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PubMed1988

Angiographic features in the infarct-related artery after intracoronary urokinase followed by prolonged anticoagulation. Role of ruptured atheromatous plaque and adherent thrombus in acute myocardial infarction in vivo.

To unravel sequential morphological features in infarct-related coronary arteries (IRCA), we performed coronary angiography (CAG) before, during, and immediately after intracoronary urokinase infusion in 43 consecutive patients. After 1 month of rigorous anticoagulation by intravenous heparin and subsequent oral warfarin or after the same period of treatment by antiplatelet agents, we repeated CAG in all patients except for one, who died 6 days after thrombolytic therapy. Thirty-two IRCAs were totally occluded, and 11 were severely occluded at baseline. With recanalization and/or reduction in luminal narrowing at the site of the occlusion by progressive removal of the overlying thrombus and plaque content, we recognized the development of extraluminal contrast pooling in an ellipsoid shape (type A), single or paired linear radiolucency(ies) with or without outpouching (type B), and definite outpouching (type C). The development of type A, B, and C lesions occurred in 4, 6, and 0 IRCAs immediately after thrombolytic therapy and in 0, 18, and 3 IRCAs 1 month later, respectively. Throughout the study, at least one of type A-C lesions developed in 23 of 43 (53.5%) IRCAs. Lesion development proceeded from total or severe occlusion to type A, then to type B or C, both accompanied by progressive reduction in luminal narrowing and frequent enlargement of outpouching. A postmortem study in one patient whose CAG immediately after thrombolytic therapy was interpreted as a type B lesion demonstrated a ruptured plaque with paired ridges. Serial observations in vivo indicate that many IRCAs are associated with a complex underlying spatial structure, probably composed of some part of ruptured atheromatous plaque with or without adherent thrombus. Recognition and identification of such complex structures beneath the accumulated thrombus are of great importance in both CAG interpretation and elucidation of the pathophysiological sequence of acute myocardial infarction in vivo and may enable prevention or more effective therapy of acute coronary events.

Aged↗
PubMed1989

ST segment shifts are poor predictors of subsequent Q wave evolution in acute myocardial infarction. A natural history study of early non-Q wave infarction.

Acute ST segment elevation is regarded generally as the sine qua non of evolving Q wave myocardial infarction (MI) because such electrocardiographic (ECG) injury is believed to be a marker of transmural ischemia and a forerunner of transmural necrosis. Alternatively, ST segment depression with or without T wave inversion is viewed as the dominant ECG feature of non-Q wave MI. However, this hypothesis has not been assessed prospectively in an acute MI population. We analyzed 2,304 serial ECGs at study entry (admission), day 2, day 3, and predischarge (mean, 10.2 +/- 2 days) from 576 patients with creatine kinase MB confirmed acute non-Q wave MI to determine what percentage of patients with early ST segment elevation culminated in subsequent Q wave development. Of this group, 187 patients (32%) exhibited 1 mm or greater ST segment elevation in two or more contiguous entry ECG leads. Of those patients whose non-Q wave MI could be localized on the basis of diagnostic admission ST segment shifts, the prevalence of early ST segment elevation was 43% (187 of 439). The sum total mean (+/- SD) peak ST segment elevation by lead group (anterior, inferior, lateral) was 4.0 +/- 2.4, 4.5 +/- 2.4, and 2.5 +/- 0.6 mm, respectively. Despite this, only 20% of patients with ST segment elevation (37 of 187) developed Q waves. Of 252 patients who exhibited early ST segment depression or T wave inversion or both, 39 (15%) evolved subsequent Q waves. Thus, while the prevalence of early ST segment elevation in acute evolving non-Q wave MI was higher than previously reported, 80% of patients with and 85% of patients without ST segment elevation and absent Q waves on the admission ECG did not develop subsequent Q waves during a 2-week period of observation (p = NS). In addition, when patients with ST segment elevation were compared with patients with ST segment depression or T wave inversions or both, there were no between-group differences in log peak creatine kinase (404 vs. 383 IU), reinfarction (6% vs. 8%), postinfarction angina (50% vs. 42%), or early recurrent ischemia (49% vs. 45%), defined as postinfarction angina with transient ECG changes. Thus, in patients who present with initial acute non-Q wave MI, ST segment shifts on admission are unreliable predictors of subsequent Q wave evolution and do not discriminate significant differences in postinfarction outcome. In particular, ST segment elevation during the early hours of evolving infarction is not an invariable harbinger of subsequent Q wave development.

