Reciprocal ST-segment Changes Research Articles

Relation of collateral circulation with reciprocal changes in patients with acute ST-elevation myocardial infarction

ObjectiveAcute STEMI is often accompanied by reciprocal ST-segment depression (RC) occurring in opposite leads, whose significance has been debated for decades. The possible role of collateral circulation in promoting RC in acute STEMI has not been identified. So our aim to find the relationship between collateral circulation and RC in STEMI patients treated with primary percutaneous intervention (PPCI). MethodsThe study included 112 pts. with acute STEMI underwent PPCI. The patients divided in to 2 groups: Group (A):66 pts. with RC, Group (B):46 pts without RC. All patients subjected to history taking, ECG [localization of infarction & RC], CKMB level, transthoracic echo [LVEF%], coronary angiography &PPCI to culprit artery and assess number of diseased vessels, site of occlusion, collaterals, TIMI flow pre and post PCI. ResultsPatients in group A with RC had shorter time to door, P < 0.001; more frequent inferior infarctions, P < 0.001; had higher CKMB level, P < 0.001; higher LVEDD, P < 0.001; LVESD, P < 0.001and lower LVEF, P = 0.004; had multi vessel diseases P = 0.02, increase incidence of RCA as a culprit artery <0.001 compared to patients with no RC. Patients with RC had significantly higher incidence of proximal LAD occlusion, distal RCA and distal LCX compared to patients without RC. The percentage of change was 61.2 ± 12.35% for ST elevation and 50.5 ± 10.87% for reciprocal ST depression post PCI with significance difference between them, t = 3.035P = 0.0023.There was no significant correlation between collateral circulation and RC. We found four significant independent predictors of RC. They were inferior infarction (P = 0.024), RCA as a culprit vessel, (P = 0.034), low EF, (P = 0.007) and multi-vessel disease, (P = 0.022). ConclusionThere is no correlation between concomitant RC and presence of collateral vessels in acute STEMI patients. So the pathogenesis of reciprocal ST-segment changes result from an interplay of ischemia at distance due to multi-vessel CAD and benign mirror electrical changes not caused by collateral circulation diverting blood to ischemic area from non-diseased artery.

Reciprocal ST segment changes reproduced in burn-induced subepicardial injury model in bullfrog heart.

In our previous studies, by simply inducing burn injuries on bullfrog hearts or partially exposing their surface to high-potassium (K+) solution, we could reproduce a ST segment elevation in the electrocardiogram (ECG), which is a characteristic finding in human ischemic heart disease. In the present study, using our burn-induced subepicardial injury model, we could additionally reproduce “reciprocal” ST segment changes for the first time in frog hearts, mimicking those observed in human acute myocardial infarction. Immunohistochemistry demonstrated markedly decreased Na+/K+-ATPase protein expression in the ventricular surface after the burn injury. The loss of this pump expression in injured cardiomyocytes was thought to be responsible for the creation of “currents of injury” and the subsequent ST segment changes observed in acute myocardial infarction.

The Pattern of reciprocal electrocardiography changes in St-segment elevation myocardial infarction patients presenting with single-vessel disease versus multi-vessel disease

Introduction: The reciprocal ST-segment depression in the electrocardiography (ECG) leads overlying noninfarcting areas was studied previously in acute myocardial ischemia. Multi-vessel disease (MVD) subset of patients have more vague and confusing presentations on ECG; they usually show less ST-segment elevation and profound and diffuse ST-segment depression compared to ST-segment elevation myocardial infarction (STEMI) patients with single-vessel disease (SVD) involving occlusion of one coronary artery only, namely the infarct-related artery (IRA). Aim of the Work: The aim was to study and compare the pattern of reciprocal ECG changes in STEMI patients presenting with SVD versus MVD. Methods and Results: A total of 125 consecutive patients admitted from April 2014 to August 2015 from the emergency room with the diagnosis of acute STEMI and treated by primary percutaneous coronary intervention (PPCI) at our cath lab at Ainshams University Hospitals (a 24/7 tertiary referral center for PPCI) were included. ST-segment deviations were measured at the J-point. Reciprocal ST-segment changes were identified as per guidelines published by the European Society of Cardiology and the American College of Cardiology, i.e., ST-segment depression ≥0.1 mV in any ECG lead other than aVR, while the cutoff value is different for leads V2 and V3 being only 0.05 mV. Coronary angiographies were evaluated by two independent operators blinded to the clinical and electrocardiographic data. Regarding the left anterior descending (LAD) occlusion, the reciprocal ST-segment depression magnitudes in lead III and in lead arteriovenous fistula (aVF) were significantly less in the MVD group compared to the SVD group, i.e., lead III (−0.08 ± 0.10 mV vs. −0.19 ± 0.15, P = 0.015) and lead aVF (−0.07 ± 0.06 mV vs. −0.15 ± 0.11, P = 0.02); while regarding the left circumflex coronary artery (LCX) occlusion, the reciprocal ST-segment depression extended significantly in V4 chest lead in the MVD group compared to the SVD group (−0.16 ± 0.08 mV vs. −0.1 ± 0.04, P = 0.025); and finally regarding the right coronary artery (RCA) occlusion, the reciprocal ST-segment depression extended significantly in V3 chest lead in the MVD group compared to the SVD group (−0.18 ± 0.07 mV vs. −0.1 ± 0.06, P = 0.02). Conclusion: The pattern of reciprocal ST-segment depression was more profound when the LAD was the culprit artery causing the anterior STEMI compared to the same case if the LAD was a part of MVD; this does not apply to the LCX and RCA when they were the culprit in cases of inferior STEMI where the MVD group showed more reciprocal ST-segment depression.

