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PubMed1998

A comparison of the early outcome of acute myocardial infarction in women and men. The Third International Study of Infarct Survival Collaborative Group.

BACKGROUND: In previous studies, unadjusted comparisons of mortality and major morbidity after acute myocardial infarction have generally indicated that women have a poorer outcome than men. Much larger studies are needed, with more complete adjustment for coexisting conditions, to determine whether this difference is explained by the older age of the women studied or by the presence of other unfavorable prognostic factors, or both. METHODS: As part of the Third International Study of Infarct Survival (ISIS-3), information was collected on deaths during days 0 to 35 and on major clinical events during hospitalization up to day 35 for 9600 women and 26,480 men with suspected acute myocardial infarction who were considered to have a clear indication for fibrinolytic therapy. We compared the outcome among women and men, first without adjustment, then with adjustment for age, and finally with adjustment for other recorded baseline characteristics by means of multiple logistic regression. RESULTS: The unadjusted odds ratio for death among women as compared with men was 1.73 (95 percent confidence interval, 1.61 to 1.86). The women were significantly older than the men, and after adjustment for age the odds ratio was reduced markedly to 1.20 (95 percent confidence interval, 1.11 to 1.29). Adjustment for other differences in base-line clinical features further reduced the odds ratio to 1.14 (95 percent confidence interval, 1.05 to 1.23). Excesses in other major clinical events among women were generally reduced to a similar extent by adjustment. CONCLUSIONS: It seems likely that there is at most only a small independent association between female sex and early mortality and morbidity after suspected acute myocardial infarction.

Adult↗

PubMed1999

Coronary angioplasty with or without stent implantation for acute myocardial infarction. Stent Primary Angioplasty in Myocardial Infarction Study Group.

BACKGROUND: Coronary-stent implantation is frequently performed for treatment of acute myocardial infarction. However, few studies have compared stent implantation with primary angioplasty alone. METHODS: We designed a multicenter study to compare primary angioplasty with angioplasty accompanied by implantation of a heparin-coated Palmaz-Schatz stent. Patients with acute myocardial infarction underwent emergency catheterization and angioplasty. Those with vessels suitable for stenting were randomly assigned to undergo angioplasty with stenting (452 patients) or angioplasty alone (448 patients). RESULTS: The mean (+/-SD) minimal luminal diameter was larger after stenting than after angioplasty alone (2.56+/-0.44 mm vs. 2.12+/-0.45 mm, P<0.001), although fewer patients assigned to stenting had grade 3 blood flow (according to the classification of the Thrombolysis in Myocardial Infarction trial) (89.4 percent, vs. 92.7 percent in the angioplasty group; P=0.10). After six months, fewer patients in the stent group than in the angioplasty group had angina (11.3 percent vs. 16.9 percent, P=0.02) or needed target-vessel revascularization because of ischemia (7.7 percent vs. 17.0 percent, P<0.001). In addition, the combined primary end point of death, reinfarction, disabling stroke, or target-vessel revascularization because of ischemia occurred in fewer patients in the stent group than in the angioplasty group (12.6 percent vs. 20.1 percent, P<0.01). The decrease in the combined end point was due entirely to the decreased need for target-vessel revascularization. The six-month mortality rates were 4.2 percent in the stent group and 2.7 percent in the angioplasty group (P=0.27). Angiographic follow-up at 6.5 months demonstrated a lower incidence of restenosis in the stent group than in the angioplasty group (20.3 percent vs. 33.5 percent, P<0.001). CONCLUSIONS: In patients with acute myocardial infarction, routine implantation of a stent has clinical benefits beyond those of primary coronary angioplasty alone.

Angioplasty, Balloon, Coronary↗

PubMed2000

Coronary stenting plus platelet glycoprotein IIb/IIIa blockade compared with tissue plasminogen activator in acute myocardial infarction. Stent versus Thrombolysis for Occluded Coronary Arteries in Patients with Acute Myocardial Infarction Study Investigators.

