Patency Of Infarct-related Coronary Artery Research Articles

Early unfractionated heparin treatment in patients with STEMI – trial design and rationale

The early unfractionated heparin (UFH) treatment in patients with ST-elevation myocardial infarction (STEMI) is a single-center, open-label, randomized controlled trial. The study population are patients with STEMI that undergo primary percutaneous coronary intervention (PPCI). The trial was designed to investigate whether early administration of unfractionated heparin immediately after diagnosis of STEMI is beneficial in terms of patency of infarct-related coronary artery (IRA) when compared to established UFH administration at the time of coronary intervention. The patients will be randomized in 1:1 fashion in one of the two groups. The primary efficacy endpoint of the study is Thrombolysis in myocardial infarction (TIMI) flow grades 2 and 3 on diagnostic coronary angiography. Secondary outcome measures are: TIMI flow after PPCI, progression to cardiogenic shock, 30-day mortality, ST-segment resolution, highest Troponin I and Troponin I values at 24 hours. The safety outcome is bleeding complications. The study of early heparin administration in patients with STEMI will address whether pretreatment with UFH can increase the rate of spontaneous reperfusion of infarct-related coronary artery.

Sustained endothelial dysfunction in the infarct-related coronary artery is associated with left ventricular adverse remodeling in survivors of ST-segment elevation myocardial infarction

BackgroundIschemia-reperfusion causes endothelial injury and dysfunction in the infarct-related coronary artery (IRA). Using serial assessment of coronary endothelial vasomotor function and left ventriculography (LVG), this study prospectively investigated the clinical impact of endothelial vasomotor dysfunction in the patent IRA on left ventricular (LV) remodeling in survivors of ST-elevation myocardial infarction (STEMI). MethodsThis study included 78 patients with STEMI due to occlusion of the left anterior descending coronary artery (LAD) and successful reperfusion therapy with percutaneous coronary intervention. All of them had LV ejection fraction (LVEF) <55%. LVG and the vasomotor responses to acetylcholine (ACh) in the LAD were examined within 2 weeks (1st test) and 6 months (2nd test) after MI. Cut-off values for coronary vasomotor dysfunction in response to ACh were based on the lower 10% of the distribution of coronary vasomotor responses to ACh in 20 control subjects. ResultsLV adverse remodeling, defined as a >10% increase in either LV end-diastolic volume index (LVEDVI) and/or end-systolic volume index (LVESVI) from the 1st to the 2nd test, occurred in 21 (70%) of 30 patients with sustained impairment of the coronary flow response to ACh at both the 1st and 2nd tests and 14 (29%) of 48 in the other coronary flow response group (p < 0.01). In multivariate logistic regression analysis, a >10% increase in LVEDVI and LVESVI was respectively associated with sustained impairment of the coronary diameter and flow responses to ACh (OR 4.9 and 3.5, 95% CI 1.7–14.1 and 1.1–10.9, p < 0.01 and p = 0.03, respectively), that was independent of hypertension, peak creatine phosphokinase, and the baseline coronary flow response to ACh at the 1st test. ConclusionsSustained endothelial vasomotor dysfunction in the IRA was associated with LV adverse remodeling in STEMI survivors with successful reperfusion therapy.

Evaluation of Infarct-Related Coronary Artery Patency and Microcirculatory Function After Facilitated Percutaneous Primary Coronary Angioplasty: The FINESSE-ANGIO (Facilitated Intervention With Enhanced Reperfusion Speed to Stop Events–Angiographic) Study

