Translate this page into:
Quantitative analysis of SPECT imaging parameters in patients with resting perfusion defects on myocardial perfusion scintigraphy
Address for correspondence: Dr. Sandip Basu, Radiation Medicine Centre, Bhabha Atomic Research Centre (BARC), Tata Memorial Hospital, Annexe Building, Jerbai Wadia Road, Parel, Mumbai-400 012, India. E-mail: drsanb@yahoo.com
This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
This article was originally published by Medknow Publications and was migrated to Scientific Scholar after the change of Publisher.
Abstract
Background:
Functional status/contractile behaviour of hibernating myocardium was analyzed objectively by analyzing the available quantitative parameters obtained on gated SPECT myocardial perfusion imaging (MPI) using Emory cardiac toolbox (ECTB) software.
Materials and Methods:
In this retrospective study, 70 patients with perfusion defects on 99Tc-Sestamibi MPI (12 females, 58 males) who also underwent 18F-FDG Cardiac PET study for assessment of hibernating myocardium were included for analysis. Patients were divided in three categories based on summed rest score (SRS) obtained from ECTB software, depicting the extent of perfusion defects. In a study population matched for extent of perfusion defects, quantitative parameters obtained from ECTB software such as left ventricular ejection fraction (LVEF), left ventricular end diastolic volume (EDV), left ventricular end systolic volume (ESV) and left ventricular stroke volume (SV) were compared between patients showing evidence of hibernating myocardium and patients showing no evidence of hibernating myocardium. Student ‘t’ test was applied on the given observations and a P-value <0.05 was considered as a significant difference between the means in two categories.
Results:
There was no significant difference in LVEF, EDV, ESV and SV measurements between those who demonstrate hibernating myocardium and those who show no evidence of hibernating myocardium across all the categories of patients. Few trends were evident in the present study in LVEF, EDV and ESV measurements i.e., fall in mean LVEF with increasing SRS and rise in mean EDV and ESV with increasing SRS.
Conclusions:
The findings were consistent with the nature of hibernating myocardium i.e., non-contractile and dysfunctional. The fall in the LVEF was suggestive of deteriorating myocardial function with increasing extent of perfusion defects. The increasing left ventricular EDV and ESV with increasing extent of perfusion defects was suggestive of rising incidence of gross morphological LV cavity dilatation or “Dilated ischemic cardiomyopathy” in these patients.
Keywords
Emory cardiac toolbox
hibernating myocardium
left ventricular failure
myocardial perfusion imaging
myocardial viability
quantitative parameters
INTRODUCTION
Hibernating myocardium is a state of persistently impaired myocardial function due to reduced coronary blood flow that can be partially or completely restored to normal if the myocardial oxygen supply/demand relationship is favorably altered, either by improving blood flow and/or by reducing demand.[167]
The concept of hibernation presupposed that a reduction in coronary blood flow was followed by a down regulation in cardiac function to a point at which the limited oxygen supply enabled the maintenance of the biochemical functions that sustained cell integrity.[1] The hibernating response of the heart is considered as an act of self-preservation.[1]
The primarily clinical concept of myocardial hibernation subsequently merged with a number of experimental observations: (a) Regional myocardial function and blood flow are reduced proportionately during ischemia i.e., a state of perfusion-contraction matching (b) Metabolic parameters such as myocardial lactate consumption, creatine phosphate content and free energy change of ATP-hydrolysis recover toward their preischemic baseline values during ongoing ischemia, consistent with the idea that the reduced function is an adaptation to reduced blood flow. (c) An inotropic reserve persists in hibernating myocardium.[3]
The phenotype of hibernating myocardium, i.e., chronic, yet reversible contractile dysfunction in the setting of coronary artery disease could arise from either continued ischemia or from repetitive cycles of ischemia/reperfusion.[3] Hibernating myocardium refers to the presence of persistent myocardial and left ventricular dysfunction at rest, associated with conditions of severely reduced coronary blood flow.[2]
Several non-invasive techniques have been developed to identify viable myocardium in the dysfunctional segments:[5]
18F-FDG cardiac PET.
99mTc-Sestamibi.
99mTc-Tetrofosmin.
201Tl rest-redistribution technique.
201Tl reinjection technique.
Low dose dobutamine stress echocardiography.
Cardiac 18F-FDG PET is the “most sensitive” marker for hibernating myocardium while Dobutamine stress echocardiography is considered to be the “most specific” marker.[5]
We sought to assess the contractile/functional behavior of hibernating myocardium by comparing quantitative parameters like left ventricular ejection fraction (LVEF), left ventricular end diastolic volume (EDV), left ventricular end systolic volumes (ESV) and left ventricular stroke volume (SV) [obtained from myocardial perfusion imaging (MPI) studies] between individuals having evidence of hibernating myocardium and individuals with no evidence of hibernating myocardium.
