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(Chest. 2004;125:831-840.)
© 2004 American College of Chest Physicians

Paradoxical Effect of Smoking in the Spanish Population With Acute Myocardial Infarction or Unstable Angina*

Results of the ARIAM Register

Manuel Ruiz-Bailén, MD, PhD; Eduardo Aguayo de Hoyos, MD, PhD; Antonio Reina-Toral, MD; Juan Miguel Torres-Ruiz, MD; Miguel Álvarez-Bueno, MD and Francisco Javier Gómez Jiménez, MD; for the ARIAM Group{dagger}

* From the Intensive Care Unit (Dr. Ruiz-Bailén), Critical Care and Emergency Department, Hospital de Poniente, El Ejido, Almería; Intensive Care Unit (Drs. Aguayo de Hoyos and Reina-Toral), Critical Care and Emergency Department, Virgen de las Nieves University Hospital, Granada; Intensive Care Unit (Dr. Torres-Ruiz), Critical Care and Emergency Department, Hospital San Cecilio, Granada; Intensive Care Unit (Dr. Álvarez-Bueno), Critical Care and Emergency Department, Carlos Haya University Hospital, Málaga, Granada; and Medicine Department (Dr. Gómez Jiménez), University of Granada, Granada, Spain.

Correspondence to: Manuel Ruiz-Bailén, MD, PhD. C/ Costa del Sol 12. Aguadulce, 04720 Roquetas de Mar. Almería, Spain; e-mail: ruizbailen{at}terra.es


   Abstract
TOP
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 Conclusions
 Appendix
 References
 
Objectives: The paradoxical effect of smoking after acute myocardial infarction (AMI) is a phenomenon consisting of a reduction in the mortality of smokers compared to nonsmokers. However, it is not known whether the benefit of this reduction in mortality is due to smoking itself or to other covariables. Despite acceptance of the paradoxical effect of smoking in AMI, it is not known whether a similar phenomenon occurs in unstable angina. The objective of this study was to investigate the paradoxical effect of smoking in AMI and unstable angina, and to study specifically whether smoking is an independent prognostic variable.

Methods and results: The study population was selected from the multicentric ARIAM (Análisis del Retraso en el Infarto Agudo de Miocardio [analysis of delay in AMI]) Register, a register of 29,532 patients with a diagnosis of unstable angina or AMI. Tobacco smokers were younger, presented fewer cardiovascular risk factors such as diabetes or hypertension, fewer previous infarcts, a lower Killip and Kimball class, and a lower crude and adjusted mortality in AMI (odds ratio, 0.774; 95% confidence interval, 0.660 to 0.909; p = 0.002). Smokers with unstable angina were younger, with less hypertension or diabetes. In the multivariate analysis, no statistically significant difference in mortality was found.

Conclusions: The reduced mortality observed in smokers with AMI during their stay in the ICU cannot be explained solely by clinical covariables such as age, sex, other cardiovascular factors, Killip and Kimball class, or treatment received. Therefore, smoking may have a direct beneficial effect on reduced mortality in the AMI population. The lower mortality rates found in smokers with unstable angina are not supported by the multivariate analysis. In this case, the difference in mortality can be explained by the other covariables.

Key Words: acute myocardial infarction • cigarette smoking • mortality • tobacco • unstable angina


   Introduction
TOP
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 Conclusions
 Appendix
 References
 
The association between smoking and heart disease was first suspected in the early 20th century. Subsequently, the direct relationship between smoking and development of coronary artery disease was confirmed.1 Smoking is associated with a higher incidence of acute myocardial infarction (AMI) and a higher incidence of death due to coronary artery disease. There is a clear dose-effect relationship that is minimized or eliminated after giving up smoking.2 Tobacco smoking is a predictive, independent variable for coronary atherosclerosis, AMI, and sudden death.3

There are multiple causes of this poor prognosis in smokers including, particularly, the following: (1) induction of states of hypercoagulability,4 as shown in human and animal studies that demonstrate that tobacco exposure increases fibrinogen levels and causes platelet aggregation,4 5 which in turn may enhance development of atherosclerosis6 and increase coronary artery occlusion in earlier stages of atheromatous disease by promoting platelet aggregation and thrombosis7 ; (2) nicotine-induced catecholamine release leads to increased heart rate, BP,8 and even arrhythmogenic effect9 ; and (3) induction of coronary artery vasoconstriction10 11 12 and reduction in oxygen delivery due to increased carbon monoxide levels.13