The FINESSE-ANGIO (Facilitated Intervention with Enhanced Reperfusion Speed to Stop Events-Angiographic) study evaluated acute treatment effects on infarct-related artery (IRA) patency and angiographic correlates of coronary microcirculatory function. The FINESSE trial evaluated the effects on clinical outcomes of primary percutaneous coronary intervention (PCI) facilitated with pre-catheterization laboratory administration of abciximab with half-dose reteplase (combination-facilitated group), abciximab alone (abciximab-facilitated group), or with abciximab administered immediately before the procedure (primary PCI). The FINESSE-ANGIO substudy compared the effects of the 3 treatment strategies on patency (TIMI [Thrombolysis In Myocardial Infarction] flow grade 2/3) of the IRA at basal coronary angiography. The secondary efficacy end points were corrected TIMI frame count, percentage of patients achieving TIMI flow grade 3, and the percentage achieving myocardial blush grade 2/3 of the IRA at post-PCI angiography. All angiographies were evaluated at a central core laboratory. Of the 2,452 FINESSE patients, 637 were included in the FINESSE-ANGIO substudy. Patients in the combination-facilitated group exhibited significantly higher rates of baseline IRA patency compared with the abciximab-facilitated and the primary PCI groups (76.1% vs. 43.7% and 32.7%, respectively; p < 0.0001 for both; p = 0.025 abciximab-facilitated vs. primary PCI). There were no significant differences in the post-PCI corrected TIMI frame count (17.1 ± 15.8, 17.4 ± 17.3, and 15.8 ± 14.1) or the rates of post-PCI TIMI flow grade 3 (79.8%, 77.7%, and 76.6%), myocardial blush grade 2/3 (85.6%, 79.5%, and 86.4%), respectively. Pre-catheterization laboratory administration of abciximab alone and especially in combination with half-dose reteplase resulted in higher rates of IRA patency at baseline coronary angiography compared with no pre-treatment. However, post-procedural angiographic and microcirculatory variables were unaffected by facilitation therapy.

Transcoronary Infusion of Bone Marrow Derived Multipotent Stem Cells to Preserve Left Ventricular Geometry and Function After Myocardial Infarction

Myocardial damage after myocardial infarction (MI) was deemed irreversible after late reperfusion. Administration of multipotent stem cell (MSC) into such infarct may regenerate the myocardium and capillary network. Transcoronary infusion of bone marrow derived multipotent stem cells into infarcted related artery after acute myocardial infarction is feasible, safe and improve left ventricular function. We conducted a pilot study in patients who survived ST-elevation MI with late reperfusion therapy and remained hemodynamically stable. Bone marrow derived MSC was infused into a patent infarct-related coronary artery during brief low pressure (2 atm) balloon inflation. A 3-T gadolinium-based MRI was performed at baseline and 8 weeks later to evaluate infarct area and LV function. We enrolled 10 patients, age 63.8 +/- 2.8 years 5.2 +/- 4.12 x 10(6) MSC were infused via coronary artery 24.8 +/- 16 days after infarction. The procedures were successful in all patients without any in-hospital event. Infarct size by MRI decreased by 5.84% (P = .018) over 8 weeks. Mean baseline left ventricular ejection fraction (LVEF) was 44.1% +/- 9% and was 46.3% +/- 9% at 8 weeks (P = .34). A trend of smaller LV end-systolic volume with 65.02 +/- 18.2 ml vs 63.04 +/- 21.89 ml (P = .09) with no change of LV end-diastolic volume observed. MSC infusion into coronary circulation was feasible and safe after myocardial infarction. Infarct size was reduced with preservation of LV geometry.

Methylenetetrahydrofolate reductase (MTHFR) C677T genetic polymorphism and late infarct-related coronary artery patency after thrombolysis

In patients with acute myocardial infarction (AMI), a persistently occluded infarct-related artery (IRA) is associated with unfavorable prognosis and genetic factors may be contributing factors to thrombolysis failure. One-hundred and one consecutive patients treated with intravenous thrombolysis during AMI were blind-tested for methylenetetrahydrofolate reductase (MTHFR) and circulating homocysteine levels and underwent protocol angiography 14 +/- 6 days after the event. IRA was patent in 61 patients and occluded in 40. Overall MTHFR 677TT frequency was 22%. Patients with MTHFR 677TT homozygosis had higher prevalence of occluded IRA (73%) versus those with MTHFR 677CT/CC genotype (30%, P < 0.001); MTHFR 677TT genotype predicted independently the risk of IRA occlusion with a specificity of 90% (odds ratio 3.8, 95% confidence interval 1.1-9.1; P = 0.03). Moreover, patients with occluded IRA and MTHFR 677TT genotype had the highest homocysteine levels (21 +/- 7.6 micromol/l vs. < or =14.9 +/- 3.8 micromol/l; P = 0.011). In patients with AMI, MTHFR 677TT homozygosis is independently associated with a persistently occluded IRA after thrombolysis. This finding may have pathophysiological and therapeutic implications for recanalization strategies in patients with AMI.

