M Frais

The phase image: its relationship to patterns of contraction and conduction.

To determine the relationship of phase changes and abnormalities of ventricular contraction and conduction, we performed phase image analysis of blood pool scintigrams in 29 patients. Eleven patients had no evidence of blood pool contraction or ECG conduction abnormalities, four had contraction abnormalities, seven had abnormal conduction and seven had abnormalities of both variables. The phase delay generally related to the degree of contraction abnormality. The mean phase delay in hypokinetic segments differed from that in normokinetic segments in the same patient (p < 0.025), the phase delay of akinetic and dyskinetic segments differed from that in normokinetic segments (p < 0.001) and the phase delay in dyskinetic segments differed from that in akinetic segments (p < 0.005), but there was a significant overlap in the phase delay in normal and hypokinetic segments. Also, in patients with conduction abnormalities, the minimal associated regional phase delay presented a phase dispersion and a pattern of contraction consistent with the pattern of conduction and different from normal. A single study performed both at rest and with stress demonstrated the effect of heart rate on phase assessment and confirmed the independent effects of contraction and conduction on phase delay. Acquisition and analytic methods should add significantly to the resolution of the phase method.

An accurate means of detecting and characterizing abnormal patterns of ventricular activation by phase image analysis

The ability of scintigraphic phase image analysis to characterize patterns of abnormal ventricular activation was investigated. The pattern of phase distribution and sequential phase changes over both right and left ventricular regions of interest were evaluated in 16 patients with normal electrical activation and wall motion and compared with those in 8 patients with an artificial pacemaker and 4 patients with sinus rhythm with the Wolff-Parkinson-White syndrome and delta waves. Normally, the site of earliest phase angle was seen at the base of the interventricular septum, with sequential change affecting the body of the septum and the cardiac apex and then spreading laterally to involve the body of both ventricles. The site of earliest phase angle was located at the apex of the right ventricle in seven patients with a right ventricular endocardial pacemaker and on the lateral left ventricular wall in one patient with a left ventricular epicardial pacemaker. In each case the site corresponded exactly to the position of the pacing electrode as seen on posteroanterior and left lateral chest X-ray films, and sequential phase changes spread from the initial focus to affect both ventricles. In each of the patients with the Wolff-Parkinson-White syndrome, the site of earliest ventricular phase angle was located, and it corresponded exactly to the site of the bypass tract as determined by endocardial mapping. In this way, four bypass pathways, two posterior left paraseptal, one left lateral and one right lateral, were correctly localized scintigraphically. On the basis of the sequence of mechanical contraction, phase image analysis provides an accurate noninvasive method of detecting abnormal foci of ventricular activation.

Phase Image Characterization of Ventricular Contraction in Left and Right Bundle Branch Block

The phase image is a computer-derived functional image, based on the analysis of the time versus radioactivity curve in each pixel location of the multiple gated blood pool scintigram. Within the ventricular regions of interest, the phase angle is roughly equivalent to the time of onset of counts reduction or to the time of onset of ventricular contraction and is expressed in degrees from 0 to 360 degrees. A gray scale-coded image of such a regional phase angle, the phase image, can be looked on as a map of sequential contraction. This method was applied in 33 patients without severe contraction abnormality including 16 patients with normal conduction, 9 with right bundle branch block and 8 with left bundle branch block. In patients with normal conduction the pattern of phase angle distribution, representing the pattern of ventricular contraction, was homogeneous and symmetric in both the left and right ventricles. Analysis in this normal group indicated a slight but significant difference between the mean (+/- standard deviation) phase angle of the left ventricle (8.5 +/- 11.8 degrees) and that of the right ventricle (13.6 +/0 12.9 degrees, p = 0.01). There was a slight, but nonsignificant difference between mean intrapatient left and right ventricular phase angle onset (1.9 +/- 6.5 degrees). The mean phase angle of the right ventricle in patients with right bundle branch block (27.6 +/- 14.2 degrees) and of the left ventricle in those with left bundle branch block (21.9 +/- 14.0 degrees) was delayed compared with that in patients with normal conduction (p less than 0.05 for both). The mean intrapatient difference between left and right ventricular mean phase angles in patients with normal conduction (-5.2 +/- 6.8 degrees) was significantly different from that in patients with right (-21.8 +/- 10.3 degrees, p less than 0.001) or left (21.8 +/- 6.8 degrees, p less than 0.001) bundle branch block. The mean intrapatient difference between onset of left and right ventricular phase angles was also significantly different from normal in patients with right (-10.6 +/- 7.5 degrees, p less than 0.005) or left (18.7 +/- 8.3 degrees, p = 0.01) bundle branch block. Although phase imaging is not without artifactual error, this study demonstrates that the phase image can characterize familiar conduction abnormalities. It presents the potential for application as a general noninvasive tool in the investigation of the timing and sequence of ventricular contraction in patients with normal or abnormal ventricular activation.

