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At least 217 records · Page 12Linked to original sources
PubMed1992

[Does reperfusion modify the risk of heart rupture? Effects of early reperfusion].

The goal of this study was to evaluate whether early fibrinolytic therapy could reduce in-hospital mortality caused by cardiac rupture in patients with acute myocardial infarction (AMI). Based on the strong correlation between occurrence of left ventricular free wall rupture and development of sudden electromechanical dissociation (EMD) in patients with a first TAMI without relevant heart failure, we compare the incidence of this mechanism of death in patients treated with streptokinase and in those from a control group. The study included 406 patients with a first transmural AMI younger than 71 years who received intravenous streptokinase (SK) with 104 similar patients not treated with fibrinolytic agents. Mortality rate in patients treated with SK was 6% compared to 11% in those from the control group. Patients treated with SK presented a lower incidence of EMD than those from the control group (17% vs 72%; p < 0.002). A necropsy study carried out in 33% of cases, confirmed the existence of left ventricular free wall rupture in each of the 7 cases who presented EMD but in none of the 6 who died in shock. We conclude that left ventricular free wall rupture is the principal cause of mortality in patients admitted to a Coronary Care Unit with a first transmural AMI, and that fibrinolytic treatment reduces mortality mainly by reducing development of cardiac rupture.

Administration, Oral↗
PubMed1993

Limitation of infarct expansion and ventricular remodeling by late reperfusion. Study of time course and mechanism in a rat model.

BACKGROUND: Reperfusion of acutely infarcted myocardium may be beneficial in limiting infarct expansion and ventricular remodeling even if established after the time that salvage of ischemic myocardium is possible. METHODS AND RESULTS: To examine the permanency, time course, and mechanism of this effect of late reperfusion, 200 rats were randomized into one of four groups: (1) infarction with reperfusion after 1 to 2 hours, (2) infarction with reperfusion after 6 to 8 hours, (3) infarction without reperfusion, and (4) sham operation. Surviving rats were killed at either 7 days, when infarct expansion has plateaued, or 21 days, when infarct healing is complete. In both 7- and 21-day analyses, late reperfusion did not reduce infarct size or degree of transmural necrosis but significantly limited infarct expansion, as measured by an index based on infarct endocardial segment lengthening and infarct wall thinning (expansion index at 7 days: no reperfusion, 2.73 +/- 0.25, n = 13; reperfusion after 1 to 2 hours, 1.56 +/- 0.13, n = 23, P < .001; reperfusion after 6 to 8 hours, 1.78 +/- 0.15, n = 16, P = .002; at 21 days: no reperfusion, 3.45 +/- 0.39, n = 13; reperfusion after 1 to 2 hours, 2.21 +/- 0.24, n = 15, P = .01; reperfusion after 6 to 8 hours, 2.02 +/- 0.20, n = 9, P = .01). Reperfusion after 6 to 8 hours was equally effective in limiting expansion as reperfusion after 1 to 2 hours. Late reperfusion also significantly reduced ventricular remodeling at 21 days, as measured by an index based on left ventricular cavity dilatation and noninfarcted myocardial hypertrophy (remodeling index at 21 days: no reperfusion, 2.67 +/- 0.15, n = 13; reperfusion after 1 to 2 hours, 2.20 +/- 0.15, n = 15, P = .035; reperfusion after 6 to 8 hours, 2.12 +/- 0.10, n = 9, P = .012). Histological examination revealed that reperfusion accelerated the clearance of residual dead myofibrils, suggesting an increase in the rate of healing, and increased the degree of myocytolysis but did not change the final degree of infarct healing, tissue density, or viable subepicardial cells. CONCLUSIONS: Late reperfusion causes a permanent reduction in postinfarction expansion that is present even after complete infarct healing. The time after coronary occlusion in which reperfusion is of benefit in reducing subsequent expansion and remodeling is substantially longer than previously established. The mechanism by which late reperfusion limits expansion may involve changing the rate of healing and the nature of myocardial necrosis but does not involve preserving subepicardial cells.

