Position statement on the non-invasive diagnosis of patients with ATTR pardiac amyloidosis, endorsed by the Hellenic Society of Nuclear Cardiology, for the Nuclear Medicine practitioners.

Cardiac amyloidosis is a rare condition characterized by the accumulation of abnormal proteins called amyloids in the heart tissue. These amyloids can disrupt the normal functioning of the heart and lead to a variety of symptoms and complications.

PET Counting Response Variability Depending on Tumor Location, Activity, and Patient Obesity: A Feasibility Study of Solitary Pulmonary Nodule Using Monte Carlo.

We aim to investigate the counting response variations of positron emission tomography (PET) scanners with different detector configurations in the presence of solitary pulmonary nodule (SPN). Using experimentally validated Monte Carlo simulations, the counting performance of four different scanner models with varying tumor activity, location, and patient obesity is represented using a noise equivalent count rate (NECR). NECR is a well-established quantitative metric which has positive correlation with clinically perceived image quality. The combined effect of tumor displacement and increased activity shows a linear ascending trend for NECR with slope ranges of (12.5-18.2)*10-3 (kBq/cm3)-1 for three-ring (3R) scanners and (15.3-21.5)*10-3 (kBq/cm3)-1 for four-ring (4R). The trend for the combined effect of tumor displacement and patient obesity is exponential decay with 3R configurations weakly dependent on the patient obesity if the tumor is located at the center of the field of view with exponent's range of (6.6-33.8)*10-2cm-1. The dependence is stronger for 4R scanners (9.6-38.5)*10-2cm-1. The analysis indicates that quantitative PET data from the same SPN patient possibly examined in different time points (e.g., during staging or for the evaluation of treatment response) are affected by the different detector configurations and need to be normalized with patient weight, activity, and tumor location to reduce unwanted bias of the diagnosis. This paper provides also with a proof of concept for the ability of properly tuned simulations to provide additional insights into the counting response variability especially in tumor types where often borderline decisions have to be made regarding their characterization.

Assessment of myocardial adrenergic innervation in patients with sick sinus syndrome: effect of asynchronous ventricular activation from ventricular apical stimulation.

OBJECTIVE: To investigate ventricular sympathetic innervation in patients with sick sinus syndrome and to detect regional deterioration of adrenergic innervation caused by asynchronous ventricular activation from right ventricular pacing. DESIGN: Prospective controlled study. SETTING: Tertiary cardiac referral centre. PATIENTS: 22 patients with sick sinus syndrome and indications for permanent dual chamber pacing; 20 healthy individuals as controls. INTERVENTIONS: All patients underwent myocardial imaging with planar and single photon emission computed tomography (SPECT) after an intravenous infusion of 5 mCi 123I-meta-iodobenzylguanidine (123I-MIBG) before and after pacemaker implantation. A SPECT thallium201 myocardial study was done during the same week as the 123I-MIBG study in all patients. MAIN OUTCOME MEASURES: The heart to mediastinum (H/M) ratio and washout rate were calculated during the 123I-MIBG study to assess the global cardiac sympathetic activity; the aim of the SPECT study was to investigate the regional distribution of adrenergic innervation. RESULTS: The H/M ratio was significantly smaller in the patients with sick sinus syndrome than in the controls (p < 0.001). In sick sinus syndrome there were regional adrenergic innervation defects, mostly in the inferior and apical walls. After a medium term pacing period, a redistribution of 123I-MIBG uptake was detected, with deterioration of adrenergic innervation in the inferior, apical, and posterior walls. The thallium201 myocardial perfusion study showed no change after three months of permanent pacing. CONCLUSIONS: Patients with sick sinus syndrome have global and regional disturbances of the adrenergic innervation of the left ventricular myocardium. These seem to deteriorate as a result of asynchronous electrical activation. The clinical significance of this finding requires further investigation.

Segmental pattern of myocardial sympathetic denervation in idiopathic dilated cardiomyopathy: relationship to regional wall motion and myocardial perfusion abnormalities.

