The role of nuclear medicine technique in evaluating electrophysiology in diabetic hearts especially with 123I-MIBG cardiac SPECT imaging.

Diabetes mellitus is a risk factor for cardiovascular morbidity and death. Cardiac autonomic diabetic neuropathy (CADN) is a common and serious complication of diabetes mellitus, which consists of damage to the autonomic nerve fibres that innervate the heart and blood vessels, resulting in alterations in heart rate control and vascular dynamics, associated with disabling clinical manifestations and increased mortality and incidence of both silent myocardial ischaemia and infarction. In vivo non-invasive radionuclide assessment of cardiac sympathetic innervation is possible with the use of radioabelled analogues of norepinephrine, which are actively taken up by the postganglionic presynaptic sympathetic nerve fibres of the heart. The catecholamine analogue 123I-metaiodobenzylguanidine (123I-MIBG) is the most commonly used tracer for imaging myocardial presynaptic sympathetic innervation on a broad clinical basis. 123I-MIBG imaging provides unique insights into the effects of diabetes on cardiac sympathetic integrity and the pathophysiological consequences of cardiac sympathetic dysinnervation. It also allows the assessment of both glycemic control on the progression of autonomic neuropathy and the effects of the autonomic derangement on myocardial blood flow regulation, function and electrophysiology, showing even potential for the prediction of adverse outcome.

[PET/CT with (11)C-choline and (18)F-FDG in patients with elevated PSA after radical treatment of a prostate cancer]. / PET/TAC con (11)C-colina y (18)F-FDG en pacientes con elevación de PSA tras tratamiento radical de un cáncer de próstata.

OBJECTIVE: To compare the diagnostic accuracy of PET/CT with (18)F-FDG and (11)C-choline for early detection and localization of recurrent prostate cancer. MATERIAL AND METHODS: Thirty-eight patients with increased PSA levels (0.8-9.5 ng/ml) after radical treatment for prostate cancer (surgery n = 20/radiation therapy n = 18) were included. Ten patients were on hormone therapy. All patients underwent a PET/CT with (11)C-choline and (18)F-FDG, respectively, on the same day. The PET imaging findings were compared with histopathology (n = 10); PSA monitoring (n = 21) and/ or other methods (n = 7). RESULTS: Focal uptake of (11)C-choline was detected in 26 patients (68%), and focal uptake of (18)F-FDG was detected in 13 patients (34%). The (11)C-choline uptake in 14 patients was suggested local recurrence, whereas this was true in only 4 patients (48%) with (18)F-FDG. Pelvic lymph nodes were detected with (11)C-choline PET/CT in 8 patients and only in 4 patients (50%) with (18)F-FDG. Mediastinal involvement was detected in 5 patients with (11)C-choline and 3 patients (60%) with (18)F-FDG. Focal bone involvement was detected in 3 patients with (11)C-choline and (18)F-FDG. (11)C-choline was able to detect 40% of recurrences in patients with PSA < 1 ng/ml, 50% of recurrences in patients with PSA 1-4 ng/ml and 87% of recurrences with PSA > 4 ng/ml. Sensitivity of (11)C-choline was higher for surgically treated patients, with no significant differences found between patients with and without hormone therapy. CONCLUSIONS: (11)C-choline PET/CT was useful for the detection of biochemical recurrence of prostate cancer, with higher yielding as compared to (18)F-FDG. (11)C-choline sensitivity was clearly related to PSA levels, was higher in patients with surgery and did not seem to be modified by hormonal therapy. Disease staging with (11)C-choline showed direct impact for the selection of the most appropriate therapeutic approach.

Computing quantitative indicators of structural renal damage in pediatric DMSA scans.