In view of the above, it would seem to be logical that tobacco smokers will have higher mortality rates than nonsmokers after AMI. However, this hypothesis has not been demonstrated. Rather, there is evidence that smokers with AMI have lower mortality, a finding known as the paradoxical effect of smoking.14 Many explanations have been proposed for the more favorable prognosis of smokers after AMI including, particularly, the following: (1) smokers are younger and less seriously ill, or have fewer comorbid conditions; (2) smokers have fewer cardiovascular risk factors; (3) coronary artery lesions are smaller; (4) there is greater myocardial preconditioning and/or greater coronary artery reperfusion, either spontaneous or due to greater efficacy of the thrombolysis acting on a thrombus, during the early phases of coronary atherosclerosis; (5) prehospital mortality is possibly higher in smokers; and (6) sudden withdrawal of smoking could have a beneficial effect.15 16 17 18

All of these explanations agree that the prognosis for these patients is better because smoking coexists with other decisive covariables of greater importance that have a direct influence on prognosis. Nevertheless, smoking itself may not have any real beneficial effect. A multivariate analysis performed to investigate whether smoking is an independent, protective variable against mortality showed a clear discrepancy in the results.15 16 17 18 19 20 21 Although there are many studies that have investigated the paradoxical phenomenon of smoking in AMI, the possible presence of this effect in unstable angina has not been studied sufficiently.

The objective of the present study was to investigate the paradoxical effect of smoking in Spanish patients with a diagnosis of acute coronary syndrome on admission to the ICU/critical care unit (CCU). The differences in the clinical outcome of smokers, ex-smokers, and nonsmokers in the AMI and unstable angina populations were studied, with particular focus on the prognosis. A multivariate analysis was also carried out to determine whether smoking is an independent, protective variable against mortality in patients with AMI or unstable angina.


   Materials and Methods
TOP
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 Conclusions
 Appendix
 References
 
Data Collection: the ARIAM Register
A descriptive study of a retrospective cohort including all patients in the ARIAM (Análisis del Retraso en el Infarto Agudo de Miocardio [analysis of delay in AMI]) Register Project, a multicentric Spanish study22 23 24 25 26 designed as an internal project to improve the quality of treatment of ischemic heart disease. The ARIAM Project was based in the ICUs and CCUs of 119 hospitals in Spain. The ARIAM Register includes all patients admitted to participating ICUs/CCUs with a diagnosis of AMI or unstable angina when the delay from symptom onset to hospital admission was < 24 h. The study period was from January 1995 to January 2001.

The patients selected for this study all had a diagnosis of AMI or unstable angina on admission to the ICU/CCU. AMI was defined as the presence of at least two of the following: coronary pain for > 30 min, ECG signs, and increase in creatine kinase (CK) level to twice the laboratory reference level. The extent of necrosis (determined according to ECG criteria) was evaluated according to four criteria: appearance of a new pathologic Q wave, ST elevation without QS development on hospital admission, no QS with ST depression on hospital admission, and nonspecifiable. Unstable angina was classified according to the criteria proposed by the Spanish Cardiology Society in 1995, which includes the following groups: initial, progressive, at rest, prolonged, variant, postinfarct, and secondary to other conditions such as arrhythmias, anemia, hypertension, etc.27

The patients were classified as ex-smokers, nonsmokers, and smokers; ex-smokers included patients who have not smoked for at least 3 months, nonsmokers included patients who have never smoked, and smokers included the remainder of the patients. Smoking was defined to include all possible forms of smoking, including pipes or cigarettes. The study population was divided into the following age groups: patients < 55 years old, patients 55 to 64 years old, patients 65 to 74 years old, and patients > 75 years old.

The following variables were studied: cardiovascular risk factors; maximum peak CK level recorded during hospital admission; severity on hospital admission, evaluated in the first 24 h using the APACHE (acute physiology and chronic health evaluation) II score28 ; poorest functional grade during admission to the emergency department or ICU/CCU using the Killip and Kimball classification29 ; mortality and mean length of stay; complications; and treatment received. The ARIAM Study Group also established a score with a range of 0 to 4 points to evaluate the efficacy of thrombolysis according to the following reperfusion criteria: fall in ST segment to < 50% of highest prethrombolysis elevation, peak CK level within the first 12 h after onset of symptoms, resolution of pain in < 30 min, and appearance of "reperfusion" arrhythmias (Table 1 and 1A ).