Infarct-Related Coronary Artery Patency and Medication Use Prior to ST-Segment Elevation Myocardial Infarction

In patients who have ST-segment elevation myocardial infarction (STEMI), a patent infarct-related artery on the initial angiogram is associated with improved clinical outcomes, including decreased mortality. The present study assessed the influence of administering aspirin, beta blockers, statins, and angiotensin-converting enzyme inhibitors before STEMI on infarct-related artery patency. Our data demonstrate that patients who have STEMI and receive these medications on an outpatient basis before the event have a higher likelihood of having a patent infarct-related artery compared with patients who do not receive these medications. Further, our data demonstrate a graded association according to the number of such medications being administered: the likelihood of a patent infarct-related artery increased to >50% as the number of these medications increased.

Correlation between infarct-related coronary artery patency and predischarge electrocardiographic patterns in patients with first anterior myocardial infarction who received thrombolytic therapy.

The aim of this study was to investigate the correlation between the ST-segment and T-wave patterns in predischarge electrocardiogram and patency of left anterior descending coronary artery in patients with a first anterior myocardial infarction (AMI). One hundred and fifty-six of 175 consecutive patients who were admitted to our clinic between January 2000 and September 2002 due to a first episode of transmural AMI and who received thrombolytic therapy were enrolled. Coronary angiography was performed by the Judkins method on the 6th-10th day after the acute infarction. The corrected TIMI frame count (CTFC) was estimated according to the previously described method. According to the combination of the ST-segment and T-wave morphology on the day (6-10) of cardiac catheterization, patients were classified into four groups: group A, ST elevation <<0.1 mV and negative T waves; group B, ST elevation >or=0.1 mV and negative T waves; group C, ST elevation <<0.1 mV and positive T waves; and group D, ST elevation >or=0.1 mV and positive T waves. Of the 99 patients with negative T waves, 47 (48%) had CTFC <or=27, 32 (32%) CTFC between 27 and 40, 15 (15%) CTFC >or=40-100, and 5 (5%) CTFC >>100. Of the 57 patients with positive T waves, CTFC was <or=27 in 14 (25%), between 27 and 40 in 17 (30%), >or=40-100 in 11 (19%), and >>100 in 15 (26%) ( P << 0.001). From the 76 patients with an isoelectric ST segment, 38 (50%) had CTFC <or=27, 29 (38%) CTFC between 27 and 40, 8 (11%) CTFC >or=40-100, and 1 (1%) CTFC >>100. Of the 80 patients with an elevated ST segment, 23 (29%) had CTFC <or=27, 20 (25%) CTFC between 27 and 40, 18 (23%) CTFC >or=40-100, and 19 (23%) CTFC >>100 ( P << 0.001). Use of the combination of two electrocardiographic parameters (ST segment and T waves) also indicated that there were significant differences between groups A and D, and groups B and D ( P << 0.001 and P << 0.05, respectively). Development of an isoelectric ST segment with negative T waves may indicate a better degree of reperfusion after AMI. In contrast, patients in whom ST-segment elevation and positive T waves remain at discharge from the coronary care unit have a higher probability of a nonpatent left anterior descending artery.

Coronary blood flow in evolving myocardial infarction preceded by preinfarction angina: a critical reevaluation of preconditioning effects in clinical cases.

This study was undertaken to reevaluate the protective effects of preinfarction (pre-MI) angina in acute MI. The mechanisms involved in the apparent protective effects of pre-MI angina have been presumed to be preconditioning effects as defined by experimental studies. The phenomenon, has not, however, been observed in diabetic and/or elderly patients or in those treated by primary percutaneous coronary intervention (PCI). A total of 202 patients with anterior wall MI without a history of MI who underwent primary PCI with coronary balloon dilation and stenting (rate: 50%) <6 hours after onset were studied. Patients included 59 with pre-MI angina (group 1) and 143 without pre-MI angina (group 2). The infarct-related coronary artery was patent on admission in 46% of group 1 and 31% of group 2 (p=0.045). Thrombolysis in Myocardial Infarction (TIMI) 1-2 flow was significantly more frequent in group 1 (29%) than in group 2 (11%, p=0.005) on admission. Among risk factors, clinical background, coronary anatomy, and clinical outcome, the only significant predictor of pre-MI angina was a patent infarct-related coronary artery on admission (odds ratio: 2.39, p = 0.015). There was no significant difference in left ventricular ejection fraction, peak creatine kinase, or the incidences of heart failure and in-hospital/follow-up deaths between these groups. In conclusion, the findings suggest that the protective effects reported in MI with pre-MI angina treated by thrombolysis are due to more fragile thrombotic occlusion, which can be more easily recanalized by thrombolysis, whereas the beneficial effects are not evident in those treated by primary PCI.