Creatine Kinase↗
PubMed1991

Identification of acute myocardial infarction patients suitable for early hospital discharge after aggressive interventional therapy. Results from the Thrombolysis and Angioplasty in Acute Myocardial Infarction Registry.

BACKGROUND: Very early (day 4) hospital discharge has recently been proposed for selected patients with acute myocardial infarction (MI). The purpose of this study was to determine the most useful factors for identifying acute MI patients treated with aggressive interventional therapy who could be safely discharged on day 4. METHODS AND RESULTS: We studied 708 patients enrolled in the Thrombolysis and Angioplasty in Acute Myocardial Infarction trials I-III. Patients dying in the first 3 days and those with early (days 1-3) emergency coronary artery bypass graft surgery (CABG), late elective CABG (greater than or equal to day 4), or urgent/emergency CABG resulting from a late elective coronary angioplasty were excluded. The remaining 580 patients were randomly divided into a training sample (group 1) that was used to build a logistic regression model for predicting the absence of a late major complication and a test sample (group 2) that was used to validate this model. For this study, patients were considered appropriate for day 4 hospital discharge if they did not experience any of the following for 30 days after MI: death, reinfarction, cardiogenic shock, pulmonary edema, sustained hypotension, sustained ventricular tachycardia, high-grade atrioventricular block, acute ventricular septal defect, and recurrent ischemia necessitating urgent CABG. In group 1, four variables were independent predictors of freedom from late major complications: absence of early sustained ventricular tachycardia or ventricular fibrillation, absence of early sustained hypotension or cardiogenic shock, fewer coronary arteries with significant (greater than or equal to 75%) stenosis, and a higher left ventricular ejection fraction. In group 2, 23% of patients had a logistic model prediction of a 3% or less chance of a late complication. These patients had no deaths or reinfarctions by day 30 and a 3% late major complication rate. CONCLUSIONS: The results of early cardiac catheterization and the absence of selected early (days 1-3) major complications do allow identification of a low risk subgroup of acute MI patients that may be suitable for very early discharge.

Angioplasty, Balloon, Coronary↗
PubMed1991

Evaluation of combination thrombolytic therapy and timing of cardiac catheterization in acute myocardial infarction. Results of thrombolysis and angioplasty in myocardial infarction--phase 5 randomized trial. TAMI Study Group.

Recent trials of myocardial reperfusion using single-agent thrombolytic therapy and sequential cardiac catheterization have supported a conservative approach to the patient with acute myocardial infarction. To evaluate combination thrombolytic therapy and the role of a previously untested strategy for the aggressive use of cardiac catheterization, we performed a multicenter clinical trial with a 3 x 2 factorial design in which 575 patients were randomly allocated to one of three drug regimens--tissue-type plasminogen activator (t-PA) (n = 191), urokinase (n = 190), or both (n = 194) - and one of two catheterization strategies--immediate catheterization with angioplasty for failed thrombolysis (n = 287) or deferred predischarge catheterization on days 5-10 (n = 288). Patients with contraindications to thrombolytic therapy, cardiogenic shock, or age of more than 75 years were excluded. Global left ventricular ejection fraction was well preserved and almost identical at predischarge catheterization (54%), regardless of the catheterization or thrombolytic strategy used (p = 0.98). Combination thrombolytic therapy was associated with a less complicated clinical course, most clearly documented by a lower rate of reocclusion (2%) compared with urokinase (7%) and t-PA (12%) (p = 0.04) and a lower rate of recurrent ischemia (25%) compared with urokinase (35%) and t-PA (31%). When a composite clinical end point (e.g., death, stroke, reinfarction, reocclusion, heart failure, or recurrent ischemia) was examined, combination thrombolytic therapy was associated with greater freedom from any adverse event (68%) compared with either single agent (urokinase, 55%; t-PA, 60%) (p = 0.04) and with a less complicated clinical course when the composite clinical end points were ranked according to clinical severity (p = 0.024). Early patency rates were greater with combination therapy, although predischarge patency rates after considering interventions to maintain patency were similar among drug regimens. No difference in bleeding complication rates was observed with any thrombolytic regimen. The aggressive catheterization strategy led to an overall early patency rate of 96% and a predischarge patency rate of 94% compared with a 90% predischarge patency in the conservative strategy (p = 0.065). The aggressive strategy improved regional wall motion in the infarct region (-2.16 SDs/chord) compared with deferred catheterization (-2.49 SDs/chord) (p = 0.004). More patients treated with the aggressive strategy were free from adverse outcomes (67% versus 55% in the conservative strategy, p = 0.004), and the clinical course was less complicated when the adverse outcomes were ranked according to severity (p = 0.016). No significant increase in use of blood products resulted from the aggressive strategy.(ABSTRACT TRUNCATED AT 400 WORDS)

