Smoking: back to the future - again?
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Adult↗
Biomedical subjects
J K French
Publications and source records attributed to J K French.
Four-year survival of patients with acute coronary syndromes without ST-segment elevation and prognostic significance of 0.5-mm ST-segment depression.
We prospectively evaluated all patients admitted to our coronary care unit during 1993 with ischemic chest pain but without ST-segment elevation on the presenting electrocardiogram, and determined the influence of the extent of ST-segment depression, measured using calipers and blinded to the outcome, on 4-year survival. The presenting symptoms of 367 patients (mean age 64 years) were coded according to the Braunwald classification, 86% being in class IIIB (primary unstable angina with rest angina within 48 hours) and 7.4% in class IIIC (postinfarction angina). Thirty-two patients (8.6%) had myocardial infarction at presentation (defined as a creatine kinase level exceeding twice the reference range within 18 hours). During hospitalization 97% of patients received aspirin, 67% received intravenous heparin, 37% underwent angiography, and 35% underwent revascularization. The vital status of 99% of the patients was determined after a median of 52 months (interquartile range 48 to 55). At follow-up, 88% of patients were taking aspirin, 45% were taking beta blockers, and 50% had undergone revascularization. The survival rate was 70% in patients with > or = 0.5-mm ST-segment depression (53%, 77%, and 82% survival for > or = 2-, 1-, and 0.5-mm ST-segment depression, respectively; p <0.0001). Patients with a normal electrocardiogram had a greater survival rate (94%) than that of patients with 0.5-mm ST-segment depression (82%, p = 0.020), but not significantly different from that of patients with T-wave inversion (84%, p = NS). Independent predictors of mortality (odds ratio [95% confidence interval]) were: age in yearly increments (1.05 [1.03 to 1.06], p = 0.003), revascularization during follow-up (0.40 [0.29 to 0.56], p = 0.006), pulmonary edema (3.45 [2.19 to 5.45], p = 0.007), and ST-segment depression (1.37 [1.20 to 1.55], p = 0.015). Thus, ST-segment depression of > or = 0.5 mm predicts 4-year survival in patients with acute ischemic syndromes.
Adrenergic beta-Antagonists↗
Usefulness of the presenting electrocardiogram in predicting successful reperfusion with streptokinase in acute myocardial infarction.
The presenting electrocardiogram may contain information indicating the probability of successful reperfusion. The relation between 3 parameters in the presenting electrocardiogram (pathologic Q waves, T-wave inversion, and the slope of ST elevation) and Thrombolysis in Myocardial Infarction trial (TIMI) grade 3 flow in the infarct-related artery was assessed angiographically 90 minutes after beginning streptokinase in 362 patients. TIMI grade 3 flow was more common in patients without Q waves (55%) than in those with Q waves (35%; p <0.001), and more common in patients without T-wave inversion (50%) than in those with T-wave inversion (30%; p <0.002). There was no relation between the slope of the ST segment or the magnitude of its deviation and the achievement of TIMI grade 3 flow. Only 20% of the 59 patients with both Q waves and T-wave inversion had TIMI grade 3 flow, compared with 50% of the remaining patients (p <0.0001). Among patients treated within 3 hours, TIMI grade 3 flow was seen in 68% of those without versus 44% of those with Q waves (p <0.01), and in 62% of those without versus 43% of those with T-wave inversion (p = 0.06). Among patients treated after 3 hours, TIMI grade 3 flow was seen in 38% of those without versus 30% of those with Q waves (p = NS), and in 38% of those without versus 23% of those with T-wave inversion (p <0.05). On multivariate analysis, the absence of Q waves, the time from the onset of chest pain to treatment, and age were independent predictors of TIMI grade 3 flow. Pathologic Q waves in the presenting electrocardiogram provide valuable information as to the probability of achieving successful reperfusion following administration of streptokinase, and may be helpful for triage of patients to alternative reperfusion strategies, including percutaneous revascularization.
Anticoagulants↗
Direct thrombin inhibitors as adjuncts to thrombolytic therapy.
