Acute Transmural Myocardial Infarction Research Articles

Fatal Hemoptysis during Coronary Thrombolysis.

Cerebral hemorrhage is the most dreaded complication of coronary thrombolysis. Significant bleeding has also been described from catheter-entry sites, the retroperitoneum, and the gastrointestinal and genitourinary tracts. However, hemoptysis induced by thrombolysis has rarely been described in the literature. We present a 66-year-old male who received front-loaded tissue plasminogen activator (tPA) for acute transmural anterior wall myocardial infarction and developed massive hemoptysis from preexisting cavitary lung disease. The patient died within 5 hours. We believe this is the first case report of fatal hemoptysis induced by coronary thrombolysis. A history of cavitary lung disease may be a risk factor for life-threatening hemoptysis in patients receiving thrombolytic therapy.

Angiotensin converting enzyme inhibitor therapy promotes remodeling in patients with left ventricular ejection fraction ⪢ 40% after acute transmural myocardial infarction

Angiotensin converting enzyme inhibitor therapy promotes remodeling in patients with left ventricular ejection fraction ⪢ 40% after acute transmural myocardial infarction

Relevance of electrocardiographic findings, heart failure, and infarct site in assessing risk and timing of left ventricular free wall rupture during acute myocardial infarction

Clinical and electrocardiographic features of 227 patients who died of an acute myocardial infarction (AMI) were compared with those or 150 survivors of a first AMI. Left ventricular (LV) free wall rupture was found in 93 patients aged >50 years, but not in 134. The incidence of healed infarct (4 [4%] vs 50 [37%], p < 0.001), heart failure (11 [12%] vs 112 [84%], p < 0.001), and bundle branch block (11 [12%] vs 54 [40%], p < 0.001) was lower in patients with than without LV rupture. In patients with anterior AMI and early rupture (1 day), admission ST elevation was higher man in those with late LV rupture (>1 day, 6.8 ± 4.0 vs 4.0 ± 2.7 mm, p < 0.01). However, lateral wall AMI had minimal ST elevation and accounted for 10% of ruptures. On day 2, the decrease in ST segment in patients with late LV rupture was less than in survivors (0.5 ± 1.6 vs 3.2 ± 2.9 mm, p < 0.001). Admission systolic blood pressure in patients who had early rupture was higher than in survivors (155 ± 22 vs 137 ± 22 mm Hg, p < 0.001) and in those with late rupture (135 ± 23 mm Hg, p < 0.001). Late rupture was associated with infarct thinning and triggered by a physical strain in 18 of 45 patients (40%); infarct thinning, however, was present only in 4 of 48 patients (8%) with early rupture (p < 0.02). We conclude that (1) patients with LV rupture are among those >50 years of age with a first transmural AMI without conduction abnormalities or heart failure; (2) patients with anterior AMI, hypertension on admission, and high ST elevation are at risk for early rupture, whereas those without initial hypertension or high ST segment that remains elevated may have late rupture in an expanded infarction, often after an undue strain.

Predictors of in-hospital and 6-month outcome after acute myocardial infarction in the reperfusion era: The primary angioplasty in myocardial infarction (PAMI) trial

Objectives. This study examined the predictors of in-hospital and 6-month outcome after different reperfusion strategies in acute myocardial infarction.Background. Thrombolytic therapy and primary angioplasty are both widely applied as reperfusion modalities in patients with myocardial infarction. Although it is accepted that restoration of early patency of the infarct-related artery can reduce mortality and salvage myocardium, the optimal reperfusion strategy remains controversial, and the predictors of outcome in the reperfusion era have been incompletely characterized.Methods. At 12 centers, 395 patients presenting within 12 h of onset of acute transmural myocardial infarction were prospectively randomized to receive tissue-type plasminogen activator (t-PA) or undergo primary angioplasty without antecedent thrombolysis. Sixteen clinical variables were examined with univariate and multiple logistic regression analysis to identify the predictors of clinical outcome.Results. By univariate analysis, in-hospital mortality was increased in the elderly, women, patients with diabetes and in patients treated with t-PA as opposed to angioplasty. Only advanced age and treatment by t-PA versus angioplasty independently correlated with increased in-hospital mortality (6.5% vs. 2.6%, respectively, p = 0.039 by multiple logistic regression analysis). Similarly, the only variables independently related to in-hospital death or nonfatal reinfarction were advanced age and treatment by t-PA versus angioplasty (12.0% vs. 5.1%, p = 0.02). The reduction in in-hospital death or reinfarction with angioplasty versus t-PA was particularly marked in patients ≥65 years of age (8.6% vs. 20.0%, p = 0.048). Furthermore, primary management with angioplasty versus t-PA was the most powerful multivariate correlate of freedom from recurrent ischemic events (10.3% vs. 28.0%, p = 0.0001). The independent beneficial effect of angioplasty on freedom from death or reinfarction was maintained at 6-month follow-up (8.2% vs. 17.0%, p = 0.02).Conclusions. In the reperfusion era, the two most powerful determinants of freedom from death, reinfarction and recurrent ischemia after myocardial infarction are young age and treatment by primary angioplasty.