Angioplasty, Balloon, Coronary↗
PubMed1991

Post-myocardial infarction mortality in patients with ventricular premature depolarizations. Canadian Amiodarone Myocardial Infarction Arrhythmia Trial Pilot Study.

BACKGROUND: Among survivors of acute myocardial infarction, frequent and repetitive ventricular premature depolarizations (VPDs) detected on ambulatory monitoring contribute independently to the risk of all-cause mortality and sudden death. Apart from the beta-blockers, no antiarrhythmic drug has been reliably demonstrated to reduce mortality among patients with VPDs. A pilot study was undertaken to gather data to aid in the design of a multicenter trial of amiodarone for the reduction of mortality from cardiac arrhythmias in such patients. METHODS AND RESULTS: Seventy-seven patients with acute myocardial infarction within the previous 6-30 days and 10 or more VPDs/hr or one or more runs of ventricular tachycardia on 24-hour electrocardiographic recording were randomized in a double-blind fashion in a 2:1 amiodarone-to-placebo ratio. The loading dose was 10 mg/kg/day for 3 weeks. The maintenance dose was 300-400 mg/day with reductions at 4-month intervals in response to VPD suppression, excessive plasma levels, or toxicity. VPD suppression at 1 week and 2 weeks was 63% and 85%, respectively, on amiodarone and 17% and 27%, respectively, on placebo. Apart from thyroid-stimulating hormone elevation and skin reactions, no side effects occurred more frequently with amiodarone. The study drug was stopped for side effects or noncompliance in 35% of amiodarone patients and 34% of placebo patients. Patients were followed for a maximum of 2 years (mean, 20 months). Arrhythmic death or resuscitated ventricular fibrillation occurred in two of 48 amiodarone patients (6%) and four of 29 placebo patients (14%), whereas the rates of all-cause mortality were five of 48 (10%) and six of 29 (21%), respectively. CONCLUSIONS: Amiodarone, in moderate loading and maintenance dosages with adjustments in response to plasma levels, VPD suppression, and side effects, results in effective VPD suppression and acceptable levels of toxicity.

Amiodarone↗
PubMed1992

Predictors of early morbidity and mortality after thrombolytic therapy of acute myocardial infarction. Analyses of patient subgroups in the Thrombolysis in Myocardial Infarction (TIMI) trial, phase II.

BACKGROUND: Thrombolysis has altered treatment of acute myocardial infarction (AMI). Therefore, reevaluation of predictors of outcome and treatment strategies is appropriate. METHODS AND RESULTS: Clinical variables collected prospectively for the 3,339 patients of the Thrombolysis in Myocardial Infarction II study were analyzed retrospectively to identify predictors of clinical events at 42 days and earlier and to identify subgroups in which an invasive or conservative strategy might be superior. Pulmonary edema/cardiogenic shock presented as the strongest independent correlate with death (relative risk, 6.0). In two subgroups, mortality differed between the invasive and conservative strategies: 1) Patients with versus without prior AMI had a higher mortality in the conservative strategy (11.5% versus 3.5%, p less than 0.001); in the invasive strategy, the mortality rates were similar (6.0% and 5.1%). 2) Patients with diabetes mellitus and no prior AMI had a higher mortality in the invasive than in the conservative strategy (14.8% versus 4.2%, p less than 0.001). Reinfarction was not independently correlated with baseline characteristics except with history of angina (relative risk, 1.9). Mortality was lower in current smokers and ex-smokers versus never-smokers (3.6% and 4.8% versus 8.0%, p less than 0.001). Current smokers had a lower risk profile (p less than 0.001), including age, pulmonary edema/cardiogenic shock, history of hypertension, and diabetes. The rate of reinfarction was lower in current smokers versus ex-smokers and never-smokers (4.6% versus 8.3% and 8.8%, p less than 0.001). "Not current smoker" was an independent correlate with reinfarction (relative risk, 1.9). The coronary anatomy did not differ among the current smokers, ex-smokers, and never-smokers. CONCLUSIONS: The strong independent correlation of pulmonary edema/cardiogenic shock with death suggests that thrombolysis is not sufficient to improve survival in these patients. The higher mortality in patients with versus without prior AMI in the conservative strategy suggests that early catheterization and revascularization of these patients might be beneficial. Conversely, the higher mortality in diabetes without prior AMI in the invasive than in the conservative strategy suggests that early aggressive management might not be suitable in this subgroup except for clinical indications. Reinfarction was not predictable by clinical variables except by history of angina. The finding that "not current smoker" was an independent correlate with reinfarction was unexpected.

