A perfect tool for comprehensive evaluation of myocardial perfusion and function: Stress PET imaging
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Pharmacologic stress cardiac positron emission tomography (PET) is a highly advanced technique for myocardial perfusion imaging (MPI). In comparison with traditional single-photon emission computed tomography (SPECT), MPI with PET provides faster acquisition, better quality, less attenuation artifact, lower radiation burden, and more accurate quantitation of myocardial blood flow (MBF) and perfusion reserve (MPR). With all the advantages, MPI with PET brings higher diagnostic accuracy and more accurate risk stratification and decision-making to patients with known or suspected coronary artery disease (CAD).1–3 In addition, applying ECG-gating technique further enables MPI with PET to simultaneously assess left ventricular (LV) functions and synchrony not only at resting but also at peak-stress status.4,5 All of these myocardial substrates produce additional values in diagnosis and prognosis6,7 and also provide wonderful opportunities for researches on the pathophysiology mechanisms in patients with CAD and heart failure.
In this issue of journal of nuclear cardiology, Juarez-Orozco et al used adenosine-stress N-13 ammonia PET to retrospectively study the relationship between traditional perfusion estimate with summed rest score (SRS, a surrogate of myocardial scar) and quantitative perfusion estimates with stress MBF (sMBF), rest MBF (rMBF), MPR, and peak-stress ventricular synchrony expressed as bandwidth (BW), standard deviation (SD), and entropy (E) in chronic heart failure patients referred for MPI with PET due to suspected myocardial ischemia.8 The authors found an inverse relationship between perfusion estimates and ventricular synchrony. However, quantitative estimates with sMBF, rMBF, and MPR were inferior to SRS for predicting ventricular mechanical synchrony in these patients. The authors further proposed that characterizing the fixed perfusion defects with SRS might be a more convenient approach for treatment in order to improve ventricular mechanical dyssynchrony. Interestingly, the same group had a similar study in which the enrolled patients were also referred for N-13 ammonia PET due to suspected myocardial ischemia but not limited to chronic heart failure;9 however, sMBF is better than MPR, SSS, and SRS in predicting peak-stress ventricular synchrony independently from other relevant cardiovascular risk factors and clinical covariates. The different results between the authors’ two studies might be caused by the more complicated mechanism of ventricular synchrony in patients with chronic heart failure and the further study is needed to answer this question.
The relationship between myocardial perfusion status and LV mechanical synchrony had been well described in previous studies. Our previous study with SPECT showed that stress-induced myocardial ischemia caused dyssynchronous contraction in the ischemic region, deteriorating LV mechanical synchrony.10 Moreover, our study showed that LV dyssynchrony at stress was more significantly reduced than that at rest in the normal and infarcted myocardium. For patients with chronic heart failure, however, the current study found myocardial scar (the extent and severity of fixed perfusion defects as SRS) was even more important in the pathophysiologic mechanism of ventricular synchrony. In our previous SPECT studies, we had similar observations that significant correlation was noted between myocardial scar (expressed as area of resting myocardial perfusion defect) and phase SD in heart failure patients with cardiac resynchronization therapy (CRT).11 In addition, we further demonstrated that myocardial scar interfered with the normal propagation of mechanical activation, resulting in more heterogeneous activation sequences and thus contributing to the development of ventricular arrhythmia.12
Compared to SPECT imaging mostly using Tc-99m agents, PET has another advantage of imaging cardiac function in the immediate peak-stress condition. Using Rb-92 MPI with PET, Dorbala et al. found that there was inverse relationship between stress-induced change in LVEF and magnitude of ischemia during peak vasodilator stress, and that the stress-induced LVEF worsening highly indicated left main or multivessel CAD and also significantly more cardiac events and all-cause death.18,19 On the other hand, Tc-99m SPECT imaging usually starts 30 to 60 minute after stress and often results in recovery of LV stunning with little or no residual detectable change in LV function. Although there are considerable disadvantages including poorer image quality and higher radiation burden to patients, Tl-201 imaging starts 5-10 minute after stress and has more chance to capture stress-induced change than Tc-99m. Our previous studies using Tl-201 SPECT showed that stress-induced worsening of LVEF or regional wall motion were associated with severe CAD and were independent predictors of major adverse cardiac events.20,21 In addition, stress-induced ischemia caused more LV dyssynchronous contraction which provided incremental value in detecting multivessel CAD.22 In the current study, the authors studied the relationship between peak-stress LV synchrony and perfusion estimates using N-13 ammonia PET. Using this perfect tool for MPI, we believe it would be even more interesting to further explore the pathophysiology mechanism or clinical significance of stress-induced LV dyssynchrony.
It has been more than a decade since phase analysis for MPI with SPECT was invented, and this technique is still expanding its applications in academic research or clinical patient care. In combination with the perfect tool for MPI, stress-rest cardiac PET will provide the most comprehensive information in perfusion, quantitative flow and function than any other nuclear imaging modalities ever. We look forward to the new era of nuclear cardiology with cardiac PET.
The authors declare that they have no conflict of interest.
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