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.

Technetium-99m labelling of human immunoglobulin and preliminary clinical evaluation in tumour patients.

In the present investigation we have human immunoglobulin labelled with 99Tc(m), applying two different systems. The radiochemical characteristics of the labelled antibody were studied by conventional, radioanalytical methods. Further on, pharmacokinetics of this 99Tc(m)-labelled biomolecule were investigated, by i.v. administration in women, checked for tumours of the ovaries, uterus and cervix. Scintigraphic findings were compared to the results of other imaging techniques (CT, US, X rays), as well as to surgical findings. Our studies indicated that 99Tc(m)-human immunoglobuline can be applied successfully for the scintigraphic detection of several malignant and benign tumours of the female genital system. Tumour accumulation is probably due to the activation of particular cells, as macrophages and lymphocytes, responsible for inflammatory and immunological responses.

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.

Assessment of left ventricular stiffness and compliance.

Invasive and non-invasive methods exist to assess left ventricular compliance (LVC). This work has two parts, one experimental and one clinical. We estimated left chamber stiffness in dogs by using volume data from radionuclide ventriculography (RNV) and left ventricular pressure data, synchronized with a gating system to the intraventricular dp/dt max to obtain volume and pressure data from a mean cardiac cycle. In five dogs after acute experimental ischaemia, the modulus chamber stiffness Kp rose from 30.2 +/- 4.4 to 55.4 +/- 5.9 (P < 0.01). In 10 dogs with experimental infarction after intra-aortic balloon pumping, Kp decreased from 33.7 +/- 5.0 to 15.5 +/- 3.9 (P < 0.01) and in five dogs with experimental infarction, after intravenous infusion of sodium nitroprusside, Kp decreased from 41.4 +/- 5.5 to 22.2 +/- 2.8 (P < 0.01). In eight normal volunteers and in 20 postmyocardial infarction patients, we estimated a parameter reflecting the LVC by using volume data with blood flow velocity at the mitral valve annulus. Assuming that the mitral flow-velocity variation reflects LV pressure changes, the formula LVC = (dv/dt)/(dp-dt) becomes (dv/dt)/(df/dt) = dv/df. Values obtained in normals were 0.841 +/- 0.295 m-1s and after myocardial infarction 0.331 +/- 0.10 m-1s. Both methods allow clear separation in groups of animals or patients according to the expected changes in LVC or stiffness.

Acute effects of external and internal pacing on ejection fraction in patients with severe cardiac failure.

The present study aims at evaluating the acute hemodynamic effects of external and internal (3 and 15 mA) pacing on 30 patients with severe cardiac failure. The global and regional ejection fraction were calculated by repeated radionuclide ventriculography at rest (control) and during increasing pacing rates. Blood pressure was measured at the end of each scintigraphy data acquisition period. The pacing rate was increased by 10 beats/min in every step and varied between +10 to +60 beats/min above the resting heart rate. The ejection fraction during pacing was lower than the resting ejection fraction in every pacing mode (resting ejection fraction = 23.30 +/- 7.67%, external pacing = 19.36 +/- 9.30%, p < 0.05, internal pacing 3 mA = 22.15 +/- 7.00%, p = N.S., internal pacing 15 mA = 19.92 +/- 6.95%, p < 0.05). The resting ejection fraction was higher than the ejection fraction in every pacing rate. In 4 out of 30 patients the ejection fraction was higher in every pacing mode and rate than the resting ejection fraction. The regional ejection fraction of the interventricular septum during internal pacing was lower (p < 0.001) than resting and/or external pacing. In conclusion, pacing in patients with severe cardiac failure reduces the control ejection fraction. This reduction increases as the pacing rate increases. The reduction is greater with internal pacing of 15 mA while the hemodynamic effect in external pacing did not differ significantly from internal pacing. Overall, the resting ejection fraction was higher than the paced ejection fraction, although in some patients pacing improved their resting ejection fraction.

I-123 metaiodobenzylguanidine--thallium-201 mismatch following myocardial infarction.