Female↗
PubMed1994

Hirudin in acute myocardial infarction. Safety report from the Thrombolysis and Thrombin Inhibition in Myocardial Infarction (TIMI) 9A Trial.

BACKGROUND: The Thrombolysis and Thrombin Inhibition in Myocardial Infarction (TIMI) 9A trial compared the efficacy and safety of intravenous hirudin with heparin as adjunctive therapy to thrombolysis and aspirin in patients with acute myocardial infarction. The primary safety end point was the occurrence of major hemorrhage or anaphylaxis. METHODS AND RESULTS: Based on experience in phase II trials, TIMI 9A used a hirudin bolus of 0.6 mg/kg followed by a fixed-dose 96-hour infusion of 0.2 mg/kg per hour. A modified weight-adjusted heparin regimen was used (5000-U bolus and infusion of 1000 U/h for patients < 80 kg or 1300 U/h for patients > or = 80 kg) with titration to a target activated partial thromboplastin time (aPTT) of 60 to 90 seconds. Because rates of hemorrhage in both treatment arms were higher than expected, randomization was suspended in TIMI 9A after 757 patients had been enrolled. Intracranial hemorrhage occurred in 1.7% of patients treated with hirudin and 1.9% of those treated with heparin (P = NS). Major spontaneous hemorrhage at a nonintracranial site occurred more frequently in hirudin--than in heparin-treated patients (7.0% versus 3.0%; P = .02), whereas major hemorrhage at instrumented sites was similar (5.2% in both hirudin and heparin groups). Patients who developed a major hemorrhage were older (P < .001) and had higher aPTT values, especially in the first 12 hours after thrombolysis (P = .001). CONCLUSIONS: The rate of major spontaneous hemorrhage for both heparin and hirudin in TIMI 9A was higher than that seen in TIMI 5, TIMI 6, and GUSTO 1. This was possibly a result of high levels of anticoagulation at the doses of heparin and hirudin used, low previous estimates of the hemorrhage risk at the doses of hirudin used in TIMI 9A due to the relatively small number of patients receiving that dose in earlier studies, and enrollment of patients at higher risk of hemorrhage. Because a prolonged aPTT was associated with an increased risk of major hemorrhage in both heparin- and hirudin-treated patients, it now appears important to monitor aPTT on a regular basis when using either antithrombin to identify those patients who require downward adjustment of the infusion. TIMI 9B has therefore been configured with a lower hirudin bolus (0.1 mg/kg) and infusion (0.1 mg/kg per hour) and lower heparin infusion (1000 U/h without weight adjustment). Infusions of both antithrombins will be titrated to a target aPTT of 55 to 85 seconds.

Aged↗
PubMed1997

Danish multicenter randomized study of invasive versus conservative treatment in patients with inducible ischemia after thrombolysis in acute myocardial infarction (DANAMI). DANish trial in Acute Myocardial Infarction.

