Cardiopulmonary complications in acute subarachnoid hemorrhage

Pathologic electrocardiogram (ECG) may be present in more than 90% of patients with subarachnoid haemorrhage. The ECG findings are often transient and may mimic acute myocardial ischaemia or infarction. These ECG findings may cause diagnostic problems in patients with subarachnoid haemorrhage who are unconscious or who have atypical symptoms. Life-threatening arrhythmias are also seen and may be responsible for sudden deaths in patients with subarachnoid haemorrhage. Other signs of myocardial injury, such as ventricular wall motion dysfunction, elevated enzymes, and histological evidence of contraction band necrosis are described. The myocardial dysfunction known as neurogenic stunned myocardium is reversible if the patient survives the acute phase, but it may lead to haemodynamic instability and contribute to the origin of neurogenic pulmonary oedema. The myocardial injury in subarachnoid haemorrhage may be due to a massive sympathetic stimulation of the myocardium in response to rapidly increasing intracranial pressure. We illustrate myocardial injury and dysfunction in a case report where a patient had subarachnoid haemorrhage with ventricular fibrillation, pulmonary oedema, left ventricular dysfunction and ST-segment elevation, initially thought to be acute myocardial infarction.     

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OBJECTIVES: To investigate the frequency of ECG abnormalities suggestive of myocardial ischaemia in patients with severe drug resistant epilepsy and without any indication of previous cardiac disease, assuming that these changes may be of significance for the group of epileptic patients with sudden unexpected death. MATERIAL AND METHODS: Twelve patients with medically intractable epilepsy were investigated with simultaneous long ECG and EEG recordings while attending either epilepsy surgery investigational procedures or the investigational programme for diagnostic purposes, and one while having an episode of status epilepticus. RESULTS: The ECG recording failed in 1 patient. This patient had chest pain and minor yet morphologically conspicuous changes in the ECG, suggestive of myocardial infarction. He died in heart arrest. Eight epilepsy patients had episodes of ST segment depression in the ECG, many of which coincided with video- and EEG documented epileptic seizures. Two patients experiencing simple partial seizures and 1 patient experiencing absence seizures had no ST segment depressions in the ECG. One patient had an episode of status epilepticus secondary to brain damage and no ST segment deviation was seen during the ECG recording which continued until 3 h before the patient died. CONCLUSION: Patients with severe drug resistant epilepsy have episodes of ST segment changes, some of which are closely related to epileptic seizures. Further studies are needed to confirm the present results and to investigate the nature of these changes and document the effect of prophylactic treatment with cardioactive drugs to reduce the risk of sudden death.     

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CONTEXT: Early risk stratification of patients with myocardial infarction is critical to determine optimum treatment strategies and enhance outcomes, but knowledge of the prognostic importance of the initial electrocardiogram (ECG) is limited. OBJECTIVE: To assess the independent value of the initial ECG for short-term risk stratification after acute myocardial infarction. DESIGN: Retrospective analysis of the Global Utilization of Streptokinase and t-PA (alteplase) for Occluded Coronary Arteries (GUSTO-I) clinical trial database. SETTING: A total of 1081 hospitals in 15 countries. PATIENTS: From the 41 021 patients enrolled in the overall study, we selected those who presented within 6 hours of chest pain onset with ST-segment elevation and no confounding factors (paced rhythms, ventricular rhythms, or left bundle-branch block) on the ECG performed before thrombolysis was administered (n=34 166). MAIN OUTCOME MEASURE: Ability of initial ECG to predict all-cause mortality at 30 days. RESULTS: Most ECG variables were associated with 30-day mortality in a univariable analysis. In a multivariable analysis combining the initial ECG variables and clinical predictors of mortality, the sum of the absolute ST-segment deviation (both ST elevation and ST depression: odds ratio [OR], 1.53; 95% confidence interval [CI], 1.38-1.69), ECG, heart rate (OR, 1.49; 95% CI, 1.41-1.59), QRS duration (for anterior infarct: OR, 1.55; 95% CI, 1.43-1.68), and ECG evidence of prior infarction (for new inferior infarct: OR, 2.47; 95% CI, 2.02-3.00) were the strongest ECG predictors of mortality. A nomogram based on the multivariable model produced excellent discrimination of 30-day mortality (C-index, 0.830). CONCLUSIONS: In patients presenting with myocardial infarction accompanied by ST-segment elevation, components of the initial ECG help predict 30-day mortality. This information should be valuable in early risk stratification, when the opportunity to reduce mortality is greatest, and may help in assessing outcomes adjusted for patient risk.     

