Sestamibi Single-photon Emission Tomography Research Articles

A Pilot Study of Neurobiological Mechanisms of Stress and Cardiovascular Risk.

Coronary heart disease is a leading cause of death and disability. Although psychological stress has been identified as an important potential contributor, mechanisms by which stress increases risk of heart disease and mortality are not fully understood. The purpose of this study was to assess mechanisms by which stress acts through the brain and heart to confer increased CHD risk. Coronary Heart Disease patients (N=10) underwent cardiac imaging with [Tc-99m] sestamibi single photon emission tomography at rest and during a public speaking mental stress task. Patients returned for a second day and underwent positron emission tomography imaging of the brain, heart, bone marrow, aorta (indicating inflammation) and subcutaneous adipose tissue, after injection of [18F]2-fluoro-2-deoxyglucose for assessment of glucose uptake followed mental stress. Patients with (N=4) and without (N=6) mental stress-induced myocardial ischemia were compared for glucose uptake in brain, heart, adipose tissue and aorta with mental stress. Patients with mental stress-induced ischemia showed a pattern of increased uptake in the heart, medial prefrontal cortex, and adipose tissue with stress. In the heart disease group as a whole, activity increase with stress in the medial prefrontal brain and amygdala correlated with stress-induced increases in spleen (r=0.69, p=0.038; and r=0.69, p=0.04 respectfully). Stress-induced frontal lobe increased uptake correlated with stress-induced aorta uptake (r=0.71, p=0.016). Activity in insula and medial prefrontal cortex was correlated with post-stress activity in bone marrow and adipose tissue. Activity in other brain areas not implicated in stress did not show similar correlations. Increases in medial prefrontal activity with stress correlated with increased cardiac glucose uptake with stress, suggestive of myocardial ischemia (r=0.85, p=0.004). These findings suggest a link between brain response to stress in key areas mediating emotion and peripheral organs involved in inflammation and hematopoietic activity, as well as myocardial ischemia, in Coronary Heart Disease patients.

English

BACKGROUND The differentiation of tumour progression from treatment-induced changes is critical in evaluating response to therapy among patients with gliomas. Although conventional magnetic resonance imaging (MRI) is invaluable in the overall assessment of such lesions, it is often difficult to differentiate between these two entities. We wanted to evaluate the role of contrast-enhanced MRI (CE MRI) and magnetic resonance spectroscopy (MRS) and correlation with 99 m Tc Sestamibi single-photon emission tomography (SPECT) in differentiating tumour progression from post-therapy changes in patients with glioma. METHODS This was a cross-sectional study. Being a rare disease, all adult patients (25 in number) with brain glioma reporting to the hospital for over a period of 12 months were included in the study. CE MRI, MRS and SPECT were performed at three months, six months and 12 months’ post-surgery and radiotherapy. The ratios for choline (Cho) / N-acetyl aspartate (NAA) and choline (Cho) creatine (Cr) were obtained from the areas suspicious for tumour progression on CE MRI and were correlated with the presence or absence of uptake on SPECT. These findings were correlated with the patients’ clinical course and tumour histopathology. RESULTS Both choline (Cho) / N-acetyl aspartate (NAA) and choline (Cho) / creatine (Cr) ratios had high detection rates for tumour progression when cut-off values of > 1.75 were used. For the Cho / NAA ratio, the sensitivity and specificity were 93.7 % and 100 %, respectively. The sensitivity and specificity for the Cho / Cr ratio were 81.3 % and 88.9 %, respectively. The sensitivity and specificity of 99 m Tc Sestamibi SPECT were 87.5 % and 100 %, respectively. CONCLUSIONS MRS and SPECT have high sensitivity and specificity for diagnosing tumour progression and must be used in conjunction with conventional CE MRI in the posttherapy setting. KEYWORDS Glioma, Progression, Post-Therapy Changes, MRI, MRS, SPECT

Brain Correlates of Mental Stress-Induced Myocardial Ischemia.