Experimental data show that myocardial infarction (MI) results in regional depletion of myocardial catecholamines more extensively than necrosis. To investigate the extent of adrenergic denervation post MI in humans, we examined 16 patients, 59 +/- 12 years old, with recent (7-12 days) MI. Resting thallium-201 (201Tl) single photon emission computerized tomography (SPECT) imaging was performed to assess necrosis; metaiodobenzylguanidine I123 (MIBG) SPECT was used to evaluate adrenergic denervation. 201Tl and I123 MIBG defects were evaluated quantitatively using polar maps, and differences in defects were expressed as percent of total polar map. In all patients, I123 MIBG defect was larger than 201Tl defect, and difference ranged from 19 to 61% (39.5 +/- 13.2%). Thrombolysis and age > 60 did not influence the difference. Anterior MI showed larger differences (44 +/- 13 vs. 32 +/- 11%, p < 0.05); patients with ischemic electrocardiographic (ECG) changes in leads without abnormal Q waves had larger differences (45 +/- 9 vs. 33 +/- 14%, p < 0.05). It was concluded that (a) patients with recent MI present denervation larger than 201Tl perfusion defect, and (b) patients with anterior MI and ischemic ECG changes present a larger area of denervation.

Antimyosin scintigraphy for detection of myocarditis. Scintigraphic follow-up.

To examine the value of antimyosin-indium 111 imaging in relation to endomyocardial biopsy in patients with suspected myocarditis, as well as the natural evolution of abnormal findings on the antimyosin scan, 12 patients with suspected myocarditis underwent endomyocardial biopsy and antimyosin scan. The heart-to-lung ratio (H/L) was used to quantify the antimyosin scan. All 12 patients had abnormal results on the scan (H/L, 1.7 to 2.9; mean, 2.1 +/- 0.3); 8 of the 12 patients also had a diagnostic endomyocardial biopsy. In four patients with abnormal findings on antimyosin scan and normal findings on biopsy, the H/L ratio did not differ from eight patients with abnormal findings on antimyosin scan and a diagnostic biopsy; also, the ejection fraction did not differ between the two groups. One patient died, and 8 patients had a repeat antimyosin scan within 2 months after the initial study. The H/L ratio returned to normal in two out of three patients with normal results on biopsy and in three out of five patients with a diagnostic biopsy; the ejection fraction improved by 8 percent or more in one out of three patients with a nondiagnostic biopsy and in two out of five patients with a biopsy diagnostic for myocarditis. We conclude that the antimyosin scan is more frequently diagnostic than biopsy in suspected myocarditis. Patients with abnormal results on antimyosin scan and a nondiagnostic biopsy, as well as those with abnormal results on antimyosin scan and a diagnostic biopsy, tend to return to normal results on scan within 2 months and improve their ejection fraction.

Detection of viable tissue in healed infarcted myocardium by dipyridamole thallium-201 reinjection and regional wall motion studies.

Reinjection imaging with thallium-201 (Tl-201) may provide a convenient method of assessing myocardial viability. Twenty patients with a previous Q-wave healed myocardial infarction were examined to evaluate the detection of viable tissue in infarcted segments. All patients underwent to evaluate the detection of viable tissue in infarcted segments. All patients underwent dipyridamole Tl-201 tomographic imaging with reinjection of 1 mCi of Tl-201 after redistribution. Radionuclide ventriculography was performed before and after administration of 5 mg of dinitrate isosorbide sublingually for regional wall motion analysis. Patients presented with 38 fixed defects, 12 of which demonstrated improved Tl-201 uptake on reinjection; 10 of 12 reinjection-reversible segments were hypokinetic or normal after administration of nitrates, whereas 22 of 26 nonreversible segments remained akinetic or dyskinetic (p < 0.001). Of 20 patients, 9 had reinjection-reversible segments; coronary angiography revealed a patent infarct-related artery or collaterals, or both, in 7 of these patients. The infarct-related artery was patent or collaterals were present, or both, in 4 of 11 patients who did not improve with reinjection. It is concluded that reinjection of Tl-201 during dipyridamole Tl-201 scintigraphy may frequently detect viable tissue in infarcted segments in patients with a Q-wave infarction. Segments with reinjection reversibility usually do not remain dyskinetic or akinetic after administration of nitrates and have some residual flow on coronary angiography.

Doxorubicin cardiotoxicity detected by indium 111 myosin-specific imaging.

A patient with primary hepatoma, treated with doxorubicin and presenting with atypical electrocardiographic findings, was investigated with myosin-specific monoclonal antibody radiolabelled with indium-111. Despite a normal ejection fraction, myosin-specific scintigraphy was positive, indicating doxorubicin cardiotoxicity.