BACKGROUND: The aim of the DANish trial in Acute Myocardial Infarction (DANAMI) study was to compare an invasive strategy of percutaneous transluminal coronary angioplasty (PTCA) or coronary artery bypass grafting (CABG) with a conservative strategy in patients with inducible myocardial ischemia who received thrombolytic treatment for a first acute myocardial infarction (AMI). METHODS AND RESULTS: Of the 503 patients randomized to an invasive strategy, PTCA was performed in 266 (52.9%) and CABG in 147 (29.2%) from 2 to 10 weeks after the AMI. Of the 505 patients in the conservative treatment group, only 8 (1.6%) had been revascularized 2 months after the AMI. The patients were followed up from 1 to 4.5 years. The primary end points were mortality, reinfarction, and admission with unstable angina. At 2.4 years' follow-up (median), mortality was 3.6% in the invasive treatment group and 4.4% in the conservative treatment group (not significant). Invasive treatment was associated with a lower incidence of AMI (5.6% versus 10.5%; P=.0038) and a lower incidence of admission for unstable angina (17.9% versus 29.5%; P<.00001). The percentages of patients with a primary end point were 15.4% and 29.5% at 1 year, 23.5% and 36.6% at 2 years, and 31.7% versus 44.0% at 4 years (P=<.00001) in the invasive and conservative treatment groups, respectively. At 12 months, stable angina pectoris was present in 21% of patients in the invasive treatment group and 43% in the conservative treatment group. CONCLUSIONS: Invasive treatment in post-AMI patients with inducible ischemia results in a reduction in the incidence of reinfarction, fewer admissions due to unstable angina, and lower prevalence of stable angina. We conclude that patients with inducible ischemia before discharge who have received treatment with thrombolytic drugs for their first AMI should be referred to coronary arteriography and revascularized accordingly.

Adult↗
PubMed1998

Indications for ACE inhibitors in the early treatment of acute myocardial infarction: systematic overview of individual data from 100,000 patients in randomized trials. ACE Inhibitor Myocardial Infarction Collaborative Group.

BACKGROUND: Several large-scale trials have demonstrated improved survival with ACE-inhibitor therapy started during acute myocardial infarction. A systematic overview was conducted to resolve uncertainties regarding time of initiation, time course of effect, and identification of patients in whom the benefits or the risks may be greater. METHODS AND RESULTS: This overview aimed to include individual data from all randomized trials involving more than 1000 patients in which ACE-inhibitor treatment was started in the acute phase (0 to 36 hours) of myocardial infarction and continued for a short time (4 to 6 weeks). Data were available for 98,496 patients from 4 eligible trials, and the results were consistent among the trials. Thirty-day mortality was 7.1% among patients allocated to ACE inhibitors and 7.6% among control subjects, corresponding to a 7% (SD, 2%) proportional reduction (95% CI, 2% to 11%; 2P<0.004). This represented avoidance of approximately 5 (SD, 2) deaths per 1000 patients, with most of the benefit observed within the first week. The proportional benefit was similar in patients at different underlying risk. The absolute benefit was particularly large in some high-risk groups (ie, Killip class 2 to 3, heart rate > or = 100 bpm at entry) and in anterior MI. ACE-inhibitor therapy also reduced the incidence of nonfatal cardiac failure (14.6% versus 15.2%, 2P=0.01) but was associated with an excess of persistent hypotension (17.6% versus 9.3%, 2P<0.01) and renal dysfunction (1.3% versus 0.6%, 2P<0.01). CONCLUSIONS: These results support the use of ACE inhibitors early in the treatment of acute MI, either to a wide range of patients or selectively in patients with anterior MI and in those at increased risk of death.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1999

Glycometabolic state at admission: important risk marker of mortality in conventionally treated patients with diabetes mellitus and acute myocardial infarction: long-term results from the Diabetes and Insulin-Glucose Infusion in Acute Myocardial Infarction (DIGAMI) study.

BACKGROUND: The Diabetes and Insulin-Glucose Infusion in Acute Myocardial Infarction (DIGAMI) study addressed prognostic factors and the effects of concomitant treatment and glycometabolic control in diabetic patients with myocardial infarction (AMI). METHODS AND RESULTS: Of 620 diabetic patients with AMI, 306 were randomly assigned to a >/=24-hour insulin-glucose infusion followed by multidose subcutaneous insulin. Three hundred fourteen patients were randomized as controls, receiving routine antidiabetic therapy. Thrombolysis and beta-blockers were administered when possible. Univariate and multivariate statistical analyses were applied to study predictors of long-term mortality. During an average follow-up of 3.4 years (range, 1.6 to 5.6 years), 102 patients (33%) in the intensive insulin group and 138 (44%) in the control group died (P=0. 011). Old age, previous heart failure, diabetes duration, admission blood glucose, and admission Hb AIc were independent predictors of mortality in the total cohort, whereas previous AMI, hypertension, smoking, or female sex did not add independent predictive value. Metabolic control, mirrored by blood glucose and Hb AIc, improved significantly more in patients on intensive insulin treatment than in the control group. beta-Blockers improved survival in control subjects, whereas thrombolysis was most efficient in the intensive insulin group. CONCLUSIONS: Mortality in diabetic patients with AMI is predicted by age, previous heart failure, and severity of the glycometabolic state at admission but not by conventional risk factors or sex. Intensive insulin treatment reduced long-term mortality despite high admission blood glucose and Hb AIc.

