Reciprocal ST segment depression in acute myocardial infarction

The significance of "reciprocal" ST segment depression and the utility of this finding in the electrocardiogram (ECG) of patients with myocardial infarction were studied in 100 cases of acute myocardial infarction. Out of these, 30 cases expired with 20 cases (66.6%) showing reciprocal ST depression in the ECG. In the remaining 70 cases, 24(34.3%) had reciprocal ST changes while 46(65.7%) had not. Twenty (83.3%) out of 24 cases had inferior wall infarction. The incidence of complications in the form of complete heart block and mortality was higher in the patients with reciprocal changes. The creatinine kinase levels were significantly elevated in patients with reciprocal changes than in the patients without. Predischarge treadmill test done in these cases having reciprocal changes showed positive stress tests. Coronary angiography was performed in the cases with reciprocal ST-T changes which revealed the presence of double-vessel disease or triple-vessel disease in most of these cases.     

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.     

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.     

Reduction of S-T segment elevation with infusion of nitroprusside in patients with acute myocardial infarction

It is pointed out that the arrival or fixation probability of a mutant gene can be easily inferred analytically. The mean first arrival time for a single overdominant mutation to reach frequency y attains its maximum when x is close to but still slightly less than y/2, where x is the equilibrium frequency of the mutant gene in an infinitely large population. For an advantageous mutation, the mean first arrival time decreases with an increasing degree of dominance if selection is strong, but it first increases, after reaching a maximum, then decreases as the degree of dominance increases, if selection is weak. Contrary to our intuition, the mean age of an advantageous mutant gene increases with increasing degree of dominance, except when selection is very strong. A simple explanation is given in terms of the sojourn time at a particular gene frequency.     

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.     

Clinical prediction of the early prognosis in acute myocardial infarct

Several clinical factors can influence the pathophysiology, clinical course and prognosis of acute myocardial by different means. Some of them may be easily detected through the history, physical examination or ECG in an early phase. The knowledge of these factors may help the therapeutic decision making of patients with myocardial infarction. The influence for the main clinical factors (age, sex, risk factors, cardiologic antecedents and evolutive findings) on the short-term prognosis of acute myocardial infarction is reviewed. An analysis of the likely mechanisms of the influence of these factors on infarct prognosis is also performed.     

Coronary artery dissection without acute myocardial infarction

A 57 year-old-man with acute aortic dissection (DeBakey type I) who developed right coronary artery dissection without acute myocardial infarction. He was successful surgically treated and became asymptomatic.     

Effect of infarct artery patency on prognosis after acute myocardial infarction. The Survival and Ventricular Enlargement Investigators

In this study, adult male rats were injected intraperitoneally with a single dose of serotonin (5-hydroxytryptamine, 5HT; 10 mg kg-1 bodyweight) for 2 h or 18 h, or daily with graded doses of 5HT (0.1-10 mg kg-1) for four days before being killed. Serum and testicular interstitial fluid (IF) concentrations of luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone and immunoreactive-inhibin were measured by radioimmunoassay, and one testis was removed for histological examination. At 2 h after a single injection, 5HT caused a significant inhibition of serum concentrations of LH and inhibin, recovered IF volume and intratesticular testosterone concentrations; testis weight and serum concentrations of testosterone and FSH were unaffected. At 18 h after injection, all parameters had returned to normal, with the exception of intratesticular testosterone concentration which remained lower than normal. The lowest 5HT dose (0.1 mg kg-1) had no effect on any parameter following four daily injections. At a dose of 1.0 mg kg-1 5HT, there was a four-fold increase in the concentration of serum LH, but testis weight, recovered IF volume, testosterone and inhibin concentrations and serum concentrations of FSH were not significantly affected. At the highest dose of 5HT (10 mg kg-1) after four daily injections, testis weight decreased, and IF volume increased nearly three-fold. Testis concentrations of inhibin and serum testosterone were reduced, whereas serum concentrations of both LH and FSH were elevated; intratesticular testosterone concentrations did not differ from controls. Only at the highest dose of 5HT was disruption to the seminiferous epithelium observed, with focal damage ranging in severity from increased degeneration of spermatogenic cell profiles, to complete loss of the germinal epithelium; however, many tubule profiles displayed completely normal spermatogenesis. The acute IF volume reduction and spermatogenic disruption in 5HT-treated rats were consistent with localized ischaemia due to constriction of the testicular arterial supply. The eventual increase in IF volume observed after 5HT treatment appeared to be secondary to the loss of germ cells. Although 5HT also inhibited pituitary LH release and Leydig cell steroidogenesis, these effects appeared to play only a minor role in the induction of spermatogenic damage.     