Coronary artery disease (CAD) is a major cause of morbidity and mortality, and despite important advances in our understanding of this disorder, the underlying mechanisms remain under investigation. Recently, increased attention has been placed on the role of behavioral factors such as emotional stress on CAD risk. Brain areas involved in memory and the stress response, including medial prefrontal cortex, insula, and parietal cortex, also have outputs to the peripheral cardiovascular system. The purpose of this study was to assess the effects of mental stress on brain and cardiac function in patients with CAD. CAD patients (N = 170) underwent cardiac imaging with [Tc-99m] sestamibi single-photon emission tomography at rest and during a public speaking mental stress task. On another day, they underwent imaging of the brain with [O-15] water positron emission tomography (PET) during mental stress (arithmetic and public speaking) and control conditions. Patients with mental stress-induced myocardial ischemia showed increased activation with stress in anterior cingulate, inferior frontal gyrus, and parietal cortex (p < .005). This was seen with both arithmetic stress and public speaking stress. Arithmetic stress was additionally associated with left insula activation, and public speaking with right pre/postcentral gyrus and middle temporal gyrus activation (p < .005). These findings suggest that mental stress-induced myocardial ischemia is associated with activation in brain areas involved in the stress response and autonomic regulation of the cardiovascular system. Altered brain reactivity to stress could possibly represent a mechanism through which stress leads to increased risk of CAD-related morbidity and mortality.

Association Between High-Sensitivity Cardiac Troponin Levels and Myocardial Ischemia During Mental Stress and Conventional Stress

ObjectivesThis study sought to investigate whether patients with mental stress–induced myocardial ischemia will have high resting and post–mental stress high-sensitivity cardiac troponin I (hs-cTnI). BackgroundHs-cTnI is a marker of myocardial necrosis, and its elevated levels are associated with adverse outcomes. Hs-cTnI levels may increase with exercise in patients with coronary artery disease. Mental stress–induced myocardial ischemia is also linked to adverse outcomes. MethodsIn this study, 587 patients with stable coronary artery disease underwent technetium Tc 99m sestamibi–single-photon emission tomography myocardial perfusion imaging during mental stress testing using a public speaking task and during conventional (pharmacological/exercise) stress testing as a control condition. Ischemia was defined as new/worsening impairment in myocardial perfusion using a 17-segment model. ResultsThe median hs-cTnI resting level was 4.3 (interquartile range [IQR]: 2.9 to 7.3) pg/ml. Overall, 16% and 34.8% of patients developed myocardial ischemia during mental and conventional stress, respectively. Compared with those without ischemia, median resting hs-cTnI levels were higher in patients who developed ischemia either during mental stress (5.9 [IQR: 3.9 to 8.3] pg/ml vs. 4.1 [IQR: 2.7 to 7.0] pg/ml; p < 0.001) or during conventional stress (5.4 [IQR: 3.9 to 9.3] pg/ml vs. 3.9 [IQR: 2.5 to 6.5] pg/ml; p < 0.001). Patients with high hs-cTnI (cutoff of 4.6 pg/ml for men and 3.9 pg/ml for women) had greater odds of developing mental (odds ratio [OR]: 2.4; 95% confidence interval [CI]: 1.5 to 3.9; p < 0.001) and conventional (OR: 2.4; 95% CI: 1.7 to 3.4; p < 0.001) stress-induced ischemia. Although there was a significant increase in 45-min post–treadmill exercise hs-cTnI levels in those who developed ischemia, there was no significant increase after mental or pharmacological stress test. ConclusionsIn patients with coronary artery disease, myocardial ischemia during either mental stress or conventional stress is associated with higher resting levels of hs-cTnI. This suggests that hs-cTnI elevation is an indicator of chronic ischemic burden experienced during everyday life. Whether elevated hs-cTnI levels are an indicator of adverse prognosis beyond inducible ischemia or whether it is amenable to intervention requires further investigation.

