Improved coronary artery flow after coronary angioplasty in patients with unstable angina

Background : Coronary artery flow is impaired after myocardial infarction but there is limited information regarding coronary flow in unstable angina.
Aim : To assess baseline coronary artery flow and the effects of coronary angioplasty on coronary flow in patients with unstable angina.
Methods : Twenty-one patients with unstable angina with a culprit lesion suitable for coronary angioplasty were enrolled in the study. Coronary flow was assessed with the Thrombolysis In Myocardial Infarction (TIMI) grade and the Corrected TIMI Frame Count (CTFC) pre and post angioplasty.
Results : Baseline flow was impaired in the culprit artery compared to the non culprit artery (42.0±28.1 vs 25.3±7.0 frames, p <0.02). Pre angioplasty coronary flow was TIMI grade 2 in 52% and TIMI grade 3 in 48% of patients. Post angioplasty flow improved with TIMI grade 2 flow in 5% and TIMI grade 3 in 95%. After angioplasty coronary flow improved from 42.0±28.1 frames to 21.6±16.3 ( p =0.0001). The culprit coronary stenosis decreased from 74±9% pre angioplasty to 28±12% after intervention ( p =0.0001).
Conclusions : Angioplasty and stenting of the culprit vessel restores normal coronary flow in most patients with unstable angina. This suggests that impaired flow in unstable angina is predominantly related to the culprit lesion residual stenosis.     

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.     

Comparative efficacy of primary angioplasty with stent implantation and thrombolysis in restoring basal coronary artery flow in acute ST segment elevation myocardial infarction: quantitative assessment using the corrected TIMI frame count

Following thrombolysis and primary percutaneous transluminal coronary angioplasty (PTCA) for acute ST segment elevation myocardial infarction, basal flow in the culprit artery is known to influence prognosis. The purpose of this study was to determine if differences exist in basal flow in culprit and nonculprit coronary arteries in patients with acute ST segment elevation myocardial infarction who were treated with thrombolysis or primary PTCA with stent implantation. Twenty patients were randomized to thrombolysis (with recombinant tissue plasminogen activator) and 24 to primary PTCA with stent implantation within 3 hours of onset of acute ST segment elevation myocardial infarction. Coronary angiography was performed 90-120 minutes after thrombolysis or immediately after PTCA with stent implantation and again at 18-36 hours after intervention in both groups. Patients who failed to achieve thrombolysis in myocardial infarction (TIMI) grade 2 or 3 flow were excluded. The corrected TIMI frame count was used as the index of basal coronary artery flow. Early after intervention the mean corrected TIMI frame count in the culprit coronary artery was significantly lower in the primary PTCA with stent group (27.4 +/- 7.7 frames) than in the thrombolysis group (39.8 +/- 10 frames, p < 0.001). Eight thrombolysis patients (40%) and 20 primary PTCA patients (83%, p < 0.01) achieved TIMI grade 3 flow early after intervention. By 18-36 hours after intervention there were no significant differences in the mean correct TIMI frame count between the thrombolysis and primary PTCA with stent groups. There were no significant differences in the mean corrected TIMI frame count between these two groups in the nonculprit coronary artery, either early after intervention or at 18-36 hours. In successfully reperfused coronary arteries following acute ST segment elevation myocardial infarction, primary angioplasty with stent implantation reestablished TIMI grade 2 or 3 flow faster and more effectively than thrombolysis did.     

Progression of the Culprit Lesion in Unstable Coronary Artery Disease With Warfarin and Aspirin Versus Aspirin Alone: Preliminary Study

