Search PubMed⌕ Search

Biomedical subjects

Y Birnbaum

Publications and source records attributed to Y Birnbaum.

At least 91 records · Page 5Linked to original sources
PubMed1997

Maximal precordial ST-segment depression in leads V4-V6 in patients with inferior wall acute myocardial infarction indicates coronary artery disease involving the left anterior descending coronary artery system.

BACKGROUND: In inferior wall acute myocardial infarction, maximal ST-segment depression in left precordial leads (V4-V6) has been shown to be associated with increased in-hospital mortality, presumably due to coronary artery disease involving the left anterior descending coronary artery system. METHODS: We measured ST-segment deviation from baseline in the initial electrocardiogram of patients with inferior wall acute myocardial infarction, who subsequently underwent coronary angiography during their in-hospital stay. Patients were divided into three groups: (I) No precordial ST-segment depression (n = 34). (II) Maximal precordial ST-segment depression in leads V1-V3 (n = 44). (III) Maximal precordial ST-segment depression in leads V4-V6 (n = 14). RESULTS: The left anterior descending coronary artery or its diagonal branch were stenosed (> 50%) in 32%, 41%, and 71% of patients in groups I, II, and III, respectively (p = 0.04), and severely stenosed (> 70%) in 18%, 18% and 57% of patients in the respective groups (p = 0.007). CONCLUSION: In patients with inferior wall acute myocardial infarction, maximal precordial ST-segment depression in leads V4-V6 is suggestive of severe coronary artery disease involving the left anterior descending coronary artery or its diagonal branch.

Adult↗
PubMed1997

Pathobiology and Clinical Impact of Reperfusion Injury.

Reperfusion injury refers to cellular death or dysfunction caused by restoration of blood flow to previously alchemic tissue. This should be differentiated from the normal reparative processes that follow an ischemic insult. Four types of reperfusion injury have been described in the literature: (1) lethal reperfusion injury, (2) nonlethal reperfusion injury, (myocardial stunning), (3) reperfusion arrhythmias, and (4) vascular injury (including the "no-reflow" phenomenon). There is continued debate whether reperfusion itself is capable of killing viable myocytes, which otherwise would have survived the ischemic insult. However, there is firm evidence for the existence of myocardial stunning following various ischemic syndromes, including reperfusion therapy for acute myocardial infarction, unstable angina pectoris, vasospastic angina, effort-induced ischemia, coronary artery bypass surgery, and cardiac transplantation. Reperfusion arrhythmia is more common after short ischemic episodes than after long ischemic periods. Thus, while reperfusion arrhythmias in the setting of acute myocardial infarction are relatively rare, reperfusion arrhythmias may be an important cause of sudden death. The "no-reflow" phenomenon has been described following reperfusion in patients with acute myocardial infarction. Three major components have been proposed as mediators of reperfusion injury: (1) oxygen free radicals, (2) the complement system, and (3) neutrophils. Numerous experimental studies have shown short-term benefit by blocking various stages of the postischemic inflammatory response. Oxygen free radicals scavengers, complement inhibition, leukocyte depletion, and the use of antibodies against various adhesion molecules have shown a reduction of infarct size in many ischemic/reperfusion experimental models. However, many of these agents failed to show a benefit in the clinical setting. Moreover, the long-term benefit of such intervention is still unknown.

Journal Article↗
PubMed1997

Estradiol, Administered Acutely, Protects Ischemic Myocardium in Both Female and Male Rabbits.

BACKGROUND: The benefits of chronic administration of estrogen to postmenopausal women are well documented; however, the acute effects of exogenous estradiol on myocardium after coronary artery occlusion and reperfusion in male and female animal models are unknown. We tested the influence of acute pretreatment with estradiol on the development of myocardial necrosis in two protocols, studying intact anesthetized female and male rabbits. METHODS AND RESULTS: 17beta-estradiol (1 mg) was given 15 minutes before coronary artery occlusion in the treated groups (n = 10 females, 10 males); control rabbits (n = 11 females, 10 males) received water. All rabbits underwent 30 minutes of coronary artery occlusion and 4 hours of reperfusion. Myocardial blood flow was similar between groups at 10 minutes after treatment and during coronary artery occlusion and reperfusion. Thus estradiol did not increase blood flow. Heart rate and systemic pressure were also similar between groups. Estradiol levels during coronary artery occlusion were 1-8 pg/mL in untreated female and male rabbits and 66 +/- 28 (male) and 352 +/- 273 (female) in treated rabbits. Although the size of the ischemic risk zones was similar in both groups in both protocols, estradiol-treated rabbits of both sexes developed significantly less necrosis. Infarct size as a percent of the risk region was 10 +/- 1% in female estradiol-treated rabbits compared with 23 +/- 5% in controls (P <.03) and 16 +/- 4% in estradiol-treated male rabbits compared with 31 +/- 5% in control males (P =.03). Although male rabbits had larger infarcts than female rabbits, sex was not a significant covariate for infarct size. CONCLUSIONS: Estradiol exerts a protective effect on ischemic myocardium that is not associated with an increase in myocardial blood flow or alteration in hemodynamics. This study shows that acute administration of estrogen before coronary artery occlusion reduces infarct size in both male and female rabbits.

