disappeared almost completely when that same type of injury was extended onto the septum.

The speed at which the excitatory process spreads through a certain segment of the myocardial syncytium depends upon the orientation of the fibers in that segment to each other and to the point of origin of excitation. Spread down a strip of fibers of which the long axis is parallel to the long axis of the strip is rapid as compared with spread down a strip in which the fibers run at a right angle to the long axis of the strip. Endocardial activation is rapid, not because of the presence of Purkinje fibers, but because the subendocardial bands of myocardium form a network through which excitation can move rapidly along the long axis of the fibers. Spread across the septum in bundle-branch block and across the free wall of the left ventricle in the normally activated heart is slow because excitation is moving through fibers the long axis of which is prependicular to the advancing wave of excitation.

Among 24 cases of small subendocardial infarctions included in this report are 10 cases of anteroseptal distribution in which the electrocardiogram was characterized by the presence of deeply inverted T waves in some or all of the precordial leads. Two other types of change encountered among the remaining 14 cases are described. Electrocardiographic changes in this group of 24 cases are compared with changes encountered in 5 cases of large and near circumferential acute subendocardial infarction described in part I of this study.

The electrocardiographic consequences of subendocardial infarction will find their most evident and characteristic expression in the acute has of a large lesion. Five cases of this kind are presented here and the associated electrocardiographic changes are described. At what level in the myocardium between the endocardium and epicardium do the electrocardiographic expressions of subendocardial infarction give way to those of transmural infarction Data in 6 cases of large nontransmural infarction are presented for comparison with findings in the 5 cases of subendocardial infarction.

This conference has been concerned with a case of primary systemic amyloidosis in which death occurred in the course of severe, congestive heart failure. Major emphasis has been attached to the diagnostic problems which were posed by a patient so afflicted. If comments regarding treatment have been of limited extent, so have been the results of treatment when applied.