Objectives. This study assessed whether combination therapy with aspirin and warfarin for 10 weeks reduces the risk of progression or reocclusion of the unstable coronary artery lesion.Background. Reocclusion of the culprit coronary artery occurs in up to one third of patients during the 3 months after myocardial infarction (MI) or unstable angina and is associated with increased morbidity and mortality.Methods. Fifty-seven patients presenting with unstable angina or MI who had an identifiable culprit lesion at coronary angiography were randomized in double-blind manner to receive warfarin (target international normalized ratio [INR] 2.0 to 2.5) or placebo in addition to aspirin (150 mg daily). Changes in the culprit lesion were assessed by quantitative angiography in 50 patients after 10 weeks of therapy or after a clinical event. Progression of the culprit lesion was defined as a decrease in minimal lumen diameter >0.4 mm or a new total occlusion. Regression was defined as an increase in minimal lumen diameter >0.4 mm.Results. In subjects randomized to receive warfarin, the culprit lesion was less likely to progress (1 [4%] vs. 8 [33%]) and more likely to regress (5[19%] vs. 2[9%]) than in subjects receiving placebo (p = 0.02). Recurrent MI or a new occlusion at angiography occurred in 2 (7%) of 29 patients receiving warfarin versus 11 (39%) of 28 patients receiving placebo (p = 0.005).Conclusions. In patients with an acute coronary syndrome, combined therapy with aspirin and warfarin with a target INR of 2.0 to 2.5 for 10 weeks reduces the risk of progression or reocclusion of the culprit coronary lesion.     

Urokinase plus heparin versus aspirin in unstable angina and non-Q-wave myocardial infarction

The pivotal role of thrombosis in unstable angina and non-Q-wave myocardial infarction has been established recently. To assess the value and safety of thrombolytic therapy compared to conventional antithrombotic therapy (aspirin) in arresting progression in this setting to recurrent ischemic end-points, 25 patients presenting with unstable angina and an electrocardiogram showing subendocardial ischemia were randomized to receive either aspirin 325 mg daily, or urokinase 3 x 10(6) U intravenously, over 30 minutes followed by heparin. Incidence of endpoints (intractable ischemia requiring mechanical intervention, new myocardial infarction or death) was determined over 7 days. Coronary arteriography was performed at 24 to 72 hours to determine extent of coronary artery disease and morphologic severity of the culprit lesion, graded by a semiquantitative scoring system ranging from 4+ (definite thrombosis) to 0 (chronic lesion). In the first 24 hours, 7 of 13 aspirin versus 1 of 12 urokinase patients exhibited ischemia progression (p less than 0.05). By 7 days, progression to a primary ischemic endpoint occurred in 8 of 13 aspirin patients (3 myocardial infarctions and 5 intractable ischemias) versus 3 of 12 urokinase patients (2 intractable ischemias and 1 death) (p = 0.18). The apparent benefit of urokinase followed by heparin compared to conventional aspirin therapy in arresting early progression of unstable angina or non-Q-wave myocardial infarction was not associated with enhanced culprit lesion morphology (mean lesion severity score 2.7 +/- 1.5 vs 2.8 +/- 1.6 in aspirin-treated patients). Large scale, randomized trials to assess the clinical utility of urokinase for unstable angina are warranted.     

Relationship between corrected TIMI frame counts at three weeks and late survival after myocardial infarction

OBJECTIVES: To evaluate the corrected Thrombolysis in Myocardial Infarction (TIMI) frame count (CTFC) as a predictor of late survival after myocardial infarction. BACKGROUND: Thrombolysis in Myocardial Infarction flow grades predict late survival after myocardial infarction. The CTFC provides a more reproducible measurement of infarct-related artery blood flow than the TIMI flow grade, and has been linked to 30-day outcomes, but it has not yet been established how the CTFC correlates with late survival. METHODS: Of 1,001 patients with acute myocardial infarction presenting within 4 h of symptom onset, 882 underwent angiography at approximately three weeks. Infarct artery flow was assessed, blinded to clinical outcomes, according to the CTFC and TIMI flow grade. Late cardiac mortality and survival were determined in 97.5% of patients. RESULTS: The mean CTFC was 40 +/- 29 in 644 patent infarct arteries (median, 34 [interquartile range, 24 to 47]). The CTFC, assessed as a continuous univariate variable, was found to be a predictor of five-year survival, as was the TIMI flow grade (both p < 0.001). On multivariate analysis, factors associated with five-year survival included the ejection fraction or end-systolic volume index (both p < 0.001); exercise duration (p = 0.005), age (p = 0.008), diabetes (p = 0.02) and CTFC (p = 0.02) or TIMI flow (p = 0.02). The same factors, except for the CTFC and TIMI flow grade, were predictors of 10-year survival. CONCLUSIONS: The CTFC three weeks after myocardial infarction was an independent predictor of five-year survival, but not 10-year survival. Although the CTFC provided additional prognostic information within TIMI flow grades, its superiority was not demonstrated.     