The electrocardiogram during physical stress and Holter monitoring in the detection of asymptomatic myocardial infarct

INTRODUCTION: In patients with myocardial infarction acute myocardial ischaemia could be manifested by characteristic ischaemic symptoms or noncharacteristic symptoms such as cardiac insufficiency or heart rhythm disturbances. Sometimes myocardial ischaemia is not followed by any symptom. This condition is known as asymptomatic myocardial ischaemia. Asymptomatic myocardial ischaemia usually could be detected by treadmill exercise tolerance test or 24-hour Holter ECG monitoring. PATIENTS AND METHODS: We analyzed a group of 58 patients suffering from myocardial infarction with ST segment depression during the treadmill exercise tolerance test. All patients were on Holter 24-hour ECG monitoring. As a criterion of myocardial ischaemia during Holter monitoring ST segment depression of 1 mm and more, lasting 1 minute and more, and 0.08" of J point was accepted. RESULTS: During the treadmill exercise tolerance test segment depression was not followed by any symptom in 18 (31%) patients. There were no differences in the number of patients with hypertension in the group with symptoms and the group without symptoms. Diabetes mellitus was more frequent in the group with asymptomatic myocardial ischaemia. The average values of maximum ST segment depression and heart rates during treadmill tests were not statistically significant in both groups (with and without symptoms). During daily activities myocardial ischaemia was found in 30 (51%) patients by a 24-hour Holter ECG monitoring. We observed 198 episodes of myocardial ischaemia of which 138 (69.1%) were asymtomatic. The amplitude of ST segment depression and duration of these changes were significantly greater in the group with symptomatic episodes than in the group with asymptomatic episodes of myocardial ischaemia. DISCUSSION: Asymptomatic myocardial ischaemia is an often appearance in patients with myocardial ischaemia. Almost in 25% of persons in whom sudden death occurred obstructive changes in coronary arteries during the autopsy were found. Asymptomatic myocardial ischaemia could be found even an a "completely healthy person" without any complaints. Asymptomatic myocardial ischaemia is usually detected in a "completely healthy person" by casual diagnosis, in patients with stable and non stable angina pectoris, in patients with stenosis of the coronary arteries proved by angiography, and in patients after myocardial infarction. Some authors considered that treadmill exercise tolerance testing is less reliable to discover asymptomatic myocardial ischaemia comparing to the continuous 24-hour Holter ECG monitoring. It is know that in patients with diabetes mellitus neuropathy precedes the onset of symptomatic myocardial ischaemia. Asymptomatic myocardial ischaemia has the same predictive value for prognosis of the disease as symptomatic myocardial ischaemia. In some patients "anginal alarm system" is defective, and perception and conduction of pain sensations are disturbed. CONCLUSION: 1. In 31% of patients who suffered from myocardial infarction with ST segment depression during the treadmill testing asymptomatic myocardial ischaemia was found. 2. By Holter monitoring ischaemia ST segment depression during the exertion is observed in 52% of patients. Most of ischaemic episodes were asymptomatic. 3. The amplitude of ST segment depression is significantly greater and duration of depression is significantly longer in symptomatic episodes of myocardial ischaemia comparing to asymptomatic myocardial ischaemia obtained by Holter ECG monitoring.     