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  		Table 1. Differences Between Nonsmokers, Smokers, and Ex-smokers in Patients With AMI*

 

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  		Table 1A. Continued*

 
All complications occurring during the prehospital period or during admission to the emergency department or ICU/CCU were studied, as long as they had been adequately documented. The most significant complications studied include the following: hemorrhagic complications; hemodynamic complications, such as right-heart failure, cardiac tamponade, severe systemic hypertension, and cardiogenic shock; electrical complications, any type of arrhythmia or intraventricular conduction defect; clinical complications, such as angina of difficult control, reinfarction, pericarditis, postinfarct angina, onset of electromechanical dissociation, development of infectious process, and pulmonary or systemic embolism, including stroke; and mechanical complications or complications due to ICU/CCU procedures or other drugs administered.

Statistical Analysis
The Spanish version of the SPSS-10.0 statistical package (SPSS; Chicago, IL) was used for the statistical analysis. A descriptive analysis of all variables was carried out to obtain the distribution by frequencies. Analysis of variance was used to study the difference between the mean scores of the quantitative variables after testing for normality of the data using the Levene test for the equality of variance. The Pearson {chi}2 and Fisher exact tests were used to compare proportions. Univariate and multivariate analyses with binary logistic regression were used to compare the independent variables to the dependent variables. A multivariate analysis was carried out to investigate whether smoking is a protective variable against death in patients with AMI or unstable angina. The crude and adjusted odds ratio (OR) was calculated for each variable, taking into account all variables in which statistically significant differences were observed or which were clinically relevant in the multivariate analysis. The OR for each independent variable is expressed with 95% confidence intervals (CIs). Numerical data are presented as mean scores ± SD. Qualitative variables are expressed as absolute values and percentages; p < 0.05 was considered statistically significant.


   Results
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 Conclusions
 Appendix
 References
 
A total of 29,532 patients were added to the ARIAM Register during the study period. The mean age of the patients was 64.80 ± 12.29 years (± SD), and 72.8% were men. AMI was diagnosed in 17,761 of these patients, and unstable angina was diagnosed in 7,795 patients. The remainder of the patients had other diagnoses secondary to coronary heart disease. Of the total number of patients, 8,022 patients (27.2%) were smokers, 6,141 patients (20.8%) were ex-smokers, and 15,369 patients (52.0%) were nonsmokers.

Effect of Smoking in Patients With AMI
The mean age of the patients with AMI was 67.46 ± 10.34 years, and 24.6% were women. A total of 8,471 patients (47.7%) were nonsmokers, 5,796 patients (32.6%) were smokers, and 3,494 patients (19.7%) were ex-smokers. The global mortality after AMI was 9.8%. The patients with AMI who were smokers were younger, with a higher incidence of inferior/inferoposterior AMI, more Q-wave infarcts, and a lower incidence of complications. In terms of severity, both the Killip and Kimball classes and the APACHE II scores were lower in patients who were smokers. The cardiovascular risk factors were also different in these groups. Smokers presented a higher frequency of hypercholesterolemia and family history of cardiovascular risk. They also had a lower incidence of diabetes, hypertension, and previous angina, and required fewer percutaneous transluminal angioplasty (PTCA) procedures and fewer coronary bypass grafts prior to current hospital admission. The clinical course in smokers presented fewer complications, such as cardiogenic shock, lower incidence of reinfarction or extent of AMI, and fewer episodes of refractory postinfarct angina, but they had more episodes of primary ventricular fibrillation.

Nonsmokers required more diagnostic-therapeutic techniques, such as insertion of Swan-Ganz catheter, coronary angiography, cardiopulmonary resuscitation, mechanical ventilation, and a greater number of temporary pacemakers. With regard to coronary artery reperfusion techniques, there was a significantly higher number of PTCA stent, primary PTCA, and rescue PTCA in the smokers. Thrombolysis was more frequent, with a shorter delay after onset of the symptoms and a higher efficacy score in the smokers. There were also minor differences in terms of treatment: smokers were administered more beta-blockers and lipid-lowering drugs, and fewer angiotensin-converting enzyme (ACE) inhibitors, whereas the results for the ex-smokers were between those of the smokers and nonsmokers (Table 1) .

