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.     

冠脉造影血流TIMI分级及计帧值与多普勒血流速度的相关性

目的：应用血管内多普勒导丝测量血流速度（DFV）评价冠脉造影血流TIMI分级（TIMI－FG）及其计帧值（TIMI－FC）的准确性。方法：在11只猪的冠状狭窄模型和36例冠脉造影及17例行血管介入治疗的病人，比较TIMI－FG，TIMI－FC与DFV的相关性。结果：（1）随着动物模型充盈球囊造成血管狭窄程度的加重，DFV减慢，TIMI－FG下降，TIMI－FG变大，P均＜0．01；（2）17例病人25支血管在介入治疗后，DFV增加，TIMI－FG上升，TIMI－FC变小（P＜0．05－＜0．01）；（3）TIMI－FC与DFV呈负相关（冠心病人r=-0.49-0.58,猪r=-0.41)；而TIMI－FC变化差值与DFV变化差值相关性则有提高（冠心病人r=-0.62-0.66,猪r=-0.71)。结论：冠脉造影TIMI－FC推测冠心病流速度具有一定准确性，对血流速度变化的推测更佳。     

Techniques in the Angiographic Analysis of Coronary Flow: Past, Present, and Future

The current method of analyzing coronary flow data is the TIMI flow grade method. This method is convenient and easy to apply, but there are limitations to this categorical method of analyzing coronary artery flow. We have developed a new method of analyzing coronary blood flow called the "TIMI frame count." Using the TIMI frame counting method, we have shown that the flow in the coronary arteries is in fact distributed as a continuous variable and that there are nondiscrete categories of slow and fast flow. This article discusses the statistical basis for the development of this new, simple, and continuous index of coronary flow and provides a "how-to manual" describing the practical implementation of the new TIMI frame count method. We also describe simple new techniques for measuring the distance to the landmark used for TIMI frame counting. Knowing the distance and the time from the TIMI frame count, velocity can easily be calculated. Tables are provided that can be used for these calculations on-line in the cardiac catheterization laboratory. If the diameter is known, flow can also be calculated from these tables. We also describe new applications of marker wires to measure distance and velocity .     

冠状动脉造影血流TIMI分级及其计帧值与血管内多普勒血流速度相关性

目的 :应用血管内多普勒导丝测量血流速度评价冠状动脉造影血流TIMI分级 (TIMI FG)及其计帧值 (TIMI FC)准确性。方法 :在 11只猪右冠状动脉狭窄动物模型和 36例冠状动脉造影及 17例行血管介入治疗患者中 ,比较TIMI FG和TIMI FC与血流速度相关性。结果 :①随动物模型充盈球囊造成血管狭窄程度加重 ,血流速度减慢、TIMI FG下降、TIMI FC变大。② 17例患者 2 5支血管介入治疗后 ,血流速度增加 ,TIMI FG上升、TIMI FC变小。③TIMI FC与血流速度呈中度负相关 ;而TIMI FG和TIMI FC变化值与血流速度变化值相关性提高。结论 :冠状动脉造影TIMI FC判断血流速度具有一定准确性 ,尤其对血流速度变化更佳     

Repeated assessment of coronary flow velocity pattern in patients with first acute myocardial infarction

