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At least 1,297 records · Page 72Linked to original sources
PubMed2005

Relation of impaired Thrombolysis In Myocardial Infarction myocardial perfusion grades to residual thrombus following the restoration of epicardial patency in ST-elevation myocardial infarction.

Clinical and angiographic data were analyzed from 929 patients who had ST-elevation myocardial infarction and open epicardial arteries after fibrinolytic therapy. Residual angiographically evident thrombus was associated with more frequent Thrombolysis In Myocardial Infarction (TIMI) grade 2 flow (33.6% vs 26.8%, p = 0.03), higher corrected TIMI frame counts (34 vs 31 frames, p = 0.0003), and lower TIMI myocardial perfusion grades (43.0% vs 32.0% TIMI myocardial perfusion grades 0/1, p = 0.001) among all patients and among patients who had TIMI grade 3 flow (33.5% vs 26.0% TIMI myocardial perfusion grades 0/1, p = 0.043). In multivariate analyses, angiographically evident thrombus was associated with higher corrected TIMI frame counts and worsened myocardial perfusion independent of clinical and angiographic covariates, including TIMI grade 3 flow.

Blood Flow Velocity↗
PubMed2005

ST-segment depression on the initial electrocardiogram in acute myocardial infarction-prognostic significance and its effect on short-term mortality: A report from the National Registry of Myocardial Infarction (NRMI-2, 3, 4).

This study analyzed 255,256 patients who had acute myocardial infarction and were enrolled in the National Registry of Myocardial Infarction 2, 3, and 4 (1994 to 2002). The objective was to determine in-hospital mortality rate among patients who had ST-segment depression on the initial electrocardiogram. Patients who had ST-segment depression had an in-hospital mortality rate (15.8%) similar to that of patients who had ST-segment elevation or left bundle branch block (15.5%). After adjusting for observed differences, ST-segment depression was associated with only a slightly lower odds ratio (0.91) of mortality compared with ST-segment elevation or left bundle branch block.

Aged↗
PubMed2006

Effect of reactive hyperemia after coronary recanalization on myocardial tissue reperfusion by thrombolysis in myocardial infarction flow grade in acute myocardial infarction.

Thrombolysis In Myocardial Infarction (TIMI) flow grade is widely used to evaluate myocardial tissue reperfusion in acute myocardial infarction (AMI), but the current grading system is incomplete. Therefore, we clarified the regulation of epicardial coronary flow velocity with the progression of microvascular dysfunction in AMI. We studied 36 patients with first anterior AMI. After intervention, we assessed TIMI flow grade and measured average peak velocity (APV) at baseline and after infusion of adenosine triphosphate (48 microg; baseline and hyperemic APVs, respectively) with a Doppler guidewire. We performed myocardial contrast echocardiography after 2 weeks to assess microvascular integrity (good reflow vs no reflow) and left ventriculography at admission and discharge (24 +/- 2 days) to measure regional wall motion (SD/chord). Patients were classified into 3 groups based on TIMI flow grade and microvascular integrity: TIMI grade 3 flow/good reflow (n = 16), TIMI grade 3 flow/no reflow (n = 12), and TIMI grade 2 flow (n = 8). Baseline APV was comparable in the patients with TIMI grade 3 flow but hyperemic APV was higher in patients with TIMI grade 3 flow/good reflow than in those with TIMI grade 3 flow/no reflow (hyperemic APV 59.3 +/- 25.8 vs 32.8 +/- 8.9 cm/s, p <0.01). All patients with TIMI grade 2 flow showed no reflow and the lowest values of baseline and hyperemic APVs. Regional wall motion at discharge was higher in patients with TIMI grade 3 flow/good reflow than in those with TIMI grade 3 flow/no reflow and TIMI grade 2 flow (-1.44 +/- 0.70, -2.69 +/- 0.31, and -2.88 +/- 0.48 SD/chord, respectively, p <0.01). In conclusion, compensatory reactive hyperemia preserves epicardial coronary flow velocity even in patients with microvascular damage, and with the progression of damage, this compensatory hyperemia can no longer preserve epicardial coronary flow velocity, and baseline APV is decreased in TIMI grade 2 flow.