Animals↗
PubMed1998

Use of a nitric oxide precursor to protect pig myocutaneous flaps from ischemia-reperfusion injury.

Nitric oxide is a radical with vasodilating properties that protects tissues from neutrophil-mediated ischemia-reperfusion injury in the heart and intestine. Previous studies in our laboratory suggested that L-arginine, a nitric oxide precursor, can protect skin flaps from ischemia-reperfusion injury. In this study, we examined the effects of L-arginine on the survival of myocutaneous flaps in a large animal model and established whether this effect was mediated by nitric oxide and neutrophils. Two superiorly based 15 x 7.5 cm epigastric myocutaneous island flaps were dissected in 15 Yorkshire pigs weighing 45 to 50 kg. One of the flaps was subjected to 6 hours of arterial ischemia and then reperfused for 4 hours (ischemia-reperfusion flaps), whereas the other flap was used as a non-ischemic control (non-ischemia-reperfusion flaps). The flaps were divided into four groups: control non-ischemia-reperfusion flaps that received only saline (group I); ischemia-reperfusion flaps that were treated with saline (group II); and flaps treated with either L-arginine (group III) or Nomega-nitro-L-arginine methylester (L-NAME), a nitric oxide synthase competitive inhibitor, plus L-arginine in equimolar amounts (group IV). These drugs were administered as an intravenous bolus 10 minutes before the onset of reperfusion, followed by a 1-hour continuous intravenous infusion. Full-thickness muscle biopsies were taken at baseline, 3 and 6 hours of ischemia, and 1 and 4 hours of reperfusion. The biopsies were evaluated by counting neutrophils and measuring myelo-peroxidase activity. At the end of the experiment, skeletal muscle necrosis was quantified using the nitroblue tetrazolium staining technique, and a full-thickness biopsy of each flap was used for determination of water content. Statistical analysis was performed using analysis of variance and the Newman-Keuls test. Non-ischemia-reperfusion flaps showed no muscle necrosis. Ischemia-reperfusion flaps treated with saline had 68.7 +/- 9.1 percent necrosis, which was reduced to 21.9 +/- 13.6 percent with L-arginine (p < 0.05). L-NAME administered concomitantly with L-arginine demonstrated a necrosis rate similar to that of saline-treated ischemia-reperfusion flaps (61.0 +/- 17.6 percent). Neutrophil counts and myeloperoxidase activity after 4 hours of reperfusion were significantly higher in ischemia-reperfusion flaps treated with L-NAME and L-arginine as compared with the other three groups (p < 0.05). Flap water content increased significantly in ischemia-reperfusion flaps treated with saline and L-NAME plus L-arginine versus non-ischemia-reperfusion flaps (p < 0.02) and L-arginine-treated ischemia-reperfusion flaps (p < 0.05). There was no difference in flap water content between ischemia-reperfusion flaps treated with L-arginine and non-ischemia-reperfusion flaps. Administration of L-arginine before and during the initial hour of reperfusion significantly reduced the extent of flap necrosis, neutrophil accumulation, and edema due to ischemia-reperfusion injury in a large animal model. This protective effect is completely negated by the use of the nitric oxide synthase blocker L-NAME. The mechanism of action seems to be related to nitric oxide-mediated suppression of ischemia-reperfusion injury through neutrophil activity inhibition.

Animals↗
PubMed1997

Early detection of successful coronary reperfusion based on serum concentration of human heart-type cytoplasmic fatty acid-binding protein.