Clinical Significance of Reciprocal ST-segment Changes in Patients With STEMI: A Cardiac Magnetic Resonance Imaging Study

Introduction and objectivesWe sought to determine the association of reciprocal change in the ST-segment with myocardial injury assessed by cardiac magnetic resonance (CMR) in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI). MethodsWe performed CMR imaging in 244 patients who underwent primary PCI for their first STEMI; CMR was performed a median 3 days after primary PCI. The first electrocardiogram was analyzed, and patients were stratified according to the presence of reciprocal change. The primary outcome was infarct size measured by CMR. Secondary outcomes were area at risk and myocardial salvage index. ResultsPatients with reciprocal change (n=133, 54.5%) had a lower incidence of anterior infarction (27.8% vs 71.2%, P < .001) and shorter symptom onset to balloon time (221.5±169.8 vs 289.7±337.3min, P=.042). Using a multiple linear regression model, we found that patients with reciprocal change had a larger area at risk (P=.002) and a greater myocardial salvage index (P=.04) than patients without reciprocal change. Consequently, myocardial infarct size was not significantly different between the 2 groups (P=.14). The rate of major adverse cardiovascular events, including all-cause death, myocardial infarction, and repeat coronary revascularization, was similar between the 2 groups after 2 years of follow-up (P=.92). ConclusionsReciprocal ST-segment change was associated with larger extent of ischemic myocardium at risk and more myocardial salvage but not with final infarct size or adverse clinical outcomes in STEMI patients undergoing primary PCI.

264Clinical significance of reciprocal ST segment changes in patients with ST-segment elevation myocardial infarction: A cardiac magnetic resonance imaging study

264Clinical significance of reciprocal ST segment changes in patients with ST-segment elevation myocardial infarction: A cardiac magnetic resonance imaging study

Interactions Between Reciprocal ST-Segment Downsloping During ST-Elevated Myocardial Infarction and Global Cardiac Perfusion and Functional Abnormalities

Reciprocal ST-segment downsloping on electrocardiogram is a frequent finding during ST-elevated myocardial infarction (STEMI), but its etiology is still disputed. We sought to evaluate the relation between reciprocal ST-segment downsloping during STEMI and major cardiac perfusion and functional parameters. One hundred eighty-five patients with STEMI underwent emergency coronary angiography. The presence of reciprocal ST-segment downsloping was assessed. At coronary angiography, the corrected TIMI frame count (cTFC) was computed both on culprit and remote vessels and the occurrence of "no/slow reflow" phenomenon after percutaneous coronary intervention (PCI) identified. The left ventricular wall motion score index ratio (discharge/admission values) at echocardiography and the slope of high-sensitivity troponin elimination were computed as measures of effective myocardial reperfusion. Reciprocal ST-segment downsloping was revealed in 91 patients (49%). They presented higher cTFC values on remote vessels than patients without reciprocal electrocardiographic abnormalities (44 ± 18 vs 37 ± 15 cineframes× second-1, p= 0.004). The presence of remote ST-segment downsloping was also associated with a higher prevalence of "no/slow reflow" phenomenon (59% vs 40%, p=0.013) as well as more abnormal values of wall motion score index ratio (p= 0.042) and high-sensitivity troponin slope (p=0.012). At multivariate analyses, a higher cTFC on remote vessels predicted the occurrence of reciprocal ST-segment changes (p= 0.018) and the development of "no/slow reflow" phenomenon after PCI (p= 0.005). In conclusion, the presence of reciprocal ST-segment downsloping during STEMI clusters with significant perfusion and cardiac functional abnormalities, predicting the development of "no reflow" phenomenon after PCI.