755-4 Does a Less Restrictive Indication for Thrombolytic Therapy Cause More Iatrogenic Complications in Acute Myocardial Infarction?

In consideration of possible severe complications thrombolytic agents are administered to only 30% of patients with acute myocardial infarction (AMI) admitted to coronary care units in Western Europe. “The 60-Minutes Myocardial Infarction Project” therefore investigates the effect of a higher lysis rate (LR) on the frequency of complications. The multicenter nationwide study includes 154 hospitals in Germany. During an 8-month period 4650 consecutive patients with proven transmural AMI were enrolled and complications occurring within 48 hours after admission were registered for clinical centers with a low and high LR (≥50% versus &gt;50%). clinical centers:allLR&lt;50%LR&gt;50%complications (within 48 h):n = 4650n = 2768n = 1882death8.0%8.3%7.5%hemorrhagic stroke0.4%0.5%0.2%ventricular rupture0.4%0.4%0.4%moderate bleeding2.4%1.8%3,3%allergic reaction0.8%0.5%1.3% Both groups were similar in age, sex and coexisting diseases. 1. 48-hour mortality was lower in clinical centers with a higher LR. 2. Severe complications showed no significant difference. 3. Minor complications were significantly more frequent in clinical centers with a higher LR. 4. These results support a less restrictive indication for thrombolytic therapy in AMI based on individual benefit-risk evaluation.

Antiaggregative Therapy with Acetylsalicylic Acid and Diclofenac in Patients with Acute Myocardial Infarction

A total of 109 male patients with acute transmural myocardial infarction (MI) were studied. 26 patients received a dose of acetylsalicylic acid (aspirin, ASA) 500 mg/d and 29 patients of 50 mg/d. 27 patients were given diclofenac (25 mg/d). 27 patients received no antiplatelet therapy. We observed thrombocyte hyperaggregation on the 1st MI day, a rapid increase in platelet activity by the 7th day and a considerable decrease in platelet aggregation during the 3rd and 4th weeks of illness in the group without antiaggregative treatment. The present study clearly demonstrated high antiaggregatory efficacy of ASA in dose of 50 mg/d which was significantly higher than that in daily dose of 500 mg ASA. Low-dose aspirin had fewer side-effects than aspirin 500 mg/d. However, although daily dose of 50 mg aspirin significantly inhibited platelet hyperaggregation on 7th day of MI, the hyperactivity of thrombocytes was not abolished. Diclofenac 25 mg daily had only a moderate antiaggregative efficacy in acute MI patients.

Thrombolysis for acute myocardial infarction.

Thrombolysis has become standard treatment in the great majority of patients with an acute transmural myocardial infarction. Large placebo-controlled trials have shown that thrombolytic therapy, when given within 6 hours after onset of symptoms, reduces infarct size, preserves left ventricular function and improves survival. Because of discrepancies observed between the effects of thrombolysis on left ventricular function and survival and since beneficial effects have also been observed in subgroups of patients treated after 6 hours, additional mechanisms of actions (besides salvage of ischemic myocardium) have been supposed: limitation of infarct expansion and left ventricular remodeling, increased electrical stability and provision of collaterals to other myocardial regions. The equal clinical outcome with different agents, in spite of proven differences in efficacy for early recanalization, in GISSI-2/International and ISIS-3 has further challenged the importance of the original pathophysiological mechanism (early reperfusion and myocardial salvage). The results of recent megatrials (GUSTO, EMERAS and LATE) and of a recent meta-analysis (FTT's collaborative Study Group) have resolved many uncertainties. The implications of these recent trials for the selection of both patients and thrombolytic strategies and for the future development of new treatment can not be overestimated.

