To Balloon or Not to Balloon? The Effects of an Intra-Aortic Balloon-Pump on Coronary Artery Flow during Extracorporeal Circulation Simulating Normal and Low Cardiac Output Syndromes

ECMO is the most frequently used mechanical support for patients suffering from low cardiac output syndrome. Combining IABP with ECMO is believed to increase coronary artery blood flow, decrease high afterload, and restore systemic pulsatile flow conditions. This study evaluates that combined effect on coronary artery flow during various load conditions using an in vitro circuit. In doing so, different clinical scenarios were simulated, such as normal cardiac output and moderate-to-severe heart failure. In the heart failure scenarios, we used peripheral ECMO support to compensate for the lowered cardiac output value and reach a default normal value. The increase in coronary blood flow using the combined IABP-ECMO setup was more noticeable in low heart rate conditions. At baseline, intermediate and severe LV failure levels, adding IABP increased coronary mean flow by 16%, 7.5%, and 3.4% (HR 60 bpm) and by 6%, 4.5%, and 2.5% (HR 100 bpm) respectively. Based on our in vitro study results, combining ECMO and IABP in a heart failure setup further improves coronary blood flow. This effect was more pronounced at a lower heart rate and decreased with heart failure, which might positively impact recovery from cardiac failure.

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Altered muscle metaboreflex control of coronary blood flow and ventricular function in heart failure

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00985.2004 ◽

2005 ◽

Vol 288 (3) ◽

pp. H1381-H1388 ◽

Cited By ~ 29

Author(s):

Eric J. Ansorge ◽

Robert A. Augustyniak ◽

Mariana L. Perinot ◽

Robert L. Hammond ◽

Jong-Kyung Kim ◽

...

Keyword(s):

Heart Failure ◽

Heart Rate ◽

Blood Flow ◽

Cardiac Output ◽

Mean Arterial Pressure ◽

Arterial Pressure ◽

Coronary Blood Flow ◽

Moderate Exercise ◽

Muscle Metaboreflex ◽

Significant Change

We investigated the effect of muscle metaboreflex activation on left circumflex coronary blood flow (CBF), coronary vascular conductance (CVC), and regional left ventricular performance in conscious, chronically instrumented dogs during treadmill exercise before and after the induction of heart failure (HF). In control experiments, muscle metaboreflex activation during mild exercise elicited significant reflex increases in mean arterial pressure, heart rate, and cardiac output. CBF increased significantly, whereas no significant change in CVC occurred. There was no significant change in the minimal rate of myocardial shortening (−d l/d tmin) with muscle metaboreflex activation during mild exercise (15.5 ± 1.3 to 16.8 ± 2.4 mm/s, P > 0.05); however, the maximal rate of myocardial relaxation (+d l/d tmax) increased (from 26.3 ± 4.0 to 33.7 ± 5.7 mm/s, P < 0.05). Similar hemodynamic responses were observed with metaboreflex activation during moderate exercise, except there were significant changes in both −d l/d tmin and d l/d tmax. In contrast, during mild exercise with metaboreflex activation during HF, no significant increase in cardiac output occurred, despite a significant increase in heart rate, inasmuch as a significant decrease in stroke volume occurred as well. The increases in mean arterial pressure and CBF were attenuated, and a significant reduction in CVC was observed (0.74 ± 0.14 vs. 0.62 ± 0.12 ml·min−1·mmHg−1; P < 0.05). Similar results were observed during moderate exercise in HF. Muscle metaboreflex activation did not elicit significant changes in either −d l/d tmin or +d l/d tmax during mild exercise in HF. We conclude that during HF the elevated muscle metaboreflex-induced increases in sympathetic tone to the heart functionally vasoconstrict the coronary vasculature, which may limit increases in myocardial performance.

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Coronary smooth muscle reactivity to muscarinic stimulation after ischemia-reperfusion in porcine myocardial infarction

Journal of Applied Physiology ◽

10.1152/japplphysiol.00119.2003 ◽

2003 ◽

Vol 95 (1) ◽

pp. 81-88 ◽

Cited By ~ 7

Author(s):

Antonio Rodríguez-Sinovas ◽

Josep Bis ◽

Inocencio Anivarro ◽

Javier de la Torre ◽

Antoni Bayés-Genís ◽

...

