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PubMed1998

Prospective, multicenter study of the safety and feasibility of primary stenting in acute myocardial infarction: in-hospital and 30-day results of the PAMI stent pilot trial. Primary Angioplasty in Myocardial Infarction Stent Pilot Trial Investigators.

OBJECTIVES: The goals of this study were to examine the safety and feasibility of a routine (primary) stent strategy in acute myocardial infarction (AMI). BACKGROUND: Limitations of reperfusion by primary percutaneous transluminal coronary angioplasty (PTCA) in AMI include in-hospital recurrent ischemia or reinfarction in 10% to 15% of patients, restenosis in 37% to 49% and late infarct-related artery reocclusion in 9% to 14%. By lowering the residual stenosis and sealing dissection planes created by PTCA, primary stenting may further improve short- and long-term outcomes after mechanical reperfusion. METHODS: Three hundred twelve consecutive patients treated with primary PTCA for AMI at nine international centers were prospectively enrolled. After PTCA, stenting was attempted in all eligible lesions (vessel size 3.0 to 4.0 mm; lesion length < or = 2 stents; and the absence of giant thrombus burden after PTCA, major side branch jeopardy or excessive proximal tortuosity or calcification). Patients with stents were treated with aspirin, ticlopidine and a 60-h tapering heparin regimen. RESULTS: Stenting was attempted in 240 (77%) of 312 patients, successfully in 236 (98%), with Thrombolysis in Myocardial Infarction grade 3 flow restored in 230 patients (96%). Patients with stents had low rates of in-hospital death (0.8%), reinfarction (1.7%), recurrent ischemia (3.8%) and predischarge target vessel revascularization for ischemia (1.3%). At 30-day follow-up, no additional deaths or reinfarctions occurred among patients with stents, and target vessel revascularization was required in only one additional patient (0.4%). CONCLUSIONS: Primary stenting is safe and feasible in the majority of patients with AMI and results in excellent short-term outcomes.

Aged↗
PubMed1998

Influence of payor on use of invasive cardiac procedures and patient outcome after myocardial infarction in the United States. Participants in the National Registry of Myocardial Infarction.

OBJECTIVES: We sought to determine the influence of payor status on the use and appropriateness of cardiac procedures. BACKGROUND: The use of invasive procedures affects the cost of cardiovascular care and may be influenced by payor status. METHODS: We compared treatment and outcomes of myocardial infarction among four payor groups: fee for service (FFS), health maintenance organization (HMO), Medicaid and uninsured. Multivariate comparison was performed on the use of invasive cardiac procedures, length of hospital stay and in-hospital mortality in 17,600 patients <65 years old enrolled in the National Registry of Myocardial Infarction from June 1994 to October 1995. To determine the appropriateness of coronary angiography, we compared its use in patients at low and high risk for cardiac events. RESULTS: Angiography was performed in 86% of FFS, 80% of HMO, 61% of Medicaid and 75% of uninsured patients. FFS patients were more likely to undergo angiography than HMO (odds ratio [OR] 1.27, 95% confidence interval [CI] 1.13 to 1.42), Medicaid (OR 2.43, 95% CI 2.11 to 2.81) and uninsured patients (OR 1.99, 95% CI 1.76 to 2.25). Similar patterns for the use of coronary revascularization were found. Among those at low risk, FFS patients were as likely to undergo angiography as HMO patients but more likely than Medicaid and uninsured patients. For those at high risk, FFS patients were more likely to undergo angiography than patients in other payor groups. Adjusted mean length of stay (7.3 days) was similar among all payor groups, but adjusted mortality was higher in the Medicaid group (Medicaid vs. FFS: OR 1.55, 95% CI 1.19 to 2.01). CONCLUSIONS: Payor status is associated with the use and appropriateness of invasive cardiac procedures but not length of hospital stay after myocardial infarction. The higher in-hospital mortality in the Medicaid cohort merits further study.

Adult↗
PubMed1999

A multicenter, randomized study of argatroban versus heparin as adjunct to tissue plasminogen activator (TPA) in acute myocardial infarction: myocardial infarction with novastan and TPA (MINT) study.