Early programmes of high and low intensity exercise and quality of life after acute myocardial infarction.

To determine whether a group programme of light exercise could improve quality of life in patients after acute myocardial infarction to the same extent as a high intensity exercise training programme. Australian teaching hospital. 224 men from a consecutive series of 339 men under 70 admitted to a coronary care unit with transmural acute myocardial infarction. Patients were randomly allocated in hospital to a group programme lasting eight weeks of either high intensity exercise training or light exercise. Physical working capacity based on metabolic equivalents achieved from treadmill exercise tests at entry, after 11 weeks, and after one year. Quality of life based on self report scores of anxiety, depression, denial, and wellbeing and interview assessments of activities and psychosocial adjustment at entry, after four months, and after one year. The two groups were well matched at entry. At 11 weeks the mean results of treadmill testing were 10.7 (95% confidence interval 10.20 to 11.20) metabolic equivalents for exercise training and 9.7 (9.26 to 10.14) for light exercise (t = 2.85, df = 181, p = 0.005). Apart from this small temporary benefit in mean physical working capacity, there were no significant differences between groups. Improvement in occupational adjustment score from baseline to four months was greater after exercise training than after light exercise, but at one year repeated measures analysis of variance showed no significant effects of treatment or interaction between treatment and time point. The effects on quality of life of a low cost programme of light exercise are similar to those obtained from a high intensity exercise training programme.

The effects of chronic oral milrinone therapy on early postinfarction left ventricular remodeling

Left ventricular remodeling following acute transmural myocardial infarction may result in early left ventricular enlargement. To characterize the effects of milrinone on components of early left ventricular dilation, rats ( n = 120) underwent left coronary artery ligation or sham surgery. In the immediate postoperative period, rats received either no treatment or milrinone (3.17 ± 0.08 mg/kg/day) dissolved in drinking water for 20 days. Twenty-one days after the initial surgery, hemodynamic measurements were made. The rats were then put to death and the hearts arrested in diastole were excised and fixed at a constant pressure for morphometric analysis. To examine the effects of milrinone on the relative contribution of infarcted and noninfarcted segments to early left ventricular dilation after acute myocardial infarction, a subgroup of infarcted rats chosen randomly was put to death 3 days after the initial surgery for morphometric analysis. Compared with infarcted untreated rats, infarcted milrinone-treated rats had a lower left ventricular volume (1.41 ± 0.07 ml/kg vs 2.16 ± 0.19 ml/kg, p < 0.001), lower left ventricular wall stress (0.64 ± 0.03 vs 0.91 ± 0.06, p < 0.001), and a lower expansion index (1.61 ± 0.12 vs 2.61 ± 0.22, p < 0.001). Morphometric analysis revealed that the noninfarcted segment length did not differ between the two infarcted groups either 3 days or 21 days after left coronary artery ligation. Infarct segment length also did not differ between the two infarcted groups at 3 days, but at 21 days infarct segment was shorter in the milrinone-treated group compared with the untreated group ( p < 0.03). An increase in infarct segment length/total endocardial circumference ratio between day 3 and day 21 was observed only in the untreated group of rats. Thus milrinone begun in the immediate postinfarction period in a rat myocardial infarction model attenuates left ventricular dilation when hearts are examined 3 weeks later. This attenuation of early postinfarction left ventricular dilation with milrinone appears to be related to its effects on infarct zone remodeling.

