Relation between Perfusion Status of Dysfunctional Myocardium and Coronary Flow Reserve in Acute Myocardial Infarction

BACKGROUND: Dydfunction of microvasculature was frequently observed despite of successful revascularization with alteration of coronary flow dynamics flow dynamics in acute myocardial infarction (AMI). Reduction of coronary vasodilatory reserve was found in poorly perfused infarcted myocardium. The objectives of this study was to evaluate the vasodilatory reserve in infarcted myocardium and determind its relationship to perfusion status of myocardium in early recovery phase of acute myocardial infarction. METHODS: The study subjects consisted of 14 patients with anterior AMI&and 6 controls with atypical chest pain and have normal coronary artery. The coronary flow pattern was assessed using intracoronary Doppler wire and vasodilatory reserve was measured after injection of 18ug of adenosine to infarct-related artery after successful revascularization by percutaneous angioplasty at average 11 days post-AMI After measurement of coronary blood flow pattern, myocardial perfusion status was evaluated by myocardial contrast echocardiography (MCE). Perfusion status by MCE was analysed semiquantitatively and compared to various parameters of coronary flow and vasodilatory reserve of infarct-related artery. RESULTS: After successful revascularization, perfusion defect by MCE was observed in 50% (n=7) of patients. The vasodilatory reserve was lower in patients with perfusion defect by MCE than those of patients without perfusion defect (p<0.05) and control (p<0.05). There was no difference in coronary flow reserve between patients with no perfusion defect and controls (p=0.54). Coronary flow reserve was more than 2.0 in patients with no perfusion defect and was below 2.0 in patients with perfusion defect except one patients. Coronary flow reserve correlated well with the degree of contrast opacification of left anterior descending artery territory (r=0.80, p=0.005). The increments of peak distolic velocity (r=0.63, p=0.016 vs r=0.3, p=0.29). CONCLUSIONS: These data showed a good correlation of coronary flow reserve with the degree of myocardial perfusion in patients of reperfused acute myocardial infarction. The increments of peak diastolic velocity was important to maintain the coronary flow than that of systolic peak velocity. This suggest that the measurement of vasodilatory reserve by intracoronary Doppler wire is a good method to assess the perfusion status of infarcted myocardium in early recovery phase of AMI.

Relation between Perfusion of Infarcted Myocardium and Exercise-induced ST Shift in Acute Myocardial Infarction

BACKGROUND: It has been demonstrated that within 2 weeks following acute myocardial infarction (AMI), exercise-induced ST-segment depression (STD) indicates subendocardial ischemia in the viable myocardium within infarcted or remote area from the infarction. Exercise-induced ST-segment elevation (STE) in leads with abnormal Q wave is associated with left ventricular dysfunction or aneurysm rather than transmural ischemia. We studied whether each pattern of ST-segment shift on exercise ECG during recovery phase following AMI is correlated with the perfusion status of infarcted myocardium evaluated by myocardial contrast echocardiog-raphy (MCE), regardless of findings of coronary angiography (CAG). METHOD: Study population was consisted of 25 patients with AMI (anteior wall: 11 patients, inferior wall: 14 patients, mean age=57.3+/-8.9years). Patients underwent exercise ECG and coronary angiography at 10 days post-AMI. After CAG, sonicated Hexabrix was injected into both coronory arteries alternatively and 2-D echocardiography was taken in parasternal short axis, apical 4, and 2 chamber views. To analyze the echocardiographic image semiquantitively, left ventricle was divided into 20 segments and perfusion status was graded as good, partial, and no opacification. RESULT: All patients with exercise-induced STE (n=8) in Q-leads had patent infarcted-related artery and poor collaterals on CAG, which was associated with poor or no opacification of infarcted myocardium on MCE. Patients with exercise-induced STD (n=9) frequently had closed infarct-related artery (67%), but good opacification of infarcted myocardium was shown by retrograde perfusion via collaterals, which was commonly seen in patients with multivessel disease. CONCLUSION: In early recovery phase of acute myocardial infarction, exercise-induced ST elevation in Q leads was associated with poor perfusional status in infarcted myocardium, even with patent infarct-related artery on CAG, while exercise-induced ST depression was frequently seen in the good perfusional status despite of closed infarted-related artery, which was commonly observed in patients with multivessel disease.