Keyword(s):

Blood Flow ◽

Smooth Muscle ◽

Coronary Artery ◽

Coronary Blood Flow ◽

Ischemia Reperfusion ◽

Left Ventricular ◽

Severe Left Ventricular Dysfunction ◽

Coronary Smooth Muscle

This study tested whether ischemia-reperfusion alters coronary smooth muscle reactivity to vasoconstrictor stimuli such as those elicited by an adventitial stimulation with methacholine. In vitro studies were performed to assess the reactivity of endothelium-denuded infarct-related coronary arteries to methacholine ( n = 18). In addition, the vasoconstrictor effects of adventitial application of methacholine to left anterior descending (LAD) coronary artery was assessed in vivo in pigs submitted to 2 h of LAD occlusion followed by reperfusion ( n = 12), LAD deendothelization ( n = 11), or a sham operation ( n = 6). Endothelial-dependent vasodilator capacity of infarct-related LAD was assessed by intracoronary injection of bradykinin ( n = 13). In vitro, smooth muscle reactivity to methacholine was unaffected by ischemia-reperfusion. In vivo, baseline methacholine administration induced a transient and reversible drop in coronary blood flow (9.6 ± 4.6 to 1.9 ± 2.6 ml/min, P < 0.01), accompanied by severe left ventricular dysfunction. After ischemia-reperfusion, methacholine induced a prolonged and severe coronary blood flow drop (9.7 ± 7.0 to 3.4 ± 3.9 ml/min), with a significant delay in recovery ( P < 0.001). Endothelial denudation mimics in part the effects of methacholine after ischemia-reperfusion, and intracoronary bradykinin confirmed the existence of endothelial dysfunction. Infarct-related epicardial coronary artery shows a delayed recovery after vasoconstrictor stimuli, because of appropriate smooth muscle reactivity and impairment of endothelial-dependent vasodilator capacity.

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Multiphysics model for blood flow and drug transport with application to patient-specific coronary artery flow

Computational Mechanics ◽

10.1007/s00466-008-0321-z ◽

2008 ◽

Vol 43 (1) ◽

pp. 161-177 ◽

Cited By ~ 36

Author(s):

V. M. Calo ◽

N. F. Brasher ◽

Y. Bazilevs ◽

T. J. R. Hughes

Keyword(s):

Blood Flow ◽

Coronary Artery ◽

Drug Transport ◽

Patient Specific ◽

Coronary Artery Flow ◽

Artery Flow

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Adrenomedullin-epinephrine cotreatment enhances cardiac output and left ventricular function by energetically neutral mechanisms

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00887.2011 ◽

2012 ◽

Vol 302 (8) ◽

pp. H1584-H1590

Author(s):

Thor Allan Stenberg ◽

Anders Benjamin Kildal ◽

Ole-Jakob How ◽

Truls Myrmel

Keyword(s):

