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Objective: The feasibility of human cardiac imaging using a prototype 256-detector row cone-beam computed tomography (256CBCT) scanner without electrocardiographic gating was examined., Methods: Two healthy male volunteers were examined by contrast-enhanced 256CBCT. The number of detectors was 912 x 256, each measuring approximately 0.5 mm x 0.5 mm at the center of rotation. The craniocaudal coverage was approximately 100 mm after reconstruction by the Feldkamp-Davis-Kress algorithm. The effective time resolution was 500 milliseconds using a half-scan algorithm., Results: Serial enhancement of the left ventricular myocardium was detected. The right and left coronary arteries at proximal and distal segments were depicted without significant blurring. Although the left ventricular wall motion on cine images was not smooth over time, it was possible to measure ventricular volume and ejection fraction., Conclusions: Using the 256CBCT, it was possible to visualize the coronary arteries, myocardial perfusion, and ventricular contraction simultaneously during a single acquisition.

123I-metaiodobenzylguanidine (MIBG) scintigraphy has been used to predict prognosis of patients with dilated cardiomyopathy (DCM), although it is unknown which parameter of MIBG is the most useful clinically. We studied MIBG in 59 patients with DCM, and followed them up to evaluate the prognosis of DCM. Single photon emission tomography (SPET) and planar imaging were performed, both early (e) and 4 h (delayed, d) post-injection. 201Tl (TL) SPET and radionuclide-ventriculography were also investigated. The total defect score of early and delayed MIBG and 201 Tl (MIBGeDS, MIBGdDS, TLDS) was analysed visually for each SPET image. The heart to mediastinum ratio (H/M) for both the early and delayed MIBG planar images and myocardial washout rate at 4 h were analysed quantitatively. Sixteen patients died during follow-up. Cox Hazards univariate analysis selected washout rate (P < 0.0001), H/Me (P = 0.0012), H/Md (P = 0.0001) and left ventricular ejection fraction (P = 0.0004) as indices for the prediction of cardiac death. Multivariate analysis selected washout rate as the most powerful independent predictor of prognosis (P < 0.0001). Survival curves with a threshold value of 52% for washout rate were able to differentiate a negative outcome from survival (P < 0.0001). TLDS, MIBGeDS and MIBGdDS were not useful in the prediction of prognosis. The washout rate of MIBG is the most potent predictor of cardiac death and is considered clinically useful.

The aim of this study was to determine whether sympathetic imbalance in congenital long QT syndrome (LQTS) can be identified by cardiac sympathetic neuronal dysinnervation. 123I-metaiodobenzylguanidine (MIBG) is a tracer of the norepinephrine analogue which reflects the regional innervation and norepinephrine kinetics in cardiac sympathetic nerves. Sixteen patients with LQTS, who were members of 12 families, and 7 normal controls underwent MIBG scintigraphy. Myocardial SPET and planar images were obtained 15 min and 4 h after the injection of MIBG in each patient. The relative regional uptake (RRU) and regional washout rate (rWR) of MIBG at 4 h in each of nine regions were compared with those in the control group. The heat-to-mediastinum ratio (H/M) and global washout rate (GWR) were also calculated. The RRU, rWR, H/M and GWR showed no significant difference between LQTS patients and normal controls. Furthermore, the RRU in 96% of all regions in LQTS was within the mean +/- 2 standard deviations of that in the control group. Patients with LQTS have normal cardiac sympathetic innervation, as assessed by MIBG. The sympathetic imbalance hypothesis is unlikely to be attributed to an abnormal distribution and different regional norepinephrine kinetics of cardiac sympathetic nerves.

Background: Sympathetic cardiopulmonary nerves arise from the cervical sympathetic trunks and the stellate ganglia and subsequently course along the origin of the great arteries and the coronary arteries to innervate the ventricles. Therefore, the sympathetic nerves may be obligatorily interrupted by the arterial switch operation (ASO) for complete transposition of the great arteries., Methods and Results: To demonstrate and characterize the possible sympathetic denervation, 51 patients after ASO, 4.8 years old (range, 1 month to 10.1 years), underwent [123I]metaiodobenzylguanidine (MIBG) imaging of the sympathetic nerve terminal. MIBG uptake to the heart was graded by quantitative analysis using the heart-to-mediastinum (H/M) ratio of MIBG uptake. A quantitative criterion for absent uptake of MIBG was set to 1.48 in the H/M ratio. Four patients < 1 month after ASO showed complete absence of MIBG uptake, which had been observed preoperatively. In contrast, 47 patients late after ASO (range, 15 months to 10.1 years) showed various degrees of uptake of MIBG. Patients operated on at < or =55 days of age showed positive MIBG uptake much more frequently than those operated on at later ages. Heart rate and rate-pressure product at peak exercise on a treadmill exercise test were significantly greater in patients with positive uptake than in those with absent uptake of MIBG., Conclusions: Cardiac sympathetic nerves were denervated early after and reinnervated late after ASO. Neonatal ASO may be favorable to facilitate sympathetic reinnervation, which may affect exercise tolerance late after surgery.