The primary result, the intra-ICU/CCU mortality, was 5% in smokers, 9.3% in ex-smokers, and 13.3% in nonsmokers. The study of mortality by age groups shows that the lower mortality rate in smokers and ex-smokers is shown in all the age subgroups (Fig 1 ). Smokers have a crude OR of 0.383 (95% CI, 0.336 to 0.437 [p < 0.0001]). After adjustment of this OR for age, other cardiovascular risk factors, site and extent of AMI, Killip and Kimball class, and treatment administered, with specific reference to thrombolysis, smoking continues to act as an independent, protective variable against mortality (OR, 0.774; 95% CI, 0.660 to 0.909 [p = 0.002]) [Table 2 ].



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  		Figure 1. AMI patient mortality by age group, subdivided into nonsmokers, smokers, and ex-smokers. See Table 1 for expansion of abbreviation.

 

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  		Table 2. Predictive Factors of Mortality in AMI Population

 
Effect of Smoking in Patients With Unstable Angina
The mean age of patients with unstable angina was 64.36 ± 11.38 years, whereas the mean age of the smokers subgroup was 7 years lower. There were 4,124 nonsmokers (52.9%), 1,721 smokers (22.1%), and 1,950 ex-smokers (25.0%). In the smokers subgroup, there was a significantly higher number of men. The only group with more men was the ex-smoker group. There were also differences between the groups in terms of the form of presentation of unstable angina: the initial form was more frequent in smokers, whereas prolonged angina was more common in nonsmokers. The higher incidence of variant angina in smokers is particularly noteworthy. A previous ischemic event was found more frequently in the ex-smokers group followed by the nonsmokers; the frequency was much lower in the group of active smokers. Both the APACHE II and the highest Killip and Kimball class scores were suggestive of lesser severity in smokers than nonsmokers (with levels of severity in between for ex-smokers). All of the cardiovascular risk factors (hypercholesterolemia, hypertension, diabetes, and cerebrovascular accidents) were more frequent in nonsmokers, with the exception of family history of a cardiovascular event (Table 3 ).


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  		Table 3. Univariate Analysis of Nonsmokers, Smokers, and Ex-smokers With Unstable Angina*

 
There were no differences between the different subgroups of patients with unstable angina in terms of progression to AMI or complications. However, there were differences in terms of treatment received, as beta-blockers were used more frequently in smokers whereas ACE inhibitors were used more frequently in nonsmokers. Nonsmokers required more reperfusion techniques such as angioplasty, stent insertion, and aortocoronary bypass. Interestingly, there was a difference in mortality; smokers had a mortality of 0.7%, ex-smokers had a mortality of 1.0%, and nonsmokers had a mortality of 1.5%. The adjusted OR for smokers in comparison to nonsmokers was 0.584 (95% CI, 0.322 to 1.059; p = 0.584). There was no statistically significant difference in the crude OR for ex-smokers in comparison to nonsmokers (OR, 0.811; 95% CI, 0.484 to 1.358; p = 0.425).


   Discussion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
Conclusions
 Appendix
 References
 
AMI
The results of this study also indicate that smoking has a paradoxical effect. The smokers group includes more men, and younger patients with fewer cardiovascular risk factors such as hypertension or diabetes. Interestingly, previously reported data have shown an association between smokers and family history of ischemic events, and it has even proposed that this may be due to a genetic interaction.30 31 A higher frequency of hypercholesterolemia was also observed, in contrast to some authors,32 and in agreement with others.3

As in previous studies,17 18 19 20 21 we found that smokers have infarcts with a possibly smaller extent, such as inferior AMIs, and fewer anterior or more complicated AMIs. They were in a higher Killip and Kimball class,17 18 19 20 21 32 and had fewer fatal complications. Interestingly, smokers had a lower incidence of previous angina or AMI. Therefore, although there is less myocardial preconditioning, they still had lower mortality rates.

