Temporal changes in myocardial perfusion patterns after AMI.
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Publications and source records attributed to C Marcassa.
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OBJECTIVES: This study investigated the value of sestamibi scintigraphy in assessing residual ischemia after anterior myocardial infarction. BACKGROUND: Serial imaging with sestamibi, the uptake and retention of which correlate with regional myocardial blood flow and viability, has been used to estimate salvaged myocardium and risk area after acute infarction. We recently documented that recovery of perfusion and contraction in the infarcted area may continue well after the subacute phase, suggesting myocardial hibernation. Some underestimation of viability in the setting of hibernating myocardium by sestamibi imaging has been reported. METHODS: We studied 58 patients in stable condition after Q wave anterior infarction. Regional perfusion and function were quantitatively assessed by sestamibi tomography and two-dimensional echocardiography at 4 to 6 weeks and at 7 months after infarction. In sestamibi polar maps, abnormal areas with tracer uptake > 2.5 SD below our reference values were computed at rest and after symptom-limited exercise. On two-dimensional echocardiography the ejection fraction and extent of rest wall motion abnormalities were assessed by a computerized system. All patients had coronary angiography between the two studies. RESULTS: At 7 months the extent of rest sestamibi defect was significantly reduced in 40 patients (69%, group 1) and unchanged in 18 (31%, group 2). Rest wall motion abnormalities and ventricular ejection fraction significantly improved in group 1 but not in group 2. Underlying coronary disease, patency of the infarct-related vessel and rest sestamibi defect extent at 5 weeks were comparable between the two groups. At 7 months, an increase in the reversible (stress-rest defect) tracer defect was observed in group 1 (p < 0.05) despite a smaller stress-induced hypoperfusion (p < 0.05). Reversible sestamibi defects and stress hypoperfusion were unchanged in group 2. In 38 (95%) of 40 group 1 patients, the area showing reversible sestamibi defects at 7 months matched the area showing fixed hypoperfusion at 5 weeks. CONCLUSIONS: The reduction in the rest tracer uptake defect that can occur late after infarction may affect the assessment of ischemic burden by sestamibi imaging early after anterior myocardial infarction.
OBJECTIVES: This study investigated whether exercise-induced myocardial ischemia influences left ventricular remodeling after anterior myocardial infarction. BACKGROUND: The effects of acute and recurrent ischemia on ventricular function are well established. However, to our knowledge the role of exertional ischemia in the remodeling response after infarction has not been investigated. METHODS: Ninety-one patients with a first anterior Q wave myocardial infarction were studied at 5 weeks by rest echocardiography and exercise scintigraphy. The echocardiographic examination was repeated 6 months later. On the basis of the presence and extent of reversible perfusion defects on exercise scintigraphy, patients were assigned to groups with no exertional ischemia (group 1, n = 20 [22%], mild to moderate ischemia (group 2, n = 45 [49%]) and severe exertional ischemia (group 3, n = 26 [29%]). RESULTS: Initial left ventricular volumes were similar, and no differences were found among the three groups in the remodeling response over the 6-month period of the study. However, patients in groups 2 and 3 with an ejection fraction < or = 40% showed significant (p < 0.01) ventricular enlargement over time, which was similar between the two groups (end-diastolic volume [mean +/- SD] from 74 +/- 13 to 80 +/- 17 ml/m2 in group 2 and from 72 +/- 11 to 81 +/- 19 ml/m2 in group 3; regional dilation from 42 +/- 16% to 52 +/- 22% in group 2 and from 38 +/- 18% to 46 +/- 27% in group 3). In contrast, ventricular dimensions did not change in group 1 patients with an ejection fraction < or = 40% as well as in patients in all three groups with an ejection fraction > 40%. CONCLUSIONS: Exercise-induced myocardial ischemia may contribute to progressive ventricular enlargement in patients with poor left ventricular function after a large anterior myocardial infarction.