Thrombolytic therapy aims to achieve rapid and sustained infarct-related artery patency, although this results in a procoagulant state. Heparin has limitations as an antithrombin agent, which has led to clinical investigation of alternative agents. Direct thrombin inhibitors, as adjuncts to thrombolytic therapy, have been shown to increase 90 minute Thrombolysis in Myocardial Infarction (TIMI)-3 flow rates and reduce reinfarction, when compared with heparin. These results have been achieved with an acceptable risk of bleeding, when administered in appropriate dosing regimens. When the direct thrombin inhibitor hirudin was administered at a mean of 34 and 50 minutes after thrombolytic therapy in large clinical trials, there was no reduction in mortality. In contrast, in several angiographic studies, direct thrombin inhibitors were administered prior to thrombolysis. The effect on mortality of the administration of hirulog prior to streptokinase is currently being examined.
Antithrombins↗
Effects of early captopril administration after thrombolysis on regional wall motion in relation to infarct artery blood flow.
OBJECTIVES: To determine whether early administration of captopril lessens infarct zone regional wall motion abnormalities when infarct artery blood flow is abnormal. BACKGROUND: The interaction between angiotensin-converting enzyme (ACE) inhibitor therapy, ventricular function and infarct artery blood flow has not been well described. METHODS: A total of 493 patients aged < or = 75 years with first infarctions, presenting within 4 h of symptom onset, were randomized to receive 6.25 mg captopril, increasing to 50 mg t.d.s. or a matching placebo 2.1+/-0.4 h after commencing intravenous streptokinase (1.5 x 10(6) U over 30 to 60 min). Trial therapy was stopped 48 h prior to angiography at 3 weeks, to determine regional wall motion and infarct artery flow. RESULTS: There were no differences in ejection fractions or end-systolic volumes between patients randomized to receive captopril and those randomized to receive a placebo. Among patients with anterior infarction (n = 216), randomization to captopril resulted in fewer hypokinetic chords (40+/-13; vs. 44+/-13; p=0.028) and a trend toward fewer chords >2 SD below normal (26+/-17 vs. 30+/-17; p=0.052) in the infarct zone. In patients randomized to receive captopril who had anterior infarction and Thrombolysis in Myocardial Infarction (TIMI) 0-2, flow there were fewer hypokinetic chords (44+/-12 vs. 50+/-9; p=0.043) and a trend toward fewer chords >2 SD below normal (33+/-15 vs. 39+/-13; p=0.057). Patients receiving captopril who had anterior infarction and corrected TIMI frame counts > 27 had fewer hypokinetic chords (42+/-13 vs. 46+/-12; p=0.015) and fewer chords >2 SD below normal (27+/-17 vs. 32+/-17; p= 0.047). Captopril had no effect in patients with inferior infarction. There were 20 late cardiac deaths (median follow-up 4 years) in the captopril group and 35 in the placebo group (p=0.036). CONCLUSIONS: Randomization to receive captopril 2 h after streptokinase improved regional wall motion at 3 weeks. The greatest benefit was seen in patients with anterior infarction particularly when infarct artery blood flow is reduced.
Adult↗
Survival 12 years after randomization to streptokinase: the influence of thrombolysis in myocardial infarction flow at three to four weeks.
OBJECTIVES: The purpose of this study was to determine whether the mortality benefit of intravenous streptokinase administered within 4 h of the onset of acute myocardial infarction is maintained at 12 years, and whether Thrombolysis in Myocardial Infarction (TIMI) flow grades independently influence late survival. BACKGROUND: Treatment with reperfusion therapies and achievement of TIMI 3 flow are associated with increased short- and medium-term survival after infarction. Whether infarct artery flow independently influences survival more than five years after infarction is unknown. METHODS: The late survival of patients randomized to receive either streptokinase (1,500,000 IU over 30 to 60 min) or a matching placebo within 4 h of symptom onset in 1984-1986 was determined. Angiography was performed in surviving patients at three to four weeks, and TIMI flow grades were assessed blind to randomization and outcomes. The late vital status was determined in 99% of patients. RESULTS: Patients randomized to receive streptokinase (n = 107) had improved survival compared with those randomized to placebo (n = 112) at five years (84% vs. 70%; p = 0.023) and 12 years (66% vs. 51%; p = 0.022). At five years 94% of patients with TIMI grade 3 flow, 81% of those with TIMI grade 2 flow and 72% of those with TIMI grade 0-1 flow survived (p = 0.005). At 12 years 72% of patients with TIMI 3, 67% of those with TIMI 2 and 54% of those with TIMI 0-1 flow survived (p = 0.023). Multivariate analysis identified the ejection fraction (p = 0.014), exercise duration (p = 0.013) and TIMI 3 flow (p = 0.04 compared with TIMI 0-2 flow) as important factors for five-year survival. At 12 years multivariate predictors of late survival were the ejection fraction (p = 0.006), exercise duration (p = 0.003) and myocardial score (p = 0.013). The end-systolic volume index was similar to the ejection fraction as a predictor of survival at five and 12 years. CONCLUSIONS: The survival benefits of streptokinase persist for 12 years after infarction. TIMI flow at three to four weeks is an independent predictor of five-year survival.
