Noninvasive evaluation of ischaemic heart disease: myocardial perfusion imaging or stress echocardiography?

Stress echocardiography and myocardial perfusion imaging are commonly used noninvasive imaging modalities for the evaluation of ischaemic heart disease. Both modalities have proved clinically useful in the entire spectrum of coronary artery disease. Both techniques can detect coronary artery disease and provide prognostic information. Both techniques can identify low-risk and high-risk subsets among patients with known or suspected coronary artery disease and thus guide patient management decisions. In patients with acute myocardial infarction, both techniques have been used to identify residual viable tissue and predict improvement of function over time. In patients with chronic ischaemic left ventricular (LV) dysfunction, viability assessment with either modality can be used to predict improvement of function after revascularisation and thus guide patient treatment

Technetium-99m sestamibi tomographic evaluation of residual ischemia after anterior myocardial infarction

Objectives.This study investigated the value of sestamibi scintigraphy in assessing residual ischemia after anterior myocardial infarction.Background.Serial imaging with sestamibi, the uptake and retention of which correlate with regional myocardial blood flow and viability, has been used to estimate salvaged myocardium and risk area after acute infarction. We recently documented that recovery of perfusion and contraction in the infarcted area may continue well after the subacute phase, suggesting myocardial hibernation. Some underestimation of viability in the setting of hibernating myocardium by sestamibi imaging has been reported.Methods.We studied 58 patients in stable condition after Q wave anterior infarction. Regional perfusion and function were quantitatively assessed by sestamibi tomography and two-dimensional echocardiography at 4 to 6 weeks and at 7 months after infarction. In sestamibi polar maps, abnormal areas with tracer uptake >2.5 SD below our reference values were computed at rest and after symptom-limited exercise. On two-dimensional echocardiography the ejection fraction and extent of rest wall motion abnormalities were assessed by a computerized system. All patients had coronary angiography between the two studies.Results.At 7 months the extent of rest sestamibi defect was significantly reduced in 40 patients (69%, group 1) and unchanged in 18 (31%, group 2). Rest wall motion abnormalities and ventricular ejection fraction significantly improved in group 1 but not in group 2. Underlying coronary disease, patency of the infarct-related vessel and rest sestamibi defect extent at 5 weeks were comparable between the two groups. At 7 months, an increase in the reversible (stress-rest defect) tracer defect was observed in group 1 (p < 0.05) despite a smaller stress-induced hypoperfusion (p < 0.05). Reversible sestamibi defects and stress hypoperfusion were unchanged in group 2. In 38 (95%) of 40 group 1 patients, the area showing reversible sestamibi defects at 7 months matched the area showing fixed hypoperfusion at 5 weeks.Conclusions.The reduction in the rest tracer uptake defect that can occur late after infarction may affect the assessment of ischemic burden by sestamibi imaging early after anterior myocardial infarction

Taxonomy of segmental myocardial systolic dysfunction.

The terms used to describe different states of myocardial health and disease are poorly defined. Imprecision and inconsistency in nomenclature can lead to difficulty in interpreting and applying trial outcomes to clinical practice. In particular, the terms 'viable' and 'hibernating' are commonly applied interchangeably and incorrectly to myocardium that exhibits chronic contractile dysfunction in patients with ischaemic heart disease. The range of inherent differences amongst imaging modalities used to define myocardial health and disease add further challenges to consistent definitions. The results of several large trials have led to renewed discussion about the classification of dysfunctional myocardial segments. This article aims to describe the diverse myocardial pathologies that may affect the myocardium in ischaemic heart disease and cardiomyopathy, and how they may be assessed with non-invasive imaging techniques in order to provide a taxonomy of myocardial dysfunction

Dysfunctional but viable myocardium - ischemic heart disease assessed by magnetic resonance imaging and single photon emission computed tomography

