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      Coronary–aortic interaction during ventricular isovolumic contraction

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          Abstract

          In earlier work, we suggested that the start of the isovolumic contraction period could be detected in arterial pressure waveforms as the start of a temporary pre-systolic pressure perturbation (AIC start, start of the Arterially detected Isovolumic Contraction), and proposed the retrograde coronary blood volume flow in combination with a backwards traveling pressure wave as its most likely origin. In this study, we tested this hypothesis by means of a coronary artery occlusion protocol. In six Yorkshire × Landrace swine, we simultaneously occluded the left anterior descending (LAD) and left circumflex (LCx) artery for 5 s followed by a 20-s reperfusion period and repeated this sequence at least two more times. A similar procedure was used to occlude only the right coronary artery (RCA) and finally all three main coronary arteries simultaneously. None of the occlusion protocols caused a decrease in the arterial pressure perturbation in the aorta during occlusion ( P > 0.20) nor an increase during reactive hyperemia ( P > 0.22), despite a higher deceleration of coronary blood volume flow ( P = 0.03) or increased coronary conductance ( P = 0.04) during hyperemia. These results show that the pre-systolic aortic pressure perturbation does not originate from the coronary arteries.

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          Most cited references16

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          Functional and structural adaptations of coronary microvessels distal to a chronic coronary artery stenosis.

          Distal to a chronic coronary artery stenosis, structural remodeling of the microvasculature occurs. The microvascular functional changes distal to the stenosis have not been studied in detail. We tested the hypothesis that microvascular structural remodeling is accompanied by altered regulation of coronary vasomotor tone with increased responsiveness to endothelin-1. Vasomotor tone was studied in coronary microvessels from healthy control swine and from swine 3 to 4 months after implantation of an occluder that causes a progressive coronary narrowing, resulting in regional left ventricular dysfunction and blunted myocardial vasodilator reserve. Arterioles (approximately 200-microm passive inner diameter at 60 mm Hg) were isolated from regions perfused by the stenotic left anterior descending and normal left circumflex coronary arteries and studied in vitro. Passive pressure-diameter curves demonstrated reduced distensibility of subendocardial left anterior descending compared with subendocardial left circumflex or control arterioles, suggestive of structural remodeling. Myogenic responses were blunted in subendocardial left anterior descending compared with left circumflex arterioles, reflecting altered smooth muscle function. However, vasodilator responses to nitroprusside and bradykinin were not different in the endocardium, suggesting preserved endothelium and smooth muscle responsiveness. Finally, vasoconstrictor responses to endothelin-1 were enhanced in left anterior descending arterioles compared with left circumflex or control arterioles. Regional myocardial vascular conductance responses to bradykinin and endothelin in vivo confirmed the in vitro observations. In conclusion, inward remodeling of coronary microvessels distal to a stenosis is accompanied by exaggerated vasoconstrictor responses to endothelin-1. These structural and functional alterations may aggravate flow abnormalities distal to a chronic coronary artery stenosis.
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            Pulse wave analysis.

            PULSE WAVE ANALYSIS IN HISTORICAL TIMES: Interpretation of the arterial pulse has been an important part of the medical examination from ancient times. Graphic methods for clinical pulse wave recording were introduced by Marey in Paris and by Mahomed in London last century. Mahomed showed how such recordings could be used to detect asymptomatic hypertension, and used them to chart the natural history of essential hypertension and to distinguish between this condition and chronic nephritis. Interest in arterial pulse analysis, as applied by Mahomed, lapsed with the introduction of the cuff sphygmomanometer 100 years ago. MODERN PULSE WAVE ANALYSIS: Analysis of the arterial pulse is now regaining favour as limitations of the cuff sphygmomanometer are better recognized (including the ability only to measure extremes of the pulse in the brachial artery). In addition, high-fidelity tonometers have been introduced for very accurate, non-invasive measurement of arterial pulse contour, and there is now a better understanding of arterial hemodynamics, and appreciation of disease and aging effects in humans. It is now possible to record the pulse wave accurately in the radial or carotid artery, to synthesize the ascending aortic pulse waveform, to identify systolic and diastolic periods and to generate indices of ventricular-vascular interaction previously only possible with invasive arterial catheterization. Pressure pulse wave analysis now permits more accurate diagnosis and more logical therapy than was ever possible in the past.
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              Wave-intensity analysis: a new approach to coronary hemodynamics.

              In 10 anesthetized dogs, we measured high-fidelity left circumflex coronary (P(LCx)), aortic (P(Ao)), and left ventricular (P(LV)) pressures and left circumflex velocity (U(LCx); Doppler) and used wave-intensity analysis (WIA) to identify the determinants of P(LCx) and U(LCx). Dogs were paced from the right atrium (control 1) or right ventricle by use of single (control 2) and then paired pacing to evaluate the effects of left ventricular contraction on P(LCx) and U(LCx). During left ventricular isovolumic contraction, P(LCx) exceeded P(Ao), paired pacing increasing the difference. Paired pacing increased DeltaP(X) (the P(LCx)-P(Ao) difference at the P(Ao)-P(LV) crossover) and average dP(LCx)/dt (P < 0.0001 for both). During this time, WIA identified a backward-going compression wave (BCW) that increased P(LCx) and decreased U(LCx); the BCW increased during paired pacing (P < 0.0001). After the aortic valve opened, the increase in P(Ao) caused a forward-going compression wave that, when it exceeded the BCW, caused U(LCx) to increase, despite P(LV) and (presumably) elastance continuing to increase. Thus WIA identifies the contributions of upstream (aortic) and downstream (microcirculatory) effects on P(LCx) and U(LCx).
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                Author and article information

                Contributors
                m.vanhouwelingen@erasmusmc.nl
                Journal
                Med Biol Eng Comput
                Medical & Biological Engineering & Computing
                Springer-Verlag (Berlin/Heidelberg )
                0140-0118
                1741-0444
                13 April 2011
                13 April 2011
                August 2011
                : 49
                : 8
                : 917-924
                Affiliations
                [1 ]Experimental Cardiology, Thoraxcenter, Cardiovascular Research Institute COEUR, Erasmus MC, University Medical Center Rotterdam, Dr Molewaterplein 50, P.O. Box 2040, 3000 CA Rotterdam, The Netherlands
                [2 ]MACAWI b.v., Eindhoven, The Netherlands
                [3 ]Biomedical Engineering, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, The Netherlands
                Article
                770
                10.1007/s11517-011-0770-y
                3139876
                21487819
                4f43717a-0dd7-473f-abcd-ddfbb3f9bce4
                © The Author(s) 2011
                History
                : 15 December 2010
                : 23 March 2011
                Categories
                Original Article
                Custom metadata
                © International Federation for Medical and Biological Engineering 2011

                Biomedical engineering
                coronary–aortic interaction,pulse wave analysis,coronary occlusion,isovolumic contraction

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