Adult↗
PubMed2005

Combination of site of infarct, unrecognized glucose intolerance, and reinfarction after acute myocardial infarction in normotensive subjects is determinant of the development of subsequent systemic hypertension: a pilot study.

BACKGROUND: The natural history of hypertension in healthy normotensive subjects has been described in the Framingham population. We aim to study the rate of progression to hypertension in normotensive subjects after acute myocardial infarction (AMI). METHODS: One hundred seventy-three consecutive normotensive subjects admitted to the Coronary Care Unit with AMI were studied retrospectively with prospective follow-up 4 years after AMI. All the patients who were not known to be diabetic on admission (n = 150) underwent glucose tolerance test (GTT) at 2 months after AMI. RESULTS: Among the 15 patients (8.7%) who developed hypertension, GTT was abnormal in 75% (diabetes = 3, impaired glucose tolerance = 9). There were significantly more Indo-Asians and fewer whites in the hypertensive than in the normotesive patients but they were similar in age and gender, creatinine kinase level, and rate of thrombolysis during admission for AMI. Multiple regression analysis showed that progression to hypertension was a function of the presence of anterior AMI on admission (P = .0297), abnormal GTT (P = .0156), and subsequent MI on follow-up (P = .0122), but was independent of age, gender, smoking habit, body weight, previous MI, thrombolysis, creatinine kinase level, subsequent development of heart failure, and intake of beta-adrenergic blockade or angiotensin-converting enzyme (ACE) inhibitor. Of the hypertensive patients, 47% (n = 7) died compared to 8% (n = 13) of the normotensive subjects (P < .0001). CONCLUSIONS: Progression to hypertension in normotensive subjects after AMI is determined by a combination of the site of the infarct, GTT 2 months after AMI, and subsequent development of a second MI. Systemic hypertension after AMI is associated with a high mortality.

Aged↗
PubMed2005

Prediction of depressive disorder following myocardial infarction data from the Myocardial INfarction and Depression-Intervention Trial (MIND-IT).

BACKGROUND: Depression following myocardial infarction (MI) is associated with complicated cardiac rehabilitation, non-compliance and poor prognosis. Whether depression following MI can be predicted from variables routinely assessed during hospitalization for MI is unknown. METHODS: Using data from the Myocardial INfarction and Depression-Intervention Trial (MIND-IT), we identified 2,177 MI patients (mean age 63 years; 23% female). Patients were randomly divided into a derivation and a validation sample. In the derivation sample, we analyzed variables potentially associated with the development of post-MI depressive disorder, which were tested in the validation sample. RESULTS: In the year following MI, 18.5% suffered from depressive disorder (ICD-10 criteria). In a multivariate model, factors associated with depression were younger age (OR 1.94; CI 1.38-2.74), hypercholesterolemia (OR 1.68; CI 1.08-2.61), the use of calcium channel blockers at discharge (OR 1.80; CI 1.20-2.71), and left ventricular ejection fraction (LVEF) (OR 4.14 for patients with LVEF <30%; CI (2.42-7.10). The derived predictors were tested in the validation sample. The final model yielded two clinical predictors, i.e., younger age and severe LV-dysfunction, which correctly predicted post-discharge depression status in 82.9% of the MI patients. The model yielded a high negative predictive value (89%). A positive depression questionnaire (BDI) during hospitalization increased the positive predictive value of 23% to 52%. CONCLUSIONS: During hospitalization for MI and using a two-step strategy with common clinical variables, i.e., younger age, severe LV-dysfunction and BDI score during hospitalization, it is possible to identify MI patients with a high risk for subsequent development of depression.

Adult↗
PubMed2006

White blood cell count adds prognostic information to the thrombolysis in myocardial infarction risk index in patients following primary percutaneous coronary intervention (ANIN Myocardial Infarction Registry).

