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An echocardiographically documented case of right ventricular infarction is reported. Electrocardiographic diagnosis was masked by concomitant true posterior left ventricular infarction. This case highlights an important limitation of electrocardiography in diagnosing 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.
Early administration of thrombolytic agents in acute myocardial infarction lowers mortality and preserves left ventricular function. Currently, only one third of infarct patients receive this treatment, the vast majority being excluded because of restrictive criteria and delayed hospital admission. When correctly administered, thrombolytic therapy achieves reperfusion in 50-85% of occluded vessels. Five to 15% of these initially recanalized vessels eventually reocclude. Possible mechanisms of failure of thrombolytic therapy to induce stable coronary reperfusion include thrombus formation during thrombolysis, platelet activation by thrombolysis, fibrin deposition during thrombolysis, and resistance to thrombolysis. Bleeding complications including intracranial haemorrhage remain a major complication. New therapeutic regimens, new thrombolytic agents and more effective anti-thrombotic drugs, together with intervention strategies that anticipate the time of treatment, promise a significant increase of the overall benefits obtainable with thrombolysis in acute myocardial infarction.
Current limitations of recombinant tissue-type plasminogen activator (rt-PA) therapy for acute myocardial infarction include failure to achieve recanalization in 25% of patients, reocclusion and reperfusion injury. Iloprost, a stable analogue of prostacyclin (PGI2), has been demonstrated to facilitate thrombolysis and reduce myocardial stunning in experimental models. To evaluate combined therapy, rt-PA (100 mg 3 h) and Iloprost (2 ng/kg per min for 48 h) were administered to 25 patients and then rt-PA alone (same dose) was given to an additional 25 patients with evolving myocardial infarction. At 90 min after drug administration, infarct-related vessel patency was observed in 11 (44%) of 25 who received rt-PA plus Iloprost compared with 15 (60%) of 25 who received rt-PA alone (p = 0.26). At 1 week, reocclusion had occurred in 3 (14%) of 21 patients who received combined therapy compared with 6 (26%) of 23 patients treated with rt-PA alone (p = 0.46). Ejection fraction increased significantly from baseline to 7 days for rt-PA alone whereas it decreased with combined therapy (rt-PA alone whereas it decreased with combined therapy (rt-PA alone: 47.3 +/- 11.5% at baseline to 50.4 +/- 9.8% at 7 days; rt-PA plus Iloprost: 51.3 +/- 10.1% at baseline to 49.0 +/- 9.4% at 7 days; difference between groups p = 0.05). At 4 h after therapy, fibrinogen decreased 33% for rt-PA plus Iloprost compared with a 52% for rt-PA alone (p = 0.001). Fibrinogen degradation products increased 60% more for rt-PA alone than for rt-PA plus Ilprost. Thus, the combination of rt-PA plus Iloprost at the doses employed did not improve immediate or follow-up coronary artery patency or left ventricular functional recovery compared with that achieved with rt-PA alone.
To determine whether a weight-adjusted high dose (2 mg/kg body weight over 3 h) rapid infusion of recombinant tissue-type plasminogen activator (rt-PA) was more efficacious than a weight-adjusted standard dose (1.25 mg/kg over 3 h) in achieving reperfusion in the setting of acute myocardial infarction, 175 patients were entered into a randomized multicenter trial. Eighty-four patients were entered into the high dose group, receiving 1.2 mg/kg (10% given as a bolus injection) over 1 h, followed by 0.8 mg/kg over the next 2 h. Ninety-one patients were given 0.75 mg/kg (10% given as a bolus injection) in 1 h, followed by 0.5 mg/kg administered over the next 2 h. The median dose in the group that received 2 mg/kg dose was 145 mg, compared with 100 mg in the group that received 1.25 mg/kg. The 90 min patency rate in the group that received 2 mg/kg was 84% compared with 70% in the group that received 1.25 mg/kg (p = 0.003). Sixty-four percent of the patients in each group underwent coronary angioplasty at the time of cardiac catheterization. The infarct-related artery patency rate at the end of catheterization was 91% in the group that received 2 mg/kg compared with 83% in the group that received 1.25 mg/kg (p = 0.08). Among patients with a patent infarct-related coronary artery after catheterization, the 6 month mortality rate in the group that received 2 mg/kg was 2.9% compared with 9.8% in the group that received 1.25 mg/kg (p = 0.15). The bleeding complication rate in the two groups was similar.(ABSTRACT TRUNCATED AT 250 WORDS)