ST-segment deviation behavior during acute myocardial ischemia in opposite ventricular regions: observations in the intact and perfused heart.

Acute myocardial ischemia in opposite regions may attenuate ST-segment changes, but whether this effect is expressed differently in extracardiac compared to direct intramyocardial recordings is not well known. The purpose of this study was to characterize ST-segment changes induced by opposite ischemic regions in intact and isolated perfused pig hearts. Left anterior descending (LAD) and right coronary arteries (RCA) were occluded in 7 closed chest pigs and in 5 isolated pig hearts. ST-segment changes were analyzed in 12-lead ECG and in local extracellular electrograms. Isolated LAD or RCA occlusion induced maximal ST-segment elevation in leads V4 (0.84 ± 0.30 mV, P = .003) and III (0.16 ± 0.11 mV, P = .04), respectively. RCA occlusion also induced reciprocal ST-segment depression maximal in lead V4 (-0.40 ± 0.16 mV, P = .005). Simultaneous LAD and RCA occlusion reduced ST-segment elevation by about 60% and blunted reciprocal ST-segment changes. Reperfusion of 1 of the 2 occluded arteries induced immediate regional reversion of ST-segment elevation with concurrent beat-to-beat re-elevation in the opposite ischemic region and reappearance of reciprocal ST-segment changes. In the isolated heart, single LAD or RCA ligature induced regional transmural ST-segment elevation that was maximal in endocardial electrograms with no appreciable reciprocal ST-segment depression. Simultaneous LAD and RCA ligature reduced ST-segment elevation by about 30% with no appreciable re-elevation after 1-vessel selective reperfusion. Acute myocardial ischemia in opposite ventricular regions attenuated ST-segment elevation and blunted reciprocal depression in conventional ECG leads but not in direct local myocardial electrograms.

Influence of the Extent of Coronary Atherosclerotic Disease on ST-Segment Changes Induced by ST Elevation Myocardial Infarction

The accuracy of the admission electrocardiogram (ECG) in predicting the site of acute coronary artery occlusion in patients with ST-segment elevation myocardial infarction (STEMI) and multivessel disease is not well known. This study aimed to assess whether the presence of multivessel coronary artery disease (CAD) modifies the artery-related ST-segment changes in patients with acute coronary artery occlusion. We reviewed the admission ECG, clinical records, and coronary angiography of 289 patients with STEMI caused by acute occlusion of left anterior descending (LAD; n = 140), right (n = 118), or left circumflex (LCx; n = 31) coronary arteries. All patients underwent primary percutaneous coronary reperfusion during the first 12 hours. The magnitude and distribution of artery-related ST-segment patterns were comparable in patients with single (n = 149) and multivessel (n = 140) CAD. Occlusion of proximal (n = 55) or mid-distal (n = 85) LAD artery induced ST-segment elevation in leads V1 to V5, but only the proximal occlusion induced reciprocal ST-segment depression in leads II, III, and aVF (p <0.001). Proximal and mid-distal occlusion of right (n = 45 and 73, respectively) or LCx (n = 15 and 16) coronary artery always induced ST-segment elevation in leads II, III, and aVF and reciprocal ST-segment depression in leads V2 and V3. ST-segment elevation in lead V6 >0.1 mV predicted LCx artery occlusion. In conclusion, patients with STEMI with single or multivessel CAD have concordant artery-related ST-segment patterns on the admission ECG; in both groups, reciprocal ST-segment depression in LAD artery occlusion predicts a large infarct. Subendocardial ischemia at a distance is not a requisite for the genesis of reciprocal ST-segment changes.

