Cardiac diastolic dysfunction in conscious dogs with heart failure induced by chronic coronary microembolization

Gill, Robert M.; Jones, Bonita D.; Corbly, Angela K.; Wang, Juan; Braz, Julian C.; Sandusky, George E.; Wang, Jie; Shen, Wen

doi:10.1152/ajpheart.00052.2006

Cited by 20 publications

(9 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The ratio of NF/left ventricle area (NF/LV) from all examined slices were calculated and averaged. Even slices (2,4,6,8,10) were used for light and transmission electron microscopic analysis.…”

Section: Evaluation the Areas Of No-flow Zonementioning

confidence: 99%

Establishment and Characterization of an Experimental Model of Coronary Thrombotic Microembolism in Rats

Bai

et al. 2010

The American Journal of Pathology

View full text Add to dashboard Cite

To establish a model of coronary thrombotic microembolism in rats, either automicrothrombotic particulates (CM group) or saline control (SHAM group) was injected into temporarily clamped aortas of male Sprague-Dawley rats. After automicrothrombotic particulate injection, serum c-troponin I and von Willebrand factor levels, the no-flow area as evaluated by Thioflavin S, myocardial leukocyte infiltration levels, myocardial expressions of tumor necrosis factor ␣ and interleukin-6, the percentage of arterioles obstructed by thrombosis, and myocardial fibrosis were all significantly increased whereas cardiac function as evaluated by echocardiography and hemodynamic measurements were significantly reduced compared with the sham group. Thus, aortic automicrothrombotic particulate injection could induce coronary microembolism in rats, and this model could be of value in improving the understanding of pathophysiology of coronary microembolism. Atherosclerotic plaque rupture is a key event in the pathogenesis of acute coronary syndrome and during coronary interventions.1 It does not always result in complete thrombotic occlusion of the epicardial coronary artery with subsequent impending myocardial infarction, but may in milder forms result in the embolization of atherosclerotic and thrombotic debris into the coronary microcirculation, which has recently been identified as a potential cause of no-reflow phenomenon, myocardium ischemia, and myocardial infarctlet. Atherosclerotic embolization in the microvasculature is associated with adverse prognosis. [1][2][3][4] Research results derived from suitable experimental models of coronary microembolism would help clinicians to understand the underlying pathological mechanisms and to develop effective therapies of coronary microembolism induced by atherosclerotic embolization in the microvasculature.5 Until now, plastic microspheres ranging from 20 to 900 m in diameter were injected into the coronary microcirculation to establish the coronary microembolism models in dog, swine and sheep.6 -11 Experimental models were also made by injecting adenosine-diphosphate or catecholamine to induce platelet aggregation in coronary microcirculation in pigs.12-13 However, injecting microspheres with unique sizing would only occlude respective vessels with comparable sizes, while thrombotic debris in patients might vary greatly in sizing and affect vessels with different diameters. Models using adenosine diphosphate or catecholamine could mimic the platelet aggregation process during coronary microthrombosis but could not reflect the influences of various embolism components of atherosclerotic plaques. Therefore, established coronary microembolism models could only partly mimic the in vivo situation of coronary microthrombosis. In the present study, we showed that coronary microembolism could be induced by intraaortic injection of automicrothrombotic particulates varying in sizing in rats. Increased myocardial inflammatory cells infiltration and fibrosis as well as reduced cardiac function w...

show abstract

Section: Evaluation the Areas Of No-flow Zonementioning

confidence: 99%

Establishment and Characterization of an Experimental Model of Coronary Thrombotic Microembolism in Rats

Bai

et al. 2010

The American Journal of Pathology

View full text Add to dashboard Cite

show abstract

“…Other investigators determined EDPVRs with EDV variation ranging from 25% to 50%. The numbers of cardiac cycles used were typically Ͻ10 in some studies (11,13,23,25). In the present study, the average EDV variation was 31 Ϯ 16% (relative to the maximum EDV) and the average diastatic volume variation was 40 Ϯ 21% (relative to the maximum diastatic volume).…”

Section: Determination Of the Edpvr And D-pvrmentioning

confidence: 48%

The diastatic pressure-volume relationship is not the same as the end-diastolic pressure-volume relationship