Both human heart-type cytoplasmic fatty acid-binding protein (H-FABPc) and myoglobin are low molecular weight proteins that are abundant in the cytoplasm of myocardial cells. Unlike myoglobin, H-FABPc content in the skeletal muscle is less than in cardiac muscle. To investigate the usefulness of the serum concentration of H-FABPc in the early detection of successful coronary reperfusion, we measured serum concentrations of H-FABPc and myoglobin in 45 patients with acute myocardial infarction treated with intracoronary thrombolysis or direct percutaneous transluminal coronary angioplasty. Coronary angiography was performed every 5 min for reperfusion therapy to identify the onset of reperfusion. Reperfusion, defined as a TIMI grade 2 or 3, was achieved within 60 min of the initiation of reperfusion therapy in 30 patients (the reperfused group), but was not achieved in 15 patients (the non-reperfused group). Blood samples were obtained before initiation of treatment and 15, 30 and 60 min after initiation of treatment in the non-reperfused group. In the reperfused group, samples were obtained before reperfusion and 15, 30 and 60 min after reperfusion. The H-FABPc ratio (the ratio of value after to value before the initiation of treatment or reperfusion) increased sharply after the onset of reperfusion, peaking at 41 +/- 18 min, and decreased rapidly thereafter. The predictive accuracy of an H-FABPc ratio of > 1.8 for the detection of reperfusion within 60 min of the initiation of treatment was 93% at 15 min after reperfusion, 98% at 30 min, and 100% at 60 min. Similar rates of predictive accuracy were observed for a myoglobin ratio > 2.4. The H-FABPc ratio detected successful reperfusion as early as 15 min after the onset of reperfusion and was highly accurate in detecting reperfusion within 60 min of the onset of reperfusion. The predictive accuracy of the H-FABPc ratio was similar to that of the myoglobin ratio for the early detection of successful coronary reperfusion.

Adult↗
PubMed1993

Late reperfusion for acute myocardial infarction limits the dilatation of left ventricle without the reduction of infarct size.

BACKGROUND: While previous clinical studies have shown a possible beneficial effect of the reperfusion performed at a relatively late phase of acute myocardial infarction ("late reperfusion") in preventing left ventricular enlargement, the mechanism has not been clarified. METHODS AND RESULTS: Of 89 patients with an initial anterior myocardial infarction, reperfusion was successful in 69. These 69 were divided into three groups according to the time required to achieve reperfusion after the onset of symptoms: early-reperfused (< 3 hours from the onset to reperfusion; n = 22), intermediate-reperfused (3 to 6 hours from the onset to reperfusion; n = 28), and late-reperfused (> 6 hours from the onset to reperfusion; n = 19). The 20 patients whose infarct-related artery were occluded in the acute phase as well as 1 month later was classified as nonreperfused. Infarct size, evaluated as defect volume by 201Tl single-photon emission computed tomography 1 month after the onset, was 1593 +/- 652 units (mean +/- SD) in the late-reperfused group, significantly larger (P < .05) than that of the intermediate-reperfused (1066 +/- 546 U) or the early-reperfused groups (372 +/- 453 U) but not different from that of the nonreperfused group (1736 +/- 562 U). Wall motion abnormality index as well as global ejection fraction evaluated by left ventriculography 1 month after the onset showed that late reperfusion did not preserve the left ventricular wall motion and function. These results indicate that the earlier reperfusion decreased the size of the infarction and preserved left ventricular function, whereas late reperfusion (> 6 hours after onset) did not limit infarct size or preserve left ventricular function. In contrast, the end-diastolic volume index did not differ significantly among the early-reperfused (50 +/- 15 mL/m2), intermediate-reperfused (54 +/- 14 mL/m2), and late-reperfused (53 +/- 19 mL/m2) groups; those were significantly smaller than that of the nonreperfused group (68 +/- 12 mL/m2; P < .05). Left ventriculographic data obtained in both the acute and chronic phase in 39 patients showed that left ventricular volumes increased significantly during the course of myocardial infarction only in the nonreperfused group. CONCLUSIONS: Late reperfusion appeared to prevent ventricular dilatation acute myocardial infarction independent of the limitation of infarct size.

Adult↗
PubMed2003

Prospective evaluation of clinical outcomes after acute ST-elevation myocardial infarction in patients who are ineligible for reperfusion therapy: preliminary results from the TETAMI registry and randomized trial.