Inducible ventricular arrhythmias and patency of infarct-related artery in survivors of acute myocardial infarction.

Patency of infarct-related artery in patients who suffered an acute myocardial infarction (AMI) has been shown to be associated with improved survival. Ventricular tachyarrhythmias induced by programmed electrical stimulation may be predictive of arrhythmic events and sudden death. The study was undertaken to assess the possible effect of a patent infarct-related coronary artery on induced ventricular tachyarrhythmias during programmed ventricular stimulation in survivors of AMI. In this prospective study, programmed electrical stimulation was performed before hospital discharge (14 +/- 2 days) in 79 patients who survived an AMI. Patients were subdivided into two groups: Group I with patent infarct-related coronary artery (n = 64) and Group 2 with occluded infarct-related artery (n = 15) at coronary angiography performed at 14 +/- 2 days. These two groups were comparable in terms of mean left ventricular ejection fraction, location of infarct-related artery, number of diseased vessels, peak creatine kinase value, and infarct location. Ventricular arrhythmias were induced in 21 patients ( 32.6%) of Group I and 4 patients (26.6%) of Group 2. This difference was not statistically significant. This study suggests that ventricular arrhythmias induced by programmed ventricular stimulation in survivors of AMI did not differ whether the infarct-related artery was patent or occluded. Other factors may play a role in electrical instability as assessed by programmed ventricular stimulation.

Early Prognostic Assessment and Treatment of Acute Myocardial Infarction in the Elderly.

The progressive aging of the population is associated with an increase in the proportion of very old patients (greater than 75 years) hospitalized with acute myocardial infarction. The lack of evidence regarding the efficacy of most therapeutic interventions for acute myocardial infarction in these patients is leading to a significant degree of uncertainty in the cardiology community with respect to their optimal management. When aggressive treatment (defined as a therapeutic strategy designed to obtain and maintain a patent infarct-related coronary artery at an early moment) of acute myocardial infarction is considered in very old patients, three main questions should be addressed: why should we treat? Whom should we treat? And how should we treat? To answer these questions, the authors reviewed the data available in the literature as well as new data from the PPRIMM75 (Pronóstico del PRimer Infarto de Miocardio en Mayores de 75 aÃ+/-os) Registry, a large, prospective database of patients aged 75 years or older, admitted to a single coronary care unit in Madrid, Spain, for their first acute myocardial infarction during the last decade. (c) 2000 by CVRR, Inc.

Complex stenosis morphology predicts late reocclusion during follow-up after myocardial infarction in patients with patent infarct–related coronary arteries

Background Whether angiographic morphology of infarct-related residual stenoses continues to affect prognosis after discharge is not known. Methods We studied 175 patients after their myocardial infarction who required nonurgent coronary angioplasty for residual myocardial ischemia. The findings at diagnostic coronary angiography were compared with those before angioplasty (mean of 7 months later). Infarct-related stenoses were classified as complex or smooth. Stenosis progression was defined as >0.5 mm diameter reduction. Results One hundred twenty-one (69%) infarct-related stenoses were complex. At restudy, total occlusion was found in 41 (35%) of the infarct-related complex stenoses compared with 7 (13%) smooth stenoses ( P = .001). Reocclusion occurred in 16 (55%) of 29 complex infarct-related stenoses with thrombus, compared with 25 (28%) of 88 without thrombus ( P = .01). During follow-up, 46 patients (26%) had cardiac events. Of these, 70% had complex lesions at study entry compared with 30% smooth ( P < .05). Conclusions Residual angiographically complex stenoses after an uncomplicated myocardial infarction are associated with a greater risk of reocclusion and may predispose to coronary events at follow-up. (Am Heart J 1998;136:877-83.)

Impact of early accelerated dose tissue plasminogen activator on in-hospital patency of the infarcted vessel in patients with acute right ventricular infarction.

OBJECTIVE: To assess the efficacy of early accelerated dose tissue plasminogen activator on in-hospital patency of the infarct related artery in patients with inferior myocardial infarction with and without right...

Gender and Acute Myocardial Infarction: Is There a Different Response to Thrombolysis?