Cardiac rupture, a clinically predictable complication of acute myocardial infarction: Report of 70 cases with clinicopathologic correlation

Objectives. To test the hypothesis that certain clinical events may precede free wall myocardial rupture and allow its prediction, we conducted a retrospective and prospective study of 70 patients with rupture.Background. Rupture of the left ventricular free wall develops in approximately 10% of patients with fatal acute transmural myocardial infarction. Clinically, its occurrence has been considered precipitous and unexpected. Pathologically, however, rupture appears to be a stuttering, progressive process characterized in many instances by an infiltrating intramural hemorrhage and a thrombus within the tear of ≥1 day's duration.Methods. The clinical course and evolutionary electrocardiographic (ECG) changes in 70 consecutive patients with rupture and 100 comprison patients with acute myocardial infarction but without rupture were reviewed to ascertain whether certain clinical symptoms, signs and ECG alterations occur in patients prone to develop rupture, allowing its anticipation, In addition, a correlation was established between the site of infarction indicated by the ECG and the site of rupture determined at autopsy or surgery,Results. Patients with rupture had a significantly greater incidence of pericarditis, repetitive emesis and restlessness and agitation than did patients without rupture. More than 80% of patients with rupture had two or more symptoms compared with 3% of patients without rupture (p < 0.002). A deviation from the expected evolutionary T wave pattern occurred in 94% of patients with rupture and 34% of control patients (p ≤ 0.02), An abrupt transient episode of hypotension and bradycardia, probably due to the initial tearing of the epicardium with a resultant small hemopericardium, was observed in 21% of patients with rapture. Rupture of the midlateral wall was most common (32%) and usually occurred in the setting of an inferoposterolateral infarction related to an acute left circumflex artery occlusion. On the basis of these clinical and ECG changes, rupture was confirmed by echocardiography and pericardiocentesis in the two most recent ptients, and the defect was successfully repaired.Conclusions. Rupture is often preceded by particular symptoms, signs—namely, one or more episodes of abrupt, transient hypotension and bradycardia and unexpected alterations of the T waves, especially directional changes of the latter. Patients displaying these symptoms, signs and ECG changes require a bedside echocardiogram and echocardiographically guided pericardiocentesis if fluid is visualized. If the pericardiocentesis identifies the fluid as blood, immediate surgery is indicated.

Platelet and neutrophil imaging techniques in the investigation of the response to thrombolytic therapy and the no-reflow phenomenon

Total coronary occlusion by thrombus is the cause of transmural acute myocardial infarction (AMI) in at least 90 % of cases, but patency may be reestablished spontaneous1y.l These total occlusions occur mostly at the site of preexisting coronary artery stenosis, which need not be severe.2, 3 The extent of myocardial damage depends on (1) the rapidity of occlusion, (2) the duration of the occlusion, (3) collateral flow, and (4) the coronary vascular and myocardial response to acute ischemia.4 Coronary thrombosis is the most common initial step in a more complex occlusion process involving anatomic and functional mechanisms. The purpose of this review is to describe the existing experimental and clinical methods available to assess platelet and neutrophil function in acute coronary arterial thrombosis. A better understanding of the functional and anatomic microvascular and myocardial changes should help in the management of evolving and recurrent myocardial infarction and its complications, in particular the so-called “no-reflow phenomenon.”

Intracellular magnesium deficiency in acute myocardial infarction.

It has been hypothesized that intracellular magnesium deficiency is a pathogenetic factor in acute myocardial infarction. This study examined the time course of changes in the erythrocyte magnesium concentration and the correlation between the erythrocyte magnesium concentration and the severity of acute myocardial infarction in 49 consecutive patients with transmural acute myocardial infarction. The data were compared with results from 20 control patients without ischemic heart disease. The erythrocyte magnesium concentration (mg/dl) decreased significantly during the acute phase of the infarction (4.86 +/- 0.09 on day 1, 4.89 +/- 0.10 on day 2 and 4.86 +/- 0.10 on day 3 versus 5.26 +/- 0.19 for controls, all P < 0.05) and then normalized gradually to 5.25 +/- 0.10 on day 28. The serum magnesium concentration (mg/dl) also decreased significantly during the acute phase of the infarction (1.93 +/- 0.04 on day 1 and 2.11 +/- 0.03 on day 2 versus 2.26 +/- 0.08 for controls, all P < 0.05), before recovering to 2.28 +/- 0.06 on day 28. There were significant correlations between the erythrocyte magnesium concentration on day 1 and maximal values of serum cardiac enzymes (r = -0.30 for creatine kinase, r = -0.34 for glutamic oxaloacetic transaminase and r = -0.57 for lactate dehydrogenase, all P < 0.05). Moreover, the erythrocyte magnesium concentration was significantly lower in patients with (4.32 +/- 0.08 mg/dl, n = 13) than in those without (5.06 +/- 0.09 mg/dl, n = 36, P < 0.0001) serious arrhythmias. These data indicate that intracellular magnesium deficiency is involved in the acute phase of myocardial infarction.