BACKGROUND: Iodine 123-labeled metaiodobenzylguanidine (MIBG) has been used to study cardiac adrenergic nerve activity. Cardiac MIBG uptake is diminished in patients with heart failure. However, it is not known how this reduction is related to regional abnormalities of myocardial wall motion or perfusion. METHODS AND RESULTS: We studied 24 patients with idiopathic dilated cardiomyopathy (ejection fraction <45%) and 15 healthy control subjects using I-123 MIBG cardiac imaging, echocardiographic assessment of wall motion abnormalities, technetium 99m sestamibi perfusion scintigraphy, and hemodynamic assessment. Cardiac MIBG was significantly correlated with ejection fraction (r = 0.67), cardiac index (r = 0.57), left ventricular wall motion score index (r = -0.68), and systolic wall stress (r = -0.61). MIBG was lower in patients than in control subjects (1.43 +/- 0.19 vs 2.05 +/- 0.02; P <.01), whereas the washout rate was higher (P <.01). Moreover, a significant correlation was found between the reduction in MIBG uptake and the severity of echocardiographic wall motion abnormalities in the anterior wall (r = 0.543), apex (r = 0.530), and septum (r = 0.675), as well as with the severity of decrease in resting myocardial perfusion in the anterior wall (r = 0.480) and septum (r = 0.580). CONCLUSIONS: Patients with idiopathic dilated cardiomyopathy show not only global but also regional abnormalities of cardiac sympathetic innervation. The severity of these changes is partially correlated with abnormalities of regional wall motion and myocardial perfusion.

Effects of asynchronous ventricular activation on myocardial adrenergic innervation in patients with permanent dual-chamber pacemakers; an I(123)-metaiodobenzylguanidine cardiac scintigraphic study.

AIMS: To evaluate myocardial sympathetic innervation abnormalities in patients with DDD pacemakers for complete heart block. METHODS: We studied 39 patients, chronically paced in DDD mode because of complete atrioventricular block. Twenty-three healthy individuals served as a control group. All patients underwent planar and single-photon emission computed tomography (SPECT) myocardial imaging 4 h after intravenous infusion of 185 MBq I(123)-MIBG. The heart to mediastinum ratio was calculated to quantify cardiac I(123)-MIBG accumulation, while the SPECT study was performed to investigate the regional distribution of adrenergic innervation. All patients underwent a SPECT thallium(201)myocardial study during the same week as the I(123)-MIBG study. RESULTS: The heart to mediastinum ratio was significantly smaller in paced patients than in the controls (P<0.001). 89.7% of paced patients had regional abnormalities of I(123)-MIBG uptake, mainly in the inferior (92.3%) and apical (38.5%) wall. 46.2% of paced patients had regional perfusion defects, also mainly in the inferior (46.2%) and apical (10.3%) wall. Neither the I(123)-MIBG abnormalities nor the perfusion defects were related to the duration of pacing. CONCLUSIONS: Stimulation from the apex of the right ventricle leads to regional disturbances of the adrenergic innervation of the left ventricular myocardium, as assessed by I(123)-MIBG activity.

Indium-111 monoclonal antimyosin cardiac scintigraphy in men with idiopathic dilated cardiomyopathy.

This study examined the prognostic value and the evolution of the heart-to-lung ratio of monoclonal antimyosin antibody (MAA) uptake in patients with a diagnosis of idiopathic dilated cardiomyopathy (IDC). Uptake of indium-111-labeled MAA occurs when the myocytes become irreversibly damaged. The study included 29 men with IDC followed up for 3 years. The diagnosis was verified by endomyocardial biopsy in all patients. Patients who survived beyond 1 year were restudied. Baseline heart-to-lung ratio of MAA was 1.74+/-0.22. Multivariate Cox regression analysis revealed that MAA and New York Heart Association class were independent predictors of late mortality, with a hazard ratio of 4.4 (95% confidence interval 1.1 to 17.9, p = 0.036) and 7.5 (95% confidence interval 2.0 to 28.4, p = 0.003), respectively, when heart-to-lung ratio of MAA uptake was > 1.74 and New York Heart Association class was >11. When these patients were divided into those with chronic IDC (group I [n = 19]) and those with subacute IDC (group II [n = 10]), baseline heart-to-lung ratio was 1.7+/-0.2 and 1.86+/-0.25, respectively (p = NS). In the surviving patients, on restudy, the heart-to-lung ratio of MAA uptake was unchanged in group I (1.64+/-0.20, p = NS), but had decreased to the level of group I (1.66+/-0.21 [p = 0.008]) in group II. Thus, men with IDC and a high heart-to-lung ratio of MAA uptake have a worse long-term prognosis than patients with a lower ratio. The heart-to-lung ratio of MAA decreases comparably over time in subacute IDC and remains stable in chronic IDC.