Mechanism and diagnostic potential of reciprocal ECG changes induced by acute coronary artery occlusion in pigs

Reciprocal ST-segment depression simulating additional subendocardial ischemia is commonly observed in ST-segment elevation myocardial infarction. To study the mechanism and characterization of the whole reciprocal electrocardiogram (ECG) patterns induced by acute coronary artery occlusion at different locations in the absence of additional subendocardial ischemia in pigs. Conventional 12-lead ECG and/or local extracellular epicardial, mid-myocardial, and endocardial electrograms were recorded during the acute occlusion of right coronary (RC) and left anterior descending (LAD) coronary arteries in the in situ (n = 9) or in the isolated perfused (n = 5) pig hearts. Mid-RC occlusion induced reciprocal ST-segment depression (-0.43 ± 0.14 mV; P<.01) and S-wave deepening (-0.74 ± 0.23 mV; P<.01) in anterior ECG leads. Mid-LAD occlusion induced reciprocal S-wave deepening (-0.43 ± 0.37 mV; P = .02) but not ST-segment depression in inferior leads. Proximal LAD induced reciprocal ST-segment depression (-0.21 ± 0.20 mV; P = .03) and S-wave deepening (-0.56 ± 0.58 mV; P = .04) in inferior leads. Reciprocal QRS widening was observed only during proximal LAD occlusion. Local extracellular recordings did not show significant reciprocal QRS and ST-segment changes. In the absence of additional subendocardial ischemia, acute coronary artery occlusion induces reciprocal ST-segment and S-wave changes in the 12-lead ECG that allow better differentiation between proximal and mid-LAD occlusion. Reciprocal ECG changes depend on conventional lead system design and not on the transmission of injury currents from the ischemic border zone to distant normal myocardium.

Reciprocal ST segment changes in acute inferior myocardial infarction: Clinical, hemodynamic and angiographic implications

To investigate the clinical significance of reciprocal ST segment depression on the presenting electrocardiogram in patients with acute inferior myocardial infarction. Design and setting: A prospective, randomized, controlled single center study done in the critical care department, Cairo university Hospital. Forty consecutive patients with acute inferior myocardial infarction were enrolled in this study divided into two groups, 20 patients with reciprocal ST depression (group 1) and 20 patients without such depression (group 2). Interventions: All patients were investigated with serial ECG, cardiac biomarkers, echocardiography and coronary angiography. There was no significant difference in the proportion of coronary disease risk factors in patients in group 1, versus those in group 2. Patients in group 1 had significant higher degree ST elevation (in inf. Leads) than patients in group 2, higher levels of peak total CPK and CKMB was also seen. In addition patients in group 1 developed complication more frequently than those in group 2. Although no statistically significant difference between the two groups was seen as regard the ejection fraction sought by echocardiography, it did show a higher incidence of mitral regurge in group 1 [14 (70%)] versus 6 (30%) in group 2 with P value of 0.01. In group 1 left anterior descending artery lesions was significantly more frequent than in group 2 with P value < 0.001, also multivessel disease was significantly more frequent in group 1. The significance of reciprocal ST depression on the electrocardiogram during the course of inferior MI remains uncertain, opinion is divided as to whether it is a benign electrical phenomenon or a sign of a greater myocardial necrosis and more frequent left coronary artery disease, from our study we support the latter opinion. This simple ECG finding may be used to differentiate high risk patients for a more aggressive approach.

Identifying False-positive ST-elevation Myocardial Infarction in Emergency Department Patients

BackgroundIn a push to treat ST-elevation myocardial infarction (STEMI) patients with primary percutaneous coronary intervention (PCI) within 90min of door-to-balloon time, emergency cardiac catheterization laboratory activation protocols bypass routine clinical assessments, raising the possibility of more frequent catheterizations in patients with no culprit coronary lesion. ObjectiveTo determine the incidence, predictors, and prognosis of false-positive STEMI. MethodsWe followed a prospective cohort of patients diagnosed with STEMI by usual criteria receiving emergency cardiac catheterization with intention of primary PCI between January 2005 and December 2007 at a tertiary care center. False-positive STEMI was defined as absence of a clear culprit lesion on coronary angiography. ResultsOf 489 patients who received emergency cardiac catheterization indicated for STEMI, 54 (11.0%, 95% confidence interval [CI] 8.3–13.8) had no culprit lesion on coronary angiography. Independent predictors of false-positive STEMI were absence of chest pain (odds ratio [OR] 18.2, 95% CI 3.7–90.1), no reciprocal ST-segment changes (OR 11.8, 95% CI 5.14–27.3), fewer than three cardiovascular risk factors (OR 9.79, 95% CI 4.0–23.8), and symptom duration longer than 6h (OR 9.2, 95% CI 3.6–23.7); all p<0.001. Using predictors, we modeled a risk score that achieved 88% (95% CI 81–94%) accuracy in identifying patients with negative coronary angiography. Among the false-positive STEMI patients, 48.1% had other serious diagnoses related to their electrocardiographic findings. ConclusionWhen the diagnosis of STEMI is in doubt, clinicians may use predictors to quickly reassess the likelihood of an alternative diagnosis.

