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ST-segment analysis to predict infarct size and functional outcome in acute myocardial infarction treated with primary coronary intervention and adjunctive abciximab therapy.

ST-segment resolution is used to classify the response to reperfusion therapy in acute myocardial infarction, but the possibility to predict outcome in individual patients is unclear, particularly in the setting of primary percutaneous coronary intervention (PCI) and abciximab therapy. We studied 213 patients who underwent successful revascularization with PCI. Maximal ST-segment elevation was measured before and 30 minutes after PCI. Patient outcome was defined on the basis of infarct size and left ventricular ejection fraction (EF) as derived from gated single-photon emission computed tomography that was acquired 1 month after infarction. Patients who had > or =50% ST resolution showed a smaller infarct (15.1 +/- 13.6% vs 19.9 +/- 15.7%, p < 0.05) but not a higher left ventricular EF (48.7 +/- 12.3% vs 45.2 +/- 11.8%) than did patients who had <50% resolution. According to cluster analysis of infarct size and left ventricular EF, 132 patients had favorable outcome (central values: infarct size 7.5%, left ventricular EF 55%) and 81 did not (central values: infarct size 30%, left ventricular EF 36%). Using receiver-operating characteristic curve analysis, the optimal ST-resolution cutoff was >60%, with 77% sensitivity and 51% specificity for predicting favorable outcome. ST-segment elevation < or =4.5 mV before PCI was 80% sensitive and 48% specific, and ST-segment elevation < or =1 mV after PCI was 74% sensitive and 60% specific for predicting favorable outcome. In conclusion, in the setting of primary PCI and abciximab therapy, ST-segment elevation resolution requires a high threshold (>60%) to effectively classify patients; the capability of ST-segment analysis to predict patient outcome is limited, with ST-segment elevation after PCI showing the best compromise between sensitivity and specificity.

Abciximab↗

Macrophage migration inhibitory factor and the risk of myocardial infarction or death due to coronary artery disease in adults without prior myocardial infarction or stroke: the EPIC-Norfolk Prospective Population study.

PURPOSE: To determine whether plasma levels of macrophage migration inhibitory factor, a proinflammatory cytokine involved in atherogenesis, are predictive of myocardial infarction or death from coronary artery disease. METHODS: We performed a prospective case-control study nested in the European Prospective Investigation into Cancer and Nutrition (EPIC)-Norfolk cohort. We selected men and women who did not report a history of myocardial infarction or stroke at baseline. Baseline concentrations of macrophage migration inhibitory factor were measured among 777 patients who had a myocardial infarction or died of coronary artery disease during follow-up, and 1554 matched controls who remained free of coronary artery disease. RESULTS: Baseline macrophage migration inhibitory factor concentrations were higher in cases than controls (median, 107.4 microg/L vs. 90.7 microg/L, P = 0.001). The risk of myocardial infarction or death from coronary artery disease increased with increasing quartiles of macrophage migration inhibitory factor (P for linearity <0.0001). Patients in the highest quartile had the greatest likelihood of myocardial infarction or death due to coronary artery disease (unadjusted odds ratio [OR] = 1.6; 95% confidence interval [CI]: 1.2 to 2.0). After adjustment for traditional risk factors and C-reactive protein level, the odds ratio decreased slightly (OR = 1.3; 95% CI: 1.0 to 1.7). Upon additional adjustment for white cell count, this association was no longer statistically significant. CONCLUSION: Prospective data suggest that the relation between macrophage migration inhibitory factor and the risk of myocardial infarction or death due to coronary artery disease in adults without a history of myocardial infarction or stroke is not very strong. However, the data support a regulatory role for macrophage migration inhibitory factor in the process of atherosclerosis.

Adult↗

Metabolic syndrome in patients with acute myocardial infarction is associated with increased infarct size and in-hospital complications.