OBJECTIVES: The proposal and implementation of a computational framework for the quantification of structural renal damage from 99mTc-dimercaptosuccinic acid (DMSA) scans. The aim of this work is to propose, implement, and validate a computational framework for the quantification of structural renal damage from DMSA scans and in an observer-independent manner. MATERIALS AND METHODS: From a set of 16 pediatric DMSA-positive scans and 16 matched controls and using both expert-guided and automatic approaches, a set of image-derived quantitative indicators was computed based on the relative size, intensity and histogram distribution of the lesion. A correlation analysis was conducted in order to investigate the association of these indicators with other clinical data of interest in this scenario, including C-reactive protein (CRP), white cell count, vesicoureteral reflux, fever, relative perfusion, and the presence of renal sequelae in a 6-month follow-up DMSA scan. RESULTS: A fully automatic lesion detection and segmentation system was able to successfully classify DMSA-positive from negative scans (AUC=0.92, sensitivity=81% and specificity=94%). The image-computed relative size of the lesion correlated with the presence of fever and CRP levels (p<0.05), and a measurement derived from the distribution histogram of the lesion obtained significant performance results in the detection of permanent renal damage (AUC=0.86, sensitivity=100% and specificity=75%). CONCLUSIONS: The proposal and implementation of a computational framework for the quantification of structural renal damage from DMSA scans showed a promising potential to complement visual diagnosis and non-imaging indicators.

Endogenous bacterial endophthalmitis. A report of 2cases. / Endoftalmitis endógenas bacterianas. A propósito de 2casos.

CLINICAL CASES: The cases are presented on 2patients with bacterial endogenous endophthalmitis. The first one was caused by Streptococcus bovis, developed after colonoscopy, which had a poor outcome and resulted in evisceration. The second case was caused by a methicillin resistant Staphylococcus aureus from an arthrodesis complicated with a para-spinal abscess. It had an excellent visual outcome. DISCUSSION: Bacterial endogenous endophthalmitis is a rare, but serious ocular disease that occurs when bacteria reach the eye via the bloodstream. It requires a very early diagnosis based on the clinical symptoms and patient history. A suitable and specific treatment with intravenous and intravitreal antibiotics may prevent a bad visual prognosis in some cases.

The usefulness of 18F-fluorocholine PET/CT in the detection of recurrence of central nervous system primary neoplasms. / Valor de la PET/TC cerebral con 18F-fluorocolina en la detección de recurrencias de neoplasias primarias del sistema nervioso central.

AIM: To study the usefulness of 18F-fluorocholine (FCH) in detecting the recurrence of primary brain tumours. MATERIAL AND METHODS: A prospective study was conducted on brain PET/CT with FCH for compassionate use in 21 patients with suspected recurrence of a primary brain tumour. The distribution by pathology was: three grade ii astrocytomas, three grade iii astrocytomas, one grade ii oligodendroglioma, three grade iii oligodendrogliomas, one grade iii oligoastrocytoma, four glioblastoma multiform, one gliomatosis cerebri, and five meningiomas. Studies in which there was a visually significant uptake in the brain parenchyma were classified as positive. RESULTS: A total of 17 patients were classified as positive, with the results being confirmed by histology (10 cases) or clinical follow-up and imaging, with no false positives or negatives. The mean SUVmax for positive patients was 8.02 and 0.94 for the negative ones, which was significantly different (P=.003) CONCLUSION: PET/CT with FCH shows encouraging results in the evaluation of patients with suspected recurrence of primary brain neoplasms.

[Dementia with Lewy bodies and Alzheimer's disease: differential diagnosis by cardiac sympathetic innervation MIBG imaging]. / Demencia con cuerpos de Lewy y enfermedad de Alzheimer: diagnóstico diferencial mediante estudio de la inervación simpática cardíaca con MIBG.

UNLABELLED: Dementia with Lewy bodies (DLB) is the second most common cause of degenerative dementia after Alzheimer's disease (AD). At present, pre-mortem diagnosis of DLB can only be made clinically using the International Consensus Criteria. However, an accurate differential diagnosis between these diseases could improve the therapeutic handling of patients with DLB, due to their supersensitivity to neuroleptic treatment and the difficult treatment of their psychotic symptoms. OBJECTIVE: To assess the utility of cardiac MIBG imaging as diagnostic study for DLB, to help in the differential diagnosis with AD. MATERIAL AND METHODS: Cardiac MIBG imaging was performed in 11 patients with clinical criteria of probable DLB (7 males, mean age 77 years [range 62-89 years], mean MMSE 17 [range 11-28], and in 9 patients with clinical criteria of probable AD (3 males, mean age 79 years [range 61-87 years], mean MMSE 17 [range 4-25]). Planar anterior images of the thorax were acquired at 15 minutes. (early study) and 4 hours (late study) after tracer injection. Myocardial MIBG activity was quantified by means of a heart-to-mediastinum ratio (HMR). A HMR > 1.8 was considered normal. RESULTS: Respect AD patients, patients with DLB showed decreased HMR in the early study (1.34 +/- 0.27 [range 1.03-1.98] vs. 1.84 +/- 0.22 [range 1.53-2.15], p<0.001) and in the late study (1.22 +/- 0.23 [range 0.95-1.75] vs. 1.73 +/- 0.08 [range 1.59-1.89], p<0.0001). CONCLUSIONS: Cardiac MIBG imaging could be a useful tool for differential diagnosis between DLB and AD.