“Benign” early repolarization versus malignant early abnormalities: Clinical-electrocardiographic distinction and genetic basis

In the great majority of cases the ECG pattern of early repolarization (ERP) is a benign phenomenon observed predominantly in teenagers, young adults, male athletes and the black race. The universally accepted criterion for its diagnosis is the presence, in at least two adjoining leads, of ≥ 1 mm or 0.1 mV ST segment elevation. In benign ERP reciprocal ST segment changes are possible only in lead aVR. In contrast, reciprocal ST segment changes can be observed in several leads in idiopathic ventricular fibrillation (IVF) and acute coronary syndrome. In benign ERP the ST segment and T wave patterns have a relative temporal stability. IVF is an entity with low prevalence, possibly familiar, and characterized by the occurrence of VF events in a young person. More frequently this occurs in male subjects without structural heart disease and with otherwise with normal ECG even using high right accessory leads and/or after ajmaline injection. Several clinical entities cause ST segment elevation include asthenic habitus, acute pericarditis, ST segment elevation myocardial infarction, Brugada syndrome, congenital short QT syndrome, and idiopathic VF. In these circumstances clinical and ECG data are most important for differential diagnosis. In IVF the modifications could be dramatic and predominantly at night during vagotonic predominance when J waves > 2 mm in amplitude. The ST/T abnormalities are dynamic, inconstant, and reversed with isoproterenol. Convex upward J waves, with horizontal/descending ST segments or "lambda-wave" ST shape are suggestive of IVF with early repolarization abnormalities. Premature ventricular contractions with very short coupling and "R on T" phenomenon are characteristics with two pattern: When originate from right ventricular outflow tract left bundle branch block morphology and from peripheral Purkinje network, left bundle branch block pattern. The inherited-familial forms are not frequent in IVF; however mutations were identified in the genes KCNJ8, DPP6, SCN5A, SCN3B, CACNA1C, CACNB2, and CACNA2D1. The management of IVF has class I indication for ICD implantation. Ablation therapy is considered additional to ICD implantation in those patients with repetitive ventricular arrhythmia. Quinidine is a highly efficient drug that prevents recurrence.

Serial analyses of ventricular late potentials in patients with reciprocal ST segment changes during acute myocardial infarction.

The aim of this study was to determine whether successful reperfusion may alter substrate that is responsible for late potentials in the presence or absence of reciprocal ST segment changes (RC). The study population consisted of 50 patients (27 with RC and 23 without RC) with anterior acute myocardial infarction (AMI) undergoing successful thrombolytic therapy (TT). The presence of reciprocal changes was defined as ST-segment depression >1 mm, measured 80 ms after the J point in at least 2 leads other than those reflecting the infarct on admission ECG. All patients were evaluated with coronary angiography at predischarge. Signal averaged ECG (SAECG) recordings were obtained before and 10 days after TT. Baseline characteristics, SAECG findings, and angiographic data were similar between the groups. The only different baseline finding was the time from symptom onset to TT (204 +/- 150 minutes for patients with RC vs 312 +/- 174 minutes for patients without RC. P = 0.021). After TT, RMS values improved in patients with RC (from 35 +/- 17 microV to 43 +/- 14 microV, P = 0.038) and LAS and RMS were significantly better in this group. However, patients without RC did not show any changes in SAECG parameters after TT. LV ejection fraction (10th day) was better in patients with RC (45 +/- 11% vs 39 +/- 6%, P = 0.014). The frequency of ventricular arrhythmias during the hospitalization period was also similar between the groups. Reciprocal ST depression that regresses simultaneously with the infarction related ECG changes after TT in anterior AMI seems to be related to the time that has elapsed since the symptom onset. The improvement in SAECG parameters after TT in these patients is probably the result of earlier reperfusion leading to less myocardial damage.