AIMS: To determine the relationship between baseline white blood cell (WBC) count, Thrombolysis in Myocardial Infarction (TIMI) risk index, and 30-day mortality in unselected patients with ST-elevation myocardial infarction (STEMI) treated with primary mechanical reperfusion (PCI). METHODS AND RESULTS: 903 patients from prospective registry admitted for primary PCI to a tertiary cardiological center. Both baseline WBC count and TIMI risk index data were dichotomized about the respective medians. Overall 30-day mortality was 4.3%. Higher WBC count was associated with adverse clinical outcome (6.3% vs. 2.4%; Kaplan-Meier p=0.004) as were higher TIMI risk index values (7.2% vs. 1.4%; Kaplan-Meier p<0.00001). In addition, median WBC count stratified patients within TIMI risk index strata into very low risk (0%), intermediate risk (3.3%) and high risk (11%) (Kaplan-Meier p=0.023 and p=0.005 for comparison of lower and higher WBC count within TIMI risk index stratas). In multivariate analysis WBC count provided independent and additional to TIMI risk index predictive information (Hosmer-Lemeshow p=0.57 and p=0.88 respectively for predictive value of TIMI risk index alone and combined with WBC count). Other independent predictors of death were current smoking (RR 0.33; 95% CI: 0.13-0.87) and previous MI (RR 3.13; 95% CI: 1.28-7.69). CONCLUSIONS: WBC count may be a simple and useful tool for risk stratification in STEMI patients, providing additional to established risk index prognostic information. Our findings stress the strong correlation of inflammation and poor outcome in STEMI patients, which may indicate directions of development of new therapies.

Aged↗
PubMed2004

A randomized trial of rescue angioplasty versus a conservative approach for failed fibrinolysis in ST-segment elevation myocardial infarction: the Middlesbrough Early Revascularization to Limit INfarction (MERLIN) trial.

OBJECTIVES: We sought to compare emergency coronary angiography with or without rescue percutaneous coronary intervention (PCI) with conservative treatment in patients with failed fibrinolysis complicating ST-segment elevation myocardial infarction (STEMI). BACKGROUND: Most patients with STEMI receive fibrinolytic therapy and aspirin. The management of failed fibrinolysis is unclear. METHODS: A total of 307 patients with STEMI and failed fibrinolysis were randomized to emergency coronary angiography with or without rescue PCI or conservative treatment. RESULTS: Thirty-day all-cause mortality was similar in the rescue and conservative groups (9.8% vs. 11%, p = 0.7, risk difference [RD] 1.2%, 95% confidence interval [CI] -5.8 to 8.3). The composite secondary end point of death/re-infarction/stroke/subsequent revascularization/heart failure occurred less frequently in the rescue group (37.3% vs. 50%, p = 0.02, RD 12.7%, 95% CI 1.6 to 23.5), driven by less subsequent revascularization (6.5% vs. 20.1%, p < 0.01, RD 13.6%, 95% CI 6.2 to 21.4). Re-infarction and clinical heart failure were less common in the rescue group (7.2% vs. 10.4%, p = 0.3, RD 3.2%, 95% CI -3.3 to 9.9; and 24.2% vs. 29.2%, p = 0.3, RD 5.7%, 95% CI -4.3 to 15.6, respectively). Strokes and transfusions were more common in the rescue group (4.6% vs. 0.6%, p = 0.03, RD 3.9%, 95% CI 0.5 to 8.6; and 11.1% vs. 1.3%, p < 0.001, RD 9.8%, 95% CI 4.9 to 19.9, respectively). Left ventricular function at 30 days was the same in the two groups. CONCLUSIONS: Rescue angioplasty did not improve survival by 30 days, but improved event-free survival, almost completely due to a reduction in subsequent revascularization. Rescue angioplasty was associated with more strokes and more transfusions and did not result in preservation of left ventricular systolic function at 30 days.

Angioplasty, Balloon, Coronary↗
PubMed2004

Accuracy of dipyridamole myocardial contrast echocardiography for the detection of residual stenosis of the infarct-related artery and multivessel disease early after acute myocardial infarction.

