Impact of spontaneous anterograde flow of the infarct artery on left ventricular function in patients with a first anterior wall acute myocardial infarction

To assess the impact of spontaneous anterograde flow of the infarct artery on outcomes in patients with acute myocardial infarction (AMI), we studied 478 patients with a first anterior wall AMI who underwent coronary angiography within 12 hours after the onset of chest pain; Thrombolysis In Myocardial Infarction (TIMI) 3 flow was obtained after reperfusion therapy. Patients were divided into 3 groups: 119 patients with spontaneous anterograde flow (initial TIMI 2 or 3 flow) of the infarct artery, 118 patients with an initially occluded artery (TIMI 0 or 1 flow) and time to angiography or=55% (odds ratio 7.13, 95% confidence interval 3.10 to 16.4, p <0.001). In conclusion, although very early reperfusion improved LV function more than late reperfusion, spontaneous anterograde flow was associated with better acute and predischarge LV function after AMI compared with very early reperfusion of an initially occluded artery.     

Impact of prodromal angina pectoris and white blood cell count on outcome of patients with acute myocardial infarction

BACKGROUND: Elevation of white blood cell (WBC) count at admission is associated with adverse outcome after acute myocardial infarction (AMI). Prodromal angina, by the mechanism of ischemic preconditioning, improves left ventricular (LV) function and survival after reperfusion therapy in patients with AMI. Recent experimental studies have reported that preconditioning has anti-inflammatory effect. METHODS: This study consisted of 598 patients with first anterior wall AMI who underwent coronary angiography within 12 h after symptom onset. WBC count was measured at the time of hospital admission. Prodromal angina was defined as angina occurring within 24 h before the onset of AMI. Serial measurements of LV ejection fraction (EF) were obtained before reperfusion therapy and before discharge in 421 patients (71%). RESULTS: High WBC count (>10.2 x 103/mm3, n=297) was associated with higher 30-day mortality (8% vs. 4%, p=0.02) and lower predischarge LVEF (51+/-15% vs. 57+/-14%, p<0.001), although there was no significant difference in acute LVEF (47+/-10% vs. 49+/-11%, p=0.07). High WBC count was an independent predictor of 30-day mortality (p=0.009) and predischarge LVEF (p=0.002). Prodromal angina was associated with lower 30-day mortality (3% vs. 7%, p=0.02) and preserved predischarge LVEF (57+/-15% vs. 53+/-14%, p=0.006). Patients with prodromal angina had lower WBC count (10.0+/-3.3 x 10(3)/mm3 vs. 11.0+/-3.9 x 10(3)/mm3, p=0.001) and prodromal angina was an independent predictor of WBC count (p<0.001). CONCLUSIONS: Elevation of WBC count and lack of prodromal angina were associated with impaired LV function and mortality after reperfusion in patients with AMI. Prodromal angina might have contributed to favorable outcome after AMI through its anti-inflammatory effect.     

Serial analyses of ventricular late potentials in patients with reciprocal ST segment changes during acute myocardial infarction

The aim of this study was to determine whether successful reperfusion may alter substrate that is responsible for late potentials in the presence or absence of reciprocal ST segment changes (RC). The study population consisted of 50 patients (27 with RC and 23 without RC) with anterior acute myocardial infarction (AMI) undergoing successful thrombolytic therapy (TT). The presence of reciprocal changes was defined as ST-segment depression >1 mm, measured 80 ms after the J point in at least 2 leads other than those reflecting the infarct on admission ECG. All patients were evaluated with coronary angiography at predischarge. Signal averaged ECG (SAECG) recordings were obtained before and 10 days after TT. Baseline characteristics, SAECG findings, and angiographic data were similar between the groups. The only different baseline finding was the time from symptom onset to TT (204 +/- 150 minutes for patients with RC vs 312 +/- 174 minutes for patients without RC. P = 0.021). After TT, RMS values improved in patients with RC (from 35 +/- 17 microV to 43 +/- 14 microV, P = 0.038) and LAS and RMS were significantly better in this group. However, patients without RC did not show any changes in SAECG parameters after TT. LV ejection fraction (10th day) was better in patients with RC (45 +/- 11% vs 39 +/- 6%, P = 0.014). The frequency of ventricular arrhythmias during the hospitalization period was also similar between the groups. Reciprocal ST depression that regresses simultaneously with the infarction related ECG changes after TT in anterior AMI seems to be related to the time that has elapsed since the symptom onset. The improvement in SAECG parameters after TT in these patients is probably the result of earlier reperfusion leading to less myocardial damage.     