High-resolution electrocardiography in acute myocardial infarct

The author starts by highlighting the importance of risk stratification in patients who have survived a myocardial infarction. High resolution electrocardiography, also called signal-averaged electrocardiography (SAECG), appears in this setting as a diagnostic tool that, by providing important information about the way the intraventricular conduction of the electrical impulse is made, contributes to the characterization of the arrhythmogenic substrate, which is the basis of ventricular tachycardia and fibrillation. By resorting to the averaging of the electrocardiographic signal, SAECG enables us to detect ventricular late potentials whenever the analysis of that signal is made in time-domain. Further details, which will enrich the information on ventricular activation, can be obtained if the analysis is made in the frequency-domain (spectral analysis). The importance of detecting abnormalities in the SAECG recordings lies in the fact that those abnormalities are related to the occurrence of ventricular tachycardia and fibrillation, which are responsible for arrhythmic death. After referring to the criteria of positivity of SAECG and its reproducibility, the author approaches the most important part of the paper: the clinical applications of SAECG. After focusing on the interest of the method in noncoronary conditions, its usefulness in patients with acute myocardial infarction is pointed out. The author then mentions the prevalence of abnormalities in SAECG in patients with acute myocardial infarction and emphasizes the interest of the method in risk stratification. The author then presents the results of his Group in what concerns prevalence and prognosis. Finally, the author refers to the application of SAECG in other forms of coronary artery disease besides myocardial infarction.     

Nutritional problems in acute myocardial infarct

Hypocaloric nutrition in patients during the first days of myocardial infarction cannot be suggested any longer. Because of several reasons the minimum calory uptake should be about 2000 kcal/per day. Patients with enddiastolic pulmonary artery pressures above 20 mm Hg which is especially a high risk group should be treated parenterally with solutions of carbohydrates, insulin, and potassium. This regimen appears to be of a special importance at beginning shock or during cardiogenic shock.     

Biochemical markers in acute myocardial infarct

Exact and early diagnosis of acute myocardial infarction is essential for the subsequent routine management of this frequent cardiovascular disease. At present, the clinical biochemistry possesses a set of more or less cardiospecific protein markers for early detection of myocardial ischemic damage. After the admission of patient to the hospital, serial estimations of rather non-specific enzyme activities (creatine kinase, its MB-izoenzyme, lactate dehydrogenase, hydroxybutyrate dehydrogenase) are currently used for the detection of acute myocardial infarction and for the further monitoring of the patient and managing his therapy. In the past decade, many cardiospecific biochemical markers were discovered and gradually introduced into the routine clinical practice. The most perspective markers are some molecules of contractile proteins of heart myofibrils (troponins, myosin chains) as well as "rediscovered" myoglobin. The aim of this review article is to inform about the commonly used, as well as about the new biochemical markers, to discuss some problems of diagnostic strategy in the early and exact detection of ischemic myocardial damage and to attract attention to the difficulties. However its disadvantage resides in its presence in both myocardium and skeletal muscles which arise when the diagnosis of acute myocardial infarction is prematurely excluded from consideration and such patients are discharged too soon from hospital. (Fig. 1, Tab. 1, Ref. 72.)     