BACKGROUND: Metabolic syndrome (MS), the combination of hypertension, obesity, dyslipidemia, and insulin resistance, is a precursor of diabetes mellitus (DM) and highly prevalent among patients with acute myocardial infarction (AMI). Diabetes mellitus is associated with larger infarct size and worse outcomes after AMI. This study examined infarct size and short-term outcomes among nondiabetic patients with MS following contemporary treatment of AMI. METHODS: Four hundred five consecutive patients with AMI treated with primary percutaneous coronary intervention were evaluated. Patients with diabetes (n=105) were excluded. Those with MS (n=167) included patients with three or more of the following criteria: hypertension, elevated fasting blood glucose, hypertriglyceridemia, low high-density lipoprotein, and obesity [body mass index (BMI)> or =30]. The control group (n=133) included patients without MS or DM. RESULTS: Baseline characteristics were similar except for hypertension, BMI, and dyslipidemia, which by study design were higher in the MS group. The MS group had larger infarct size as determined by peak creatine kinase-MB (79.8+/-133.8 vs. 30.84+/-51.5, P<.001). Overall in-hospital complications were higher in patients with MS (21.1% vs. 9.2%, P=.003). Metabolic syndrome is associated with a 10-fold increased risk of acute renal failure after myocardial infarction (7.9% vs. 0.8%, P=.007). CONCLUSION: Metabolic syndrome in nondiabetic patients with AMI is associated with larger infarct size, more in-hospital complications, and a marked increase of acute renal failure. Awareness of MS and preventative measures is crucial in this population to minimize infarct size and decrease morbidity after AMI.

Acute Kidney Injury↗

Characterization of the infarct substrate and ventricular tachycardia circuits with noncontact unipolar mapping in a porcine model of myocardial infarction.

BACKGROUND: Conventional mapping of ventricular tachycardia (VT) after myocardial infarction is limited in patients with hemodynamically untolerated or noninducible VT. OBJECTIVES: The purpose of this study was to develop a unique strategy using noncontact unipolar mapping to define infarct substrate and VT circuits. METHODS: Dynamic substrate mapping (DSM) was performed in seven pigs with healed anterior myocardial infarction. This technique defined substrate as the intersection of low-voltage areas identified in sinus rhythm and during pacing around the infarct. Pacing was also performed within the substrate to determine exit sites. RESULTS: Anteroapical transmural scar was identified in all animals. A mean of three pacing sites was used for substrate definition. The mean area (+/- SD) was 18.4 +/- 8.8 cm2 by DSM and 15.4 +/- 6.9 cm2 by pathology (P >.5). A mean of 4.5 sites was paced within substrate. Ten of 18 paced wavefronts exited substrate adjacent to the pacing area, seven exited at distant areas, and one had two exits. VT was induced in five animals (1.6 morphologies per animal). Except for one VT, circuit exit sites were identified at substrate borders on the endocardium. VT exit sites were at (n = 6) or near (n = 3) a pacing exit site. Electrogram voltages differed significantly between substrate, border, and nonsubstrate areas in infarcted animals and in comparison with control animals. No substrate was identified in two control animals. CONCLUSION: DSM is a reliable method for infarct substrate localization in this model. Pacing within substrate can predict VT exit sites and may prove useful for ablation of unmappable VT after myocardial infarction.

Animals↗

Exercise-induced prolongation of the infarct-related Q-waves as a marker of myocardial viability in the infarcted area.

OBJECTIVE: It is known that exercise-induced ischemia in patients with coronary artery disease (CAD) may produce QRS prolongation in the surface electrocardiogram (ECG). To investigate the presence of exercise-induced Q-wave prolongation in patients with single-vessel CAD and Q-wave myocardial infarction (MI), in association with the presence of reversible perfusion defects during thallium scintigraphy in the infarcted area. METHODS: 107 consecutive patients (89 males, mean age 56+/-8 years) were evaluated. All patients underwent coronary arteriography, maximal treadmill exercise testing and thallium-201 scintigraphy. Q-wave duration was measured both before exercise testing and during maximal heart rate from 12-lead ECGs recorded with a paper speed of 50 mm/s. RESULTS: Only 57 out of the 107 studied patients showed reversible perfusion defects in the infarcted area during thallium scintigraphy. Q-wave duration was significantly increased from the resting to the stress ECG (DeltaQ-wave duration) in patients with reversible perfusion defects in the infarcted areas (10+/-13 ms), but not in patients with fixed defects in the infarcted zone (-2.0+/-5 ms, p<0.01). The sensitivities and the specificities of Q-wave prolongation, ST segment elevation, and the combination of ST segment elevation with ST segment depression in the reciprocal leads for the detection of myocardial viability in the infarcted area were 82%, 48%, 29% and 88%, 50%, and 90%, respectively. CONCLUSIONS: Exercise-induced Q-wave prolongation is demonstrated in those patients with single-vessel CAD and a recent MI who show reversible perfusion defects in thallium scintigraphy. Exercise-induced Q-wave prolongation was found to be a sensitive and specific ECG marker for the detection of myocardial viability in the infarcted area.