BACKGROUND: Prevention of myocardial damage is the main goal of all reperfusion therapies in patients with acute myocardial infarction. The relative efficacy of various reperfusion strategies is under intensive investigation. We assessed whether coronary stenting combined with the blockade of platelet glycoprotein IIb/IIIa receptors produces a greater degree of myocardial salvage than fibrinolysis with an accelerated infusion of alteplase, a tissue plasminogen activator, in patients with acute myocardial infarction. METHODS: A total of 140 patients were enrolled in the randomized trial; 71 were assigned to receive a stent plus abciximab, and 69 to receive intravenous alteplase. The primary end point was the degree of myocardial salvage, determined by means of serial scintigraphic studies with technetium Tc 99m sestamibi. The secondary end point was a composite of death, reinfarction, and stroke within six months after randomization. RESULTS: In the group that received a stent plus abciximab, the median size of the final infarct was 14.3 percent of the left ventricle (25th and 75th percentiles, 6.8 and 24.5 percent), as compared with a median of 19.4 percent (25th and 75th percentiles, 7.9 and 34.2 percent) in the alteplase group (P=0.02). This difference was due to the larger salvage index (the percentage of the left ventricle that was salvaged, divided by the percentage that was compromised by the initial perfusion defect) in the stent group: 0.57 (25th and 75th percentiles, 0.35 and 0.69), as compared with 0.26 (25th and 75th percentiles, 0.09 and 0.61; P<0.001). The cumulative incidence of death, reinfarction, or stroke at six months was lower in the stent group than in the alteplase group (8.5 vs. 23.2 percent. P=0.02; relative risk, 0.34; 95 percent confidence interval, 0.13 to 0.88). CONCLUSIONS: In patients with acute myocardial infarction, coronary stenting plus abciximab leads to a greater degree of myocardial salvage and a better clinical outcome than does fibrinolysis with a tissue plasminogen activator.

Abciximab↗

PubMed2001

Six-month angiographic follow-up after intravascular ultrasound-guided stenting of infarct-related artery: comparison with non-infarct-related artery.

BACKGROUND: Compared with balloon angioplasty, stenting has been established as an effective treatment modality to reduce restenosis in patients with acute myocardial infarction. However, the immediate results that predict favorable long-term outcomes in the acute infarct stenting are unknown. Therefore, we evaluated long-term outcomes of stenting for infarct-related artery (IRA) lesions by using intravascular ultrasound (IVUS) compared with that of stenting for non-IRA lesions. METHODS: IVUS-guided coronary stenting was successfully performed in 510 native coronary lesions (105 IRA vs 405 non-IRA). A 6-month follow-up angiogram was performed in 419 (82.2%) lesions: 87 (82.9%) IRA lesions and 332 (82.0%) non-IRA lesions. Coronary stenting on the IRA lesions was successfully performed within 7 to 10 days after onset of infarction in 42 patients and within 12 hours in 45 patients. Results were evaluated by clinical, angiographic, and IVUS methods. RESULTS: There were no significant differences in clinical and angiographic variables between the two groups. IVUS variables including reference vessel area and minimal stent area were also similar between the two groups. There was no significant difference in angiographic restenosis rate between the two groups in cases of minimal stent area > or = 7 mm(2): 12.8% (6 of 47) in IRA versus 19.1% (33 of 173) in non-IRA lesions (P = .315). However, the angiographic restenosis rate in cases of minimal stent area <7 mm(2) was 50% (20 of 40) in IRA lesions versus 31.5% (50 of 159) in non-IRA lesions (P = .028). CONCLUSIONS: Angiographic restenosis is significantly higher in stenting for IRA lesions compared with that for non-IRA lesions in cases of minimal stent area < 7 mm(2).

Angioplasty, Balloon, Coronary↗

PubMed2001

Myoglobin levels at 12 hours identify patients at low risk for 30-day mortality after thrombolysis in acute myocardial infarction: a Thrombolysis in Myocardial Infarction 10B substudy.