BACKGROUND: Treatment with lytics or primary percutaneous coronary interventions (PCI) reduces the mortality rate of patients with ST-elevation myocardial infarction (STEMI) presenting within 12 hours. Patients presenting >12 hours are generally considered to be ineligible for reperfusion therapy, and there are currently no specific treatment recommendations for this subgroup.Methods- All patients with STEMI <24 hours were included in the Treatment with Enoxaparin and Tirofiban in Acute Myocardial Infarction (TETAMI) randomized trial or registry. Those patients who were ineligible for acute reperfusion, had no cardiogenic shock, and were not planned for revascularization within 48 hours were randomized to 1 of 4 antithrombotic regimens involving enoxaparin or unfractionated heparin (UFH), in combination with tirofiban or placebo for 2 to 8 days. A concurrent registry tracked STEMI patients coming in within <12 hours, and who underwent reperfusion. This registry also tracked the remaining STEMI patients who neither received reperfusion nor were enrolled in the TETAMI randomized trial. The demographics and clinical outcomes of all three groups (received reperfusion therapy, too late for reperfusion and enrolled in the randomized trial, neither received reperfusion therapy nor were enrolled in the randomized trial) were prospectively tracked. RESULTS AND CONCLUSIONS: There were 2,737 patients who presented with STEMI or a new left branch bundle block (LBBB), of which 1,654 (60%) presented < or =12 hours. There were 1,196 (72%) of 1,654 patients who received reperfusion therapy. There were 458 (28%) of the 1,654 patients deemed "ineligible" for reperfusion, mostly because of a contraindication to lytics or for being "too old." In contrast, 1,083 (40%) of 2,737 patients presented >12 hours. Apart from 34 of these patients who had a stuttering infarction and were referred for reperfusion, the remaining patients did not receive reperfusion therapy. Registry patients who received reperfusion therapy, compared with TETAMI randomized patients (all of whom received antithrombotic therapy) and registry patients who did not receive reperfusion, were younger (61 years versus 63 years and 67 years), were more likely to be male (78% versus 73% and 63%), and had persistent ST-segment elevation as opposed to LBBB or Q waves. Registry patients who received reperfusion therapy had better clinical outcomes, even after adjusting for admission Killip class, compared with TETAMI randomized patients and registry patients who did not receive reperfusion therapy. TETAMI randomized patients had better outcomes than registry patients who did not receive reperfusion therapy. The major obstacle to expanding the delivery of reperfusion therapy to patients with STEMI is the large fraction of patients who present too late for reperfusion therapy. Examination of prospectively gathered data on STEMI patients who are ineligible for reperfusion may help optimize their treatment.

Age Factors↗
PubMed1996

Improvement in functional recovery of the isolated guinea pig heart after hyperkalemic reperfusion with adenosine.