Objectives. This study sought to 1) determine the effect of gender on early and late infarct-related artery patency and reocclusion after thrombolytic therapy for acute myocardial infarction; 2) examine the effect of gender on left ventricular function in response to injury/reperfusion; and 3) assess the independent contribution of gender to early (30-day) mortality after acute myocardial infarction.Background. Women have a higher mortality rate than men after myocardial infarction. However, the effect of gender on infarct-related coronary artery patency and left ventricular response to injury/reperfusion have not been fully defined in the thrombolytic era.Methods. Patency rates and global and regional left ventricular function were determined in patients at 90 min and 5 to 7 days after thrombolytic therapy for acute myocardial infarction. The effect of gender on infarct-related artery patency and left ventricular function was determined. Thirty-day mortality differences between women and men were compared.Results. Women were significantly older and had more hypertension, diabetes, hypercholesterolemia, heart failure and shock. They were less likely to have had a previous myocardial infarction, history of smoking or previous bypass surgery. Ninety-minute patency rates (Thrombolysis in Myocardial Infarction [TIMI] flow grade 3) in women and men were 39% and 38%, respectively (p = 0.5). Reocclusion rates were 8.7% in women versus 5.1% in men (p = 0.14). Women had more recurrent ischemia than men (21.4% vs. 17.0%, respectively, p = 0.01). Ninety-minute ejection fraction and regional ventricular function were clinically similar in women and men with TIMI 2 or 3 flow (ejection fraction [mean ± SD]: 63.4 ± 6% vs. 59.4 ± 0.7%, p = 0.02; number of chords: 21.4 ± 0.9 vs. 21.0 ± 1.9, p = 0.7; SD/chord: −2.4 ± 08 vs. −2.4 ± 0.2, p = 0.9, respectively). No clinically significant differences in left ventricular function were noted at 5- to 7-day follow-up. Women had a greater hyperkinetic response than men in the noninfarct zone (SD/chord: 2.4 ± 0.2 vs. 1.7 ± 0.1, p = 0.005). The 30-day mortality rate was 13.1% in women versus 4.8% in men (p ≤ 0.0001). After adjustment for other clinical and angiographic variables, gender remained an independent determinant of 30-day mortality.Conclusions. Women do not differ significantly from men with regard to either early infarct-related artery patency rates or reocclusion after thrombolytic therapy or ventricular functional response to injury/reperfusion. Gender was an independent determinant of 30-day mortality after acute myocardial infarction.(J Am Coll Cardiol 1997;29:35–42)>

Patency of infarct-related coronary artery.

HomeCirculationVol. 90, No. 3Patency of infarct-related coronary artery. Free AccessAbstractPDF/EPUBAboutView PDFSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessAbstractPDF/EPUBPatency of infarct-related coronary artery. J E Madias J E MadiasJ E Madias Search for more papers by this author Originally published21 Mar 2018https://doi.org/10.1161/circ.90.3.8087968Circulation. 1994;90:1578"Patency of infarct-related coronary artery.." Circulation, 90(3), p. 1578 Previous Back to top Next FiguresReferencesRelatedDetails September 1, 1994Vol 90, Issue 3 Advertisement Article InformationMetrics Copyright © 1994 by American Heart Associationhttps://doi.org/10.1161/circ.90.3.8087968PMID: 8087968 Originally publishedMarch 21, 2018 PDF download Advertisement

Factors influencing changes in the signal-averaged electrocardiogram within the first year after a first myocardial infarction

One hundred twenty-nine patients were prospectively studied after a first myocardial infarction. A first signal-averaged electrocardiogram (SAECG-1) was performed in the acute phase (within 48 hours after onset of symptoms) and a second one (SAECG-2) in the late phase (6 to 18 months after hospital discharge). We studied the influence of nine parameters on the evolution of the signal-averaged electrocardiogram: age, gender, myocardial infarction location, number of diseased coronary vessels, infarct-related coronary artery patency, use of thrombolytic therapy or percutaneous transluminal coronary angioplasty in the acute phase, left ventricular ejection fraction, and recurrence of ischemic events. No follow-up data were available in 15 patients. Of the remaining 114 patients, an ischemic event occurred in 25 (22%). The signal-averaged electrocardiogram remained unchanged in 97 (85%) (remaining normal in 78 and abnormal in 19). It became abnormal in 13 (11.5%) and became normal in 4 (3.5%). In patients with a normal SAECG-1, two factors were associated with the change to an abnormal SAECG-2: (1) an ischemic event occurred in 11 (85%) of 13 patients whose SAECG-2 was abnormal compared with only 13 (17%) of 78 patients whose SAECG-2 remained normal (p < 0.0001), and (2) 100% of patients with an abnormal SAECG-2 had an inferior myocardial infarction compared with 54% of patients with a normal SAECG-2 (p = 0.004). In conclusion, our findings suggest that in the setting of myocardial infarction, changes from an early (<48 hours) normal to a late (>6 months) abnormal signal-averaged electrocardiogram is highly indicative of recurrences of ischemic events and an inferior location of the myocardial infarction.