Thrombosis in Cardiovascular Disorders

The seminal discovery more than a decade ago that coronary artery thrombosis, usually caused by atherosclerotic plaque disruption, is the cause of virtually all cases of acute transmural myocardial infarction and plays a critical role in the development of unstable angina and other ischemic syndromes brought about an intense clinical and scientific interest in the process of thrombosis. The fruits of these investigations are detailed in in Cardiovascular Disorders, a remarkably up-to-date and comprehensive book. Although somewhat weighted towards thrombosis relative to cardiologic problems (fully one third of the book is concerned with coronary ischemic syndromes and thromboembolism from cardiac chambers and valves), there is in-depth coverage of thrombotic problems in other arterial beds and excellent chapters on venous thromboembolism and disseminated intravascular coagulation. On the whole the book is well balanced and reflects the backgrounds of the two editors, both distinguished leaders in cardiology and hematology from opposite sides of the Atlantic Ocean. They have selected an international group of 49 expert contributors representing the disciplines of cardiology, hematology, neurology, epidemiology, biochemistry, pharmacology, clinical medicine, and surgery. This eclectic lineup of authors is appropriate because thrombotic diseases are unusual in that they are included in the practice of most doctors, regardless of training, background, or subspecialty practice. Although the book is clinically oriented and practical, there are lucid and pithy summaries of the biochemical, pharmacologic, and molecular mechanisms involved in thrombosis and antithrombotic drugs, anticoagulants, and thrombolytic agents. In addition new agents and future therapeutic directions are nicely covered in a chapter entitled Novelties in Antithrombotic and Thrombolytic Therapy: A Latest Update. The basic pathogenesis of thrombosis is well summarized in introductory chapters that emphasize the interrelationship between cell to cell, molecular, and biochemical interactions as influenced by changes in the deformation of blood flow. There is a fascinating early chapter entitled Interrelationship Between Atherosclerosis and Thrombosis that lends compelling modern scientific support for Duguid's encrustation theory of atherogenesis. The bulk of this book, however, is intensely practical, with solid advice from experts on the management of thrombotic disease. A hallmark is that the opinions are backed by scholarship based on data from sound clinical trials and a thorough understanding of basic and theoretic considerations. The book is well edited. Each editor independently refereed each chapter, most of which were resubmitted in revised form within a 3-month deadline. The entire project was completed within 6 months, and many of the references are within I year of the 1992 publication date. Although there is variation in emphasis and opinion, there is a minimum of overlap and redundancy. There are two reservations. First, the chapter on peripheral arterial disease is disappointing. That it is written by European internists (angiologists) is apparent in the idiomatic phrasing (terminoterminal anastomosis in the aorta for end-to-end anastomosis), occasional misstatements (Streptokinase has been the most widely used agent for peripheral arterial occlusion), and curious misunderstandings (the . . . so-called blue toe syndrome is secondary to obstruction of the microcirculation in patients with essential or secondary thrombocythemia). Although there is useful information to be gleaned from this chapter, most American vascaflar surgeons will find it somewhat rambling and difficult to understand. The second reservation is the paucity of coverage of prethrombotic or hypercoagulable states. Although mentioned in passing in several chapters, the book would benefit from an in-depth chapter on congenital and acquired hypercoagulable syndromes. Despite these reservations this book can be recommended as an up-to-date, authoritative, and scholarly resource on thrombotic disorders. Anyone treating patients with arterial and thromboembolic disease would benefit from owning it; obviously, this includes vascular surgeons.

Late potentials in an ovine model of acute transmural myocardial infarction.