Myocyte cell damage after administration of doxorubicin or mitoxantrone in breast cancer patients assessed by indium 111 antimyosin monoclonal antibody studies.

PURPOSE: To compare myocyte cell damage induced by doxorubicin or mitoxantrone, we performed left ventricular ejection fraction (LVEF) measurements and indium 111 antimyosin antibody studies in a group of patients with advanced breast cancer who had been treated with these anthracycline derivatives. PATIENTS AND METHODS: We studied 35 patients eligible to receive chemotherapy including the anthracyclines: doxorubicin or mitoxantrone (cumulative dose of doxorubicin, 500 mg/m2; or mitoxantrone, 120 mg/m2). LVEF was measured before and after 10 cycles of chemotherapy. Antimyosin uptake in the myocardium was quantified by means of a heart-to-lung ratio (HLR). RESULTS: Patients treated with doxorubicin presented with a significant decrease in LVEF after chemotherapy (before, 60.4% +/- 8.92%; after, 49.8% +/- 9.71%; P = .001). Antimyosin uptake was observed in all patients with a HLR of 2.03 +/- 0.25. Seven of eight patients with a HLR greater than 2.03 had a greater than 10% decrease in LVEF. Patients treated with mitoxantrone did not present with a decrease in LVEF after chemotherapy (before, 55.4% +/- 6.25%; after, 55.8% +/- 7.25%; not significant). Antimyosin uptake was observed in 14 of 17 patients with a HLR of 1.77 +/- 0.18 (P < .05). CONCLUSION: 111In antimyosin monoclonal antibodies defect myocardial cell damage produced by doxorubicin and mitoxantrone. In patients with advanced breast cancer, cumulative doses of 120 mg/m2 of mitoxantrone produce less myocardial cell damage than cumulative doses of 500 mg/m2 of doxorubicin. 111In antimyosin uptake without decrease in LVEF after treatment with mitoxantrone indicates the presence of myocyte cell damage, but not to the extent necessary to deteriorate function. These results indicate that 111In antimyosin antibody studies are useful in the noninvasive comparative assessment of cardiotoxicity produced by different anthracycline derivatives.

High prevalence of myocardial monoclonal antimyosin antibody uptake in patients with chronic idiopathic dilated cardiomyopathy.

Monoclonal antimyosin antibody studies were undertaken to assess the presence of myocardial uptake in patients with chronic idiopathic dilated cardiomyopathy. Three groups were studied: 17 patients with chronic (greater than 12 months) idiopathic dilated cardiomyopathy, 12 patients with a large, poorly contracting left ventricle not due to dilated cardiomyopathy (control patients) and 8 normal individuals. The patients in the cardiomyopathy and control groups showed a similar degree of clinical and functional impairment. Imaging was undertaken 48 h after antimyosin injection. The heart/lung ratio of antimyosin uptake was used to assess the results. The mean ratio in the cardiomyopathy group was 1.83 +/- 0.36 (range 1.40 to 2.80), a value significantly higher than that obtained in the control patients without cardiomyopathy (mean 1.46 +/- 0.04, range 1.38 to 1.50) or normal subjects (mean 1.46 +/- 0.13, range 1.31 to 1.6) (p less than 0.01). No difference in the ratio was noted between the normal subjects and control patients. Abnormal antimyosin uptake was seen in 12 (70%) of the 17 patients with cardiomyopathy and in only 1 (8%) of the 12 control patients. Positive monoclonal antimyosin antibody studies are highly prevalent in chronic idiopathic dilated cardiomyopathy.

Marked ventricular repolarization abnormalities in highly trained athletes' electrocardiograms: clinical and prognostic implications.