In view of the high risk of sudden cardiac death and the prognostic importance of complex ventricular ectopic activity, the effects of prophylactic antiarrhythmic treatment were investigated prospectively in patients with persisting asymptomatic complex arrhythmias after myocardial infarction. End points were total mortality and arrhythmic events (sudden death, sustained ventricular tachycardia and ventricular fibrillation). Of 1,220 consecutively screened survivors of myocardial infarction, 312 had Lown class 3 or 4b arrhythmia on 24 h electrocardiographic recordings before hospital discharge and consented to the study. They were randomized to individualized antiarrhythmic treatment (Group 1, n = 100), treatment with low dose amiodarone, 200 mg/day (Group 2, n = 98) or no antiarrhythmic therapy (Group 3 [control group], n = 114). During the 1 year follow-up period, 10 patients in Group 1 died, as did 5 in Group 2 and 15 in Group 3. On the basis of an intention to treat analysis, the probability of survival of patients given amiodarone was significantly greater than that of control patients (p less than 0.05). In addition, arrhythmic events were significantly reduced by amiodarone (p less than 0.01). These effects were less marked and not significant for individually treated patients (Group 1). These findings suggest that low dose amiodarone decreases mortality in the 1st year after myocardial infarction in patients at high risk of sudden death.
OBJECTIVES: The purpose of this study was to determine the incidence of ventricular tachycardia and fibrillation without hypotension or heart failure after treatment with recombinant tissue-type plasminogen activator (rt-PA), anatomic correlates of their development, the effect of immediate intravenous metoprolol on their occurrence and the outcome of patients with these arrhythmias. BACKGROUND: Malignant arrhythmias after thrombolytic therapy have been reported to occur as a result of coronary reperfusion, which is associated with reduced mortality in patients receiving thrombolytic therapy. METHODS: We analyzed data from 2,546 patients in the Thrombolysis in Myocardial Infarction (TIMI) Phase II trial without congestive heart failure or hypotension during the 1st 24 h after study entry. Forty-nine patients (1.9%) developed sustained ventricular tachycardia or ventricular fibrillation within 24 h of study entry (group 1), and 2,497 patients (98.1%) did not (group 2). RESULTS: Baseline characteristics and admission laboratory values were similar in the two groups. In patients undergoing protocol angiography 18 to 48 h after rt-PA, the infarct-related artery was patient in a greater percent of group 2 patients (87% [1,015 of 1,169]) than group 1 patients (68% [15 of 22], p = 0.01), although angiography was performed less frequently in group 1 than in group 2. More group 1 than group 2 patients died within 21 days (20.4%) (1.6%, p < 0.001). For patients surviving to 21 days, there was no difference in mortality between patients in the two groups in the following year. CONCLUSIONS: Ventricular tachycardia and fibrillation are not markers for reperfusion after thrombolytic therapy. These arrhythmias are associated with occlusion, not patency, of the infarct-related artery. Early mortality is increased in patients who develop ventricular tachycardia and fibrillation, even in the absence of congestive heart failure and hypotension.
A new mouse monoclonal antibody that recognizes alpha- and beta-heavy chains of human atrial and ventricular myosin and beta-heavy chain of human slow skeletal muscle myosin was obtained. The 125I- and 111In-labelled antibody, and its F(ab')2 and Fab fragments localize in isoproterenol induced infarcted rat heart, with the F(ab')2 fragment showing the highest uptake. Comparison with 99Tc-pyrophosphate uptake in infarcted dog heart, induced by selective obstruction of a coronary artery, suggest that the 111In-labelled F(ab')2 localizes specifically in infarcted myocardium only.