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AIMS: To assess the ability of clinical characteristics, admission ECG and continuous ST segment monitoring in determining long-term prognosis in unstable angina. METHODS: Two hundred and twelve patients with unstable angina (mean age 59 years), presenting within 24 h of an acute episode of angina were recruited at three hospitals and treated with standardized medical therapy. All patients kept chest pain charts and underwent ST segment monitoring for 48 h. The occurrence of death, myocardial infarction, and need for revascularization was assessed over a median follow-up of 2.6 years. RESULTS: The risk of death of myocardial infarction was greatest in the first 6-8 weeks after admission. Admission ECG ST depression and the presence of transient ischaemia predicted increased risk of subsequent death or myocardial infarction, whereas a normal ECG predicted a good prognosis. In 14 patients, ST segment monitoring provided the only evidence of recurrent ischaemia, and 72% of this group suffered an adverse event. Transient ischaemia and a history of hypertension were the most powerful independent predictors of death or myocardial infarction. CONCLUSIONS: Adverse events in unstable angina occur early after admission and can be predicted by clinical and ECG characteristics, and by the presence of transient ischaemia during ST segment monitoring. Risk stratification by these simple assessments can identify patients with unstable angina at high risk.     

Chain elongation in the isoprenoid biosynthetic pathway

PURPOSE: To investigate the associations between specific preoperative 12-lead electrocardiogram (ECG) abnormalities, perioperative ischemia, and postoperative myocardial infarction or cardiac death in major vascular surgery. METHODS: Two prospective studies on perioperative myocardial ischemia performed in two tertiary university hospitals were combined to include 405 patients. All preoperative ECGs were analyzed according to the Sokolow-Lyon criteria for left ventricular hypertrophy by investigators who were blinded to the patients' perioperative clinical course. Perioperative myocardial ischemia was detected by continuous ECG recording, and postoperative cardiac complications included myocardial infarction and cardiac death. RESULTS: A total of 19 postoperative cardiac complications occurred (two cardiac deaths and 17 myocardial infarctions). Voltage criteria for left ventricular hypertrophy (78 patients, 19%) and ST segment depression greater than 0.5 mm (98 patients, 24.2%) on preoperative ECGs were both significantly associated with postoperative myocardial infarction or cardiac death (odds ratio, 4.2 and 4.7; p = 0.001 and 0.0005, respectively) and with longer intraoperative and postoperative myocardial ischemia. In each of the two study groups, a preoperative ECG abnormality that involved voltage criteria, ST segment depression, or both (134 patients, 33.1%) was more predictive of postoperative cardiac complications than any other preoperative clinical variable, including a history of myocardial infarction or angina pectoris, diabetes mellitus, pathologic Q-wave by ECG, or preoperative myocardial ischemia. The combined duration of intraoperative and postoperative ischemia and the preoperative ECG with either voltage criteria or ST segment depression were the only independent factors associated with adverse cardiac events by multivariate analysis (p < or = 0.0001 and p = 0.02, respectively). CONCLUSION: Left ventricular hypertrophy and ST segment depression on preoperative 12-lead ECGs are important markers of increased risk for myocardial infarction or cardiac death after major vascular surgery.     

Precordial mapping in acute myocardial infarction

Serial precordial mapping was done in 30 patients with acute anterior myocardial infarction, 27 transmural and 3 subendorcardial. The sum of ST elevations in the 48 lead map was designated as sigma ST. Normal sigma ST was calculated as 27.1+/-3.1 in males and 14.3+/-2.8 in females. In infarction it was 100.4+/-58.2 in males and 84.8+/-50.9 in females on the 1st day of admission. Sigma ST was elevated on day 1 and tended to fall gradually. In 6 patients it was normal by day 7 and in 7 it was still abnormal by day 21. This fall roughly correlated with fall in SGOT and CPK levels. Significant elevation of sigma ST occurred in 14 of 27 cases after day 1. In 10 of 27 cases significant re-elevation occurred on day 4 or after i.e. when the patient was outside the ICCU. In 10 of the 14 re-elevations there was pain or worsening of clinical picture and in 12 there was re-elevation of SGOT. This elevation presumably implied infarct extension. There was a tendency to more arrhythmias in the patients with higher sigma ST and of the 4 deaths in the series 3 had very high sigma ST and high levels of SGOT. The patient with the highest sigma ST 295 died in cardiogenic shock. The number of risk factors was found to be higher in the high sigma ST group.     