OBJECTIVES: This study examined the effect of a small-molecule, direct thrombin inhibitor, argatroban, on reperfusion induced by tissue plasminogen activator (TPA) in patients with acute myocardial infarction (AMI). BACKGROUND: Thrombin plays a crucial role in thrombosis and thrombolysis. In vitro and in vivo studies have shown that argatroban has advantages over heparin for the inhibition of clot-bound thrombin and for the enhancement of thrombolysis with TPA. METHODS: One hundred and twenty-five patients with AMI within 6 h were randomized to heparin, low-dose argatroban or high-dose argatroban in addition to TPA. The primary end point was the rate of thrombolysis in myocardial infarction (TIMI) grade 3 flow at 90 min. RESULTS: TIMI grade 3 flow was achieved in 42.1% of heparin, 56.8% of low-dose argatroban (p = 0.20 vs. heparin) and 58.7% of high-dose argatroban patients (p = 0.13 vs. heparin). In patients presenting after 3 h, TIMI grade 3 flow was significantly more frequent in high-dose argatroban versus heparin patients: 57.1% versus 20.0% (p = 0.03 vs. heparin). Major bleeding was observed in 10.0% of heparin, and in 2.6% and 4.3% of low-dose and high-dose argatroban patients, respectively. The composite of death, recurrent myocardial infarction, cardiogenic shock or congestive heart failure, revascularization and recurrent ischemia at 30 days occurred in 37.5% of heparin, 32.0% of low-dose argatroban and 25.5% of high-dose argatroban patients (p = 0.23). CONCLUSIONS: Argatroban, as compared with heparin, appears to enhance reperfusion with TPA in patients with AMI, particularly in those patients with delayed presentation. The incidences of major bleeding and adverse clinical outcome were lower in the patients receiving argatroban.

Adult↗
PubMed1999

Impaired coronary blood flow in nonculprit arteries in the setting of acute myocardial infarction. The TIMI Study Group. Thrombolysis in myocardial infarction.

OBJECTIVES AND BACKGROUND: While attention has focused on coronary blood flow in the culprit artery in acute myocardia infarction (MI), flow in the nonculprit artery has not been studied widely, in part because it has been assumed to be normal. We hypothesized that slower flow in culprit arteries, larger territories infarcted and hemodynamic perturbations may be associated with slow flow in nonculprit arteries. METHODS: The number of frames for dye to first reach distal landmarks (corrected TIMI [Thrombolysis in Acute Myocardial Infarction] frame count [CTFC]) were counted in 1,817 nonculprit arteries from the TIMI 4, 10A, 10B and 14 thrombolytic trials. RESULTS: Nonculprit artery flow was slowed to 30.9 +/- 15.0 frames at 90 min after thrombolytic administration, which is 45% slower than normal flow in the absence of acute MI (21 +/- 3.1, p < 0.0001). Patients with TIMI grade 3 flow in the culprit artery had faster nonculprit artery CTFCs than those patients with TIMI grades 0, 1 or 2 flow (29.1 +/- 13.7, n = 1,050 vs. 33.3 +/- 16.1, n = 752, p < 0.0001). The nonculprit artery CTFC improved between 60 and 90 min (3.3 +/- 17.9 frames, n = 432, p = 0.0001), and improvements were related to improved culprit artery flow (p = 0.0005). Correlates of slower nonculprit artery flow included a pulsatile flow pattern (i.e., systolic flow reversal) in the nonculprit artery (p < 0.0001) and in the culprit artery (p = 0.01), a left anterior descending artery culprit artery location (p < 0.0001), a decreased systolic blood pressure (p = 0.01), a decreased ventriculographic cardiac output (p = 0.02), a decreased double product (p = 0.0002), a greater percent diameter stenosis of the nonculprit artery (p = 0.01) and a greater percent of the culprit artery bed lying distal to the stenosis (p = 0.04). Adjunctive percutaneous transluminal coronary angioplasty (PTCA) of the culprit artery restored a culprit artery CTFC (30.4 +/- 22.2) that was similar to that in the nonculprit artery at 90 min (30.2 +/- 13.5), but both were slower than normal CTFCs (21 +/- 3.1, p < 0.0005 for both). If flow in the nonculprit artery was abnormal (CTFC > or = 28 frames) then the CTFC after PTCA in the culprit artery was 17% slower (p = 0.01). Patients who died had slower global CTFCs (mean CTFC for the three arteries) than patients who survived (46.8 +/- 21.3, n = 47 vs. 39.4 +/- 16.7, n = 1,055, p = 0.02). CONCLUSIONS: Acute MI slows flow globally, and slower global flow is associated with adverse outcomes. Relief of the culprit artery stenosis by PTCA restored culprit artery flow to that in the nonculprit artery, but both were 45% slower than normal flow.

