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PubMed1990

[Late potentials and computerized averaging electrocardiogram in acute myocardial infarct: evaluation of myocardial reperfusion].

Myocardial reperfusion after thrombolytic therapy in acute myocardial infarction can be directly demonstrated with coronary angiography or it can be assessed thanks to indirect markers of reperfusion, such as modifications in the "averaged" QRS complex. We assessed the presence of late potentials in 37 patients within 5 hours of acute myocardial infarction onset and evaluated their disappearance or modification after reperfusion. Signal-averaged electrocardiogram, obtained computerizing QRS complexes filtered through Simson's bidirectional filter (25-250 Hz), was serially recorded in each patient: at admission, as well as 12 hours, 3 and 10 days following urokinase and/or heparin therapy. Other indirect markers of reperfusion (incidence of ventricular arrhythmias, serum CK-MB level, ST elevation) were contemporaneously evaluated. All patients underwent coronary angiography between 6 and 83 days after acute myocardial infarction. Late potentials (Total QRS greater than 115 ms; Under 40 microV greater than 39 ms; RMS Last 40 ms less than 25 microV) were present only in 25% of patients, and they always disappeared after successful thrombolysis. On the contrary if ischemia-related vessel occlusion persisted, late potentials persisted as well or else were first recorded on the 3rd or 10th day following acute myocardial infarction. Quantitative analysis of the "averaged" QRS complex showed a statistically significant reduction in QRS duration (-9.1 +/- 12.7 ms) 3 days after acute myocardial infarction in reperfused patients (group A, n = 24), while no significant reduction in the total QRS (-1 +/- 6.7 ms) was observed in non-reperfused cases (group B, n = 13), (p less than 0.05 group A vs group B). So, 10 ms reduction in total QRS duration was a good marker of reperfusion, with specificity = 92% and sensitivity = 54%; marker sensitivity was even higher (= 79%) when coupled with serum CK-MB peak within 12 hours of therapy (diagnostic accuracy = 84%). In conclusion, even if late potentials have a low prevalence in acute myocardial infarction (25%) their disappearance correlates with myocardial reperfusion. Furthermore, a reduction in total QRS duration greater than or equal to 10 ms can itself be a good marker of successful thrombolysis.

Adult↗
PubMed1992

[The era of myocardial reperfusion].

Myocardial reperfusion is the single most useful therapeutic approach in patients with acute myocardial infarction. The thousands of lives saved each year by this treatment are the result of scientific progress in very different areas, including the biopathology of myocardial ischemia and reperfusion, the mechanisms of coronary occlusion, the pharmacology of the fibrinolytic system, and clinical research. The 30% reduction in mortality achieved by fibrinolytic treatment in patients with acute myocardial infarction does not fit, apparently, with the short time-window during which restoration of blood flow results in significant myocardial salvage in animal models with few collaterals. This discrepancy could be due to the protective effect of intermittent coronary occlusions immediately preceding stable occlusive thrombosis (ischemic preconditioning), or to other possible beneficial effects of reperfusion independent of myocardial salvage, as limitation of ventricular remodelling or reduction of the risk of cardiac rupture or severe arrhythmias. Clearly, the best approach to increase the beneficial effects of reperfusion therapy is to perform it as early as possible; the cost-effectiveness of pre-hospital treatment strategies is now under investigation. In the other hand, current reperfusion therapy cannot be considered optimal. Thrombolytic agents fail to achieve recanalization of the infarct related vessel in 20-30% of patients, and 10-15% of the successfully opened arteries present early reocclusion. In certain subgroups of patients, such in those with cardiogenic shock, failure rate is higher. Mechanical recanalization by "direct" angioplasty represent an alternative reperfusion method, which utility has been established in certain circumstances only. So, well in the "reperfusion era", many questions remain open.(ABSTRACT TRUNCATED AT 250 WORDS)

Angioplasty, Balloon, Coronary↗
PubMed1989

Role of free radicals and neutrophils in canine myocardial reperfusion injury: myocardial salvage by a novel free radical scavenger, 2-octadecylascorbic acid.