Reverse redistribution: fact or fiction?

It has been well documented that it is not uncommon for a thallium-201 perfusion defect to develop or become more evident on delayed exercise thallium scintigraphic imaging, as compared with the initial image immediately following stress. The pathophysiology and clinical significance of the phenomenon are currently unclear. Literature on this subject is reviewed, and it is concluded that reverse redistribution of 201Tl in the post-myocardial infarction patient is indeed a "fact". In this context it represents a low-risk condition and may imply successful thrombolysis, patent infarct-related coronary artery, improved wall motion at the infarct site and retained myocardial viability in that segment.

Efficacy of 100 mg of double-bolus alteplase in achieving complete perfusion in the treatment of acute myocardial infarction

Objectives. The purpose of this study was to assess the efficacy of 150 mg of aspirin plus 100 mg of alteplase, administered as two intravenous bolus injections of 50 mg each given 30 min apart, and followed by intravenous heparin, on infarct-related coronary artery patency (Thrombolysis in Myocardial Infarction [TIMI] flow grade 3).Background. previous workers have shown in animals that reducing the duration of an infusion of recombinant tissue-type plasminogen activator increases the initial rate of thrombolysis, resulting in high early infarct-related coronary artery patenecy rates. The logical progression of this idea is bolus administration.Methods, Consecutive patients presenting up to 6 h from the onset of symptoms were recruited for the study. Angiography was performed at 60 and 90 min after the first bolus and between 19 to 48 h after study entry. Patients were followed up for 1 month.Results. At 60 min, angiography revealed infarct-related coronary artery patency of TIMI flow grade 3 in 55 (86%) of 64 patients (95% confidence interval [CI] 75% to 93%) and TIMI flow grade 2 or 3 in 58 (91%) of 64 patients (95% CI 81% to 97%). At 90 min, infarct-related artery patency of TIMI flow grade 3 was achieved in 74 (88%) of 84 patients (95% CI 79% to 94%) and TIMI flow grade 2 or 3 in 78 (93%) of 84 patients (95% CI 85% to 97%). Two patients (2.4%) had early angiographic reocclusion whereas 10 (11.9%) had late reinfarction. Bleeding episodes were mostly minor, and there was no cerebrovascular bleeding. Five patients (6.0%) died within 1 month of the acute myocardial infarction.Conclusions. In 84 patients with acute myocardial infarction, administration of 100 mg of double-bolus (2 × 50 mg) alteplase, aspirin and heparin is associated with remarkably high early infarct-related coronary artery patency rates (TIMI flow grade 3) of 86% and 88%, respectively, at 60 and 90 min.

Influence of infarct-related artery patency on the indexes of parasympathetic activity and prevalence of late potentials in survivors of acute myocardial infarction

Objectives. The purpose of this study was to determine whether infarct-related coronary artery patency influence myocardial electrical stability as measured by the prevalence of late potentials or heart rate variability.Background. Several studies have suggested that loss of vagal activity is associated with an increased incidence of arrhythmic death after myocardial infarction.Methods. A short-duration, high resolution electrocardiogram (ECG) was performed before hospital discharge in 175 patients with a first myocardial infarction. Seventy-three patients received thrombolytic therapy. All patients underwent coronary angiography. Coronary occlusion was defined as minimal or no anterograde flow. Eighty-eight patients (50.3%) had an occluded infarct-related artery. Sixty-two healthy subjects served as control subjects to determine the normal range of heart rate variability.Results. Comparison between the control group and patients without patency of the infarct-related artery in the time domain and spectral analyses revealed in the latter patients a reduced heart rate variability (p < 0.0001) and a lower power spectrum density in both the 0.05- to 0.15-Hz band (p < 0.0001) and the 0.15- to 0.35-Hz band (p < 0.0001). The heart rate variability in patient with late potentials was lower than in those with a normal signal-averaged ECG. Those patients with spontaneous or thrombolysis-induced reperfusion have less occurrence of late potentials and higher parasympathetic activity than do patients with a closed artery.Conclusions. This study suggests that the patency of the infarct-related artery determines both the absence of late potentials and the preservation of vagal tone and may explain the reduction in mortality induced by thrombolytic therapy in myocardial infarction.