MATERIALS AND METHODS
A retrospective analysis was carried out on 70 patients with perfusion defects on 99mTc-Sestamibi MPI [Table 1] who also underwent 18F-FDG cardiac PET study for the assessment of hibernating myocardium. Assessment was done visually by a single nuclear medicine physician and “Perfusion-metabolism mismatch” in any one segment on visual analysis was taken as the criterion for diagnosing hibernating myocardium.[6]
| Total patients | 70 |
|---|---|
| Sex | |
| Males | 58 |
| Females | 12 |
| History of myocardial infarction | 54 |
| No history of myocardial infarction | 14 |
Patients were divided in three categories on the basis of summed rest score (SRS) depicting the extent of defects:
SRS between 0 and 10.
SRS between 11 and 20.
SRS between 21 and 30.
In this study population matched for the extent of defects, quantitative parameters such as LVEF, EDV, ESV and SV obtained from Emory Cardiac toolbox (ECTB) software were compared between patients showing evidence of hibernating myocardium and patients showing no evidence of hibernating myocardium [Figures 1–3].
Inclusion criteria
All left ventricular failure patients irrespective of prior myocardial infarction, who underwent Tc-99m Sestamibi (hexakis methoxy isobutyl isonitrile) MPI and 18- FDG (Fluoro deoxy glucose) cardiac PET study for assessment of hibernating myocardium (from January 2008 to March 2010 at our institute) were included in the study.
Imaging protocol
Rest myocardial perfusion scintigraphy was performed 1 hour following intravenous administration of 99mTc-Sestamibi. Images were obtained on Siemens dual head γ-camera (E cam) by Gated SPECT in supine position from RAO 45°to LPO 225°. The images were reconstructed into vertical long, horizontal long and short-axis slices. Quantitative parameters such as LVEF in percentage, EDV in ml, ESV in ml, SV in ml and SRS were obtained along with a polar map depicting “17 segment model” using ECTB software using a semi-automatic approach. The role of operator was limited to defining correctly the left ventricular endocardial and epicardial borders.
On another day (within 3 days of the MPI study), 90 minutes after intravenous injection of 18F-FDG, which was administered 1 hour after oral glucose load of 75 g, a regional cardiac PET study was acquired using a whole-body full-ring dedicated GE Advance BGO PET camera. Images acquired were processed into short axis, vertical long axis and horizontal long axis. A polar map depicting “17 segment model” was also generated.
Analysis
Assessment of hibernating myocardium was done visually by single physician. “Perfusion-metabolism mismatch” in any one segment on visual analysis was taken as the sole crieterion for hibernating myocardium.
Statistical analysis
Mean values and standard deviations of the quantitative parameters in different categories were calculated. Unpaired “Student ‘t’ test” was applied to the data in each category for each parameter and P-value <0.05 was considered as significant difference between the mean values.
RESULTS
Results are shown in Tables 2–5
| Group with evidence of hibernating myocardium (39 patients) | Group with no evidence of hibernating myocardium (31 patients) | P-value (obtained on student ‘t’ test) | |
|---|---|---|---|
| Mean LVEF (%) | 39.10 ± 16.75 | 41.35 ± 16.61 | 0.5767 |
| Mean EDV (ml) | 173.71 ± 74.57 | 186.71 ± 111.86 | 0.562999 |
| Mean ESV (ml) | 113.67 ± 67.74 | 121.90 ± 102.05 | 0.687087 |
| Mean SV (ml) | 60.05 ± 22.77 | 64.81 ± 17.77 | 0.3435744 |
LVEF: left ventricular ejection fraction; EDV: left ventricular end diastolic volume; ESV: left ventricular end systolic volume; SV: left ventricular stroke volume (Mean ± Standard Deviation)
| Group with evidence of hibernating myocardium (7 patients) | Group with no evidence of hibernating myocardium (8 patients) | P-value (obtained on student ‘t’ test) | |
|---|---|---|---|
| Mean LVEF (%) | 42.57 ± 19.06 | 55.12 ± 14.79 | 0.1748 |
| Mean EDV (ml) | 188.14 ± 75.67 | 121.37 ± 52.11 | 0.065251 |
| Mean ESV (ml) | 118.85 ± 79.61 | 60 ± 36.93 | 0.082737 |
| Mean SV (ml) | 69.28 ± 24.44 | 61.37 ± 17.78 | 0.4820809 |
LVEF: left ventricular ejection fraction; EDV: left ventricular end diastolic volume; ESV: left ventricular end systolic volume; SV: left ventricular stroke volume (Mean ± Standard Deviation)
| Group with evidence of hibernating myocardium (26 patients) | Group with no evidence of hibernating myocardium (14 patients) | P-value (obtained on student ‘t’ test) | |
|---|---|---|---|
| Mean LVEF (%) | 40.61 ± 17.10 | 43.35 ± 14.40 | 0.6133 |