Association between anger and mental stress–induced myocardial ischemia

Mental stress-induced myocardial ischemia is associated with adverse prognosis in coronary artery disease patients. Anger is thought to be a trigger of acute coronary syndromes and is associated with increased cardiovascular risk; however, little direct evidence exists for a link between anger and myocardial ischemia. [(99m)Tc]-sestamibi single-photon emission tomography was performed at rest, after mental stress (a social stressor with a speech task) and after exercise/pharmacologic stress. Summed scores of perfusion abnormalities were obtained by observer-independent software. A summed-difference score, the difference between stress and rest scores, was used to quantify myocardial ischemia under both stress conditions. The Spielberger's State-Trait Anger Expression Inventory was used to assess different anger dimensions. The mean age was 50 years, 50% were female, and 60% were non-white. After adjusting for demographic factors, smoking, coronary artery disease severity, depressive, and anxiety symptoms, each IQR increment in state-anger score was associated with 0.36 U-adjusted increase in ischemia as measured by the summed-difference score (95% CI 0.14-0.59); the corresponding association for trait anger was 0.95 (95% CI 0.21-1.69). Anger expression scales were not associated with ischemia. None of the anger dimensions was related to ischemia during exercise/pharmacologic stress. Anger, both as an emotional state and as a personality trait, is significantly associated with propensity to develop myocardial ischemia during mental stress but not during exercise/pharmacologic stress. Patients with this psychologic profile may be at increased risk for silent ischemia induced by emotional stress, and this may translate into worse prognosis.

Measuring myocardial salvage

The efficacy of cardioprotective strategies can be quantified by myocardial salvage as an indicator of therapeutic benefit. Salvage is calculated as the difference between the area at risk (AAR) and the final infarct size (FIS). AAR has been quantified by angiographic assessment followed by quantification of FIS by biochemical ischaemic markers or imaging modalities such as cardiovascular magnetic resonance (CMR). Angiographical methods may overestimate AAR and since methodological differences may exist between different modalities, the use of different modalities for estimating AAR and FIS may not be recommended. (99m)Technetium (Tc)-Sestamibi single-photon emission tomography (SPECT) allows quantification of AAR and FIS by tracer injection prior to revascularization and after 1 month, respectively. SPECT provides the most validated measure of myocardial salvage and has been utilized in multiple randomized clinical trials. However, SPECT is logistically challenging, expensive, and includes radiation exposure. More recently, a large number of studies have suggested that CMR can determine salvage in a single examination by combining measures of myocardial oedema in the AAR exposed to ischaemia reperfusion with FIS quantification by late gadolinium enhancement. The T1- and T2-weighted CMR approaches for quantification of AAR utilize non-contrast, early and late gadolinium enhancement techniques. The technical progress, high spatial resolution and the potential for retrospective quantification of the AAR makes CMR the most appropriate technique for assessment of myocardial salvage. However, the optimum CMR technique for assessment of myocardial AAR remains to be defined. Consequently, we recommend a comprehensive CMR protocol to ensure reliable assessment of myocardial salvage.

Myocardial perfusion imaging using a technetium-99m Sestamibi in asymptomatic and low risk for coronary artery disease patients with diagnosed systemic lupus erythematosus

The aim of the present study was to evaluate technetium-99m sestamibi single photon emission tomography (SPECT) myocardial perfusion imaging (MPI) and its association with some clinical and laboratory parameters in an asymptomatic systemic lupus erythematosus (SLE) population. Twenty-one subjects with SLE and no suspected or documented coronary artery disease (CAD) accomplished myocardial perfusion imaging. Some SLE and CAD parameters were also evaluated in association with myocardial SPECT. Twenty-one women with a diagnosis of SLE (mean age 36.9 ± 12.8) entered the study. All patients were in the low-risk category for CAD pretest; however, abnormal myocardial perfusion results were found in eight (38%) patients. Amongst the traditional CAD risk factors, there was a significant association between the presence of dyslipidemia and myocardial perfusion abnormalities (P= 0.047). However, we found no significant association between other traditional and SLE-specific risk factors. This study's significant finding was that asymptomatic CAD is common in SLE patients, even in those thought to be low risk for CAD and in the absence of cardiac symptoms.

Symptomatic Sternal Metastasis Mimicking Cardiac Angina Discovered by Tc-99m Sestamibi Myocardial Perfusion Scintigraphy

Tc-99m sestamibi has been reported to accumulate in several tissues with increased metabolism and particularly in solid tumors. Although the clinical utility of this radiopharmaceutical has been described in primary breast cancer and its axillary involvement, it has not been fully evaluated in local recurrence or distant metastasis. We illustrate the case of a post-mastectomy patient in whom Tc-99m sestamibi single photon emission tomography (SPET) myocardial perfusion scintigraphy, performed to evaluate chest pain mimicking angina, aided in discovering local recurrence of breast cancer in the chest wall. This example underlines that myocardial scintigraphy requires--particularly in a selected group of patients with previous neoplasms of the chest or neck--careful scrutiny for extracardiac uptake and why any unusual or unexpected localization should be pursued and clarified for diagnosis.