Myocardial sestamibi uptake reflects regional flow distribution and cellular integrity; however, some segments showing reduced tracer uptake at rest may consist of viable, although hypoperfused, myocardium. It is speculated that the administration of nitroglycerin (NTG) before the sestamibi injection would improve the tracer uptake in resting hypoperfused regions. Thirty-six stable patients with previous myocardial infarction (56 +/- 2 years; mean ejection fraction 42 +/- 2%), in whom perfusion defects could be seen at resting sestamibi tomography, repeated the scintigraphic study 2 to 6 days later, receiving NTG (0.3 to 0.6 mg sublingually) before the tracer injection. The size of the tracer uptake defect was quantified from circumferential profiles in 3 short-axis slices by integrating the area below the lower normal limit (mean -2 SD). After NTG, the mean perfusion defect significantly decreased (from 6,324 +/- 619 to 5,365 +/- 516, p < 0.01). The defect was reduced beyond the reproducibility limits in 20 patients (56%, group 1) and was unchanged or increased in 16 (44%, group 2). The resting sestamibi defect size was comparable between the 2 groups. The average percent reduction of the perfusion defect after NTG was 29 +/- 4% (range 7 to 74).(ABSTRACT TRUNCATED AT 250 WORDS)
Early poststress thallium-201 reinjection to obviate the need for two sets of redistribution images has been proposed as an alternative reinjection protocol although, in a preliminary study, it did not reduce the frequency of late redistribution. The efficacy of the early reinjection protocol was assessed in 102 patients with chronic ischemic heart disease and left ventricular dysfunction who showed severe thallium-201 defects on planar stress images. Thallium-201 was reinjected immediately after the poststress study, and redistribution images were acquired 4 and 24 hours later. By quantitative analysis, a further increase in thallium-201 uptake on 24-hour imaging was documented in only 48 (6%) of 740 segments still abnormal on 4-hour images, 26 (54%) of which were represented by partially reversible or not severe fixed defects. Overall, late thallium-201 uptake was less frequently observed in patients with depressed ejection fraction (p < 0.05). Clinically relevant late reversibility was found in only 3 (3%) of 94 patients. Scans were repeated after revascularization in 20 patients. Tracer uptake improved in 40 (34%) of 118 segments with 4-hour defect: the improvement mainly (85%) involved those segments already showing partial 4-hour reversibility or mild fixed defects on the preoperative study. Thus a negligible late tracer redistribution was found in patients with severe stress thallium-201 defects undergoing early reinjection and 4-hour imaging; no significant 24-hour improvement was observed in those patients with depressed ventricular function and fixed 4-hour defects. This simpler imaging protocol could obviate the need for additional late imaging to detect residual viability.
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BACKGROUND: In patients with ventricular dysfunction caused by stunning or hibernation, it is not clear when complete recovery of the salvaged myocardium occurs after acute myocardial infarction. The purpose of this study was to determine whether a delayed recovery of perfusion and contraction continues even after the subacute phase. METHODS AND RESULTS: We prospectively studied 71 consecutive male patients with first uncomplicated Q-wave anterior infarction. Resting regional blood flow distribution and contraction were assessed quantitatively 5 weeks and 7 months after the acute phase by serial sestamibi tomography and two-dimensional echocardiography. Coronary angiography also was performed in 52 patients. Overall, at 7 months there was an improvement in the perfusion defect severity (1019 +/- 811 versus 1365 +/- 821 at 5 weeks, P < .001) as well as in the extent of abnormal wall motion (28 +/- 19% versus 32 +/- 15%, P < .001) and left ventricular ejection fraction (53 +/- 14% versus 50 +/- 13%, P < .01). Among the 68 of 71 patients showing resting perfusion defects at 5 weeks, two groups were identified: 47 (group 1) who showed a significant (beyond the reproducibility limits) 7-month reduction of the resting perfusion defect, and 21 patients (group 2) in whom the perfusion defect remained unchanged. Ejection fraction and the extent of abnormal wall motion significantly (P < .01) improved in group 1 but not in group 2. Despite the presence of a comparable perfusion defect size between the two groups at 5 weeks after infarction, group 1 already showed a better regional and global ventricular function (P < .05). No significant differences were found between the two groups regarding age, medical therapy, the extent of underlying coronary disease, thrombolysis in the acute phase, Thrombolysis in Myocardial Infarction grade of the infarct-related vessel, and presence of collaterals on angiography. CONCLUSIONS: After anterior Q-wave infarction, the recovery of perfusion and wall motion may continue well after the subacute phase. Several patients exhibit relative hypoperfusion in viable tissue as late as 5 weeks after infarction, and a significant improvement of perfusion in the infarcted area commonly is observed between 5 weeks and 7 months. This delayed improvement of perfusion is associated with a delayed improvement of contractile function in the infarcted area after the first 5 weeks, which may continue for up to 7 months, suggesting the presence of hibernating myocardium in the infarcted area. Despite similar perfusion defect sizes, the level of regional function can be different at 5 weeks, and measurements taken around this time may not accurately estimate the eventual recovery of function.