The influence of the resolution of reciprocal ST segment changes on in‐hospital complications of acute myocardial infarction after percutaneous coronary angioplasty

We studied 120 patients (M:F 105:15, mean age 57.5 ± l0.l years) with acute myocardial infarction (MI) successfully treated with percutaneous coronary angioplasty (PTCA) to analyze the influence of the resolution of the ST segment elevation and depression after intervention to 1 month composite endpoints of reinfarction or reocclusion, development of congestive heart failure (CF) and death. Sum of preintervention and postintervention ST segment elevation and depression and the rate of resolution of these ST segment elevations and depressions were recorded for every patient. A total of 17 (14.2 %) composite endpoint events (events group) were recorded (7 reocclusion or recurrent MI, 9 CF, and 1 death). On univariate analysis, events group patients were older (53.3 ± 9.9 vs. 58.8 ± 9.1 years, P = 0.032), had lesser resolution of ST segment elevations (85 ± 24 % vs. 44 ± 55%, P = 0.017) and depression (72 ± 26% vs. 52 ± 30%, P = 0.009), had greater preintervention ST segment elevation (17.49 ± 12.95 mm vs. 28.38 ± 20.41 mm, P = 0.045), had lower ejection fraction (59.3 ± 10.2% vs. 43.6 ± 9.4%, P < 0.001), and had more frequent multivessel disease (71% vs. 47%, P = 0.048) compared to the nonevents group. Time from angina to reperfusion, residual stenosis, sex, infarct location and infarct-related vessel distribution were similar. On multivariate analysis (logistic regression with backward likelihood ratio) only older age (P = 0.0752), lesser rate of resolution of ST segment depression (P = 0.0262) and lower ejection fractions (P = 0.0014) were retained as predictors of the composite endpoints. Relative risk conferred by less than 50% resolution of ST segment depressions for composite endpoints were 3.78 (95% CI 1.63–8.73). We conclude that the lack of resolution of the sum of reciprocal ST segment depressions identifies a subgroup of acute MI patients with greater morbidity after primary PTCA. Cathet. Cardiovasc. Diagn. 45:240–245, 1998. © 1998 Wiley-Liss, Inc.

A computer heart model incorporating anisotropic propagation: IV. Simulation of regional myocardial ischemia

The main goal of this study was to simulate clinical body surface potential maps, recorded during percutaneous transluminal coronary angioplasty protocols, using a realistic geometry computer heart model. Other objectives were to address the question of reciprocal ST-segment changes observed in the 12-lead electrocardiogram during ischemia and to verify the hypothesis that the shortening of the QRS duration observed in left anterior descending (LAD) coronary artery occlusion may be explained by conduction delay in the septal His-Purkinje system. Simulation was achieved by first introducing into the heart model three transmural zones of mild, moderate, and severe ischemia for assumed occlusions in the LAD, left circumflex, and right coronary arteries. The heart model was then excited, in turn, with these three zones present for assumed occlusions in the LAD, left circumflex, and right coronary arteries. Myocardial conduction velocities in the regions of moderate and severe ischemia were assumed to be reduced to 75 and 50% of normal, respectively. Model action potentials in the mild, moderate, and severely ischemic zones were also altered to reflect known ischemic changes in these action potentials. Body surface potential maps and electrocardiograms were computed by placing the heart model inside a numerical torso model. Simulated map patterns during both ST-segment and QRS were qualitatively similar to clinical maps. Reciprocal ST-segment depression was observed for all three occlusions in remote leads that did not overlie the ischemic zones. QRS shortening due to septal His-Purkinje conduction delay was verified. The simulation results attest to the model's ability to reproduce body surface potential distributions recorded following percutaneous transluminal coronary angioplasty protocols. The simulations also showed that reciprocal ST-segment changes occur as a natural consequence of the primary ischemic region and that there is no need to invoke a second region of ischemia. Finally, the model demonstrated that QRS shortening can occur in LAD occlusion despite a slowing of conduction down the septal His-Purkinje system.