Most studies20 32 that have shown a paradoxical effect of smoking attribute this effect to the covariables mentioned above, particularly with regard to lower age and lower comorbidity. They do not consider that the results of the multivariate analysis indicate the benefits of smoking. There are few studies21 33 34 that find smoking to be a protective variable against mortality, which is still valid after adjusting for the different variables. The disparity in the findings could be related to methodologic differences such as selection of patients receiving thrombolysis, sample size, or the variables included in the multivariate study.

The present study obtained data from unselected patients on a register. This was also the case in the National Register of Myocardial Infarction 2,35 a study with 510,044 patients in which smoking was found to be an independent variable for mortality that still had a protective effect after adjusting for the different variables. Our study agrees with the data obtained from this register. The results of the multivariate analysis show that, after adjusting for the different clinical covariables, tobacco smoking continues to act as an independent, protective variable against mortality. Therefore, the benefits or the "smokers’ paradox" cannot be explained solely by other covariables of severity associated with nonsmokers. In spite of the recognized harmful health effects, tobacco smoking may have a protective effect against mortality in patients who have an AMI. The factors by which smoking directly induces benefits are unknown. It may be that the type of coronary artery disease induced by smoking is different from that seen in nonsmokers.17 32 At any rate, tobacco smoking as an independent variable is associated with a better prognosis.

Unstable Angina
The term smokers’ paradox was first used for patients with AMI, since it has only been observed with AMI and not with unstable angina. The present study found that smokers clearly have a better prognosis. This may be influenced by the fact that the smokers are younger, have fewer cardiovascular risk factors, and fewer, less severe previous episodes of ischemia. These results are not compatible with possible greater myocardial preconditioning. Although smokers have a lower mortality, the multivariate analysis did not find that smoking was an independent variable for mortality. In this case, mortality can be explained by the other covariables mentioned.36 37

Ex-smokers
The results for ex-smokers were between those of smokers and nonsmokers, and ex-smokers had a better prognosis than nonsmokers. This finding would support the differences found between smokers and nonsmokers. Interestingly, as occurs with smokers, ex-smoker status is predictive of good prognosis in AMI.

Study Limitations
Despite the unequivocal results obtained, the findings of this study must be considered with caution since they are based on a register and, consequently, have all of the defects inherent in registers. Therefore, it may not include some clinical covariables. Smoking has been adjusted for the different clinical variables using the variables included in the register. The results might have been different if variables such as left ventricular ejection fraction or variables specific to coronary angiography, such as coronary artery lesions or the number of coronary arteries affected, were taken into account. There may be a selection bias since only those patients admitted to an ICU/CCU were studied, and patients not admitted to these units were not considered. Nevertheless, since the study was in patients with acute coronary syndrome, most of the patients were probably admitted to these units for intensive care and monitoring. Another possible selection bias, particularly for the patients with AMI, is that the study did not include the population that did not receive hospital or prehospital care. Therefore, we do not know how many patients died before receiving care in either of these settings. As this study was limited only to the period of ICU/CCU admission, the subsequent prognosis is not known.


   Conclusions
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 Conclusions
Appendix
 References
 
The reduced mortality observed in smokers with AMI during their stay in the ICU/CCU cannot be explained solely by clinical covariables such as age, sex, other cardiovascular factors, Killip and Kimball class, or treatment received. Therefore, smoking may have a direct beneficial effect on reduction of mortality in the AMI population. The reduced mortality observed in smokers with unstable angina can be explained by the different covariables.


   Appendix
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 Conclusions
 Appendix
References
 