Background: Excellent results regarding mortality are well recognized in the long-term period after intracardiac repair of tetralogy of Fallot. However, it is still unclear how postoperative sequelae affect cardiac performance during exercise., Methods and Results: Twenty-nine patients with tetralogy of Fallot were studied 16 +/- 2 years after intracardiac repair by use of radionuclide first-pass ventriculography with an ultra-high-sensitive gamma camera at rest and at peak exercise on a semi-upright bicycle ergometer. The results were compared with those from 10 age- and sex-matched control subjects. Left and right ventricular ejection fraction and absolute ventricular volume were measured at rest and peak exercise. Regional right ventricular wall motion and diastolic function of the left ventricle were also assessed. Cardiac output of tetralogy was normally preserved both at rest and during exercise. Nevertheless, the incremental response of left ventricular ejection fraction during exercise was depressed in the patients. Left ventricular ejection fraction during exercise was inversely correlated with the right ventricular end-diastolic volume and the severity of pulmonary regurgitation. Regional wall motion at the right ventricular outflow tract was not decreased in the patients. Left ventricular diastolic function was not impaired in the patients compared with control subjects., Conclusions: Latent left ventricular dysfunction during exercise is related to an enlarged right ventricle due to pulmonary regurgitation after intracardiac repair of tetralogy. Careful follow-up is required in patients having significant pulmonary regurgitation.

Background: The therapeutic value of doxorubicin (DOX) is limited by its cardiotoxicity, which is dose dependent. To improve the detection of such myocardial damage, this study was designed to determine whether the 111In antimyosin antibody Fab could serve as a marker for cardiotoxicity in treated versus control rats on the basis of comparative morphological and hemodynamic findings., Methods and Results: DOX was administered by intravenous injection to rats at a dose of 3 mg.kg-1.week-1 for 5 weeks. Three weeks after the final injection, an intravenous dose of 111In antimyosin, 740 kBq (20 microCi), was administered, and tissue distribution of the radioisotope (percent kilogram dose per gram) was assessed in 48 hours. Myocardial uptake of radioactivity by both ventricles was more prominent in the DOX-treated rats than in control rats (p < 0.001). The heart-to-blood and heart-to-lung uptake ratios were markedly higher in the treated rats than in controls (p < 0.001). As the severity of the myocardial damage increased, there was a progressive increase in myocardial uptake. There was a strong correlation between the severity of myocardial damage and the ventricular end-diastolic pressure (r = 0.84 and r = 0.83 in the left and right ventricles, respectively). On microscopic immunoautoradiography of the DOX-treated heart, there was a specific immunolocalization of the radiotracer in the injured myocytes but no radioactivity in the control myocytes., Conclusions: 111In antimyosin antibody appears to be a useful immunoradiotracer in detecting cardiac damage induced by DOX administration and in assessing the severity of cardiotoxicity. These data reinforce the clinical observation that myocardial imaging using 111In antimyosin Fab is able to provide information to guide the course of patients receiving DOX treatment.

We compared combination therapy with low-dose aspirin plus ticlopidine to therapy with aspirin alone or ticlopidine alone in patients suffering transient ischemic attack or cerebral infarction. In 17, 24, and 23 patients, respectively, 300 mg/day aspirin, 200 mg/day ticlopidine, and 81 mg/day aspirin plus 100 mg/day ticlopidine were administered orally. Aspirin alone markedly inhibited platelet aggregation induced by arachidonic acid, partially inhibited platelet aggregation induced by adenosine diphosphate, and did not inhibit platelet aggregation induced by platelet activating factor. Ticlopidine alone inhibited platelet aggregation induced by adenosine diphosphate and platelet activating factor, but did not inhibit platelet aggregation induced by arachidonic acid. Combination therapy with aspirin plus ticlopidine markedly inhibited platelet aggregation induced by all three agonists. Plasma concentrations of beta-thromboglobulin and platelet factor 4 remained unchanged by aspirin alone, were slightly reduced by ticlopidine alone, and were markedly reduced by aspirin plus ticlopidine. Plasma concentration of thromboxane B2 was reduced by aspirin alone or with ticlopidine, but not by ticlopidine alone. The level of 6-ketoprostaglandin F1 alpha was reduced only by aspirin alone. Bleeding time was significantly prolonged by aspirin alone and by ticlopidine alone, although the greatest prolongation was produced by aspirin plus ticlopidine. Our results indicate that the combination of aspirin plus ticlopidine is a potent antiplatelet strategy, although the clinical importance of the changes observed need to be determined by a properly designed and controlled prospective study.