140 consecutive cases of minimally invasive, radio-guided parathyroidectomy

The advent of highly accurate parathyroid imaging and the ever-increasing trend towards minimally invasive procedures have changed considerably the surgical approach to the patient with primary hyperparathyroidism (PHPT) caused by a single parathyroid adenoma. This study analyzes the short- and longer-term results of 140 patients who underwent minimally invasive, radio-guided parathyroidectomy. Demographic, clinical, and pre-operative imaging data, operative findings, and short- and long-term results of 140 consecutive patients operated within a 20 months period (8/1999-4/2002), were prospectively entered into a database. Immediate pre-operative sestamibi scintigraphy with skin marking of focal adenoma uptake were followed by intraoperative hand-held gamma probe for the removal of the parathyroid adenoma by unilateral minimal access surgery. Preoperative and surgical data were analyzed and correlated to outcomes, measured by success or failure to cure PHPT, associated morbidity and mortality, predictive value of localizing studies, and postoperative laboratory results in the immediate as well as long-term period. 140 patients, mean age: 55.1 +/- 14.1 years (range 19-88 years), female to male ratio 94:46 with PHPT proven by concomitantly elevated serum calcium and parathormone (PTH) levels, with a single adenoma identified by sestamibi single photon emission tomography (SPECT) scintigraphy and high-resolution sonography, underwent minimally invasive, radio-guided parathyroidectomy. Mean serum levels of preoperative calcium, phosphorus, and PTH were 11.6 +/- 0.8 mg/dL (range 9.1-14), 3.0 +/- 0.3 mg/dL, and 147.1 +/- 94.3 pg/mL (range 68-784), respectively. Overall, in 3 out of 140 patients (2.1%), focused, minimally invasive surgery failed to identify and remove the adenoma. Positive predictive value when both localizing modalities concurred was 99.2%. Positive predictive value of SPECT scan alone was 97.2%. Overall success rate was 97.8% (137/140). 24 hours postoperative mean serum calcium was 9.2 +/- 0.8 mg/dL and at 6 months mean serum calcium, phosphorus, and PTH were 9.4 +/- 1.06 mg/dL, 3.2 +/- 0.8 mg/dL, and 32.1 +/- 11.9 pg/mL, respectively (p = 0.0001). There was no mortality. In 2 patients (1.4%) there was transient vocal cord paresis and there were 8 instances of clinically significant hypocalcemia. In 3 cases (2.1%), a second adenoma manifested itself 9-14 months following surgery and was removed by minimal access procedure. Minimally invasive, radio-guided focused parathyroidectomy for a single adenoma is safe and effective in curing hyperparathyroidism with a 97% success rate. A second adenoma occurring in less than 3% may be successfully treated with a second minimal access operation. The combined positive predictive value of concurring sestamibi SPECT scintigraphy and sonography of 99.2% may increase success rate, and thus implementing this technique in patients with concurring sonography and scintigraphy may be advocated.

Detection and reproducibility of mental stress induced ischemia utilizing Tc-99m sestamibi single-photon emission tomography in normal and coronary artery disease population

Detection and reproducibility of mental stress induced ischemia utilizing Tc-99m sestamibi single-photon emission tomography in normal and coronary artery disease population

Prediction of functional outcome by quantification of sestamibi and BMIPP after acute myocardial infarction.