Evaluation of the condition of the peri-infarct zone in acute myocardial infarct according to 35 precordial leads

The condition of the peri-infarction and the necrotic zones was assessed by cartographic analysis of ECG recorded from 35 precordial leads. During a 4-week follow-up functional mobility of indices characterising the prenecrotic zone and the stability of the zone of necrosis was noted. The indices sigma ST (overall index of ST segment elevation), AST (area of ST segment elevation), and AQS (area of QS recording), as well as the AST/AQS ratio possess definite prognostic significance: the lower the value of sigma ST, AST, and AQS and AQS and the greater the AST/AQS coefficient, the more favourable is the prognosis in myocardial infarction.     

ST-segment elevation in right precordial leads implies depressed right ventricular function after acute inferior myocardial infarction

BACKGROUND: The prognosis of acute inferior myocardial infarction is worse when it is complicated by right ventricular infarction. ST elevation in the right precordial leads is one of the reliable methods for detecting acute right ventricular infarction. The purpose of the study was to examine the relation between ST elevation in the right precordial electrocardiographic leads during acute inferior infarction and the severity of right ventricular systolic dysfunction. METHODS: This study analyzed the relation between ST elevation > or = 0.1 mV in V4R and the severity of right ventricular systolic dysfunction in 43 consecutive patients (men/women: 35/8; average age 62+/-9 years) with acute inferior myocardial infarction with a rapid-response Swan-Ganz catheter to measure the right ventricular ejection fraction (RVEF). RESULTS: RVEF was significantly lower in patients with ST elevation (n = 18) than in those without (n = 25) (33%+/-6% vs 40%+/-9%, p = 0.010). If the infarct-related lesion was located in the proximal right coronary artery, RVEF tended to be lower than if the lesion was located in the distal right coronary artery or the left circumflex coronary artery (33%+/-10% vs 37%+/-9% vs 42%+/-9%, p = 0.101). Logistic regression analysis demonstrated that ST elevation in V4R was the only independent predictor of depressed RVEF (odds ratio = 5.31, 95% confidence interval = 1.28 to 22.1, p = 0.022). CONCLUSION: ST elevation in lead V4R during acute inferior myocardial infarction predicts right ventricular systolic dysfunction.     

Natural history and evaluation of ST segment changes and MB CK release in acute myocardial infarction

The experimental evidence relating ST segment elevation in the electrocardiogram to the progress and extent of ischaemic myocardial damage is discussed. There are difficulties in applying this to patients: the reproducibility of praecordial mapping was tested using a multiple analysis of variance. This showed that factors such as time after the onset of myocardial infarction and posture can affect measurements of sigmaST elevation significantly. There was a pattern of changes in segmaST elevation and of changes in plasma MB CK activity in a group of patients with uncomplicated anterior infarction. A significant byt weak correlation was found between sigmaST elevation in the first hour and the total MB CK activity released into the plasma, but not at any other time. The use of sigmaST elevation as a measure of the extent of ischaemic damage is unreliable. In 5 patients with a variety of complications of acute anterior infarction, changes in sigmaST elevation werr significantly different from the uncomplicated group, and MB CK release profiles suggested further necrosis. The pattern and time course of ST segment changes may be of use in assessing the progress of ischaemic myocardial damage.     

Should survivors of myocardial infarction with low ejection fraction be routinely referred to arrhythmia specialists?

