Limitations of myocardial blush grade in the evaluation of myocardial perfusion in patients with acute myocardial infarction and TIMI grade 3 flow

INTRODUCTION AND OBJECTIVES: An analysis was made of variability in the measurement of the angiographic index blush between a university hospital and an independent core laboratory, as well as its correlation with perfusion analyzed by intracoronary myocardial contrast echocardiography (MCE) and the ventricular function at the sixth month. METHODS: The study comprised 40 patients with a first ST-segment elevation myocardial infarction, single-vessel disease and open infarct-related artery. Perfusion was quantified by angiography (median fifth day, range 3-7) with blush in our laboratory and in an independent core laboratory. MCE was performed. Ejection fraction at the sixth month was determined with magnetic resonance imaging. RESULTS: We found a weak correlation (r=0.38) between both laboratories. In the comparison of blush measurements concordance was 80%, kappa=0.43 if normality was defined by blush 2-3; and concordance 55%, kappa=0.1 for blush 3. Neither perfusion analyzed by MCE (r= 0.23, P=.2) nor ejection fraction by resonance (r=0.20, P=.3) did correlate to blush. CONCLUSIONS: After infarction in patients with TIMI 3, variability is observed in blush measurements between a university hospital and an independent core laboratory, therefore it seems advisable to centralize blush measures in highly specialized core laboratories. A weak correlation was detected with perfusion analyzed by MCE and with late systolic function.     

Prognostic implications of TIMI flow grade in the infarct related artery compared with continuous 12-lead ST-segment resolution analysis. Reexamining the "gold standard" for myocardial reperfusion assessment

OBJECTIVE: To compare the prognostic significance of reperfusion assessment by Thrombolysis in Myocardial Infarction (TIMI) flow grade in the infarct related artery and ST-segment resolution analysis, by correlating with clinical outcomes in patients with acute myocardial infarction (AMI). BACKGROUND: Angiographic assessment, based on epicardial coronary anatomy, has been considered the "gold standard" for reperfusion. The electrocardiogram (ECG) monitoring provides a noninvasive, real-time physiologic marker of cellular reperfusion and may better predict clinical outcomes. METHODS: Two hundred fifty-eight AMI patients from the Thrombolytics and Myocardia Infarction phase 7 and Global Utilization of Streptokinase tPA for Occluded coronary arteries phase 1 trials were stratified based on blinded, simultaneous reperfusion assessment on the acute angiogram (divided into TIMI grades 0 & 1, TIMI grade 2 and TIMI grade 3) and ST-segment resolution analysis (divided into: <50% ST-segment elevation resolution or reelevation and > or =50% ST-segment elevation resolution). In-hospital mortality, congestive heart failure (CHF) and combined mortality or CHF were compared to determine the prognostic significance of reperfusion assessment by each modality using chi-square and Fisher's Exact tests for univariable correlation and logistic regression analysis for univariable and multivariable prediction models. RESULTS: By logistic regression analysis, ST-segment resolution patterns were an independent predictor of the combined outcome of mortality or CHF (p = 0.024), whereas TIMI flow grade was not (p = 0.693). Among the patients determined to have failed reperfusion by TIMI flow grade assessment (TIMI flow grade 0 & 1), the ST-segment resolution of > or =50% identified a subgroup with relatively benign outcomes with the incidence of the combined end point of mortality or CHF 17.2% versus 37.2% in those without ST-segment resolution (p = 0.06). CONCLUSION: Continuous 12-lead ECG monitoring can be an inexpensive and reliable modality for monitoring nutritive reperfusion status and to obtain prognostic information in patients with AMI.     