Ariam Group Investigators (Analysis of the Delay in Acute Myocardial Infarction)
Hospital de Poniente, El Ejido: Manuel Ruiz Bailén, J.A. Ramos Cuadra, J.L. Fierro Rosón, A. Cárdenas Cruz. H. de Torrecárdenas, Almería: J.F. Martínez Coronel, F. Barrero Acedo, S. Martínez Escobar. H. de la Inmaculada, Huercal Overa: FJ. Rodríguez Pérez, FJ. Delgado Vilchez, J. Córdoba Escames. H. Puerta el Mar, Cádiz: A. Sánchez Rodríguez. H. Punta Europa, Algeciras: P. Cobos Castellanos, J. Rodríguez Medina. H. General de Puerto, Real: J.C. Rodríguez Yáñez, J. Gil Cebrián. H. Jerez: José Arias Garrido, Antonio Rodríguez Zapallo, L. Vallejo Sánchez. Hospital Naval San Carlos, Cádiz. Hospital Infanta Margarita, Cabra, Córdoba: C. de la Fuente Martos, R. Toro Sánchez. Hospital de la Cruz Roja, Córdoba: A. Guerrero Arjona. H. Reina Sofía, Córdoba: F. Dios Torronteras. Hospital Valle de los Pedroches, Pozoblanco, Córdoba: E. Lopera Lopera, F. Contreras Molina, JM. Molina Cantero. Hospital Comarcal de Baza, Baza, Granada: JL. Bellot Iglesias, MI. Rodríguez Higueras, P. Ramos, S. Ruiz Navarro. H. Virgen de las Nieves, Granada: A. Reina Toral, E. Aguayo de Hoyos. M Colmenero Ruiz, MM. Jiménez Quintana. H. Clínico de Granada: F. Barranco Ruiz, S. Shiaffino Cano, JM. Torres Ruiz. H. Santa Ana, Motril: JM. Mercado Ramos, I. Macias Guarasa. Hospital Alto Guadalquivir, Andújar, Jaén: MA. Fernández Sacristán, E. del Campo Molina, A. Bayona Gómez. Complejo Hospitalario Ciudad de Jaén: Ll. Rucabado Aguilar, JL. Muñoz Muñoz, E. Castillo Lorente. H. Princesa de España, Jaén: A. Carrillo Garrido. H. San Agustín, Linares: A. de Molina Ortega, JA. Camacho Pulido, A. Montijano Vizcaíno. H. San Juan de la Cruz, Úbeda: A. Bartolomé Sanz, MM. Sánchez Zorrilla Sanz. H. Carlos Haya, Málaga: JA. Ferriz Martín, T. García Paredes, JC. Escudero Valera. H. Clínico Universitario de Málaga: A. García Alcántara, María Victoria de la Torre Prados, Javier Merino Vega. H. Básico de Antequera: A. Varela López, G. Quesada García, M. Zaheri Beryanaki, A. Vázquez Vicente. H. de la Serranía, Ronda: JI. Mateo Sánchez, JM. García Álvarez, A. Poullet Brea. H. de la Axarquía, Vélez-Málaga: A. García García, F. Castillo Guerrero. H. Costa del Sol, Marbella: JA. Arboleda, R. Siendones, J. Prieto de Paula, Y. Fernández Jurado. H. Na Sa de la Merced, Osuna, Sevilla: B. Maza, R. Enamorado. Hospital Universitario Virgen del Rocío, Sevilla: J. Maraví Petri, A. García Lombardo. Hospital Vigil de Quiñones, Sevilla: J. Fajardo López-Cuervo. H. Comarcal de Melilla: F. Ríos Ortíz. Hospital Clínico Lozano Blesa, Zaragoza: E. Civeira, I. Gutiérrez Cia, J. González Cortijo. Hospital Royo Vilanova, Zaragoza, G. Olivar Duplá. Hospital de San Agustín, Avilés, Asturias: JM. Vega. Hospital de Cabueñes, Gijón, Asturias: JA. Lapuerta, M. González. Hospital Valle del Nalón, Sama de Langreo, Asturias: J. Megido. Hospital Verge del Toro, Mahó: Illes Balears. R. Fernández-Cid Bouza, MA. González López. Hospital General de Fuerteventura, Las Palmas: C. de la Rubia de Gracia, F. Cabeza Cabeza, P. Ventura Ventura, L. Fajardo Feo. Hospital Santos Reyes, Aranda de Duero, Burgos: P. Cancelo Suarez. Hospital General Yagüe, Burgos: A. Montón Rodríguez, M. Arroyo García, A. Zabalegui Pérez. Hospital Santiago Apóstol, Miranda de Ebro, Burgos: J. Armentia Fructuoso. Hospital del Bierzo, Ponferrada, León: Z. Ferreras Paez, C. Ruiz Pardo, F. Cañizares Castellanos, Ch. Martínez Jiménez, B. Álvarez Martínez, JJ. Sandoval Garzón. Hospital Río Carrión, Palencia: JB. López Messa, C. Berrocal de la Fuente. Hospital General de Segovia, Segovia: JJ. Cortina Gómez, P. Ancillo García, MA. Taberna Izquierdo. Hospital General de Soria, Soria: P. Medina Santaolalla. Hospital Río Hortega, Valladolid: JJ. Sanz Hernán. Hospital Virgen de la Concha, Zamora: A. Caballero Zirena. Hospital General de Catalunya, Sant Cugat, Barcelona: M. Nolla, R. Diaz Boladeras. Hospital de Tarrassa, Tarrassa, Barcelona: M. Valdés. Hospital Mútua de Terrassa, Terrassa, Barcelona: J. Nava. Hospital de Barcelona, Barcelona: J. Costa. Hospital Parc Tauli, Badalona, Barcelona: A. Ochagavia, F. Baigorri. Hospital Calella y Blanes, Calella, Barcelona: C. Sala. Hospital de Granollers, Granollers, Barcelona: P. Velasco. Creu Roja de L’Hospitalet, L’Hospitalet, Barcelona: A. Rovira. Centre Hospitalari de Manresa, Manresa, Barcelona: JM. Alcoberro. Hospital de Mataró, Mataró, Barcelona: X. Balanzó. Hospital Sant Joan, Reus, Barcelona: I. Vallverdú, B. Balsera. Hospital Joan XXIII, Tarragona: S. Alonso, J. Rello. Hospital Verge de la Cinta, Tortosa, Tarragona: R. Claramonte Porcar, I. Forcadell Ferré, G. Masdeu Eixarch. Hospital de Sant Pau i Santa Tecla de Tarragona, Tarragona: F. Bodí. Hospital de la Cruz Roja, Ceuta. ML. Centeno. Hospital Juan Canalejo, A Coruña: S. Calvo Barros, P. Jiménez Gómez, JM. Gulias López. Hospital Arquitecto Marcide, Ferrol, A Coruña: J. González Tutor, CJ. Fernández González. Complejo Hospitalario Xeral-Calde/Hospital Xeral-Calde, Lugo: AM. Ferreiro González, ML. Martínez Rodríguez. Hospital Cristal Piñor, Ourense: A. Díaz Lamas, R. Rodríguez Álvarez-Granados. Hospital Nosa Señora Nai: E. Rodríguez García, MJ. de la Torre Fernández. Hospital de Montecelo, Pontevedra: C. Miguez Baños, A. País Almozara. Hospital do Meixoeiro/Hospital Meixoeiro, Vigo, Pontevedra: D. Vila Fernández. H. Xeral de Vigo/Hospital Xeral-Cies, Vigo, Pontevedra: J. Fandiño Pena, S. López Astral. Hospital General La Mancha-Centro, Alcázar de San Juan, Ciudad Real: A. Canabal. Hospital General, Cuenca: L. Navarro, JC. Pérez. Hospital Príncipe de Asturias, Alcalá de Henares, Madrid: E. de la Fuente. Fundación Hospital Alcorcón, Alcorcón, Madrid: S. Temprano Vázquez. Hospital Severo Ochoa, Leganés, Madrid: F. del Nogal Sáez, J. Rebollo Ternero, J. López Martín. Clínica ICE, Madrid: T. Grau. Clínica Moncloa, Madrid: JJ. Oñoro Cañavera, V. Gómez Tello, JL. Moreno Hurtrez. Hospital del Aire, Madrid: JD. García. Hospital Militar Gómez Ulla, Madrid: JL. Soria. Hospital Nuestra Señora del Rosario, Madrid: A. García de la Gandara, S. Plaza García, V. Barrio Nebreda. Hospital La Paz, Madrid: P. López Lorente. Hospital de la Princesa, Madrid: E. Cereijo. Hospital Universitario San Carlos, Madrid: J. Miquel. Hospital de Móstoles, Mostoles, Madrid: FJ. Goizueta. Hospital Nuestra Señora del Prado, Talavera de la Reina, Toledo: M. Quintana, A. Simón Martín, J. González Rodríguez. Hospital Nuestra Señora del Rosario, Toledo: S. García Plaza, V. Barrio Nebreda. Hospital Virgen de la Salud, Toledo: M. Rodríguez. Hospital Comarcal, Melilla: Francisco Ríos. Hospital La Arrixaca, Murcia: A. Sánchez, G. Torres, FA. Jaime. Hospital General Universitario, Murcia: F. Felices Abad, C. Palazón Sánchez. Hospital Virgen del Rosell, Cartagena, Murcia: J. A. Melgarejo, FJ. Gil. Hospital Rafael Méndez, Lorca, Murcia: S. Nicolás Franco, J. Rodríguez. Hospital Morales Meseguer, Murcia: A. Carrillo Alcaraz, P. Jara. Hospital Virgen del Camino, Pamplona, Navarra: A. Manrique. Hospital García Orcoyen, Estella, Navarra: F. Sos. Hospital Santiago Apostol, Vitoria-Gasteiz. Hospital de Galdakao, Vizcaya: G. Hernando. Hospital San Millán, Logroño, La Rioja: FJ. Ochoa. Hospital General Universitario, Alicante: J. Cánovas Robles, C. García-Romeu García, M. Díaz Barranco, C. Ruiperez Cebrian. Clínica Vistahermosa, Alicante: M. Pérez Avilés, F. Ballenilla Antón, R. Nogueira Collado. Hospital Virgen de los Lirios, Alcoy, Alicante: F. Guardiola Navarro, A. Roche. Hospital Comarcal de Villajoyosa, Villajoyosa, Alicante: F. Criado Rodríguez, JM. Carrasco Barea.