Relation between Perfusion of Infarcted Myocardium and Exercise-induced ST Shift in Acute Myocardial Infarction

BACKGROUND: It has been demonstrated that within 2 weeks following acute myocardial infarction (AMI), exercise-induced ST-segment depression (STD) indicates subendocardial ischemia in the viable myocardium within infarcted or remote area from the infarction. Exercise-induced ST-segment elevation (STE) in leads with abnormal Q wave is associated with left ventricular dysfunction or aneurysm rather than transmural ischemia. We studied whether each pattern of ST-segment shift on exercise ECG during recovery phase following AMI is correlated with the perfusion status of infarcted myocardium evaluated by myocardial contrast echocardiog-raphy (MCE), regardless of findings of coronary angiography (CAG). METHOD: Study population was consisted of 25 patients with AMI (anteior wall: 11 patients, inferior wall: 14 patients, mean age=57.3+/-8.9years). Patients underwent exercise ECG and coronary angiography at 10 days post-AMI. After CAG, sonicated Hexabrix was injected into both coronory arteries alternatively and 2-D echocardiography was taken in parasternal short axis, apical 4, and 2 chamber views. To analyze the echocardiographic image semiquantitively, left ventricle was divided into 20 segments and perfusion status was graded as good, partial, and no opacification. RESULT: All patients with exercise-induced STE (n=8) in Q-leads had patent infarcted-related artery and poor collaterals on CAG, which was associated with poor or no opacification of infarcted myocardium on MCE. Patients with exercise-induced STD (n=9) frequently had closed infarct-related artery (67%), but good opacification of infarcted myocardium was shown by retrograde perfusion via collaterals, which was commonly seen in patients with multivessel disease. CONCLUSION: In early recovery phase of acute myocardial infarction, exercise-induced ST elevation in Q leads was associated with poor perfusional status in infarcted myocardium, even with patent infarct-related artery on CAG, while exercise-induced ST depression was frequently seen in the good perfusional status despite of closed infarted-related artery, which was commonly observed in patients with multivessel disease.

Clinical Experiences of Intravenous Urokinase in Acute Myocardial Infarction / 대한내과학회지

OBJECTIVES: The most important therapeutic strategy in acute myocardial infarction(AMI) is early recanalization of infarct-related artery(IRA). In Korea the commonly used method for recanalization is urokinase infusion in early phase of disease. But total dosage and method of urokinase infusion are still arbitary. Thus this study was undertaken to evaluate the patency rate of infarct-related artery by urokinase in AMI patients. METHODS: 42 acute myocardial infarction patients were treated with intravenous urokinase(40.000U/kg in 32 patients, 3,00,000U in 10 patients). IRA patency was evaluated with coronary angiography at 90 minutes and 7-10 days after intravenous urokinase. The clinical findings and coronary angiographic findings according to dose of urokinase or pain to time for urokinase injection were analysed prospectively. RESULTS: Mean pain to Door time was 251 minutes and door to urokinase time was 74 minutes. Early patiency of IRA was 61.8%(21/42) and no difference was observed between the dosage of intravenous urokinase. In open IRA group(21 patients) the reocclusion was not observed at 7-10 days later. The ejection fraction on admission was similiar in patent or non-patent IRA group, but follow up ejection fraction was significantly lower in closed IRA group than open IRA group(P=0.0185). Life- threatened bleeding complications were developed in 2 cases(4.8%, I intracranial hemorrhage, 1 gastrointestinal bleeding). CONCLUSION: IRA patency was achieved in 61.8% of acute myocardial infarction by intravenous urokinase as evaluated by coronary angiography. The patency of IRA at 90 minutes was important in preserving the global left ventricular function in early recovery phase of acute myocardial infarction. But large, prospective study may be needed to determine optimal and effective intravenous urokinase dosage in acute myocardial infarction.

Serial Changes of Transmitral Inflow Patterns after Acute Myocardial Infarction

BACKGROUND: Although determination of Doppler echocardiographic transmitral inflow patterns(DETIP) is used as an indrect method assessing LV diastolic function. It is known that DETIP can be affected by certain hemodynamic variables. The aim of this investigation is to assess the serial changes of DETIP and to determine the relation of DETIP with clinical parameter such as initial left ventricular end-diastolic volume(LVEDV), ejection fraction(EF), Killip class and thrombolytic therapy in acute myocardial infarction (AMI) patients. METHOD: Four serial Doppler and 2-D echocardiographic studies were performed at 1 day, 1 week, 1mouth, and 3 months after development of AMI in 24 patients(M:F=19:5, aged 58+/-11 year , 15 anterior MI) and 13 normal adults (aged 47+/-9 years) as reference group. On admission 14 patients were in Killip class I and 10 patients in class II. Thrombolytic therapy with IV urokinase were done in 11 patients. E velocity, pressure half-time (PHT), and isovolumic relaxation time(IVRT) were analyzed and LV systolic function was determined in apical 4 chamber view. RESULTS: DETIP did not change until 1month after development of AMI. However, E/A ratio was decreased, and PHT and IVRT were increased at 3 months after AMI. Doppler transmitral flow parameters were not related with Killip class and LV systolic function. Patiens who recieved urokinase intravenously and who had greater intial LVEDV(>118cm3) showed higher E/A ratio and shorter PHTand IVRT than those who did not. These findings indicate that changes in Doppler transmitral inflow pattern in AMI patients are not uniform over a period of 3 months and thrombolytic therapy causes favorable effect on Doppler transmitral flow parameters. CONCLUSION: Changes in Doppler trasmitral inflow pattern may be variable over post-AMI period and this should be taken into account in evaluating LV diastolic function after AMI. Thrombolytic therapy may improve LV diastolic function in AMI patients.