Corrected TIMI frame counts correlate with stenosis severity and infarct zone wall motion after thrombolytic therapy

BACKGROUND: The majority of patients with patent infarct-related arteries after thrombolytic therapy have slower than normal flow, which relates to myocardial perfusion. METHODS: To evaluate the relationships between blood levels of creatine kinase (CK) and the corrected Thrombolysis in Myocardial Infarction (TIMI) frame count (CTFC), infarct artery stenosis, and left ventricular function, we studied 397 patients with a first myocardial infarction who underwent angiography at 3 weeks. TIMI flow grades, the CTFC, infarct artery stenosis, and infarct zone wall motion (by contrast ventriculography using the centerline method) were assessed, and CK levels (in units per liter) were measured hourly for the first 4 hours after streptokinase (1.5 x 10(6) U over 30-60 minutes) and then every 4 hours over the next 20 hours, all blinded to treatment and outcome. RESULTS: Infarct artery stenosis and the CTFC, assessed as continuous variables, correlated in patients with patent infarct arteries (r = 0.33, P <.001). Also, there was a significant correlation between the CTFC and the sum of hypokinetic chords in the infarct zone (r = 0.15, P =.01). Patients with total occlusion or markedly slowed infarct artery flow (CTFC >100) had a higher fraction of chords with wall motion >2 SDs below normal (0.65 [0.41, 0.80] vs 0.37 [0.0, 0.67]) compared with patients with normal flow (CTFC < or =27) (P <.001). The rates of increase of median CK levels with respect to TIMI flow grades were 342 U/L/h for TIMI 3 versus 212 U/L/h for TIMI 2 versus 140 U/L/h for TIMI 0-1 (P <.0001). CONCLUSIONS: Prolonged corrected TIMI frame counts correlate with stenosis severity in the infarct artery after infarction, infarct zone regional wall motion, and CK levels.     

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.     

Three episodes of inferior acute myocardial infarction due to thrombotic occlusion of the right coronary artery: a case report

A 77-year-old female with two previous inferior myocardial infarctions was transferred to our medical center with a third inferior acute myocardial infarction. Coronary angiography revealed 99% stenosis with rich thrombus in the distal right coronary artery [Thrombolysis in Myocardial Infarction (TIMI) grade 2 flow]. The angiographic appearance of the right coronary artery was similar to the two previous myocardial infarctions. Coronary aspiration was performed and TIMI grade 3 flow was established. To confirm the presence of thrombus, intravascular ultrasound (IVUS) and coronary angioscopy were performed at pre-discharge. IVUS showed a thrombus-like low-density area at the mid right coronary artery. Red thrombi were observed in the same area using coronary angioscopy. Although warfarin had been prescribed for secondary prevention since the first acute myocardial infarction, both the second and third acute myocardial infarction occurred after cessation of warfarin. Patients with acute myocardial infarction due to thrombotic occlusion, confirmed by IVUS or angioscopy, might be good candidates for permanent warfarin therapy.     

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 (≥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 patent infarct-related arteries had a 'normal' CTFC of ≥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.     

