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Background The relation between culprit plaque morphology and the clinical presentation of an acute myocardial infarction (AMI) has not been examined in detail. Purpose To study the culprit plaque morphology in patients with AMI with or without preinfarction angina using optical coherence tomography (OCT) imaging. Methods A total of 102 patients with AMI (32 STEMI, 70 NSTEMI) who underwent OCT imaging before percutaneous coronary intervention were enrolled. Patients were classified as: i) having either intermittent chest pain in the six hours preceding the final episode of pain, or unstable angina (or both) in the week preceding AMI (preinfarction angina group); or ii) having a single episode of chest pain without unstable symptoms in the preceding week (no preinfarction angina group). Culprit plaque was classified as plaque rupture (PR) or intact fibrous cap (IFC), as previously described. Prati thrombus score was calculated, and the prevalence of calcification, neovascularization, and OCT-defined macrophage accumulation was assessed. Results Patients with preinfarction angina showed a significantly higher prevalence of IFC than PR, while those without preinfarction angina showed a significantly higher prevalence of PR than IFC (Figure). PR in patients with preinfarction angina were more frequently associated with macrophage accumulation, while those in patients without preinfarction angina were not (Figure). White thrombus tended to be more frequent in patients with preinfarction angina than in those without (85.7% vs. 63.6%, p=0.097), and Prati thrombus score tended to be lower [22.0 (15.8–30.3) vs. 38.5 (12.8–67.5), p=0.145]. Calcifications were significantly less frequent in patients with preinfarction angina than in those without (22.0% vs. 40.4%, p=0.045), while neovascularization tended to be more frequent (58.0% vs. 42.3%, p=0.113). Conclusions Patients with preinfarction angina have a distinct culprit plaque phenotype, frequently characterized by IFC and a relatively lower thrombotic burden, probably reflecting a prevalence of reparative mechanisms and spontaneous thrombolytic activity in these patients.

Objective: The appearance of collaterals during ST-elevation myocardial infarction (STEMI) and clinical factors potentially associated with their early appearance were studied. Background: The appearance of collaterals is associated with the duration of chronic coronary occlusion. Nevertheless, the question remains as to whether collaterals are already apparent shortly after an acute coronary occlusion. Results: The appearance of collaterals was studied during STEMI, in 187 patients who underwent angiography at various times after the onset of symptoms. For the onset-to-angiography groups of 0–6 h, >6–9 h, >9–24 h, >1–7 days, >7–14 days and >14 days, the prevalence of angiographic collaterals (Rentrop classification 2–3) were 19, 31, 41, 40, 50 and 68%, respectively (p < 0.001). Among the clinical factors, preinfarction angina was the only independent determinant (odds ratio 3.1; 95% CI: 1.2–8.5). Conclusion: As in chronic coronary occlusion, after acute occlusion the appearance of angiographic visible co...

OBJECTIVE The objective of this study was to investigate the predictors of preinfarction angina (PA) and to show the association between PA and coronary ectasia (CE). METHODS A total of 222 patients with acute myocardial infarction were included. All patients were treated with primary coronary intervention and interviewed by the staff physicians within 24 h of presentation after reperfusion had succeeded. The patients were classified according to the presence of PA and CE. All groups were compared statistically according to their clinicodemographic characteristics and angiographic results. Regression analysis was performed to show the predictors of PA. RESULTS Half of the patients were defined as preinfarction angina (48.2%) and the success rate of primary coronary intervention did not differ statistically in the PA present group. More than half of the patients had multivessel disease and coronary ectasia was found in the 11.7%. The right coronary artery (RCA) was the most common localization for ectasia and 61.5% of the ectatic vessels were also infarct-related. Diabetes mellitus, hypertension and previous coronary heart disease were slightly more common in the PA present group. In the regression analysis, coronary ectasia, multivessel disease and previously diagnosed coronary artery disease were independent predictors of PA (P = 0.001, P = 0.01 and P = 0.03, respectively) CONCLUSIONS CE is more common in patients with PA and more than half of the patients showed CE in the infarct-related vessel. CE and multivessel disease are independent predictors of PA. The success rate of primary coronary intervention in ectatic infarct-related vessels did not differ in the PA group.