Weight-adjusted dosing of TNK-tissue plasminogen activator and its relation to angiographic outcomes in the thrombolysis in myocardial infarction 10B trial. TIMI 10B Investigators

Fixed doses of thrombolytic agents are generally administered to patients of varying body weights, and the dose-response relation may be confounded by the variability in patient weight. We hypothesized that higher doses of TNK-tissue plasminogen activator (tPA) per unit body weight would be related to improved flow at 90 minutes after thrombolytic administration. A total of 886 patients with acute myocardial infarction were randomized to receive either a single bolus of 30, 40, or 50 mg of TNK-tPA or front-loaded tPA in the Thrombolysis In Myocardial Infarction (TIMI) 10B trial. The dose of TNK-tPA administered was divided by the patient's weight to arrive at the TNK-tPA dose (mg) per unit body weight (kg), and patients were stratified into tertiles based on mg/kg of TNK-tPA: low dose, 0.2 to 0.39 mg/kg; mid-dose, 0.40 to 0.51 mg/kg; high dose, 0.52 to 1.24 mg/kg. Flow in the culprit and nonculprit arteries was analyzed using the TIMI flow grades and the corrected TIMI frame count (CTFC). The median CTFC in culprit arteries differed between the tertiles (3-way p = 0.007), with the CTFC being 7.2 frames faster in high-dose than in low-dose patients (43.1 +/- 30.1, median 31.2, n = 171 vs 54.6 +/- 34.8, median 38.4, n = 166, 2-way p = 0.002). Patients in the mid- and high-dose tertiles achieved patency more frequently (TIMI grade 2 or 3 flow) by 60 minutes (p = 0.02), and the 90-minute percent diameter stenosis was less severe in patients in the high- versus low-dose tertile (p = 0.03). In nonculprit arteries, the CTFC was faster in high- than in low-dose tertiles (29.6 +/- 13.4, median 26.9, n = 130 vs 34.7 +/- 16.3, median 32.8, n = 108, 3-way p = 0.03, 2-way p = 0.008). In patients who underwent percutaneous transluminal coronary angioplasty (PTCA), the CTFC in culprit arteries after PTCA was fastest in the high- and mid-dose tertiles than in those receiving low doses (2-way p = 0.05). Thus, higher doses per unit body weight of TNK-tPA result in not only faster culprit artery flow, but also faster nonculprit, global, and post-PTCA flow, which may reflect earlier opening, reduced stunning, or improved microvascular function. The greater effectiveness of thrombolysis must be weighed against any increase in risk.     

Comparison of angiographic center and local site analysis of PTCA results in a multicenter angioplasty-restenosis trial. The M Heart Group.

We compared three methods of coronary stenosis (S) sizing in a multihospital PTCA restenosis trial: visual analysis by independent observers, single point caliper measurements, and quantitative coronary angiography (QCA). Cine films from 50 patients were submitted from the clinical site to the quantitative angiographic center, where visual analysis and computer quantitation were performed. Regression analysis revealed a correlation coefficient of .857 for caliper vs. QCA (p less than .0001) and .876 for visual observation vs. QCA (p less than .0001). No significant differences were found between any of the 3 methods for pre- or post-PTCA stenosis values. However, QCA yielded smaller PTCA changes in stenosis severity than either caliper or visual observation (p less than .05). Both caliper and visual methods correlated well with QCA in assessing stenosis size pre- and post-PTCA. Trained observers can visually assess lesion severity with accuracy approaching QCA. QCA is likely to be less expensive when compared to visual analysis by three experienced observers and should be the method used for estimating the results of PTCA in clinical trials.     

Determinants of coronary blood flow after thrombolytic administration. TIMI Study Group. Thrombolysis in Myocardial Infarction.