Journal Article↗
PubMed1996

Distortion of the terminal portion of the QRS on the admission electrocardiogram in acute myocardial infarction and correlation with infarct size and long-term prognosis (Thrombolysis in Myocardial Infarction 4 Trial).

Previous studies have shown an association between distortion of the terminal portion of the QRS (QRS[+] pattern: emergence of the J point > or = 50%. of the R wave in leads with qR configuration or disappearance of the S wave in leads with an Rs configuration) on admission and in-hospital mortality in acute myocardial infarction (AMI). However, the mechanism for this association is not known. We assessed the relation between QRS(+) pattern and coronary angiographic findings, infarct size, and long-term prognosis in the Thrombolysis In Myocardial Infarction 4 trial. Patients were allocated into 2 groups based on the presence (QRS[+], n = 85) or absence (QRS[-], n = 293) of QRS distortion. The QRS(+) patients were older (mean +/- SD: 61.1 +/- 10.6 vs 57.5 +/- 10.6 years, p = 0.004), had more anterior AMI (49% vs 37%, p = 0.04), and less previous angina (42% vs 54%, p = 0.05). QRS(+) patients had larger infarct size as assessed by creatine kinase release over 24 hours (209 +/- 147 vs 155 +/- 129, p = 0.003), and predischarge sestamibi (MIBI) defect (17.9 +/- 15.9% vs 11.2 +/- 13.4%, p <0.001). When adjusting for difference in baseline characteristics, p values for the differences in 24-hour creatine kinase release were 0.03 and 0.64 for anterior and nonanterior AMI, respectively, and for MIBI defect size 0.03 and 0.02, respectively. One-year mortality (18% vs 6%, p = 0.03) was higher and the weighted end point of death, reinfarction, heart failure, or left ventricular ejection fraction <40% (0.33 +/- 0.37 vs 0.24 +/- 0.32, p = 0. 13), tended to be higher in the anterior AMI patients with QRS(+). No difference in clinical outcome was found in patients with non-anterior AMI. These findings suggest that this simple electrocardiographic definition of presence of QRS(+) pattern on admission may provide an early estimation of infarct size and long-term prognosis, especially in anterior AMI.

Adult↗
PubMed1996

Prognostic significance of the initial electrocardiographic pattern in patients with inferior wall acute myocardial infarction.

The purpose of the study was to determine whether the initial electrocardiographic pattern is predictive of in-hospital mortality in inferior wall acute myocardial infarction. It is commonly perceived that patients with acute myocardial infarction presenting with greater ST elevation have a worse prognosis. The initial electrocardiogram of patients (n = 213) with inferior wall myocardial infarction was categorized based on the pattern of ST-segment elevation in inferior leads: (A) ST <1 mm with tall T waves, (B) ST > or = 1 mm with normal terminal QRS, and (C) ST > or = 1 mm with distortion of terminal QRS. ST deviation from baseline was calculated for all leads. Patients with maximal precordial ST depression in V4-V6 and pattern A had an in-hospital mortality rate of 68.8% compared with 16.9% for the entire study group. By univariate analysis, only pattern A was significantly predictive of in-hospital mortality [odds ratio = 2.91, 95% confidence interval (CI) 1.22-6.93], but by multivariate analysis adjusted for (1) age, (2) diabetes mellitus, (3) previous myocardial infarction, (4) thrombolytic therapy, (5) precordial ST-depression pattern, and (6) patterns of ST elevation, maximal ST depression in V4-V6 was significantly predictive (odds ratio = 4.93, 95% CI 1.79-13.56), whereas pattern A was not (odds ratio = 1.12, 95% CI 0.36-3.52). Contrary to popular perception, patients with inferior wall myocardial infarction presenting with minimal ST-segment elevation are at highest risk for in-hospital mortality, especially if accompanied by maximal precordial ST depression in V4-V6.