肌钙蛋白升高的非ST段抬高型急性冠状动脉综合征造影特点

目的观察肌钙蛋白升高的非ST段抬高型急性冠状动脉综合征患冠状动脉造影特点．包括冠状动脉造影下的心肌微灌注特点。方法291例行冠状动脉造影的非ST段抬高型急性冠状动脉综合征患．冠状动脉造影术前测定心肌钙蛋白T(cardiac troponin T,cTnT),cTnT阳性界限值为0．01μg／L(ng／ml)。应用心肌梗死溶栓治疗临床实验(thrombolysis in myocardial infarction,TIMI)血流分级和校正的TIMI帧数评价冠状动脉血流,应用TIMI心肌灌注分数评价心肌微灌注。结果与cTnT阴性组患相比,cTnT阳性组患中冠状动脉血流通畅(TIMI2／3)发生率较低(P=0．001)．血流完全正常的发生率也较低(P=0．040)。cTnT阳性组患比阴性组患有更高的血栓发生率(P=0．012)、较重的狭窄率(P=0．027)、较高的血管闭塞率(P=0．001)、较大的校正的TIMI帧数,(P=0．026)。与cTnT阴性组患相比,cTnT阳性组患微血管堵塞(TMP0／1)发生率高(P=10．009)。多因素回归模型显示,TIMI心肌灌注分数(TIMI myocairdial perfusion,TMP0／1)是独立于TIMI、CTFC、狭窄程度和血栓之外的cTnT阳性的预测因子(OR=2．647;P=0．002)。结论肌钙蛋白升高的非ST段抬高型急性冠状动脉综合征患冠状动脉造影特点为血栓发生率高、狭窄较重、血管闭塞率高、血流较慢、心肌组织灌注不良多。TMP0／1是独立于TIMI、CTFC、狭窄程度和血栓之外的cTnT阳性的预测因子。     

Relationship of clinical presentation and calcification of culprit coronary artery stenoses

Coronary artery calcification is increased in the presence of atherosclerosis. However, there is great variability in the calcification of individual coronary stenoses, and the clinical significance of this finding remains unknown. We tested the hypothesis that culprit lesions associated with myocardial infarction or unstable angina are less calcified than are stenoses associated with stable angina. The study consisted of 78 patients who underwent intravascular ultrasound imaging of culprit stenoses after the placement of a stent. Seventeen patients presented with stable angina; 43, with unstable angina; and 18, with myocardial infarction. The extent of coronary calcification was measured by the angle of its arc and was quantified with a computer-based protractor. The arc of calcium was measured in the stented area at the point of maximal calcification and also as an average of the calcification found at proximal, middle, and distal stent segments. The maximal arc of calcium decreased progressively from patients with stable angina (91+/-10 degrees ) to those with unstable angina (59+/-8 degrees ) and to those with myocardial infarction (49+/-11 degrees, P=0.014). Similarly, the average arc of calcium was greatest (32+/-7 degrees ) in patients with stable angina, less (15+/-4 degrees ) in patients with unstable angina, and least (10+/-5 degrees ) in patients with acute myocardial infarction (P=0.014). These associations remained significant after adjustment for other factors that potentially affect arterial calcification. Acute coronary syndromes are associated with a relative lack of calcium in the culprit stenoses compared with stenoses of patients with stable angina. These findings have implications for the understanding of the biology of acute coronary syndromes as well as for the identification of coronary stenoses by methods that rely solely on the presence of calcium.     

Intracoronary temperature in patients with coronary artery disease

OBJECTIVES: Measurements of changes in plaque temperature may predict plaque rupture. The present study investigated variations in temperature within the atherosclerotic coronary artery using a pressure guide wire with thermal sensor (dual sensor guide wire). METHODS AND RESULTS: Seventy-seven patients (78 lesions), who had no significant lesion at the orifice of the culprit coronary artery, were studied. The patients had acute myocardial infarction (22 patients), unstable angina pectoris (20 patients), and stable angina pectoris (35 patients). The thermal sensor was calibrated at the orifice of the coronary artery, and then inserted into the culprit coronary artery. deltaT was defined as the difference between the intracoronary temperature at the position of the pressure gradient and at the orifice. deltaT was higher in patients with acute myocardial infarction and unstable angina pectoris than in patients with stable angina pectoris (0.09 +/- 0.07 and 0.07 +/- 0.07 vs 0.03 +/- 0.04 degrees C, p < 0.001, p = 0.02, respectively). There was no significant difference in deltaT between patients with acute myocardial infarction and unstable angina pectoris (p = 0.48). Patients with acute myocardial infarction and unstable angina pectoris showed a significant relationship between deltaT and C-reactive protein (r = 0.59, p = 0.0004). CONCLUSIONS: The variations in intracoronary temperature of the culprit coronary arteries in patients with acute coronary syndrome were higher than those in patients with stable angina pectoris. These variations may be related to inflammation of vulnerable plaque.     