To define the role of oxygen free radicals and neutrophil involvement in evolving myocardial reperfusion injury, we evaluated the effect of 2-octadecylascorbic acid (CV-3611), a novel free radical scavenger, on neutrophil function and the extent of myocardial damage resulting from 90 min of ischaemia followed by 5 h of reperfusion in an experimental model of myocardial infarction. Dogs were randomly assigned to receive CV-3611 (5 mg.kg-1.[5 min]-1, intravenously) just before the onset of reperfusion. Infarct size, as a percent of area at risk, was reduced by 60% in CV-3611 treated group as compared with control, at 16.7(SEM 3.1)% v 41.5(4.5)%, p less than 0.01. Administration of CV-3611 markedly reduced function of neutrophils isolated from peripheral circulation during reperfusion ex vivo as estimated by free radical generation (ferricytochrome c reduction and luminol enhanced chemiluminescence), chemotactic activity, and aggregation induced by A23187. Under these conditions, the enhancement in neutrophil infiltration and free radical generation (luminol enhanced chemiluminescence) in myocardium within area at risk, especially in the border zone between viable and irreversible injured myocardium, was markedly reduced. Haemodynamic profiles were similar between control and CV-3611 treated group. These results suggest that activated neutrophils, especially their generation of oxygen free radicals, contribute to reperfusion induced myocardial injury.

Animals↗
PubMed1992

Perfluorochemical reperfusion limits myocardial reperfusion injury after prolonged hypothermic global ischemia.

The ability of an oxygenated perfluorochemical (Fluosol) to limit myocardial reperfusion injury following global hypothermic ischemic insult was investigated. Neonatal piglet hearts were arrested with cold crystalloid cardioplegia and stored for 12 hours in 2 degrees C saline. Reperfusion was carried out using an isolated, blood-perfused, working heart preparation. Hearts were initially reperfused (10 minutes) with either whole blood (WB, n = 6), unmodified perfluorochemical (PFC, n = 8), or aspartate/glutamate-enriched perfluorochemical cardioplegia (PFC+, n = 6), prior to institution of whole blood perfusion, functional evaluation and left ventricular biopsy. A control group (C, n = 7) was evaluated without an intervening period of ischemia. At a left ventricular diastolic pressure of 9 mm Hg WB hearts developed a left-ventricular stroke work index (SWI) of 3.8 +/- 2.3 x 10(3) erg/g (mean +/- standard error of the mean). Under similar conditions, PFC-reperfused hearts achieved a SWI of 14.6 +/- 1.3 x 10(3), significantly greater than that of WB (p less than 0.001). SWI for PFC+ hearts was 19.8 +/- 1.6 x 10(3), significantly increased over that of PFC (p less than 0.01), and not different from values obtained for C (19.2 +/- 0.8 x 10(3)). In addition, PFC-reperfused hearts demonstrated superior maintenance (p less than 0.05) of ATP (2.08 +/- 0.16 umole/g), compared to WB (1.50 +/- 0.19), while preservation of ATP in PFC+ hearts (2.99 +/- 0.12), was significantly increased over that of PFC (p less than 0.001), and not significantly different from that for C (2.68 +/- 0.17).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed2001

Predictive value of markers of myocardial reperfusion in acute myocardial infarction for follow-up left ventricular function.

