Abstract 15835: Cold Air Inhalation Induces Differential Effects on Coronary Microvascular Resistance and Flow Depending on Presence of Significant Coronary Artery Disease
Introduction: Cold temperatures increase the incidence of myocardial infarction. Precise mechanisms remain unclear. Sudden severe myocardial oxygen supply/demand mismatch may be responsible. We measured coronary flow and myocardial work during cold air inhalation (CAI), invasively and with cardiac magnetic resonance imaging (CMR), aiming to elucidate the dominant mechanisms.
Methods: All data were acquired at rest and peak stress during CAI: 5minutes -15oC via a face-mask. Simultaneous intracoronary pressure and flow velocity data were acquired in a target artery from 20 patients (10 with normal coronary arteries, 10 with a significant stenosis (CAD). Coronary flow average peak velocity (APV), microvascular resistance (MVR) and buckberg index (BI: a surrogate for subendocardial ischemia) were calculated. Wave intensity analysis also differentiated waves that accelerate and decelerate coronary flow. Separately CMR perfusion was performed in 7 patients with a significant stenosis to quantify myocardial perfusion reserve (MPR) and transmural perfusion gradients (TPG).
Results: At rest MVR is lower in CAD patients, maintaining APV (1a,b). During CAI, although myocardial work increased similarly in normal and CAD patients (rate pressure product mean difference 2312 and 2651mmHg.min-1 respectively), there was a differential response in coronary flow, with a significant increase and a downward trend in APV respectively (1a). Relative hypoperfusion of stenosed segments was also noted on MPR (2a). This inability of CAD patients to augment APV is explained by a significant increase in MVR (1b) collaborating with a reduction in accelerating flow waves (1c). These cause a relative subendocardial perfusion deficit, demonstrated by a significant decrease in BI (1d) and increase in TPG (2b).
Conclusions: CAI increases myocardial work but CAD patients are unable to augment flow due to microvascular vasoconstriction and adverse ventricular-vascular coupling.
Author Disclosures: R. Williams: None. K. Asrress: None. M. Lumley: None. S. Arri: None. T. Patterson: None. V. Manou-Stathopoulou: None. C. Macfarlane: None. H. Ellis: None. Z. Khawaja: None. N. Briceno: None. B. Clapp: None. D. Perera: None. A. Chiribiri: None. S. Plein: None. M. Marber: None. S. Redwood: None.
- © 2015 by American Heart Association, Inc.