Iodine-123 15-(p-iodophenyl)-3-R,S-methylpentadecanoic acid (BMIPP) can be used to image myocardial fatty acid regional distribution and utilisation with single-photon emission tomography (SPET). By visual analysis, a mismatching with regional uptake of BMIPP less than that of a perfusion tracer has been shown to predict myocardial viability and functional improvement after restoration of flow in patients with myocardial infarction. The current study aimed to evaluate a newly developed quantitative method of analysis of sestamibi and BMIPP uptake for the prediction of functional recovery after revascularization in patients with acute infarction. BMIPP and gated sestamibi SPET studies at rest were obtained before and >3 months after revascularization in 18 patients with recent infarction. A colour-coded polar map was generated from the comparison of sestamibi and BMIPP uptake. Depending on the relative distribution of the two tracers, different patterns of uptake were identified and their extent expressed as percentages of the surface of the whole left ventricle and of the three main coronary artery territories. At follow-up, recovery was defined as a > or =5% increase in ejection fraction compared with baseline. Receiver-operating characteristic curve analysis was performed to analyse the data. At baseline, significant correlations were found between ejection fraction and the % surface with decreased sestamibi or BMIPP uptake (r=-0.68, P= 0.001, and r=-0.72, P<0.0001, respectively). When combining both tracers, ejection fraction was significantly associated with the extent of myocardium showing decreased sestamibi uptake with lower BMIPP uptake (mismatching; r=-0.68, P=0.001). At follow-up, significant functional recovery was found in 13/18 patients. By ROC curve analysis, the optimal pattern of distribution predicting recovery was a mismatching with uptake of sestamibi <70% and uptake of BMIPP at least 10% lower. For this parameter, optimal cut-off of extent was 10% of the whole left ventricle surface (sensitivity 69%, specificity 80%, accuracy 72%) and 25% of the infarct-related arterial territory (sensitivity 77%, specificity 80%, accuracy 78%). The areas under the curve were 79% for the left ventricle surface and 72% for the individual arterial territories. These results suggest that in patients with acute infarction, quantitative analysis of sestamibi and BMIPP could offer an objective and reproducible method for estimating the severity of cardiac dysfunction and predicting the evolution of ejection fraction after revascularization.

Technetium-99m sestamibi single-photon emission tomography detects subclinical myocardial perfusion abnormalities in patients with systemic lupus erythematosus.

In patients with systemic lupus erythematosus, involvement of the cardiovascular system is the third leading cause of death. However, although autopsy studies have demonstrated a high incidence of abnormalities in both the myocardium and coronary vessels, clinical manifestations have been reported in only a small percentage of cases. The aim of this study was to evaluate myocardial perfusion in asymptomatic lupus patients using technetium-99m sestamibi single-photon emission tomography (SPET). Twenty-eight patients without overt cardiac involvement and risk factors were studied with 99mTc-sestamibi SPET at rest and after dipyridamole infusion. Perfusion abnormalities were detected in 18 cases: six had persistent defects, three had reversible defects, seven had both persistent and reversible defects, and two showed rest defects which normalized on dipyridamole images ("reverse redistribution pattern"). Coronary angiography was performed in eight patients with positive 99mTc-sestamibi SPET, and showed normal epicardial vessels in all the cases. These results indicate that 99mTc-sestamibi SPET reveals a high prevalence (18 out of 28 patients in this study, i.e. 64%) of myocardial perfusion abnormalities in asymptomatic lupus patients, probably due to the primary immunological damage of this autoimmune disease. In conclusion, rest/dipyridamole 99mTc-sestamibi SPET can be a useful non-invasive method to identify subclinical myocardial involvement in systemic lupus erythematosus, and patients potentially at risk of later cardiac events.

The role of technetium-99m sestamibi single photon emission tomography in the follow-up of malignant melanoma and the detection of lymph node metastases.

In the follow-up of patients with malignant melanoma treated by surgical resection of the cutaneous tumour, it is important to achieve early detection of possible lymph node metastasis. In many cases, clinical examination alone will not be sufficient. In our study, single-photon emission tomography (SPET) with technetium-99m sestamibi (MIBI) was used in the assessment of 30 patients with previously resected malignant melanoma when the clinical examination raised the suspicion of lymph node metastasis. Using MIBI, 16 out of 17 lymph node metastases were detected and confirmed by histology. No false-positive results were obtained during this prospective study. It is concluded that MIBI scintigraphy may be useful in the early detection of lymph node metastases of malignant melanomas. If our preliminary results are confirmed, early detection of lymph node metastasis of previously resected malignant melanoma by 99mTc-MIBI scintigraphy may have a significant impact on the management of these patients.