OBJECTIVES: This study evaluated the determinants of coronary blood flow following thrombolytic administration in a large cohort of patients. BACKGROUND: Tighter residual stenoses following thrombolysis have been associated with slower coronary blood flow, but the independent contribution of other variables to delayed flow has not been fully explored. METHODS: The univariate and multivariate correlates of coronary blood flow at 90 min after thrombolytic administration were examined in a total of 2,195 patients from the Thrombolysis in Myocardial Infarction (TIMI) 4, 10A, 10B and 14 trials. The cineframes needed for dye to first reach distal landmarks (corrected TIMI frame count, CTFC) were counted as an index of coronary blood flow. RESULTS: The following were validated as univariate predictors of delayed 90-min flow in two cohorts of patients: a greater percent diameter stenosis (p < 0.0001 for both cohorts), a decreased minimum lumen diameter (p = 0.0003, p = 0.0008), a greater percent of the culprit artery distal to the stenosis (p = 0.03, p = 0.02) and the presence of any of the following: delayed achievement of patency (i.e., between 60 and 90 min) (p < 0.0001 for both cohorts), a culprit location in the left coronary circulation (left anterior descending or circumflex) (p = 0.02, p < 0.0001), pulsatile flow (i.e., reversal of flow in systole, a marker of heightened microvascular resistance, p = 0.0003, p < 0.0001) and thrombus (p = 0.002, p = 0.03). Despite a minimal 16.4% residual stenosis following stent placement, the mean post-stent CTFC (25.8 +/- 17.2, n = 181) remained significantly slower than normal (21.0 +/- 3.1, n = 78, p = 0.02), and likewise 34% of patients did not achieve a CTFC within normal limits (i.e., <28 frames, the upper limit of the 95th percent confidence interval previously reported for normal flow). Those patients who failed to achieve normal CTFCs following stent placement had a higher mortality than did those patients who achieved normal flow (6/62 or 9.7% vs. 1/118 or 0.8%, p = 0.003). CONCLUSIONS: Lumen geometry is not the sole determinant of coronary blood flow at 90 min following thrombolytic administration. Other variables such as the location of the culprit artery, the duration of patency, a pulsatile flow pattern and thrombus are also related to slower flow. Despite a minimal 16% residual stenosis, one-third of the patients treated with adjunctive stenting still have a persistent flow delay following thrombolysis, which carries a poor prognosis.     

Mitral regurgitation in early myocardial infarction. Incidence, clinical detection, and prognostic implications. TIMI Study Group.

OBJECTIVE: To investigate mitral regurgitation occurring early in the course of acute myocardial infarction with respect to its incidence, the impact of infarct size and location, the accuracy of clinical detection, the contribution of global and regional left ventricular performance, and its influence on prognosis. DESIGN: Prospective observational study derived from patients entering Phase I of the Thrombolysis in Myocardial Infarction (TIMI) trial. SETTING: Multicenter trial involving 13 university-affiliated medical centers. PATIENTS: A total of 206 patients studied within 7 hours of symptom onset during their first myocardial infarction. MEASUREMENTS: Contrast left ventriculography was used to document mitral regurgitation. RESULTS: Mitral regurgitation was present in 27 patients (13%). Although the presence of regurgitation correlated with the site of infarction (20 of 27 had anterior infarctions) and the number of akinetic chords, it was not statistically related to the peak creatine kinase value or to left ventricular chamber size or filling pressure. A murmur of mitral regurgitation was heard in only 2 patients (1 incorrectly). The presence of early mitral regurgitation predicted cardiovascular mortality at 1 year by univariate (relative risk, 12.2; 95% Cl, 3.5 to 42; P less than 0.0001) and multivariate (relative risk, 7.5; Cl, 2.0 to 28.6; P = 0.0008) analyses. CONCLUSIONS: Mitral regurgitation in early myocardial infarction is generally clinically "silent," is more common in anterior infarction, is associated with regional dysfunction but not early ventricular dilation or peak enzyme release, and is an important predictor of cardiovascular mortality.     

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.     

The role of adrenergic activity in slow coronary flow and its relationship to TIMI frame count

The aim of this study was to investigate the role of adrenergic activity in patients with slow coronary flow (SCF) and its relationship to TIMI frame count on the pathogenesis of SCF. Plasma noradrenalin and adrenalin concentrations at rest were compared in 51 patients diagnosed with SCF through coronary angiography and TIMI frame count; and 44 healthy controls with normal coronary flow (NCF). Furthermore, the relationship between TIMI frame count and noradrenalin and adrenalin levels was investigated. Plasma noradrenalin (127.9 +/-9.2 and 79.3 +/- 7.3 ng/mL, p < 0.0001) and adrenalin levels (63.9 +/- 2.6 and 44.7 +/- 2.8 ng/mL, p < 0.0001) were higher in patients with SCF when compared to patients with NCF. Noradrenalin and adrenalin levels were effected with SCF-dominant vessels with respect to TIMI frame count (p = 0.012 and p < 0.0001). Patients with SCF in 1, 2, or 3 vessels had different noradrenalin and adrenalin levels (p <0.003 and p < 0.0001). Patients with TIMI frame count above the 75th percentile had significantly higher noradrenalin and adrenalin levels when compared with those between the 25th-50th percentiles and below (p < 0.001 and p = 0.011, respectively). Correlation analysis established that both adrenalin and noradrenalin levels were correlated with TIMI frame counts of left anterior descending (LAD) and circumflex (Cx) arteries. Exercise testing revealed ischemia in 6 patients. Their TIMI frame counts were above the 75th percentile, and they had higher noradrenalin and adrenalin levels when compared with those without ischemia (p = 0.029, p = 0.045). Higher noradrenalin and adrenalin levels and correlation between TIMI frame count and ischemia in patients with SCF suggest that increased adrenergic activity may be the manifestation of slow coronary flow.     