Evidence for the delayed effect in human ischemic preconditioning: prospective multicenter study for preconditioning in acute myocardial infarction

OBJECTIVES

This study aimed to investigate prospectively the protective effect of a first preinfarction angina attack against acute myocardial infarction (AMI) in human hearts without significant collaterals.

BACKGROUND

Several retrospective studies and the prospective studies have demonstrated the existence of the preconditioning (PC) effect in humans. However, collaterals were not examined in the prospective studies. In animal models, the PC effect on myocardial infarct size appears soon after PC reperfusion (classic) but disappears within 1 to 2 h. It then reappears 24 to 48 h after reperfusion (the delayed PC effect). Meanwhile, the PC effect on stunning appears 12 h after PC reperfusion (the delayed PC effect). The concept of the classic and delayed PC effects has not been investigated in human AMI studies. If the above concept is also correct in humans, the infarct size and/or impairment of the left ventricular function should be inversely correlated with the time interval between the first preinfarction angina attack and the onset of AMI when that time interval is limited to between 2 and 48 h.

METHODS

The subjects were 25 patients with first AMI of the proximal left anterior descending artery who underwent successful direct percutaneous transluminal coronary angioplasty (PTCA) 2 to 6 h after the onset and with no (or poor) collateral circulation (grade 0 or 1). They were divided into two groups: preinfarction angina (PA)(+) group: 11 patients with new onset preinfarction angina from 2 to 48 h before the onset, PA(−) group: 14 patients without angina before infarction. Peak creatine kinase (CK) and cumulative CK were examined, and the left ventricular ejection fraction (LVEF) and the regional wall motion (RWM) were determined from the left ventriculograms during the acute (immediately after the coronary reperfusion) and chronic (four weeks after the onset of AMI) phases. The RWM index (RWMI) was then calculated as the mean motion of chords (standard deviation [SD]/chord) lying in the area of chords of RWM ≤ −2 SD in the acute phase (ischemic risk area).

RESULTS

The increase in the RWMI between the acute and chronic phases was significantly larger in the PA(+) group than in the PA(−) group (1.55 ± 1.32 and 0.69 ± 0.75, p < 0.05, respectively) although no significant difference in the enzymatic infarct size was seen between the two groups. The increases in the LVEF and the RWMI were significantly correlated with the time interval from the first preinfarction angina attack to the onset of AMI (r = 0.622, p < 0.05 and r = 0.646, p < 0.05, respectively), but the enzymatic infarct size was not.

CONCLUSIONS

The beneficial effect of preinfarction angina on left ventricular wall motion, independently of collateral flows, indicates the existence of the PC effect in humans. The greater protective effect of a longer time interval between angina pectoris and AMI suggests that the protection is due to a delayed PC effect.     

Effect of preinfarction angina pectoris on myocardial blush grade after reperfusion in first anterior wall acute myocardial infarction.

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<0.0001, respectively). Multivariate logistic regression analysis showed that PIA (p=0.004) and diabetes mellitus (p=0.03) were independently associated with MBG 2 or 3 after reperfusion. CONCLUSIONS: PIA has beneficial effects on myocardial tissue-level reperfusion evaluated by MBG in first anterior wall AMI.     

Immediate and long-term results of delayed recanalization of occluded acute myocardial infarction-related arteries using coronary angioplasty.

Recent evidence suggests that late reperfusion of an occluded infarct-related artery after acute myocardial infarction (AMI) may convey a better prognosis. The clinical outcome of percutaneous transluminal coronary angioplasty (PTCA) as a means of mechanical reperfusion in this particular setting has not been clearly delineated. Ninety-seven patients with AMI underwent PTCA of the occluded infarct-related artery after the acute phase of the AMI (48 hours to 2 weeks, mean 8 +/- 4 days). The study consisted of 72 men (74%) (mean age 56.5 +/- 12 years) and 25 women. Seventy-seven patients (79%) had a Q-wave AMI and 20 patients (21%) a non-Q-wave AMI. Seventy-six patients (79%) had angina after AMI and 4 had previously undergone coronary bypass surgery. Clinical success was achieved in 85 patients (87%). Angiographic success was obtained in 90 of the 97 occluded arteries (93%) and was similar for all 3 major vessels: right coronary 97%, left anterior descending 93% and circumflex 85% (p = not significant). Major complications (AMI, emergency bypass and death) occurred in 3 patients (3.1%). Long-term follow up (3.7 +/- 0.8 years) revealed symptomatic recurrence in 20 (23%), whereas 51 (58%) remained asymptomatic. Most recurrences (16 of 20) were in the form of restenosis rather than reocclusion, with a high success rate for repeat dilation (93%). These results indicate that mechanical reperfusion of an occluded infarct artery, performing PTCA 48 hours to 2 weeks after AMI, has a high success rate, a low complication rate and low symptomatic restenosis.     