Because survivors of myocardial infarction are at risk for ventricular arrhythmias and sudden death, physicians must decide whether to refer these patients to specialists for arrhythmia assessment and therapy. However, this decision is complex as few randomized data are available concerning either diagnostic or therapeutic options. Therefore, we modeled the potential impact of current arrhythmia detection and management strategies on mortality in survivors of myocardial infarction with reduced left ventricular function who are managed in a contemporary manner. Based on recent data we estimated that the mortality for myocardial infarction survivors with left ventricular ejection fraction less than 0.40 is 20 percent over 3.5 years and that half of the deaths are sudden. The sensitivity and specificity of a Holter electrocardiogram (ECG), a signal-averaged ECG, and an invasive electrophysiology study for predicting sudden death were obtained from a literature review of trials published after 1990 that included more than 300 patients. A series of models were constructed to predict mortality achieved by different arrhythmia management strategies that reduced sudden death by 50 percent and 75 percent--reductions estimated to be within the range for amiodarone and implantable defibrillators. We found that, when routinely applied to all infarct survivors with depressed ventricular function, a therapy that reduces sudden death by 50 percent with 1 percent fatal adverse effects (potentially amiodarone) saves approximately 1 life for every 25 patients treated. Therapy that reduces sudden death by 75 percent with 2 percent fatal adverse effects (potentially implantable defibrillators) saves 1 life for every 14 patients treated. Using Holter ECG recordings, a signal-averaged ECG, or an invasive electrophysiology study to select higher-risk groups, 1 life can be saved for every 4 to 11 patients treated, and the negative impact of adverse effects can be reduced. However, to achieve this benefit, additional and potentially invasive arrhythmia testing must be applied to 28 to 47 patients for each life saved. Thus, with contemporary management of acute myocardial infarction, the risk of sudden death for survivors is sufficiently low that broad application of available antiarrhythmic therapies has limited potential for further improving survival, particularly if therapy also has significant adverse effects. Thus, routine referral to arrhythmia specialists is not warranted for the majority of infarct survivors and should be largely reserved for patients with serious, symptomatic arrhythmias.     

Relation of absence of ST reelevation immediately after reperfusion and success of reperfusion with myocardial salvage

To examine whether resolution in ST elevation without ST reelevation immediately after reperfusion indicates successful reperfusion with myocardial salvage, we studied 40 patients who had an extensive acute myocardial infarction with early reperfusion: 24 patients had ST reelevation and 16 patients had no ST reelevation. Results indicate that (1) in the group with ST reelevation, rapid progression of myocardial damage occurs by reperfusion itself (i.e., reperfusion injury) and (2) in the group without ST reelevation, myocardial damage had already been extensive and irreversible at the time of reperfusion; thus, the absence of ST reelevation is not always a sign of reperfusion with myocardial salvage.     

Silent myocardial ischemia in patients with different clinical forms of IHD

70 IHD patients underwent ambulatory Holter ECG monitoring two times. Out of 357 episodes of transitory ischemia registered in the course of exercise and presenting primarily as ST depression the proportion of silent episodes reached 75.6%. The number of episodes, their duration and mean value of ST depression were significantly greater in subjects 1 year after myocardial infarction. These patients more frequently developed ventricular arrhythmia and had ejection fraction below 50%. The findings evidence a significant clinical value of silent myocardial ischemia. It may serve a predictor of repeated acute coronary accidents in postmyocardial infarction patients.     

Value of signal-averaged electrocardiography, radionuclide ventriculography, Holter monitoring and clinical variables for prediction of arrhythmic events in survivors of acute myocardial infarction in the thrombolytic era

