C oronary artery disease accounts for ≈1 in every 6 deaths in the United States, with acute ST-segment-elevation myocardial infarction (STEMI) contributing significantly to the overall morbidity associated with this disease. 1 Postmortem studies in patients dying of myocardial infarction consistently demonstrate that the majority of STEMIs are triggered by rupture of a thin-fibrous cap overlying a lipidrich necrotic core. 2-5Intracoronary near-infrared spectroscopy (NIRS) is a catheter-based imaging modality developed and validated to detect lipid-rich plaques (LRPs) in patients undergoing coronary angiography. 6,7 In an exploratory analysis in a small number of STEMI patients, NIRS demonstrated large, significant differences in the lipid content between culprit and nonculprit segments.8 A potential NIRS signature of STEMI culprit lesions was identified, defined by a maximum lipid core burden index within a 4-mm coronary section (maxL-CBI 4mm ) being >400. These initial observations were limited by a modest sample size, single-center enrollment, and post hoc selection of the maxLCBI 4mm ≥400 threshold. This study was designed a priori to confirm the ability of NIRS to discriminate STEMI culprit from nonculprit segments and to determine the sensitivity and specificity of the maxLCBI 4mm ≥400 threshold. Secondary aims were to evaluate the ability of the NIRS block chemogram to differentiate culprit from nonculprit segments and to evaluate the regional deposition of lipid within coronary segments adjacent to the angiographically defined culprit segment.© 2016 American Heart Association, Inc. Objective-In a previous exploratory analysis, intracoronary near-infrared spectroscopy (NIRS) found the majority of culprit lesions in ST-segment-elevation myocardial infarction (STEMI) to contain a maximum lipid core burden index in 4 mm (maxLCBI 4mm ) of >400. This initial study was limited by a small sample size, enrollment at a single center, and post hoc selection of the maxLCBI 4mm ≥400 threshold. This study was designed a priori to substantiate the ability of NIRS to discriminate STEMI culprit from nonculprit segments and to confirm the performance of the maxLCBI 4mm ≥400 threshold. Approach and Results-At 2 centers in the United States and Sweden, 75 STEMI patients underwent intracoronary NIRS imaging after establishing thrombolysis in myocardial infarction 3 flow, but before stenting. Blinded core laboratory analysis defined the culprit segment as the 10-mm segment distal to the proximal angiographic culprit margin. The remaining vessel was divided into contiguous 10-mm nonculprit segments.

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A large body of evidence demonstrates an independent association between arterial stiffness and prospective risk of cardiovascular events. A reduction in coronary perfusion is presumed to underscore this association; however, studies confirming this are lacking. This study compared invasive measures of coronary blood flow (CBF) with cardiac magnetic resonance (CMR)-derived aortic distensibility (AD). Following coronary angiography, a Doppler FloWire and infusion microcatheter were advanced into the study vessel. Average peak velocity (APV) was acquired at baseline and following intracoronary adenosine to derive coronary flow velocity reserve (CFVR = hyperemic APV/resting APV) and CBF [π × (diameter)2 × APV × 0.125]. Following angiography, patients underwent CMR to evaluate distensibility at the ascending aorta (AA), proximal descending aorta (PDA) and distal descending aorta (DDA). Fifteen participants (53 ± 13 yr) with minor epicardial disease (maximum stenosis <30%) were enrolled. Resting CBF was 44.1 ± 11.9 mL/min, hyperemic CBF was 143.8 ± 37.4 mL/min, and CFVR was 3.15 ± 0.48. AD was 3.89 ± 1.72·10−3mmHg−1 at the AA, 4.08 ± 1.80·10−3mmHg−1 at the PDA, and 4.42 ± 1.67·10−3mmHg−1 at the DDA. All levels of distensibility correlated with resting CBF ( R2 = 0.350–0.373, P < 0.05), hyperemic CBF ( R2 = 0.453–0.464, P < 0.01), and CFVR ( R2 = 0.442–0.511, P < 0.01). This study demonstrates that hyperemic and, to a lesser extent resting CBF, are significantly associated with measures of aortic stiffness in patients with only minor angiographic disease. These findings provide further in vivo support for the observed prognostic capacity of large artery function in cardiovascular event prediction. NEW & NOTEWORTHY Cardiac magnetic resonance-derived aortic distensibility is associated with invasive measures of coronary blood flow. Large artery function is more strongly correlated with hyperemic than resting blood flow. Increased stiffness may represent a potential target for novel antianginal medications.

Aim: Preclinical studies have demonstrated improvements in renal blood flow after renal sympathetic denervation (RSDN); however, such effects are yet to be confirmed in patients with resistant hypertension. Herein, we assessed the effects of RSDN on renal artery blood flow and diameter at multiple time points post-RSDN. Methods and results: Patients (n=11) with systolic blood pressures ≥160 mmHg despite taking three or more antihypertensive medications at maximum tolerated dose were recruited into this single-center, prospective, non-blinded study. Magnetic resonance imaging indices included renal blood flow and renal artery diameters at baseline, 1 month and 6 months. In addition to significant decreases in blood pressures (p<0.0001), total volume of blood flow per cardiac cycle increased by 20% from 6.9±2 mL at baseline to 8.4±2 mL (p=0.003) at 1 month and to 8.0±2 mL (p=0.04) 6 months post-procedure, with no changes in the renal blood flow. There was a significant decrease in renal artery diameters from 7±2 mm at baseline to 6±1 mm (p=0.03) at 1 month post-procedure. This decrease was associated with increases in maximum velocity of blood flow from 73±20 cm/s at baseline to 78±19 cm/s at 1 month post-procedure. Notably, both parameters reverted to 7±2 mm and 72±18 cm/s, respectively, 6 months after procedure. Conclusion: RSDN improves renal physiology as evidenced by significant improvements in total volume of blood flow per cardiac cycle. Additionally, for the first time, we identified a transient decrease in renal artery diameters immediately after procedure potentially caused by edema and inflammation that reverted to baseline values 6 months post-procedure.

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S169 136The importance of evaluating patients with MINOCA (Myocardial infarction with non-obstructive coronary arteries)