Aged↗
PubMed1981

Dobutamine infusion in conscious dogs with and without acute myocardial infarction. Effects on systemic hemodynamics, myocardial blood flow, and infarct size.

We infused dobutamine (20 microgram/kg per min) intravenously, once before and once after coronary artery occlusion, in 10 chronically instrumented dogs. Both infusions increased cardiac output and left ventricular dP/dt and dP/dt/P, but divergent effects on heart rate and aortic blood pressure were observed. Dobutamine decreased heart rate and increased mean aortic blood pressure before coronary artery occlusion, whereas after occlusion it increased heart rate while mean aortic blood pressure remained unchanged. A greater decrease in total peripheral vascular resistance occurred during dobutamine infusion after coronary artery occlusion than before. These differences may relate to withdrawal of enhanced sympathetic tone after coronary occlusion. Similar infusions of normal saline (n = 9) produced no systemic hemodynamic changes either before or after coronary artery occlusion. Myocardial blood flow increased to both non-ischemic and ischemic regions of the heart during dobutamine infusion, but the endocardial:epicardial blood flow ratio did not change significantly. In addition, infarct size, measured by nitroblue tetrazolium stain, was smaller in the dobutamine group (10 +/- 1 g) than in the normal saline group (15 +/- 2 g). Neither left ventricular weight nor risk zone differed between the two groups. These results indicate that dobutamine may be a useful inotropic agent during acute myocardial infarction.

Animals↗
PubMed2006

Intracoronary bone marrow cell transfer after myocardial infarction: eighteen months' follow-up data from the randomized, controlled BOOST (BOne marrOw transfer to enhance ST-elevation infarct regeneration) trial.

BACKGROUND: Intracoronary transfer of autologous bone marrow cells (BMCs) may enhance recovery of left ventricular (LV) function in patients after acute myocardial infarction (AMI). However, clinical studies addressing the effects of BMCs after AMI have covered only limited time frames ranging from 3 to 6 months. The critical question of whether BMC transfer can have a sustained impact on LV function remains unanswered. METHODS AND RESULTS: After percutaneous coronary intervention with stent implantation (PCI) of the infarct-related artery, 60 patients were randomized 1:1 to a control group with optimal postinfarction therapy and a BMC transfer group that also received an intracoronary BMC infusion 4.8+/-1.3 days after PCI. Cardiac MRI was performed 3.5+/-1.5 days, 6+/-1 months, and 18+/-6 months after PCI. BMC transfer was not associated with adverse clinical events. In the control group, mean global LV ejection fraction increased by 0.7 and 3.1 percentage points after 6 and 18 months, respectively. LV ejection fraction in the BMC transfer group increased by 6.7 and 5.9 percentage points. The difference in LVEF improvement between groups was significant after 6 months but not after 18 months (P=0.27). The speed of LV ejection fraction recovery over the course of 18 months was significantly higher in the BMC transfer group (P=0.001). CONCLUSIONS: In this study, a single dose of intracoronary BMCs did not provide long-term benefit on LV systolic function after AMI compared with a randomized control group; however, the study suggests an acceleration of LV ejection fraction recovery after AMI by BMC therapy.

Adult↗
PubMedDate not supplied

Differentiating the infarct-related artery on initial electrocardiogram in single or multi-vessel disease in acute inferior myocardial infarction and evaluating involvement of vessels using correspondence analysis.