OBJECTIVES: We aimed to evaluate the ability of vasodilator myocardial contrast echocardiography (MCE) to detect significant infarct-related artery (IRA) stenosis and multivessel disease (MVD) after thrombolysis. BACKGROUND: The detection of residual IRA stenosis subtending significant viable myocardium and the identification of MVD may help to triage patients who may benefit from mechanical revascularization after acute myocardial infarction (AMI) and thrombolysis. METHODS: Patients with AMI underwent low-power MCE at rest and after dipyridamole stress during SonoVue infusion seven to 10 days after thrombolysis. RESULTS: Of the 73 patients, 61 demonstrated significant myocardial viability, of whom 57 (93%) showed significant IRA stenosis. Sensitivities to detect >50% IRA stenosis and MVD were 88% and 72%, respectively. The accuracy of detecting significant coronary stenosis in the anterior (left anterior descending coronary artery) versus inferoposterior (right coronary artery/left circumflex artery) circulation was similar for both IRA (85% vs. 91%) and remote territories (91% vs. 81%). Quantitative peak contrast intensity (p = 0.02), microbubble velocity (p = 0.0001), and myocardial blood flow (p < 0.0001) were significantly lower in patients with significant coronary stenosis during dipyridamole compared with rest. Only beta reserve discriminated various grades of coronary stenosis. CONCLUSIONS: Use of MCE accurately predicted significant IRA stenosis and MVD after thrombolysis. This information is valuable for identifying patients who may benefit from mechanical revascularization.

Aged↗
PubMed2005

Antiarrhythmic effect of carvedilol after acute myocardial infarction: results of the Carvedilol Post-Infarct Survival Control in Left Ventricular Dysfunction (CAPRICORN) trial.

OBJECTIVES: Whether beta-blockers reduce atrial arrhythmias and, when added to an angiotensin-converting enzyme (ACE) inhibitor, ventricular arrhythmia is unknown. BACKGROUND: Ventricular and atrial arrhythmias are common after acute myocardial infarction (AMI) and are associated with a poor prognosis. Angiotensin-converting enzyme inhibitors reduce the incidence of both types of arrhythmia. METHODS: The antiarrhythmic effect of carvedilol was examined in a placebo-controlled multicenter trial, the Carvedilol Post-Infarct Survival Control in Left Ventricular Dysfunction (CAPRICORN) study, which enrolled 1,959 patients with reduced left ventricular systolic function after AMI, 98% of whom were treated with an ACE inhibitor. RESULTS: The incidence of atrial fibrillation/flutter was 53 to 984 (5.4%) in the placebo group and 22 to 975 (2.3%) in the carvedilol group, giving a carvedilol/placebo hazard ratio (HR) of 0.41 (95% confidence interval [CI] 0.25 to 0.68; p = 0.0003). The corresponding rates of ventricular tachycardia/flutter/fibrillation were 38 to 984 (3.9%) and 9 to 975 (0.9%) (HR 0.24, 95% CI 0.11 to 0.49; p < 0.0001). CONCLUSIONS: Carvedilol has a powerful antiarrhythmic effect after AMI, even in patients already treated with an ACE inhibitor. Carvedilol suppresses atrial as well as ventricular arrhythmias in these patients.

Adrenergic beta-Antagonists↗
PubMed2006

Fractional flow reserve of infarct-related arteries identifies reversible defects on noninvasive myocardial perfusion imaging early after myocardial infarction.

OBJECTIVES: We hypothesized that fractional flow reserve (FFR) of an infarct-related artery (IRA) early after myocardial infarction (MI) identifies inducible ischemia on noninvasive imaging. BACKGROUND: Early after MI, IRAs frequently have angiographically indeterminant lesions. Whether FFR can detect reversible perfusion defects early after MI when dynamic microvascular abnormalities are present is not known. METHODS: Rest and dipyridamole (DP)-stress 99mTc sestamibi single-photon emission computed tomography (SPECT) were performed in 48 patients 3.7 +/- 1.3 days after MI, with 23 patients undergoing concurrent myocardial contrast echocardiography (MCE). Angiography, FFR, and percutaneous coronary intervention (PCI) of the IRA (as necessary) were subsequently performed. Follow-up SPECT was performed 11 weeks after PCI to identify true reversibility on baseline SPECT. RESULTS: The sensitivity, specificity, positive and negative predictive value, and concordance of FFR < or =0.75 for detecting reversibility on SPECT were 88%, 50%, 68%, 89%, and 71% (chi-square <0.001), respectively; which improved to 88%, 93%, 88%, 93%, and 91% (chi-square <0.001), respectively, for the detection of true reversibility. The corresponding values of FFR < or =0.75 for detecting reversibility on DP-MCE were 90%, 100%, 100%, 75%, and 93% (chi-square <0.001), respectively, and on either SPECT or MCE were 88%, 93%, 91%, 91%, and 91% (chi-square <0.001), respectively. The optimal FFR value for discriminating inducible ischemia on noninvasive imaging was 0.78. CONCLUSIONS: Fractional flow reserve of the IRA accurately identifies reversibility on noninvasive imaging early after MI. These findings support the utility of FFR early after MI.