This study evaluated recently suggested invasive and noninvasive parameters of myocardial reperfusion after acute myocardial infarction (AMI), assessing their predictive value for left ventricular function 4 weeks after AMI and reperfusion defined by myocardial contrast echocardiography (MCE). In 38 patients, angiographic myocardial blush grade, corrected Thrombolysis In Myocardial Infarction frame count, ST-segment elevation index, and coronary flow reserve (n = 25) were determined immediately after primary percutaneous transluminal coronary angioplasty (PTCA) for first AMI, and intravenous MCE was determined before, and at 1 and 24 hours after PTCA to evaluate myocardial reperfusion. Results were related to global wall motion index (GWMI) at 4 weeks. MCE 1 hour after PTCA showed good correlation with GWMI at 4 weeks (r = 0.684, p <0.001) and was in an analysis of variance the best parameter to predict GWMI 4 weeks after AMI. The ST-segment elevation index was close in its predictive value. Considering only invasive parameters of reperfusion myocardial blush grade was the best predictor of GWMI at 4 weeks (R(2) = 0.3107, p <0.001). A MCE perfusion defect size at 24 hours of > or =50% of the MCE perfusion defect size before PTCA was used to define myocardial nonreperfusion. In a multivariate analysis, low myocardial blush grade class was the best predictor of nonreperfusion defined by MCE. Thus, intravenous MCE allows better prediction of left ventricular function 4 weeks after AMI than other evaluated parameters of myocardial reperfusion. Myocardial blush grade is the best predictor of nonreperfusion defined by MCE and is the invasive parameter with the greatest predictive value for left ventricular function after AMI. Coronary flow parameters are less predictive.

Aged↗
PubMed2006

Thrombus aspiration before primary angioplasty improves myocardial reperfusion in acute myocardial infarction: the DEAR-MI (Dethrombosis to Enhance Acute Reperfusion in Myocardial Infarction) study.

OBJECTIVES: This study sought to test the hypothesis that thrombus removal, with a new manual thrombus-aspirating device, before primary percutaneous coronary intervention (PPCI) may improve myocardial reperfusion compared with standard PPCI in patients with ST-segment elevation acute myocardial infarction (STEMI). BACKGROUND: In STEMI patients, PPCI may cause thrombus dislodgment and impaired microcirculatory reperfusion. Controversial results have been reported with different systems of distal protection or thrombus removal. METHODS: One-hundred forty-eight consecutive STEMI patients, admitted within 12 h of symptom onset and scheduled for PPCI, were randomly assigned to PPCI (group 1) or manual thrombus aspiration before standard PPCI (group 2). Patients with cardiogenic shock, previous infarction, or thrombolytic therapy were excluded. Primary end points were complete (>70%) ST-segment resolution (STR) and myocardial blush grade (MBG) 3. RESULTS: Baseline clinical and angiographic characteristics were similar in the 2 groups. Comparing groups 1 and 2: complete STR 50% versus 68% (p < 0.05); MBG-3 44% versus 88% (p < 0.0001); coronary Thrombolysis In Myocardial Infarction (TIMI) flow grade 3 78% versus 89% (p = NS); corrected TIMI frame count 21.5 +/- 12 versus 17.3 +/- 6 (p < 0.01); no reflow 15% versus 3% (p < 0.05); angiographic embolization 19% versus 5% (p < 0.05); direct stenting 24% versus 70% (p < 0.0001); and peak creatine kinase-mass band fraction 910 +/- 128 mug/l versus 790 +/- 132 mug/l (p < 0001). In-hospital clinical events were similar in the 2 groups. After adjusting for confounding factors, multivariate analysis showed thrombus aspiration to be an independent predictor of complete STR and MBG-3. CONCLUSIONS: Manual thrombus aspiration before PPCI leads to better myocardial reperfusion and is associated with lower creatine kinase mass band fraction release, lower risk of distal embolization, and no reflow compared with standard PPCI. (Thrombus Aspiration Before Standard Primary Angioplasty Improves Myocardial Reperfusion in Acute Myocardial Infarction; http://clinicaltrials.gov/ct/show/NCT00257153).

Angioplasty, Balloon, Coronary↗
PubMed1992

Protective effect of puerarin against myocardial reperfusion injury. Myocardial metabolism and ultrastructure.