OBJECTIVE: We sought to study the functional, clinical and prognostic implications of marked repolarization abnormalities (MRA) sometimes seen in athletes' electrocardiograms (ECGs). BACKGROUND: The clinical meaning of ECG MRA in athletes is unknown. No relationship has been drawn between either training intensity or any particular type of sport and MRA. Athletes are usually symptom free and do not show any decrease in their physical performance. It is as yet unclear whether MRA may have a negative effect on the performance of such athletes in competitive sports. METHODS: We studied 26 athletes with MRA (negative T waves > or =2 mm in three or more ECG leads at rest). No athletes presented clinical symptoms of cardiac disease or decrease in their physical performance. Clinical and physical examinations, ECG at rest, exercise test and echocardiographic and antimyosin studies were performed in all athletes. Rest/exercise myocardial perfusion single-photon emission computed tomography studies were performed in 17 athletes. The follow-up ranged from 4 to 20 years (mean 6.7 years). RESULTS: Four athletes were excluded due to hypertrophic cardiomyopathy. Echocardiographic studies showed right and left normal ventricular dimensions for highly conditioned athletes. In the exercise test, heart rate was 166 +/- 12.4 beats/min, and exercise tolerance was 15.2 +/- 2.7 metabolic equivalents of the task. All athletes had ECG at rest simulating myocardial ischemia or "pseudoischemia" with a tendency to normalize during exercise. Myocardial perfusion studies were normal in the studied athletes. Antimyosin studies showed mild and diffuse myocardial radiotracer uptake in 15 athletes (68%). No adverse clinical events were observed in the follow-up. CONCLUSIONS: These results suggest that MRA have no clinical or pathological implications in athletes and should, therefore, not preclude physical training or participation in sporting events.

Evaluation of biopsy classification for rejection: relation to detection of myocardial damage by monoclonal antimyosin antibody imaging.

OBJECTIVES: This study sought to compare the histologic grades of rejection in endomyocardial biopsy specimens with the global estimate of myocardial transplant-related cardiac damage detected by myocardial uptake of monoclonal antimyosin antibodies. BACKGROUND: The diagnosis and treatment of acute cardiac allograft rejection is based on the interpretation of endomyocardial biopsies. Because allograft rejection is a multifocal process and biopsy is obtained from a small area of the right ventricle, sampling error may occur. Global assessment of myocardial damage associated with graft rejection is now possible with the use of antimyosin scintigraphy. The present study was undertaken to compare the histologic grades of rejection in endomyocardial biopsy specimens with the global assessment of transplant-related myocardial damage detected by antimyosin scintigraphy. METHODS: Biopsies (n=395) from 112 patients were independently interpreted by three pathologists in a blinded manner according to the original Stanford four-grade (normal, mild, moderate and severe) and the current International Society of Heart and Lung Transplantation (ISHLT) seven-grade (0, 1A, 1B, 2, 3A, 3B and 4) classifications. The results were correlated with 395 antimyosin studies performed at the time of the biopsies. The heart/lung ratio of antimyosin antibody uptake was used to assess the severity of myocardial damage. RESULTS: In the Stanford biopsy grade classification, significantly higher antimyosin uptake, indicating increasing degrees of myocardial damage, were associated with normal (1.78+/-0.26), mild (1.88+/-0.31) and moderate (1.95+/-0.38) biopsy classifications for rejection (p < 0.01). In the ISHLT classification, significant differences were detected only for antimyosin uptake associated with grades 0 (1.77+/-0.26) and 3A (1.98+/-0.39) but not for intermediate scores (1A, 1B and 2). In view of the similar intensity of antibody uptake among the various grades, ISHLT biopsy scores were regrouped: normal biopsies in grade A; 1A and 1B as grade B; and 2 and 3A as grade C. Antimyosin uptake in grades A, B and C was 1.78+/-0.26, 1.88+/-0.31, 1.95+/-0.38, respectively (p < 0.01). CONCLUSIONS: The current ISHLT seven-grade scoring system does not reflect the progressive severity of myocardial damage associated with heart transplant rejection. Because myocardial damage constitutes the basis of treatment for allograft rejection, there is a need to reevaluate the ISHLT grading system, given its importance for multicenter trials.

Myocardial cell damage in human hypertension.