This review outlines the development and current use of the rat coronary artery ligation model of heart failure. The techniques to ligate the left coronary artery and to obtain morphologic/hemodynamic measurements are described. The authors show how the pathology seen in this model relates to clinical ischemic heart disease. An effort is made throughout the review to relate the changes that occur in this model to clinically relevant observations. For example, the progression to heart failure in these rats is similar to what happens when a patient sustains a large myocardial infarction, survives, but goes on to develop heart failure without another ischemic insult. In both rats and people with large infarctions, the noninfarcted myocardium, even though not damaged at the time of the infarct, cannot compensate sufficiently to prevent the eventual development of heart failure. In addition to being a good approximation of human disease, the responses to pharmacologic interventions, like angiotensin converting enzyme inhibitors, in rats has proved useful in predicting what will happen in humans given the same treatment. More recent data on the molecular control of ventricular remodeling emphasizes how this model will provide important information in the study of integrated physiology by examining biochemical, pharmacologic, and physiologic changes in the same tissue.
BACKGROUND: Results from a number of studies indicate that primary percutaneous coronary intervention (PCI) is superior to fibrinolysis for treatment of acute ST-elevation myocardial infarction. Modern adjunctive antithrombotic treatment with systematic use of low-molecular-weight heparins, fibrin-specific thrombolysis, and glycoprotein IIb/IIIa receptor inhibitors may improve the outcome compared with what was achieved in previous studies. METHODS: Patients with ST-elevation myocardial infarction were randomized to receive enoxaparin followed by reteplase (group A; n = 104) or enoxaparin followed by abciximab and transfer to invasive center for optional PCI (group B; n = 101). Primary end points were ST-segment resolution 120 minutes and TIMI flow at coronary angiography 5 to 7 days after randomization. RESULTS: Forty-two percent of the patients started therapy in the prehospital phase. Time from symptom to treatment was 114 minutes in group A and 202 minutes in group B. Baseline characteristics were similar in the 2 groups. Sixty-four percent in group A and 68% in group B had ST resolution of > 50% at 120 minutes (not significant). At control angiography, 54% in the fibrinolytic group and 71% in the invasive group had TIMI 3 flow (P = .04). At 30 days, the composite of death, stroke, or reinfarction occurred in 8% in the fibrinolytic group compared with 3% in the invasive group (not significant). CONCLUSIONS: Despite much shorter time delay to start of fibrinolysis than PCI, this did not result in signs of superior myocardial reperfusion. Epicardial flow in the infarct-related artery was better after invasive therapy, and there was a trend toward better clinical outcome after this treatment compared with after fibrinolysis.
The present study investigated any seasonal variation in myocardial perfusion, enzymatic infarct size, and 1-year mortality in 1,548 patients who underwent primary angioplasty for ST-segment elevation myocardial infarction. No seasonal variation was observed in patients' demographic and clinical characteristics. No difference was observed in the prevalence of heart failure at presentation and in myocardial perfusion, enzymatic infarct size, and 1-year mortality.
We investigated whether N-terminal pro-brain natriuretic peptide (NT-pro-BNP) that was measured on admission in patients with acute myocardial infarction (AMI) predicts the efficacy of reperfusion or whether NT-pro-BNP provides prognostic information independent of infarct size as estimated by single-photon emission computed tomographic scintigraphy. The study included 174 patients with ST-segment elevation AMI who were admitted within 24 hours of pain onset. NT-pro-BNP level was measured on admission. Paired scintigraphic studies (before and 7 to 14 days after reperfusion) were performed to assess infarct size and define myocardial salvage. One-year clinical follow-up was assessed. Patients were categorized into the high NT-pro-BNP group (57 patients in the upper tertile of NT-pro-BNP) and low NT-pro-BNP group (117 patients in the middle and lower tertiles of NT-pro-BNP). Initial median perfusion defect was 35.0% (interquartile rage 20.0 to 53.0%) of the left ventricle in the high NT-pro-BNP group versus 19.0% (interquartile range 10.0 to 32.2) of the left ventricle in the low NT-pro-BNP group (p <0.001). Median salvage index was 0.36 (interquartile range 0.16 to 0.86) in the high NT-pro-BNP group versus 0.53 (interquartile range 0.31 to 0.75) in the low NT-pro-BNP group (p = 0.22). After adjustment in Cox's proportional hazards model, NT-pro-BNP remained an independent correlate of 1-year mortality (adjusted hazard ratio 2.31, 95% confidence interval 1.09 to 4.89, p = 0.03, high vs low NT-pro-BNP group). In conclusion, NT-pro-BNP measured on admission in patients with AMI correlates with scintigraphic area at risk and predicts prognosis but does not predict the efficacy of mechanical reperfusion by stenting or angioplasty.