Determinants of collateral development in patients with acute myocardial infarction.

BACKGROUND: The presence or absence of collateral circulation to the infarct-related coronary artery in acute myocardial infarction (AMI) significantly impacts on infarct size and resulting left ventricular function. However, the determinants of collateral development have not been clarified. HYPOTHESIS: The purpose of this study was to elucidate the determinants of collateral development in humans. METHODS: The study group consisted of 248 patients (178 men, 70 women; mean age 63 years) undergoing coronary angiography within 12 h after the onset of a first AMI. All patients exhibited complete occlusion of the infarct-related artery. The extent of collateral circulation to the area perfused by the infarct-related artery was graded as none, or poorly or well developed, depending on the degree of opacification of the occluded coronary artery on the contralateral injection of contrast. RESULTS: Well-developed collateral circulation was observed in 92 of the 248 patients (37.1%). The prevalence of well-developed collaterals was 57% in patients with a history of angina pectoris prior to AMI, which was significantly (p < 0.0001) higher than the 26% in those without a history of angina. Multivariate stepwise logistic regression analysis was then applied to identify predictors of collateral development. Possible determinants of collateral development were long-standing preinfarction angina, severity of coronary artery disease, age, gender, and coronary risk factors (hypertension, diabetes, hypercholesterolemia, smoking). This analysis revealed that only the presence of a history of angina pectoris prior to AMI was a significant predictor of collateral development (p < 0.0001). CONCLUSIONS: A history of angina pectoris prior to AMI is a clinical marker for coronary stenoses. Since severe coronary stenoses can provide stimuli that lead to collateral development, it is reasonable that a history of angina would also be a clinical marker for collateral vessels.     

Diabetes mellitus prevents ischemic preconditioning in patients with a first acute anterior wall myocardial infarction

OBJECTIVES: This study was undertaken to assess whether prodromal angina could have beneficial effects in diabetic patients with acute myocardial infarction (AMI). BACKGROUND: Prodromal angina occurring shortly before the onset of AMI is associated with favorable outcomes by the mechanism of ischemic preconditioning. However, little is known about the impact of diabetes on ischemic preconditioning. METHODS: We studied 611 patients with a first anterior wall AMI who underwent emergency catheterization within 12 h after the onset of chest pain: 490 patients without diabetes and 121 patients with non-insulin treated diabetes. Prodromal angina was defined as angina episode(s) occurring within 24 h before the onset of AMI. Serial contrast left ventriculograms were obtained in 424 patients at the time of acute and predischarge catheterization. RESULTS: In non-diabetic patients, prodromal angina was associated with lower peak creatine kinase (CK) value (3,068 +/- 2,647 IU/l vs. 3,601 +/- 2,462 IU/l, p = 0.037), larger increase in left ventricular ejection fraction (LVEF) (10.1 +/- 13.0% vs. 5.8 +/- 13.4%, p = 0.004) and lower in-hospital mortality (3.4% vs. 9.3%, p = 0.015). On the contrary, in diabetic patients, there was no significant difference in peak CK value (3,382 +/- 2,520 IU/l vs. 3,233 +/- 2,412 IU/l, p = NS), the change in LVEF (6.7 +/- 13.8% vs. 7.1 +/- 12.4%, p = NS) and in-hospital mortality (8.8% vs. 11.0%, p = NS) between patients with and patients without prodromal angina. CONCLUSIONS: Prodromal angina limited infarct size, enhanced recovery of LV function and improved survival in non-diabetic patients with AMI. However, such beneficial effects of prodromal angina were not observed in diabetic patients, suggesting that diabetes might prevent ischemic preconditioning.     