Angiographically evident thrombus following fibrinolytic therapy is associated with impaired myocardial perfusion in STEMI: a CLARITY-TIMI 28 substudy.

AIMS: The presence of residual thrombus following fibrinolytic therapy for ST-segment elevation myocardial infarction (STEMI) may predispose to greater embolization and microvascular dysfunction. METHODS AND RESULTS: We hypothesized that even in the presence of a patent epicardial artery, residual thrombus would be associated with worsened TIMI myocardial perfusion grades (TMPG), independent of epicardial flow. Data were analysed from the angiograms of 2684 patients enrolled in the CLARITY-TIMI 28 trial, with angiographically patent arteries (TIMI 2/3 flow) at a median of 88 h following fibrinolytic therapy. Thrombus in a patent epicardial artery was observed more frequently among patients with shorter times from randomization to angiography, among patients with non-left anterior descending infarctions, and among patients treated with placebo (vs. clopidogrel). Thrombus was associated with more frequent TIMI 2 flow (35.1 vs. 22.1%, P < 0.001), higher corrected TIMI frame counts (CTFC) (42 vs. 33 frames, P < 0.001), and a lower incidence of normal TMPG 3 (48.7 vs. 63.9%, P < 0.001), irrespective of treatment with clopidogrel or placebo. In multivariable analyses, thrombus remained associated with higher CTFC (P < 0.001) and worse TMPG (OR 1.6 for TMPG 0/1/2, P < 0.001) after adjustment for baseline covariates as well as known correlates of TMPG. The association between thrombus and impaired TMPG remained even after further adjustment for CTFC or TIMI flow grade. CONCLUSION: Residual angiographic thrombus following fibrinolytic therapy in STEMI patients is associated with impaired myocardial perfusion, independent of epicardial flow. This finding emphasizes the roles of platelet aggregation and distal embolization in the pathogenesis of microvascular dysfunction in STEMI.     

Usefulness of coronary flow velocity measurement by transthoracic Doppler echocardiography in patients with acute coronary syndrome

OBJECTIVES: To evaluate the usefulness of left anterior descending coronary artery (LAD) flow measured by transthoracic Doppler echocardiography (TTDE) in patients with acute coronary syndrome. METHODS: Thirty consecutive patients with acute coronary syndrome in the LAD territory and unstable angina or non-ST-segment elevation myocardial infarction required decisions on the need for emergency coronary angiography. The diastolic peak flow velocity was measured in the distal segment of the LAD under guidance of color Doppler echocardiography in the emergency room. If LAD flow was not detected within 10 min, the coronary flow was judged as under the detection limit. The results of TTDE were compared with the Thrombolysis in Myocardial Infarction (TIMI) grade of LAD determined by coronary angiography, which was performed within 1 week (mean 2.5 +/- 1.5 days) in all patients. RESULTS: Coronary flow was not detected by TTDE in six patients who had TIMI grade 1 or 0. The diastolic peak flow velocity in 19 patients with TIMI 3 was higher than that in 5 patients with TIMI 2 (20.1 +/- 4.1 vs 10.9 +/- 2.3 cm/sec, p = 0.0001). A diastolic peak flow velocity of 14 cm/sec was the optimal cut-off value for the prediction of TIMI 3, with a sensitivity of 95% and a specificity of 100%. CONCLUSIONS: Coronary flow velocity measured by TTDE closely reflected the TIMI grade. Coronary flow measurement by TTDE is useful to decide the treatment strategy for patients with acute coronary syndrome in the emergency room.     