The development of slow conduction during the first hours of acute transmural myocardial infarction (ATMI) was studied by signal-averaged electrocardiograms (SAE) in 19 adult anesthetized sheep. SAEs were recorded before and after intravenous infusions of lidocaine and bretylium were begun and 10, 30, and 60 min after ATMI produced by ligation of the left anterior descending and second diagonal coronary arteries. Four sheep died promptly of ventricular tachyarrhythmias; two others developed sustained ventricular arrhythmias, which precluded additional data. Biphasic changes in QRS duration, root mean square voltage of the terminal 40 ms of the QRS complex, and duration of terminal low-amplitude (less than 30 microV) signal were observed. Peak changes in conduction occurred 30 min after infarction and regressed toward baseline thereafter. At 30 min, all animals developed late potentials, which were defined as signals that exceeded both after-drug QRS duration and duration of terminal low-amplitude signal less than 30 microV by more than two standard deviations. At 60 min, only 3 of 13 (23%) animals had late potentials. Conduction is slowest 30 min after ATMI in sheep but may not be related to development of ventricular arrhythmias. In five of six sheep (83%), ventricular arrhythmias occurred within 15 min of infarction before peak slowing was observed by SAE.

Detection of acute myocardial infarction with digital image processing of two-dimensional echocardiograms

We have previously described the ability of a computer-based image digitizing system to assess early textural changes in acute canine myocardial infarction. To determine whether this technique could be applied to human beings, we studied 12 patients with a first acute transmural myocardial infarction and five normal subjects. Two-dimensional echocardiograms were performed on days 1 and 8 in normal subjects and on days 1 (day of admission), 2, 3, 5, and 14 in the patient population. All recording parameters on the echocardiography machine were kept identical for serial studies. The mean period between hospitalization and first echocardiogram was 11.1 hours (range 4 to 20 hours). End-diastolic frames from the two-dimensional echocardiographic images were digitized and displayed on a monitor. The mean pixel intensity (MPI) (±SD) in the region of asynergy (area of myocardial infarction) and a normal area were determined. In normal volunteers, no significant change in MPI was noted between anteroseptal and lateral areas on two separate two-dimensional echocardiographic studies, which were performed 7 days apart (anteroseptal: MPI, 21.6 ± 1.1 vs 21.8 ± 0.4, p = not significant) and (lateral: MPI, 21.5 ± 1.2 vs 21.4 ± 1.4, p = not significant). In patients with myocardial infarction, a significant increase in MPI was noted on the first day of myocardial infarction between normal and infarcted myocardium (20.4 ± 2.0 vs 24.3 ± 2.3, p < 0.05) and progressively increased thereafter until day 14 (20.5 ± 1.7 vs 31.9 ± 3.7, p < 0.05). In conclusion, two-dimensional echocardiograms, which were obtained when the transducer was placed on the chest wall and digital image processing was performed, enabled the differentiation of normal myocardium from infarcted myocardium in its early stages. This technique may be clinically useful, especially when conventional electrocardiography does not provide a diagnosis.

EAMI—Exercise Training in Anterior Myocardial Infarction: An Ongoing Multicenter Randomized Study : Preliminary Results on Left Ventricular Function and Remodeling