Vessel heterogeneity of TIMI frame count and its relation to P-wave dispersion in patients with coronary slow flow

Background

The vessel heterogeneity of thrombolysis in myocardial infarction (TIMI) frame count (TFC) in patients with coronary slow flow (CSF) remains to be further evaluated, and the correlation between TFC heterogeneity and P-wave dispersion (PWD) has not been elucidated. We aim to investigate the vessel heterogeneity of TFC in coronary arteries, and its relation to PWD in patients with CSF and otherwise normal coronary arteries.

Methods

We studied 72 patients with angiographically documented CSF and 66 age- and gender-matched control subjects. The coefficient of variation (CV) and mean TFC of the three vessels were calculated. P-wave duration and PWD were measured on the standard electrocardiograms (ECGs).

Results

The mean TFC and CV were both significantly higher in CSF patients than in controls (P<0.001 for both comparisons). The maximum P-wave duration (Pmax) and PWD were found to be significantly higher in CSF patients than in controls (P<0.001 for both comparisons). In patients with CSF, both Pmax and PWD were mildly correlated to mean TFC (r=0.318, P=0.009; and r=0.307, P=0.010), and were more significantly correlated to CV (r=0.506, P<0.001; and r=0.579, P<0.001).

Conclusions

These data demonstrate that variability of TFC in three coronary arteries is increased in CSF patients, and that the vessel heterogeneity in coronary flow might be intimately associated with PWD.     

Thrombolysis in Myocardial Infarction (TIMI) phase II trial: outcome comparison of a "conservative strategy" in community versus tertiary hospitals. The TIMI Research Group

In the conservative strategy arm of phase II of the Thrombolysis in Myocardial Infarction (TIMI) trial, 1,461 patients were treated with intravenous recombinant tissue-type plasminogen activator (rt-PA). Coronary angiography, with angioplasty if feasible, was to be performed only for recurrent spontaneous or exercise-induced ischemia. In this study results in patients treated by this strategy in community and tertiary hospitals are compared. Despite similar baseline findings in the two groups, coronary angiography was performed within 42 days in more patients (542 [48%] of 1,155) initially admitted to a tertiary hospital (on-site coronary angiography/angioplasty available) than in those (94 [32%] of 306) admitted to a community hospital (transfer to tertiary hospital for coronary angiography/angioplasty) (p less than 0.001). This different approach resulted in a greater use of coronary angioplasty (203 [18%] of 1,155 versus 32 [11%] of 306, p less than 0.01), coronary artery bypass surgery (133 [12%] of 1,155 versus 23 [8%] of 306, p less than 0.05) and blood transfusions (139 [12%] of 1,155 versus 17 [5.5%] of 306, p less than 0.001) in patients admitted to a tertiary than to a community hospital. However, there were no significant differences between the two groups in mortality, recurrent myocardial infarction or left ventricular function. These results demonstrate that a conservative strategy after treatment of acute myocardial infarction with rt-PA is applicable in the community hospital setting.     

Effects of a timely therapy with doxycycline on the left ventricular remodeling according to the pre-procedural TIMI flow grade in patients with ST-elevation acute myocardial infarction