OBJECTIVES: The goal of this study was to investigate the presence of myocardial cell damage in patients with systemic hypertension and its relationship with left ventricular hypertrophy (LVH). BACKGROUND: Although initially compensatory, LVH adversely affects myocellular integrity and contributes to congestive heart failure in hypertensive patients. Noninvasive detection of myocardial damage can be of value. METHODS: We performed imaging studies with 111In-labeled monoclonal antimyosin antibodies to identify myocardial damage in 39 patients with systemic hypertension and variable degrees of LVH. Three groups were considered: 16 asymptomatic patients with normal echocardiographic left ventricular mass (LVM) (group I); 14 asymptomatic patients with LVH (group II) and 9 patients with symptomatic hypertensive heart disease and advanced LVH (group III). The severity of myocardial damage was represented as heart-to-lung (target-to-background) antibody uptake ratio (normal: <1.55). RESULTS: Mean LVM index was 105+/-14 g/m2 in group I, 124+/-24 in group II and 174+/-29 in group III. Heart-to-lung ratios of antimyosin uptake were: 1.45+/-0.14 in group I, 4 of the 16 (25%) patients showing an abnormal scan; 1.50+/-0.07 in group II with abnormal scans in 2 of the 14 (16%) patients and 1.77+/-0.16 (p < 0.001) in group III, all 9 patients presenting with abnormal antimyosin scans. On multivariate regression analysis LVM index was the main variable that independently correlated with the degree of myocardial uptake of antimyosin (r = 0.815; p = 0.001). CONCLUSIONS: This study provides the first in vivo evidence of myocyte damage in patients with hypertension. The severity of myocardial damage can be related to the magnitude of LVH.

Active myocardial damage without attending inflammatory response in dilated cardiomyopathy.

OBJECTIVES: This study aimed to compare indium-111 (111In)-monoclonal antimyosin antibody uptake in patients with dilated cardiomyopathy before heart transplantation with the histologic findings in the explanted hearts. BACKGROUND: A high prevalence of 111In-monoclonal antimyosin antibody uptake has been described in patients with dilated cardiomyopathy, suggesting the presence of active, ongoing myocyte damage; however, no correlation between monoclonal antimyosin antibodies and histologic findings is available in these patients. METHODS: A consecutive series of 21 patients with dilated cardiomyopathy awaiting heart transplantation were studied with monoclonal antimyosin antibodies before the operation, and the results were compared with the histologic analysis of the explanted hearts. The interval between monoclonal antimyosin antibody studies and transplantation was 1 to 90 days (mean 58 +/- 31). RESULTS: Using a semiquantitative method (heart/lung ratio), monoclonal antimyosin antibody uptake was present in 15 (71%) of 21 patients, but active myocarditis in the explanted hearts was detected in only 7. In 11 patients, intense monoclonal antimyosin antibody uptake coexisting with absent myocyte damage or cellular infiltration of explanted hearts was noted. One patient who showed preoperative monoclonal antimyosin antibody uptake underwent transplantation 11 h later, and ex vivo diffuse myocardial antimyosin uptake was detected, but active myocarditis was seen only at cardiectomy in only a small area of the heart; the rest of the myocardium showed no signs of myocyte damage. CONCLUSIONS: In dilated cardiomyopathy, monoclonal antimyosin antibody uptake cannot be equated with the presence of an inflammatory response detected in the myocardium of the explanted heart.

Efficacy of augmented immunosuppressive therapy for early vasculopathy in heart transplantation.