OBJECTIVE: We sought to identify, by use of serum cardiac markers, patients at low risk for 30-day mortality after ST-segment elevation myocardial infarction. BACKGROUND: Baseline cardiac markers are currently used to identify patients at increased risk for short-term events. We hypothesized that serum markers measured after treatment could identify patients at low risk for 30-day mortality. METHODS: A total of 839 patients from the Thrombolysis in Myocardial Infarction (TIMI) 10B study had myoglobin, cardiac-specific troponin-I, creatine kinase (CK)-MB measurements at the following time points; baseline, 90 minutes, and 3 and 12 hours after thrombolysis. By use of receiver operating characteristic analysis, thresholds were derived to predict 30-day mortality with at least 95% negative predictive value. RESULTS: Ninety minutes after thrombolysis myoglobin was superior to troponin-I or CK-MB in identifying patients at low risk for mortality. The 30-day mortality for 12-hour myoglobin < or = 239 ng/mL was 1.4% compared with 9.1% for levels > 239 ng/mL (P < .001). For 12-hour troponin-I (threshold 81.5 ng/mL), mortality was 1.9% versus 6.6% (P = .001) if above threshold; similarly for CK-MB at 12 hours (threshold 191 ng/mL) it was 3.3% versus 7.9% (P = .02). Multivariate analysis of baseline and posttreatment cardiac markers, age, sex, infarct artery location, and 90-minute TIMI flow grade identified only 12-hour myoglobin among the cardiac markers as independently predicting a low 30-day mortality (odds ratio 0.11, 95% confidence interval 0.02-0.50, P < .004). CONCLUSION: Serum cardiac markers can identify greater than two thirds of patients at low risk for 30-day mortality. A low 12-hour myoglobin level (< or = 239 ng/mL in this substudy) identifies such patients at low risk and could potentially assist in early risk stratification and triage after ST-segment elevation myocardial infarction.

Aged↗

PubMed2001

Direct infarct artery stenting without predilation and no-reflow in patients with acute myocardial infarction.

BACKGROUND: In patients with acute myocardial infarction (AMI), the rate of microvascular embolization and no-reflow promoted by coronary stenting with the use of conventional techniques (CS) appears to be greater than the one that occurs with balloon angioplasty. The minor invasiveness of direct stenting (DS) of the infarct artery without predilation could be expected to reduce embolization in the coronary microvasculature and no-reflow in patients with AMI. METHODS: In a cohort of 423 consecutive patients with AMI who underwent infarct-artery stenting, we compared CS and DS in terms of angiographic no-reflow rate and 1-month clinical outcome. RESULTS: At baseline patients who underwent DS (n = 110) had a better risk profile compared with the use of CS (n = 313). The incidence of angiographic no-reflow was 12% in the CS group and 5.5% in the DS group (P =.040). The 1-month mortality rate was 8% in the CS group and 1% in the DS group (P =.008). The mortality rate was 11% in patients with no-reflow and 5.6% in patients with a normal flow. Multivariate analysis showed that age, preprocedure patent infarct artery, and lesion length were related to the risk of no-reflow. In the subset of patients with a target lesion length </=15 mm, the variables independently related to the risk of no-reflow were age, DS, and final balloon inflation pressure. CONCLUSIONS: DS in patients with AMI may reduce the incidence of angiographic no-reflow, thereby increasing ultimate effective myocardial reperfusion.

Acute Disease↗

PubMed2002

Early ST-segment recovery, infarct artery blood flow, and long-term outcome after acute myocardial infarction.

BACKGROUND: Early resolution of ST-segment deviation (ST recovery) on the postthrombolytic electrocardiograms and restoration of "normal" blood flow in the infarct-related artery are associated with improved outcomes after myocardial infarction (MI). METHODS AND RESULTS: To evaluate the relationships between ST recovery, infarct-related artery flow, and late survival we studied 766 patients with electrocardiograms recorded at a median of 167 minutes after thrombolytic therapy. Angiography was performed at 3 weeks, and follow-up was done at a median of 6.3 years (interquartile range [IQR] 5.0-8.4). At 10 years, the survival rates were 55% (95% CI 43-70) in patients with <30% ST recovery in the single lead with maximum ST elevation, 71% (95% CI 64-79) in those with 30% to 70% ST recovery, and 74% (95% CI 68-82) in those with >70% ST recovery (P =.0005), whereas ST recovery measured as the sum of voltage changes of either ST deviation (elevation or depression) or ST elevation was not associated with 10-year survival (log-rank test, P =.06 and P =.34, respectively). In patients with Thrombolysis In Myocardial Infarction (TIMI) grade 3 flow, ST recovery of >70% (vs <30% and 30% to 70%) in the lead with maximum ST elevation was associated with increased late survival (P =.04). On multivariate analysis, the predictors, at admission, of 5-year survival were age (P <.001), ST recovery (measured as a continuous variable, P =.001), diabetes (P =.003) and female gender (P =.02). When the ejection fraction (P =.003) and TIMI flow grade (P =.02) at 3 weeks were included in the analysis, the P value for ST recovery was.08. CONCLUSIONS: ST recovery measured in the single lead with maximum ST elevation was a predictor of late survival, even in patients with TIMI grade 3 flow but ST recovery measured as the sum of voltage changes in all leads with ST deviation was not. This simple electrocardiographic parameter can identify patients with a reduced chance of survival who might benefit from additional therapies.