Adult↗
PubMed2000

Myocardial infarction in diabetic vs non-diabetic subjects. Survival and infarct size following therapy with sulfonylureas (glibenclamide)

AIMS: Sulfonylureas may interfere with 'ischaemic preconditioning' and worsen the prognosis in diabetic patients with acute myocardial infarction. METHODS AND RESULTS: Three hundred and fifty-seven non-diabetic patients admitted with acute myocardial infarction to one hospital over 6.5 years (72 deaths, in-hospital mortality 20.2%) were compared to 245 Type 2 diabetic patients categorized as having taken sulfonylureas (glibenclamide 7+/-3 mg x day(-1); n = 76, 25 deaths = 32.9%;P = 0.025), not having taken sulfonylureas (n = 89, 29 deaths = 33.0%;P = 0.012), and newly diagnosed as having diabetes (n = 80, 20 deaths = 25.0%). Survival was significantly different (log-rank test: P = 0.03). Increments in creatine kinase and creatine kinase(MB)activity were higher in non-diabetic patients (P<0.01). CONCLUSIONS: In-hospital mortality in Type 2 diabetic patients is higher than in non-diabetic patients suffering acute myocardial infarction regardless of whether or not they had been treated with sulfonylureas. Glibenclamide does not enlarge myocardial necroses.

Aged↗
PubMed2000

Effect of 48-h intravenous trimetazidine on short- and long-term outcomes of patients with acute myocardial infarction, with and without thrombolytic therapy; A double-blind, placebo-controlled, randomized trial. The EMIP-FR Group. European Myocardial Infarction Project--Free Radicals.

AIMS: To compare the effect of trimetazidine (TMZ) versus placebo administered during the acute phase of myocardial infarction on long- and short-term mortality. METHODS AND RESULTS: EMIP-FR (European Myocardial Infarction Project - Free Radicals) was a prospective, double-blind, European multicentre trial in which 19 725 patients, presenting symptoms of acute myocardial infarction within the previous 24 h were randomized. Stratification was according to thrombolytic therapy (56%) or not (44%). An intravenous bolus injection of trimetazidine (40 mg) was given just before or simultaneously with thrombolysis, followed by continuous infusion (60 mg. 24 h(-1)) for 48 h. Overall, no difference was found between trimetazidine and placebo for the main end-point, short-term (35-day) mortality, (P = 0.98) in an intention-to-treat analysis. This was the result of opposing trends in the two strata. Thrombolysed patients showed a tendency towards more short-term deaths with trimetazidine, compared to placebo (trimetazidine: 11.3%, placebo: 10.5%, P = 0.15) and non-thrombolysed patients the converse (trimetazidine: 14.0%, placebo: 15.1%, P = 0.14). In a per-protocol analysis the beneficial effect of trimetazidine for non-thrombolysed patients became statistically significant (trimetazidine: 13.3%, placebo: 15.1%, P = 0.027). CONCLUSION: Trimetazidine does not reduce mortality in patients undergoing thrombolytic therapy; however, it might have some beneficial effect for non-thrombolysed patients.

Adult↗
PubMed1993

A comparison of immediate angioplasty with thrombolytic therapy for acute myocardial infarction. The Primary Angioplasty in Myocardial Infarction Study Group.

