Effect of Coronary Perfusion Pressure or Coronary Flow on Oxygen Usage of the Myocardium

Gregg, Donald E.

doi:10.1161/01.res.13.6.497

Cited by 254 publications

(143 citation statements)

References 5 publications

Supporting

Mentioning

133

Contrasting

Unclassified

Order By: Relevance

“…This could be explained by increased coronary micro-vascular filling and thus stretch of the sarcomeres and/or release of positive inotropic factors, leading to increased contractility. [38][39][40] Also the nitroprusside experiments support the theory that coronary vasodilation could improve RV function. We found that nitroprusside, which can be considered a "pure" vasodilator, improved RV contractility in the control hearts and the hypertrophic hearts where the coronary flow was increased.…”

Section: A C C E P T E Dmentioning

confidence: 66%

Inotropic Effects of Prostacyclins on the Right Ventricle Are Abolished in Isolated Rat Hearts With Right-Ventricular Hypertrophy and Failure

Holmboe

Andersen

Johnsen

et al. 2017

Journal of Cardiovascular Pharmacology

View full text Add to dashboard Cite

Background:Prostacyclin mimetics are vasodilatory agents used in the treatment of pulmonary arterial hypertension. The direct effects of prostanoids on right ventricular (RV) function are unknown.We aimed to investigate the direct effects of prostacyclin mimetics on RV function in hearts with and without RV hypertrophy and failure. Methods:Wistar rats were subjected to pulmonary trunk banding to induce compensated RV hypertrophy (n=32) or manifest RV failure (n=32). Rats without banding served as healthy controls (n=30).The hearts were excised and perfused in a Langendorff system and subjected to iloprost, treprostinil, epoprostenol or MRE-269 in increasing concentrations. The effect on RV function was evaluated using a balloon-tipped catheter inserted into the RV. Results:In control hearts iloprost, treprostinil and MRE-269, improved RV function. The effect was, however, absent in hearts with RV hypertrophy and failure. Treprostinil and MRE-269 even impaired RV function in hearts with manifest RV failure.Copyright Ó 2016 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited. A C C E P T E D 3 Conclusion:Iloprost, treprostinil and MRE-269 improved RV function in the healthy rat heart. RV hypertrophy abolished the positive inotropic effect and in the failing right ventricle, MRE-269 and treprostinil impaired RV function. This may be related to changes in prostanoid receptor expression and reduced coronary flow reserve in the hypertrophic and failing right ventricle.

show abstract

Section: A C C E P T E Dmentioning

confidence: 66%

Inotropic Effects of Prostacyclins on the Right Ventricle Are Abolished in Isolated Rat Hearts With Right-Ventricular Hypertrophy and Failure

Holmboe

Andersen

Johnsen

et al. 2017

Journal of Cardiovascular Pharmacology

View full text Add to dashboard Cite

show abstract

“…However, there is rapid improvement in systolic performance during reperfusion at 1 minute because of increased coronary flow. During reactive hyperemia, LV function can be augmented to suprabaseline levels, a phenomenon known as the Gregg effect 28. Increased volume of the microvasculature following reperfusion causes stretch‐activated calcium channels to open.…”

Section: Discussionmentioning

confidence: 99%

Stunning and Right Ventricular Dysfunction Is Induced by Coronary Balloon Occlusion and Rapid Pacing in Humans: Insights From Right Ventricular Conductance Catheter Studies