Eur J Clin Invest 2011; 41 (11): 1220–1226 Abstract Background Preinfarction angina, a possible form of ischaemic preconditioning, improves the prognosis in patients who experience a major ischaemic event; though the associated pathophysiology is not yet fully understood. The aim of this study was to determine the possible involvement of endothelial progenitor cells (EPC), the vascular endothelial growth factor (VEGF) and the hepatocyte growth factor (HGF) in the development of preinfarction angina. Methods and results We studied 41 patients (60·5 ± 12 years; 34% women) and 14 healthy controls; 43·9% of the patients had preinfarction angina. No differences were found in the baseline characteristics of the two groups. Although the EPC, VEGF and HGF were raised as compared with the control group, no significant differences were found according to the presence or absence of preinfarction angina in the levels of EPC (baseline, P = 0·25; day 3, P = 0·11; day 7, P = 0·32), VEGF (baseline, P = 0·96; day 3, P = 0·06; day 7, P = 0·57) or HGF (baseline, P = 0·18; day 3, P = 1; day 7, P = 0·86). An association was seen in the patients who had preinfarction angina between the EPC levels at baseline and on days 3 and 7 and the HGF on admission with the time from the angina to the STEMI (β = −0·070; β = −0·066; β = −0·081; β = −80·16; P

BACKGROUND AND HYPOTHESIS: Although prodromal angina occurring shortly before an acute myocardial infarction (MI) has protective effects against in‐hospital complications, this effect has not been well documented after initial hospitalization, especially in older or diabetic patients. We examined whether angina 1 week before a first MI provides protection in these patients. METHODS: A total of 290 consecutive patients, 143 elderly (>64 years of age) and 147 adults (

In animals, brief episodes of ischemia before a total coronary occlusion protect the heart and result in a smaller myocardial infarct size. In humans, episodes of angina before acute myocardial infarction might also confer a preconditioning or protective effect; numerous studies show that preinfarction angina is associated with smaller infarcts. Preinfarction angina is also associated with reductions in ventricular dysfunction, arrhythmias and incidence of no-reflow phenomena, and, in some cases, improved survival. The protective effect of preconditioning in humans is characterized by marked individual variations and seems to be attenuated in women, people with diabetes and the elderly. Exercise seems to be an important way to induce preconditioning in humans and preserves it in the elderly.

An approximate model for nonlinear self-induced vibrations of a myocardium pump which involves in situ experiments on evaluation of the resonance, Q-factor, and elastic parameters of a cardiac circuit (cavity) in the frequency range of 0.1–15 Hz is presented. A concept of a fast diagnosis of human preinfarction angina by the pulse at the wrist is proposed.

The present study investigated the relationship between myocardial damage and C-reactive protein (CRP) levels, with no increase in creatine kinase (CK) activity, immediately after the onset of acute myocardial infarction (AMI) in 85 patients with their first reperfused anterior AMI without CK elevation on admission and no ischemic events during hospitalization. Patients were classified into those with low levels (0.3 mg/dl) of CRP (Group L; n=67) and those with high levels (or =0.3 mg/dl) of CRP (Group H; n=18). Group H had a higher proportion of patients with a history of preinfarction angina (89 vs 55%, p0.01), especially unstable angina. SigmaST in leads V1-6 on admission ECG was lower in Group H than in Group L (14+/-7 vs 21+/-13 mm, p0.05). Predischarge left ventriculography showed that the left ventricular global ejection fraction (55+/-11 vs 48+/-10%, p0.01) and SD/chord at the left anterior descending artery lesion (-1.7+/-0.9 vs -2.3+/-0.9, p0.01) were better in Group H. Multivariate analysis demonstrated that both CRP on admission (p=0.011) and preinfarction angina (p=0.002) were independently associated with better regional wall motion (SD/chord-2.0) before discharge. These results suggest that the clinical situation of elevated CRP immediately after onset is associated with less myocardial damage and better left ventricular function in reperfused anterior AMI.