To determine the effects of a 6-month exercise training program on left ventricular (LV) function and remodeling, 49 consecutive patients (pts) with first Q anterior myocardial infarction (51 ± 8 years), in I-II NYHA class, were studied 4 to 8 weeks after the acute episode and 6 months later by 2D-ECHO and upright bicycle ergometric test. At entry, pts were randomly allocated to physical training (T = 25pts) or control (C = 24pts). Global endocardial surface area (ESA), LV volumes and EF, extent of abnormal wall motion (%WMA), of regional dilatation (%REG DIL), and the shape distortion (DIST) index were analyzed. After 6 months, a significant increase in work capacity (4,589 ± 1,417 to 5,379 ± 1,485 KPM/min, p<0.03) and in lactic anaerobic threshold (45 ± 13 to 63 ± 15 W, p<0.01) was observed only in T. Initial ESA, EDV, EF, %WMA, %REG DIL, and DIST index were similar and they did not change after 6 months in both groups. However, pts with <40%EF had greater (p<0.0001) EDV and %WMA with marked DIST index at entry and showed further (p<0.01) deterioration after 6 months both in C and in T (EDV, ml/ m 2 Erlebacher JA Weiss JL Weisfeldt ML Bulkley BH Early dilatation of the infarcted segment in acute transmural myocardial infarction: role of infarct expansion in acute left ventricular enlargement.. J Am Coll Cardiol. 1984; 4: 201-208 Abstract Full Text PDF PubMed Scopus (209) Google Scholar : 68 ± 12 to T7 ± 18 in C, 71 ± 12 to 74 ± 18 in T; %REG DIL: 39 ± 20 to 49 ± 24 in C, 32 ± 12 to 35 ± 23 in T; DIST index: 0.16 ± 0.07 to 0.21 ± 0.09 in C, 0.2 ± 0.07 to 0.22 ± 0.1 in T). These variables did not change in pts with >40%EF. Thus, from these preliminary data, pts with <40%EF at entry are prone to further global and regional LV deterioration. Physical training does not seem to increase this spontaneous deterioration. To determine the effects of a 6-month exercise training program on left ventricular (LV) function and remodeling, 49 consecutive patients (pts) with first Q anterior myocardial infarction (51 ± 8 years), in I-II NYHA class, were studied 4 to 8 weeks after the acute episode and 6 months later by 2D-ECHO and upright bicycle ergometric test. At entry, pts were randomly allocated to physical training (T = 25pts) or control (C = 24pts). Global endocardial surface area (ESA), LV volumes and EF, extent of abnormal wall motion (%WMA), of regional dilatation (%REG DIL), and the shape distortion (DIST) index were analyzed. After 6 months, a significant increase in work capacity (4,589 ± 1,417 to 5,379 ± 1,485 KPM/min, p<0.03) and in lactic anaerobic threshold (45 ± 13 to 63 ± 15 W, p<0.01) was observed only in T. Initial ESA, EDV, EF, %WMA, %REG DIL, and DIST index were similar and they did not change after 6 months in both groups. However, pts with <40%EF had greater (p<0.0001) EDV and %WMA with marked DIST index at entry and showed further (p<0.01) deterioration after 6 months both in C and in T (EDV, ml/ m 2 Erlebacher JA Weiss JL Weisfeldt ML Bulkley BH Early dilatation of the infarcted segment in acute transmural myocardial infarction: role of infarct expansion in acute left ventricular enlargement.. J Am Coll Cardiol. 1984; 4: 201-208 Abstract Full Text PDF PubMed Scopus (209) Google Scholar : 68 ± 12 to T7 ± 18 in C, 71 ± 12 to 74 ± 18 in T; %REG DIL: 39 ± 20 to 49 ± 24 in C, 32 ± 12 to 35 ± 23 in T; DIST index: 0.16 ± 0.07 to 0.21 ± 0.09 in C, 0.2 ± 0.07 to 0.22 ± 0.1 in T). These variables did not change in pts with >40%EF. Thus, from these preliminary data, pts with <40%EF at entry are prone to further global and regional LV deterioration. Physical training does not seem to increase this spontaneous deterioration.

Anteroseptal myocardial infarction clinically mimicking right ventricular infarction

Acute transmural anteroseptal myocardial infarction with acute left ventricular failure can also raise systemic venous pressure in the absence of right ventricular infarction. Right ventricular infarction, therefore, should not be diagnosed simply by the presence of systemic venous congestion.