Phase image characterization of localized and generalized left ventricular contraction abnormalities

To evaluate their phase image characteristics, 61 patients with varying left ventricular contraction abnormalities were studied. In 16 normal patients, the left ventricular phase image revealed a homogeneous pattern, a narrow bell-shaped histogram and an orderly spatial progression of phase angle (phi). In 16 patients with segmental abnormalities, the left ventricular phase image showed a region of uniformly delayed phase angle corresponding to the site of segmental abnormality, a discrete secondary histogram peak and a discontinuous, but orderly, spatial progression of phase angle. The mean phase angle (phi) (23.6 +/- 15.7 degrees) and its standard deviation (17.6 +/- 7.2 degrees) differed from the normal group (7.6 +/- 11.1 degrees, p less than 0.002 and 8.9 +/- 2.8 degrees, p less than 0.001). The percent of end-diastolic volume involved in the segmental abnormality, calculated using phase data in 13 of these and in 11 additional patients with a left ventricular aneurysm on ventriculography, correlated well with the percent akinetic segment on scintigraphic (r = 0.78) and angiographic (r = 0.84) study. In 18 patients with generalized abnormalities, the left ventricular phase image revealed multiple regions of inhomogeneous phase angle, a grossly irregular histogram and a disorderly spatial progression of phase angle. The mean phase angle (56.4 +/- 23.9 degrees) and standard deviation (27.3 +/- 7.1 degrees) differed from values in the normal group and from patients with segmental contraction abnormalities (both p less than 0.001). The mean phase angle and its standard deviation in scattered regions with abnormally prolonged phase angle differed significantly from abnormal regions in patients with segmental abnormalities (both p less than 0.001). These patterns of left ventricular phase angle demonstrate characteristics that may help differentiate between ventricles with segmental and generalized contraction abnormalities. Their relation to underlying pathophysiology and potential clinical implications should be considered.

Exercise-induced T wave normalization is not specific for myocardial ischemia detected by perfusion scintigraphy

1. Heger JJ, Prystowsky EN, Jackman WM, et al. Amiodarone, clinical efficacy and electrophysiology during long-term therapy for recurrent ventricular tachycardia or ventricular fibrillation. N Engl J Med 1981;305:539-45. 2. Meier C, Kauer B, Muller U, Ludin HP. Neuromyopathy during chronic amiodarone treatment. J Neurol 1979;220: 231-9. 3. Adams PC, Holt DW, Storey GCA, Morley AR, Callaghan J, Campbell RWF. Amiodarone and its desethyl metabolite: tissue distribution and morphologic changes during long-term therapy. Circulation 1985;72:1064-75. 4. Dake MD, Madison JM, Montgomery CK, et al. Electron microscopic demonstration of lysosomal inclusion bodies in lung, liver, lymph nodes, and blood leukocytes of patients with amiodarone pulmonary toxicity. Am J Med 1985;78:504-12. 5. Kuncl RW, Duncan G, Watson D, Alderson K, Rogawski MA, Peper M. Colchicine myopathy and neuropathy. N Engl J Med 1987;316:1562-8. Exercise-induced T wave normalization is not specific for myocardial ischemia detected by perfusion scintigraphy

Are regions of ischaemia detected on stress perfusion scintigraphy predictive of sites of subsequent myocardial infarction

To determine the relation between scintigraphic regions of stress-induced ischaemia and subsequent myocardial infarction, a select group of 21 patients was investigated. Each patient had undergone stress perfusion scintigraphy before myocardial infarction was recorded. After acute infarction, thallium-201 perfusion scintigraphy was performed in 16 patients (76%) and 99mTc (stannous) pyrophosphate in 14 patients (67%). All patients had at least one post-myocardial infarction scintigram and nine (42%) had both perfusion scintigraphy and infarct imaging. Nineteen patients (90%) had scintigraphic evidence of stress-induced ischaemia pre-infarction. Scintigraphic regions of infarction were compared with regions of previously demonstrated stress-induced ischaemia. In 11 patients (53%) the myocardial infarction was more extensive; in one of these patients, reimaged one week before myocardial infarction, and in four others (19%) there were matching defects; in three patients (14%) the infarction was less extensive, and in two patients (9%) the infarction was less extensive but also involved regions not previously shown to develop ischaemia. In the final patient (5%) there was no match. Stress perfusion scintigraphy was generally abnormal before acute infarction in this group of patients. Acute infarction frequently involved regions previously shown to develop stress-induced ischaemia, though these often underestimated the extent of myocardium at risk.

The functional implications of scintigraphic measures of myocardial ischemia and infarction

To compare serial functional and perfusion scintigraphic changes after myocardial infarction, we performed left ventricular (LV) cineangiograms and thallium (TI)-201 myocardial perfusion scintigrams before and 1 hour, 2 days, 9 days, and 1 month after closed chest coronary occlusion in 14 dogs as survival permitted. Survivors were studied with technetium-99m (stannous) pyrophosphate (TcPYP) scintigrams at 48 hours, and at postmortem examination infarction was documented and measured after nitroblue tetrazolium (NBT) staining. The TcPYP image was abnormal in 10 dogs, each of which had infarcts on NBT staining measuring 3 to 23 gm. In all 14 dogs, perfusion scintigrams became abnormal and LV ejection fraction (EF) fell when measured within 48 hours of occlusion. In the nine late survivors studied over 1 week after the event, perfusion scintigrams and EF improved in those which developed infarcts and normalized in those without infarction. The decrement in LVEF after coronary occlusion generally showed serial improvement and correlated with the size of the defect in the accompanying TI-201 scintigram (r = 0.74). TI-201 defect size seen in late studies correlated well with NBT infarct size (r = 0.89) and TcPYP image infarct size (r = 0.82), as it did with the decrement in LVEF noted in late studies (r = 0.86). The results suggest that early perfusion scintigrams together with TcPYP images may be useful for estimating the amount of reversible dysfunction after coronary occlusion.