Initial electrocardiography changes were compared prospectively with the findings of coronary angiography to predict the infarct-related artery (IRA) in cases of single- and multi-vessel disease and to demonstrate the relationship between other coexisting coronary involvements and IRA in patients who presented with acute inferior myocardial infarction (AMI). ST elevations or depressions of at least 1 mm (0.1 mV) were evaluated in the leads I, aVL, and V1-V6. Of the 160 patients hospitalized due to inferior AMI, 153 (96%) underwent coronary angiography using standard methods. The angiograms were screened for stenotic lesions using quantitative coronary angiography to confirm significance, which was considered >50% vessel lumen diameter reduction. Among single-vessel involvements, the IRA was either the circumflex artery (Cx) or right coronary artery (RCA). In conditions in which IRA was detected as either Cx or RCA, 1-, 2-, and 3-vessel involvements were also detected. Correspondence analysis was performed to show the vessel involvements accompanying IRA. Compared with patients with IRA as RCA, the presence of ST depressions in the leads V1 or V2 and aVL were more frequently seen in patients with IRA as Cx (p=0.000, p=0.015, respectively). Among all vessel involvements in which IRA was either Cx or RCA, a ST-segment depression in leads V1 or V2 (p=0.000) and aVL (p=0.000) and a ST-segment elevation in lead I (p=0.005) were considered to be significant for Cx, and a ST-segment depression in lead I for RCA involvement (p=0.010). According to correspondence analysis, the most frequent single-vessel involvement seen in inferior AMI was RCA; when IRA was RCA, a multi-vessel involvement included RCA and Cx; and when IRA was Cx, a single-vessel involvement included the left anterior descending (LAD) artery most frequently, and RCA+LAD less frequently (p=0.000). In inferior AMI, RCA was the most common IRA; however, the possibility of multi-vessel disease is increased when Cx is found to be the IRA. In patients presenting with inferior AMI, the presence of ST-depression in the leads aVL and V1-2 is a sensitive finding that indicates Cx stenosis rather than RCA stenosis and is not affected by coexisting other coronary artery involvements.

Electrocardiography↗
PubMed1996

The value of nifedipine in the treatment of hypertension, coronary heart disease and myocardial infarction (post-infarction therapy).

Calcium antagonists are among the drugs most often prescribed in the treatment of cardiovascular diseases. Among the 2000 preparations most often prescribed in Germany in 1994, there were 48 calcium antagonists which presented a prescription rate of 1268 million defined daily doses. Calcium antagonists of the nifedipine type are by far the most often prescribed preparations of this group. They are targeted mainly against hypertension and coronary heart disease, with post-infarction angina pectoris also featuring among their indications. Recent publications have, in consideration of indications on possible risks associated with nifedipine medication, fanned discussions on the pros and cons of nifedipine medication and thus the value of calcium antagonists in treating hypertension and CHD as well as post-infarction patients. The purpose of this report is to analyze the current situation and to draw conclusions for the practical use of calcium antagonists.

Adult↗
PubMed2005

The impact of glucose-insulin-potassium infusion in acute myocardial infarction on infarct size and left ventricular ejection fraction [ISRCTN56720616].

BACKGROUND: Favorable clinical outcomes have been observed with glucose-insulin-potassium infusion (GIK) in acute myocardial infarction (MI). The mechanisms of this beneficial effect have not been delineated clearly. GIK has metabolic, anti-inflammatory and profibrinolytic effects and it may preserve the ischemic myocardium. We sought to assess the effect of GIK infusion on infarct size and left ventricular function, as part of a randomized controlled trial. METHODS: Patients (n = 940) treated for acute MI by primary percutaneous coronary intervention (PCI) were randomized to GIK infusion or no infusion. Endpoints were the creatinine kinase MB-fraction (CK-MB) and left ventricular ejection fraction (LVEF). CK-MB levels were determined 0, 2, 4, 6, 24, 48, 72 and 96 hours after admission and the LVEF was measured before discharge. RESULTS: There were no differences between the two groups in the time course or magnitude of CK-MB release: the peak CK-MB level was 249 +/- 228 U/L in the GIK group and 240 +/- 200 U/L in the control group (NS). The mean LVEF was 43.7 +/- 11.0 % in the GIK group and 42.4 +/- 11.7% in the control group (P = 0.12). A LVEF < or = 30% was observed in 18% in the controls and in 12% of the GIK group (P = 0.01). CONCLUSION: Treatment with GIK has no effect on myocardial function as determined by LVEF and by the pattern or magnitude of enzyme release. However, left ventricular function was preserved in GIK treated patients.

Aged↗
PubMed2004

The association between white blood cell count and acute myocardial infarction in-hospital mortality: findings from the National Registry of Myocardial Infarction.