OBJECTIVES: The aim of this study was to evaluate the coronary blood flow velocity pattern immediately and 24 h after percutaneous transluminal coronary angioplasty (PTCA) for acute myocardial infarction (AMI) in relation to myocardial reperfusion and follow-up left ventricular (LV) function. BACKGROUND: Analysis of coronary blood flow velocity pattern after AMI may provide information about microvascular damage and the occurrence of a reperfusion injury. METHODS: Measurement of coronary blood flow velocity pattern was performed immediately after PTCA and after 24 h in 25 patients with first AMI using a Doppler guidewire. Measurements were related to reperfusion determined by intravenous myocardial contrast echocardiography (MCE) performed before PTCA and at 24 h and to LV function at four weeks. RESULTS: Using MCE, 13 patients showed reperfusion and 12 patients showed nonreperfusion. Compared with patients with reperfusion, patients with MCE nonreperfusion had a lower systolic peak flow velocity immediately after PTCA (10.0 +/- 0.3 cm/s vs. 19.3 +/- 0.8 cm/s, respectively) and after 24 h (12.3 +/- 0.4 cm/s vs. 21.3 +/- 0.1 cm/s, respectively, p = 0.0022), more frequent early systolic retrograde flow (6/12 vs. 0/13, p = 0.0052 immediately after PTCA and 24 h later) and a shorter diastolic deceleration time immediately after PTCA (483 +/- 6 ms vs. 737 +/- 0 ms, respectively) and after 24 h (551 +/- 9 ms vs. 823 +/- 2 ms, respectively, p = 0.0091). Similarly, patients with impaired LV function at four weeks had altered coronary flow pattern compared with patients with preserved function. The coronary flow velocity pattern showed a tendency for improvement after 24 h in the reperfusion and the nonreperfusion groups. CONCLUSIONS: The coronary flow velocity pattern immediately and 24 h after PTCA for AMI relates to myocardial perfusion determined by MCE and LV function at four weeks. The flow velocity pattern shows slight improvement during the first 24 h after revascularization, indicating the absence of a major reperfusion injury.     

Intracoronary verapamil for reversal of no-reflow during coronary angioplasty for acute myocardial infarction.

No-reflow is a frequent observation during direct PTCA for acute myocardial infarction (AMI) and associated with a poor clinical outcome. This study assesses the value of verapamil for reversal of no-reflow during PTCA for AMI. In a consecutive series of 212 direct or rescue PTCAs for AMI, a TIMI flow grade < 3 was observed in 23 patients (10.8%). Ten of these patients had received GP IIb/IIIa antagonists before PTCA. Seven patients with AMI and TIMI grade 3 flow served as controls. All lesions were treated by stents. In 18 patients with systolic blood pressure > 90 mm Hg, nitroglycerine (0.1 mg i.c.) was given. Verapamil (1 mg over 2 min) was given via an infusion catheter distal to the angioplasty site. Before and after nitroglycerine, after verapamil, and 15 min later coronary flow was assessed by the TIMI frame count method (TFC). Nitroglycerine had no effect on TFC. Verapamil reduced TFC from 56 +/- 9 frames to 24 +/- 4 (P < 0.001). In controls, TFC did not change significantly. The TIMI flow grade was restored to TIMI flow grade 3 in 65%. In two of seven right coronary and one of three circumflex arteries, intermittent AV block II occurred during verapamil injection, which disappeared after atropine. No-reflow after PTCA for AMI can be reversed by intracoronary verapamil. This supports the hypothesis that no-reflow is caused by acute microvascular dysfunction probably because of a disorder in calcium homeostasis or microvascular spasm.     

Effect of reactive hyperemia after coronary recanalization on myocardial tissue reperfusion by thrombolysis in myocardial infarction flow grade in acute myocardial infarction