OBJECTIVES: This study assessed the ability of signal-averaged electrocardiography, radionuclide ventriculography and Holter electrocardiographic (ECG) monitoring and clinical variables to identify patients at risk of serious arrhythmic events after myocardial infarction in the thrombolytic era. BACKGROUND: Most studies of signal-averaged electrocardiography, radionuclide ventriculography and Holter ECG monitoring in risk stratification after myocardial infarction preceded the introduction of thrombolytic therapy. METHODS: A consecutive series of 301 survivors of myocardial infarction, 205 (68%) of whom received thrombolytic agents, underwent signal-averaged electrocardiography (1st 48 h, day 6 and discharge), Holter ECG monitoring (days 6 to 7) and radionuclide left ventriculography (days 7 to 14). Median follow-up time was 1.03 years. RESULTS: Thirteen patients (4.3%) had an arrhythmic event (sudden death in 11, sustained ventricular tachyarrhythmia in 2). The 25-Hz high pass filtered signal-averaged ECG at discharge was 64% sensitive (95% confidence intervals [CI] 36% to 92%) and 81% specific (95% CI 76% to 86%). High grade ventricular ectopic activity on the Holter ECG was only 38% sensitive (95% CI 12% to 64%) and 74% specific (95% CI 71% to 77%). Left ventricular ejection fraction < 0.4 was the best test for prediction of arrhythmic events (sensitivity 75% [95% CI 50% to 100%] and specificity 81% [95% CI 76% to 85%]). In multivariate analysis, in rank order, digoxin therapy at discharge, an abnormal 25-Hz signal-averaged ECG before discharge, absence of angina before index infarction and previous infarction were predictive of arrhythmic events. With digoxin therapy excluded, ejection fraction was an independent predictor. Discriminant analysis identified a high risk group (12% of the study patients) with an event rate of 26%. CONCLUSIONS: The signal-averaged ECG and left ventricular ejection fraction are each independently predictive of arrhythmic events after myocardial infarction, but the Holter ECG is not. A combination of clinical and investigative variables, including the signal-averaged ECG, best identifies patients at highest risk.     

Usefulness of ST-segment elevation in lead III exceeding that of lead II for identifying the location of the totally occluded coronary artery in inferior wall myocardial infarction

The presence of ST-segment elevation in lead III exceeding that of lead II, particularly if combined with ST elevation in lead V1, proved to be a powerful marker for occlusion of the proximal or midportion of the right coronary artery. These findings helped to determine the extent of myocardium at risk in inferior wall myocardial infarction and may further guide the decision to administer thrombolytics.     

A simple electrocardiographic predictor of the outcome of patients with acute myocardial infarction treated with a thrombolytic agent. A Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto Miocardico (GISSI-2)-Derived Analysis

OBJECTIVES: This analysis aimed to evaluate in a large patient cohort the relation between ST segment alterations after fibrinolytic therapy for acute myocardial infarction and 1) the combined end point of in-hospital mortality plus clinical congestive heart failure or extensive left ventricular damage, and 2) mortality 30 and 180 days after randomization. BACKGROUND: Angina relief, enzyme release acceleration and ST segment normalization are related to coronary artery reperfusion and prognosis. Electrocardiographic (ECG) evaluation before and after fibrinolytic drug administration has been used to predict short- and long-term clinical outcome in acute myocardial infarction. METHODS: Patients enrolled in the Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto Miocardico (GISSI-2) trial underwent a standard ECG on admission and after 4 h of alteplase or streptokinase therapy; 7,426 recordings were suitable for ST segment analysis. A decrease > or = 50% in the sum of ST segment elevation in all ECG leads was adopted as the cutoff for predicting coronary artery patency. Recanalization was deemed to have occurred in 4,951 patients (group A) versus 2,475 patients without reperfusion (group B). RESULTS: Group A patients experienced a lower incidence of the combined end point than did group B patients (16.2% vs. 22.9%, respectively), as well as of all its components (death, clinical heart failure, ejection fraction < 35%, injured myocardial segment > 45%, QRS score > 10). Thirty- and 180-day mortality rates were lower in group A than group B (3.5% and 5.7% vs. 7.4% and 9.9%, respectively); relative risk (Cox) was 0.46 (95% confidence interval [CI] 0.37 to 0.57) for 30-day and 0.58 (95% CI 0.48 to 0.70) for 180-day mortality. Patients in group A had significantly less ventricular fibrillation and sustained ventricular tachycardia but more ischemic episodes (early recurrent angina plus myocardial infarction recurrence). CONCLUSIONS: A simple, inexpensive instrumental evaluation, unaffected by different epidemiologic and clinical characteristics of the population analyzed, can allow early assessment of the effectiveness of fibrinolytic treatment with respect to the main clinical outcomes.     