This study assesses the effects of early and late reperfusion of the infarct-related coronary artery and collateral circulation developed after infarction on left ventricular morphology and function in 22 patients with a first acute anterior myocardial infarction and without long-standing preinfarction angina. The patients were categorized into 4 groups: group A-5 patients with successful reperfusion within 6 h after the onset of infarction: group B-6 patients with late patency of the infarct-related coronary artery; group C-6 patients without recanalization of the infarct-related coronary artery who had good collateral circulation (collateral index (CI) = 2 or 3); and group D-5 patients without recanalization who had either poor or no collateral circulation (CI = 0 or 1). The left ventricular size and function were evaluated by means of contrast left ventriculography during the chronic stage of infarction. The left ventricular global and regional functions were preserved better (p < 0.05) in group A than in the other three groups. Although there was no difference in regional wall motion of the infarct area among groups B, C and D, the ejection fraction was greater (p < 0.05) and the percentage perimetric circumference was smaller (p < 0.05) in groups B and C than in group D. Among the 4 groups, the left ventricular end-diastolic volume index tended to be greater in group D. Thus, these results suggest that blood supply to the infarct area is essential for the preservation of left ventricular size and function regardless of the timing and route.

Background Preinfarction angina (PrA), clinical equivalent of ischemic preconditioning, confers protection against inhospital mortality for acute myocardial infarction (AMI) in adult but not in elderly patients. This study aims to examine the interaction between physical activity and body mass index (BMI) in preserving the cardioprotective effect of PrA in elderly patients with AMI. Design Elderly patients (Z65 years old) with AMI admitted to Coronary Care Unit. Methods Elderly patients with AMI were retrospectively stratified for the presence and absence of PrA, and for quartiles of BMI and physical activity. In-hospital outcomes (death, cardiogenic shock, and reinfarction and creatine kinase-MB peak) were evaluated. Results In-hospital mortality of 1014 elderly patients with AMI was 19.2% in those with PrA and 22.7% in those without (P = 0.18, NS). Mortality further decreased with increased physical activity and reduced BMI, a trend that was not observed in patients without PrA. When physical activity and BMI were considered together, lowest in-hospital mortality was observed in patients with highest physical activity and normal BMI (from 18.2 to 9.6%; P < 0.01) with the greatest reduction observed in patients with PrA (from 18.3 to 5.1%; P =0.02). Multivariate analysis showed that PrA did not exert a protective effect in all patients irrespective of physical activity and BMI. A protective role was, however, observed in patients with highest physical activity or normal BMI and reached a maximum protective role in patients who showed both highest physical activity and normal BMI [odds ratio =0.08; 95% confidence interval = 0.02–0.72; P < 0.01]. Conclusion The cardioprotective effect of PrA was preserved in elderly patients who showed the highest physical activity and a normal BMI.

FUNDAMENTO: A angina pré-infarto (API) pode ser um marcador de pré-condicionamento isquêmico. Foi demonstrada redução da área infartada, do remodelamento ventricular, da incidência de insuficiência cardíaca, choque cardiogênico ou morte, quando a API estava presente. Esses resultados foram mais evidentes em adultos, porém, não em idosos. OBJETIVO: Avaliar a relação entre API e a evolução clínica de pacientes idosos com infarto agudo do miocárdio (IAM). MÉTODOS: Estudo tipo série de casos com grupo de comparação. Foram incluídos 36 pacientes com diagnóstico de IAM com elevação do segmento ST. Os pacientes foram distribuídos em grupo A (21 pacientes com API) e grupo B (15 pacientes sem API). RESULTADOS: A idade média da população estudada foi 70,5 anos. A maioria (73%) dos pacientes era do sexo masculino. O índice de massa corpórea médio foi 25,3 kg/m2. A amostra era constituída por 77,8% de hipertensos, 27,8% de diabéticos e 32,4% de dislipidêmicos. Dor torácica tipo A foi relatada por 71,4% dos estudados. A maioria (72,2%) dos idosos foi classificada em Killip I. Os desfechos clínicos nos grupos A e B foram: angina pós-infarto 9,5% versus 20%, p=0,630; insuficiência cardíaca 23,8% versus 13,3%, p=0,674; revascularização de urgência 4,8% versus 6,7%, p=1; arritmia cardíaca 0% versus 6,7%, p=0,417. Não foi constatado nenhum caso de reinfarto, choque cardiogênico e morte até 30 dias em ambos os grupos. CONCLUSÃO: A presença da angina pré-infarto não se associou com uma melhor evolução clínica em idosos acometidos por IAM nesta série de casos.