Thrombolysis In Myocardial Infarction (TIMI) flow grade is widely used to evaluate myocardial tissue reperfusion in acute myocardial infarction (AMI), but the current grading system is incomplete. Therefore, we clarified the regulation of epicardial coronary flow velocity with the progression of microvascular dysfunction in AMI. We studied 36 patients with first anterior AMI. After intervention, we assessed TIMI flow grade and measured average peak velocity (APV) at baseline and after infusion of adenosine triphosphate (48 microg; baseline and hyperemic APVs, respectively) with a Doppler guidewire. We performed myocardial contrast echocardiography after 2 weeks to assess microvascular integrity (good reflow vs no reflow) and left ventriculography at admission and discharge (24 +/- 2 days) to measure regional wall motion (SD/chord). Patients were classified into 3 groups based on TIMI flow grade and microvascular integrity: TIMI grade 3 flow/good reflow (n = 16), TIMI grade 3 flow/no reflow (n = 12), and TIMI grade 2 flow (n = 8). Baseline APV was comparable in the patients with TIMI grade 3 flow but hyperemic APV was higher in patients with TIMI grade 3 flow/good reflow than in those with TIMI grade 3 flow/no reflow (hyperemic APV 59.3 +/- 25.8 vs 32.8 +/- 8.9 cm/s, p <0.01). All patients with TIMI grade 2 flow showed no reflow and the lowest values of baseline and hyperemic APVs. Regional wall motion at discharge was higher in patients with TIMI grade 3 flow/good reflow than in those with TIMI grade 3 flow/no reflow and TIMI grade 2 flow (-1.44 +/- 0.70, -2.69 +/- 0.31, and -2.88 +/- 0.48 SD/chord, respectively, p <0.01). In conclusion, compensatory reactive hyperemia preserves epicardial coronary flow velocity even in patients with microvascular damage, and with the progression of damage, this compensatory hyperemia can no longer preserve epicardial coronary flow velocity, and baseline APV is decreased in TIMI grade 2 flow.     

“Rescue” Utilization of Abciximab for the Dissolution of Coronary Thrombus Developing as a Complication of Coronary Angioplasty

Objectives. This study sought to test the effect on thrombus score of the “rescue” utilization of the glycoprotein IIb/IIIa antagonist abciximab given to patients in whom intracoronary thrombus has developed as a complication after percutaneous transluminal coronary angioplasty (PTCA) and to determine its clinical utility.

Background. Abciximab is effective in the prevention of acute ischemic complications when given prophylactically to patients during high risk PTCA. However, its ability to therapeutically dissolve newly formed intracoronary thrombus occurring as a complication after PTCA is not known.

Methods. We performed an observational study in 29 consecutive patients who received abciximab (0.25 mg/kg body weight intravenous bolus, followed by a 12-h infusion at 10 μg/min) after attempted PTCA caused either the new development or further progression of thrombus. Angiograms were analyzed to determine thrombus score and Thrombolysis in Myocardial Infarction (TIMI) flow grade before and after abciximab. Procedural and clinical success and long-term outcome were also determined.

Results. Thrombus score decreased from 3.0 ± 0.9 (mean ± SD) to 0.86 ± 0.92 (p < 0.001), and TIMI flow grade increased from 2.5 ± 0.7 to 2.9 ± 0.3 (p = 0.008). No instances of distal embolization or no-reflow were noted. The procedural success (≤50% residual stenosis) rate was 97%. The clinical success (procedural success with no in-hospital myocardial infarction, bypass surgery or death) rate was 93%.

Conclusions. Dissolution of thrombus and restoration of TIMI grade 3 flow were readily achieved after administration of abciximab when delivered in a “rescue” manner after the development of thrombosis after PTCA. This novel use of abciximab will need to be validated in randomized trials.     

Differences in TIMI frame count following successful reperfusion with stenting or percutaneous transluminal coronary angioplasty for acute myocardial infarction

The Thrombolysis In Myocardial Infarction (TIMI) flow grade achieved in the infarct-related artery (IRA) during reperfusion therapy for acute myocardial infarction (AMI) is directly related to myocardial salvage. Recently, several series have demonstrated the safety of stenting in AMI and documented a larger postprocedure luminal diameter than that found at angioplasty, although no study has compared the effect of PTCA and stenting in AMI on flow characteristics of the IRA. The residual stenosis and the number of frames required to opacify standardized angiographic landmarks normalized for vessel length (corrected TIMI frame count) or compared with flow in a corresponding normal coronary artery (TIMI frame count index) were determined for the IRA of 39 patients who underwent angioplasty or stenting for AMI. Baseline characteristics were similar for the 20 patients who underwent stenting and the 19 patients who underwent percutaneous transluminal coronary angioplasty. After intervention, the luminal diameter was greater (3.24 vs 2.09 mm, p <0.0001) and the residual stenosis was less (-9.4% vs. 26.7%, p <0.0001) after stenting than after percutaneous transluminal coronary angioplasty. These changes in vessel geometry were associated with a lower corrected TIMI frame count (16.1 vs 30.7, p <0.002) and a lower TIMI frame count index (0.68 vs 1.3, p <0.002). Thus, stenting in AMI is associated with a greater postprocedure luminal diameter and improvement in coronary blood flow as measured by the TIMI frame count method.     