Accelerated infusion of streptokinase in acute myocardial infarction results in better TIMI flow grade in infarct-related artery

Bolus followed by rapid infusion of tissue plasminogen activator results in higher grade of TIMI flow in infarct-related artery as compared to slow infusion. In the present study, an accelerated regimen of streptokinase given over 15 minutes was compared with conventional infusion over one hour in 47 patients presenting within 12 hours of acute myocardial infarction. Forty-seven patients (44 males, 3 females; mean age 54.0 +/- 1.1 years) were randomly allocated to receive 1.5 million units of streptokinase either over 15 minutes (group 1, n = 24) or over one hour (group 2, n = 23) at a mean interval of 5.4 +/- 3.6 hours after onset of symptoms. All the patients received aspirin and intravenous heparin (1000 U/hr) for 96 hours after thrombolysis. Coronary angiography was performed in 43 patients (22 in group 1, 21 in group 2) prior to discharge from the hospital (mean 7 +/- 2.1 days after acute myocardial infarction) and patency of the infarct-related artery and grade of TIMI flow were determined. Infarct-related artery was patent (TIMI 2/3 flow) in 19 (86.4%) patients in group 1 as compared to 12 (57.1%) in group 2 (p < 0.05). TIMI grade 3 flow in the infarct-related artery was present in 13 (59.1%) in group 1 as compared to 7 (33.3%) in group 2 (p = 0.1). There was no significant difference between group 1 and 2 in time of presentation (mean 5.3 +/- 3.9 hrs vs 5.5 +/- 3.2 hrs), time to needle in hospital (25.6 +/- 11.2 min vs 26.3 +/- 6.2 min), site of infarct (anterior myocardial infarction 12 in group 1 vs 11 in group 2), relief of pain at 90 min (13 vs 12), more than 50 percent reduction of ST elevation at 90 minutes (17 vs 12) and left ventricular ejection fraction (48.8 +/- 9.1% vs 49.8 +/- 16.0%), respectively. Streptokinase was well tolerated in both the groups, although hypotension was more common with the accelerated regimen (5 in group 1 vs 3 in group 2; p = NS). Thus, 'accelerated' streptokinase given over 15 minutes in patients presenting within 12 hours of acute myocardial infarction is well tolerated and results in higher grades of TIMI flow in the infarct-related artery as compared to the "conventional" one-hour infusion regimen.     

A pilot study with a new, rapid-exchange, thrombus-aspirating device in patients with thrombus-containing lesions: the Diver C.E. study.

BACKGROUND: In patients with acute coronary syndromes (ACS), distal embolization of thrombotic material is more likely to play a key role in the pathogenesis of myocardial no-reflow during percutaneous coronary intervention (PCI). Thus, interventional techniques able to reduce thrombus burden at the culprit vessel might improve final myocardial reperfusion. OBJECTIVE: To evaluate a new rapid-exchange thrombus-aspirating catheter, the Diver C.E., in patients with thrombotic coronary lesions undergoing PCI. METHODS: Fifty patients with acute myocardial infarction (n = 44) or with non-ST-elevation ACS and angiographic evidence of coronary thrombus (n = 6) undergoing urgent PCI were prospectively enrolled. The Diver C.E. was used to aspirate coronary thrombus from the culprit lesion after placement of the guidewire. Adjunctive balloon inflations and stent implantation were used to achieve good angiographic result. Angiographic coronary flow (by means of TIMI score and corrected TIMI frame count, cTFC), thrombus score (TS), and myocardial perfusion (by means of postintervention myocardial blush grade, MBG) were assessed in all patients. RESULTS: The device could be successfully employed in 96% of the cases (48/50) and yielded significant (P < 0.0001) acute reduction in thrombus burden (TS: predevice 3.5 +/- 0.8, postdevice 2.5 +/- 0.9) and improvement in coronary flow (TIMI grade: predevice 1.0 +/- 0.9, postdevice 2.0 +/- 0.9; CTFC predevice 71 +/- 31, postdevice 39 +/- 26). Final TIMI grade 0-1 was observed in one patient only (2%). A significant (P = 0.02) correlation was found between preintervention TS and efficacy of thrombus aspiration. A more pronounced acute reduction of thrombus burden after thrombus aspiration (TS reduction > or = 2) was associated with a better postintervention angiographic myocardial perfusion (MBG 2.3 +/- 0.9 vs 1.7 +/- 0.8; P = 0.05). CONCLUSIONS: This new, easy-to-use, device is able to reduce thrombus burden and to improve coronary flow in patients with thrombus-containing lesions. The improvement in myocardial perfusion associated to greater thrombus removal highlights the importance of thrombus aspiration in the management of thrombus-burdened coronary lesions.     