Adult↗
PubMed1996

Exercise-induced syncope and Holter-documented asystole in an endurance runner with moderate aortic stenosis.

The case of an endurance runner with moderate aortic stenosis, who had recurrent syncope, is reported. A Holter recording during syncope revealed asystole lasting 57 s. Head-up tilt table test with isoproterenol was abnormal. No important abnormality was found in sinus or atrioventricular nodal functions. It was postulated that the syncope was due to exaggerated left ventricular baroreflex response, probably aggravated by the increased vagal tone in an endurance runner. The patient was given a beta-adrenergic blocker, and a pacemaker was implanted because of the profound cardio-inhibitory response. The arguments for this approach are discussed.

Adrenergic beta-Antagonists↗
PubMed1996

Progressive decrease in the ST segment elevation during ischemic preconditioning: is it related to recruitment of collateral vessels?

This study assesses the effect of ischemic preconditioning (IP) on the magnitude of ST segment shift. Anesthetized rabbits were subjected to IP (four periods of 5-min coronary artery occlusion followed by 5-min reperfusion; n = 9) or control (no IP; n = 9). Thereafter, both groups were subjected to 60 min of ischemia. There was a gradual decline in the magnitude of ST segment elevation, recorded by an epicardial lead overlying the ischemic zone. ST amplitude after 1 min of ischemia was 2.19 +/- 0.51, 1.29 +/- 0.44, 0.72 +/- 0.26, 0.20 +/- 0.10, and 0.26 +/- 0.13 mV, during the first, second, third, fourth IP episodes and the final ischemic period respectively (P = 0.0003). ST amplitude after 2 min of ischemia was 2.56 +/- 0.69, 2.47 +/- 0.55, 1.82 +/- 0.42, 1.13 +/- 0.23, and 1.02 +/- 0.14 mV, respectively (P = 0.0043). While heart rate and mean blood pressure at 1, 2, 30, and 60 min of the final long ischemia were similar in both groups, the IP group had less ST elevation (P = 0.0074). There was no change in RMBF between the first IP and the final occlusion. Both groups were equally ischemic during the long occlusion. In the rabbit, progressive reduction in ST segment shift with repeated ischemia is caused by preconditioning and is independent of the recruitment of collaterals or of hemodynamic changes.

Animals↗
PubMed1996

Prognostic significance of the admission electrocardiogram in acute myocardial infarction.

OBJECTIONS: We sought to access the ST segment and the terminal portion of the QRS complex in the initial electrocardiogram (ECG) as tools to predict outcome in patients with acute myocardial infarction given thrombolytic therapy. BACKGROUND: Previous studies assessing early risk stratification of patients with acute myocardial infarction by ECG criteria have focused on the number of leads with ST segment elevation or the absolute magnitude of ST deviation. A new classification independent of the absolute values of ST deviation was pursued. METHODS: Patients with ST elevation and positive T waves in at least two adjacent leads who received thrombolytic therapy were classified into two groups based on the absence (1,232 patients) or presence (1,371 patients) of distortion of the terminal portion of the QRS complex on the admission ECG. RESULTS: There were no differences between groups in the prevalence of previous angina, hypertension, current smoking, anterior infarction, time from onset of symptoms to therapy of type of thrombolytic regimen. Patients with QRS distortion were less likely to have had a previous infarction (12.0% vs. 18.4%, p = 0.02) or diabetes mellitus (16.9% vs. 21.4%, p = 0.003). They had higher peak creatine kinase levels (1,617 +/- 1,670 vs. 1,080 +/- 1,343 IU, p = 0.00001). Hospital mortality for those with and without QRS distortion was 6.8% and 3.8%, respectively (p = 0.0008). Multivariable logistic regression analysis confirmed that hospital mortality was independently associated with distortion of terminal portion of the QRS complex (odds ratio 1.78, 95% confidence interval 1.19 to 2.68, p = 0.004). CONCLUSIONS: Distortion of the terminal portion of the QRS complex on the admission ECG is independently associated with a higher hospital mortality rate in patients with acute myocardial infarction given thrombolytic therapy.

Acute Disease↗
PubMed1996

Prognostic significance of precordial ST segment depression on admission electrocardiogram in patients with inferior wall myocardial infarction.