Effect of preinfarction angina pectoris on microcirculation in patients with reperfused acute myocardial infarction

Preinfarction angina pectoris has been suggested in some studies to have a beneficial effect on left ventricular function after acute myocardial infarction (AMI). The precise mechanisms of this protection have not been fully elucidated. The effect of preinfarction angina on myocardial tissue perfusion also needs to be clarified. In this study, we investigated the influence of preinfarction angina on microvasculatory damage by using ST-segment resolution and pressure-derived collateral flow index (CFIp) as a marker of microcirculatory perfusion. METHODS: We studied 41 patients with a first AMI in whom thrombolysis in myocardial infarction (TIMI) grade 3 flow in the infarct-related artery was established by thrombolytic therapy. The percent resolution of ST-segment deviation (deltasigma ST) after thrombolysis was determined. All of the patients had TIMI grade 3 flow in IRA at the coronary angiography, which was done a mean of 4 days after AMI. Intracoronary pressure measurements and stent implantation to the IRA were performed. After angiography, CFIp was calculated as the ratio of simultaneously measured coronary wedge pressure-central venous pressure (Pv) to mean aortic pressure-Pv. RESULTS: Patients with preinfarction angina pectoris had greater percent deltasigma ST than those without PA (67 +/- 18% vs. 44 +/- 24%, p = 0.03).The mean of the coronary wedge pressure (16.4 +/- 7.4 compared with 23.2 +/- 9.4, P < 0.03) and the pressure-derived collateral flow index (0.15 +/- 0.10 compared with 0.22 +/- 0.08, P < 0.03) were significantly lower in patients with preinfarction angina compared to those without. CONCLUSION: Preinfarction angina is associated with a greater degree of ST-segment resolution and lower CFI-p in patients with TIMI-3 reflow after thrombolysis. These findings suggest that a protective effect of preinfarction angina against reperfusion injury may result in greater ST resolution and lower CFIp after AMI.     

Effect of preinfarction angina pectoris on ST-segment resolution after primary coronary angioplasty for acute myocardial infarction

The presence of preinfarction angina has been shown to exert a favorable effect on left ventricular function after acute myocardial infarction (AMI). Whether or not preinfarction angina is beneficial for myocardial tissue reperfusion, however, remains to be determined. We sought to evaluate the influence of preinfarction angina on resolution of ST-segment elevation, which could be affected by microcirculatory damage after recanalization therapy. We studied 96 patients with a first AMI in whom Thrombolysis In Myocardial Infarction (TIMI)-3 flow in the infarct-related artery was established by primary angioplasty. Percent reduction in the sum of ST elevation from baseline to 1 hour after angioplasty (percent delta summation operator ST) was examined. Poor ST resolution, defined as percent delta summation operator ST <50%, was observed in 25 patients, who had a worse clinical outcome, larger infarct size, and poorer left ventricular function. On multivariate analysis, the absence of preinfarction angina, as well as anterior wall infarction, were major independent predictors of poor ST resolution, whereas age, sex, coronary risk factors, ischemic time, Killip class on admission, multivessel disease, initial TIMI flow grade, and extent of collaterals were not significant. Patients with preinfarction angina had a greater degree of ST-segment resolution than those without angina (71 +/- 21% vs 49 +/- 43%, p = 0.02). Additional ST elevation after reperfusion was noted exclusively in patients without preinfarction angina (p = 0.02). Preinfarction angina is associated with a greater degree of ST-segment resolution in patients with TIMI-3 flow after primary angioplasty, suggesting a protective effect of preinfarction angina against microcirculatory damage after reperfusion.     

Predictive factors for development of the no-reflow phenomenon in patients with reperfused anterior wall acute myocardial infarction