Actuarial Analysis↗
Antithrombin agents as adjuncts to thrombolytic therapy.
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Adjuvants, Pharmaceutic↗
Waiting times and prioritization for coronary artery bypass surgery in New Zealand.
OBJECTIVES: To review the New Zealand coronary artery bypass priority score instituted in May 1996, and specifically to determine whether it prioritizes patients at high risk of cardiac events while waiting. The New Zealand score is compared with the Ontario urgency rating score, and waiting times for surgery are compared with the maximum times recommended by the Ontario consensus panel. DESIGN: Retrospective review of patients accepted for isolated coronary artery bypass surgery between 1 January 1993 and 31 January 1996. SETTING: Green Lane Hospital, Auckland, New Zealand. MAIN OUTCOME MEASURES: Waiting time, cardiac death, myocardial infarction, and cardiac readmission. RESULTS: The median waiting times were five days for hospital cases (n = 721) and 146 days for out of hospital cases (n = 701). Of the latter group, 28% waited more than a year, 33% had their surgery expedited because of worsening symptoms, and 19% failed to meet the cut off point set by the New Zealand score for acceptance onto the list. Twenty two patients died, 18 on the outpatient waiting list (waiting list mortality 2.6%, risk 0.28% per month of waiting), and 132 were readmitted, 12% with myocardial infarction and 76% with unstable angina. Risk factors for a composite end point of death or myocardial infarction and/or cardiac readmission were: previous coronary artery bypass surgery (p = 0. 001), class III or IV angina (p = 0.002), and hypertension (p = 0. 005). The New Zealand score did not identify those at risk. Excluding hospital cases, 32% had surgery within the time recommended by the Ontario consensus panel. CONCLUSIONS: Waiting times for coronary artery bypass surgery in New Zealand are considerably longer than those in Ontario, Canada. By using a numerical cut off point, implementation of the New Zealand priority scoring system has restricted access to coronary surgery on the basis of funding constraints rather than clinical appropriateness. The score does not add greatly to the clinicians' prioritization in predicting those patients who will suffer events while waiting.
Adult↗
Angiographic frame counts 90 minutes after streptokinase predict left ventricular function at 48 hours following myocardial infarction.
OBJECTIVE: To assess whether the 90 minute corrected thrombolysis in myocardial infarction frame count (CTFC) in the infarct related artery predicts left ventricular function at 48 hours in patients with myocardial infarction treated with aspirin, streptokinase, and either heparin or Hirulog. DESIGN AND SETTING: Analysis of 251 patients with acute myocardial infarction enrolled in the international, multicentre Hirulog early reperfusion/occlusion (HERO-1) trial, who underwent both 90 minute coronary angiography and 48 hour left ventriculography. MAIN OUTCOME VARIABLES: The CTFC was determined in the infarct related artery 90 minutes after starting intravenous streptokinase (1.5 x 106 U over 30 to 60 minutes), and compared with indices of left ventricular function assessed by contrast ventriculography at 48 hours. RESULTS: A CTFC of </= 27 frames (previously reported mean + 2 SD in coronary arteries of patients without acute infarction) occurred in 29% of infarct related arteries, and was associated with a lower infarct zone mean chord score (-2.06 v -2.54, p = 0.01), a lower fraction of chords > 2 SD below normal (37% v 51%, p = 0.005), and trends towards higher left ventricular ejection fractions (60.9% v 58.2%, p = 0.11) and lower end systolic volumes (50.1 ml v 55.9 ml, p = 0.23). A CTFC of </= 40 at 90 minutes occurred in 50% of infarct related arteries, and was associated with a significantly lower mean chord score (-2.20 v -2.60, p = 0.02), a smaller fraction of chords > 2 SD below normal (41% v 52%, p = 0.025), a smaller end systolic volume (49.1 ml v 59.3 ml, p = 0.02), and a higher left ventricular ejection fraction (60.4% v 56.5%, p = 0.03). CONCLUSIONS: The 90 minute CTFC predicts left ventricular function at 48 hours following streptokinase. The CTFC associated with better ventricular function may be higher than values determined from a non-infarct population.