To ascertain the beneficial effect of puerarin on the myocardium against reperfusion injury, studies on myocardial metabolism and ultrastructure were made. Twelve dogs divided into two equal groups were placed on moderate hypothermic cardiopulmonary bypass, and their hearts were subjected to 140 minutes cold cardioplegic arrest and 60 minute reperfusion. In the control group, the hearts were perfused with crystalloid cardioplegic solution (CPS) every 20 minutes during arrest. In the treated group, the hearts received CPS containing puerarin (2 mg/kg). Myocardial oxygen consumption, lactate production, creatine phosphokinase (CPK) release, water content and ultrastructural alterations were determined before ischemia, during cardiac arrest and at reperfusion. The results showed that intermittent infusion of CPS containing puerarin significantly decreased myocardial lactate production during ischemia, as well as myocardial oxygen consumption, CPK release and water content during reperfusion. Under electronmicroscopy, the degree of ischemic damage judged by a scoring method was less pronounced in the puerarin group than in the control. The authors conclude that puerarin has protective effects on the function of hearts that have undergone long periods of arrest and reperfusion.

Animals↗
PubMed2004

Assessment of myocardial reperfusion after myocardial infarction using automatic 3-dimensional quantification and template matching.

UNLABELLED: Assessment of perfusion defect extent is essential for determining prognosis after a myocardial infarction (MI), but quantification methods usually rely on segmental analysis, which may lack accuracy. We present an automated voxel-based and template-based approach for precise quantification of perfusion defect extent and reperfusion evolution. METHODS: Coronary angiography and stress/reinjection (201)Tl tomography were performed prospectively on 49 patients with recent MI (45 men; mean age +/- SD, 54 +/- 10 y), before and 3 mo after revascularization (40 angioplasties and 9 bypasses). Perfusion defect extent was quantified using expert 16-segment visual scoring of the slices and a 3-dimensional (3D) method with spatial normalization between times 1 and 2. Briefly, the latter automatically extracted myocardial edges, matched them to a reference template, and compared the perfusion intensity in each voxel with the intensity of the corresponding voxel in a control population of 100 healthy subjects. RESULTS: Reocclusion occurred in 12 patients within 3 mo of surgery (all had undergone angioplasty). The perfusion gain between times 1 and 2, assessed by visual analysis, was significantly higher in permeable patients than in reoccluded patients: 12.4% +/- 13.3% and 2.3% +/- 8.2% of the initial stress defect, respectively (P = 0.02). Proportional gains, measured with the quantitative 3D method, were 4.5% +/- 3.6% and 1.9% +/- 2.7%, respectively (P = 0.02). Furthermore, the 3D method allowed measurement within the initial ischemic defect (reversible part of the stress defect at time 1), the extent of myocardium whose perfusion improved at time 2 (reperfusion), and the extent of myocardium whose perfusion remained unchanged (residual ischemia). A voxel-by-voxel analysis of these regions revealed that the proportion of reperfusion was significantly higher in permeable patients than in reoccluded patients: 60.0% +/- 21.3% versus 40.0% +/- 22.5%, respectively (P = 0.008). This was cumbersome to quantify using visual analysis and did not reach statistical significance, likely because of segmental division (partial-volume effect) and absence of spatial normalization. CONCLUSION: The 3D voxel-based quantification allows satisfying assessment of reperfusion 3 mo after MI. Moreover, the automated analysis using spatial normalization should facilitate a reproducible assessment of large populations over time.

Aged↗
PubMedDate not supplied

[Ischemia-reperfusion myocardial injury].

In this article, we present some considerations on the myocardial damage due to a deficit of oxygen supply. In fact, this damage properly constitutes a partial diastolic depolarization or injury, i.e., a moderate reduction of the rest transmembrane potential. This phenomenon is characteristic of the acute phase of the myocardial infarction syndrome and is responsible for the main electrical manifestations appearing in this phase: disorders of rhythm and conduction, as well as a reduced contractility of the involved myocardial fibers. All the mentioned phenomena are due to a defect of the myocardial energetic mechanisms, owing to the mitochondrial alterations in myocytes: early reduction of the nicotinamide adenine nucleotides, accumulation of calcium ("calcium overload") into mitochondria, and a drop in oxidative phosphorylation. These changes can present again, more exaggerated, in a following phase of evolution of the myocardial infarction due to myocardial reperfusion. Its severity is related to the duration of the initial ischemia period. Moreover, consequences of the oxidative stress can add producing cellular damage by liberation of reactive oxygen species. Oxidant stress causes also alterations in the mitochondrial DNA, i.e., mutations due to oxidation of nitrogenous bases. During the initial ischemia phase, as well as during reperfusion, metabolic therapy can be very useful as, for example, glucose-insulin-potassium solutions (G-I-K). These could act as scavengers of the free radicals derived from oxygen and avoid or reduce the myocardial damage due to reperfused myocytes. Metabolic drugs, as for example trimetazidine, antioxidants, etc, can also be used in the myocardial reperfusion phase.