BACKGROUND: The success of thrombolytic therapy for acute myocardial infarction is limited by bleeding complications, the impossibility of reperfusing all occluded coronary arteries, recurrent myocardial ischemia, and the relatively small number of patients who are appropriate candidates for this therapy. We hypothesized that these problems could be overcome by the use of immediate percutaneous transluminal coronary angioplasty (PTCA), without previous thrombolytic therapy. METHODS: At 12 clinical centers, 395 patients who presented within 12 hours of the onset of myocardial infarction were treated with intravenous heparin and aspirin and then randomly assigned to undergo immediate PTCA (without previous thrombolytic therapy, 195 patients) or to receive intravenous tissue plasminogen activator (t-PA, 200 patients) followed by conservative care. Radionuclide ventriculography was performed to assess ventricular function within 24 hours and at six weeks. RESULTS: Among the patients randomly assigned to PTCA, 90 percent underwent the procedure; the success rate was 97 percent, and no patient required emergency coronary-artery bypass surgery. The in-hospital mortality rates in the t-PA and PTCA groups were 6.5 and 2.6 percent, respectively (P = 0.06). In a post hoc analysis, the mortality rates in the subgroups classified as "not low risk" were 10.4 and 2.0 percent, respectively (P = 0.01). Reinfarction or death in the hospital occurred in 12.0 percent of the patients treated with t-PA and 5.1 percent of those treated with PTCA (P = 0.02). Intracranial bleeding occurred more frequently among patients who received t-PA than among those who underwent PTCA (2.0 vs. 0 percent, P = 0.05). The mean (+/- SD) ejection fractions at rest (53 +/- 13 vs. 53 +/- 13 percent) and during exercise (56 +/- 13 vs. 56 +/- 14 percent) were similar in the t-PA and PTCA groups at six weeks. By six months, reinfarction or death had occurred in 32 patients who received t-PA (16.8 percent) and 16 treated with PTCA (8.5 percent, P = 0.02). CONCLUSIONS: As compared with t-PA therapy for acute myocardial infarction, immediate PTCA reduced the combined occurrence of nonfatal reinfarction or death, was associated with a lower rate of intracranial hemorrhage, and resulted in similar left ventricular systolic function.

Adult↗
PubMed2000

The volume of primary angioplasty procedures and survival after acute myocardial infarction. National Registry of Myocardial Infarction 2 Investigators.

BACKGROUND: There is an inverse relation between mortality from cardiovascular causes and the number of elective cardiac procedures (coronary angioplasty, stenting, or coronary bypass surgery) performed by individual practitioners or hospitals. However, it is not known whether patients with acute myocardial infarction fare better at centers where more patients undergo primary angioplasty or thrombolytic therapy than at centers with lower volumes. METHODS: We analyzed data from the National Registry of Myocardial Infarction to determine the relation between the number of patients receiving reperfusion therapy (primary angioplasty or thrombolytic therapy) and subsequent in-hospital mortality. A total of 450 hospitals were divided into quartiles according to the volume of primary angioplasty. Multiple logistic-regression models were used to determine whether the volume of primary angioplasty procedures was an independent predictor of in-hospital mortality among patients undergoing this procedure. Similar analyses were performed for patients receiving thrombolytic therapy at 516 hospitals. RESULTS: In-hospital mortality was 28 percent lower among patients who underwent primary angioplasty at hospitals with the highest volume than among those who underwent angioplasty at hospitals with the lowest volume (adjusted relative risk, 0.72; 95 percent confidence interval, 0.60 to 0.87; P<0.001). This lower rate, which represented 2.0 fewer deaths per 100 patients treated, was independent of the total volume of patients with myocardial infarction at each hospital, year of admission, and use or nonuse of adjunctive pharmacologic therapies. There was no significant relation between the volume of thrombolytic interventions and in-hospital mortality among patients who received thrombolytic therapy (7.0 percent for patients in the highest-volume hospitals vs. 6.9 percent for those in the lowest-volume hospitals, P=0.36). CONCLUSIONS: Among hospitals in the United States that have full interventional capabilities, a higher volume of angioplasty procedures is associated with a lower mortality rate among patients undergoing primary angioplasty, but there is no association between volume and mortality for thrombolytic therapy.

Angioplasty, Balloon, Coronary↗
PubMed2001

Recent magnitude of and temporal trends (1994-1997) in the incidence and hospital death rates of cardiogenic shock complicating acute myocardial infarction: the second national registry of myocardial infarction.