Coronary Angiography↗
Inadequate control of lipid levels in patients with a previous myocardial infarction.
AIM: To access the current lipid management of late survivors of acute myocardial infarction. METHODS: A systematic follow-up of all survivors who had previously been screened for enrolment into one of three randomised clinical trials in Auckland was undertaken from December 1995 to January 1997. All contacted survivors were asked to answer a questionnaire regarding their current therapy and were invited to undergo venepuncture for a lipid assay. RESULTS: Of the 1036 patients with acute myocardial infarction screened for enrolment in the three trials there were 984 (95%) who survived 30 days. At a median of 5.5 years (interquartile range 3.2-8.5) follow-up, 641 (86%) survivors agreed to have a fasting lipid test. The mean total cholesterol level was 5.7 +/- 1.1 mmol/L high density lipoprotein cholesterol 1.1 +/- 0.3 mmol/L, low density lipoprotein cholesterol 3.8 +/- 0.9 mmol/L and triglyceride level 1.9 +/- 1.1 mmol/L. Two hundred and seven (32%) patients were treated with a lipid-modifying agent. Four hundred and forty-five (69%) patients had a cholesterol level > or = 5.2 mmol/L 381 (59%) patients had a level > or = 5.5 mmol/L and 72 (11%) patients had a level > or = 7.0 mmol/L of whom 62 patients were not being treated with a lipid-modifying agent. For the 107 patients with coronary artery bypass grafts, the mean cholesterol level was 5.4 mmol/L and the mean low density lipoprotein cholesterol level was 3.7 +/- 0.9 mmol/L, with 57 (53%) patients not being treated with a "statin" or "fibrate". CONCLUSION: Lipid management is suboptimal in this high risk population of patients post-infarction and greater efforts need to be made to achieve better control. Diet is frequently inadequate in these patients at high risk and statin therapy is indicated.
Aged↗
Results of percutaneous coronary angioplasty in patients <40 years of age.
This study examined factors influencing the outcome of percutaneous transluminal coronary angioplasty (PTCA) in patients <40 years of age. We followed 86 patients (mean age 37 years) treated from 1982 to 1994. The primary procedural success was 90%. At follow-up of 83 patients (97%) at a mean of 48 +/- 33 months (range 5 to 147), there had been 3 late deaths. Actuarial survival at 5 and 10 years was 95% and 91%, respectively. At review only 5% of patients had class III angina and no patient had class IV angina. Repeat revascularization (PTCA alone in 21 [25%], surgery in 8 [10%], or both in 10 [12%] patients) was performed for restenosis in 29 patients (35%) and for disease progression at other sites in 10 patients (12%). On multivariate analysis, a history of diabetes mellitus (p <0.02) was the only factor associated with death or a subsequent cardiovascular event (myocardial infarction, stroke, or hospital admission with unstable angina). At follow-up, 20 patients (24%) still smoked, 64 (77%) had a total cholesterol level > or = 200 mg/dl, 20 (24%) had a body mass index > or = 30, and 15 (18%) were not taking aspirin. In conclusion, PTCA in adults <40 years of age has excellent early results with a low morbidity and mortality. The medium-term prognosis and control of symptoms was good, although by 5 years, further revascularization was required in almost half of the patients.
Adult↗
Abnormal coronary flow in infarct arteries 1 year after myocardial infarction is predicted at 4 weeks by corrected Thrombolysis in Myocardial Infarction (TIMI) frame count and stenosis severity.