Aged↗

Macrophage colony-stimulating factor treatment after myocardial infarction attenuates left ventricular dysfunction by accelerating infarct repair.

OBJECTIVES: We aimed to determine the effects of macrophage colony-stimulating factor (M-CSF) and granulocyte colony-stimulating factor (G-CSF) treatment on both the repair process and ventricular function after myocardial infarction (MI). BACKGROUND: The M-CSF and G-CSF have multiple potential effects on cells involved in wound repair. METHODS: Myocardial infarction was induced by 45- or 90-min coronary occlusion and reperfusion in rats with or without subsequent injection of M-CSF (10(6) IU/kg/day) or G-CSF (50 microg/kg/day) for five days. We examined histology and messenger ribonucleic acid (mRNA), and assessed left ventricular function in situ using a conductance catheter. RESULTS: Five days after MI, M-CSF increased the number of ED-1-positive cells, mRNA levels of transforming growth factor-beta-1, collagen I and III, and collagen fibers within the infarct. Fourteen days after MI, induced by 45-min ischemia, left ventricular end-systolic elastance (Ees) was reduced (1,191 +/- 87 mm Hg/ml vs. 1,812 +/- 150 mm Hg/ml) and both isovolumic relaxation time constant (tau) (11.9 +/- 0.9 ms vs. 8.5 +/- 0.4 ms) and left ventricular end-diastolic volume (LVEDV) (0.225 +/- 0.014 ml vs. 0.172 +/- 0.011 ml) increased versus sham-operated rats. These alterations after MI were attenuated by M-CSF (Ees = 1,650 +/- 146, tau = 9.7 +/- 0.7, LVEDV = 0.199 +/- 0.012) but not by G-CSF. This beneficial effect of M-CSF on Ees was also detected in hearts with MI induced by 90-min ischemia. Furthermore, M-CSF increased collagen content within infarcts and reduced the proportion of thin collagen fibers 14 days after MI. The Ees significantly correlated with infarct collagen content. Nevertheless, neither M-CSF nor G-CSF modified infarct size. CONCLUSIONS: The M-CSF treatment attenuates deterioration of left ventricular function after MI by accelerating infarct repair.

Animals↗

Rheolytic thrombectomy with percutaneous coronary intervention for infarct size reduction in acute myocardial infarction: 30-day results from a multicenter randomized study.

OBJECTIVES: The goal of this work was to determine whether rheolytic thrombectomy (RT) as an adjunct to primary percutaneous coronary intervention (PCI) reduces infarction size and improves myocardial perfusion during treatment of ST-segment elevation myocardial infarction (STEMI). BACKGROUND: Primary PCI for STEMI achieves brisk epicardial flow in most patients, but myocardial perfusion often remains suboptimal. Distal embolization of thrombus during treatment may be a contributing factor. METHODS: This prospective, multicenter trial enrolled 480 patients presenting within 12 h of symptom onset and randomized to treatment with RT as an adjunct to PCI (n = 240) or to PCI alone (n = 240). Visible thrombus was not required. The primary end point was infarct size measured by sestamibi imaging at 14 to 28 days. Secondary end points included final Thrombolysis In Myocardial Infarction (TIMI) flow grade, tissue myocardial perfusion (TMP) blush, ST-segment resolution, and major adverse cardiac events (MACE), defined as the occurrence of death, new Q-wave myocardial infarction, emergent coronary artery bypass grafting, target lesion revascularization, stroke, or stent thrombosis at 30 days. RESULTS: Final infarct size was higher in the adjunct RT group compared with PCI alone (9.8 +/- 10.9% vs. 12.5 +/- 12.13%; p = 0.03). Final TIMI flow grade 3 was lower in the adjunct RT group (91.8% vs. 97.0% in the PCI alone group; p < 0.02), although fewer patients had baseline TIMI flow grade 3 in the adjunct RT group (44% vs. 63% in the PCI alone group; p < 0.05). There were no significant differences in TMP blush scores or ST-segment resolution. Thirty-day MACE was higher in the adjunct RT group (6.7% vs. 1.7% in the PCI alone group; p = 0.01), a difference primarily driven by very low mortality rate in patients treated with PCI alone (0.8% vs. 4.6% in patients treated with adjunct RT; p = 0.02). CONCLUSIONS: Despite effective thrombus removal, RT with primary PCI did not reduce infarct size or improve TIMI flow grade, TMP blush, ST-segment resolution, or 30-day MACE.