The extent and severity of residual myocardial ischaemia are well-known as major determinants of mortality after myocardial infarction, and non-invasive assessment of these parameters still plays a critical role in the management of patients. Most of the published data on this topic derive from observations collected before the widespread use of thrombolysis. The results of large multicentre trials assessing the most appropriate therapies after thrombolysis have shown that the more conservative strategy of reserving catheterization and revascularization for patients with recurrent spontaneous or induced ischaemia may be the best approach. Sophisticated techniques to detect more accurately the residual ischaemic burden after infarction have been suggested that would have a major impact on clinical decision making and on the cost of health care. The relative influence of residual ischaemic on the prognosis after myocardial infarction, however, has recently been questioned. The relative risk associated with residual ischaemia seems to be low compared with other predictors of mortality. The progression of coronary artery disease is variable and highly unpredictable, and this may be a major limitation of our ability to predict further ischaemic events.
Since myocardial 99mTc-Sestamibi uptake is closely related to coronary blood flow and the tracer does not redistribute, resting perfusion defects may be observed even in viable regions supplied by vessels with severe stenosis. The incidence and the clinical significance of 99mTc-Sestamibi uptake defects at rest were investigated in 60 men with suspected coronary artery disease and no previous myocardial infarction, in a multicenter study. Of 60 patients, 12 showed normal coronary arteries and 48 significant coronary artery disease (> 50% luminal narrowing). Based on the presence or absence of tracer uptake defects at resting planar scans, the patients were divided into Group 1 (27 patients) and Group 2 (33 patients), respectively. A greater incidence of coronary artery disease (100% versus 64%, p < 0.01) and of multivessel disease (70% versus 36%, p < 0.05) was observed in patients of Group 1. All patients underwent dipyridamole (up to 0.84 mg/kg in 10 min) 99mTc-Sestamibi scintigraphy, which more frequently induced transient 99mTc-Sestamibi uptake defects in Group 1 than in Group 2 (85% versus 42%, p < 0.001). A high incidence of resting 99mTc-Sestamibi uptake defects was observed in patients without previous myocardial infarction; this identified a subset of patients with a higher prevalence of coronary artery disease and multivessel involvement and with a greater impairment of the coronary reserve, as evidenced by a dipyridamole test.
The behavior of myocardial blood flow (MBF) regulation in territories supplied by angiographically normal vessels of patients with coronary artery disease (CAD) has been poorly investigated. Resting MBF and coronary reserve were evaluated in 32 patients with stable angina, no previous myocardial infarction, and isolated left anterior descending or left circumflex coronary artery stenosis (> or = 50% diameter narrowing). MBF was measured, in the absence of any medical therapy, by means of dynamic positron emission tomography and 13N-ammonia. MBF measurements at baseline and after intravenous dipyridamole (0.56 mg/kg administered over 4 minutes), were obtained both in the stenosis-related regions and in contralateral territories. As a control group, 14 normal subjects were evaluated according to the same protocol. At rest, the 32 patients with CAD had similar MBF values in the stenotic and remote regions (0.76 +/- 0.21 and 0.77 +/- 0.19 ml/min/g, respectively, p = NS); both these values were significantly (p < 0.01) reduced with respect to mean MBF in normal subjects (1.03 +/- 0.25 ml/min/g). The dipyridamole study was completed in 30 patients; these patients had lower values of maximal MBF in the stenotic than in the remote regions (1.52 +/- 0.65 vs 1.76 +/- 0.68 ml/min/g, p < 0.05); however, both these values were significantly reduced (p < 0.01) with respect to mean dipyridamole MBF in normal subjects (3.66 +/- 0.92 ml/min/g). Thus, in patients with CAD, resting and maximal MBF can be reduced not only in myocardial territories supplied by stenotic arteries, but also in territories supplied by angiographically normal arteries.