OBJECTIVES: This study assessed retrospectively the correlation between the pattern of precordial ST segment depression on the admission electrocardiogram (ECG) and hospital mortality in patients with an inferior myocardial infarction treated with intravenous thrombolytic therapy. BACKGROUND: Previous studies have shown that in acute inferior myocardial infarction, ST segment depression in the precordial leads is associated with increased hospital mortality. However, the significance of the different patterns of precordial ST segment depression has been evaluated in only two previous studies. METHODS: The study included 1,321 patients (1,020 men) who enrolled in the Global Utilization of Streptokinase and t-PA for Occluded Coronary Arteries (GUSTO-I) trial in Israel and received intravenous thrombolytic therapy. Patients with an ST segment elevation > or = 0.1 mV in at least two of the inferior leads were included. Patients were classified into four groups on the basis of their admission ECG: group I = patients with no precordial ST segment depression (n = 346); group II = those for whom the sum of ST segment depression in leads V1 to V3 was greater than that in leads V4 to V6 (n = 700); group III = those for whom the sum of ST depression in leads V1 to V3 was equal to that in leads V4 to V6 (n = 162); group IV = those with maximal ST depression in leads V4 to V6 (n = 113). RESULTS: The overall hospital mortality rate was 3.6% (48 patients): for groups I, II, III and IV it was 2.9%, 2.8%, 4.3% and 9.7%, respectively. Multivariable logistic regression analysis confirmed that hospital mortality was independently associated with the pattern of precordial ST segment depression. The odd ratios in group IV relative to group I was 2.78 (95% confidence interval 1.26 to 6.13, p = 0.007). CONCLUSIONS: The risk of mortality is higher in patients with an inferior myocardial infarction and maximal ST segment depression in precordial leads V4 to V6 versus precordial leads V1 to V3 on the admission ECG.

Case-Control Studies↗
PubMed1996

Acute myocardial infarction entailing ST-segment elevation in lead aVL: electrocardiographic differentiation among occlusion of the left anterior descending, first diagonal, and first obtuse marginal coronary arteries.

Acute myocardial infarction with ST elevation in lead aVL may represent involvement of the first diagonal or the first obtuse marginal branch. This study assesses the correlation among different electrocardiographic patterns of acute myocardial infarction with ST elevation in aVL and the site of the infarct-related artery occlusion. Patients who underwent coronary angiography within 14 days of infarction with an unequivocal culprit lesion were included. Fifty-seven patients were evaluated. The culprit lesion was in the left anterior descending coronary artery proximal to the first diagonal, first diagonal, and first obtuse marginal branches, in 38, 8, and 11 patients, respectively. ST elevation in aVL and V2 through V5 signifies left anterior descending artery occlusion proximal to the first diagonal branch (positive predictive value [PPV] and negative predictive value [NPV] of 95% and 94%, respectively). ST elevation in aVL and V2, not accompanied by ST elevation in V3 through V5, favors occlusion of the first diagonal branch (PPV, 89%; NPV, 100%). ST elevation in aVL accompanied by ST depression in V2 predicts obstruction of the first obtuse marginal branch (PPV, 100%; NPV, 98%).

Cineradiography↗
PubMed1996

beta-Estradiol, but not alpha-estradiol, reduced myocardial necrosis in rabbits after ischemia and reperfusion.

Recent studies in several animal models have suggested that estrogen, given for the short term, may protect ischemic myocardium. Our objective was to test the effect of exogenous estradiol on the development of myocardial necrosis. Twenty minutes before coronary occlusion, rabbits were given an IV bolus of either 17 beta-estradiol, a form of the hormone that stimulates the estrogen receptor (10 micrograms) or 17 alpha-estradiol, a natural form of the hormone lacking estrogenic effects (1 mg), or vehicle. Regional myocardial blood flow (RMBF) was measured after treatment and during occlusion and reperfusion, and heart rate and blood pressure were monitored throughout. All rabbits underwent 30 minutes of coronary artery occlusion and 4 hours of reperfusion. Estradiol levels were 6 +/- 2 pg/ml in untreated rabbits, 392 +/- 78 pg/ml in rabbits given 17 beta-estradiol, and 413 +/- 68 pg/ml in rabbits given 17 alpha-estradiol. The size of the ischemic region was similar in all groups, but rabbits treated with 17 beta-estradiol developed significantly less necrosis than did control rabbits (0.33 +/- 0.04 vs 0.53 +/- 0.05 of the area at risk; p < 0.05), whereas rabbits treated with 17 alpha-estradiol did not (0.43 +/- 0.03; p = NS vs control group). Heart rate, systemic pressure, and RMBF were comparable among groups throughout the protocol. In conclusion, 17 beta-estradiol exerts a protective effect on ischemic myocardium, reducing infarct size. This beneficial effect is not associated with an increase in myocardial blood flow or alteration in hemodynamics. Because 17 alpha-estradiol did not affect infarct size, the cardioprotective effect of 17 beta-estradiol is probably receptor mediated.