BACKGROUND: Limited recent data are available to describe the magnitude of, and temporal trends in, the incidence and case-fatality rates associated with cardiogenic shock complicating acute myocardial infarction. The purpose of this study was to examine recent (1994-1997) trends in the incidence of, and hospital death rates from, cardiogenic shock complicating acute myocardial infarction from a large, multihospital national perspective. METHODS: An observational study was performed of 426,253 patients hospitalized with acute myocardial infarction in 1662 hospitals throughout the United States between 1994 and 1997. RESULTS: The incidence rates of cardiogenic shock averaged 6.2%. There was evidence for a slight decline in these rates between 1994 (6.6%) and 1997 (6.0%). Results of a multivariable regression analysis controlling for factors that might affect the risk of development of cardiogenic shock indicated that patients hospitalized in more recent years were at significantly lower risk for shock. Patients with shock had a markedly increased risk for dying during hospitalization compared with patients not having shock (74% vs 10%). Significant, albeit small, absolute differences were observed in the risk of dying after cardiogenic shock over time (76% dying in 1997, 72% dying in 1994). These improving trends were magnified, however, after potentially confounding prognostic factors were controlled: patients having shock in 1997 were at approximately one fifth lower risk of dying (odds ratio 0.79, 95% confidence interval 0.71-0.87) than those hospitalized in 1994. CONCLUSIONS: Our findings indicate a slight decline in the incidence rates of cardiogenic shock and improving trends in the hospital survival of patients with shock. Despite these trends, it remains of considerable importance to prevent this clinical syndrome, given its high lethality.

Aged↗
PubMed2001

Randomized comparison of a novel anticoagulant, vasoflux, and heparin as adjunctive therapy to streptokinase for acute myocardial infarction: results of the VITAL study (Vasoflux International Trial for Acute Myocardial Infarction Lysis).

BACKGROUND: Vasoflux is a low-molecular-weight heparin derivative that inhibits factor IXa activation of factor X and catalyzes fibrin-bound thrombin inactivation by heparin cofactor II. We studied whether vasoflux improves the results of thrombolysis with streptokinase for acute myocardial infarction. METHODS AND RESULTS: We randomized 277 patients with acute myocardial infarction to standard intravenous unfractionated heparin (UFH) or intravenous vasoflux 1, 4, 8, or 16 mg/kg as a bolus followed by 1, 4, 8, or 16 mg/kg per hour infusion, on top of streptokinase and aspirin, until angiography at 90 minutes. Patency and corrected Thrombolysis in Myocardial Infarction (TIMI) frame count were studied at 60 and 90 minutes. Rates of TIMI grade 3 flow with vasoflux at any dose (35% to 42%) were not different from UFH (41%) at either time point, nor was the corrected TIMI frame count. However, there was an excess of bleeding in the patients randomized to vasoflux 8 or 16 mg/kg: 78% and 71%, compared with 53% for UFH (P =.004 and.043, respectively). Major bleeding was observed in 13% and 28% at these vasoflux doses compared with 8% with UFH (P =.558 and.01, respectively). CONCLUSION: At doses that increase the risk of bleeding, the addition of vasoflux to streptokinase and aspirin did not lead to improved patency rates compared with UFH. Targeting factor IXa and heparin cofactor II may not be a useful adjunct to thrombolysis.

Adult↗
PubMed2002

Multicenter, dose-ranging study of efegatran sulfate versus heparin with thrombolysis for acute myocardial infarction: The Promotion of Reperfusion in Myocardial Infarction Evolution (PRIME) trial.

