Reduction in Infarct Size, Arrhythmias, Chest Pain and Morbidity by Early Intravenous β-Blockade in Suspected Acute Myocardial Infarction

Yusuf, Salim; Rossi, P; Ramsdale, David R.; Pető, Richárd; Furse, L.; Motwani, Reena; Parish, S; Gray, Richard; Bennett, David; Bray, Colin; Sleight, Peter

doi:10.2165/00003495-198300252-00090

Cited by 42 publications

(41 citation statements)

References 15 publications

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“…For correlation analysis of the ranks of variables, Spearman correlation coefficients were calculated. In all other cases, pairwise signifi- (12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24) ... NS Antiarrhythmic drugs on day 1, n (%) 23 (27) 27 (33) 19 (25) 69 (28) ... NS Antiarrhythmic drugs after day 1, n (%) 12 (14) 9 (11) 11 (14) 32 (13) ... cance tests combined with a Bonferroni correction were used.…”

Section: Methodsmentioning

confidence: 96%

Significance of arrhythmias during the first 24 hours of acute myocardial infarction treated with alteplase and effect of early administration of a beta-blocker or a bradycardiac agent on their incidence.

et al. 1994

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BACKGROUND Although early intravenous beta-blocker therapy during acute myocardial infarction (AMI) reduces the incidence of fatal arrhythmias in patients not treated with thrombolytic agents, its antiarrhythmic effect in thrombolysed patients remains controversial. We investigated prospectively the arrhythmia incidence in 244 patients with AMI receiving alteplase and a double-blind randomized adjunctive therapy with intravenous atenolol, alinidine, or placebo. Moreover, the characteristics and prognostic significance of early arrhythmias and their relation with infarct size and coronary patency were evaluated. METHODS AND RESULTS All patients underwent 24-hour Holter monitoring on day 1 and were clinically followed in the hospital for 10 to 14 days. Coronary angiography was performed on day 10 to 14. Atenolol and alinidine significantly decreased the basic heart rate without causing more sinus arrest or higher-degree atrioventricular block. The prevalence of atrial fibrillation in alinidine patients was lower than in the atenolol patients (P = .007) but not lower than in placebo patients (P = .11). There was no effect of either agent on the incidence and frequency distribution of ventricular or supraventricular premature beats or on the incidence and characteristics of nonsustained ventricular tachycardia, accelerated idioventricular rhythm, sustained ventricular tachycardia (VT), or ventricular fibrillation (VF). On day 1, seven VF episodes were recorded in six patients (2.5%) and five VT episodes in five patients (2%). VF always started at < 2.5 hours after start of thrombolytic treatment and VT always at > 2.5 hours (average of 6 hours). Five of the seven VF and three of the five VT episodes started with an R-on-T. However, for all VT, the morphology of the first beat was the same as that of the following beats, suggesting that the sustained arrhythmia was not induced by an extrasystole. After day 1 and before hospital discharge, VF and VT developed in one and six patients, respectively. Three of the seven patients who developed VF during the first 2 weeks underwent coronary angiography; all three had an occluded infarct-related artery. In contrast, only one of nine patients with early or late VT had an occluded vessel. Patients with VT and VF on day 1 had a significantly larger enzymatic infarct size than those without the arrhythmia (P = .02), and a similar trend was noted for VT or VF after day 1 (P = .19). However, none of the patients with VT or VF on day 1 developed a life-threatening arrhythmia later during the hospital stay. Also, none of the seven patients with VT or VF after day 1 had experienced a major rhythm disturbance during the first 24 hours. CONCLUSIONS (1) Our data do not support the hypothesis that beta-blockers or bradycardiac agents might reduce the incidence of major arrhythmias when used in conjunction with thrombolytic therapy. (2) The pathogeneses of VT and VF early during AMI are clearly distinct. (3) VT or VF during the first 2 weeks is a marker for a larger infarct. (4) We could not detect a relation between malignant arrhythmias on day 1 and recurrences within the following 2 weeks.

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Section: Methodsmentioning

confidence: 96%

Significance of arrhythmias during the first 24 hours of acute myocardial infarction treated with alteplase and effect of early administration of a beta-blocker or a bradycardiac agent on their incidence.

et al. 1994

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“…7 Most analyses of the infarctlimiting effects of β-blockers were done in the prereperfusion era and yielded conflicting results. [8][9][10][11] Data on the cardioprotective effect of β-blockers during thrombolytic reperfusion are scarce, with just 1 randomized 12 and 1 nonrandomized 13 study, with contradictory results. In the era of primary PCI as the treatment of choice for STEMI, no randomized trials aiming to test the infarct-limiting effect of β-blockers have been published.…”

