Physiological basis for angina and ST-segment change PET-verified thresholds of quantitative stress myocardial perfusion and coronary flow reserve.

Weatherhead PET Center For Preventing and Reversing Atherosclerosis, Division of Cardiology, Department of Medicine, University of Texas Medical School and Memorial Hermann Hospital, Houston, Texas, USA.
JACC. Cardiovascular imaging (Impact Factor: 14.29). 09/2011; 4(9):990-8. DOI:10.1016/j.jcmg.2011.06.015
Source: PubMed

ABSTRACT This study aimed to determine the quantitative low-flow threshold for stress-induced perfusion defects with severe angina and/or significant ST-segment depression during dipyridamole hyperemia.
Vasodilator stress reveals differences in regional perfusion without ischemia in most patients. However, in patients with a perfusion defect, angina, and/or significant ST-segment depression during dipyridamole stress, quantitative absolute myocardial perfusion and coronary flow reserve (CFR) at the exact moment of definite ischemia have not been established. Defining these low-flow thresholds of angina or ST-segment changes may offer insight into physiological disease severity in patients with atherosclerosis.
Patients underwent rest-dipyridamole stress positron emission tomography (PET) with absolute flow quantification in ml/min/g. Definite ischemia was defined as a new or worse perfusion defect during dipyridamole stress with significant ST-segment depression and/or severe angina requiring pharmacological treatment. Indeterminate clinical features required only 1 of these 3 abnormalities. The comparison group included patients without prior myocardial infarction, or angina or electrocardiographic changes after dipyridamole.
In 1,674 sequential PET studies, we identified 194 (12%) with definite ischemia, 840 (50%) studies with no ischemia, and 301 (18%) that were clinically indeterminate. A vasodilator stress perfusion cutoff of 0.91 ml/min/g optimally separated definite from no ischemia with an area under the receiver-operator characteristic curve (AUC) of 0.98 and a CFR cutoff of 1.74 with an AUC = 0.91, reflecting excellent discrimination at the exact moment of definite ischemia.
Thresholds of low myocardial vasodilator stress perfusion in ml/min/g and CFR sharply separate patients with angina or ST-segment change from those without these manifestations of ischemia during dipyridamole stress with excellent discrimination. Stress flow below 0.91 ml/min/g in dipyridamole-induced PET perfusion defects causes significant ST-segment depression and/or severe angina. However, when the worst vasodilator stress flow exceeds 1.12 ml/min/g, these manifestations of ischemia occur rarely.

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  • Journal of Nuclear Cardiology 10/2012; · 2.85 Impact Factor
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    ABSTRACT: The noninvasive diagnosis of coronary artery disease (CAD) is a challenging task. Although a large armamentarium of imaging modalities is available to evaluate the functional consequences of the extent and severity of CAD, cardiac perfusion positron emission tomography (PET) is considered the gold standard for this purpose. Alternatively, noninvasive anatomical imaging of coronary atherosclerosis with coronary computed tomography angiography (CCTA) has recently been successfully implemented in clinical practice. Although each of these diagnostic approaches has its own merits and caveats, functional and morphological imaging techniques provide fundamentally different insights into the disease process and should be considered to be complementary rather than overlapping. Hybrid imaging with PET/CT offers the possibility to evaluate both aspects nearly simultaneously, and studies have demonstrated that such a comprehensive assessment results in superior diagnostic accuracy, better prognostication, and helps in guiding clinical patient management. The aim of this review is to discuss the value of stand-alone CCTA and PET in CAD, and to summarize the available data on the surplus value of hybrid PET/CT including its strengths and limitations.
    Journal of Nuclear Cardiology 07/2013; · 2.85 Impact Factor
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    ABSTRACT: Heterogeneity of resting perfusion may be due in part to up-regulation of coronary vasoconstriction via endothelin (ET) type A receptors, as homogeneity increases during subsequent vasodilatory hyperemia. Therefore, we conducted a mechanistic study using an ET receptor antagonist to determine if it could alter the homogeneity of myocardial perfusion. Included subjects demonstrated a low myocardial perfusion homogeneity index (HI) compared to normal volunteers. Four serial cardiac positron emission tomography Rb-82 scans were performed 2 weeks apart. Before the middle two scans, subjects were randomized to receive either darusentan first then placebo or visa versa. Absolute flow and coronary flow reserve were quantified for each study. Rest flow was adjusted for the pressure-rate product (PRP). We screened 37 subjects and randomized 20 who satisfied entry criteria. Rest HI increased significantly while taking darusentan (0.39 ± 0.10 vs 0.33 ± 0.04 on placebo, P = .030, compared to a normal range of 0.52 ± 0.10) without an increase in the PRP (6,859 ± 1,503 vs 6,976 ± 1,092, P = .79), leading to a higher adjusted flow at rest (0.69 ± 0.18 cc/minute/g at 7,000 PRP vs 0.59 ± 0.07 with placebo). Antagonism of the type A ET receptor increases homogeneity of resting myocardial perfusion. The mechanism appears to be increased absolute rest flow without an increase in either the PRP or myocardial perfusion during hyperemia. Our translational results are consistent with one mechanism for the observed heterogeneity of myocardial perfusion in humans.
    Journal of Nuclear Cardiology 07/2013; · 2.85 Impact Factor


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Nils P Johnson