Axell

Giblett

White

et al. 2017

JAHA

View full text Add to dashboard Cite

BackgroundWe sought to determine whether right ventricular stunning could be detected after supply (during coronary balloon occlusion [BO]) and supply/demand ischemia (induced by rapid pacing [RP] during transcatheter aortic valve replacement) in humans.Methods and ResultsTen subjects with single‐vessel right coronary artery disease undergoing percutaneous coronary intervention with normal ventricular function were studied in the BO group. Ten subjects undergoing transfemoral transcatheter aortic valve replacement were studied in the RP group. In both, a conductance catheter was placed into the right ventricle, and pressure volume loops were recorded at baseline and for intervals over 15 minutes after a low‐pressure BO for 1 minute or a cumulative duration of RP for up to 1 minute. Ischemia‐induced diastolic dysfunction was seen 1 minute after RP (end‐diastolic pressure [mm Hg]: 8.1±4.2 versus 12.1±4.1, P<0.001) and BO (end‐diastolic pressure [mm Hg]: 8.1±4.0 versus 8.7±4.0, P=0.03). Impairment of systolic and diastolic function after BO remained at 15‐minutes recovery (ejection fraction [%]: 55.7±9.0 versus 47.8±6.3, P<0.01; end‐diastolic pressure [mm Hg]: 8.1±4.0 versus 9.2±3.9, P<0.01). Persistent diastolic dysfunction was also evident in the RP group at 15‐minutes recovery (end‐diastolic pressure [mm Hg]: 8.1±4.1 versus 9.9±4.4, P=0.03) and there was also sustained impairment of load‐independent indices of systolic function at 15 minutes after RP (end‐systolic elastance and ventriculo‐arterial coupling [mm Hg/mL]: 1.25±0.31 versus 0.85±0.43, P<0.01).ConclusionsRP and right coronary artery balloon occlusion both cause ischemic right ventricular dysfunction with stunning observed later during the procedure. This may have intraoperative implications in patients without right ventricular functional reserve.

show abstract

“…22 Thus, in the clinical setting, if function is not seen to improve with dipyridamole, the presence of coronary stenosis could be inferred. The wide variability in the reported sensitivity of dipyridamole stress may in part be related to the criterion for abnormality-inducible regional systolic dysfunction versus lack of improvement in regional function-as well as the subjective nature of such calls.…”

Section: Discussionmentioning

confidence: 99%

Mechanism of Inducible Regional Dysfunction During Dipyridamole Stress

Bin

Pelberg

et al. 2002

Circulation

View full text Add to dashboard Cite

Background-We hypothesized that increased myocardial oxygen demand resulting from hypotension and reflex tachycardia unmasking a reduced endocardial myocardial blood flow (MBF) reserve is the mechanism of dipyridamole-induced regional dysfunction in chronic coronary artery disease. Methods and Results-Ameroid constrictors were placed around the proximal coronary arteries and their major branches in 15 dogs to create chronic coronary stenosis. Seven days later, radiolabeled microsphere-derived MBF and 2-dimensional echocardiography-derived percent wall thickening (%WT) were measured at rest and after 0.56 mg/kg dipyridamole. Dipyridamole caused an increase (mean, 21%) in the rate-pressure product secondary to reflex tachycardia resulting from mild systemic hypotension. %WT in myocardial segments with an endocardial MBF reserve (dipyridamole/resting MBF) of 1.5 to 2.5 (nϭ35) did not change after dipyridamole, whereas it decreased in segments with an endocardial MBF reserve of Ͻ1.5 (nϭ30) and increased in those with an endocardial MBF reserve of Ն2.5 (nϭ45) (PϽ0.05). Most (80%) segments with endocardial MBF reserve of Ͻ1.5 and 14% with an endocardial MBF reserve of 1.5 to 2.5 showed inducible dysfunction after dipyridamole, whereas none of the segments with an endocardial MBF reserve of Ն2.

show abstract

Effect of Coronary Perfusion Pressure or Coronary Flow on Oxygen Usage of the Myocardium

Cited by 254 publications

References 5 publications

Inotropic Effects of Prostacyclins on the Right Ventricle Are Abolished in Isolated Rat Hearts With Right-Ventricular Hypertrophy and Failure

Inotropic Effects of Prostacyclins on the Right Ventricle Are Abolished in Isolated Rat Hearts With Right-Ventricular Hypertrophy and Failure

Stunning and Right Ventricular Dysfunction Is Induced by Coronary Balloon Occlusion and Rapid Pacing in Humans: Insights From Right Ventricular Conductance Catheter Studies

Mechanism of Inducible Regional Dysfunction During Dipyridamole Stress

Contact Info

Product

Resources

About