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The ECG changes of myocardial infarction during permanent or transient right ventricular pacing were studied in 32 patients with transvenous pacemakers who developed myocardial infarction. During right ventricular pacing the electrocardiogram resembled left bundle branch block in 29 patients, right bundle branch block in two, and in one patient the pattern could not be determined. Myocardial infarction induced new ECG changes during pacemaker rhythm in 20 of the 32 patients. There were only QS complexes in 5 cases, ST segment abnormalities in 4 and T wave inversions in 4, negative Q and T waves were simultaneously observed in one patient, Q wave and S-T segment changes in 3 and S-T segment change and T wave inversion in 3 patients. It is concluded that knowledge of the ECG changes induced by myocardial infarction in most patients under artificial pacing can be useful for diagnosis.     

Use of changes in ST segment elevation for prediction of infarct artery recanalization in acute myocardial infarction

BACKGROUND: The role of the ECG in evaluating reperfusion status after thrombolytic treatment in acute myocardial infarction is not clear. Dramatic ST segment changes have been observed during recanalization of an infarct-related artery, but ST criteria have not been definitively established for prediction of coronary artery patency. Differences in ST segment changes in relation to infarct localization have not been evaluated, and further investigation is required into reciprocal ST depression, which provides information independent from ST elevation. Therefore, the aim of this study was to evaluate how early changes in ST segment elevations and depressions predict vessel patency after fibrinolysis for patients with anterior and inferior/lateral infarcts. METHODS AND RESULTS: Two hundred patients with a Pardee wave in the ECG and chest pain of less than 6 h duration were given thrombolytic treatment. The result of the therapy was assessed simultaneously with coronary angiography. Patients were divided into two groups: I (50 patients) without recanalization (TIMI grade 0, 1 or 2), and II (150 patients) with successful recanalization (TIMI grade 3). Before and after therapy, analysis of the 12 lead ECG included maximum ST elevation measurement (H1, H2 respectively), the sum of ST elevations (sigma H1, sigma H2), the sum of ST segment depressions (sigma h1, sigma h2), and the ratios of ST segment changes (R1 = H2:H1, R2 = sigma H2:sigma H1, R3 = sigma h2:sigma h1). The mean interval from the first to the second ECG was 3.5 +/- 1 h. Successive values of R1 and R2 were examined to find that which best distinguished between the two groups. The best values for prediction of reperfusion were: (1) For anterior wall infarct [table: see text] (2) For inferior and lateral infarct [table: see text] In 13 patients with a complete right or left bundle branch block in the first or second ECG, the result of treatment was predicted in 11 patients using criteria for factor R1 and in 12 patients using criteria for R2. Analysis of ST segment depressions revealed a significant correlation between normalization of ST segment depressions and elevations (R3 vs R1: r = 0.60, P < 0.05; R3 vs R2 r = 0.59, P < 0.05). Multivariate discriminant analysis showed an independent value of R3 for discrimination between the two groups, but only in patients with inferior/lateral infarcts. The overall accuracy of the common algorithm in predicting reperfusion was significantly better in patients with inferior/lateral infarcts (Chi2 test, P = 0.0078). When separate algorithms were used, there was no significant difference between patients with anterior or inferior/lateral infarcts because of the significant improvement in prediction of reperfusion in patients with anterior infarcts (McNemar's test: P = 0.041). CONCLUSIONS: We conclude that analysis of ST segments on the standard 12-lead ECG offers valuable help in the early identification of successful recanalization of infarct-related arteries after thrombolytic therapy in patients with acute myocardial infarction. Use of the ratio of ST segment normalization according to the separate criteria for anterior and inferior/lateral infarcts gives the test a high sensitivity and specificity, even in the presence of interventricular conduction disturbances.     