Adenosine technetium-99m sestamibi single-photon emission tomography for the assessment of jeopardized myocardium early after acute myocardial infarction

Adenosine technetium-99m sestamibi single-photon emission tomography for the assessment of jeopardized myocardium early after acute myocardial infarction

Adenosine technetium-99m sestamibi single-photon emission tomography for the assessment of jeopardized myocardium early after acute myocardial infarction

This study investigated the value of technetium-99m sestamibi scintigraphy in identifying patients at risk for post-infarct ischaemia (=jeopardized myocardium), especially within the reperfused infarct region. In 51 patients with a recent (<1 month) myocardial infarction, adenosine 99mTc-sestamibi single-photon emission tomography (SPET) and dobutamine stress echocardiography (DSE) were performed and correlated with the presence of significant coronary artery stenosis [% diameter stenosis (DS) >50%] on quantitative coronary angiography. Regional perfusion activity was analysed semi-quantitatively (score 0-4) on a 13-segment left ventricular model. DSE was used for the estimation of the infarct size (low-dose DSE) and for concomitant evaluation of ischaemia (high-dose DSE). A reversible perfusion defect within the infarct region was observed in 20 of the 37 patients with a significant infarct-related lesion (sensitivity of 54%) and only in one patient without a significant infarct-related lesion (specificity of 93%). Further analysis revealed that the scintigraphic assessment of jeopardized myocardium was fairly good in patients with a moderate (DS 51%-64%) infarct-related stenosis but was inadequate in patients with a severe (DS>/=65%) infarct-related stenosis (sensitivity of 80% vs 36%, P<0.01), while the echocardiographic detection of ischaemia was not influenced by stenosis severity (sensitivity of 73% in both subgroups). This scintigraphic underestimation of jeopardized myocardium was mainly related to a severely impaired myocardial perfusion under baseline conditions, as was evidenced by a significantly more severe rest perfusion score in the infarct region in patients with a severe stenosis as compared to those with a moderate stenosis (average score: 1.5+/-0.7 vs 2.1+/-0.6, P<0.01), while infarct size on echocardiography was similar for both subgroups. It may be concluded that early after an acute myocardial infarction, adenosine 99mTc-sestamibi SPET may underestimate reperfused but still jeopardized myocardium, particularly in patients with a severe infarct-related stenosis. In these patients the evaluation of the ischaemic burden on rest-stress scintigraphy is hampered by the presence of a severely impaired myocardial perfusion in resting conditions.

Cardiac sympathetic denervation in patients with coronary artery disease without previous myocardial infarction.

Myocardial infarction damages sympathetic nerve fibers coursing through the infarct zone. In this study we investigated whether coronary artery disease without myocardial infarction results in sympathetic denervation. We examined 12 patients without a history of previous myocardial infarction and 19 postinfarction patients. 1-123 metaiodobenzylguanidine (MIBG) and technetium-99m sestamibi (MIBI) single-photon emission tomography were conducted at rest to determine the extent of denervated myocardium and the extent of myocardium with reduced perfusion, respectively. In addition, myocardial perfusion during exercise was assessed with MIBI. A MIBG or MIBI defect was determined as being regional uptake of < or =30% of the maximal myocardial activity. All but 1 patient without previous infarction had MIBG defects. MIBG defects (10.3 +/- 8.5% of left ventricular mass) were significantly larger than MIBI defects at rest (2.4 +/- 3.2%, p <0.001) and during exercise (4.8 +/- 6.1%, p <0.05). In multiregression analysis, the size of an MIBG defect was associated with severity of coronary stenoses (> or =90% of lumen diameter; p <0.05), but not with age, number of significant stenoses (> or =50% of lumen diameter), left main disease, functional class, left ventricular ejection fraction, angina pectoris, maximal ST depression, or mean workload during exercise test. MIBG and MIBI defects were significantly larger in patients with severe coronary stenoses than in patients with moderate stenoses (50% to 89% of lumen diameter) (16.4 +/- 8.9% vs 6.0 +/- 5.2% [p <0.05] and 5.0 +/- 3.1% vs 0.6 +/- 1.3% [p <0.001], respectively). The size of MIBG (16.1 +/- 8.9%) and MIBI defects (7.3 +/- 6.5%) at rest in postinfarction patients did not differ from patients with severe stenoses. Our study demonstrates that cardiac adrenergic tissue is very sensitive to ischemia and that regional cardiac sympathetic denervation can occur in patients with stable coronary artery disease without previous myocardial infarction.

Myocardial sestamibi single-photon emission tomography: variations in reference values with gender, age and rest versus stress?

Myocardial sestamibi single-photon emission tomography: variations in reference values with gender, age and rest versus stress?