The assessment of ischemic heart disease (IHD) often focuses on the detection of dysfunctional but viable myocardium which may improve in function following revascularization. Dysfunctional but viable myocardium is identified by distinct characteristics with regards to function, perfusion and viability. Therefore, in Paper I we developed a method for quantitative polar representation of left ventricular myocardial function, perfusion and viability using single photon emission computed tomography (SPECT) and cardiac magnetic resonance (CMR). Polar representation of these parameters was feasible, and the quantitative method agreed with visual assessment. Paper II showed that wall thickening decreases with increasing infarct transmurality. However, the variation in wall thickening was large, and importantly, influenced more so by the function of adjacent myocardium than by infarct transmurality. This underscores the difficulty of using resting function alone to accurately assess myocardial infarction in revascularized IHD. In Paper III we assessed the relationship between left ventricular ejection fraction (LVEF) and infarct size and found that LVEF cannot be used to estimate infarct size, and vice versa. However, the study showed that LVEF can be used to estimate a maximum predicted infarct size, and that infarct size can be used to estimate a maximum predicted LVEF. These results emphasize the importance of direct infarct imaging by CMR when attempting to estimate the size of infarction in patients with IHD. Paper IV was designed to assess the time course of recovery of myocardial perfusion and function after revascularization. The recovery of perfusion was found to occur in the first month, while the recovery of function was delayed in segments with non-transmural infarction. In summary, the presented studies emphasize the importance of direct infarct imaging by CMR for the accurate identification of infarction in the assessment of dysfunctional myocardium. Neither regional nor global myocardial function have a close correlation to infarction, but the presence of non-transmural infarction is a marker for delayed recovery of function following revascularization

New nuclear medicine techniques for the assessment of myocardial viability

Een dotterbehandeling of een bypassoperatie heeft alleen zin als er nog voldoende hartspierweefsel over is dat zich kan herstellen. Momenteel wordt de vitaliteit van de hartspier voor de ingreep nog onderzocht met een PET-scan, maar deze techniek is duur en maar in een paar ziekenhuizen in Nederland aanwezig. Riemer Slart constateert in zijn proefschrift dat een goedkopere scan het succes van een bypass of dotteren ook kan voorspellen.

Prevalence of scarred and dysfunctional myocardium in patients with heart failure of ischaemic origin: a cardiovascular magnetic resonance study

BACKGROUND: Cardiovascular magnetic resonance (CMR) with late gadolinium enhancement (LGE) can provide unique data on the transmural extent of scar/viability. We assessed the prevalence of dysfunctional myocardium, including partial thickness scar, which could contribute to left ventricular contractile dysfunction in patients with heart failure and ischaemic heart disease who denied angina symptoms. METHODS: We invited patients with ischaemic heart disease and a left ventricular ejection fraction < 50% by echocardiography to have LGE CMR. Myocardial contractility and transmural extent of scar were assessed using a 17-segment model. RESULTS: The median age of the 193 patients enrolled was 70 (interquartile range: 63-76) years and 167 (87%) were men. Of 3281 myocardial segments assessed, 1759 (54%) were dysfunctional, of which 581 (33%) showed no scar, 623 (35%) had scar affecting ≤50% of wall thickness and 555 (32%) had scar affecting > 50% of wall thickness. Of 1522 segments with normal contractile function, only 98 (6%) had evidence of scar on CMR. Overall, 182 (94%) patients had ≥1 and 107 (55%) patients had ≥5 segments with contractile dysfunction that had no scar or ≤50% transmural scar suggesting viability. CONCLUSIONS: In this cohort of patients with left ventricular systolic dysfunction and ischaemic heart disease, about half of all segments had contractile dysfunction but only one third of these had > 50% of the wall thickness affected by scar, suggesting that most dysfunctional segments could improve in response to an appropriate intervention

Evaluation of changes in perfusion defect and left ventricular systolic function using Tc-99m Tetrofosmin single photon emission computed tomography over 3 month period in patients of Acute Myocardial Infarction undergoing primary angioplasty