Because 24% to 30% of patent infarct-related arteries occlude in the year following thrombolytic therapy for acute myocardial infarction, angiographic factors including corrected Thrombolysis in Myocardial Infarction (TIMI) frame count which may predict abnormal infarct-artery flow, require definition. We examined changes in coronary flow and infarct-artery lesion severity by computerized quantitative angiography over 1 year in 154 patients with a patent infarct-related artery 4 weeks after myocardial infarction. These patients were randomized to receive either ongoing daily therapy of 50 mg aspirin and 400 mg dipyridamole, or placebo. All angiograms were interpreted blind in our core angiographic laboratory. Infarct-artery flow, assessed by corrected TIMI frame counts, was normal (< or = 27) in 46% and 45% of patients at 4 weeks and 1 year, respectively. At 4 weeks, patients with corrected TIMI frame counts < or = 27 had higher ejection fractions (60+/-11% vs 56+/-12%; p = 0.04) than those with corrected TIMI frame counts >27. On multivariate analysis, corrected TIMI frame count and stenosis severity were predictive of late abnormal infarct-artery flow (TIMI 0 to 2 flow, both p <0.01). Only stenosis severity at 4 weeks predicted reocclusion at 1 year (p <0.0001). Aspirin and dipyridamole had no effect on flow or reocclusion. Thus, corrected TIMI frame count and stenosis severity at 4 weeks was highly correlated with infarct-artery flow at 1 year.
Aged↗
Early noninvasive identification of failed reperfusion after intravenous thrombolytic therapy in acute myocardial infarction.
OBJECTIVES: This study sought to evaluate a biochemical approach to the early noninvasive assessment of reperfusion. BACKGROUND: In patients with an acute myocardial infarction, a rapid noninvasive method of detecting failure of intravenous thrombolytic therapy to restore early Thrombolysis in Myocardial Infarction (TIMI) grade 3 flow in the infarct-related artery (IRA) is needed. METHODS: Serial blood samples were collected to assay creatine kinase-MB fraction (CKMB mass), cardiac troponin T and myoglobin concentrations in 105 patients with a myocardial infarction who underwent early angiography after intravenous streptokinase. The ratios of the 60- and 90-min concentrations to prethrombolytic values were used to determine an index that could identify failure to achieve TIMI grade 3 flow in the IRA at 90 min. RESULTS: Significant increases in serum concentrations of markers at 60 min were more likely with TIMI grade 3 flow (59 patients) than with TIMI grade 0 to 2 flow (46 patients). Ratios < or = 5 at 60 min after thrombolysis detected failure to achieve 90-min TIMI grade 3 flow with 92% to 97% sensitivity, 43% to 60% specificity and 63% to 76% positive and 86% to 94% negative predictive values. Ratios < or = 10 at 90 min showed 88% to 95% sensitivity, 49% to 65% specificity and 61% to 69% positive and 86% to 94% negative predictive values for TIMI flow grade < 3. The overall predictive values were thus similar for all three markers. CONCLUSIONS: In acute myocardial infarction treated with intravenous streptokinase, a simple measurement of increased serum concentrations of CKMB mass, cardiac troponin T or myoglobin at 60 and 90 min can accurately predict failure to achieve TIMI grade 3 flow in the IRA at 90 min.
Aged↗
Thrombolytic eligibility.
The Fibrinolytic Therapy Trialists' Collaborative Group has demonstrated that patients without clear contraindications who present with ischaemic chest pain within 12 hours of the onset of symptoms and who have ST segment elevation or bundle branch block on their electrocardiogram (ECG), will benefit from thrombolytic therapy. Therefore the treatment of patients presenting with ischaemic chest pain is guided by the initial ECG. This paper addresses the question of thrombolytic eligibility in several subsets of patients who may benefit from treatment. It also explores the data which confirm the benefit for patients presenting with an inferior myocardial infarction and for those presenting from six-12 hours after the onset of symptoms. In conclusion, thrombolytic therapy should not be routinely withheld from diabetic or elderly patients, menstruating women and patients who have had cardiopulmonary resuscitation.
Age Factors↗
Hirudin (desirudin) and Hirulog (bivalirudin) in acute ischaemic syndromes and the rationale for the Hirulog/Early Reperfusion Occlusion (HERO-2) Study.
Unlike unfractionated heparin, direct thrombin inhibitors such as hirudin and Hirulog inhibit clot-bound as well as fluid-phase thrombin, escape neutralisation by platelet secretion products, do not require monitoring, and are unassociated with immune thrombocytopenia. They have been shown to have modest advantages over heparin when given after thrombolytic therapy, reducing reinfarction by 14%. In the Global Use of Strategies to Open Occluded Coronary Arteries (GUSTO 2b) trial, patients treated with streptokinase and adjunctive hirudin had a reduction in death or myocardial infarction of 40% at 30 days (8.6% with hirudin versus 14.4% with heparin, p = 0.004). In the Hirulog Early Reperfusion/Occlusion (HERO 1) trial, 48% of patients who received Hirulog as adjunctive therapy with streptokinase had Thrombolysis in Myocardial Infarction (TIMI) trial grade 3 flow in the infarct-related artery, compared with 35% of patients who received heparin with streptokinase (p < 0.05). The HERO 2 study, involving 17,000 patients, will test the hypothesis that Hirulog and aspirin given before streptokinase will reduce mortality compared with aspirin plus heparin. Early administration of direct thrombin inhibitors may potentially improve the outcome of patients treated with thrombolytic therapy.