OBJECTIVES: The present study was undertaken to prospectively and comparatively evaluate the role of serial myocardial perfusion imaging and coronary angiography for the detection of early vasculopathy in a large patient population and also to determine the short- and long-term efficacy of augmented immunosuppressive therapy in the potential reversal of the early vasculopathy. BACKGROUND: Allograft vasculopathy is the commonest cause of death after the first year of heart transplantation. Anecdotal studies have reported the efficacy of augmented immunosuppressive therapy after early detection of vascular involvement. However, no prospective study has evaluated the feasibility of early detection and treatment of allograft vasculopathy. METHODS: In 76 cardiac allograft recipients, 230 coronary angiographic and 376 scintigraphic studies were performed in a follow-up period of 8 years. Angiography was performed at 1 month and every year after transplantation, and thallium-201 scintigraphy at 1, 3, 6 and 12 months after transplantation and twice a year thereafter. Prospective follow-up of 76 patients showed that 18 developed either angiographic or scintigraphic evidence of coronary vasculopathy. All episodes were treated with 3-day methylprednisolone pulse and antithymocyte globulin. RESULTS: Twenty-two episodes of vasculopathy were diagnosed and treated in these 18 patients. Of these 22 episodes, two were detected only by angiography, seven by both angiography and scintigraphy, four by scintigraphy and histologic evidence of vasculitis and nine episodes only by thallium-201 scintigraphy studies. Angiographic and/or scintigraphic resolution was observed in 15 of the 22 episodes (68%) with augmented immunosuppression. The likelihood of regression was higher when treatment was instituted within the first year of transplantation (92%) than after the first year (40%) (p = 0.033). Eighty percent of patients who responded to follow-up. CONCLUSIONS: The present study suggests that early detection of allograft coronary vasculopathy is feasible with surveillance myocardial perfusion or coronary angiographic studies. When identified early after transplantation, immunosuppressive treatment may result in regression of coronary disease.

Spectrum of alcohol-induced myocardial damage detected by indium-111-labeled monoclonal antimyosin antibodies.

OBJECTIVES: We sought to determine the prevalence, intensity and evolving changes of myocardial damage detected by myocardial uptake of antimyosin antibodies in patients with alcohol-induced dilated cardiomyopathy, alcohol addicts attending a detoxification unit and healthy subjects with short-term alcohol consumption. BACKGROUND: Evidence of alcohol-induced myocardial damage may be provided by myocardial uptake of indium-111-labeled monoclonal antimyosin antibodies. The spectrum of such damage in patients who are heavy drinkers (> 100 g for > 10 years), with or without cardiomyopathy, and the impact of short-term alcohol ingestion on antimyosin antibody uptake have not been adequately explored. METHODS: One hundred twenty antimyosin studies were performed in 56 patients with dilated cardiomyopathy (group I), 15 alcohol addicts attending a detoxification unit (group II) and 6 volunteers for short-term alcohol ingestion (group III). Estimation of antibody uptake was calculated through a heart/lung ratio (HLR) (normal < 1.55). RESULTS: The 56 patients in group I (54 men, 2 women; mean [+/-SD] age 46 +/- 11 years) had consumed 123 +/- 60 g/day of alcohol for 21 +/- 9 years, for a cumulative intake of 914 +/- 478 kg. Mean duration of symptoms was 46 +/- 49 months. Mean left ventricular end-diastolic diameter was 71 +/- 10 mm, and mean ejection fraction was 28 +/- 12%. No differences in New York Heart Association functional class, ventricular size or ejection fraction were noted between 28 active and 28 past consumers, except for the prevalence and intensity of antibody uptake (75% vs. 32%, p < 0.001) and HLR (1.75 +/- 0.26 vs. 1.49 +/- 0.17, p = 0.0001). In 19 patients in the active group restudied after alcohol withdrawal, antibody uptake decreased (from 1.76 +/- 0.17 to 1.55 +/- 0.19, p < 0.001), and ejection fraction improved (from 30 +/- 12% to 43 +/- 16%, (p < 0.001). No changes occurred in the 15 past consumers restudied. The 15 male patients in group II (mean age 36 +/- 4 years) had consumed 156 +/- 59 g/day for 17 +/- 5 years, for a cumulative alcohol intake of 978 +/- 537 kg, an amount similar to that in patients in group I, but antimyosin antibody uptake was detected in only 3 (20%) of 15 patients. None of six group III subjects developed antibody uptake after short-term ethanol ingestion. Despite the small sample size, the power to detect clinically relevant differences in most variables that did not reach statistical significance was amply sufficient. CONCLUSIONS: In alcohol-induced dilated cardiomyopathy, alcohol withdrawal is associated with the reduction or disappearance of myocardial damage and improvement of function. The difference in prevalence of antimyosin antibody uptake in patients with and without cardiac disease who consume similar amounts of alcohol suggests the presence of those with different myocardial susceptibilities to alcohol. Short-term ethanol ingestion in healthy subjects does not induce detectable uptake of antimyosin antibodies.