Electrophysiology↗
PubMed1995

Early spontaneous intermittent myocardial reperfusion during acute myocardial infarction is associated with augmented thrombogenic activity and less myocardial damage.

OBJECTIVES: This study investigated the influence of early spontaneous intermittent reperfusion on the extent of myocardial damage and its relation to endogenous hemostatic activity. BACKGROUND: In the early phase of acute myocardial infarction coronary occlusion is often intermittent, even before thrombolytic therapy is administered. The relation between this phenomenon, myocardial damage and hemostatic activity is unknown. METHODS: Holter ST segment recording and pretreatment plasma tissue-type plasminogen activator (t-PA) antigen, plasminogen activator inhibitor-1 (PAI-1) antigen, prothrombin fragment F1 + 2 and soluble fibrin levels were measured in 57 patients with acute evolving myocardial infarction. Spontaneous intermittent myocardial reperfusion, defined as two or more episodes of transient resolution of ST segment elevation to within 0.05 mV of baseline, lasting > or = 1 min, before the start of recombinant t-PA (rt-PA) treatment was present in 28 patients (group 1) and absent in 29 (group 2). Left ventriculography and coronary angiography were performed 90 min after intravenous rt-PA administration. Plasma creatine kinase-MB fraction (CK-MB) levels were measured every 6 h for 24 h, and C-reactive protein levels were measured daily for 3 days. RESULTS: Group 1 had lower peak plasma CK-MB (141.9 +/- 28.3 vs. 203.8 +/- 23.3 IU/liter [mean +/- SEM], p < 0.014) and C-reactive protein levels (16 +/- 4 vs. 28 +/- 4 mg/liter on day 1; 26.6 +/- 5.5 vs. 61.8 +/- 14.4 mg/liter on day 2; 19.6 +/- 4.2 vs. 40.6 +/- 6.5 mg/liter on day 3, p < 0.012) and a higher left ventricular ejection fraction (62.9 +/- 4% vs. 51.1 +/- 5%, p < 0.04) than group 2. Group 1 had lower plasma t-PA antigen levels (15.6 vs. 27 micrograms/liter, p < 0.006) but higher prothrombin fragment F1 + 2 (1.8 vs. 1.1 nmol/liter, p < 0.003) and soluble fibrin levels (66.8 vs. 31 nmol/liter, p < 0.01). Coronary patency at 90 min was similar. CONCLUSIONS: Early spontaneous intermittent reperfusion during acute myocardial infarction is associated with augmented thrombogenic activity and less subsequent myocardial damage. This finding is consistent with a protective effect of intermittency on the myocardium and a procoagulant effect of spontaneous lysis on blood. It may also reflect a different rate of evolution of coronary thrombosis and myocardial infarction in patients with and those without spontaneous intermittent myocardial reperfusion.

Analysis of Variance↗
PubMed2000

Assessment of myocardial reperfusion by intravenous myocardial contrast echocardiography and coronary flow reserve after primary percutaneous transluminal coronary angioplasty [correction of angiography] in patients with acute myocardial infarction.