Assessing myocardial perfusion with the transthoracic Doppler technique in patients with reperfused anterior myocardial infarction: comparison with angiographic, enzymatic and electrocardiographic indices.

AIMS: Doppler guidewire studies demonstrated that the no-reflow phenomenon in acute myocardial infarction is associated with characteristic coronary blood flow pattern. We investigated the potential of coronary flow measurement with transthoracic Doppler technique to detect the no-flow in the patients with reperfused infarction, and compared it to that of other modalities. METHODS AND RESULTS: We performed intracoronary myocardial contrast echocardiography after successful primary coronary intervention in the 94 patients with first, anterior wall infarction. Coronary blood flow in the left anterior descending artery was detected with transthoracic Doppler echocardiography within 24 h after reperfusion in 83 patients (88.3%). Twenty-two patients with the no-reflow had significantly lower systolic peak velocity (5.1 +/- 4.2 vs. 8.1 +/- 6.2 cm/s, p = 0.04), higher diastolic peak velocity (38.2 +/- 10.3 vs. 30.8 +/- 15.7 cm/s; p = 0.04), and shorter diastolic deceleration time (134 +/- 41 vs. 424 +/- 202 ms; p < 0.0001) than those with good-reflow. Systolic flow reversal was more frequently observed in those with no-reflow (18.2% vs. 3.3%, p = 0 .02). Diastolic deceleration time < 185 ms detected the no-reflow with far higher sensitivity/specificity (95.5%/95.1%) than TIMI frame count (45.5%/91.8%), ST resolution (54.5%/73.8%) and creatinine kinase-MB (54.5%/88.5%). CONCLUSION: Analysing coronary blood flow pattern can detect the no-reflow after anterior infarction better than other angiographic, electrocardiographic and enzymatic modalities.     

Evaluation of an active coronary perfusion balloon device using Doppler flow wire during PTCA

The aim of this study was to assess whether active coronary perfusion catheters (APC) can provide a sufficient coronary flow in large caliber vessels during balloon inflation. To prevent myocardial ischemia during PTCA, these APC may be employed. However, it is as yet unknown whether the active flow rate of these devices approaches the flow rate prior to PTCA during balloon inflation. Therefore, we measured the efficacy of the APC during balloon inflation in vessels supplying a large amount of myocardium. In 12 patients (1 female, 11 males, 53 ± 12.6 yr) with stenosed vessels (average diameter 3.4 ± 0.26 mm), the coronary flow velocity was measured using a 0.014“ Doppler guidewire, which was placed distally bypassing the balloon of the APC. The active perfusion balloon catheter was advanced through a 7F guiding catheter along a 0.014” guidewire. After removal of the guidewire, arterial blood being withdrawn from the side port of the femoral angioplasty sheath was pumped through the catheter to the distal coronary vessel. The perfusion volumes of the pump were set to different levels between 30 to 60 ml/min. Intracoronary flow rate was calculated by the angiographically assessed vessel luminal area × average peak velocity × 0.5. The mean coronary flow rate prior to PTCA was 43 ± 17.7 ml/min. Maximum flow during PTCA was 55 ± 19.6 ml/min. We found a good correlation between the preset external pump rate and the coronary flow in situ (r=0.92). Pre-PTCA flow rates were achieved in 11 of 12 patients (92%) during balloon inflation. No relevant decrease in the arterial pressure occurred during dilation times of 4.6 ± 1.63 min. Only two patients showed significant ECG changes during these balloon inflations. After an average follow-up period of 13 ± 6.3 mo, only one patient (8%) had a significant re-stenosis requiring the implantation of a stent. The combination of intravascular Doppler velocity measurements with quantitative coronary angiography offers the opportunity of exact online flow registration during angioplasty. Using APC, it is possible to maintain a sufficient coronary flow in the distal vessel during balloon inflation even in large vessels. Therefore, as compared with mechanical circulatory assist devices, coronary assist by APC is a little invasive, but according to our measurements it might be a sufficient tool for performing PTCA also in high-risk patients. Cathet. Cardiovasc. Diagn. 42:84-89, 1997. © 1997 Wiley-Liss, Inc.     