Background The aim of the present study was to clarify the effect of preinfarction angina pectoris (PIA) on myocardial blush grade (MBG), a simple marker of myocardial tissue-level reperfusion, in acute myocardial infarction (AMI). Methods and Results One hundred forty-two patients with first anterior wall AMI who were admitted within 6 h after onset of symptoms were examined. PIA was defined as typical chest pain within 48 h before onset of symptoms. MBG was evaluated by coronary angiography after reperfusion. Patients with MBG 2 or 3 (n=103) had a higher frequency of PIA and a lower frequency of diabetes mellitus than those with MBG 0 or 1 (n=39) (57% vs 28%, p=0.004, and 23% vs 44%, p=0.03, respectively). The former had a lower peak creatine kinase level and a greater left ventricular ejection fraction at predischarge than the latter (3,652±2,440 vs 5,507±3,058 IU/L, p=0.0002, and 57±12% vs 45±11%, p

Introduction and objectives. The occurrence of preinfarction angina (PA) reduces the extent of myocardial necrosis, increases the volume of viable myocardium, and improves left ventricular function. However, there is no agreement about the effect of PA on mortality. The objective of this study was to determine whether PA is associated with in-hospital mortality. Method. A meta-analysis (fixed effects model) of all published reports evaluating in-hospital mortality in patients with acute myocardial infarction according to the presence or absence of PA was performed. PA was defined as the occurrence of angina in the 24 hours before onset of the infarction. We searched the Medline and Embase databases in June 2004 using “preinfarction angina or prodromal angina and mortality” as search terms. Six studies involving a total of 3497 patients were finally identified. Results. Only one study reported that PA had a statistically significant beneficial effect on in-hospital mortality. However, combining the data showed that the presence of PA was associated with a significant decrease in the probability of in-hospital death (odds ratio=0.61; 95% CI, 0.48-0.78; P

Transient episodes of angina preceding acute myocardial infarction may both, protect the myocardium by ischemic preconditioning or damage it when associated with coronary microembolization. We now studied the potential loss of ischemic preconditioning with coronary microembolization. Anesthetized pigs (group 1; n=8) were subjected to 90 min sustained low-flow ischemia. Group 2 (n=8) was subjected to coronary microembolization (i.e. microspheres; 42 microm slashed circle; 3000 per ml min-1 inflow) 35 min before sustained ischemia. In group 3, coronary microembolization was followed 10 min later by one cycle of ischemic preconditioning (10 min ischemia/15 min reperfusion) before subsequent sustained ischemia. Infarct size was determined after 2 h reperfusion by triphenyl tetrazolium chloride staining. Infarct size after sustained ischemia alone (group 1) was 19.4+/-3.4% of the area at risk (mean+/-S.E.M.). With coronary microembolization before sustained ischemia (group 2) infarct size was only slightly larger (23.6+/-4.6%, ns). In group 3 with microembolization followed by ischemic preconditioning, infarct size was reduced to 12.7+/-3.0% (P0.05 vs. group 2). The relationships between infarct size and transmural blood flow in groups 1 and 3 were not different, giving the impression that ischemic preconditioning failed to protect microembolized myocardium. However, additional coronary microembolization shifted the relationship between infarct size and blood flow upwards to a larger infarct size at any given blood flow. Thus when comparing the relationship of group 3 to its true control (group 2), it was shifted downwards (P0.05; analysis of covariance (ANCOVA)) indicating persistent protection of microembolized myocardium by ischemic preconditioning. Coronary microembolization induces additional infarction when superimposed on sustained ischemia but does not interfere with the endogenous protection by ischemic preconditioning.