Aged↗
PubMed2006

Acute anterior myocardial infarction followed by acute inferoposterior myocardial infarction: the case of the necrotic QRS counterpoise.

A case of a 55-year-old man who suffered an acute anterior myocardial infarction (MI) followed by an acute inferoposterior MI 1 month later, which led to his demise from cardiogenic shock, is presented. The electrocardiogram after his second MI resulted in profound decrease in the amplitude of the QRS complexes and cancellation of the features of the previous anterior MI (necrotic QRS counterpoise). The implications of these electrocardiogram alterations, particularly when using this modality in QRS scoring systems for estimation of infarct size or left ventricular function, are discussed.

Electrocardiography↗
PubMedDate not supplied

Influence of infarct-zone viability detected by rest Tc-99m sestamibi gated SPECT on left ventricular remodeling after acute myocardial infarction treated by percutaneous transluminal coronary angioplasty in the acute phase.

BACKGROUND: The purpose of this study was to assess the value of technetium 99m sestamibi gated single photon emission computed tomography (SPECT) in predicting the evolution of left ventricular volumes in patients treated successfully in the acute phase of a myocardial infarction (MI). METHODS AND RESULTS: Twenty-nine patients with acute MI and early percutaneous transluminal coronary angioplasty (PTCA) were included in this study. A rest Tc-99m sestamibi electrocardiography (ECG)-gated SPECT study was performed 21 +/- 5 days after PTCA. The myocardial perfusion index was calculated by use of a semiautomatic sectorial analysis. All patients had contrast ventriculography performed during the acute phase and 6 months later. The patients were separated into two groups according to the absence (group I, n = 21) or presence (group II, n = 8) of end-systolic enlargement. The perfusion index in the infarct sectors was -2.29 +/- 2.90 SD in group I and -6.40 +/- 2.85 SD in group II ( P < .01). With a cutoff value of -2.46 SD, the sensitivity and specificity of Tc-99m sestamibi SPECT for the prediction of end-systolic volume enlargement were 100% and 62%, respectively. When the functional data from ECG-gated acquisitions were added, specificity increased to 86%. CONCLUSIONS: Despite successful PTCA in the acute phase of MI, an increase in end-systolic volume was observed at 6 months in 28% of patients. Tc-99m sestamibi ECG-gated SPECT performed 3 weeks after the acute phase could predict this enlargement with a high accuracy.

Angioplasty, Balloon↗
PubMedDate not supplied

Reducing infarct size in the setting of acute myocardial infarction.

Acute myocardial infarction is caused by coronary occlusion, and the mainstay of treatment has become reperfusion by either coronary angioplasty with possible stenting or surgical bypass grafting. Unfortunately, reperfusion can seldom be done soon enough to prevent infarction. Thus, the search for effective cardioprotection has been ongoing for more than 3 decades. After establishment of a suitable animal model to test the efficacy of pharmacological agents and other interventions, investigators found ischemic preconditioning to be a powerful and reproducible cardioprotectant. Much of the signaling pathway from cell receptor to end-effector has now been established even if the identity of the latter has not been proven. Remarkably, the actual protection is believed to occur during reperfusion rather than during ischemia. Yet, the clinical applicability of ischemic preconditioning is limited because of the obligate need to initiate it before ischemia. However, several strategies have been developed that can be applied at the time of reperfusion and which, therefore, hold clinical promise. These interventions are thought to trigger the same signaling cascades as ischemic preconditioning, which include activation of extracellular signal-regulated kinase and phosphatidylinositol 3-kinase and also somehow prevent mitochondrial permeability transition pore formation. Ultimately, deployment of any of these strategies for clinical use must involve the pharmaceutical industry, which is becoming increasingly reluctant to be involved. Before any approach is tested in the clinical arena, however, it should be thoroughly vetted in preclinical settings. Only then can industry maximize the chances that its application in man will have the highest chance of success.