Variations of coronary blood flow measured by intracoronary doppler in the acute phase of myocardial infarction before and after revascularization by angioplasty]

The authors studied the changes in coronary blood flow before, during and after reperfusion by angioplasty of the disease coronary vessel responsible for myocardial infarction using intracoronary Doppler. Forty patients aged 60.2 +/- 15.4 years, admitted for primary myocardial infarction (inferior: 22, anterior: 18) were included. Before reperfusion, the peak velocity of the collateral coronary circulation was 14.8 +/- 8.1 cm/s. The flow was bidirectional, mainly retrograde (N = 32), negative (N = 1) or positive (N = 5). The five Rentrop 0 patients had velocities similar to Rentrop 1, 2 or 3 patients (Rentrop 0: 14.9 +/- 6.4 cm/s; Rentrop 1: 12.3 +/- 9.9 cm/s; Rentrop 2: 15.2 +/- 8.2 cm/s; Rentrop 3: 17.5 +/- 6.3 cm/s). Patients with TIMI 3 reperfusion flow had the highest APV Doppler velocities (average peak velocities during the cardiac cycle) (APV TIMI 3 = 20.2 cm/s versus APV TIMI 1 and 2 = 10.9 cm/s, p = 0.05). After angioplasty, the APV was 18.7 +/- 10.4 cm/s (p < 0.001). Diastolic flow was dominant. Seventeen patients had retrograde systolic flow, 12 had minimal systolic flow and 17 had a steep diastolic deceleration slope. Intracoronary Doppler demonstrates the wide range of coronary flow in TIMI 3 flow patients, both from the morphological and the quantitative points of view, which seems to be independent of the presence of residual stenosis and could be related to abnormalities of the microcirculation. This could allow identification of a subgroup of patients at high risk and candidates for a complementary therapeutic intervention (intra-aortic balloon pumping...).     

Coronary Flow Reserve During Coronary Angioplasty in Patients With a Recent Myocardial Infarction: Relation to Stenosis and Myocardial Viability

Objectives. In the present study, we examined post-stenotic coronary flow before and after percutaneous transluminal coronary angioplasty (PTCA) in patients with and without a recent myocardial infarction (MI) and related it to stenosis severity and residual viability.

Background. Post-stenotic coronary blood flow velocity reserve (CFVR) has been used with success to estimate functional stenosis severity in patients with stable angina. However, in patients with a recent MI, the impaired coronary vasodilator response of the reperfused myocardium may substantially alter the flow dynamics of the infarct-related artery.

Methods. Distal coronary flow velocities were recorded before and after PTCA in 36 patients at day 13 ± 7 (mean ± SD) after acute MI and in 38 patients without MI. The CFVR was assessed by the ratio of distal hyperemic to baseline average peak velocity, using a 0.014-in. Doppler guide wire. Stenosis severity was analyzed by quantitative coronary angiography, and infarct size was assessed scintigraphically.