Adult↗

Beneficial effect of residual flow to the infarct region on left ventricular volume changes after acute myocardial infarction.

To determine the relationship between alterations in left ventricular (LV) volumes and residual flow to the infarct region after myocardial infarction (MI), 57 patients with a first acute transmural MI underwent two-dimensional echocardiography within 48 hours of infarction and after 1 month. A reduction in ST segment elevation by greater than or equal to 35% of the peak value of ST segment elevation within the initial 6 hours was used as an indirect indicator for early reperfusion of the infarct-related artery (IRA). IRA patency and collateral circulation were assessed by coronary arteriography performed at 1 month. LV volumes increased in patients with a persistent ST segment elevation within the initial 6 hours of infarction and in those with a totally occluded IRA without collaterals. However, LV volumes were unchanged in patients with early reperfusion and in those who had subtotally occluded IRA or who had collateral circulation. LV dilation (greater than or equal to 20% increase in end-diastolic volume) occurred less often when early reperfusion and angiographically patent IRA or collateral supply to the infarct zone were present. This prospective study indicates that residual flow to the infarct region may exert a beneficial effect on LV volume changes after acute MI.

Cardiac Catheterization↗

Complex stenosis morphology predicts late reocclusion during follow-up after myocardial infarction in patients with patent infarct-related coronary arteries.

BACKGROUND: Whether angiographic morphology of infarct-related residual stenoses continues to affect prognosis after discharge is not known. METHODS: We studied 175 patients after their myocardial infarction who required nonurgent coronary angioplasty for residual myocardial ischemia. The findings at diagnostic coronary angiography were compared with those before angioplasty (mean of 7 months later). Infarct-related stenoses were classified as complex or smooth. Stenosis progression was defined as >0.5 mm diameter reduction. RESULTS: One hundred twenty-one (69%) infarct-related stenoses were complex. At restudy, total occlusion was found in 41 (35%) of the infarct-related complex stenoses compared with 7 (13%) smooth stenoses (P = .001). Reocclusion occurred in 16 (55%) of 29 complex infarct-related stenoses with thrombus, compared with 25 (28%) of 88 without thrombus (P = .01). During follow-up, 46 patients (26%) had cardiac events. Of these, 70% had complex lesions at study entry compared with 30% smooth (P < .05). CONCLUSIONS: Residual angiographically complex stenoses after an uncomplicated myocardial infarction are associated with a greater risk of reocclusion and may predispose to coronary events at follow-up.

Adult↗

Early patency of the infarct-related artery after myocardial infarction preserves diastolic filling.

A patent infarct-related artery (IRA) following myocardial infarction has been associated with lower mortality, increased systolic function, decreased left ventricular remodeling, and electrical stability. The purpose of this study was to determine whether coronary artery patency early after myocardial infarction is associated with greater early diastolic filling than a closed artery. Radionuclide ventriculograms were performed at a central laboratory on 167 patients who received alteplase for an acute myocardial infarction and had infarct artery patency determined by cardiac catheterization. The peak early filling rate (PEFR) was assessed by 4 different methods: (1) PEFR (EDV/s)--normalized to the end-diastolic volume; (2) PEFR (SV/s)--normalized to the stroke volume; (3) PEFR (ml/s/m(2))--an absolute diastolic filling rate; and (4) PEFR (PER)--normalized to the peak ejection rate. Patients with a closed IRA (n = 16, Thrombolysis In Myocardial Infarction [TIMI] 0 or 1 flow) and patients with an open IRA (n = 151, TIMI 2 or 3 flow) had similar ages, ejection fractions, and cardiac volumes. However, among patients with an occluded IRA, the PEFR was decreased by 12% to 18% by the 4 measures of diastolic filling (3 of 4 methods, p <0.05). PEFR (EDV/s) was 1.69 +/- 0.9 in the occluded group versus 2.06 +/- 0.4 EDV/s in the open artery group (p = 0.005). By multivariate analysis, IRA patency was an independent predictor of the PEFR by all 4 methods. Early coronary artery patency after an acute myocardial infarction preserves diastolic filling. Improved diastolic function may in part explain part of the long-term benefits of a patent IRA after thrombolytic therapy when there is no documented improvement in the ejection fraction.