BACKGROUND: This study investigated whether the extent of perfusion defect determined by intravenous myocardial contrast echocardiography (MCE) in patients with acute myocardial infarction (AMI) treated by primary percutaneous transluminal coronary angioplasty (PTCA) relates to coronary flow reserve (CRF) for assessment of myocardial reperfusion and is predictive for left ventricular recovery. METHODS AND RESULTS: Twenty-five patients with first AMI underwent intravenous MCE with NC100100 with intermittent harmonic imaging before PTCA and after 24 hours. MCE before PTCA defined the risk region and MCE at 24 hours the "no-reflow" region. The no-reflow region divided by the risk region determined the ratio to the risk region. CFR was assessed immediately after PTCA and 24 hours later. Left ventricular wall motion score indexes were calculated before PTCA and after 4 weeks. CFR at 24 hours defined a recovery (CFR >/=1.6; n=17) and a nonrecovery group (CFR <1.6; n=8). Baseline CFR did not differ between groups. MCE ratio to the risk region was smaller in the recovery group compared with the nonrecovery group (34+/-49% vs 81+/-46%, P=0.009). A ratio to the risk region of </=50% defined an MCE reperfusion group. It was associated with improvement of CFR from 1.67+/-0.47 at baseline to 2. 15+/-0.53 at 24 hours (P<0.001) and of regional wall motion score index from 2.6+/-0.5 to 1.9+/-0.5 at 4 weeks (P<0.001). CONCLUSIONS: Intravenous MCE can be used to define perfusion defects after AMI. Assessment of microcirculation by MCE corresponds to evaluation by CFR. Serial intravenous MCE has the potential to identify patients likely to have improved left ventricular function after AMI.

Aged↗
PubMed1991

[Effect of echinochrom on experimental myocardial reperfusion injury].

Echinochrom, a new antioxidant of the polyhydroxynaphthaquinone class, was tested for its cardioprotective activity in a model of occlusive reperfusion myocardial infarction (90-min occlusion and 4-hour reperfusion) in the acute experiments with open-chest dogs. The bolus intravenous injection of echinochrom in a dose of 1 mg/kg 5 min before reperfusion caused a significant (over 40%) reduction in the size of a necrotic focus. A supplementary administration of echinochrom 5 min after the onset of ischemia failed to contribute to a significant enhancement of its protective effect, suggesting that there is no substantial effect of the agent on ischemic lesion. The efficacy of echinochrom given after prolonged ischemia, low effective doses, and no adverse effects create prerequisites for using the drug in the clinical setting.

Animals↗
PubMed1990

Sustained limitation of myocardial reperfusion injury by a monoclonal antibody that alters leukocyte function.

Pentobarbital anesthetized dogs were subjected to 90 minutes of left circumflex coronary artery (LCCA) occlusion followed by 72 hours of reperfusion. Control or anti-Mo1 (904) F(ab')2 fragments of monoclonal antibodies were administered intravenously at a dose of 1 mg/kg beginning 45 minutes after occlusion and at a dose of 0.5 mg/kg at 12, 24, 36, and 48 hours after reperfusion. Myocardial infarct size expressed as a percentage of the area at risk (IN/AR) measured postmortem after 72 hours of reperfusion was significantly reduced by 904 F(ab')2 (21.6 +/- 2.8%, n = 8) compared with control F(ab')2 (37.4 +/- 5.8%, n = 8; p less than 0.025). There were no significant differences between groups in heart rate, mean arterial blood pressure, rate-pressure product, or LCCA blood flow that could account for a reduced infarct size. Regional myocardial blood flow (RMBF) was determined with 15-microns radiolabeled microspheres. Transmural blood flows (ml/min/g) within the region of myocardium at risk were not statistically different between treatment groups. Infarct size in both groups was related to regional myocardial blood flow, and the relation was shifted downward in the group treated with the anti-Mo1 F(ab')2 antibody (analysis of covariance, p = 0.01). Thus, anti-Mo1 F(ab')2 produces a sustained limitation of myocardial infarct size compared with controls under similar hemodynamic conditions and a similar degree of myocardial ischemia as determined by RMBF. These data suggest that inhibition of neutrophil adhesive interactions (as suggested by the inhibitory effect of anti-Mo1 on canine neutrophil aggregation) may be an effective mechanism for protection against myocardial injury secondary to myocardial ischemia and reperfusion.