Animals↗
PubMed1996

The effect of coenzyme Q10 on infarct size in a rabbit model of ischemia/reperfusion.

OBJECTIVE: Coenzyme Q10 has been found to enhance recovery of function after reperfusion in numerous experimental acute ischemia-reperfusion models. We assessed whether coenzyme Q10, administered intravenously either during or 1 h before ischemia, can limit infarct size in the rabbit. METHODS: Anesthetized open-chest rabbits were subjected to 30 min of coronary artery occlusion and 4 h of reperfusion. In Protocol 1, 12 min after beginning of ischemia rabbits were randomized to intravenous infusion of 30 mg coenzyme Q10 (Eisai Co., Japan) (n = 10) or vehicle (n = 10). In Protocol 2, rabbits were randomized to 30 mg coenzyme Q10 (n = 6) or vehicle (n = 6) treatment 60 min before ischemia. Ischemic zone at risk (IZ) was assessed by blue dye and necrotic zone (NZ) by tetrazolium staining. RESULTS: In both protocols, coenzyme Q10 did not alter heart rate, mean blood pressure, or regional myocardial blood flows in either the ischemic or non-ischemic zones during ischemia or reperfusion. No difference was found in IZ (as fraction of LV weight) (Protocol 1: 0.24 +/- 0.02 vs. 0.25 +/- 0.02; Protocol 2: 0.28 +/- 0.02 vs. 0.28 +/- 0.03, in the control vs. coenzyme Q10 groups, respectively). The NZ/IZ ratio was comparable between the groups in both protocols (Protocol 1: 0.22 +/- 0.04 vs. 0.26 +/- 0.04; Protocol 2: 0.21 +/- 0.06 vs. 0.30 +/- 0.06, in the control vs. coenzyme Q10 groups, respectively). CONCLUSIONS: Coenzyme Q10, administered acutely either during or 60 min before myocardial ischemia, does not attenuate infarct size in the rabbit.

Animals↗
PubMed1996

Myocardial viability.

Left ventricular function is a major predictor of outcome in patients with coronary artery disease. Acute ischemia, postischemic dysfunction (stunning), myocardial hibernation, or a combination of these 3 are among the reversible forms of myocardial dysfunction. In myocardial stunning, dysfunction occurs despite normal myocardial perfusion, and function recovers spontaneously over time. In acute ischemia and hibernation, there is regional hypoperfusion. Function improves only after revascularization. Evidence of myocardial viability usually relies on the demonstration of uptake of various metabolic tracers, such as thallium (thallous chloride TI 201) or fludeoxyglucose F 18, by dysfunctional myocardium or by the demonstration of contractile reserve in a dysfunctional region. This can be shown as an augmentation of function during the infusion of various sympathomimetic agents. The response of ventricular segments to increasing doses of dobutamine may indicate the underlying mechanism of dysfunction. Stunned segments that have normal perfusion show dose-dependent augmentation of function. If perfusion is reduced as in hibernating myocardium, however, a biphasic response usually occurs: function improves at low doses of dobutamine, whereas higher doses may induce ischemia and, hence, dysfunction. But in patients with severely impaired perfusion, even low doses may cause ischemia. Myocardial regions with subendocardial infarction or diffuse scarring may also have augmented contractility during catecholamine infusion due to stimulation of the subepicardial layers. In these cases, augmentation of function after revascularization is not expected. Because the underlying mechanism, prognosis, and therapy may differ among these conditions, it is crucial to differentiate among dysfunctional myocardial segments that are nonviable and have no potential to regain function, hibernating or ischemic segments in which recovery of function occurs only after revascularization, and myocardial stunning in which function is expected to recover spontaneously. Because combinations of all of these disorders may occur, even in the same segments, caution should be used in interpreting the imaging results.

Coronary Circulation↗
PubMed1995

ST segment reelevation after acute myocardial infarction: marked differences in the electrocardiographic pattern between early and late episodes.