It has not been concluded whether there is a relation between pre-myocardial infarction angina pectoris (pre-MIAP) and reperfusion arrhythmia, although pre-MIAP has been reported to have a beneficial effect in preserving left ventricular function. Moreover, factors that are associated with reperfusion arrhythmias in patients with acute myocardial infarction (AMI) who have been successfully reperfused by reperfusion therapy are unknown. This study examined the predictive factors of reperfusion arrhythmias in patients with AMI who underwent successful reperfusion. The Japanese Intervention Trial in Myocardial Infarction study is a prospective, randomized trial that compares the outcome in patients with AMI who undergo intracoronary thrombolysis or primary percutaneous conventional coronary balloon angioplasty. One hundred ten consecutive patients with AMI who had been successfully reperfused in this study were categorized into 2 groups according to whether or not patients showed reperfusion arrhythmias. Multivariate logistic regression analysis was performed using 11 clinical factors to clarify the determinants of reperfusion arrhythmia. Reperfusion arrhythmias developed in 65 of 110 patients (59%). Multivariate logistic regression analysis confirmed that inferior AMI and pre-MIAP were independently associated with reperfusion arrhythmia. The odds ratio that predicted reperfusion arrhythmias was 2.37 (p = 0.0056) for inferior AMI. In contrast, the odds ratio was minimal at 0.24 for pre-MIAP (p = 0.036). In conclusion, pre-MIAP suppresses reperfusion arrhythmias, and inferior AMI is an independent factor for reperfusion arrhythmias.
AIM: To compare the assessment of infarct size using MRI and peak CK value. POPULATION AND METHODS: 16 patients presenting with a first MI and seriall measurement of CK underwent gadolinium-enhanced MRI. RESULTS: A significant correlation was observed between both estimates of infarct size (r=0.56, p=0.0025). In addition, an inverse correlation was found between residual viability and peak CK (r=-0.51; p=0.043). CONCLUSION: After a first episode of MI, infarct size estimate by MRI correlates with that determined by peak CK measurement.
AIMS: We analyzed the usefulness of quantitative intravenous myocardial contrast echocardiography to study microvasculature perfusion after infarction in comparison with intracoronary myocardial contrast echocardiography. METHODS AND RESULTS: Thirty-two patients with a first ST elevation myocardial infarction, single-vessel disease and an open artery (TIMI 3) were studied before discharge. Myocardial perfusion in the risk area was quantified with intracoronary and intravenous myocardial contrast echocardiography. Perfusion was normal (intracoronary contrast echocardiography normalized videointensity >0.75) in 78 out of 97 dysfunctional segments (80%). Sensitivity and specificity of intravenous contrast echocardiography to predict normal perfusion were 87% and 63% for 'first-pass myocardial blood flow' (upslope of contrast arrival x peak intensity after intravenous bolus injection of contrast) and 91% and 89% for end-systolic single-triggered images captured every 6 cycles, respectively. In an analysis per patients, normal perfusion (0 or 1 hypoperfused segments with intracoronary contrast echocardiography) was observed in 22 cases (69%). End-systolic single-triggered images showed a strong correlation with intracoronary contrast echocardiography (R2 = 0.82, p = 0.0001). CONCLUSIONS: Intravenous contrast echocardiography is a useful technique to analyze microvasculature perfusion soon after infarction. A quantitative analysis of single-triggered images is an easy-to-obtain and reliable method to define perfusion when compared with intracoronary contrast echocardiography.