Thrombolysis in postinfarction angina

Postinfarction angina carries a poor prognosis, with a 20–70% incidence of recurrent myocardial infarction (MI) or death within the subsequent 3–6 months. The pathophysiologic mechanisms causing postinfarction angina may include thrombus, complex coronary arterial lesions that form a nidus for thrombus formation, inadequate collateral supply following acute MI, or intimal endothelial dysfunction. The role of thrombus has been established in the pathophysiology of Q-wave MI, and thrombolytic treatment of patients presenting with acute transmural MI has been shown to salvage left ventricular function and to reduce mortality. However, thrombolytic therapy for the acute MI does not reduce the incidence of recurrent ischemia or infarction, as is evident from the 18–26% incidence of recurrent ischemia reported in the Thrombolysis and Angioplasty in Myocardial Infarction (TAMI) and Thrombolysis in Myocardial Infarction (TIMI) trials. In the Gruppo Itaiiano per lo Studio della Streptochinasi nell Infarto Miocardico (GISSI) study the incidence of reinfarction was documented as 4% in the streptokinase group, which was actually significantly greater than in the placebo group (2%). In a randomized placebo-controlled study of thrombolysis for postinfarction angina, 29 patients were randomized to placebo (P group, n = 17) or to thrombolytic therapy (T group, n = 12). Patient groups were similar with respect to age, location of MI, ejection fraction, severity of coronary artery disease, and antianginal therapy. Patients underwent coronary angtography 6 ± 1 days postinfarction. Filling defects consistent with intracoronary thrombus was seen in 11 of 12 T group patients and in 11 of 17 P group patients prior to treatment. Lysis occurred in 7 of 11 T patients and 1 of 11P (p < 0.02). Holter-detected silent ischemia was compared pre- and posttherapy. Of patients with pretherapy Holter studies, silent ischemia occurred in 8 of 15 P patients (1.7 ± 0.33 episodes/24 hr, lasting 27.9 ± 12.1 min/24 hr) and in 2 of 9 T patients (0.6 ± 0.4 episodes/24 hr lasting 9.4 ± 3.1 min/24 hr). There was no significant change in the amount of silent ischemia following therapy in either group. Clinical ischemic events occurred in 3 of 12 T patients and in 5 of 17 P patients (no difference between the 2 groups). This study showed that thrombus was commonly seen in patients with postinfarction angina, and thrombolytic therapy could successfully lyse the clot 6 days postinfarction. However, despite achieving successful thrombolysis, in patients who were already receiving an intensive antianginal regimen for postinfarction angina, thrombolytic therapy did not result in an improvement in Holter-detected or clinical ischemia.

Prevalence of non-Q-wave acute myocardial infarction with total angiographic occlusion of the left circumflex coronary artery within eight weeks of infarction

The genesis of Q waves in acute myocardial infarction (AMI) has been associated with complete occlusion of the infarct-related coronary artery by coronary arteriography and autopsy studies. 1 In contrast, subtotal coronary stenosis is described in association with non-Q-wave AMI. 2 Mapping studies of depolarization sequences in the isolated human heart show late activation of the lateral and posterobasal walls (≤70 ms after the earliest ventricular sites of excitation). 3 Transmural AMI involving these regions may result in no Q-wave genesis owing to this late activation sequence. Earlier studies that relate Q waves to transmural lateral AMI involved necropsy data. These studies are more likely biased toward large infarctions than clinical studies in living patients. This report evaluates the incidence of Q-wave AMI in patients with acute complete occlusion of the left circumflex coronary artery.

Effect of early programmes of high and low intensity exercise on physical performance after transmural acute myocardial infarction.

Does a programme of light exercise training after acute myocardial infarction produce the same improvement in treadmill performance as aerobic exercise training? Three hundred and eight men from a consecutive series of 479 men with transmural (Q wave) acute myocardial infarction, admitted to a single coronary care unit, were randomly allocated to eight weeks of group aerobic exercise training or group light exercise. Groups were well matched for all characteristics other than site of infarction, which did not significantly affect results. Mean (SD) physical working capacity (metabolic equivalents) determined by treadmill testing at the start of the study (in the third week after infarction) was 6.8 (2.2) v 6.7 (2.5) METs, at the end (in the eleventh week after infarction) 10.8 (2.3) v 9.9 (2.4) METs, and at 12 month review 10.8 (2.4) v 10.7 (1.9) METs for the exercise training group and the light exercise group respectively. The difference of 0.9 METs at the end of the study was the only significant difference between groups. There were no significant intergroup differences at any stage in resting and maximal heart rate, resting and maximal systolic blood pressure, or rate-pressure product. Apart from a small temporarily greater physical working capacity, the physical benefits of aerobic exercise training were equally well achieved by group light exercise.