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IT has been proposed that iodine-123 15-(p-iodophenyl)-3-R,S-methylpentadecanoic acid (123I-BMIPP) is an agent for myocardial fatty acid metabolism in animal models. The aim of the present study was to determine whether alterations in fatty acid uptake and/or utilization in patients with hypertrophic cardiomyopathy (HCM) could be detected by 123I-BMIPP. Myocardial imaging with 123I-BMIPP and thallium-201 (201Tl) was performed in 14 fasted patients. A dose of 111 MBq of 123I-BMIPP was administered intravenously at rest, and myocardial emission computed tomography was obtained 20 min and 3 h after injection. The 201Tl imaging was also performed within 1 week after the 123I-BMIPP study. The regional myocardial uptake and clearance of 123I-BMIPP and 201Tl were assessed quantitatively. The myocardial distribution of 123I-BMIPP was more heterogeneous than that of 201Tl in patients with HCM. The myocardial uptake of 123I-BMIPP was lower in the anteroseptal region of the left ventricle than in the posterolateral region (74% vs. 85%, P less than 0.001). The anteroseptal wall showed a faster clearance of 123I-BMIPP than the posterolateral wall (33% vs. 27%, P less than 0.01). Both a decreased uptake and rapid clearance of 123I-BMIPP were observed in the hypertrophied myocardium of the anteroseptal wall, where 201Tl uptake was normal or even increased. Myocardial segments with a markedly increased thickness showed a lower uptake and faster clearance of 123I-BMIPP than those with mild hypertrophy (uptake 73% vs. 82%, P less than 0.05; clearance 30% vs. 25%, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

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ST segment elevation in right precordial leads is thought to be a good predictor of right ventricular involvement in patients with acute inferior myocardial infarction. This view, however, is rapidly disappearing. Therefore, using QRS changes in body surface potential maps in the chronic phase, we have attempted to differentiate patients with or without right ventricular involvement. Thirty patients with chronic inferior myocardial infarction (2 or more months after onset) were studied, in whom 87 unipolar ECGs and right ventriculograms were recorded. The patients were then divided into three groups depending on the locations of their abnormal QRS potentials (-2SD area) exceeding the normal range (mean -2SD). In group A, the -2SD area was located predominantly on the right inferior chest, in group B on the left inferior chest, and in group N on both the right and left inferior chests equally. The results showed that group A had a lower right ventricular ejection fraction (RVEF) compared with group B (A, 40 ± 7%; B, 53 10%; p < .001), while there was no difference in left ventricular ejection fraction between the two groups (49 ± 11% and 49 ± 11%, respectively). Moreover, right ventricular asynergy occurred in 14 of the 18 patients (78%) of group A but in only one of the 10 patients (10%) of group B. Group N was presumed to be intermediate between groups A and B. We also found that patients without Q waves in lead I of the 12-lead electrocardiogram (ECG) or patients with the 20 msec QRS vector in the left upper position on the vectorcardiogram (VCG) both had lower RVEF and tended to have a higher incidence of right ventricular asynergy. For recognition of right ventricular asynergy, each of the studies (mapping, ECG, and VCG) had high sensitivities (81% to 88%). For determining spdcificity, the mapping criteria were superior to both the VCG criteria and the ECG criteria. This QRS change was characterized as loss of electrical activity in right lower chest. Information of this sort will be beneficial in managing such patients with myocardial infarction. Circulation 77, No. 6, 1283-1290, 1988 ST SEGMENT elevation in right precordial lead is thought to be a good indicator of right ventricular involvement in patients with acute inferior myocardial infarction.' However, because of the short duration of ST segment elevation,5', diagnostic accuracy was low after completion of the study period. Moreover, ST segment elevation does not identify necrotic tissue but myocardial ischemia. On the other hand, the loss of electrical activity in the right ventricle should alter the QRS potential.9' 10 Some experimental results have shown the occurrence of QRS changes in the right precordial chest caused by right ventricular infarction.In human beings, however, the effect of right ventricular infarction on the QRS complex in the chronic stage

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