| Mean EDV (ml) | 154.65 ± 61.68 | 169.35 ± 63.54 | 0.481003 |
| Mean ESV (ml) | 98.34 ± 55.89 | 102.85 ± 53.78 | 0.80655 |
| Mean SV (ml) | 56.31 ± 21.97 | 66.5 ± 14.02 | 0.1253484 |
LVEF: left ventricular ejection fraction; EDV: left ventricular end diastolic volume; ESV: left ventricular end systolic volume; SV: left ventricular stroke volume (Mean ± Standard Deviation)
| Group with evidence of hibernating myocardium (5 patients) | Group with no evidence of hibernating myocardium (10 patients) | P-value (obtained on student ‘t’ test) | |
|---|---|---|---|
| Mean LVEF (%) | 30.6 ± 7.30 | 29.9 ± 10.35 | 0.8953 |
| Mean EDV (ml) | 252.2 ± 100.21 | 209.4 ± 55.92 | 0.300641 |
| Mean ESV (ml) | 180 ± 85.20 | 149.9 ± 60.84 | 0.441727 |
| Mean SV (ml) | 72.2 ± 19.84 | 59.5 ± 15.34 | 0.1921704 |
LVEF: left ventricular ejection fraction; EDV: left ventricular end diastolic volume; ESV: left ventricular end systolic volume; SV: left ventricular stroke volume (Mean ± Standard Deviation)
DISCUSSION
To summarize the overall results, the following observations were made:
There was no significant difference in LVEF, EDV, ESV and SV measurements between those who demonstrate hibernating myocardium and those who show no evidence of hibernating myocardium across all the categories of patients.
Few trends were evident in the present study in LVEF, EDV and ESV measurements:
Fall in mean LVEF with increasing SRS.
-
Mean EDV and ESV rising with increasing SRS.
In review of the literature, Schinkel et al, and Rahimtoola et al, have described hibernating myocardium as non-contractile and dysfunctional.[17] Our study is in concordance with the known description of hibernating myocardium and is an indirect and objective reference of its non-contractile behavior. Phenotypically, hibernating myocardium was found to behave similar to infracted myocardium in terms of LVEF and left ventricular volumes. Our study was able to assess the contractile behavior of hibernating myocardium without the use of 2D-echocardiograpy.
LVEF was found to be inversely proportional to the SRS i.e., systolic dysfunction was found to increase with increase in extent of perfusion defect.
In their study Carluccio E et al,[8] have presented thatin patients with either non–Q-wave MI or no previous MIbut with LV wall motion abnormality and hibernating myocardium, there is remodellingof the LV i.e., LV EDV and ESV are increased and the LV is more spherical. Thus, they have documented that the mere presence of LV systolic dysfunctionwith hibernating myocardium can lead to LV remodelling. They have also documentedthat revascularization in patients with hibernating myocardium results in reverseremodelling i.e., there is a reduction of the increased LVEDVand LVESV, the LV is less spherical and LVEF increases.
Findings of our study are in agreement with the above study. Our study shows increment in left ventricular systolic and diastolic volumes or left ventricular cavity dilatation with increase in extent of perfusion defects.
CONCLUSIONS
The quantitative parameters obtained didn’t show any significant difference in any of the categories of patients. These findings were consistent with the nature of hibernating myocardium i.e., non-contractile and dysfunctional myocardium.
The trends in the LVEF, EDV and ESV were suggestive of deteriorating myocardial function with increasing extent of perfusion defects.
The increase in left ventricular EDV and ESV with increasing extent of perfusion defects was suggestive of increasing incidence of gross morphological LV cavity dilatation or “Dilated ischemic cardiomyopathy” in these patients.
Source of Support: Nil
Conflict of Interest: None declared.
REFERENCES
- Hibernating myocardium--mechanisms and clinical implications. Acta Medica (Hradec Kralove). 1996;39:95-9.
- [Google Scholar]
- Myocardial hibernation: A delicate balance. Am J Physiol Heart Circ Physiol. 2005;288:H984-99.
- [Google Scholar]
- Sensitivity, specificity, and predictive accuracies of various non-invasive techniques for detecting hibernating myocardium. Curr Probl Cardiol. 2001;26:147-86.
- [Google Scholar]
- Diagnostic nuclear medicine (4th ed). Philadelphia: Lippincott Williams and Wilkins; 2003. p. :319-25.
- Clinical relevance of hibernating myocardium in ischemic left ventricular dysfunction. Am J Med. 2010;123:978-86.
- [Google Scholar]
- Patients with hibernating myocardium show altered left ventricular volumes and shape, which revert after revascularization: Evidence that dyssynergy might directly induce cardiac remodelling. J Am Coll Cardiol. 2006;47:969-77.
- [Google Scholar]