The aim of this study was to examine the effect of initial hyperkalemic reperfusion (HKR), with and without added adenosine, on coronary flow, myocardial function, and endothelium-dependent and endothelium-independent coronary vascular function. Cardioplegic arrest was induced in 40 isolated guinea pig hearts by infusing oxygenated cardioplegic (high in potassium ion) Krebs solution for 5 minutes. Hearts were then stored at room temperature for 3.5 hours. On reperfusion, hearts were divided into four groups of 10 hearts each: control, reperfusion with regular Krebs solution (4.6 mmol/L potassium chloride); base hyperkalemic reperfusion, initial reperfusion with 37 degrees C oxygenated, cardioplegic Krebs solution for 5 minutes; hyperkalemic reperfusion with addition of 1 mmol/L adenosine during HKR; and hyperkalemic reperfusion with addition of 5 mmol/L adenosine. Coronary reserve (adenosine bolus 2 mmol/L) and responses to acetylcholine (1 mumol/L) and nitroprusside (100 mumol/L) were examined before and after ischemia and reperfusion. Flow did not return to preischemic values in any group after reperfusion. Adenosine treatment during initial reperfusion increased coronary flow (percentage of baseline +/- standard error of the mean) from 57% +/- 4% in control and 45% +/- 3% in hearts with hyperkalemic reperfusion to 79% +/- 3% and 83% +/- 5% in hearts with hyperkalemic reperfusion also treated with, respectively, 1 mmol/L adenosine and 5 mmol/L adenosine (p < 0.05). At 30 and 60 minutes of reperfusion, however, flow remained elevated only in the group treated with 5 mmol/L adenosine. Coronary reserve and responses to acetylcholine and nitroprusside were equivalently depressed in all groups after reperfusion. Recovery of left ventricular systolic and diastolic function was improved in all groups after hyperkalemic reperfusion (54% +/- 4% of preischemic value) compared with control (39% +/- 3%), and recovery was further enhanced in the group treated with 5 mmol/L adenosine (60% +/- 4%). In this ex vivo model, hyperkalemic reperfusion improved myocardial function after cardioplegic arrest and the addition of 5 mmol/L adenosine improved coronary flow. Adenosine may counteract the potassium chloride-induced vasoconstriction that occurs during hyperkalemic reperfusion and may thus improve coronary flow and myocardial function. Postischemic depression of endothelium-dependent or endothelium-independent vascular functions, however, was not alleviated by hyperkalemic reperfusion with or without adenosine.

Acetylcholine↗
PubMed1998

Controlled reperfusion after lung ischemia: implications for improved function after lung transplantation.

OBJECTIVES: Despite improvements in organ preservation, reperfusion injury remains a major source of morbidity and mortality after lung transplantation. This pilot study was designed to investigate the effects of controlled reperfusion after lung ischemia. METHODS: Twenty adult pigs underwent 2 hours of warm lung ischemia by crossclamping the left bronchus and pulmonary artery. In five (group 1), the clamp was simply removed at the end of ischemia (uncontrolled reperfusion). The 15 other pigs underwent modified reperfusion using blood from the femoral artery to perfuse the lung through the pulmonary artery (pressure 40 to 50 mm Hg) for 10 minutes before removing the pulmonary artery clamp. In five (group 2), the blood was mixed with crystalloid, resulting in a substrate-enriched, hypocalcemic, hyperosmolar, alkaline solution. In five (group 3), the blood was circulated through a leukocyte-depleting filter, and the last five (group 4) underwent reperfusion with both a modified solution and white blood cell filter. Lung function was assessed 60 minutes after reperfusion, and biopsy specimens were taken. RESULTS: Controlled reperfusion with both a white blood cell filter and modified solution (group 4) completely eliminated the reperfusion injury that occurred with uncontrolled reperfusion (group 1), resulting in complete preservation of compliance (98% +/- 1% vs 77% +/- 1%; p < 0.001, and arterial/alveolar ratio (97% +/- 2% vs 27% +/- 2%; p < 0.001); no increase in pulmonary vascular resistance (106% +/- 1% vs 198% +/- 1%; p < 0.001); lowered tissue edema (82.1% +/- 0.4% vs 84.3% +/- 0.2%; p < 0.001), and myeloperoxidase activity (0.18 +/- 0.02 vs 0.35 +/- 0.02 deltaOD/min/mg protein; p < 0.001). In contrast, using either a white blood cell filter or modified solution separately improved but did not avoid the reperfusion injury, resulting in pulmonary function and tissue edema levels that were intermediate between group 1 (uncontrolled reperfusion) and group 4 (white blood cell filter and modified solution). CONCLUSION: After 2 hours of warm pulmonary ischemia, (1) a severe lung injury occurs after uncontrolled reperfusion, (2) controlled reperfusion with either a modified reperfusion solution or white blood cell filter limits, but does not avoid, a lung reperfusion injury, (3) reperfusion using both a modified reperfusate and white blood cell filter results in complete preservation of pulmonary function. We therefore believe surgeons should control the reperfusate after lung transplantation to improve postoperative pulmonary function.

Animals↗