Aged↗

PubMed2003

Comparison of the predischarge exercise thallium-201 perfusion defect after myocardial infarction with myocardium at risk measured during acute infarction with technetium-99m sestamibi imaging.

BACKGROUND: Exercise thallium-201 imaging provides a noninvasive estimate of the amount of myocardium presumed to be at risk of infarcting should a complete occlusion of the coronary stenosis occur. The relationship between the size of the exercise thallium perfusion defect and the extent of myocardium supplied by a diseased coronary artery has not been established. This study evaluates that presumed correlation. METHODS: Patients were injected intravenously with technetium-99m sestamibi during acute myocardial infarction before thrombolysis or conventional therapy to quantify the myocardium at risk. Twenty-six patients who underwent risk-area assessment subsequently underwent clinically driven, predischarge, submaximal exercise imaging with thallium-201. The exercise testing was performed on day 7 +/- 2 days. A conventional polar map display was used to quantify the perfusion defect. RESULTS: The myocardium at risk determined by technetium-99m sestamibi at the time of infarction was 30% +/- 20% of the left ventricle. The mean exercise thallium-201 defect was 34% +/- 22% of the left ventricle. The exercise defect tended to be slightly larger than the myocardium at risk (4% +/- 10% of the left ventricle, P =.05). There was a close correlation between the 2 measurements (r = 0.89, SE = 9.4, P <.0001). CONCLUSIONS: This study shows a close correlation between the myocardium "at risk" assessed acutely by technetium-99m sestamibi and the "presumed at-risk area" determined by thallium-201 imaging on predischarge exercise testing. This finding supports the concept that the size of the exercise thallium defect caused by coronary stenosis indicates the likely size of a myocardial infarction resulting from occlusion of that stenosis.

Adult↗

PubMed1996

How ACE inhibitors reduce death from myocardial infarction: hypotheses from the AIRE study. Acute Infarction Ramipril Efficacy study.

Doctors treat patients, not populations. 'Evidence-based' practice is essential but extrapolation to the individual patient is always necessary and this fact is well illustrated by data from trials of ACE inhibitors post-myocardial infarction. In the AIRE (Acute Infarction Ramipril Efficacy) study, 2,006 patients with some evidence of heart failure, even if transient, after a myocardial infarction, were randomised to receive oral ramipril or placebo in addition to standard treatment. Follow-up was for a minimum of six and an average of 15 months. The risk reduction in total mortality was 27% (95% CI 11-40%; p = 0.002); approximately 40 lives might be expected to be saved for every 1000 patients treated for one year. Benefit was apparent within weeks of starting treatment. Additional data from the AIRE study are considered in relation to the findings of other mortality trials. It is argued that ACE inhibitors offer most to those patients with impaired left ventricular function through a mechanism not related to the prevention of myocardial re-infarction.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1985

Infarct size limitation by the xanthine oxidase inhibitor, allopurinol, in closed-chest dogs with small infarcts.

The present study was designed to evaluate the ability of allopurinol to limit infarct size following permanent coronary occlusion in the greyhound. Coronary occlusion was produced by injecting 2.5 mm plastic beads into the coronary artery of the closed chest dog. Non-perfused myocardium, the area at risk, was visualised by autoradiography of 141Cerium labelled microspheres which were infused immediately following coronary embolization. The treated dogs (n = 12) received 400 mg of allopurinol orally one day before surgery. A 25 mg . kg-1 bolus was administered (iv) immediately before occlusion, and repeated every 8 h. 11 dogs served as controls. After 24 h, the dogs were killed and the hearts were sliced into 5.0 mm transverse sections. The infarcted myocardium was visualised by triphenyl tetrazolium chloride staining. The percentage of the risk zone which evolved to infarct was calculated. This percentage was 18.1 +/- 3.95% in the allopurinol group vs 58.4 +/- 2.81% in the control group (p less than 0.001). We conclude that allopurinol is a potent drug for the limitation of infarct size in the dog with permanent coronary occlusion.