Background: Preinfarction angina (PA) and early reperfusion of infarct-related arteries have been shown to reduce infarct size in patients with acute myocardial infarction (AMI). The beneficial effects of PA on infarct size have been attributed to the development of ischemic preconditioning and faster coronary recanalization in patients treated with thrombolytic therapy (TT). Objective: To evaluate the effect of PA on clinical coronary reperfusion time in patients with AMI receiving successful TT. Methods: Seventy-five patients presenting with AMI (within 6 h after the initial onset of symptoms) were studied. All patients received TT and were evaluated with coronary angiography (CA) at predischarge. The patients were divided into two groups: group 1 (PA-positive) comprised those who experienced a new onset of prodromal angina within 72 h before the onset of AMI. Group 2 (PA-negative) comprised those who had a sudden onset of AMI without the preceding angina. The successful myocardial reperfusion criteria after TT were ST segment resolution of 50% or greater, the appearance of reperfusion arrhythmias and the resolution of chest pain. The time of reperfusion criteria was recorded after TT. CA was performed in all patients at predischarge. Patients with no patent infarct-related arteries on CA and clinical failure of reperfusion were excluded from the study. Results: Clinical characteristics, risk factors and angiographic findings did not differ significantly between the groups. The time interval from the start of continuous chest pain to TT was also similar between the groups. The left ventricular ejection fraction was higher and there were less frequent ventricular arrhythmias in patients with PA than in those without PA (47.9±7.4 versus 44.4±8.1, P=0.041, and 17.1% versus 37.5%, P=0.043, respectively). The clinical reperfusion time was significantly shorter in the patients with PA than in those without PA (68.2±24.5 min versus 81.4±19.3, P=0.012). The clinical reperfusion time was positively correlated with age and the time interval from the start of continuous chest pain to TT but inversely related to the presence of PA. Conclusions: In patients with AMI preceded by PA, TT resulted in more rapid clinical reperfusion than in patients without PA. Thus, earlier myocardial reperfusion may account for smaller infarct size and better prognosis in patients with PA. © 2005 Pulsus Group Inc. All rights reserved.

BACKGROUND: Preinfarction angina (PA) and early reperfusion of infarct-related arteries have been shown to reduce infarct size in patients with acute myocardial infarction (AMI). The beneficial effects of PA on infarct size have been attributed to the development of ischemic preconditioning and faster coronary recanalization in patients treated with thrombolytic therapy (TT).

WOS: 000221490800003, PubMed: 15090697, Immune-mediated mechanisms are thought to play a key role in the,development of coronary artery disease and its thrombotic complications. Preinfarction angina has been suggested to improve left ventricular function and short-term outcomes. The purpose of the present study was to investigate the relation between the immune response and in-hospital clinical course in preinfarction angina. We prospectively evaluated 93 patients. Forty-three patients exhibited. preinfarction angina within 24 hours before the onset of acute myocardial infarction (AMI) (preinfarction angina group) and 50 patients were free from preinfarction angina (sudden onset group). The incidence of complications (heart failure, recurrent angina, arrhythmia and coronary interventions) and in-hospital mortality were assessed in the two study groups. We detected some immune markers, including white blood cells, C-reactive protein, immunoglobulins, and complement. White blood cells and CRP were significantly lower in the preinfarction angina group than in the sudden onset group (P < 0.001, P < 0.005, respectively). Conversely, IgE and C-4 were significantly higher in the preinfarction angina group than in the sudden onset group (P < 0.001, P < 0.001, respectively). The incidences of heart failure and severe arrhythmias were lower in the preinfarction group than in the Sudden onset group (P < 0.005, P < 0.05 respectively). The beneficial effect of preinfarction angina may be associated with an immune-inflammatory response modified by a brief ischemic episode.