OBJECTIVES: We sought to elucidate the clinical factors related to the development of no-reflow phenomenon after successful coronary reperfusion in patients with an acute myocardial infarction (AMI). BACKGROUND: Myocardial contrast echocardiography revealed that the no-reflow phenomenon is observed in some patients with a reperfused AMI, and those patients usually have poor functional and clinical outcomes. It is still unknown what clinical factors are related to the development of the no-reflow phenomenon. METHODS: Myocardial contrast echocardiography was performed 15 min after successful coronary reperfusion therapy in 199 patients with an anterior wall AMI who underwent successful coronary reperfusion with primary coronary angioplasty within 24 h after the onset of AMI. Multiple logistic regression analysis was used to identify independent predictors of the no-reflow phenomenon. RESULTS: Seventy-nine patients showed the no-reflow phenomenon. Univariate analysis indicated that pre-infarction angina within 48 h before symptom onset, Killip class, Thrombolysis in Myocardial Infarction flow grade 0 on the initial coronary angiogram, the number of abnormal Q-waves and the wall motion score (WMS) on the echocardiogram obtained at hospital admission are related to the no-reflow phenomenon. Multivariate logistic regression analysis revealed that all of these factors, except for Killip class, are independent predictive factors of the no-reflow phenomenon. CONCLUSIONS: Development of the no-reflow phenomenon is related to the severity of myocardial damage (number of Q-waves), the size of the risk area (WMS) and the occlusion status of infarct-related artery. In addition, ischemic preconditioning (pre-infarction angina) seems to be the factor that attenuates the no-reflow phenomenon.     

Planar myocardial scintigraphy with 99mTc sestamibi for the evaluation of the infarct area and the efficacy of the thrombolytic therapy]

BACKGROUND: Nuclear cardiology permits the estimation of myocardial infarction size and the result of the thrombolytic therapy. The aim of the study was to demonstrate the feasibility of the planar myocardial scintigraphy with tecnetium-99m-sestamibi in the coronary intensive care unit for the early identification of the infarct size and the results of the thrombolytic therapy. MATERIAL AND METHODS: We studied 15 patients affected by a first acute myocardial infarction (AMI), 10 anterior and 5 inferior wall, treated with thrombolysis (APSAC 30U i.v.) within and interval of 3 hours from the symptoms onset, tecnetium-99m-sestamibi was injected before thrombolysis and after 3 +/- 1 hours the planar imaging was registered with a mobile gamma-camera. Scintigraphic evaluation was repeated after 24 hours and before patient discharge. Within 48 hours from the thrombolytic therapy the coronary angiography was performed for the demonstration of patency of the infarct-related artery. The left ventricle myocardial perfusion was divided in the 3 planar projections into 13 segments. The perfusion in each segment was evaluated with a perfusion score: 0 = normal, 1 = moderately reduced, 2 = severely reduced, 3 = absent. The sum of the hypoperfused segments represented the infarct size. A perfusion score improvement greater than 40% was considered a marker of reperfusion. RESULTS: The infarct size involved 4.2 +/- 1.5 segments in the anterior and 2 +/- 0.8 segments in the inferior wall infarctions (p < 0.05). The scintigraphic imaging made 24 hours after AMI allowed the diagnosis of coronary reperfusion in 10 patients. The coronarography demonstrated the infarct related artery patency in 14 patients. The nuclear imaging at patient discharge provided the diagnosis or reperfusion in 11 cases and demonstrated an improvement of the myocardial perfusion score in 8 cases. CONCLUSIONS: In patients with AMI treated with thrombolysis the scintigraphic imaging with tecnetium-99m-sestamibi is feasible with a mobile gamma-camera in the intensive coronary care unit. The quality of planar imaging is good and allows the evaluation of myocardial infarct size and the efficiency of thrombolytic therapy. An earlier scintigraphic imaging should be taken into consideration for a more timely non-invasive evaluation of patients who need coronary angiography and, if necessary, a rescue-PTCA.     

重组组织型纤溶酶原激活剂与直接冠状动脉内支架术治疗心肌梗死的疗效比较

目的　比较小剂量重组组织型纤溶酶原激活剂 (rt PA)与直接冠状动脉 (冠脉 )支架术治疗急性心肌梗死 (AMI)的临床疗效。方法　 131例患者接受小剂量rt PA 5 0mg静脉溶栓治疗 (溶栓组 ) ,130例患者接受梗死相关动脉 (IRA)直接冠脉支架术 (支架组 ) ,比较两组之间患者的临床治疗效果。结果　小剂量rt PA溶栓治疗组IRA再通率为 81 7%,直接冠脉支架组再通率为 98 5 %,两组差异有显著性 (P <0 0 0 0 0 1)。溶栓组再发心肌梗死、需要择期冠脉支架术明显高于支架组 (分别为7 6 %比 1 5 %,P <0 0 5 ;2 0 6 %比 0 ,P <0 0 0 0 1)。溶栓组住院期间左心室射血分数明显低于支架组[(5 5 6± 13 4 ) %比 (6 5 8± 9 2 ) %,P <0 0 0 0 1]。溶栓组平均住院天数也明显多于支架组 (16± 7比11± 4,P <0 0 0 0 1)。溶栓组住院病死率高于支架组 ,但差异无显著性 (6 1%比 3 1%,P >0 0 5 )。结论　与小剂量rt PA静脉溶栓比较 ,直接冠脉支架术可明显增加IRA的再通率 ,更好地保护心功能 ,并缩短患者的住院时间。     