The electrocardiographic diagnosis of acute myocardial infarction in the thrombolytic era

The 12-lead ECG remains a simple and inexpensive technique to diagnose AMI in its early phases. The diagnostic accuracy of the ECG depends upon the extent of myocardial necrosis and its localization. The ECG is most sensitive in patients with occlusion of the LAD artery, followed by the RCA and the left CFA. In 10% to 20% of patients with AMI the initial ECG either shows nonspecific changes or is normal. The correlation between the ECG and infarct-related artery varies according to the involved vessel. Classic ECG changes are seen in 90% of the LAD artery, in 70% to 80% of RCA, and in only 50% of CFA occlusions. A second important issue is the mechanism and clinical significance of reciprocal ST segment changes, which usually indicate larger MI, more impaired ventricular function, worse prognosis, and in some patients, significant disease of a noninfarct-related artery. Furthermore, the value of the ECG in estimating myocardial injury and infarct size remains controversial. The ECG plays an important role in coronary reperfusion. ST segment elevation is one of the principal criteria for instituting thrombolytic therapy, and helps predict those who will most likely benefit from coronary reperfusion. The role of the ECG in evaluating the reperfusion status after coronary thrombolysis is not clear. Rapid return to baseline or normalization of the ST segment suggests opening of the occluded vessel, though a small or negligible change does not exclude successful reperfusion.

Reciprocal ST Segment Changes in Acute Myocardial Infarction; Informative or Incidental?

The majority of patients show elevation of the ST segment of the surface electrocardiogram during the acute phase of transmural myocardial infarction. In a significant proportion of such patients, depression of the ST segment is observed in an area of myocardium away from the infarcted territory. In spite of the recognition of this reciprocal ST segment depression for some decades, its aetiology and diagnostic and prognostic significance have been elusive and the subject of controversy. There is general, but not uniform, agreement that patients showing reciprocal ST segment depression usually have more extensive myocardial damage than those without reciprocal changes. Assessments have included echocardiography [1], radionuclide ventriculography for ejection fraction and wall motion abnormalities [2, 3], thallium perfusion scintigraphy [4], enzyme release [2, 5] and in-hospital complications including heart failure and dysrhythmias [6]. It is logical to assume that the longer-term prognosis of such patients is somewhat less good, although evidence is limited and based on series too small to provide reliable prognostic information [7, 8]. Two general views have been advanced to explain reciprocal ST segment changes in acute myocardial infarction. The first contends that ST segment depression in areas presumably remote from the infarct territory is an electrical phenomenon related to the extent of ST segment elevation over the infarct territory. The second contends that ischaemia 'at a distance' underlies the ST segment depression, related to compromise of myocardial perfusion either from the same or a different artery to that supplying the infarct territory. It is likely that neither view is exclusively correct because of time-related changes in currents of injury after myocardial infarction. Thus, it was shown over 25 years ago in a canine model that ST segment elevation from the anterior epicardial electrogram after left anterior descending coronary artery ligation was associated immediately with ST segment depression on the epicardial surface of the posterior wall, directly opposite the evolving infarct [9]. Within 20 min, however electrodes on the periphery of the infarct that had recorded ST segment elevation initially showed ST segment depression as a marker of local myocardial injury. Clearly, the 12 lead body surface electrocardiogram is insufficient to differentiate reliably between such non-infarct and peri-infarct phenomena. Transient reciprocal ST segment changes, for example during coronary angioplasty [10,11], do not necessarily reflect currents of injury during evolving myocardial infarction. Protagonists of these two viewpoints have examined the predictive value of reciprocal ST

Reciprocal ST segment changes in acute inferior myocardial infarction: clinical, haemodynamic and angiographic implications

Reciprocal ST segment changes are frequent during acute inferior myocardial infarction, yet their significance remains controversial. In order to investigate the implications of these changes, the ECG obtained on admission for 83 patients with acute inferior myocardial infarction was compared with the clinical course and the results of angiographic and coronary arteriographic studies performed an average of 3 weeks after the onset of symptoms. Group 1 consisted of 59 patients with at least 1 mm of horizontal on downsloping ST segment depression in at least 1 of leads V1 to V4. Groups 2 consisted of 24 patients without precordial ST depression in this area. Group 1 patients were generally older than group 2 patients (59.6 +/- 6.4 versus 54 +/- 5.3 yr, P less than 0.01) had higher total creatine kinase (CK) levels and MB fractions (1835 +/- 940 versus 875 +/- 305, P less than 0.01, 269 +/- 102 versus 95 +/- 35 for MB fraction) and more complications during the hospital course (80% versus 38% P less than 0.01) and greater left ventricular dysfunction (ejection fraction 52.2 +/- 6% for group 1 versus 59.2 +/- 7% for group 2; cardiac index 2.75 +/- 0.41 min-1 m-2 for group 1 versus 3.25 +/- 0.31 min-1 m-2 for group 2 P less than 0.005). No difference was observed on biplane angiography as far as left ventricular wall kinesis was concerned.(ABSTRACT TRUNCATED AT 250 WORDS)