Myocardial sestamibi single-photon emission tomography: Variations in reference values with gender, age and rest versus stress?

Reference data files support the evaluation of myocardial perfusion single-photon emission tomography (SPET). The aim of this study was to create a large reference data base for technetium-99m sestamibi SPET, age and gender matched to the general patient population. One hundred and twenty-eight healthy volunteers (76 males and 52 females) with a likelihood of coronary artery disease of less than 5% underwent rest and maximal exercise 99mTc-sestamibi SPET with a 2-day protocol and 180 degrees elliptical rotation. The normalized activity values of 99mTc-sestamibi in the inferior wall differed significantly between men and women. Age variations were found for men in the anterior wall. Normalized activity values in all four walls were strikingly similar during rest and stress. Our results suggest that the use of reference files in 99mTc-sestamibi SPET requires a gender- and, for males, possibly an age-matched reference population. Different reference files at rest and during stress might not be necessary.

ECG-manifest and ECG-silent dipyridamole technetium-99m sestamibi SPET perfusion defects in patients with ischaemic heart disease.

At dipyridamole myocardial scintigraphy, perfusion defects are seldom backed up by significant ECG changes. This would suggest myocardial blood flow heterogeneity, rather than true ischaemia, as the cause of the scintigraphic abnormalities. Electrocardiographic surface mapping has been documented to be more accurate than standard 12-lead ECG in the detection of provoked ischaemia. Thus, to investigate the relationship between ECG changes and perfusion abnormalities, body surface maps were recorded during dipyridamole infusion in 55 subjects (11 normals and 44 patients with ischaemic heart disease) undergoing dipyridamole technetium-99m sestamibi single-photon emission tomography (SPET). All had a normal resting ECG. The extent and severity of the sestamibi defect were quantified. New negative areas in the isointegral maps and rest-dipyridamole map differences >2 SD from normal limits were considered abnormal. After dipyridamole in normals, neither perfusion defects nor >/=1 mm ST segment depression on 12-lead ECG nor new negative areas in isointegral maps occurred. In patients, dipyridamole induced new perfusion defects in 35 (80%) but ST segment depression in only 18 (41%, P<0.001). Of the 35 patients with perfusion defects, 17 (49%, group 1) showed ST segment depression, while the other 18 (51%, group 2) did not. Abnormal body surface maps were found in 100% of group 1 and 88% of group 2 patients (NS). In group 1, the provoked hypoperfusion was of greater extent (P=0.007) and severity (P=0.01) and the onset of map abnormalities was significantly earlier (P<0. 001) than in group 2; time to map abnormalities was also significantly shorter than time to ST segment depression (P=0.01). In the 35 patients with complete scintigraphic, body map and angiographic data, the severity of reversible perfusion defect proved to be the strongest correlate of ST segment depression upon logistic regression analysis. Thus, sestamibi SPET abnormalities after dipyridamole are almost always associated with electrical changes on body surface maps, suggesting myocardial ischaemia as their cause. The much less common 12-lead ECG changes are slower to appear and reflect a more severe hypoperfusion.

Breast cancer staging using technetium-99m sestamibi and indium-111 pentetreotide single-photon emission tomography.

We evaluated the clinical usefulness of single-photon emission tomography (SPET) with technetium-99m sestamibi and indium-111 pentetreotide in breast cancer staging. Fifteen patients with clinical and/or mammographic findings suggesting T1-2N0-1 breast cancer were studied. SPET images were acquired 20 min after 99mTc-sestamibi injection and 4 and 24 h after 111In-pentetreotide injection. Patients underwent surgery the day after the later 111In-pentetreotide acquisition. Pathological examination showed 16 tumours in the 15 patients, with one bilateral carcinoma. The mean tumour diameter was 18.7 mm. Metastatic axillary involvement was found in 6/16 tumours, with a mean of five metastatic nodes per axilla. Both tracers correctly identified 15/16 primary tumours and five of the six cases of metastatic axillary node involvement. No difference between the tracers was observed in breast cancer staging. 99mTc-sestamibi seems to be the better tracer in terms of physical characteristics, execution time and cost-effectiveness. Our data suggest the future possibility of using nuclear medicine imaging to avoid axillary dissection in patients with T1 breast cancer.