Animals↗
PubMed2004

[Myocardial reperfusion injury].

Myocardial reperfusion injury is defined as the adverse effects that ensue upon restoration of the circulation, which allows blood and nutrients to reach cells previously subjected to ischemia. Restoration of blood flow can be accompanied by the release of oxygen free radicals, the appearance of intracellular calcium overload, and alterations in cell metabolism -all situations that can give rise to functional or structural myocardial injury. Clinical signs of injury may appear after circulation is restored or after the use of extracorporeal circulation during heart surgery, and are manifested as stunned or hibernating myocardium after acute coronary syndromes, as the no-reflow phenomenon (microvascular injury) after blood flow is restored during angioplasty or after < >, and especially after surgical revascularization. This review examines the pathophysiological substrates, clinical manifestations and current approaches to treatment for each of these entities.

Animals↗
PubMed2004

Effect of intracoronary adenosine infusion during coronary intervention on myocardial reperfusion injury in patients with acute myocardial infarction.

Despite early recanalization of an occluded infarct artery, up to 33% of patients with acute myocardial infarction do not obtain complete myocardial reperfusion due to a process of reperfusion injury. This study assessed whether adjunctive therapy with adenosine might prevent or attenuate the phenomenon of myocardial reperfusion injury. Myocardial reperfusion was assessed in 79 consecutive patients receiving a 20-minute intracoronary infusion of adenosine during percutaneous coronary intervention (PCI) and in a historical cohort of 200 patients with acute myocardial infarction who were treated with PCI (controls). Myocardial reperfusion injury was defined as persistent (> or =50% of initial value) ST-segment elevation after successful recanalization. Its effect on infarct size was evaluated by calculating the Selvester QRS score before intervention and at follow-up. Myocardial reperfusion injury was present in 19% of patients receiving adenosine versus 35% of control patients (p = 0.004). Evaluation of infarct expansion over time showed almost no change in the QRS score in patients receiving adenosine (3.4 +/- 3.0 before PCI; 3.5 +/- 3.1 at follow-up). In contrast, infarct QRS score in the control group worsened from 3.1 +/- 2.7 before PCI to 4.5 +/- 3.2 at follow-up (p = 0.003 treatment with adenosine vs control). Multivariate analysis identified adjunctive therapy with adenosine as an independent protective determinant of myocardial reperfusion injury and of infarct expansion. The rate of major adverse cardiac events (death and myocardial infarction) at 1 month tended to be lower in patients receiving adenosine (4% vs 6.5%, p = 0.7) and was mainly observed in patients with evidence of myocardial reperfusion injury (cardiac event rate 2% in patients with ST-segment elevation of <50% vs 14% in patients with ST-segment elevation > or =50%, p = 0.003). Thus, impaired myocardial reperfusion is the most important determinant of clinical outcome in patients with acute myocardial infarction treated with PCI. Adjunctive therapy with intracoronary infusion of adenosine during PCI prevents the occurrence of severe myocardial reperfusion injury and is associated with less infarct expansion.

Adenosine↗
PubMed1991

Myocardial reperfusion injury. Platelet-activating factor stimulates polymorphonuclear leukocyte hydrogen peroxide production during myocardial reperfusion.