Results. For similar angiographic stenosis severity, pre- and post-PTCA values of CFVR were significantly lower in patients with than without MI: 1.22 ± 0.26 versus 1.50 ± 0.45 before PTCA (p < 0.05) and 1.72 ± 0.43 versus 2.21 ± 0.74 after PTCA, respectively (p < 0.01). Although CFVR increased significantly (p < 0.0001) after angiographically successful PTCA in both study groups, abnormal CFVR (≤2.0) was still observed in 80% of patients with MI and in 44% of those without MI (MI vs. no MI, p = 0.001). Patients with an extensive infarction (relative infarct size ≥50%) and those with a small infarction (relative infarct size <50%) had comparable levels of post-PTCA CFVR (1.6 ± 0.3 vs. 1.8 ± 0.5, p = NS). Among a variety of factors, angiographic stenosis severity was the most important determinant of CFVR in both study groups.

Conclusions. In patients with a recent MI, CFVR was significantly lower than in those without MI, both before and after PTCA. Besides the presence of this postreperfusion-related impairment of the coronary vasodilating response, CFVR was mainly influenced by stenosis severity and not by residual viability.

(J Am Coll Cardiol 1996;28:1712–9)>     

Functional, angiographic and intracoronary doppler flow characteristics in symptomatic patients with myocardial bridging: Effect of short-term intravenous beta-blocker medication

Objectives. We sought to define the effects of short-term beta-adrenergic blocking medication on intracoronary flow characteristics, clinical symptoms and angiographic diameter changes in patients with severe myocarding bridging of the left anterior descending coronary artery.

Background. Controversy exists regarding the pathophysiology, clinical relevance and optimal therapy in symptomatic patients with myocardial bridges because antianginal drugs have not been systematically tested.

Methods. In 15 symptomatic patients with myocardial bridging of the left anterior descending coronary artery, maximal lumen diameter reductions were evaluated by quantitative coronary angiography. There were no angiographic signs of coronary artery disease. Coronary blood flow velocities (using a 0.014-in. [0.035 cm] Doppler guide wire) were measured at rest, during atrial pacing and during intravenous administration of a short-acting beta-blocker (esmolol, 50 to 500 μg/kg body weight per min) with continuous atrial pacing.

Results. The maximal angiographic systolic lumen diameter reduction within the myocardial bridges was 83 ± 9% at rest, with a persistent diastolic diameter reduction of 41 ± 11% (mean ± SD). Short-term intravenous beta-blocker therapy decreased the diameter reduction during both systole (from 83 ± 9% to 62 ± 11%) and diastole (from 41 ± 11% to 30 ± 9%, both p < 0.001). The average diastolic peak flow velocity was higher within the myocardial bridges (33 ± 13 cm/s) than the proximal (26 ± 13 cm/s) and distal bridges (17 ± 4 cm/s, both p < 0.001). During tachypacing average diastolic peak flow velocity increased within the bridged segments to 63 ± 21 cm/s versus 29 ± 12 cm/s in the proximal and 20 ± 4 cm/s in the distal bridges (both p < 0.001). Beta-receptor blockade produced a return to baseline values (average diastolic peak flow velocity within bridge 35 ± 16 cm/s, p < 0.001). ST segment changes and symptoms were abolished with beta-blocker administration.

Conclusions. In patients with myocardial bridges, administration of short-acting beta-blockers during atrial pacing alleviates anginal symptoms and signs of ischemia. This effect was mediated by a reduction of vascular compression and maximal flow velocities within the bridged coronary artery segment.     

Cardiac Release and Kinetics of Endothelin After Uncomplicated Percutaneous Transluminal Coronary Angioplasty