Female↗

Significance of spontaneous normalization of negative T waves in infarct-related leads during healing of anterior wall acute myocardial infarction.

This study was conducted to elucidate the significance of spontaneous normalization of negative T waves in infarct-related leads during the chronic phase of anterior wall acute myocardial infarction. Results of this study indicate that patients with spontaneous normalization of negative T waves in infarct-related leads between 1 and 6 months after anterior wall acute myocardial infarction have smaller infarct size, decreased left ventricular dysfunction, and greater improvement in left ventricular wall motion in the infarct area, suggesting that T-wave normalization represents functional recovery of viable myocardium in the infarct area.

Biomarkers↗

Predictors of coronary artery disease in patients with cocaine-associated myocardial infarction. Cocaine-Associated Myocardial Infarction (CAMI) Study Group.

PURPOSE: To identify clinical criteria predictive of underlying coronary artery disease in patients with cocaine-associated myocardial infarction. PATIENTS AND METHODS: Using a retrospective cross-sectional study design at 29 acute care hospitals, we identified 70 patients with cocaine-associated myocardial infarction who had a determination of the presence or absence of coronary artery disease. Clinical characteristics of patients with coronary artery disease (> 50% stenosis on cardiac catheterization or reversible ischemia on stress test) were compared with patients without coronary artery disease (< 50% stenosis on cardiac catheterization). RESULTS: Compared with patients without coronary artery disease (n = 21), patients with coronary artery disease (n = 49) were older (42 versus 31 years; P < 0.001), had more traditional cardiac risk factors (2.3 versus 1.5; P < 0.001), more frequent history of hypertension (odds ratio [OR], 5.3; 95% confidence interval [CI], 1.4 to 20.4); more frequent family history of myocardial infarction (OR, 4.4; 95% CI, 1.3 to 15.1), more bradydysrhythmias (OR, 8.0; 95% CI, 1.0 to 65.5), and more likely to have an inferior infarct location (P = 0.04). CONCLUSION: Age, number of cardiac risk factors, location of myocardial infarction, and bradydysrhythmias predict underlying coronary artery disease in patients with cocaine-associated myocardial infarction. If validated, this knowledge may be used to develop a medically appropriate, cost-effective evaluation strategy for patients following cocaine-associated myocardial infarction.

Adult↗

The Na(+)/H(+) exchange inhibitor eniporide as an adjunct to early reperfusion therapy for acute myocardial infarction. Results of the evaluation of the safety and cardioprotective effects of eniporide in acute myocardial infarction (ESCAMI) trial.

OBJECTIVES: We conducted an international, prospective, randomized, double-blind, placebo-controlled phase 2 trial in patients undergoing thrombolytic therapy or primary angioplasty for acute ST-elevation myocardial infarction (MI) to investigate the effect of eniporide on infarct size and clinical outcome. BACKGROUND: Experimental studies suggest that the activity of the Na(+)/H(+) exchange (NHE) plays an important role in the unfavorable sequels of myocardial ischemia and reperfusion. Eniporide specifically inhibits the NHE-1 isoform and has been shown to limit infarct size in experimental models. METHODS: The primary efficacy end point was the infarct size measured by the cumulative release of alpha-hydroxybutyrate dehydrogenase (alpha-HDBH) (area under the curve [AUC] 0 to 72 h). In stage 1, 50, 100, 150 or 200 mg eniporide given as a 10-min infusion before start of reperfusion therapy were compared with placebo in 430 patients, and in stage 2, 100 and 150 mg eniporide were compared with placebo in 959 patients. RESULTS: In stage 1, the administration of 100 mg and 150 mg eniporide resulted in smaller infarct sizes (mean alpha-HBDH AUC in U/ml x h, placebo: 44.2, 100 mg eniporide: 40.2, 150 mg eniporide: 33.9), especially in the angioplasty group. In contrast, in stage 2 there was no difference in the enzymatic infarct size between the three groups (placebo: 41.2, 100 mg eniporide: 43.0, 150 mg eniporide: 41.5). Overall there was no effect of eniporide on clinical outcome (death, cardiogenic shock, heart failure, life-threatening arrhythmias). However, there was a significant reduction of the incidence of heart failure in patients reperfused late (>4 h). CONCLUSIONS: In this large study administration of the NHE-1 inhibitor eniporide, before reperfusion therapy in patients with acute ST elevation MI, did not limit infarct size or improve clinical outcome.