Scleroderma heart disease: an unusual cause of positive antimyosin cardiac imaging.

In-antimyosin scintigraphy offers a valuable noninvasive method for early detection of clinically silent cardiac involvement in patients with systemic sclerosis, even in the absence of left ventricular dysfunction. In these patients with positive antimyosin study results, intense pharmacologic treatment with vasodilators may be warranted.

Cold-induced coronary Raynaud's phenomenon in patients with systemic sclerosis.

OBJECTIVE: Cardiac involvement with myocardial-band necrosis is common in systemic sclerosis. One possible explanation is that an underlying vasomotor abnormality accounts for these histologic findings. To shed light on this issue we investigated the existence of "myocardial Raynaud's phenomenon" in such patients. METHODS: We examined 25 patients with systemic sclerosis and 14 patients with systemic lupus erythematosus or rheumatoid arthritis, using cold pressor and dipyridamole-thallium-201 scintigraphy. RESULTS: Twenty-three patients with systemic sclerosis and 13 patients with lupus erythematosus or rheumatoid arthritis had normal perfusion during dipyridamole imaging. Seven scleroderma patients with normal dipyridamole test presented cold-induced transient myocardial ischemia, while none of the control patients had cold-induced ischemia (p = 0.034). All patients with cold-induced ischemic defects presented long-standing Raynaud's phenomenon (> 5 years); of the 14 patients with long-standing Raynaud's phenomenon 7 presented ischemic thallium-201 defects; of the remaining 9 patients with Raynaud's phenomenon of short duration (< 5 years) none presented cold-induced ischemia (p = 0.019). CONCLUSION: Patients with systemic sclerosis and long-standing Raynaud's phenomenon, even in the presence of normal myocardial perfusion during pharmacological vasodilation with dipyridamole, may present cold-induced myocardial ischemia, a functional Raynaud's phenomenon of the heart.

Antimyosin scintigraphy for detection of cardiac amyloidosis.

The diagnostic value of antimyosin scanning in 7 patients with biopsy-proven cardiac amyloidosis was examined in this study. Antimyosin imaging was positive in all amyloid patients, with more intense uptake in patients with heart failure.

Acute estrogen administration can reverse cold-induced coronary Raynaud's phenomenon in systemic sclerosis.

A 52-year-old postmenopausal woman with long-standing progressive systemic sclerosis and Raynaud's phenomenon was examined by dipyridamole-thallium-201 myocardial imaging and cold pressor thallium-201 myocardial scintigraphy. The dipyridamole test revealed normal myocardial perfusion, while the cold pressor test showed reversible ischemia to the anteroapical myocardial wall, indicating coronary Raynaud's phenomenon. Acute intravenous administration of conjugated estrogens led to normalization of the cold-induced thallium-201 defect. This is the first reported case of the beneficial effect of estrogens in coronary Raynaud's phenomenon.

Doxorubicin-induced cardiac neurotoxicity: study with iodine 123-labeled metaiodobenzylguanidine scintigraphy.

BACKGROUND: Iodine 123-labeled metaiodobenzylguanidine (123I-MIBG) can be used to generate a scintigraphic image of the adrenergic nervous innervation of the heart. METHODS AND RESULTS: To test the hypothesis that doxorubicin may lead to damage of cardiac neurons, we examined 37 patients with various malignant neoplasms, 14 of whom were on therapy with doxorubicin. All patients were examined with 123I-MIBG scintigraphy and radionuclide ventriculography. Cardiac 123I-MIBG uptake was assessed by means of a heart to mediastinum activity ratio (H/M). Left ventricular ejection fraction was not different in patients with or without doxorubicin. In patients receiving doxorubicin, the H/M ratio was significantly lower (1.73 +/- 0.25 vs 2.13 +/- 0.25, p < 0.001) and correlated with doxorubicin cumulative dose (r = -0.51, p < 0.001). By using a H/M ratio of 1.73 as a cutoff point, 123I-MIBG uptake was abnormal in none of the 23 patients not receiving and 6 of 14 patients receiving doxorubicin therapy (p < 0.001). In 10 patients initially not receiving doxorubicin, 123I-MIBG scintigraphy was repeated after receiving 236 +/- 47 mg/m2 of doxorubicin. The H/M became abnormal in 3 of 10 patients, whereas the ejection fraction became abnormal in 2 of 10 patients. CONCLUSION: 123I-MIBG cardiac uptake decreases in a doxorubicin dose-dependent way, indicating a cardiac adrenergic neurotoxic effect of doxorubicin. This phenomenon appears early and generally before deterioration of the ejection fraction.