Background The aim of this study was assessment of left ventricular (LV) systolic and diastolic function by pulsed wave Doppler tissue imaging (DTI) in patients with or without preinfarction angina in acute myocardial infarction. Methods We prospectively evaluated 31 consecutive patients (4 women, 27 men; age 58 ± 10 years) with a first acute myocardial infarction. LV systolic and diastolic function was assessed by classic methods and DTI on the third day during acute myocardial infarction. Patients were divided into 2 groups according to the presence (group 1; n=10) or absence (group 2; n=21) of preinfarction angina. Mitral inflow velocities and early diastolic mitral annular velocity (Em), late diastolic mitral annular velocity (Am), peak systolic mitral annular velocity, Em/Am, the ratio of early diastolic mitral inflow velocity (E) to Em, and myocardial performance index were calculated by DTI. Results Group 1 had significantly higher Em and Em/Am than group 2 (11.3 ± 3.34 cm/s vs 7.4 ± 2.07 cm/s, P P = .001, respectively). The E/Em ratio and myocardial performance index were significantly lower in group 1 than in group 2 (5.1 ± 2.92 vs 8.10 ± 3.15, P = .018; 0.49 ± 0.15 vs 0.65 ± 0.24, P = .042, respectively). Wall-motion score index was lower in those with preinfarction angina than in those without (1.6 ± 0.36 vs 1.9 ± 0.39; P = .04, respectively). Peak systolic mitral annular velocity and Am were not statistically different between groups (9.4 ± 1.84 vs 8.3 ± 2.03, P = .172; 11.7 ± 3.07 vs 12.1 ± 3.34, P = .72, respectively). There were no significant differences between the 2 groups regarding transmitral E velocity, atrial contraction mitral inflow velocity (A), E/A ratio, isovolumetric relaxation time, and deceleration time of the mitral E wave ( P = .91, P = .08, P = .58, P = .81, and P = .71, respectively). Conclusion LV diastolic function was better in patients with preinfarction angina than in patients without. This condition could not be detected by conventional mitral inflow Doppler velocities, but could be detected by DTI. This preliminary evidence shows that DTI is better than conventional mitral Doppler indices in the assessment of a favorable LV diastolic function in patients with preinfarction angina.

We studied the effect of preinfarction angina on in-hospital outcomes after percutaneous coronary intervention for anterior and nonanterior acute myocardial infarction. Beneficial effects of preinfarction angina on infarct size and in-hospital outcome are evident in patients with anterior infarction, but not in those with nonanterior infarction.

OBJECTIVES: To evaluate the influence of preinfarction angina on the long-term survival rate of non-thrombolized patients. MATERIAL AND METHODS: A prospective, observational study, in which 122 patients admitted at the coronary care unit at Hospital Nacional Edgardo Rebagliati Martins with a diagnosis of acute myocardial infarction (AMI) who did not undergo thrombolysis and survived to the acute intrahospitalary period, who were followed through a period of 5 years, was made. The main outcome measures were overall mortality and cardiac events. Patients were divided into 4 groups according to the presence or not, and characteristics of preinfarction angina. RESULTS: Kaplan-Meier analysis showed that those with preinfarction angina had a shorter survival and more cardiac events, as compared with those without preinfarction angina (p < 0,05). History of angina more than 30 days before AMI also correlates with shorter survival and more cardiac events, as compared with those without preinfarction angina or with recent onset angina (p

Despite the cardioprotective effect of rapid coronary reperfusion, the effects of spontaneous recanalization on myocardial viability and metabolism are unknown. We studied whether preinfarction angina affords cardioprotection when spontaneous coronary reperfusion occurred in acute infarct patients. Myocardial tomographies with thallium and I-123-labeled-beta-methyl-p-iodophenyl penta-decanoic acid (BMIPP) were performed in 27 acute myocardial infarct patients treated medically: 15 patients had preexisting angina before infarction (group A) and 12 did not (group B). Thallium and BMIPP abnormalities and regional function were quantified by a polar map and contrast ventriculography, respectively. There was no significant difference between thallium and BMIPP in the severity index in groups A and B (89 +/- 97 vs. 85 +/- 68, 97 +/- 28 vs. 95 +/- 27, respectively), and no significant difference between the groups in the thallium or BMIPP severity index. The ratio of the thallium severity index to that of BMIPP and the regional wall-motion abnormality index were identical in groups A and B. Both patient groups were divided into 2 subgroups based on the presence or absence of spontaneous coronary reperfusion: subgroups A1 and A2, and subgroups B1 and B2, respectively. There were no significant differences among the 4 subgroups in severity indexes for both tracers, the thallium/BMIPP ratio, or the asynergy score. The BMIPP severity index correlated significantly with that of thallium in all subgroups, but no significant difference between the regression lines was found. It is therefore unlikely that spontaneous coronary recanalization affords beneficial effects through preservation of myocardial viability in an ischemia-related zone, suggesting that the cardioprotective effect of preinfarction angina is a limited phenomenon in patients undergoing rapid coronary reperfusion.