The apexcardiogram in acute myocardial infarct

The relation between intracardial haemodynamics and apicocardiogram (ACG) parameters is explained. A wave (amplitude and duration), A/H ratio, true and total TCI, total systole, total expulsion, RIV, RFW, TE/TCI (total) and TE/TCI (true) findings in 22 patients with acute myocardial infarct are presented. Attention is also given to clinical and radiological signs of cardiac insufficiency and the infarct site. Constant and significant increases in the A wave, A/H ratio and RIV, together with a decrease in total expulsion, were noted, particularly in cases with clinical evident insufficiency. In the pre-expulsive stage, ACG Data could not be taken as a reliable index of myocardial contractility in cases where insufficiency was not manifest. It is felt, therefore, that ACG may be of assistance in the evaluation of changes in myocardial performance, even where clinical and radiological signs of decompensation are absent.     

Use of composite endpoints in thrombolysis trials of acute myocardial infarction

Although preventing early mortality following acute myocardial infarction (MI) is the most important goal of thrombolytic therapy, insistence on its use as the only or principal endpoint in trials of acute MI will limit the number of new thrombolytic-antithrombotic regimens that can be tested, and thus may inhibit future progress of this important area of cardiovascular therapeutics. Trials of thrombolytic therapy over the past decade, as discussed in this article, have demonstrated that: (1) thrombolytic therapy improves both mortality and intermediate endpoints, and (2) intermediate nonfatal endpoints are strongly linked to long-term mortality. Taken together, these facts provide strong evidence that intermediate nonfatal events can be used as valid endpoints in future trials of thrombolytic therapy. The unsatisfactory outcome composite endpoint, which incorporates mortality and important intermediate endpoints, will make it possible to compare innovative new regimens in much smaller trials. Ultimately, both of these approaches (i.e., megatrials using a mortality endpoint and smaller trials utilizing a composite unsatisfactory outcome endpoint) can be used in a complementary fashion. A new regimen could first be tested using the unsatisfactory outcome endpoint; if it showed particular promise, it could then become a candidate for testing in a megatrial. Conversely, if it did not prove better than standard regimens, futile research in tens of thousands of patients might be prevented. Thus, the use of composite endpoints will expand the number of new thrombolytic-antithrombotic regimens that can be tested and, it is hoped, accelerate progress in the treatment of acute MI.     

Use of thrombolytic agents and other drugs in acute myocardial infarction

Data on all patients with acute myocardial infarction who were treated in the ten hospitals in Health region 1 in Norway were extensively analysed over a two month period. Of all the 487 patients 32% received thrombolytic treatment; i.e 36% of those with definite or suspected myocardial infarction on admission. Thrombolytics were withheld, mainly because only 58% of the patients showed ST elevation or bundle branch block on their ECG, and because of a long delay from onset of symptoms to admission to hospital. With increasing age use of thrombolytics decreased, and high age seemed to some degree to act as a contraindication. Relative contraindications such as history of stroke or peptic ulcer contributed modestly to the limited use of thrombolytics. Aspirin was used by 72% of the patients, and either aspirin or anticoagulants in 87%. At six month follow-up 50% used aspirin and 32% warfarin. Betablockers were given to 57% of the patients in hospital, but were not used to any extent in the acute phase of the disease; at six months the proportion of patients on betablockers was about the same. Oral nitrates were used more extensively than betablockers and there is a clear indication that angiotensin converting enzyme inhibitors are used increasingly for secondary prevention.     