Natural evolution of antimyosin scan and cardiac function in patients with acute myocarditis.

Indium-111 monoclonal antimyosin antibody imaging is a convenient method to diagnose acute myocarditis. The present study examined the natural evolution of a positive antimyosin scan in 10 patients with acute myocarditis, in relation to left ventricular ejection fraction. All patients underwent myosin-specific monoclonal antibody imaging and radionuclide ventriculography; in all patients endomyocardial biopsy was performed. Repeat assessment of left ventricular function and antimyosin uptake was performed 1, 2 and 6 months later. A heart-to-lung ratio was used to quantify antimyosin uptake. Heart-to-lung ratio in patients with myocarditis was 2.12 +/- 0.31, significantly higher than that observed in eight controls (1.35 +/- 0.08, P < 0.001). During follow-up 2.2 repeat scans per patient were performed. Heart-to-lung ratio normalized (< 1.6) within 1 month in four patients, within 2 months in one patient and within 6 months in two patients; three patients continued to have a positive antimyosin uptake at 6 months, suggesting ongoing myocardial necrosis. At the end of follow-up, ejection fraction improved by > 5% in four patients; normalization or persistence of tracer uptake could not predict an improvement of ejection fraction. It is concluded that antimyosin scintigraphy is useful for diagnosing myocarditis in its subacute or chronic stage during which unknown or immune mechanisms may be in operation. An improvement in left ventricular function cannot be predicted on the basis of persistence or not of tracer uptake.

Dobutamine-induced ST-segment elevation in patients with healed myocardial infarction. A marker of myocardial viability.

The purpose of this study was to determine the significance of transient ST-segment elevation during dobutamine infusions in patients with healed Q wave myocardial infarction. Twenty-seven patients with previous Q wave myocardial infarction were studied prospectively with dobutamine-thallium-201 single-photon emission computed tomography. The presence of ST-segment elevation in leads with Q waves was related to thallium reversibility at 4-hour redistribution imaging or after reinjection, to residual flow, as well as to wall motion abnormalities in the infarcted zone. ST-segment elevation in infarct-related leads was observed in 15 patients; 11 (73%) showed viability by thallium-201 in the infarcted zone. In patients without ST-segment elevation, viability was shown less frequently (33%, P < .05). Hypokinesis in infarcted segments was present in 60% of patients with ST-segment elevation and in 25% of patients without ST-segment elevation (.05 < P < .1). Finally, infarct-related artery was patent and/or collaterals were present in 10 patients with ST-segment elevation (67%) and in 4 patients without (33%, .05 < P < .1). In conclusion, ST-segment elevation during dobutamine infusion is a marker of residual viability in infarcted segments.

Detection of microinfarction in patients with unstable angina: study by 111In-antimyosin imaging.

To examine the incidence of a positive indium-111 antimyosin scintigraphy in patients with unstable angina, we prospectively examined 25 patients with unstable angina and 11 patients with stable angina. All patients were injected with 2 mCi of indium-111 on admission and planar scintigraphy was performed 48 h later. Symptoms and signs of ischemia indicating severity of ischemia were monitored during the period between injection and scanning. None of the patients developed a rise in cardiac enzymes suggesting myocardial necrosis. Seven (28%) of the 25 patients with unstable angina had positive antimyosin scanning; no stable patients had positive scanning. All seven patients with unstable angina and positive scanning had signs of severe ischemia (four patients had multiple episodes of > 2/day, three patients had prolonged episodes of > 15 min, three patients had ST depression in > 3 EKG leads) while only one of the eighteen unstable patients with negative scannings had signs of severe ischemia (P < 0.001). In conclusion, (1) a significant number of unstable angina patients present positive antimyosin scanning without an elevation of cardiac enzymes and (2) these patients usually present multiple or severe episodes of ischemia indicating that during these episodes, minor myocardial necrosis, undetected by enzymes, may occur.