The protective effects of preinfarction angina were evaluated in acute myocardial infarction (AMI) treated by primary percutaneous transluminal coronary angioplasty (PTCA) and stenting. We studied 613 patients with AMI. Group 1 (n = 306) was treated by conventional medical therapies and coronary thrombolysis and group 2 (n = 307) was treated by primary PTCA supported by stenting. Each group was subdivided into those with and without preinfarction angina within 24 hours before the onset of AMI. There was no significant difference in clinical characteristics between the subgroups of groups 1 and 2. In group 1, there were differences between patients with preinfarction angina (n = 84) and those without (n = 222) in in-hospital mortality (11% vs 18%), pump failure (Killip classes 3 and 4) (11% vs 21%, p0.05), left ventricular ejection fraction at discharge (52 +/- 13% vs 48 +/- 14%, p0.05), and peak creatine kinase (2,106 +/- 1,637 vs 2,764 +/- 2,154 U/L, p0.02). In group 2, however, there was no significant difference between those with preinfarction angina (n = 82) and those without (n = 225) in mortality (6% vs 6%), pump failure (12% vs 12%), left ventricular ejection fraction (50 +/- 13% vs 50 +/- 13%) and peak creatine kinase (3,285 +/- 2,306 vs 3,291 +/- 2,262 U/L). Multivariate analysis indicated that preinfarction angina was an independent determinant of in-hospital death and pump failure in group 1, but not in group 2. We conclude that the protective effects of preinfarction angina in AMI are not evident in those treated by primary PTCA and stenting, possibly because of the overwhelming protective effects of complete coronary revascularization provided by primary PTCA and stenting.

To resolve the question of whether coronary thrombolysis for acute myocardial infarction is more effective in patients with or in those without chronic preinfarction angina, we retrospectively analyzed cineventriculograms in 54 patients with the first anterior Q-wave myocardial infarction during the chronic stage of myocardial infarction. Patients were divided into 2 groups according to the presence (group A, n = 24) or absence (group B, n = 30) of chronic preinfarction angina. In group A, 16 had either intracoronary (n = 6) or intravenous (n = 10) coronary thrombolysis with urokinase within 6 h after the onset of acute myocardial infarction. In group B, 11 had either intracoronary (n = 4) or intravenous (n = 7) coronary thrombolysis within 6 h after the onset of acute myocardial infarction. Global left ventricular ejection fraction and regional wall motion in infarct areas were evaluated quantitatively. In group A, the percentage of systolic segment shortening in infarct areas was 20 +/- (SD) 16% in patients with thrombolytic therapy and 17 +/- 15% in those with conventional therapy (p = NS). By contrast, in group B, the regional wall motion in infarct areas was significantly (p0.01) better in patients with thrombolytic therapy compared to those with conventional therapy (13 +/- 10 vs. 3 +/- 8%). Thus, patients without chronic preinfarction angina might benefit from coronary thrombolysis, while in those with preinfarction angina the beneficial effect of thrombolytic therapy may be relatively limited.

Background and Objectives:By measuring the coronary flow reserve (CFR) and echocardiographic left ventricular function, the purpose of this study was to evaluate the effect of pre-infarction angina (PA) on myocardial protection in patients with acute myocardial infarction (AMI). Subjects and Methods:Sixty-two patients (mean 54±10 years, 51 males) with first anterior AMI were studied. CFR, defined as the ratio of hyperemic (hAPV) to baseline APV (bAPV), was measured at least 24 hours after the onset of AMI at the left anterior descending artery (mean 7±4 days) with a Doppler wire. Echocardiography was performed at admission (baseline) and during follow-up periods (mean 9±7 month). All patients were divided into two groups according to the presence of PA within 72 hours prior to AMI:group A (with PA, n=27) and group B (without PA, n=35). Results:Between the two groups, CFR were higher in group A (2.1±0.5 vs.1.6±0.5, p