Section: Editorial See P 1487 Clinical Perspective On P 1503mentioning

confidence: 99%

Effect of Early Metoprolol on Infarct Size in ST-Segment–Elevation Myocardial Infarction Patients Undergoing Primary Percutaneous Coronary Intervention

et al. 2013

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Background-The effect of β-blockers on infarct size when used in conjunction with primary percutaneous coronary intervention is unknown. We hypothesize that metoprolol reduces infarct size when administered early (intravenously before reperfusion). Methods and Results-Patients with Killip class II or less anterior ST-segment-elevation myocardial infarction (STEMI) undergoing percutaneous coronary intervention within 6 hours of symptoms onset were randomized to receive intravenous metoprolol (n=131) or not (control, n=139) before reperfusion. All patients without contraindications received oral metoprolol within 24 hours. The predefined primary end point was infarct size on magnetic resonance imaging performed 5 to 7 days after STEMI. Magnetic resonance imaging was performed in 220 patients (81%). Mean±SD infarct size by magnetic resonance imaging was smaller after intravenous metoprolol compared with control (25.6±15.3 versus 32.0±22.2 g; adjusted difference, −6.52; 95% confidence interval, −11.39 to −1.78; P=0.012). In patients with pre-percutaneous coronary intervention Thrombolysis in Myocardial Infarction grade 0 to 1 flow, the adjusted treatment difference in infarct size was −8.13 (95% confidence interval, −13.10 to −3.16; P=0.0024). Infarct size estimated by peak and area under the curve creatine kinase release was measured in all study populations and was significantly reduced by intravenous metoprolol. Left ventricular ejection fraction was higher in the intravenous metoprolol group (adjusted difference, 2.67%; 95% confidence interval, 0.09-5.21; P=0.045). The composite of death, malignant ventricular arrhythmia, cardiogenic shock, atrioventricular block, and reinfarction at 24 hours in the intravenous metoprolol and control groups was 7.1% and 12.3%, respectively (P=0.21). Conclusions-In patients with anterior Killip class II or less ST-segment-elevation myocardial infarction undergoing primary percutaneous coronary intervention, early intravenous metoprolol before reperfusion reduced infarct size and increased left ventricular ejection fraction with no excess of adverse events during the first 24 hours after STEMI.

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“…5,[21][22][23][24] In these investigations, MI size was usually quantified either by postmortem analysis [15][16][17][18][19][20] or in vivo by indirect surrogates such as creatine kinase-MB fraction levels or ECG changes. 5,[21][22][23] With the advent of delayed-enhancement (DE) cardiac magnetic resonance imaging (CMR), it is now possible to accu-rately quantify the extent of myocardial necrosis in vivo. 25 It also has been shown that CMR can depict the area of myocardium at risk, which displays high signal intensity on T2-weighted images early after MI as a result of the presence of edema.…”

Section: Editorial P 2904 Clinical Perspective P 2916mentioning

confidence: 99%

Early Metoprolol Administration Before Coronary Reperfusion Results in Increased Myocardial Salvage

et al. 2007

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Background-␤-Blockers improve clinical outcome when administered early after acute myocardial infarction. However, whether ␤-blockers actually reduce the myocardial infarction size is still in dispute. Cardiac magnetic resonance imaging can accurately depict the left ventricular (LV) ischemic myocardium at risk (T2-weighted hyperintense region) early after myocardial infarction, as well as the extent of necrosis (delayed gadolinium enhancement). The aim of this study was to determine whether early administration of metoprolol could increase myocardial salvage, measured as the difference between the extent of myocardium at risk and myocardial necrosis. Methods and Results-Twelve Yorkshire pigs underwent a 90-minute left anterior descending coronary occlusion, followed by reperfusion. They were randomized to metoprolol (7.5 mg during myocardial infarction) or placebo. Global and regional LV function, extent of myocardium at risk, and myocardial necrosis were quantified by cardiac magnetic resonance imaging studies performed 4 and 22 days after reperfusion in 10 survivors. Despite similar extent of myocardium at risk in metoprolol-and placebo-treated pigs (30.9% of LV versus 30.6%; PϭNS), metoprolol resulted in 5-fold-larger salvaged myocardium (32.4% versus 6.2% of myocardium at risk; Pϭ0.015). The LV ejection fraction significantly improved in metoprolol-treated pigs between days 4 and 22 (37.2% versus 43.0%; Pϭ0.037), whereas it remained unchanged in pigs treated with placebo (35.1% versus 35.0%; PϭNS). The extent of myocardial salvage was related directly to LV ejection fraction improvement (Pϭ0.031) and regional LV wall motion recovery (Pϭ0.039) at day 22. Conclusions-Early metoprolol administration during acute coronary occlusion increases myocardial salvage. The extent of myocardial salvage, measured as the difference between myocardium at risk and myocardial necrosis, was associated with regional and global LV motion improvement. (Circulation. 2007;115:2909-2916.)

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Reduction in Infarct Size, Arrhythmias, Chest Pain and Morbidity by Early Intravenous β-Blockade in Suspected Acute Myocardial Infarction

Cited by 42 publications

References 15 publications

Significance of arrhythmias during the first 24 hours of acute myocardial infarction treated with alteplase and effect of early administration of a beta-blocker or a bradycardiac agent on their incidence.

Significance of arrhythmias during the first 24 hours of acute myocardial infarction treated with alteplase and effect of early administration of a beta-blocker or a bradycardiac agent on their incidence.

Effect of Early Metoprolol on Infarct Size in ST-Segment–Elevation Myocardial Infarction Patients Undergoing Primary Percutaneous Coronary Intervention

Early Metoprolol Administration Before Coronary Reperfusion Results in Increased Myocardial Salvage

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