Inferior ST segment depression as a useful marker for identifying proximal left anterior descending artery occlusion during acute anterior myocardial infarction

To determine whether or not ST segment deviation on admission electrocardiograms can identify patients with anterior acute myocardial infarction due to proximal left anterior descending artery occlusion, the magnitude and location of ST segment elevation or depression were compared between patients with proximal left anterior descending artery occlusion (group A, n = 47) and those with distal left anterior descending artery occlusion (group B, n = 59). ST segment depression in each of the inferior leads was significantly greater in group A than in group B. The incidence of ST segment depression > or = 1 mm in each of the inferior leads (II; 81% vs 27%, III; 85% vs 54%, aVF; 87% vs 47%, P < 0.01) was significantly higher in group A than in group B. In addition, the incidence of ST segment depression > or = 1 mm in all of the inferior leads was significantly greater in group A than in group B (77% vs 22%, P < 0.01). In group A, maximal ST segment elevation was more frequent in lead V2 alone (43% vs 14%, P < 0.01). Group A had greater ST segment elevation in lead aVL than group B, and the incidence of ST segment elevation > or = 1 mm in lead aVL was significantly higher in group A than in group B (66% vs 47%, P < 0.05). ST segment depression > or = 1 mm in all of the inferior leads was most valuable for identifying group A patients (77% sensitivity and 78% specificity). In contrast, the maximal ST segment elevation in lead V2 alone or ST segment elevation > or = 1 mm in lead aVL had a low diagnostic value (43% sensitivity and 86% specificity, 66% sensitivity and 53% specificity, respectively). In conclusion, this study indicates that analysis of ST segment deviation in the inferior leads is useful for identifying patients with acute anterior myocardial infarction due to proximal left anterior descending occlusion.     

Prognostic significance of ST segment shift early after resolution of ST elevation in patients with myocardial infarction treated with thrombolytic therapy: the GUSTO-I ST Segment Monitoring Substudy

OBJECTIVES: We sought to study the relation between recurrent ST segment shift within 6 to 24 h of initial resolution of ST elevation after thrombolytic therapy and 30-day and 1-year mortality. BACKGROUND: Rapid and stable resolution of ST segment elevation in relation to thrombolytic therapy in patients with an acute myocardial infarction is an indicator of culprit artery patency. Whether recurrence of ST segment shift during continuous ST monitoring after initial resolution is related to poor prognosis has not been studied. METHODS: ST segment monitoring was performed within 30 min after thrombolytic therapy for acute myocardial infarction. The predictive value of a new ST segment shift (assessed as > or = 0.1-mV deviation from the baseline) 6 to 24 h after thrombolytic therapy was studied with respect to 30-day and 1-year mortality. RESULTS: Of 734 patients, 243 had a new ST segment shift (33%). The 30-day mortality rate in patients with an ST shift (7.8%) was significantly higher than that in patients without an ST shift (2.25%, p = 0.001), as was the 1-year mortality rate (10.3% vs. 5.7%, respectively, p = 0.025). Multivariable analysis revealed an independent predictive value of ST shift with respect to 30-day mortality (p = 0.008), even after consideration of multiple clinical risk factors in the overall Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries (GUSTO)-I mortality model (p = 0.0001). Moreover, the duration of the ST shift bore a direct relation with 1-year mortality (p = 0.008). CONCLUSIONS: Detection of ST segment shift early after thrombolytic therapy for acute myocardial infarction is a simple, noninvasive means of identifying patients at high risk and is superior to other commonly assessed clinical risk factors. Thus, patients with a new ST shift after the first 6 h, but within 24 h, represent a high risk group that may benefit from more aggressive intervention, whereas patients without evidence of an ST shift represent a low risk subgroup.