Impact of tissue plasminogen activator and heparin versus heparin alone on quantitative coronary angiographic findings in myocardial infarction

The influence of tissue plasminogen activator (tPA) and heparin versus heparin alone on anatomic characteristics of patent infarct-related coronary arteries and the development of these angiographic descriptors in coronary arteries that remain patent during the hospital course was examined in 108 patients who participated in a placebo-controlled trial of recombinant tissue-type plasminogen activator in acute myocardial infarc tion. Coronary angiography was performed 18 ± 6 hours after treatment in 47 patients (group A) and at 10 days in 61 patients (group B). Quantitative coronary angiography of the infarct-related lesion was performed, and luminal irregularity was quantitated with an ulceration index. Of the 47 patients in group A, 7 (29%) treated with placebo had Thrombolysis in Myocardial Infarction grade 2 or 3 perfusion, whereas 18 (78%) treated with t-PA had grade 2 or 3 (p <0.001); there was no difference between patients who had grade 2 or 3 perfusion in group B (placebo 59% vs t-PA 75%). In group A, at 10 days, the luminal area of the infarct artery had increased from 0.59 ± 0.11 to 0.9 ± 0.24 mm 2 and from 0.75 ± 0.16 to 1.31 ± 0.39 mm 2 for placebo- and t-PA-treated patients, respectively (p <0.04). There was no change in the ulcerative index over time in either placebo- or t-PA-treated patients. It is concluded that early after infarction, t-PA produces marked and rapid improvement in overall patency as compared with heparin, although this difference was attenuated at 10 days because of spontaneous recanalization in the placebo group. Future studies of thrombolytic agents should consider the substantial improvement in luminal area of patients receiving heparin alone.

Non-invasive diagnosis of arterial patency after thrombolytic treatment and its relation to prognosis.

To validate a simple noninvasive method with serial creatine kinase measurements for diagnosis of early patency of the infarct related artery after thrombolytic treatment with streptokinase. To investigate the relation between early patency of the infarct related artery and prognosis. Patients under 76 years of age and seen within six hours of the start of prolonged chest pain and ST segment elevation were treated with streptokinase (1.5 x 10(6) U) intravenously over 30-60 minutes. Blood for measurement of total creatine kinase activity was taken at baseline and at 1, 2, 3, 4, 8, 12, 16, 20, and 24 hours after starting treatment. The rise in enzyme activity at each time from baseline was expressed as a proportion of the total rise from baseline to peak. Patients studied were in the following groups: (a) Sixty patients took part in a validation study with angiographic determination of patency of the infarct related coronary artery at 2.6 (0.3) hours (mean (SD)) after starting streptokinase. (b) A further 258 patients did not have early arteriography, but data were added to those from the 60 validation patients to find the relation between enzymatically determined early patency of the infarct related artery and 30 day mortality. (c) A further subset of 232 patients with first infarctions (including patients from groups (a) and (b) had angiocardiography at three weeks after infarction, and data were used to investigate the relation between early patency of the infarct related artery and left ventricular function. Normalised rate of rise of creatine kinase activity at three hours after starting streptokinase in relation to angiographic patency of the infarct related coronary artery at 2.5 hours; 30 day cardiac mortality; and left ventricular function at three weeks in survivors of first infarction. In the validation study, a rise in three hour creatine kinase activity of > 20% of peak occurred in 34/37 patients with initially patent infarct related coronary arteries (sensitivity 92%), and a rise to < 20% of peak occurred in 21/23 patients with initially occluded arteries (specificity 91%). In the prognostic study, 30 day mortality was 2.1% in the 191 patients with three hour creatine kinase > 20% of peak and 8.7% in the 127 patients with three hour creatine kinase < 20% of peak (p < 0.01). Angiocardiography in three week survivors of anterior infarction (n = 95) showed better left ventricular function when three hour creatine kinase was > or = 20% than when it was < 20% of peak (mean (SEM) end systolic volume 71 (5) v 96 (9) ml, p < 0.02; ejection fraction 56% (2%) v 51% (2%), NS). Non-invasive determination of early patency of the infarct related artery by the normalised rate of rise of creatine kinase activity at three hours seems to be reliable, and may be prognostically important and of value for use in clinical trials.