This study was designed to assess the release kinetics of endothelin after percutaneous transluminal coronary angioplasty (PTCA) and to prove the coronary endothelium as the source of the endothelin release. Twenty-seven patients with single-vessel coronary artery disease underwent PTCA. Endothelin, troponin T, myoglobin, and creatine phosphokinase paired blood samples were withdrawn from the coronary sinus and a peripheral vein before the balloon maneuver and at 1, 5, 10, 30, 45 minute(s), and at 1, 2, 3, 6, 12, and 24 hour(s) after the last balloon maneuver. Myocardial ischemia was monitored by means of cardiac lactate metabolism and 12-lead electrocardiogram. Thirteen patients who underwent a diagnostic cardiac catheterization served as a control group. In the left coronary artery, PTCA (n = 19) endothelin concentrations increased from 4.1 pg/ml as a common mean baseline level before intervention to 13.9 ± 2.6 pg/ml (mean ± SD) in the coronary sinus and 7.9 ± 2.2 pg/ml (mean ± SD) in the peripheral vein at 1 minute after the intervention (p <0.001). The levels remained elevated for 3 hours with higher coronary sinus than peripheral venous concentrations due to persistant cardiac endothelin release. PTCA of the right coronary artery (n = 8) also led to an instantaneous endothelin increase from a mean concentration of 4.4 before intervention to 8.3 pg/ml after intervention with identical coronary sinus and peripheral venous levels (p <0.001). Endothelin levels gradually decreased to normal within 6 hours. No patient developed a measurable myocardial ischemia or a myocardial infarction. In the control group all parameters remained unchanged. Uncomplicated PTCA was followed by a significant cardiac endothelin release that seems to indicate endothelial injury and not myocardial ischemia.     

中-重度主动脉瓣反流患者的主动脉根部形态与冠状动脉血流速度的关系

目的:探讨中-重度主动脉瓣反流患者的冠状动脉血流速度变化,同时了解主动脉根部形态对冠状动脉血流速度的影响.方法:收集我院2018年8月至2019年5月期间中-重度主动脉瓣反流患者41例(反流组),术前行经食道三维超声心动图检查,通过半自动方法获得主动脉根部形态参数.同时选取20例主动脉瓣功能正常的院内就诊者作为对照组,...     

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.     

Prevalence of microvascular disease in patients with significant coronary artery disease

Coronary flow velocity reserve (CFVR) measurement using intracoronary Doppler techniques has been increasing accepted for the assessment of physiological significance of epicardial stenosis and the functional changes after coronary interventions. However, large discrepancy exists concerning the acute changes of CFVR immediately after intervention. The purpose of this study was to investigate the prevalence of microvascular dysfunction in patients with significant coronary artery disease. Intracoronary Doppler flow measurements were performed in a total of 212 patients who underwent coronary interventions because of significant epicardial stenosis using 0.014" Doppler flow wire (Cardiometrics, Inc, Mountain View, CA). Intracoronary bolus injection of adenosine (12 micrograms for the right coronary and 18 micrograms for the left coronary arteries) was used to induce hyperemic reaction. CFVR was registered as the ratio of average peak velocity during hyperemia (hAPV) to at baseline (bAPV). Successful coronary interventions either by percutaneous transluminal coronary balloon angioplasty (PTCA) or by stenting could significantly improve the CFVR. In 80 patients with PTCA, the bAPV elevated from 16.6 +/- 2.1 cm/s to 20.6 +/- 13.4 cm/s and hAPV from 30.1 +/- 15.9 cm/s to 45.2 +/- 17.7 cm/s (both p < 0.001) with PTCA and the CFVR increased from 1.94 +/- 0.78 to 2.58 +/- 0.87 correspondingly (p < 0.001). Significant elevation of coronary flow parameters were also found in 132 patients with subsequent stent implantation (bAPV from 15.3 +/- 6.7 cm/s to 18.7 +/- 9.1 cm/s, hAPV from 28.7 +/- 14.4 cm/s to 44.3 +/- 17.7 cm/s and CFVR from 1.90 +/- 0.70 to 2.59 +/- 0.87, all p < 0.001). Reduction of CFVR (< 3.0) after intervention still existed in 46 (61.3%) of 80 patients after PTCA and 88 (66.7%) of 132 patients after stenting. Moreover, CFVR < 3.0 were found in 50 (45.9%) of 109 reference vessels in patients with single vessel disease. Significant improvement of coronary flow velocity and coronary flow velocity reserve could be obtained after successful angioplasty. However, microvascualr dysfunction existed in a large proportion of patients either in normal reference vessels or in target vessels after interventions.     