Animals↗
PubMed1998

TIMI 11B. Enoxaparin versus unfractionated heparin for unstable angina or non-Q-wave myocardial infarction: a double-blind, placebo-controlled, parallel-group, multicenter trial. Rationale, study design, and methods. Thrombolysis in Myocardial Infarction (TIMI) 11B Trial Investigators.

Continuous intravenous (i.v.) heparin administered in the acute period after unstable coronary artery disease reduces the likelihood and severity of subsequent ischemic events. However, reactivation of the thrombotic process may occur when heparin therapy is withdrawn. Low-molecular-weight heparin provides more reliable anticoagulation and less need for patient monitoring and dosage adjustment than standard unfractionated heparin (UFH) and therefore is well suited for long-term anticoagulation on an outpatient basis. TIMI 11B is a randomized, double-blind, placebo-controlled clinical trial designed to compare the strategy of combined short-term and long-term administration of the low-molecular-weight heparin enoxaparin for unstable angina/non-Q-wave myocardial infarction versus the standard strategy of UFH administration only during the acute phase. Patients are randomized to receive either enoxaparin (30 mg i.v. bolus followed by subcutaneous (s.c.) injections of 1.0 mg/kg every 12 hours) or UFH (70 U/kg bolus followed by an infusion of 15 U/kg per hour, titrated to an activated partial thromboplastin time of 1.5 to 2.5 times control). Infusion of i.v. UFH or placebo continues for a minimum of 72 hours. S.c. weight-adjusted enoxaparin or placebo continues until hospital discharge or day 8, whichever comes first, at which time the long-term phase of the study begins. Patients randomized to receive enoxaparin in the acute phase receive fixed-dose s.c. enoxaparin (60 mg every 12 hours for patients > or =65 kg, 40 mg every 12 hours for patients <65 kg). Patients randomized to receive UFH in the acute phase receive s.c. placebo injections during the chronic phase. The primary efficacy endpoint is the sum, through day 43, of the occurrence of death, nonfatal myocardial infarction not present at enrollment, or severe recurrent ischemia requiring urgent revascularization. The primary safety endpoint is the occurrence of either major bleeding or other serious adverse events.

Angina, Unstable↗
PubMed1999

Value of ST-segment elevation pattern in predicting infarct size and left ventricular function at discharge in patients with reperfused acute anterior myocardial infarction.

BACKGROUND: The implication of the shape of ST elevation in the acute phase of myocardial infarction (MI) remains unclear. METHODS AND RESULTS: We examined the relation between the shape of ST elevation and infarct size in 77 patients who had a first acute anterior MI with successful reperfusion within 6 hours from symptom onset. A 12-lead electrocardiogram was recorded immediately before reperfusion confirmed by coronary angiography. The shape of ST elevation in lead V3 was classified into 3 types: concave type (n = 24), straight type (n = 41), and convex type (n = 12). For concave type, straight type, and convex type, a median value of peak creatine kinase was 2287, 4371, and 5322 mU/mL, and left ventricular ejection fraction measured by left ventriculography at discharge (14 days after MI) was 58%, 48%, and 41% (P <.05; concave type versus the other 2 types), respectively. A multivariate logistic regression model demonstrated that the concave type of ST elevation was a strong predicting factor for preserved left ventricular function (left ventricular ejection fraction >/=50% at discharge; odds ratio 6.2, 95% confidence interval 1.6 to 20.8, P =.019). CONCLUSIONS: In patients with reperfused acute anterior MI, left ventricular function was excellent in patients with concave type, intermediate in those with straight type, and relatively poor in those with convex type ST elevation at discharge. This simple classification is useful for predicting left ventricular function at discharge.

Adult↗
PubMed2000

Trends in acute myocardial infarction management: use of the National Registry ofMyocardial Infarction in quality improvement.