Doxycycline has been demonstrated to reduced left ventricular (LV) remodeling, but its effect in patients with ST-elevation myocardial infarction (STEMI) and a baseline occluded [thrombolysis in myocardial infarction (TIMI) flow grade ≤1] infarct-related artery (IRA) is unknown. According to the baseline TIMI flow grade, 110 patients with a first STEMI were divided into 2 groups. Group 1: 77 patients with TIMI flow ≤1 (40 patients treated with doxycycline and 37 with standard therapy, respectively), and a Group 2: 33 patients with TIMI flow 2–3 (15 patients treated with doxycycline and 18 with standard therapy, respectively). The two randomized groups were well matched in baseline characteristics. A 2D-Echo was performed at baseline and at 6 months, together with a coronary angiography, for the remodeling and IRA patency assessment, respectively. The LV end-diastolic volume index (LVEDVi) decreased in Group 2 [?3 mL/m² (IQR: ?12 to 4 mL/m²)], and increased in Group 1 [6 mL/m² (IQR: ?2 to 14 mL/m²)], (p = 0.001). In Group 2, LVEDVi reduction was similar regardless of drug therapy, while in Group 1 the LVEDVi was smaller in patients treated with doxycycline as compared to control [3 mL/m² (IQR: ?3 to 8 mL/m²) vs. 10 mL/m² (IQR: 1–27 mL/m²), p = 0.006]. A similar pattern was observed also for LV end-systolic volume and ejection fraction. In STEMI patients at higher risk, as those with a baseline TIMI flow grade ≤1, doxycycline reduces LV remodeling.     

Combination reperfusion therapy with abciximab and reduced dose reteplase: results from TIMI 14. The Thrombolysis in Myocardial Infarction (TIMI) 14 Investigators.

Aims Abciximab has previously been shown to enhance thrombolysis and improve myocardial perfusion when combined with reduced doses of alteplase. The purpose of the reteplase phase of TIMI 14 was to evaluate the effects of abciximab when used in combination with a reduced dose of reteplase for ST-elevation myocardial infarction. Methods and Results Patients (n=299) with ST-elevation myocardial infarction were treated with aspirin and randomized to a control arm with standard dose reteplase (10+10 U given 30 min apart) or abciximab (bolus of 0.25 mg. kg(-1)and 12-h infusion of 0.125 microg. kg(-1). min(-1)) in combination with reduced doses of reteplase (5+5 U or 10+5 U). Control patients received standard weight-adjusted heparin (bolus of 70 U. kg(-1); infusion of 15 U. kg(-1). h(-1)), while each of the combination arms with abciximab and reduced dose reteplase received either low dose heparin (bolus of 60 U. kg(-1); infusion of 7 U. kg(-1). h(-1)) or very low dose heparin (bolus of 30 U. kg(-1); infusion of 4 U. kg(-1). h(-1)). The rate of TIMI 3 flow at 90 min was 70% for patients treated with 10+10 U of reteplase alone (n=87), 73% for those treated with 5+5 U of reteplase with abciximab (n=88), and 77% for those treated with 10+5 U of reteplase with abciximab (n=75). Complete (>/=70%) ST resolution at 90 min was seen in 56% of patients receiving a reduced dose of reteplase in combination with abciximab compared with 48% of patients receiving reteplase alone.Conclusions Reduced doses of reteplase when administered in combination with abciximab were associated with higher TIMI 3 flow rates than reported previously for reduced doses of reteplase without abciximab and were at least as high as for full dose reteplase alone Copyright 2000 The European Society of Cardiology.     

Incidence and prognostic implications of heart block complicating inferior myocardial infarction treated with thrombolytic therapy: results from TIMI II.