Early treatment of acute myocardial infarction with intravenous streptokinase. A high-risk syndrome

Fifty-one successive patients treated with intravenous streptokinase 1.7 +/- 0.8 (mean +/- SD) hours after onset of symptoms of acute myocardial infarction were evaluated during a three-month posthospital follow-up period. Coronary angiography was performed four to nine days after the initial hospital admission. Twenty-eight patients had a second late angiogram. Forty-one patients had successful reperfusion but only 25% of all patients were without significant clinical cardiovascular manifestations during this period. Postmyocardial infarction angina pectoris occurred in 21 patients, an abnormal stress test result was present in 28 patients, eight patients developed congestive heart failure, and five patients had reinfarction. An intervention with percutaneous transluminal coronary angioplasty or coronary artery bypass graft was performed in 15 (37%) of 41 reperfused patients. A significantly higher intervention rate was present in patients treated with streptokinase within one hour following the onset of symptoms. Early reocclusion (within three months of the infarct) was noted in patients with 60% or more residual stenosis in their infarct-related coronary artery. These patients also had a significantly greater incidence of angina pectoris. Our findings indicate that early thrombolytic therapy of acute myocardial infarction preserves myocardium, and since the infarct-related artery is patent, but narrowed, the jeopardized area is responsible for a high-risk syndrome with an increased likelihood of ischemic symptoms. An early aggressive approach may be indicated, especially for patients with greater than 60% residual stenosis in their infarct-related coronary artery.     

Correlates of bundle-branch block in patients undergoing primary angioplasty for acute myocardial infarction.

BACKGROUND: Early reperfusion therapy has reduced the infarct size and mortality rate in patients with acute myocardial infarction (AMI). The occurrence of bundle-branch block in AMI is related to the amount of myocardial damage and the insult to the conduction system. HYPOTHESIS: To evaluate the clinical and angiographic factors related to the occurrence of bundle-branch block (BBB) in patients with primary percutaneous transluminal coronary angioplasty (PTCA), we investigated consecutive series of patients with their first Q-wave AMI and successful PTCA. METHODS: Coronary angiogram at the time of admission, electrocardiogram, and echocardiogram were evaluated in 279 patients with their first Q-wave AMI and successful PTCA. RESULTS: Bundle-branch block was detected in 26 patients (9%); 16 patients had transient and 10 patients had persistent block, while 16 patients had bifascicular block and 10 patients had right BBB. The patients with BBB had a significantly larger number of left ventricular asynergic segments, higher incidence of total occlusion of infarct-related artery, angiographic no reflow, and pericardial rub than those without BBB. When the multivariate analysis was performed using five clinical markers of infarct severity, angiographic no reflow (F = 20.2, p < 0.001) and total occlusion of infarct-re-lated artery (F = 4.2, p = 0.04) were found to be the significant variables related to BBB. CONCLUSIONS: Despite successful primary PTCA, absence of antegrade flow in the infarct-related artery at the onset of AMI and/or angiographic no reflow resulted in more severe transmural myocardial damage and, hence, the occurrence of BBB.     

Increased urinary leukotriene excretion in patients with cardiac ischemia. In vivo evidence for 5-lipoxygenase activation.

