Authors:

C M Pawhay¹ , T Nakajima¹ , ¹Saitama Cardiovascular and Respiratory Center, Division of Cardiology - Kumagaya - Japan ,

Background: Stress-induced myocardial ischemia causes left ventricular (LV) systolic and diastolic dysfunction manifested as abnormal myocardial wall motion and relaxation. The assessment of LV diastolic dysfunction is a sensitive predictor of the presence of coronary artery disease (CAD), as this precedes and is independent of systolic dysfunction, but this has not been widely implemented. With electrocardiography (ECG)-gated myocardial perfusion single photon emission computed tomography (SPECT), it is possible to quantitatively detect LV diastolic dysfunction and determine the presence and extent of CAD in its early phase in the ischemic cascade.

Objective: To evaluate the utility of pharmacologic stress-induced LV diastolic dysfunction assessed by 99mTc-tetrofosmin gated-SPECT in determining the presence and extent of coronary artery disease.

Methodology: Two hundred and one patients (135 men; mean age of 70 years) who underwent a one-day adenosine stress-rest 99mTc-tetrofosmin myocardial perfusion imaging with subsequent coronary anatomy evaluation by invasive or computed tomographic coronary angiography were included. The summed stress scores (SSS) and summed difference scores (SDS) were calculated for each patient to describe the presence and extent of perfusion defects. Indicators of diastolic function including the peak filling rate (PFR), 1/3 mean filling rate (MFR/3) and time to PFR (TTPFR) after stress and at rest were computed from first order derivative of the LV volume curve produced from standard 16-frame gated SPECT images. The percent stress-to-rest differences of these parameters were then computed to describe stress-induced diastolic dysfunction.

Results: Our study showed that stress-induced perfusion abnormalities increased significantly with the presence and extent of CAD.  There is also a significant correlation (p<0.05) between increasing CAD severity and worsening diastolic function. This study also showed that increasing CAD severity is associated with a worsening trend of percent stress-to-rest difference, indicating stress-induced LV diastolic dysfunction. The independent determinants of the presence and extent of CAD in this study are the percent stress-to-rest TTPF difference (p=0.006) and the stress TTPF value (p=0.006). Other significant determinants noted are myocardial SDS (p=0.002), resting ejection fraction (p=0.001), indexed resting end-systolic volume (p=0.007) and indexed end-diastolic volume at stress (p=0.009).

Conclusion: The combined evaluation of regional myocardial perfusion, LV diastolic function as well as contractile function both at rest and after stress using quantitative gated SPECT aids in the detection of the presence and extent of CAD among patients at risk.