Coronary ectasia resulting in thrombotic coronary occlusion after warfarin interruption: a case report

A 68-year-old man taking aspirin and warfarin for ectatic right coronary artery complained of chest pain and was admitted to our hospital with acute myocardial infarction. He had discontinued taking warfarin due to nail bleeding for a month. Coronary angiography revealed total occlusion at segment 3 of the ectatic right coronary artery with massive thrombus. Because of unsuccessful reperfusion by an aspiration device, a 5F straight catheter was inserted into the ectatic right coronary artery to aspirate the massive thrombus, and Thrombolysis in Myocardial Infarction grade 3 flow reperfusion was obtained. Intravascular ultrasonography showed "moyamoya" vessels in the ectatic right coronary artery, suggesting an abnormal coronary flow pattern, but there was no evidence of unstable plaque. Warfarization should be considered to treat ectatic coronary artery.     

The use of a distal occlusion balloon protection device in acute coronary syndrome

We report our early experience in using the PercuSurge GuardWire Plus system as a distal protection device in patients with acute coronary syndrome and acute myocardial infarction. Forty-three patients received percutaneous coronary intervention with the GuardWire Plus system. Thirteen had unstable angina, five had non-Q myocardial infarction and 25 had ST segment elevation myocardial infarction. Forty-one target lesions were in native coronary vessels and two were in saphenous vein grafts. Total occlusion occurred in 18 patients. The mean occlusion time by the distal protective balloon was 262.8 +/- 114.1 s. Preoperatively, TIMI 0 flow was present in 18, TIMI II flow in two and TIMI III flow in 23 patients. Post-operatively, TIMI II and TIMI III flow were established in two and 41 patients, respectively. All procedures were successful and the GuardWire Plus system was successfully deployed in all but two patients. There was no procedure-related major adverse clinical event. There was no major adverse clinical event at 30 days. There was no device-related complication. We believe that the GuardWire Plus system is safe and feasible in patients with acute coronary syndrome and acute myocardial infarction.     

TIMI frame count immediately after primary coronary angioplasty as a predictor of functional recovery in patients with TIMI 3 reperfused acute myocardial infarction

OBJECTIVES: The purpose of this study was to evaluate whether higher coronary blood flow, estimated by the corrected Thrombolysis In Myocardial Infarction (TIMI) frame count (CTFC), is related to better functional and clinical outcome after successful percutaneous transluminal coronary angioplasty (PTCA) in patients with acute myocardial infarction (AMI). BACKGROUND: Experimental studies have found that functional recovery of the infarcted myocardium was associated with increased blood flow (reactive hyperemia) to the infarcted bed shortly after reperfusion. METHODS: We measured CTFC immediately after successful (TIMI 3) primary PTCA in 104 consecutive patients with their first AMI. Wall motion score index (WMSI) and the presence of pericardial effusion were assessed by two-dimensional echocardiography before and one month after PTCA. RESULTS: The patients were divided into two groups according to mean CTFC for corresponding coronary artery of the control group: TIMI 3 slow group (45 patients, 40 > CTFC > or = 23) and TIMI 3 fast group (59 patients, CTFC < 23). There were no significant differences in the baseline characteristics and WMSI before reperfusion between the two groups. Improvement of WMSI in the TIMI 3 fast group was significantly greater than that of the TIMI 3 slow group (1.33 +/- 0.52 vs. 0.60 +/- 0.34, p < 0.001). Pericardial effusion and intractable heart failure were observed more frequently in the TIMI 3 slow group than in the TIMI 3 fast group (27 vs. 10%; p < 0.05, 36 vs. 17%; p < 0.05). Corrected TIMI frame count, assessed as a continuous variable, had a significant correlation with the change in WMSI (r = 0.60, p < 0.001) after adjusting for age, gender, history of hypertension, history of diabetes, elapsed time to PTCA, collateral grade, presence of antegrade flow before PTCA and number of diseased vessels. CONCLUSIONS: Lower CTFC of the infarct-related artery immediately after PTCA was associated with greater functional recovery; and hence, CTFC can predict clinical and functional outcome in patients with successful PTCA.