Thrombolysis for acute myocardial infarction

Thrombolytic therapy has been a major advance in the management of acute myocardial infarction. Unfortunately, it continues to be underused or is administered later than is optimal. Thrombolytic therapy works by lysing infarct artery thrombi and achieving reperfusion, thereby reducing infarct size, preserving left ventricular function, and improving survival. The most effective thrombolytic regimens achieve angiographic epicardial infarct-artery patency in only approximately 50% of patients within 90 minutes. Bleeding requiring transfusion occurs in approximately 5% of patients and stroke in approximately 1.8% with these regimens, which include adjunctive aspirin and intravenous heparin. There are several ways in which reperfusion rates and thus patient outcomes might be improved, such as different dosing regimens of established agents; combinations of different agents; improved adjunctive therapy such as direct antithrombin agents, low-molecular-weight heparin, or glycoprotein IIb/IIIa receptor antagonists; or the development of novel thrombolytic agents with enhanced fibrin specificity, resistance to native inhibitors, or prolonged half-lives allowing bolus administration. All of these strategies are being tested in clinical trials. The best approach currently is to administer thrombolytic therapy as soon as possible to all patients without contraindications who present within 12 hours of symptom onset and have ST-segment elevation on the ECG or new-onset left bundle-branch block, unless an alternative reperfusion strategy is planned.     

Analysis of reperfusion by thrombolysis of the artery responsible for acute myocardial infarction

OBJECTIVE: To analyze the role of the culprit coronary artery in myocardial infarction, its evolution and mortality. And to correlate with clinical criteria of reperfussion. MATERIALS AND METHODS: We included patients with clinical diagnosis of acute myocardial infarction (MI) treated with thrombolytic therapy, and coronariography. We used the TIMI study angiographic scale to evaluate the level of permeability of the culprit artery. RESULTS: Of 473 patients with of acute MI; coronariography was made in 377. The most frequent culprit vessel was anterior descending artery in 168 patients (45%) and right coronary artery in 139 patients (36%). In 276 patients the culprit vessel was permeable (73%). Of them in 30 patients, had TIMI 1 alterations, TIMI 2 in 97 patients, had TIMI 3 in 148 patients, only 102 patients had TIMI 0. In anterior MI the most frequent reperfussion arrhythmia was ventricular ectopic beats followed by slow ventricular tachycardia and ventricular tachycardia in 54%, ventricular fibrillation was observed only in six patients, of whom TIMI scale was 2 and 3 in five patients. In inferior MI, ventricular ectopic beats and slow ventricular tachycardia was seen in 25% of patients. In patients with permeable culprit artery we observed significant depression of ST segment, (159 patients, 42%), and significant increase in CK-MB levels, seen in 191 patients (51%). In the group of patients with total occlusion of the culprit artery, twenty-one (30%) had left ventricular disfuntion, and only six of them were in cardiogenic shock. In the group of patients with permeable culprit artery only two percent had cardiogenic shock. Therefore the analysis of the clinical evolution is the maia marker to take into consideration to send patients to early coronary arteriography with the objective to look for other therapeutic alternatives.     

The pre-hospitalization period in acute myocardial infarct

The article reviews the possibilities of biochemical markers in coincidence with the assessment of prognosis in acute coronary syndromes and in the revealing of effectivity of their therapy. The current options of clinical biochemistry in many cases allow to supplement, confirm, or exclude the results of modern physical and other clinical examination methods and in this way to contribute to the accuracy of the diagnostic process, and enable to comment the prognosis and the risk measure of the patient. A significant progress has been achieved in the assessment of effectivity in thrombolytic therapy in acute myocardial infarction, where especially the series assessment of myoglobin levels or specific troponin cardiomarkers can facilitate the process of physician's decision as to the assessment of the subsequent procedure in the treatment of patients. The assessment of levels of both specific and partly less specific cardiomarkers becomes one of the criteria of the decision in coincidence with ischaemic episodes in the peri and postoperative periods (the diagnosis of peri-operative myocardial infarction). Specific troponin cardiomarkers acquire an extraordinary significance in the prediction of the measure of risk in patients with unstable angina pectoris where already one single assessment of the level of these markers is sufficient for hospitalization of the patient and thus enables to change the physician's strategy of further therapy. (Ref. 95.).