Aged↗
Low molecular weight heparins in acute ischaemic syndromes.
Thrombus formation and ongoing generation play a major role in the pathogenesis of unstable angina and myocardial infarction (MI). Unfractionated heparin is widely used as an adjunctive therapy in the management of acute ischaemic syndromes, but it has a number of limitations including inter-patient variability, need for monitoring, and the fact that its use may be associated with thrombocytopenia. Low molecular weight heparins have pharmacological and pharmacokinetic properties that may result in better clinical outcomes and safety. They are easy to administer and do not require monitoring. Low molecular weight heparins have been shown to reduce mortality and the incidence of MI and recurrent ischaemia compared with placebo in patients with unstable angina and non-Q-wave MI, and have a more predictable anticoagulant effect than standard unfractionated heparin. They also can be used long term in the outpatient setting, in the form of self-administered subcutaneous injections. The clinical relevance of these new developments is still being defined in ongoing clinical trials and cost-effectiveness analyses.
Angina, Unstable↗
New antiplatelet agents.
Aspirin is an established therapy for the management of acute myocardial infarction (AMI) and unstable angina. Secondary prevention with chronic aspirin therapy is also indicated for patients with stable angina. Aspirin inhibits cyclo-oxygenase-I, a key enzyme in the biosynthetic pathway leading to the production of thromboxane A2. It therefore inhibits only one of the many activation pathways leading to platelet aggregation. Other antiplatelet agents that have also been evaluated in clinical trials include ticlopidine and clopidogrel, which inhibit adenosine diphosphate-mediated platelet aggregation, but these agents are known to be effective against only one of the 90 known agonists that stimulate platelet aggregation. The final common pathway for platelet aggregation involves the glycoprotein IIb/IIIa receptor combining with fibrinogen. Several inhibitors of the glycoprotein IIb/IIIa receptor have been developed and have an important role as adjunctive therapy in angioplasty. Recent trials have been performed in patients with unstable angina, and trials of adjunctive therapy are currently underway in patients receiving thrombolysis for AMI, and for secondary prevention. These drugs have various different features, including specificity for blockade of the glycoprotein IIb/IIIa receptor, half life, duration of the haemostatic effect and potential for antigenicity. Recently concluded and ongoing trials of both intravenous and oral agents are expected to provide further support for the introduction of these agents into clinical management of patients with acute coronary syndromes.
Abciximab↗
The corrected TIMI frame count. The new gold standard?
Over the last decade Thrombolysis in Myocardial Infarction (TIMI) flow grades have been the gold standard for the assessment of efficacy of infarct-artery reperfusion. However, with the introduction of core angiographic laboratories, the reproducibility of TIMI flow grades has been questioned. The corrected TIMI frame count (CTFC) has been developed as a more reproducible method of quantifying infarct artery blood flow after myocardial infarction (MI). We have utilised the CTFC in two studies to examine infarct-artery blood flow. In the Hirulog in Early Reperfusion and Occlusion (HERO 1) study, the CTFC was measured at 90-120 minutes after administration of aspirin, streptokinase and either Hirulog or heparin. Only 27% of patients had a normal CTFC (< or = 27) in the infarct-related artery. Patients with a prolonged CTFC (> 27) had more abnormal left ventricular function (LVF) as measured by the mean chord score in the 'area at risk' (-2.51 vs -2.06, p = 0.02), on left ventriculography. In a second study, infarct-artery flow was examined four weeks and one year after MI. At four weeks, only 43% of patients with patient infarct-related arteries had a 'normal' CTFC of < or = 27. A prolonged CTFC at four weeks was a univariate predictor of increased reocclusion at one year (p = 0.001). CTFCs are frequently abnormal in patent infarct-related arteries, and predict reocclusion. Whether frame counting is a better predictor of late clinical outcomes than the TIMI flow grade needs to be prospectively examined in large clinical trials.
Blood Flow Velocity↗