Background After a primary transluminal coronary angioplasty (PTCA) following AMI (acute myocardial infarction), the perfusion defect and LV (left ventricular) function recover/change over a period of time. The analysis immediately after the procedure may not be true depiction of the exact success of the procedure. There is varying and scanty information available on the natural course of changes in these parameters after a successful PTCA. We hypothesized that majority of change occurs at 3–4 month period. Hence, we undertook this study on the natural course of recovery/changes occurring in perfusion defect size and LV function in first 3 months after primary angioplasty Material and methods 30 consecutive cases of first AMI who were taken up for Primary angioplasty were enrolled into the study. Resting MPI(Myocardial perfusion imaging) was done within 24–72 hrs of admission using Tc-99m–Tetrofosmin and after 10–14 weeks. Analysis of LVEF (left ventricular ejection fraction), summed segmental score and extent of perfusion defect was done. Images were processed using autocardiac software of emory tool box and quantification was done using QPS (quantitative perfusion SPECT) and QGS (qualitative perfusion SPECT) softwares. 20 segment scoring method was used for quantification on bull’s eye images. Student t test (two tailed, dependent) was used to find the significance of study parameters on continuous scale within each group. Effect size was computed to find the effect. Pearson correlation between perfusion defect and LVEF was performed at acute stage and after 10–14 weeks. Results The average acute perfusion defect extent was 19.76 ± 12.89% which after 3months became 16.79 ± 12.61%. The summed segmental score changed from 14.31 ± 10.58 to 11.38 ± 10.03 and LVEF improved from 48.40 ± 13.15% to 53.37 ± 12.8%. There was significant improvement in LVEF from acute setting to 10–14 weeks (p = 0.001). There was significant lowering of summed score (p = 0.007). Perfusion defect size showed significant reduction (p = 0.030). Three patients showed deterioration in perfusion defect size and in summed score with reduction in LVEF. Four patients had no change in any of the parameters. Correlation between perfusion defect and LVEF was strong both at baseline (r = -0.705, p &lt; 0.001) and after 10-18 weeks (r = -0.766, p &lt; 0.001). Conclusion The changes we found in 3 months are similar to earlier studies and also to studies using follow up at 6 months to 1 year. We feel that 3 months is a good enough time to accurately assess the success of primary angioplasty.BACKGROUND. After a primary transluminal coronary angioplasty (PTCA) following AMI (acute myocardial infarction), the perfusion defect and LV (left ventricular) function recover/change over a period of time. The analysis immediately after the pro­cedure may not be true depiction of the exact success of the procedure. There is varying and scanty information available on the natural course of changes in these parameters after a successful PTCA. We hypothesized that majority of change occurs at 3–4 month period. Hence, we undertook this study on the natural course of recovery/changes occurring in perfusion defect size and LV function in first 3 months after primary angioplasty. MATERIAL AND METHODS. 30 consecutive cases of first AMI who were taken up for Primary angioplasty were enrolled into the study. Resting MPI (Myocardial perfusion imaging) was done within 24–72 hrs of admission using Tc-99m–Tetrofosmin and after 10–14 weeks. Analysis of LVEF (left ventricular ejection fraction), summed segmental score and extent of perfusion defect was done. Images were processed using autocardiac software of emory tool box and quantification was done using QPS (quantitative perfusion SPECT) and QGS (qualitative perfusion SPECT) softwares. 20 segment scoring method was used for quantification on bull’s eye images. Student t test (two tailed, dependent) was used to find the significance of study parameters on continuous scale within each group. Effect size was computed to find the effect. Pearson correlation between perfusion defect and LVEF was performed at acute stage and after 10–14 weeks. RESULTS. The average acute perfusion defect extent was 19.76 ± 12.89% which after 3 months became 16.79 ± 12.61%. The summed segmental score changed from 14.31 ± 10.58 to 11.38 ± 10.03 and LVEF improved from 48.40 ± 13.15% to 53.37 ± 12.8%. There was significant improvement in LVEF from acute setting to 10–14 weeks (p = 0.001). There was significant lowering of summed score (p = 0.007). Perfusion defect size showed significant reduction (p = 0.030). Three patients showed deterioration in perfusion defect size and in summed score with reduction in LVEF. Four patients had no change in any of the parameters. Correlation between perfusion defect and LVEF was strong both at baseline (r = -0.705, p < 0.001) and after 10–18 weeks (r = -0.766, p < 0.001). CONCLUSION. The changes we found in 3 months are similar to earlier studies and also to studies using follow up at 6 months to 1 year. We feel that 3 months is a good enough time to accurately assess the success of primary angioplasty.