To assess whether myocardial stunning occurs after brief periods of ischemia, global and regional ventricular function assessed by radionuclide angiography was studied in 52 patients. Patients were divided into 3 groups according to the type of ischemic episodes. Group 1 consisted of 15 patients studied before, during and after episodes of angina at rest. Seventeen patients studied immediately before and after coronary angioplasty constituted group 2. Group 3 consisted of 20 patients with stable angina studied before, during and after exercise-induced ischemia. Medical therapy was discontinued 48 hours before the study in all patients except those undergoing coronary angioplasty who were receiving diltiazem 180 mg/day. No difference in baseline ejection fraction was found between groups, whereas peak filling rate was statistically lower in group 3 patients. Evidence of left ventricular dysfunction during ischemia was seen in patients in groups 1 and 3, whereas transient ischemia was documented by ST-segment displacement and/or typical chest pain during balloon inflation in group 2. Persistence of systolic or diastolic dysfunction was not observed in any of the 3 groups in the recovery phase after ischemia. In conclusion, transient ischemia caused either by a primary reduction in oxygen supply (angina at rest, coronary angioplasty) or by an increase in oxygen demand (angina on effort) did not reproduce the phenomenon of systolic and diastolic stunning observed in animal experiments, although in all patients the ischemia was of sufficient duration and severity to induce marked ventricular dysfunction. The search for stunned myocardium should be extended to other different clinical models characterized by prolonged ischemia such as unstable angina or myocardial infarction.
Sestamibi allows ECG-gated acquisition and similarly to radionuclide angiography a time-activity curve from a defined myocardial region can be derived and analysed. Diastolic (peak relaxation velocity) and systolic (per cent thickening) functional parameters from Sestamibi ECG-gated acquisition were obtained; this data were compared in 10 patients with radionuclide angiographic data (peak filling rate and ejection fraction, respectively). A high correlation was found between peak relaxation velocity and peak filling rate (r = 0.792), while no significant correlation was found between thickening and ejection fraction (r = 0.577). Sestamibi parameters were calculated in 15 patients with known or suspected coronary artery disease and compared with those obtained in 10 normal subjects. In regions supplied by stenotic vessels the average values of peak relaxation velocity and thickening were significantly lower than those obtained in control subjects in the corresponding vascular territory. The average regional values of the diastolic parameter were significantly lower than the corresponding normal range also in regions with preserved systolic function, i.e. with thickening values within 1SD from the mean value of normals. In conclusion, from the ECG-gated acquisition of Sestamibi regional diastolic and systolic functional parameter may be derived; this completes the spectrum of information that can be obtained by a single injection of tracer.
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Most patients with chronic Chagas' heart disease complain of chest pain. The pathophysiology of this symptom is unknown, although myocardial necrosis and fibrosis are frequent necropsy findings and cardiac autonomic impairment is a prominent feature of the disease. To evaluate the possibility of an ischemic cause for these abnormalities in 23 patients (18 men, aged 32 to 60 years, mean 42) with chronic Chagas' disease complaining of chest pain, thallium-201 myocardial scintigraphy was performed after maximal effort and 4-hour redistribution. Regional wall motion was assessed by radionuclide and contrast angiography. Heart rate responses to sinus respiratory arrhythmia, atropine, phenylephrine and Valsalva maneuver were evaluated in all patients and in 22 normal control subjects. Coronary angiography was performed in 16 patients. Only 1 patient had chest pain and no ischemic electrocardiographic changes occurred in any case during the effort test. Scintigraphic analysis of 7 segments per patient showed perfusion defects in at least 1 segment in all patients. Of 161 myocardial segments 16 showed fixed, 10 reversible, and 22 paradox defects (reverse redistribution). The majority (75%) of the fixed perfusion defects occurred in dyssynergic regions, whereas reverse redistribution predominated in regions with normal wall motion (82%). The reversible defects were present in normal or mildly hypokinetic regions. Markedly impaired parasympathetic cardiac control was present but no significant coronary abnormalities were seen in any of the 16 patients undergoing angiography. It is concluded that whereas fixed defects are likely to correspond to fibrotic or necrotic lesions, reversible and paradox perfusion defects may be caused by regional flow or metabolism derangements, possibly related to abnormal parasympathetic control of the coronary microcirculation.