BACKGROUND. Experimental cardiac ischemia in some animal models results in the activation of the enzyme 5-lipoxygenase and the subsequent production of leukotrienes, potent proinflammatory lipid mediators, by the affected myocardium. Furthermore, prototype antileukotriene drugs can show some beneficial effects on infarct size and cardiac function in these models. Accordingly, urinary excretion of leukotriene E4 (LTE4), the major urinary metabolite of peptide leukotrienes in humans, was measured in patients admitted to the hospital with evidence of acute myocardial ischemia to assess in vivo release of 5-lipoxygenase products during and after the ischemic episode. METHODS AND RESULTS. Urinary leukotriene excretion was measured by reversed-phase high-performance liquid chromatography and specific radioimmunoassay on admission with acute chest pain and again on day 3 in the following patient groups: acute myocardial infarction (AMI), AMI and clinical evidence of early reperfusion after treatment with recombinant tissue-type plasminogen activator (rt-PA), diagnosis of unstable angina (UA) based on clinical history and coronary arteriography, controls with nonischemic chest pain who underwent coronary arteriography, and age-matched controls and normal hospital employees. In 16 patients with diagnosis of AMI, LTE4 excretion on admission (331 +/- 99 pg/mg creatinine sulfate; mean +/- SEM) was considerably higher than that measured on day 3 (195 +/- 59 pg/mg creatinine sulfate). In a subgroup of seven subjects treated with rt-PA resulting in early reperfusion, day 1 excretion was similar (215 +/- 50 pg/mg) but had significantly declined by day 3 (65 +/- 16 pg/mg; p less than 0.01). Urinary LTE4 excretion at admission for chest pain was also elevated in 14 patients having unstable angina (UA; 370 +/- 125 pg LTE4/mg creatinine sulfate). This had declined significantly (p less than 0.05) by day 3 (at which time chest pain had resolved) to 94 +/- 31 pg/mg creatinine sulfate, an excretion rate comparable with that measured in eight similarly aged subjects (64 +/- 12 pg/mg creatinine). CONCLUSIONS. This study suggests that peptide leukotrienes are released during episodes of myocardial ischemia and provides clinical evidence for involvement of their biosynthetic enzyme, 5-lipoxygenase, during and after acute myocardial infarction and unstable angina attacks. Thus, potent and specific orally active leukotriene biosynthesis inhibitors may have therapeutic potential in limiting myocardial damage and functional abnormalities after acute ischemia.     

Transient Increase in ST-segment Changes at Time of Reperfusion in Acute Myocardial Infarction Treated by Coronary Angioplasty

PURPOSE: The clinical significance of early ST-segment re-elevation, a so called òreperfusion peakó in patients with acute myocardial infarction (AMI) treated with thrombolysis is unclear. We examined the incidence and significance of early ST-segment re-elevation immediately upon reperfusion in patients undergoing percutaneous transluminal coronary angioplasty (PTCA) where the time of reperfusion can be precisely established. METHODS: Thirty-two patients (6 women, 26 men, age 61.5 +/- 10.2 years) with an AMI, admitted less than four hours after the onset of chest pain, were included. Twenty-four patients were treated with primary PTCA and eight with rescue PTCA. Computerized on-line vectorcardiography was used for continuous ischemia monitoring. A reperfusion peak was defined as an increase in ST-vector magnitude (ST-VM) of > 50 μV, starting within two minutes after the re-opening of the infarct-related coronary artery and followed by an immediate decrease in the ST segment. RESULTS: Primary success was achieved in all treated patients. Twenty of the patients (63%) developed a reperfusion peak. ST-VM before coronary angiography was significantly larger (p = 0.004) and peak enzyme levels were higher (p = 0.014) in patients who developed a reperfusion peak. Thrombolytic treatment prior to rescue angioplasty, time to reperfusion, target vessel, presence of collaterals or medication on admission did not differ significantly between the groups. CONCLUSION: The occurrence of a reperfusion peak during the minutes after the onset of reperfusion is a common finding in patients with AMI treated at an early stage with angioplasty. There is a relationship with the occurrence of a reperfusion peak and the extent of the initial ST deviation (presumably reflecting the myocardium at risk) and peak enzyme levels. The importance of a reperfusion peak for clinical outcome and prognosis is so far not known.     