OBJECTIVES: Although cross-sectional and prospective studies have shown that the white blood cell (WBC) count is associated with long-term mortality for patients with ischemic heart disease, the role of the WBC count as an independent predictor of short-term mortality in patients with acute myocardial infarction (AMI) has not been examined as extensively. The objective of this study was to determine whether the WBC count is associated with in-hospital mortality for patients with ischemic heart disease after controlling for potential confounders. METHODS: From July 31, 2000, to July 31, 2001, the National Registry of Myocardial Infarction 4 enrolled 186,727 AMI patients. A total of 115,273 patients were included in the analysis. RESULTS: WBC counts were subdivided into intervals of 1,000/mL, and in-hospital mortality rates were determined for each interval. The distribution revealed a J-shaped curve. Patients with WBC counts >5,000/mL were subdivided into quartiles, whereas patients with WBC counts <5,000/mL were assigned to a separate category labeled "subquartile" and were analyzed separately. A linear increase in in-hospital mortality by WBC count quartile was found. The unadjusted odds ratio (OR) for the fourth versus the first quartile showed strong associations with in-hospital mortality among the entire population and by gender: 4.09 (95% confidence interval [95% CI] = 3.83 to 4.73) for all patients, 4.31 (95% CI = 3.93 to 4.73) for men, and 3.65 (95% CI = 3.32 to 4.01) for women. Following adjustment for covariates, the magnitude of the ORs attenuated, but the ORs remained highly significant (OR, 2.71 [95% CI = 2.53 to 2.90] for all patients; OR, 2.87 [95% CI = 2.59 to 3.19] for men; OR, 2.61 [95% CI = 2.36 to 2.99] for women). Reperfused patients had consistently lower in-hospital mortality rates for all patients and by gender (p < 0.0001). CONCLUSIONS: The WBC count is an independent predictor of in-hospital AMI mortality and may be useful in assessing the prognosis of AMI in conjunction with other early risk-stratification factors. Whether elevated WBC count is a marker of the inflammatory process or is a direct risk factor for AMI remains unclear. Given the simplicity and availability of the WBC count, the authors conclude that the WBC count should be used in conjunction with other ancillary tests to assess the prognosis of a patient with AMI.

Age Distribution↗
PubMed1990

Reevaluation of perioperative myocardial infarction in patients with prior myocardial infarction undergoing noncardiac operations.

We studied 275 patients with prior myocardial infarctions undergoing noncardiac operations to determine the incidence and outcome of perioperative myocardial reinfarction. Perioperative myocardial reinfarction developed in 13 patients (4.7%) of whom 3 (23%) died of cardiac causes. When time between prior myocardial infarction and the date of anesthesia was analyzed, the incidence of perioperative myocardial reinfarction was 4.3% at 0-3 mo, 0 at 4-6 mo, 5.7% at greater than 6 mo, and 3.3% at an indeterminate exact interval. None of the variables analyzed showed any significant correlation with the rate of reinfarction. The urgency of operation and aortic or vascular procedures were the only variables that approached, but failed to achieve, statistical significance.

Adult↗
PubMed2002

Risk factors indicating recurrent myocardial infarction after recovery from acute myocardial infarction.

Little is known of the risk factors of recurrent myocardial infarction (MI) among Japanese patients who have survived their first MI. The risk factors for the second MI were studied in 808 of 1,042 consecutive patients who recovered from an acute MI in Iwakuni National Hospital. Multivariate logistic regression analysis revealed that only 3 of 21 variables measured were closely related with the recurrence of MI during a follow-up period of 3.2 +/- 4.3 years: (1) transient atrial fibrillation (relative risk (RR) 3.16), (2) previous cerebrovascular accident (RR 3.05), and (3) dyslipidemia (RR 2.19). Of the parameters of dyslipidemia, a low ratio of high-density lipoprotein-cholesterol (HDL-C) to low-density lipoprotein-cholesterol (LDL-C) alone indicated subsequent MI. None of age, gender, location of the infarction, hypertension, diabetes mellitus, pulmonary congestion (Killip's class > or = 2), peak serum creatine kinase activity, serum total-cholesterol, HDL- and LDL-cholesterol levels, nor smoking habit on admission was a statistically significant predictor for the second MI. The result suggests that more intensive treatment is needed for patients with the 3 risk factors.

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