Clínica Benidorm. Hospital Marina Alta, Denia, Alicante: C. Ortega Andrés, J. Cardona Peretó, P. Marzal Sorolla. Hospital Universitario de Elche, Alicante: J. Latour Pérez, FJ. Coves Orts, A. Mota López, JA. Martín. Hospital Comarcal de Elda, Alicante: JA. Rodríguez, JA. Martín, E. de Miguel Balsa. Hospital del S.V.S. Benidorm. Hospital Comarcal Vega Baja, Orihuela, Alicante: MD. Martínez, D. Olivares Toledo. Hospital Universitario de San Juan, Alicante: G. Pérez Planelles. Hospital General de Castellón, Castellón: A. Ferrandiz, A. Belenguer Muncharaz. Hospital Universitario La Fe, Valencia: R. Clemente García, J. Cuñat de la Hoz, MP. Fuset Cabanes. Hospital General Dr. Peset, Valencia: Ll. Miralles Serrano. Hospital General Arnau de Vilanova, Valencia: M. García Sanz, M. Francés Sempere. Hospital Clínico Universitario, Valencia: R. Oltra Chorna. Hospital Santa Lucía. Hospital Militar, Valencia: M. Rico Sola, M. Roig Dasi. Hospital Francesc Borja, Gandia, Valencia: J. Miñana Lorente. Hospital Lluis Alcanys, Xátiva, Valencia: JL. Martín Ruiz, V. Borillo Moles, S. Ferrandis Borras. Hospital Comarcal de Sagunto, Valencia: R. Calvo Embuena. H. 9 de Octubre. Valencia.

ARIAM Project Secretariat: Carlos Haya Regional University Hospital/Virgen de la Victoria University Hospital, Málaga. JM. Álvarez Bueno, JJ. Rodríguez García, E. Torrado González, J. Benitez Parejo/A. García Alcántara.


   Acknowledgements
 
We would like to express our thanks to Nohemi Gil Cortés, librarian of Poniente de Almería Hospital, for providing the reference material requested. We would also like to thank all those who participated in the ARIAM Project for their work and express our appreciation for the support provided by Boehringer-Ingelheim, which has enabled this register to continue active.


   Footnotes
 
Abbreviations: ACE = angiotensin-converting enzyme; AMI = acute myocardial infarction; APACHE = acute physiology and chronic health evaluation; ARIAM = Análisis del Retraso en el Infarto Agudo de Miocardio; CCU = critical care unit; CI = confidence interval; CK = creatine kinase; OR = odds ratio; PTCA = percutaneous transluminal coronary angioplasty

{dagger} The investigators and institutions participating in the ARIAM Group (www.ariam.net) are listed in the Appendix. Back

Received for publication March 12, 2003. Accepted for publication August 19, 2003.


   References
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 Conclusions
 Appendix
 References
 

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