Myocardial blood volume and coronary resistance during and after coronary angioplasty

2011 ◽  
Vol 300 (3) ◽  
pp. H1119-H1124 ◽  
Author(s):  
Andreas Indermühle ◽  
Rolf Vogel ◽  
Pascal Meier ◽  
Rainer Zbinden ◽  
Christian Seiler
Keyword(s):  
Blood Volume ◽  
Coronary Arteries ◽  
Coronary Angioplasty ◽  
Coronary Circulation ◽  
Perfusion Pressure ◽  
Contrast Echocardiography ◽  
Coronary Perfusion ◽  
Collateral Flow ◽  
Coronary Resistance ◽  
Myocardial Blood Volume

Animal experiments have shown that the coronary circulation is pressure distensible, i.e., myocardial blood volume (MBV) increases with perfusion pressure. In humans, however, corresponding measurements are lacking so far. We sought to quantify parameters reflecting coronary distensibility such as MBV and coronary resistance (CR) during and after coronary angioplasty. Thirty patients with stable coronary artery disease underwent simultaneous coronary perfusion pressure assessment and myocardial contrast echocardiography (MCE) of 37 coronary arteries and their territories during and after angioplasty. MCE yielded MBV and myocardial blood flow (MBF; in ml·min−1·g−1). Complete data sets were obtained in 32 coronary arteries and their territories from 26 patients. During angioplasty, perfusion pressure, i.e., coronary occlusive pressure, and MBV varied between 9 and 57 mmHg (26.9 ± 11.9 mmHg) and between 1.2 and 14.5 ml/100 g (6.7 ± 3.7 ml/100 g), respectively. After successful angioplasty, perfusion pressure and MBV increased significantly ( P < 0.001 for both) and varied between 64 and 118 mmHg (93.5 ± 12.8 mmHg) and between 3.7 and 17.3 ml/100 g (9.8 ± 3.4 ml/100 g), respectively. Mean MBF increased from 31 ± 20 ml·min−1·g−1 during coronary occlusion, reflecting collateral flow, to 121 ± 33 ml·min−1·g−1 ( P < 0.01), whereas mean CR, i.e., the ratio of perfusion pressure and MBF, decreased by 20% ( P < 0.001). In conclusion, the human coronary circulation is pressure distensible. MCE allows for the quantification of CR and MBV in humans.

Abstract 2085: Increased Regional Coronary Vascular Resistance During Hyperemia in Hypertrophic Cardiomyopathy Is Associated with Reduced Myocardial Blood Volume

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Hiroshi Komatsu ◽  
Satoshi Yamada ◽  
Masanao Naya ◽  
Hisao Onozuka ◽  
Taisei Mikami ◽  
...  
Keyword(s):  
Hypertrophic Cardiomyopathy ◽  
Blood Volume ◽  
Vascular Resistance ◽  
Contrast Echocardiography ◽  
Interventricular Septum ◽  
Power Doppler ◽  
Doppler Imaging ◽  
Coronary Vascular Resistance ◽  
Coronary Resistance ◽  
Myocardial Blood Volume

Introduction: In patients with hypertrophic cardiomyopathy ( HCM ), myocardial blood flow ( MBF ) is decreased during hyperemia because of high coronary vascular resistance. Recently myocardial blood volume ( MBV ) can be estimated in vivo using myocardial contrast echocardiography ( MCE ) with the compensation for acoustic field inhomogeneity. The relationship between MBV and coronary resistance, however, has not been investigated. We thus assessed the hypothesis that increased regional coronary vascular resistance during hyperemia in HCM is associated with reduced MBV. Methods: In 13 patients with HCM ( H , 53±16 years) with asymmetric septal hypertrophy and 9 normal volunteers ( N , 54±11 years), MCE was performed under infusion of Levovist at rest and during hyperemia induced by ATP. Apical 4-chamber views of intermittent harmonic power Doppler imaging were acquired at end-diastole of every sixth beat. MBV was calculated as 10 X/10 ×100%, where X was myocardial contrast intensity minus contrast intensity of the adjacent intracavity blood pool in dB. 15 O-water PET was performed to measure regional MBF. These parameters were measured in the interventricular septum ( IVS ) and LV posterolateral ( PL ) wall. Regional coronary vascular resistance was calculated as (mean blood pressure)/MBF. Results: Wall thickness was significantly greater in H than in N (IVS: 19±4 vs 10±1 mm, p<0.0001; PL: 10±1 vs 9±1 mm, p<0.05). MBV of IVS was lower in H than in N (rest: 2.1±0.7 vs 3.5±1.1%, p<0.01; hyperemia: 2.1±1.3 vs 4.3±1.7%, p<0.01), whereas MBV of PL wall did not differ between groups. Coronary resistance at rest did not differ between groups, but the resistance during hyperemia was significantly greater in H than in N (IVS: 59±16 vs 31±14 mmHg·min·g·ml −1 , p<0.001; PL: 40±10 vs 30±11 mmHg·min·g·ml −1 , p<0.05). Coronary resistance at rest did not correlate with MBV, whereas that during hyperemia inversely correlated with MBV during hyperemia (r=−0.77, p<0.0001) as well as MBV at rest (r=−0.65, p<0.0001). Conclusions: Increased coronary vascular resistance during hyperemia in HCM was significantly associated with reduced MBV. MCE is useful for assessing the dynamic function of coronary circulation in the clinical setting.