BACKGROUND: Adjunctive therapies that increase the incidence of normal reperfusion after thrombolysis for acute myocardial infarction (MI) could enhance clinical outcomes. Direct thrombin inhibitors may offer an advantage over standard adjunctive therapies. METHODS: We randomized 336 patients with acute MI at 33 sites to receive 1 of 5 doses of efegatran sulfate, a direct thrombin inhibitor, or heparin for 72 to 96 hours, both with accelerated alteplase and aspirin. The primary end point was the incidence of thrombolytic failure (death, reinfarction, or TIMI grade 0-2 flow in the infarct artery from 90 minutes to discharge or 30 days, whichever occurred earlier). RESULTS: Significantly more patients randomized to efegatran had evidence of heart failure at admission. The lowest-dose efegatran arm was terminated at 15 patients because of unacceptably increased thrombolytic failure. The primary end point occurred in 53.0% of patients treated with heparin, in 53.8% of patients treated with efegatran overall (P =.90), and in 55.4% of patients given intermediate-dose efegatran (P =.74). These findings were unaffected after adjustment was done for baseline differences. Most bleeding was minor; major bleeding and the use of blood transfusions did not differ significantly by treatment. Three patients in the high-dose efegatran group had intracranial hemorrhage, as did 1 patient in the heparin group. Continuous ST monitoring showed a shorter time to recovery for the efegatran group (median 107 minutes) compared with the heparin group (154 minutes; P =.025). CONCLUSIONS: Efegatran sulfate appeared to offer no clear advantage over heparin as an adjunct to thrombolysis for acute myocardial infarction, although there may be a modest improvement in time to reperfusion.

Adult↗
PubMed2003

Ergometric score systems after myocardial infarction: prognostic performance of the Duke Treadmill Score, Veterans Administration Medical Center Score, and of a novel score system, GISSI-2 Index, in a cohort of survivors of acute myocardial infarction.

BACKGROUND: The aims of the study were to evaluate the performance of the Duke Treadmill Score (DTS) and the Veteran Affairs Medical Center Score (VAMCS) in predicting 6-month death in GISSI-2 study survivors of acute myocardial infarction treated with thrombolytic agents, and to develop a simple predictive scoring system from the same database. METHODS: Patients of the GISSI-2 study (n = 6251) performed a maximal symptom-limited exercise test 1 month after myocardial infarction. We calculated for each patient the DTS and the VAMCS. Based on the coefficients of a multivariate analysis of our database, we developed a simple predictive scoring system and performed an internal validation. The prognostic value of each scoring system was assessed by multivariate analysis. RESULTS: Six-month mortality rates in the subgroups of each scoring system were as follows: DTS: low risk 0.6%, moderate risk 1.8%, high risk 3.4% (P < or =.0001); VAMCS: low risk 0.6%, moderate risk 1.9%, high risk 4.7% (P < or =.0001); GISSI-2 Index: low risk 0.5%, moderate risk 1.9%, high risk 6.1% (P < or =.0001). The results of multivariate analysis (relative risk [RR] and 95% CI) were as follows: DTS: moderate risk 2.50 (1.47-12.59), high risk 5.13 (3.61-15.55); VAMCS: moderate risk 2.65 (1.53-4.59), high risk 5.97 (3.10-11.49); GISSI-2 Index: moderate risk 3.16 (1.81-5.52), high risk 8.65 (4.36-17.18). CONCLUSIONS: The use of ergometric-derived prognostic score systems in a population of survivors of acute myocardial infarction treated with thrombolytic drugs distinguishes subgroups at different risks of death and allows an appropriate recourse to more costly procedures.

Acute Disease↗
PubMed1997

Endovascular suture occlusion of the middle cerebral artery in rats: effect of suture insertion distance on cerebral blood flow, infarct distribution and infarct volume.

Sprague-Dawley rats anesthetized with isoflurane, underwent MCA occlusion by intraluminal 3-0 suture insertion, either 22 mm (n = 8) or 18 mm (n = 6) beyond the CCA bifurcation or were sham-operated as controls (n = 3) for autoradiographic analysis of cerebral blood flow. Infarct volume was measured 24 hours after the onset of ischemia (22 mm, n = 11; 18 mm, n = 10); neurological examinations were performed at 6 and 24 hours. Cerebral blood flow in the MCA distribution was significantly lower in the 22 mm suture insertion group than in the 18 mm group (p < 0.05). The total infarct volume was significantly larger (197 +/- 15 versus 135 +/- 19 mm3, p < 0.05) and the coefficient of variance was significantly smaller (23.8% versus 43.9%, p < 0.05) in the 22 mm group. Border zone regions of medial caudoputamen and dorsolateral cortex were often spared in the 18 mm group but never in the 22 mm group. The neurological deficit was more severe in the 22 mm group at 24 hours (p < 0.05), but not at 6 hours. The greater blood flow reduction and the less variable histological damage in dorsolateral cortex (a watershed area between the middle and anterior cerebral arteries) and the greater histological damage in medial caudate in the 22 mm group further characterizes this focal ischemia model for two potential applications: 22 mm insertion for studies requiring extensive and reproducible infarcts; 18 mm insertion for studies requiring less severe and more variable lesions after permanent MCA occlusion.