OBJECTIVES. The aim of this study was to determine the incidence and significance of second- or third-degree heart block among patients with inferior myocardial infarction treated with thrombolytic therapy. BACKGROUND. Data from the prethrombolytic era suggest that heart block occurs in approximately 20% of patients with acute inferior myocardial infarction and is associated with a marked increase in mortality. Little is known about the incidence and prognostic implications of heart block among patients receiving thrombolytic therapy. METHODS. We studied 1,786 patients with acute inferior myocardial infarction enrolled in the Thrombolysis in Myocardial Infarction (TIMI) II Trial who received recombinant tissue-type plasminogen activator (rt-PA) within 4 h of the onset of symptoms. RESULTS. Heart block occurred in 214 patients (12%); 113 (6.3%) had heart block on presentation and 101 (5.7%) developed heart block in the 24 h after treatment with rt-PA. Patients with heart block at entry were slightly older and a greater proportion had cardiogenic shock. The 21-day mortality rate among patients with heart block at entry was 7.1% (8 of 113), compared with 2.7% (45 of 1,673) among patients without heart block at study entry (relative risk 2.6, p = 0.007). However, heart block was not independently associated with 21-day mortality after adjustment for other variables, including shock. Mortality and other adverse cardiac events in the following year were similar among patients with and without heart block. Among patients without heart block at study entry, coronary angiography among patients randomly assigned to coronary catheterization 18 to 48 h after admission revealed that the infarct-related artery was occluded in 28.2% (11 of 39) of patients who developed heart block versus 15.5% (112 of 723) of patients without heart block (p = 0.04). The 21-day mortality rate was increased among patients in whom heart block developed after thrombolytic therapy (9.9% [10 of 101] versus 2.2% [35 of 1,572] of patients without heart block, relative risk 4.5, p less than 0.001). Analysis of the increased mortality among patients who developed heart block suggests that mortality was due to severe cardiac dysfunction; no patient was considered to have died as a result of the heart block or its treatment. CONCLUSIONS. Heart block is common among patients with inferior infarction given thrombolytic therapy and is associated with increased mortality. These clinical and anatomic data provide insight into the mechanism of heart block and increased mortality among such patients.     

Prognostic value of noninvasive markers of coronary reperfusion compared to TIMI 3 flow in patients treated with primary angioplasty

INTRODUCTION AND OBJECTIVES: The aim of this study was to compare the prognostic value of TIMI 3 flow versus noninvasive markers of coronary artery reperfusion on the outcome of patients with a recent acute myocardial infarction (AMI) treated with primary angioplasty. PATIENTS AND METHOD We analyzed 172 consecutive patients with AMI and ST-segment elevation, who were treated with primary angioplasty within 12 hours of admission. Mean age was 6113 years, 77% were men, and 56% had a history of previous AMI. RESULTS: In-hospital mortality was 3.6%; 16.6% developed heart failure, and 11.1% had complex arrhythmias during their hospital stay. The noninvasive criterion for successful reperfusion was the presence of two or more markers of reperfusion based on ECG changes or CK levels after angioplasty. Reperfusion was successful in 87.7% of the patients, and TIMI 3 flow was achieved in 87%. There was no significant concordance between the two methods (kappa index = 0.012). Multivariate analysis showed that both successful reperfusion (OR=0.028; 95% CI, 0.003-0.268) and TIMI 3 flow (OR=0.104; 95% CI, 0.019-0.563) were protective for in-hospital mortality. However, in the multivariate analysis only successful reperfusion was a protective factor for heart failure and complex arrhythmias. CONCLUSION: Our findings confirm that both TIMI 3 flow and successful coronary reperfusion evaluated noninvasively show independent prognostic value in patients with AMI treated with primary angioplasty. Noninvasive markers of coronary reperfusion should be used as complementary to angiography in these patients.     

Relationship between longitudinal morphology of ruptured plaques and TIMI flow grade in acute coronary syndrome: a three-dimensional intravascular ultrasound imaging study.

AIMS: In this study, we investigated the relationship between longitudinal morphology reconstructed from pre-intervention intravascular ultrasound (IVUS) images and thrombolysis in myocardial infarction (TIMI) flow grade at initial angiograms in the acute phase of acute coronary syndrome (ACS). METHODS AND RESULTS: Our patient population comprised 72 ACS patients in whom we obtained successful reconstructed longitudinal images. On the basis of the site of the maximum aperture of rupture in the longitudinally reconstructed IVUS images, patients were divided into three groups: plaques with rupture in the proximal shoulder (proximal type; n = 28), mid-portion (mid-type; n = 18), and distal shoulder (distal type; n = 26) of the plaque. There were no differences in terms of coronary risk factors or the angiographic findings. The proximal-type group more frequently showed TIMI 0 on initial angiogram (proximal type, 86%; mid-type, 50%; and distal type, 31%; P = 0.002). A multivariable logistic regression model revealed that the presence of a proximal-type rupture correlated with the presentation of ST-elevation myocardial infarction (P = 0.019; odds ratio, 8.12; 95% CI, 1.404-49.996). CONCLUSIONS: Longitudinal morphological features in a ruptured plaque may affect the formation of obstructive thrombus in ACS. Our results suggest that longitudinal morphology may be an important determinant of coronary artery occlusion.