Zhang

Kovács

2008

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

The end-diastolic pressure-volume (P-V) relationship (EDPVR) is routinely used to determine the passive left ventricular (LV) stiffness, although the diastatic P-V relationship (D-PVR) has also been measured. Based on the physiological difference between diastasis (the LV and atrium are relaxed and static) and end diastole (LV volume increased by atrial systole and the atrium is contracted), we hypothesized that, although both D-PVR and EDPVR include LV chamber stiffness information, they are two different, distinguishable P-V relations. Cardiac catheterization determined LV pressures, and conductance volumes in 31 subjects were analyzed. Physiological, beat-to-beat variation of the diastatic and end-diastolic P-V points were fit by linear and exponential functions to generate the D-PVR and EDPVR. The extrapolated exponential D-PVR underestimated LVEDP in 82% of the heart beats (P < 0.001). The extrapolated EDPVR overestimated pressure at diastasis in 84% of the heart beats (P < 0.001). If each subject's diastatic and end-diastolic P-V data were combined to form a continuous data set to be fit by one exponential relation, the goodness of fit was always worse than if the diastatic and end-diastolic data were grouped separately and fit by two distinct exponential relations. Diastatic chamber stiffness was less than EDPVR stiffness (defined by the slope of P-V relation) for all 31 subjects (0.16 +/- 0.11 vs. 0.24 +/- 0.15 mmHg/ml, P < 0.001). We conclude that the D-PVR and EDPVR are distinguishable. Because it is not coupled to a contracted atrium, the D-PVR conveys passive LV stiffness better than the EDPVR. Additional studies that fully elucidate the physiology and biology of diastasis in health and disease are in progress.

show abstract

“…Kass et al previously demonstrated that increased coronary perfusion during IABP support improves tissue elasticity, a major determinant of diastolic dysfunction [18,19]. Similarly, Gill et al showed that the development of diastolic dysfunction was related to decreased coronary perfusion induced by recurrent coronary embolization [20]. Furthermore, metabolic disturbances and increased central blood volume both seem to be contributing factors for the development and continued prevalence of diastolic dysfunction [21].…”

Section: Discussionmentioning

confidence: 99%

Influence of Intraaortic Balloon Pump Counterpulsation on Transesophageal Echocardiography Derived Determinants of Diastolic Function

et al. 2015

View full text Add to dashboard Cite

IntroductionIntraaortic balloon pump counterpulsation (IABP) is often used in patients with acute coronary syndrome for its favourable effects on left ventricular (LV) systolic function and coronary perfusion. However, the effects of IABP on LV diastolic function have not been comprehensively investigated. Acute diastolic dysfunction has been linked to increased morbidity and mortality. The aim of this study was to examine the influence of IABP on LV diastolic dysfunction using standard TEE derived parameters.MethodsIntraoperative TEE was performed in 10 patients (mean age 65 ± 11 yrs) undergoing urgent coronary artery bypass graft surgery (CABG), who had received an IABP preoperatively. TEE derived measures of diastolic dysfunction included early to late transmitral Doppler inflow velocity ratio (E/A), deceleration time (Dt), pulmonary venous systolic to diastolic Doppler velocity ratio (S/D), transmitral propagation velocity (Vp), and the ratio of early to late mitral annular tissue Doppler velocities (e’/a’). Statistical analyses included the Wilcoxon Sign-Rank test, and a p<0.05 was considered significant.ResultsTransmitral inflow E/A ratios increased significantly from 0.86 to 1.07 (p < 0.05), while Dt decreased significantly from 218 to 180 ms (p < 0.05) with the use of IABP. Significant increases in Vp (34 cm/s to 43 cm/s; p < 0.05), and e’/a’ (0.58 to 0.71; p < 0.05) suggested a favourable influence of intraaortic counterpulsation on diastolic function.ConclusionThe use of perioperative IABP significantly improves TEE derived parameters of diastolic function consistent with a favourable impact on LV relaxation in cardiac surgery patients undergoing CABG.

show abstract

Cardiac diastolic dysfunction in conscious dogs with heart failure induced by chronic coronary microembolization

Cited by 20 publications

References 20 publications

Establishment and Characterization of an Experimental Model of Coronary Thrombotic Microembolism in Rats

Establishment and Characterization of an Experimental Model of Coronary Thrombotic Microembolism in Rats

The diastatic pressure-volume relationship is not the same as the end-diastolic pressure-volume relationship

Influence of Intraaortic Balloon Pump Counterpulsation on Transesophageal Echocardiography Derived Determinants of Diastolic Function

Contact Info

Product

Resources

About