Clinical implication of persistent ischemic chest pain on admission in patients with late reperfused acute myocardial infarction

OBJECT: Although previous studies reported that late reperfusion might prevent left ventricular dilation after acute myocardial infarction (AMI), implication of persistent ischemic chest pain on admission remains to be investigated. This study was undertaken to assess the implication of persistent ischemic chest pain on in-hospital outcome and left ventricular function after late reperfused AMI. METHODS AND PATIENTS: We studied 63 patients with a first anterior AMI who underwent percutaneous coronary intervention 6 to 24 hours (11.2+/-4.5 hours) after the onset. Of 63 patients, 48 (76%) had persistent ischemic chest pain on admission. RESULTS: Incidence of in-hospital death, reinfarction or congestive heart failure was similar between the 2 groups. Pretreatment left ventricular ejection fraction and end-diastolic volume were similar between the 2 groups. Predischarge angiography was performed at 17+/-5 days after the onset. Late reperfusion prevented the dilation of left ventricular end-diastolic volume in patients with chest pain (78+/-12 to 75+/-17 ml/m2, p=0.15), but did not in those without (75+/-20 to 93+/-28 ml/m2, p=0.03). A multivariate analysis revealed that absence of persistent ischemic chest pain was an independent predictor of predischarge left ventricular end-diastolic volume >100 ml/m2 (odds ratio 0.10, p=0.04). CONCLUSIONS: Our data demonstrated that absence of persistent ischemic chest pain appears to be a simple and reliable marker which predicts left ventricular dilation after late reperfused AMI.     

Absence of preinfarction angina is associated with a risk of no-reflow phenomenon after primary coronary angioplasty for a first anterior wall acute myocardial infarction

BACKGROUND: No-reflow phenomenon after primary coronary angioplasty is associated with poorer left ventricular (LV) function and prognosis after acute myocardial infarction (AMI). The purpose of this study was to determine the clinical significance of preinfarction angina in the no-reflow phenomenon. METHODS AND RESULTS: A total of 40 patients with first anterior AMI were examined. All patients underwent primary balloon angioplasty or stenting within 12 h of the onset of AMI. No-reflow, defined as TIMI grade 2 flow or less without residual stenosis after angioplasty, was observed in 15 patients. Patients with no-reflow were older (67+/-9 vs. 58+/-10 years, P=0.006) and had a lower incidence of preinfarction angina (7% vs. 48%, P=0.01) than those without no-reflow. Patients with no-reflow had poorer LV function at predischarge and a higher incidence of pump failure, LV aneurysm, malignant ventricular arrhythmias or cardiac death during the hospital course in association with higher peak serum C-reactive protein levels (12.7+/-8.0 vs. 7.1+/-5.5 mg/dl, P=0.02). Multivariate analysis showed that the absence of preinfarction angina was a major independent determinant of no-reflow (RR=17.1, P=0.02). CONCLUSIONS: The absence of preinfarction angina is more frequently observed in patients with no-reflow. The beneficial effect of preinfarction angina on LV function may be explained, at least in part, by prevention of no-reflow after reperfusion.     

Rescue use of abciximab improves regional left ventricular function after early incomplete reperfusion in acute myocardial infarction

BACKGROUND: Abciximab was shown to have important beneficial effects beyond the maintenance of epicardial coronary artery patency. However, it remains uncertain whether abciximab may lead to a better functional outcome in patients with acute myocardial infarction (AMI) and with incomplete reperfusion after primary angioplasty (PA). HYPOTHESIS: The study aimed to evaluate whether rescue use of abciximab may lead to a better functional outcome in such patients. METHODS: The study included 25 patients with first AMI who met the following criteria: (1) total occlusion of the infarct-related artery, (2) PA within 12 h of symptom onset, (3) postprocedural diameter stenosis < 30%, and final Thrombolysis in Myocardial Infarction (TIMI) flow grade 2. Echocardiographic examination was performed before and on Days 7 and 30 after PA. The study population was divided into two groups: Group 1 (usual care, n = 13) and Group 2 (rescue use of abciximab, n = 12). Baseline characteristics were similar between the two groups. RESULTS: Peak level of creatine kinase was higher in Group 1 than in Group 2 (5,800+/-2,700 vs. 3,800+/-2,000 U/I, p < 0.05). At 1 month follow-up, infarct zone wall motion score index (2.71+/-0.26 vs. 2.05+/-0.63, p < 0.01) and left ventricular (LV) volume indices were smaller in Group 2 than in Group 1, whereas LV ejection fraction was higher in Group 2 than in Group 1 (52.1+/-7.8 vs. 42.1+/-6.4, p < 0.01). At 1-month, abciximab was the only independent predictor of wall motion recovery index by multiple regression analysis. CONCLUSIONS: Rescue use of abciximab may reduce the infarct size in patients with AMI and TIMI grade 2 flow after PA, which may improve the recovery of regional LV function.