To study the roles of platelet-activating factor, polymorphonuclear leukocytes, and oxygen free radicals in myocardial reperfusion injury, we subjected 10 sheep to 90 minutes of mid-left anterior descending coronary artery followed by 6 hours of reperfusion. Stainings with gentian violet and tetratriphenyl ammonium chloride demonstrated 20% +/- 3% of the left ventricular mass at risk for ischemia, of which 75% +/- 10% underwent infarction. Coronary sinus blood was assayed for platelet-activating factor and neutrophil hydrogen peroxide production before and during coronary occlusion and during reperfusion. Platelet-activating factor was isolated by column chromatography and lipid extraction and quantified by radioimmunoassay. Neutrophil hydrogen peroxide production was measured by a 2',7'-dichlorofluorescein flow-cytometric assay. Platelet-activating factor was elevated to 899 +/- 210 pg/ml at 15 minutes of reperfusion, compared with the preocclusion level of 271 +/- 55 pg/ml and coronary occlusion level of 359 +/- 64 pg/ml (p less than 0.05; analysis of variance). Neutrophil hydrogen peroxide production, measured on a relative fluorescence scale, was also elevated to a level of 141 +/- 27 at 1 hour of reperfusion, compared with the preocclusion level of 103 +/- 6 and the coronary occlusion level of 114 +/- 13 (p less than 0.01; analysis of variance). Both of these parameters returned toward baselines at the end of 6 hours of reperfusion. Histologic examination revealed infiltration of polymorphonuclear leukocytes into the interstitium of the reperfused myocardium. Neutrophils isolated from unoperated and healthy sheep demonstrated a graded dose response in hydrogen peroxide production when stimulated by purified platelet-activating factor in vitro. These findings suggest that platelet-activating factor is released in the coronary circulation and is a mediator of oxygen free radical production in polymorphonuclear leukocytes during myocardial reperfusion.

Animals↗
PubMed1992

[Myocardial reperfusion syndrome].

Myocardial reperfusion is associated with a number of clinical, electrocardiographic (arrhythmias, conduction defects, ST segment changes), haemodynamic and biological events. The commonest arrhythmias are ventricular extra-systoles, rapid ventricular tachycardias, and accelerated idio-ventricular rhythms. Reperfusion bradycardias are less common. When the arrhythmia is related to ischaemia it usually regresses when perfusion is restored. Reperfusion of the inferior wall of the left ventricle is often associated with sinus bradycardia and hypotension. The ST segment changes may evolve in two different ways: progressive regression or accentuation of ST elevation. When the responsible artery is recanalized, there is an immediate rise in plasma enzyme and myoglobin concentrations. The peak CPK concentration is usually observed after the 12th hours. The diagnostic value of the reperfusion syndrome lies in the interpretation of rapid ventricular tachycardias, accelerated idio-ventricular rhythms, ST segment changes and immediate rise in plasma CPK levels. The clinical risks of the reperfusion syndrome are low, practically never rhythmic and only exceptionally haemodynamic.

Arrhythmias, Cardiac↗
PubMed1991

Hydroxyethyl starch macromolecule and superoxide dismutase effects on myocardial reperfusion injury.

Myocardial reperfusion injury may be due to biophysical changes (e.g., endothelial cell junctional separations), as well as biochemical mechanisms (e.g., oxygen free radical activity). Superoxide dismutase (SOD), a free radical scavenger, may be effective in reducing chemical injury. Fractions of hydroxyethyl starch (HES-Pz), a large macromolecule, have been shown to decrease microvascular permeability associated with reperfusion-induced biophysical alterations. A comparison of SOD to HES-Pz was performed using a canine model of 1-hour left anterior descending coronary artery (LAD) clamping followed by 24 hours of reperfusion. Amounts of the test solution equal to 10% of the dog's blood volume were administered intraatrially to the animals just before release of the LAD clamp. Six dogs received Ringer's lactate, 7 were given 600,000 IU of SOD, 13 received 6% HES-Pz, and 9 were given SOD and HES-Pz. The ratio of infarct to area at risk was 20 +/- 3% in the control dogs receiving Ringer's lactate, 16 +/- 4% in animals receiving SOD alone (p = NS), 6 +/- 3% in dogs receiving HES-Pz alone (p less than 0.05), and 8 +/- 3% in dogs given a combination of SOD and HES-Pz (p less than 0.05). HES-Pz alone and with SOD significantly reduced reperfusion injury, although addition of SOD to HES-Pz did not have an additive effect. Appropriate-sized macromolecules may act by reducing ischemia-induced microvascular permeability.

Animals↗