scholarly journals Progesterone modulates endothelium-dependent coronary vascular reactivity in SHR

2021 ◽  
Author(s):  
Débora Tacon da Costa ◽  
Leticia Tinoco Gonçalves ◽  
Jéssyca Aparecida Soares Giesen ◽  
Roger Lyrio dos Santos
Keyword(s):  
Vascular Reactivity ◽  
Sham Group ◽  
Coronary Circulation ◽  
Perfusion Pressure ◽  
Coronary Perfusion Pressure ◽  
Ovariectomized Rats ◽  
Coronary Perfusion ◽  
Coronary Vasodilation ◽  
Progesterone Treatment ◽  
Before And After

Although progesterone has the ability to promote dilation of vascular smooth muscle, its role in coronary circulation is still poorly characterized, especially in essential hypertension and in a model of endogenous deficiency of ovarian hormones. Thus, this study evaluated the effect of progesterone treatment on endothelium-dependent coronary vascular reactivity in hypertensive (SHR) and ovariectomized rats. Adult SHR aged 8 to 10 weeks were divided into: SHAM, Ovariectomized (OVX) and Ovariectomized + treatment with 2 mg/kg/day of progesterone for 15 days (OVX-P4). Coronary vascular reactivity was investigated using modified Langendorff method. After stabilization, baseline coronary perfusion pressure (CPP) was recorded and vascular reactivity to bradykinin (BK, 0.1-1000 ng) assessed before and after infusion, either individually or in combination, with Nω-nitro-L-arginine methyl ester (L-NAME), indomethacin or clotrimazole. Scanning electron microscopy was used for qualitative analysis of the endothelium. OVX and OVX-P4 groups had a higher baseline CPP compared to that of the SHAM group. BK was able to promote vasodilation in all groups. However, relaxation to BK was less pronounced in the OVX group when compared to SHAM, with architecture loss and areas of cell atrophy having been observed. Progesterone treatment prevented this injury. Perfusion with L-NAME induced greater damage to the SHAM group, while the use of indomethacin led to a significant reduction in the vasodilator response to BK in the OVX-P4 group. Taken together, our results show that progesterone modulates endothelium-dependent coronary vasodilation in SHR ovariectomized, preventing damage caused by ovarian hormonal deficiency through a mechanism that involves prostanoid pathway.

Shunting of microspheres across the canine coronary circulation

1979 ◽  
Vol 236 (1) ◽  
pp. H7-H12 ◽  
Author(s):  
G. J. Crystal ◽  
R. B. Boatwright ◽  
H. F. Downey ◽  
F. A. Bashour
Keyword(s):  
Coronary Circulation ◽  
Perfusion Pressure ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Coronary Perfusion ◽  
Blood Samples ◽  
Ventricular Afterload ◽  
The Difference ◽  
Inspired Oxygen ◽  
Coronary Sinus Blood

Coronary shunting of 9 +/-1 micrometer and 25 +/- 5 micrometer radiolabeled microspheres was examined in anesthetized, open-chest dogs, whose left common coronary arteries were perfused at controlled pressures. Shunting was estimated from the difference in radioactivity between perfusion line and coronary sinus blood samples during selective elevations of coronary perfusion pressure (CPP), left ventricular afterload, and inspired oxygen. A linear relationship was found between coronary shunting of 9-micrometer microspheres and CPP over the range 100-200 mmHg. According to regression analysis, percent shunt flow was 4.0% at control CPP (100 mmHg) and 10.0% at CPP of 200 mmHg. No shunting of 25-micrometer microspheres occurred at any CPP. Raising afterload did not affect shunting at control CPP but attenuated the increase in shunting at elevated CPP. Changing inspired gas from room air to 100% oxygen did not influence shunting at control or elevated CPP. Raising CPP to 150 and 200 mmHg also released 2.5% and 5.9% of pretrapped 9-micrometer microspheres, respectively. This study demonstrates that vessels permitting passage of microspheres across coronary circulation are sensitive to elevated perfusion pressure.

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