Heart Failure ◽

Blood Flow ◽

Cardiac Output ◽

Acute Heart Failure ◽

Coronary Blood Flow ◽

Drug Effects ◽

Left Ventricular ◽

Experimental Myocardial Infarction ◽

Energetic Cost ◽

Lv Function

Adrenomedullin (AM) used therapeutically reduces mortality in the acute phase of experimental myocardial infarction. However, AM is potentially deleterious in acute heart failure as it is vasodilative and inotropically neutral. AM and epinephrine (EPI) are cosecreted from chromaffin cells, indicating a physiological interaction. We assessed the hemodynamic and energetic profile of AM-EPI cotreatment, exploring whether drug interaction improves cardiac function. Left ventricular (LV) mechanoenergetics were evaluated in 14 open-chest pigs using pressure-volume analysis and the pressure-volume area-myocardial O2 consumption (PVA-MV˙o2) framework. AM (15 ng·kg−1·min−1, n = 8) or saline (controls, n = 6) was infused for 120 min. Subsequently, a concurrent infusion of EPI (50 ng·kg−1·min−1) was added in both groups (AM-EPI vs. EPI). AM increased cardiac output (CO) and coronary blood flow by 20 ± 10% and 39 ± 14% (means ± SD, P < 0.05 vs. baseline), whereas controls were unaffected. AM-EPI increased CO and coronary blood flow by 55 ± 17% and 75 ± 16% ( P < 0.05, AM-EPI interaction) compared with 13 ± 12% ( P < 0.05 vs. baseline) and 18 ± 31% ( P = not significant) with EPI. LV systolic capacitance decreased by −37 ± 22% and peak positive derivative of LV pressure (dP/d tmax) increased by 32 ± 7% with AM-EPI ( P < 0.05, AM-EPI interaction), whereas no significant effects were observed with EPI. Mean arterial pressure was maintained by AM-EPI and tended to decrease with EPI (+2 ± 13% vs. −11 ± 10%, P = not significant). PVA-MV˙o2 relationships were unaffected by all treatments. In conclusion, AM-EPI cotreatment has an inodilator profile with CO and LV function augmented beyond individual drug effects and is not associated with relative increases in energetic cost. This can possibly take the inodilator treatment strategy beyond hemodynamic goals and exploit the cardioprotective effects of AM in acute heart failure.

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ANTI-THROMBOTIC EFFECT IN CANINE CORONARY ARTERIES OF A COMBINED TXA2 synthetase/TXA2-prostaglandin ENDOPEROXIDE RECEPTOR INHIBITOR (R 68070)

10.1055/s-0038-1643463 ◽

1987 ◽

Author(s):

A Van de Water ◽

R Xhonneux ◽

F De Clerck

Keyword(s):

Heart Rate ◽

Blood Flow ◽

Electrical Stimulation ◽

Coronary Artery ◽

Coronary Blood Flow ◽

Coronary Arteries ◽

Endothelial Injury ◽

Receptor Blockade ◽

Steel Electrode ◽

Prostaglandin Endoperoxide

The effects of R 68070 an oxime-alkane carboxylic acid derivative combining specific thromboxane A2 (TXA2) synthetase inhibition with TXA2/prostaglandin endoperoxide receptor blockade in one molecule, on thrombus formation in a coronary artery following electrically-induced endothelial injury and on its myocardial repercussions were examined in dogs. In an open-chest model in anaesthetized dogs, a stainless steel electrode was inserted into the left anterior descending coronary artery (LAD) distally (+ 1 cm) from an electromagnetic flow probe. ECG and heart rate were derived from limb leads. Serum TXB2 levels were measured by RIA on venous spontaneously coagulated blood (1 h, 37°C). Endothelial cell injury in the LAD coronary artery was induced by the application of an anodal current of 300 μA during 30 min; after an additional 60 min observation period, the thrombus wet weight was determined.In comparison with solvent treatment (n = 8), R 68070 (1.25 mg/kg I.V. 10 min before electrical stimulation, n = 7), significantly reduced the thrombus mass (solvent : 43 mg; R 68070 : 18 mg median value, p < 0.05), the incidence of ECG changes indicative for myocardial ischemia (fibrillation : solvent 1/8; R 68070 0/7; arrhythmias : solvent 3/8; R 68070 2/7; ST changes : solvent 7/8; R 68070 1/7, p < 0.05) and the decrease in coronary blood flow after electrical stimulation (solvent : from 13 to 6.5 ml/min; R 68070 : from 13 to 11 ml/min median values, p < 0.05). Serum TXB2 levels were reduced by 92 % at 100 min after the injection of the active compound (median value, n = 7).Heart rate and coronary blood flow measured before the induction of the endothelial injury were not modified by R 68070.The present study thus demostrates that R 68070 exerts a potent anti-thrombotic effect in canine coronary arteries. The relative contributions to this effect of TXA2 synthetase inhibition and of TXA2/prostaglandin endoperoxide receptor blockade exerted by the compound are being investigated.