BACKGROUND: To prospectively validate artificial neural network (ANN)-algorithms for early diagnosis of myocardial infarction (AMI) and prediction of 'major infarct' size in patients with chest pain and without ECG changes diagnostic for AMI. METHODS: Results of early and frequent Stratus CS measurements of troponin I (TnI) and myoglobin in 310 patients were used to validate four prespecified ANN-algorithms with use of cross-validation techniques. Two separate biochemical criteria for diagnosis of AMI were applied: TnI > or = 0.1 microg/L within 24 h ('TnI 0.1 AMI') and TnI > or = 0.4 microg/L within 24 h ('TnI 0.4 AMI'). To be considered clinically useful, the ANN-indications of AMI had to achieve a predefined positive predictive value (PPV) > or = 78% and a negative predictive value (NPV) > or = 94% at 2 h after admission. 'Major infarct' size was defined by peak levels of CK-MB within 24 h. RESULTS: For the best performing ANN-algorithms, the PPV and NPV for the indication of 'TnI 0.1 AMI' were 87% (p=0.009) and 99% (p=0.0001) at 2 h, respectively. For the indication of 'TnI 0.4 AMI', the PPV and NPV were 90% (p=0.006) and 99% (p=0.0004), respectively. Another ANN-algorithm predicted 'major AMI' at 2 h with a sensitivity of 96% and a specificity of 78%. Corresponding PPV and NPV were 73% and 97%, respectively. CONCLUSIONS: Specially designed ANN-algorithms allow diagnosis of AMI within 2 h of monitoring. These algorithms also allow early prediction of 'major AMI' size and could thus, be used as a valuable instrument for rapid assessment of chest pain patients.
OBJECTIVES: The purpose of this study was to investigate the hypothesis that circulation via collateral vessels to an infarct-related artery (IRA) is impaired with aging in patients with acute myocardial infarction (AMI). BACKGROUND: Animal experiments have shown that advanced age blunts the development of new vessels in response to angiogenic cytokines. METHODS: Of 3,573 consecutive patients with AMI, 1,934 patients who fulfilled the following criteria were enrolled in this study: 1) coronary angiograms were obtained within 72 h after the onset of AMI; and 2) IRA showed complete occlusion (Thrombolysis In Myocardial Infarction [TIMI] flow grade 0 or 1). Collaterals to the IRA were angiographically evaluated using the Rentrop score. Rentrop scores 1 to 3 were defined as demonstrating significant collaterals. RESULTS: The prevalence of collaterals decreased with age, from 47.9%, 45.8%, 43.4%, to 34.0% in patients <50 years, 50 to 59 years, 60 to 69 years, > or =70 years, respectively (p < 0.001). Advanced age was an independent factor predicting the absence of collateral circulation to the IRA. In contrast, time to catheterization, history of angina pectoris, and preinfarction angina were independent predictors for the presence of collaterals. Multivariate analysis showed that the absence of collaterals was an independent predictor of in-hospital mortality in elderly patients > or =70 years (odds ratio, 15.6; 95% confidence interval, 3.5 to 69.6), although this finding was not significant in patients <70 years. CONCLUSIONS: Advanced age is associated with decreased angiographic presence of collaterals to the IRA in patients with AMI. This abnormality may contribute to the poor prognosis of elderly patients with AMI.
OBJECTIVES: To identify an accurate and reproducible method to define myocardial infarct (MI) size, we conducted a study in a closed-chest canine model of acute myocardial infarction, in which MI size was measured using different thresholding techniques and by imaging at different delay times after contrast administration. BACKGROUND: The MI size by contrast-enhanced magnetic resonance imaging (CE-MRI) is directly related to long-term prognosis. However, previous measurements were done using nonuniform methods and tended to overestimate nonviable areas. METHODS: Thirteen animals underwent 90 min of coronary artery occlusion, followed by reperfusion. The CE-MRI data were acquired within 24 h after reperfusion and compared with triphenyltetrazolium chloride pathology. In the first nine animals, images were obtained approximately 15 min after gadolinium diethylene triamine penta-acetic acid (Gd-DTPA) using an inversion-recovery gradient-echo pulse sequence. To identify the most accurate method, MI size by CE-MRI was measured visually and by semi-automatic thresholding techniques, using different criteria. In four additional animals, images were acquired every 6 min until 30 min after Gd-DTPA. RESULTS: Postmortem MI size was 13.5 +/- 2.6% of left ventricular volume. Semi-automatic techniques, using full-width at half-maximum (FWHM) criterion, correlated best with postmortem data (r(2) = 0.94, p < 0.001; results confirmed by Bland-Altman plots). Using FWHM, there was no difference in MI size between different delay times after contrast (15.2 +/- 2.9% to 14.5 +/- 4.2% at 6 and 30 min, respectively; p = NS). CONCLUSIONS: When an objective technique is used to define MI size by CE-MRI, accurate infarct size measurements can be obtained from images obtained up to 30 min after contrast administration.