Adult↗

The prognostic significance of first myocardial infarction type (Q wave versus non-Q wave) and Q wave location. The Multicenter Diltiazem Post-Infarction Research Group.

The prognostic significance of the type of first acute myocardial infarction (Q wave versus non-Q wave) and Q wave location (anterior versus inferoposterior) was determined from a multicenter data base involving 777 placebo-treated patients who were participants in the Multicenter Diltiazem Post-Infarction Trial. There were 224 patients (29%) with a non-Q wave infarction, 326 (42%) with an inferoposterior Q wave infarction and 227 (29%) with an anterior Q wave infarction. Mean left ventricular ejection fraction was significantly (p less than 0.001) lower in patients with an anterior Q wave infarction than in the other two groups (anterior Q wave 0.39; inferior Q wave 0.52; non-Q wave 0.53). Nevertheless, the total cardiac mortality rate during the follow-up period (average 25 months per patient) was only marginally higher (p = 0.42) in the anterior Q wave group (8.4%) than in the other two groups (inferoposterior Q wave 7.1%; non-Q wave 6.3%). The total first recurrent cardiac event was somewhat higher (p = 0.08) in the anterior Q wave group (18.1%) than in the other two groups (inferoposterior Q wave 11.7%; non-Q wave 15.6%). Survivorship analyses extending over 3 years revealed that electrocardiographic classification of the type of first infarction and Q wave location did not make significant independent contributions to the risk of postinfarction cardiac death or first recurrent cardiac event, either before or after adjustment for baseline clinical variables.

Adult↗

Fate of patients with acute myocardial infarction with patency of the infarct-related vessel achieved with successful thrombolysis versus rescue angioplasty.

Patients with failure of infarct-related artery recanalization after thrombolytic therapy have a poor clinical outcome. These patients have been considered for rescue angioplasty 90 min after thrombolytic therapy at the time of emergency catheterization in the course of five Thrombolysis and Angioplasty in Myocardial Infarction (TAMI) trials. The outcome of 776 patients with patent infarct-related vessels after emergency catheterization was analyzed--607 with thrombolysis-mediated patency of the infarct-related vessel and 169 with patency achieved by angioplasty. Baseline characteristics of the thrombolysis and angioplasty patency groups were similar except for a higher acute left ventricular ejection fraction (51.3% versus 48.2%) in the thrombolysis group (p = 0.003). Seven to 10 day left ventricular ejection fraction was higher (52.3% versus 48.1%), infarct zone functional recovery was greater (0.44 versus 0.21 standard deviation/chord, or 18% versus 7%, p = 0.001) and reocclusion was less (11% versus 21%) in the thrombolysis compared with the angioplasty group. Despite these differences, angioplasty patency was associated with the same low in-hospital mortality rate (5.9% versus 4.6%) and long-term mortality rate (3% versus 2%) as thrombolysis patency. Reocclusion adversely affected the mortality rate and ventricular functional recovery. Technical failure of rescue angioplasty was associated with a much higher mortality rate than was technical success (39.1% versus 5.9%). Thrombolysis patency was preferable to angioplasty patency after thrombolytic therapy in acute myocardial infarction, but both were associated with the same low in-hospital and long-term mortality rates, suggesting that rescue angioplasty is beneficial in some patients with failure of infarct-related artery recanalization after thrombolytic therapy.

Angioplasty, Balloon, Coronary↗

First transit and equilibrium radionuclide angiography in patients with inferior transmural myocardial infarction: criteria for the diagnosis of associated hemodynamically significant right ventricular infarction.