Allopurinol↗

PubMed1988

Lignocaine in experimental myocardial infarction: failure to prevent neutrophil accumulation and ventricular fibrillation and to reduce infarct size.

Growing evidence supports the concept that neutrophils accumulating in reperfused ischaemic myocardium play a detrimental role in evolving infarction. Lignocaine, an antiarrhythmic drug commonly used clinically, interferes with neutrophil function in vitro and potentially in vivo. To test the hypothesis that lignocaine may influence infarct size by reducing neutrophil accumulation in reperfused ischaemic myocardium, 31 dogs underwent a 2 h occlusion of the left anterior descending coronary artery, followed by 6 h of reperfusion. One group of dogs received saline (controls) the other a perfusion of lignocaine 0.06 mg.kg-1.min-1 starting 30 min before coronary occlusion and lasting for the duration of the experiment. Blood lignocaine concentrations at the onset of reperfusion were 3.3(0.6) micrograms.ml-1. 111Indium labelled autologous neutrophils were injected at the time of occlusion and their accumulation in the myocardium measured by digital scintigraphy of heart slices. The area at risk and infarct size were evaluated by planimetry of the heart slices (7 mm) after perfusion of Evans blue dye and triphenyltetrazolium staining. Ventricular fibrillation occurred in six controls and in five dogs receiving lignocaine. The phenomenon occurred early during the occlusion period in the lignocaine group (five dogs) and at reperfusion in controls (five dogs; p less than 0.05). In the remaining 20 dogs, 10 in each group, a linear correlation was found between myocardial 111In labelled neutrophil and circulating neutrophil counts at the onset of reperfusion (r = 0.076, p less than 0.05) and with infarct size (r = 0.96 and 0.74, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1988

Myosin light chains release in acute myocardial infarction: non-invasive estimation of infarct size.

After the loss of membrane integrity cardiospecific myosin light chains are released as a result of proteolytic degradation of the insoluble myosin pool. Thus, as with cytosolic enzymes, the measurement of the serum concentration changes of myosin light chains may allow a non-invasive estimation of infarct size. A two compartment model was used to describe the serum concentration changes of myosin light chains after a bolus injection into awake beagle dogs. The initial distribution volume was 7.4% of body weight, whereas the second compartment accounted for 4.7% of body weight. The fractional disappearance rate of 0.0092.min-1 resulted in a serum half life of myosin light chains of 75 min. In 30 patients with acute non-reperfused myocardial infarction a close correlation was found between the cumulative appearance of myosin light chains and their maximal serum concentration. In these patients the cumulative appearance of myosin light chains correlated with serum creatine kinase estimates of infarct size, with impairment of left ventricular ejection fraction, and with mortality during hospital admission. Thus the maximal serum concentration and the cumulative appearance of myosin light chains allow a non-invasive estimation of infarct size and may serve as a serological indicator of the patient's prognosis.

Adult↗

PubMed1993

The effect of verapamil on major events in patients with impaired cardiac function recovering from acute myocardial infarction. The Danish Study Group on Verapamil in Myocardial Infarction.

