Wave speed in human coronary arteries is not influenced by microvascular vasodilation: implications for wave intensity analysis

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• 作者：M. Cristina Rolandi (1)
  Kalpa De Silva (2)
  Matthew Lumley (2)
  Timothy P. E. Lockie (2)
  Brian Clapp (2)
  Jos A. E. Spaan (1)
  Divaka Perera (2)
  Maria Siebes (1)
  
• 关键词：Coronary artery ; Coronary physiology ; Pulse wave velocity ; Wave intensity analysis
• 刊名：Basic Research in Cardiology
• 出版年：2014
• 出版时间：March 2014
• 年：2014
• 卷：109
• 期：2
• 全文大小：1,212 KB
• 作者单位：M. Cristina Rolandi (1)
  Kalpa De Silva (2)
  Matthew Lumley (2)
  Timothy P. E. Lockie (2)
  Brian Clapp (2)
  Jos A. E. Spaan (1)
  Divaka Perera (2)
  Maria Siebes (1)
  
  1. Department of Biomedical Engineering and Physics, Academic Medical Center, University of Amsterdam, Meibergdreef 9, P.O. Box 2270, 1105 AZ, Amsterdam, The Netherlands
  2. Cardiovascular Division, King’s College London British Heart Foundation Centre of Excellence at Guy’s and St. Thomas-National Health Service Foundation Trust, London, UK
  
• ISSN：1435-1803

文摘

Wave intensity analysis and wave separation are powerful tools for interrogating coronary, myocardial and microvascular physiology. Wave speed is integral to these calculations and is usually estimated by the single-point technique (SPc), a feasible but as yet unvalidated approach in coronary vessels. We aimed to directly measure wave speed in human coronary arteries and assess the impact of adenosine and nitrate administration. In 14 patients, the transit time Δt between two pressure signals was measured in angiographically normal coronary arteries using a microcatheter equipped with two high-fidelity pressure sensors located Δs?=?5?cm apart. Simultaneously, intracoronary pressure and flow velocity were measured with a dual-sensor wire to derive SPc. Actual wave speed was calculated as DNc?=?Δs/Δt. Hemodynamic signals were recorded at baseline and during adenosine-induced hyperemia, before and after nitroglycerin administration. The energy of separated wave intensity components was assessed using SPc and DNc. At baseline, DNc equaled SPc (15.9?±?1.8 vs. 16.6?±?1.5?m/s). Adenosine-induced hyperemia lowered SPc by 40?% (p?<?0.005), while DNc remained unchanged, leading to marked differences in respective separated wave energies. Nitroglycerin did not affect DNc, whereas SPc transiently fell to 12.0?±?1.2?m/s (p?<?0.02). Human coronary wave speed is reliably estimated by SPc under resting conditions but not during adenosine-induced vasodilation. Since coronary wave speed is unaffected by microvascular dilation, the SPc estimate at rest can serve as surrogate for separating wave intensity signals obtained during hyperemia, thus greatly extending the scope of WIA to study coronary physiology in humans.