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Coronary-aortic interaction during ventricular isovolumic contraction.

van Houwelingen MJ, Merkus D, Te Lintel Hekkert M, van Dijk G, Hoeks AP, Duncker DJ - Med Biol Eng Comput (2011)

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: 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. m.vanhouwelingen@erasmusmc.nl

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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Example of an aortic pressure curve with the pressure perturbation enlarged on the right. AICstart (start of the arterially-detected isovolumic contraction) is indicated by the dash-dot vertical line and the preceding Q-top of the ECG by a triangle. The enlargement shows the touching tangent (dotted line) and the area between the pressure perturbation and this tangent (PPA)
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Fig1: Example of an aortic pressure curve with the pressure perturbation enlarged on the right. AICstart (start of the arterially-detected isovolumic contraction) is indicated by the dash-dot vertical line and the preceding Q-top of the ECG by a triangle. The enlargement shows the touching tangent (dotted line) and the area between the pressure perturbation and this tangent (PPA)

Mentions: Measurement equipment introduced a >10 ms delay in the ECG compared to the aortic pressure and coronary blood volume flow signals. The delay was compensated for during post processing prior to extracting hemodynamic features. All signals were low pass filtered with a cut-off frequency of 80 Hz to remove noise. The onset of each heart cycle was identified using the Q-top of the ECG. From the aortic pressure recording, the maximum systolic (SBP), minimum diastolic (DBP), and mean blood pressure (MBP) values were determined. The onset of the arterial pressure perturbation, termed AICstart (start of the Arterially detected Isovolumic Contraction, Fig. 1) was identified as the position of the maximum of the second derivative of the aortic blood pressure (d2P/dtmax2) preceding the aortic valve opening [23]. To quantify the pressure perturbation in the aortic pressure following AICstart, the pressure perturbation area (PPA) enclosed by the aortic pressure and a tangent was calculated. The tangent started at AICstart and ran through the point where it touched the aortic pressure curve again (Fig. 1). The results from the occlusion and reactive hyperemia data were normalized to the five cycle pre-occlusion PPA average.Fig. 1


Coronary-aortic interaction during ventricular isovolumic contraction.

van Houwelingen MJ, Merkus D, Te Lintel Hekkert M, van Dijk G, Hoeks AP, Duncker DJ - Med Biol Eng Comput (2011)

Example of an aortic pressure curve with the pressure perturbation enlarged on the right. AICstart (start of the arterially-detected isovolumic contraction) is indicated by the dash-dot vertical line and the preceding Q-top of the ECG by a triangle. The enlargement shows the touching tangent (dotted line) and the area between the pressure perturbation and this tangent (PPA)
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3139876&req=5

Fig1: Example of an aortic pressure curve with the pressure perturbation enlarged on the right. AICstart (start of the arterially-detected isovolumic contraction) is indicated by the dash-dot vertical line and the preceding Q-top of the ECG by a triangle. The enlargement shows the touching tangent (dotted line) and the area between the pressure perturbation and this tangent (PPA)
Mentions: Measurement equipment introduced a >10 ms delay in the ECG compared to the aortic pressure and coronary blood volume flow signals. The delay was compensated for during post processing prior to extracting hemodynamic features. All signals were low pass filtered with a cut-off frequency of 80 Hz to remove noise. The onset of each heart cycle was identified using the Q-top of the ECG. From the aortic pressure recording, the maximum systolic (SBP), minimum diastolic (DBP), and mean blood pressure (MBP) values were determined. The onset of the arterial pressure perturbation, termed AICstart (start of the Arterially detected Isovolumic Contraction, Fig. 1) was identified as the position of the maximum of the second derivative of the aortic blood pressure (d2P/dtmax2) preceding the aortic valve opening [23]. To quantify the pressure perturbation in the aortic pressure following AICstart, the pressure perturbation area (PPA) enclosed by the aortic pressure and a tangent was calculated. The tangent started at AICstart and ran through the point where it touched the aortic pressure curve again (Fig. 1). The results from the occlusion and reactive hyperemia data were normalized to the five cycle pre-occlusion PPA average.Fig. 1

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: 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. m.vanhouwelingen@erasmusmc.nl

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.

Show MeSH
Related in: MedlinePlus