Cardiovascular disease, including acute myocardial infarction (AMI), is the leading cause of death in the United States and was the primary disease category among hospital discharges in 1996. Efforts to improve hospital care of patients with AMI should be measured and assessed routinely for appropriateness of care and improvement of medical staff performance. The National Registry of Myocardial Infarction (NRMI), an observational Phase IV study, has enrolled > 1 million AMI patients since 1990, and is now in its third phase. NRMI 3 collects patient data and facilitates the measurement of improvement in care and outcomes, while allowing participating institutions to benchmark their performance against national, state, and like-hospital data. Three measures from NRMI 3 are accepted for the Joint Commission on Accreditation of Healthcare Organizations' ORYX initiative: (1) aspirin use within 24 hours of AMI diagnosis; (2) door-to-drug time for fibrinolysis; and (3) no initial reperfusion strategy given to eligible patients.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2001

Effect of preinfarction angina pectoris on outcome in patients with acute myocardial infarction treated with primary angioplasty (results from the Myocardial Infarction Registry.

Preinfarction angina is associated with better clinical outcome in patients with acute myocardial infarction (AMI) who receive intravenous thrombolysis. This has not been proved in patients with AMI treated with primary angioplasty. We analyzed the data of the prospective multicenter Myocardial Infarction Registry (MIR). Of 14,440 patients with AMI, 774 with a prehospital delay of < or =12 hours were treated with primary angioplasty. Five hundred thirty-two patients (68.7%) had preinfarction angina. Patients with preinfarction angina were slightly older than patients without (63 vs 62 years, p = 0.042), prehospital delay was 1 hour longer (180 vs 120 minutes, p = 0.001), and arterial hypertension was more prevalent (47.6% vs 32.2%, odds ratio [OR] 1.91, 95% confidence intervals [CI] 1.39 to 2.62). There was no significant difference in hospital mortality (5.6% vs 3.3%, OR 1.75, 95% CI 0.79 to 3.87), reinfarction, stroke, or the combined end point of death, reinfarction, or stroke between the 2 groups. Logistic regression analysis showed no association of preinfarction angina with the occurrence of either death (OR 2.21, 95% CI 0.91 to 6.08) or the combined end points (OR 1.10, 95% CI 0.55 to 2.31). There was also no significant difference in mortality (6% vs 5.1%, OR 1.19, 95% CI 0.56 to 2.52), reinfarction, stroke, postinfarction angina, or the combined end points between patients with preinfarction angina within 48 hours compared with patients with preinfarction angina between 49 hours and 4 weeks before the AMI. Thus, the MIR data showed no protective effects of preinfarction angina in patients with AMI treated with primary angioplasty.

Angina Pectoris↗
PubMed2001

Magnesium use in the treatment of acute myocardial infarction in the United States (observations from the Second National Registry of Myocardial Infarction).

The use of magnesium in patients with acute myocardial infarction (AMI) is debated, largely as a result of conflicting data from randomized controlled trials. This study evaluated the use and impact on mortality of intravenous magnesium in the treatment of patients with AMI in the United States based on data from the Second National Registry of Myocardial Infarction. Only 5.1% of 173,728 patients from 1,326 hospitals received intravenous magnesium within the first 24 hours after an AMI, and this was more common in the 59,798 patients who received thrombolytic therapy or who underwent primary percutaneous transluminal coronary angioplasty (PTCA) or coronary bypass grafting (CABG) than in the 113,930 patients who did not receive any reperfusion therapy (8.5% vs 3.4%, p <0.01). Magnesium use was associated with younger age, Q-wave AMI, congestive heart failure on admission, thrombolytic therapy, primary PTCA or CABG, ventricular tachycardia or ventricular fibrillation, and beta blocker or lidocaine use in the first 24 hours (all odds ratio > 1.2, p <0.001). Magnesium use was associated with increased mortality (odds ratio 1.25, 95% confidence interval 1.12 to 1.34) and with a higher mortality in patients without initial reperfusion therapy (20.2% vs 13.2%, p <0.0001) or who underwent primary PTCA or CABG (10.2% vs 7.3%, p = 0.002), but not in patients who received thrombolytic therapy (6.2% vs 5.9%, p = NS). Thus, magnesium is used infrequently in the treatment of AMI and may be associated with worse outcome.

Aged↗