Comparison of Collateral Vascular Responses in the Donor and Recipient Coronary Artery During Transient Coronary Occlusion Assessed by Intracoronary Blood Flow Velocity Analysis in Patients

Objectives. This study was designed to evaluate the hemodynamic variables of the collateral circulation during acute coronary occlusion.

Background. There is limited information on the physiology of the collateral circulation in coronary artery disease.

Methods. Angiography of the contralateral donor artery was performed before and during balloon coronary occlusion in 57 patients with one-vessel disease. Recruitable collateral flow was assessed during coronary occlusion by blood flow analysis of the contralateral donor artery (n = 19) or the ipsilateral recipient artery (n = 15), or both (n = 23), using a Doppler catheter or guide wire. Ischemia was evaluated by the ST segment shift (≥0.1 mV) on a 12-lead electrocardiogram at 1 min of coronary occlusion.

Results. The presence (n = 39), compared with the absence (n = 18), of recruitable collateral vessels was associated with an increase of blood flow velocity in the donor artery (20 ± 19% vs. 4.8 ± 5.9% [mean ± SD], p = 0.003) and the recipient artery (velocity integral 7.2 ± 5.5 vs. 2.8 ± 2.2 cm, p = 0.02) related to a reduced relative collateral vascular resistance (9.2 ± 10 vs. 20 ± 11, p = 0.003). Collateral flow in the donor artery yielded a similar predictive value for recruitability of collateral vessels as collateral flow determined in the recipient artery or the coronary wedge/aortic pressure ratio (areas under the receiver operating characteristics curves 0.76 ± 0.07, 0.78 ± 0.08, 0.77 ± 0.07, respectively, p = NS). Collateral flow in the recipient artery was a better predictor for ischemia than collateral flow in the donor artery or angiographic grading of collateral vessels (areas 0.90 ± 0.05, 0.64 ± 0.10, 0.73 ± 0.07, respectively, p < 0.05).

Conclusions. Coronary blood flow velocity analysis of the donor and recipient coronary arteries can characterize the dynamics of the collateral circulation during acute coronary occlusion. The protective effect of recruitable collateral vessels relates to an increase of flow in the donor and recipient coronary arteries due to a reduced collateral vascular resistance. This study underscores the importance of physiologic variables for the evaluation of the function of recruitable collateral vessels.

(J Am Coll Cardiol 1997;29:1528–35)     

Antiischämische Wirkung von Verapamil im Rahmen einer interventionellen Rekanalisation

We report on a 46-year-old male with unstable angina pectoris due to a total proximal occlusion of the left circumflex artery. At the side of a plaque rupture there was a thrombotic occlusion. With PTCA recanalization was possible, but a dissection occurred, therefore coronary stents were implanted. Besides an optimal morphological result and recurrent applications of nitroglycerin, the baseline blood flow velocity declined from initial 16 cm/s to 11 cm/s after PTCA down to 8.4 cm/s after stent implantation. Because peak flow velocity remained almost unchanged, the low baseline velocity ("slow flow phenomenon") did not lead to an impaired coronary flow velocity reserve (CFVR). Only after application of 1 mg verapamil, a sustained flow velocity on a higher baseline level was reached (17 cm/s), at the same time typical signs of ischemia in the ECG (ST-segment depressions) improved. Additionally, in the non-treated LAD there was an increase in coronary blood flow velocity from 10 cm/s up to 25 cm/s. The reduction in coronary blood flow velocity with increasing manipulations might be due to an impairment of the coronary microcirculations with increasing alpha-adrenergic vasoconstriction, a distribution of vasoactive agents and peripheral microembolizations. Only after administration of verapamil, a calcium channel blocker with non-specific anti-adrenergic effects, the slow flow was removed and ECG signs of ischemia improved. The blood flow velocity in the non-treated LAD was low at baseline and improved after verapamil. This phenomenon leads to the conclusion that mechanisms with vasoconstrictive effect are present in the whole coronary system, but these mechanisms are less pronounced in non-treated vessels.