To define radionuclide criteria for identifying hemodynamically significant right ventricular infarction, 33 consecutive men with inferior transmural infarction were evaluated prospectively by right heart catheterization and first transit and equilibrium radionuclide angiography within 36 hours of the onset of symptoms. Hemodynamically significant right ventricular infarction was present in 6 of the 33 patients (Group I); the remaining 27 patients did not demonstrate the hemodynamics characteristic of right ventricular infarction (Group II). A right ventricular ejection fraction of less than 40% separated Group I and Group II patients by equilibrium (p = 0.003) but not by first transit (p = NS) radionuclide angiography. However, a right ventricular ejection fraction of less than 35% separated Group I and II patients by both techniques (p = 0.02 and p = 0.005, respectively). The presence of a right ventricular regional wall motion abnormality on either first transit or equilibrium radionuclide angiograms separated Group I and II patients (p less than 0.001). The combination of both a right ventricular ejection fraction of less than 40% and a regional wall motion abnormality separated Group I and II patients using either equilibrium (p less than 0.001) or first transit (p = 0.02) radionuclide angiography. It is concluded that in patients with acute inferior transmural myocardial infarction, a right ventricular regional wall motion abnormality alone or in combination with a right ventricular ejection fraction of less than 40% by either first transit or equilibrium radionuclide angiography is a useful criterion for establishing the presence of hemodynamically significant right ventricular infarction, while its absence argues against the diagnosis of right ventricular infarction.

Aged↗

Influence of treatment delay on infarct size and clinical outcome in patients with acute myocardial infarction treated with primary angioplasty.

OBJECTIVES: The purpose of this analysis was to determine the influence of an additional treatment delay inherent in transfer to an angioplasty center for primary angioplasty of patients with acute myocardial infarction who are first admitted to hospitals without angioplasty facilities. BACKGROUND: Several randomized trials have demonstrated the benefits of primary angioplasty in acute myocardial infarction. In recent years, increasing numbers of patients with myocardial infarction, initially admitted to hospitals without angioplasty facilities are transported to our hospital for primary angioplasty. However, the additional delay due to the transport may have a deleterious effect on infarct size and clinical outcome. METHODS: In a three-year period (December 1993 to November 1996), 207 consecutive patients who were transferred for primary angioplasty were analyzed in a matched comparison with non-transferred patients. Matching criteria were age, sex, infarct location, presentation delay and Killip class. RESULTS: Patients who were transferred had an additional median delay of 43 min. This resulted in a more extensive enzymatic infarct size and a lower ejection fraction measured at 6 months. The rate of angioplasty success defined as TIMI grade 3 flow, and the 6-month mortality rate (7%) were comparable in both groups. CONCLUSIONS: The additional delay had a deleterious effect on myocardial salvage, reflected by a larger infarct size and a lower left ventricular function. However, the patency rate and 6-month clinical outcome were not affected by this delay.

Adult↗

Acute myocardial infarction with isolated ST-segment elevation in posterior chest leads V7-9: "hidden" ST-segment elevations revealing acute posterior infarction.

OBJECTIVES: This study was done to determine whether electrocardiographic (ECG) isolated ST-segment elevation (ST) in posterior chest leads can establish the diagnosis of acute posterior infarction in patients with ischemic chest pain and to describe the clinical and echocardiographic characteristics of these patients. BACKGROUND: The absence of ST on the standard 12-lead ECG in many patients with acute posterior infarction hampers the early diagnosis of these infarcts and thus may result in inadequate triage and treatment. Although 4% of all acute myocardial infarction (AMI) patients reveal the presence of isolated ST in posterior chest leads, the significance of this finding has not yet been determined. METHODS: We studied 33 consecutive patients with ischemic chest pain suggestive of AMI without ST in the standard ECG who had isolated ST in posterior chest leads V7 through V9. All patients had echocardiographic imaging within 48 h of admission, and 20 patients underwent coronary angiography. RESULTS: Acute myocardial infarction was confirmed enzymatically in all patients and on discharge ECG pathologic Q-waves appeared in leads V7 through V9 in 75% of the patients. On echocardiography, posterior wall-motion abnormality was visible in 97% of the patients, and 69% had evidence of mitral regurgitation (MR), which was moderate or severe in one-third of the patients. Four patients (12%), all with significant MR, had heart failure, and one died from free-wall rupture. The circumflex coronary artery was the infarct related artery in all catheterized patients. CONCLUSIONS: Isolated ST in leads V7 through V9 identify patients with acute posterior wall myocardial infarction. Early identification of those patients is important for adequate triage and treatment of patients with ischemic chest pain without ST on standard 12-lead ECG.

Adult↗