The aim of this study was to assess the reliability of the quantitative analysis of regional wall thickening with electrocardiographic-gated technetium-99m 2-methoxyisobutylisonitrile (SESTAMIBI) in predicting the reversibility of stress-induced perfusion defects. The assumption was that a preserved resting wall thickening in a segment with stress-induced perfusion defect would predict normal resting perfusion. Twenty-five patients with suspected coronary artery disease underwent planar stress-rest SESTAMIBI scintigraphy. The wall thickening was quantitatively evaluated as percentage increase in counts from diastole to systole; a ratio defined as the wall thickening index (WTI) between patient and normal profile (mean - 2 SD) below 1 was considered abnormal. Improvement of the perfusion pattern at rest was observed in 76% (54/71) of segments with a stress-induced perfusion defect; 90% of these segments had a (WTI) greater than 0.8. Five segments (9%) showed fixed perfusion defects despite a WTI value greater than 0.8. In conclusion, quantitative analysis of regional wall thickening by electrocardiographic-gated SESTAMIBI identifies segments with reversible perfusion defects; this may overcome the need for studies at rest and may direct the detection of hypoperfused but viable myocardium.
Technetium-99m methoxy-isobutyl-isonitrile (SESTAMIBI) has been recently introduced to trace regional myocardial perfusion. Beyond blood flow distribution, a quantitative index of regional myocardial wall motion from SESTAMIBI electrocardiogram (ECG)-gated images was obtained, according to the assumption that changes in the detected radioactivity reflect changes in myocardial wall thickness during the cardiac cycle. As a preliminary study, 20 patients with coronary artery disease and regional wall motion abnormalities and 15 normal subjects were studied by SESTAMIBI scintigraphy and contrast ventriculography. Regional wall motion was analyzed by a radial method applied to both techniques. Absolute systolic changes in radioactivity and its ratio to reference normal values (wall thickening index, WTI) were determined in 9 anatomical cardiac regions according to the formula (endsystolic counting profile-enddiastolic counting profile/enddiastolic counting profile) x 100. The overall agreement between radioisotopic and ventriculographic techniques was 88% (158 of 180 segments). Normal, hypokinetic and akinetic ventriculographic segments showed WTI values of 1.1 +/- 0.2, 0.8 +/- 0.2 and 0.4 +/- 0.3 respectively (P less than 0.001). A second clinical study was performed in 25 patients studied by stress/rest ECG-gated SESTAMIBI scintigraphy. The assumption of this part of the study was to investigate if a preserved wall thickening in segments with stress defects might predict those areas with normal resting perfusion. Partial or total normalization of regional perfusion was observed in 90% of segments with a WTI greater than or equal to 0.8. These studies indicate the ECG-gated SESTAMIBI may represent a suitable technique for the simultaneous analysis of flow distribution and function. Analysis of post-exercise ECG-gated SESTAMIBI can predict the reversibility of transient perfusion defects.
Clinical and physiologic evidence indicates that maximal coronary vasodilation is not achieved in a large number of patients with use of the standard dose of dipyridamole (0.56 mg/kg body weight over 4 min). The feasibility, safety and accuracy of technetium-99m hexakis 2-methoxy-2-isobutyl isonitrile (Sestamibi) scintigraphy associated with intravenous high dose dipyridamole (0.56 mg/kg over 4 min followed 4 min later by an additional 0.28 mg/kg over 2 min) were evaluated in a multicenter study. Planar myocardial perfusion images were obtained at rest and after dipyridamole in 101 patients with effort chest pain and no prior myocardial infarction. High dose dipyridamole (62 patients) was used when typical chest pain or electrocardiographic (ECG) signs of ischemia, or both, did not occur during or after the standard dose (39 patients). With high dose dipyridamole, 34 patients had pain (18 patients) or ECG signs of ischemia (ST depression greater than or equal to 2 mm) (8 patients), or both (8 patients), whereas the other 28 patients had Sestamibi injection in the absence of symptoms or ECG changes. All patients underwent coronary angiography: 81 had significant coronary artery disease (greater than or equal to 50% reduction of lumen diameter) (affecting one vessel in 38, two vessels in 19 and three vessels in 24 patients) and 20 patients had normal coronary arteries. The overall sensitivity, specificity and predictive accuracy of Sestamibi scintigraphy were 81%, 90% and 83%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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