In the Danish Verapamil Infarction Trial II (DAVIT II) intervention with verapamil significantly decreased the first major event rate (i.e. reinfarction or death) in patients recovering from acute myocardial infarction. As calcium channel antagonists might have a detrimental effect in patients with heart failure, the effect of verapamil on major events in patients with and without impaired left ventricular function was analysed. Eight hundred and seventy-eight patients were randomized to verapamil 120 mg t.i.d. and 897 to placebo. Patients were followed up to 18 months. The endpoint was the first major event while on trial medication. In patients treated for heart failure during the acute phase of myocardial infarction, the lowest 18-month event rate was seen in the verapamil group (21.2% vs 22.2%) (absolute numbers: events/patients verapamil 47/291; placebo 60/323) (ns). Similarly, in patients treated with diuretics at randomization, the lowest 18-month event rate was seen in those randomized to verapamil (22.4 vs 24.3%) (absolute numbers: events/patients verapamil 57/349; placebo 76/375 (ns). When patients were subdivided according to New York Heart Association functional classes, verapamil reduced the event rate in all classes, but none of these differences was statistically significant. In patients without heart failure during the acute phase and in patients without diuretic treatment at randomization, treatment with verapamil caused a significant reduction in major events (hazard ratio (95% confidence limits): 0.66 (0.47, 0.92); 0.66 (0.45, 0.96) respectively). Long-term treatment with verapamil after acute myocardial infarction caused a significant reduction in major events.(ABSTRACT TRUNCATED AT 250 WORDS)

Denmark↗

PubMed2005

Early eptifibatide improves TIMI 3 patency before primary percutaneous coronary intervention for acute ST elevation myocardial infarction: results of the randomized integrilin in acute myocardial infarction (INTAMI) pilot trial.

AIMS: Adjunctive therapy with glycoprotein IIb/IIIa inhibitors has been shown to reduce ischaemic complications and improve clinical outcome in patients with primary percutaneous coronary intervention (PCI) for acute ST elevation myocardial infarction. Little is known about the use of eptifibatide in this setting. METHODS AND RESULTS: One hundred and two patients with ST elevation myocardial infarction <12 h scheduled for primary percutaneous intervention were randomly assigned to early eptifibatide given in the emergency room (early) or optional eptifibatide at the time of PCI (late or no). Primary endpoint was the patency of the infarct vessel before PCI. Patients in the early group received their first eptifibatide bolus, a mean of 45 min before angiography. TIMI 3 patency before PCI was observed in 34% in the early group and 10% in late or no group (P=0.01). The incidence of complete ST resolution 1 h after PCI was 61% in early group and 66% in the late or no group, respectively (P=n.s.). There were no significant differences in the rates of TIMI 3 flow after PCI, death, reinfarction, stroke, and major bleeding complications until day 30. CONCLUSION: In this pilot trial, double bolus eptifibatide given in the emergency room improved TIMI 3 grade flow of the infarct-related coronary artery before PCI. These results should be confirmed in a larger trial and whether this advantage translates into an improvement in clinical outcome should be tested in a trial with primary clinical endpoints.

Adult↗

PubMed1997

Pre-hospital and hospital time delays in thrombolytic treatment in patients with suspected acute myocardial infarction. Analysis of data from the EMIP study. European Myocardial Infarction Project.

OBJECTIVES: To compare the components of the time delay involved in pre-hospital and hospital thrombolytic therapy in patients presenting with suspected acute myocardial infarction. MATERIAL AND METHODS: From October 1988 to January 1992 a total of 198 mobile emergency units in 15 European countries and Canada randomized 5469 patients to receive either pre-hospital thrombolytic treatment, followed by placebo in hospital (pre-hospital group), or pre-hospital (hospital group) in the European Myocardial Infarction Project trial. We performed a post hoc analysis of these data to correlate components of the interval between symptom onset and treatment with baseline patient characteristics. RESULTS: The delay between onset of symptoms and calling for an ambulance was significantly longer for female patients (P = 0.0001), older patients (> 65 years old; P = 0.0001), those who had experienced pain within the previous 24 h (P = 0.0001), and those with pulmonary oedema (P = 0.04). This delay was significantly shorter in patients with previous myocardial infarction (P = 0.02), those with ventricular fibrillation (P = 0.0001), and those in shock (P = 0.0001). The delay between the two injections was significantly longer for older patients (> 65 years old; P = 0.02), those with previous myocardial infarction (P = 0.03), and those in shock (P = 0.003). CONCLUSIONS: Action undertaken to reduce delays between symptom onset and treatment should focus on modifiable factors such as patients who are likely to be late callers i.e. women and those over 65 years of age.

Aged↗

PubMed1992

Prognostic importance of predischarge exercise capacity for long-term mortality and non-fatal myocardial infarction in patients admitted for suspected acute myocardial infarction and treated with metoprolol.