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Effects of vasopressin on left anterior descending coronary artery blood flow during extremely low cardiac output

Resuscitation ◽

10.1016/j.resuscitation.2004.03.012 ◽

2004 ◽

Vol 62 (2) ◽

pp. 229-235 ◽

Cited By ~ 12

Author(s):

Viktoria D Mayr ◽

Volker Wenzel ◽

Tilko Müller ◽

Herwig Antretter ◽

Klaus Rheinberger ◽

...

Keyword(s):

Blood Flow ◽

Cardiac Output ◽

Coronary Artery ◽

Artery Blood Flow ◽

Low Cardiac Output

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Development of an In Vitro Model to Characterize the Effects of Transcatheter Aortic Valve on Coronary Artery Flow

Artificial Organs ◽

10.1111/aor.12589 ◽

2015 ◽

Vol 40 (6) ◽

pp. 612-619 ◽

Cited By ~ 6

Author(s):

Joseph Calderan ◽

Wenbin Mao ◽

Eric Sirois ◽

Wei Sun

Keyword(s):

Coronary Artery ◽

Aortic Valve ◽

In Vitro Model ◽

Transcatheter Aortic Valve ◽

Coronary Artery Flow ◽

Vitro Model ◽

Artery Flow

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Effects of levosimendan on coronary artery flow and cardiac performance in patients with advanced heart failure

European Journal of Heart Failure ◽

10.1016/j.ejheart.2007.10.002 ◽

2007 ◽

Vol 9 (12) ◽

pp. 1172-1177 ◽

Cited By ~ 24

Author(s):

Ignatios Ikonomidis ◽

John T. Parissis ◽

Ioannis Paraskevaidis ◽

Kallirrhoe Kourea ◽

Vasiliki Bistola ◽

...

Keyword(s):

Heart Failure ◽

Coronary Artery ◽

Advanced Heart Failure ◽

Cardiac Performance ◽

Coronary Artery Flow ◽

Artery Flow

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Cardiodepressant Activity of 90% Alcoholic Extract of Terminalia Arjuna and its Probable Mechanism of Action

International Journal of Medical and Dental Sciences ◽

10.19056/ijmdsjssmes/2013/v2i2/86772 ◽

2013 ◽

Vol 2 (2) ◽

pp. 144

Author(s):

B. Jassal ◽

B. Kumar ◽

V. Bajaj ◽

R. Walia

Keyword(s):

Heart Rate ◽

Blood Flow ◽

Coronary Blood Flow ◽

Mechanism Of Action ◽

Adrenergic Receptors ◽

Probable Mechanism ◽

Terminalia Arjuna ◽

Alcoholic Extract ◽

Adrenergic Blockers

Background:Terminalia arjuna is being used in various cardiovascular diseases as cardiotonic, diuretic&in hypercholesterolemia. Studies conflict each other for its mechanism of action. This study aims to investigate effect of 90% alcoholic extract of Terminalia arjuna on in vitro isolated rabbit's heart&to find its probable mechanism of action.Objective: To study the preliminary pharmacological effects of 90% alcoholic extract of Terminalia arjuna in-vitro on isolated heart, coronary blood flow, and to study its probable mechanism of action.Material&Methods: Effect of Terminalia arjuna was observed on heart rate, coronary blood flow, amplitude on in vitro isolated perfused rabbit's heart mounted on langendorff apparatus&further cholinergic&adrenergic blockers were used to study the mechanism of action. Six experiments were conducted for each parameter&data was analysed using Student's t test.Results: Terminalia arjuna causes mean percentage decrease of 7.26%, 9.31%&20.51% in heart rate, decrease of 10.34%, 16.64%, 20.51% in coronary blood flow&decrease of 15.11%, 12.61%, 11.65% in amplitude at 25μg, 50μg&100μg doses respectively. The decrease in heart rate, coronary blood flow&amplitude persists even after cholinergic&adrenergic blockers suggesting that cholinergic&adrenergic receptors are not involved in mechanism of Terminalia arjuna.Conclusion: Terminalia arjuna cardiodepressant effect does not involve cholinergic&adrenergic receptors.

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