Animals↗
PubMed1979

Estimation of circulatory parameters in patients with acute myocardial infarction. Significance for calculation of enzymatic infarct size.

Estimation of infarct size from enzyme activities in plasma or serum presupposes known values of circulatory parameters such as the extravascular distribution volume Ve and the permeability constant P for the transport of enzyme between intravascular volume Vi and Ve. In man, parameter values are used that are extrapolated either from values found in the dog or from turnover studies of non-myocardial proteins. Large systematic errors can be introduced in this way, as demonstrated in this study. It is shown that by simultaneous determination of two different enzymes in the same patient, estimates of circulatory parameters are obtained. The method is applied to creatine kinase (CK) and alpha-hydroxybutyrate dehydrogenase (HBDH) plasma activities in 36 patients with acute myocardial infarction (AMI). The following results are obtained: 1. Exchange of enzyme between Vi and Ve is much slower and clearance of CK is much faster than presently assumed in the literature. 2. Release of CK and HBDH into the circulation is proportional to the amounts of these enzymes present in the myocardium. This finding is supported by data on early enzyme release. 3. Quantitation of HBDH release needs a two-compartment model, while for CK a one-compartment model can be used in good approximation. 4. Release of CK and HBDH after AMI continues up to 96 hours. 5. Using obtained parameter values, a simulated model demonstrates that estimation of clearance rates of CK from exponential fits on plasma levels results in large errors. This may explain recent conflicting results in validation of enzymatic estimates of infarct size.

Acute Disease↗
PubMed2006

A comparison of pharmacologic therapy with/without timely coronary intervention vs. primary percutaneous intervention early after ST-elevation myocardial infarction: the WEST (Which Early ST-elevation myocardial infarction Therapy) study.

AIMS: Uncertainty exists as to which reperfusion strategy for ST-elevation myocardial infarction (MI) is optimal. We evaluated whether optimal pharmacologic therapy at the earliest point of care, emphasizing pre-hospital randomization and treatment was non-inferior to expeditious primary percutaneous coronary intervention (PCI). METHODS AND RESULTS: Which Early ST-elevation myocardial infarction Therapy (WEST) was a four-city Canadian, open-label, randomized, feasibility study of 304 STEMI patients (> 4 mm ST-elevation/deviation) within 6 h of symptom onset, emphasizing pre-hospital ambulance treatment and participation of community and tertiary care centres. All received aspirin, subcutaneous enoxaparin (1 mg/kg), and were randomized to one of three groups: (A) tenecteplase (TNK) and usual care, (B) TNK and mandatory invasive study < or = 24 h, including rescue PCI for reperfusion failure, and (C) primary PCI with 300 mg loading dose of clopidogrel. Time from symptom onset to treatment was rapid (to TNK for A = 113 and B = 130 min and for PCI in C = 176 min). The primary outcome, a composite of 30-day death, re-infarction, refractory ischaemia, congestive heart failure, cardiogenic shock, and major ventricular arrhythmia, was 25% (Group A), 24% (Group B), and 23% (Group C), respectively. However, there was a higher frequency of the combination of death and recurrent MI in Group A vs. Group C (13.0 vs. 4.0%, respectively, P-logrank = 0.021), yet no difference between Group B (6.7%, P-logrank = 0.378) and C. CONCLUSION: These data suggest that a contemporary pharmacologic regimen rapidly delivered, coupled with a strategy of regimented rescue and routine coronary intervention within 24 h of initial treatment, may not be different from timely expert PCI.

Abciximab↗
PubMed2006

Reduction in infarct size, but no functional improvement after bone marrow cell administration in a porcine model of reperfused myocardial infarction.