To evaluate the influence of acute beta-blockade on the ability of predischarge exercise test data to predict long-term prognosis in patients admitted for suspected acute myocardial infarction, patients randomized at hospital admission to intravenous metoprolol or placebo were studied. Among 190 patients discharged alive, total 4-year mortality was 20.5% (n = 39); (33 cardiac deaths, 6 non-cardiac deaths). Non-fatal infarction rate was 6.8% (n = 13). Multiple logistic regression analysis revealed that total mortality and non-fatal infarctions were independently predicted by (a) inability to perform predischarge stress testing (event-free survival for patients exercise tested 79.5% vs 56.9% for patients not eligible for testing; relative risk (RR) 1.40, 95% confidence interval (CI) 1.10-1.78; P = 0.01), and (b) low predischarge exercise capacity (RR 1.44, CI 1.08-1.93; P = 0.034). ST segment shift > or = 1 mm did not predict mortality or reinfarction. Administration of metoprolol in the acute phase did not influence the predictive value of these parametres. It is concluded that assessment of exercise capacity at early exercise testing yields independent information for later death and myocardial infarctions, and that beta-blockade with metoprolol does not influence the predictive value of early exercise testing.

Double-Blind Method↗

PubMed1994

Release of chemoattractants and neutrophil activation in acute myocardial infarction immediately after successful recanalization of the infarct-related vessel by angioplasty.

The study investigated inflammatory responses in evolving myocardial infarction. Fifteen patients with acute myocardial infarction, who had undergone balloon recanalization of the infarct-related coronary artery within 4 h after onset of symptoms, were examined. Blood samples were obtained through the guiding catheter and from the pulmonary artery before and immediately after successful recanalization. After recanalization, plasma from the pulmonary artery was 47% (quartiles: 19%, 78%; P = 0.001) more chemotactic to neutrophils from normal donors than before recanalization. Furthermore, significant changes in neutrophil function were found in the pulmonary artery. Compared to the values before recanalization, the nitroblue tetrazolium score rose by 31% (quartiles: 4%, 37%; P = 0.003), FMLP-stimulated superoxide anion production by 10% (quartiles: 0%, 39%; P = 0.020), and chemotaxis by 46% (quartiles: 0%, 81%; P = 0.011), while neutrophil filterability decreased by 28% (quartiles: 15%, 47%; P = 0.010). No significant changes in neutrophil parameters were found in the arterial blood. The study indicates that chemoattractants are released in the early reperfusion period of evolving myocardial infarction. These chemoattractants may act as inflammatory mediators causing neutrophil activation.

Aged↗

PubMed1995

Bundle branch block in acute Q wave inferior wall myocardial infarction. A high risk subgroup of inferior myocardial infarction patients. The SPRINT Study Group. Secondary Prevention Reinfarction Israeli Nifedipine Trial.

The aim of this study was to determine the incidence and impact of right and left bundle branch block on the in-hospital, 5-year and 10-year mortality of patients with acute inferior Q wave myocardial infarction. A retrospective analysis of clinical characteristics, hospital, 1-, 5-, and 10-year mortality of 2215 consecutive patients with acute inferior Q wave myocardial infarction hospitalized in 13 coronary care units in Israel was performed. Bundle branch block during acute Q wave inferior wall myocardial infarction was present in 108 patients (4.9%), 85 of whom had right and 23 left bundle branch block. Patients with bundle branch block had more in-hospital complications than those without, irrespective of the site and time of appearance of the block. In addition, atrial fibrillation (19%), complete atrioventricular block (21%) and congestive heart failure (45%) appeared more frequently in patients with, than in those without, bundle branch block (11%, 9% and 31%, respectively), and in-hospital and 5-year mortality were higher in patients with the block (22%, 33%) than in those without it (13% and 23%, respectively). Bundle branch block emerged as an independent predictor of death only among patients with new right bundle branch block, and right bundle branch block emerged as an independent predictor for the development of complete atrioventricular block (odds ratio 2.13; 90% confidence interval 1.39-3.28). However, hospital mortality among patients with inferior myocardial infarction and complete atrioventricular block was virtually independent of bundle branch block (39% with vs 36% without bundle branch block, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