This study assesses the electrocardiographic (ECG) morphologic differences between early (< 24 h) and late (> 24 h) episodes of ST segment reelevation after acute myocardial infarction. We studied the records of 101 consecutive patients with acute myocardial infarction whose admission ECG demonstrated ST segment elevation with positive T waves, without pathological Q waves in the relevant leads, and without signs of bundle branch block or left ventricular hypertrophy. Thirty-five patients had 44 episodes of early ST segment reelevation, while 22 patients experienced 26 late episodes of ST segment reelevation. Seven patients experienced both early and late episodes. Early episodes of ST segment reelevation was seen more often after thrombolytic therapy: 43% (32 of 74 patients) versus 11% (3 of 27 patients) (P < 0.006). No differences were found in the incidence of late episodes between those who underwent (23%) or did not undergo (19%) thrombolytic therapy. Two patterns of ST segment elevation were distinguished. Pattern A with positive T waves, ST segment elevation (> or = 0.1 mV), but without distortion of the terminal portion of the QRS complex. Pattern B characterized by positive T waves, ST segment elevation (> or = 0.1 mV) with distortion of the terminal portion of the QRS complex. Each ECG was categorized according to these two patterns. The admission ECG pattern was A in 75 patients, and B in 26. No significant differences were found between patients with early, late, or no episodes of ST segment reelevation in the appearance of pattern A or B on admission.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1995

The predictive value of the electrocardiographic pattern of acute Q-wave myocardial infarction for recurrent ischemia.

A total of 140 consecutive patients with acute Q-wave myocardial infarction was evaluated to assess the relationship between different electrocardiographic patterns of evolution and the incidence of recurrent ischemia within 10 days of infarction. Patients were allocated to three groups according to the electrocardiogram at 12 h after admission: Group A: ST elevation of < 2 mm and negative T waves (75 patients); Group B: ST elevation of > 2 mm and negative T waves (35 patients); Group C: ST elevation of > 2 mm and positive T waves (30 patients). Patients in Group C had more anterior wall infarctions (82%) than Group A (40%) or Group B (58%) (p = 0.0001). Peak creatine kinase levels were lower in Group A (782 +/- 115 IU) than in Groups B (1415 +/- 257 IU) and C (1501 +/- 287 IU) (p < 0.0001). The occurrence of post-infarction recurrent ischemia was more frequent in Group A (79.2%) than in Groups B (33.3%) and C (14.8%) (p < 0.0001). Patients in Group A had relatively smaller infarctions and a higher incidence of recurrent ischemia, whereas patients in Group C had larger infarctions and a lower incidence of recurrent ischemia. The electrocardiographic pattern 12 h after admission for acute myocardial infarction is helpful in identifying a subgroup at high risk of recurrent ischemia.

Adult↗
PubMed1995

Pathobiology and Clinical Impact of Reperfusion Injury.

Reperfusion injury refers to cellular death or dysfunction caused by restoration of blood flow to previously ischemic tissue. This should be differentiated from the normal reparative processes that follow an ischemic insult. Four types of reperfusion injury have been described in the literature: (1) lethal reperfusion injury, (2) nonlethal reperfusion injury (myocardial stunning), (3) reperfusion arrhythmias, and (4) vascular injury (including the "no-reflow" phenomenon). There is continued debate whether reperfusion itself is capable of killing viable myocytes, which otherwise would have survived the ischemic insult. However, there is firm evidence for the existence of myocardial stunning following various ischemic syndromes, including reperfusion therapy for acute myocardial infarction, unstable angina pectoris, vasospastic angina, effort-induced ischemia, coronary artery bypass surgery, and cardiac transplantation. Reperfusion arrhythmia is more common after short ischemic episodes than after long ischemic periods. Thus, while reperfusion arrhythmias in the setting of acute myocardial infarction are relatively rare, reperfusion arrhythmias may be an important cause of sudden death. The "no-reflow" phenomenon has been described following reperfusion in patients with acute myocardial infarction. Three major components have been proposed as mediators of reperfusion injury: (1) oxygen free radicals, (2) the complement system, and (3) neutrophils. Numerous experimental studies have shown short-term benefit by blocking various stages of the postischemic inflammatory response. Oxygen free radicals scavangers, complement inhibition, leukocyte depletion, and the use of antibodies against various adhesion molecules have shown a reduction of infarct size in many ischemic/reperfusion experimental models. However, many of these agents failed to show a benefit in the clinical setting. Moreover, the long-term benefit of such intervention is still unknown.

Journal Article↗