AIMS: Stem cell therapy after myocardial infarction (MI) has been studied in models of permanent coronary occlusion. We studied the effect of intracoronary administration of unselected bone marrow (BM) and mononuclear cells (MNC) in a porcine model of reperfused MI. METHODS AND RESULTS: In 34 swine, the left circumflex coronary artery was balloon-occluded for 2 h followed by reperfusion. Ten swine without MI served as controls. All swine underwent magnetic resonance imaging (MRI) 1 week post-MI. The next day, 10 of the 30 surviving MI swine received BM, 10 other MI swine received MNC, and the remaining MI swine received medium intracoronary. Four weeks later, all swine underwent a follow-up MRI. One week after MI, end-diastolic volume (92+/-16 mL) and left ventricular (LV) weight (78+/-12 g) were greater, whereas ejection fraction (40+/-8%) was lower than in controls (69+/-11 mL, 62+/-13 g, and 53+/-6%). Injection of BM or MNC had no effect on the MI-induced changes in global or regional LV-function. However, there was a significant reduction in infarct size 4 weeks after MNC injection (-6+/-3%) compared with the medium (-3+/-5%). CONCLUSION: Intracoronary injection of BM or MNC in swine does not improve regional or global LV-function 4 weeks after injection. However, a reduction in infarct-size was noted after MNC injection.

Animals↗
PubMed2000

Age-dependent increase in infarct volume following photochemically induced cerebral infarction: putative role of astroglia.

This study demonstrates that the photochemically induced model of stroke is an extremely viable method of inducing cerebral infarction in old animals. The lesions are reproducible both in terms of location and size and compatible with long-term survival of the animal. With this model we demonstrated, one week following surgery, a significantly larger infarct in rats 20 and 24 months of age compared to 4-month-old rats. The older rats also sustained greater neurologic deficits as assessed on a rotarod task. Older rats also were characterized by a glial response that was far less intense than in young animals. While the precise relationship between glia activation and cerebral damage remains to be determined, it would appear that a better understanding of those factors that contribute to the astrocytic response in the aged rat may be of particular benefit in designing therapeutic strategies aimed at reducing the pathologic consequences of cerebral infarction in elderly humans.

Aging↗
PubMed1996

Endothelial dysfunction of the non-infarct related, angiographically normal, coronary artery in patients with an acute myocardial infarction.

BACKGROUND: Patients with acute myocardial infarction and single-vessel disease may have early atherosclerosis in other angiographically normal coronary arteries. METHODS: Coronary endothelial responses were analysed in 20 non-diabetic patients with an acute myocardial infarction and one-vessel disease. In an angiographically normal, non-infarct related, coronary artery serial acetylcholine doses of 10(-7) M, 10(-6) M, 10(-5) M and 10(-4) M and nitroglycerin 40 micrograms were infused over 3 min. The responses of the coronary vessel were measured with quantitative angiography. Coronary blood flow was also measured with a Doppler catheter in 11 of the 20 patients. RESULTS: Four patients showed a trend towards vasodilation during acetylcholine infusion in the proximal and distal segments: from 2.49 +/- 0.23 mm to 2.95 +/- 0.42 mm and 2.43 +/- 0.56 mm to 2.81 +/- 0.66 mm, respectively. Coronary vascular resistance decreased to 57 +/- 4% (P = 0.03). The other 16 patients presented vasoconstriction in the proximal and distal segments: 2.61 +/- 0.75 mm to 2.03 +/- 0.65 mm (P = 0.0001), and 2.40 +/- 0.58 to 1.81 +/- 0.56 mm (P = 0.0036), respectively. Nitroglycerin caused vasodilation in the proximal (2.69 +/- 0.61 mm, P = 0.017, ANOVA) and distal segments (2.48 +/- 0.45 mm, P = 0.009, ANOVA). Coronary vascular resistance increased to 141 +/- 43% (P = 0.03) over the basal value in this group of patients. CONCLUSION: Endothelial dysfunction of the epicardial and resistance vessels was found in angiographically normal coronary arteries of patients with one-vessel disease in 75% of this population.

Adult↗