Additional value of systolic wall thickening in myocardial stunning evaluated by stress-rest gated perfusion SPECT

2017 ◽  
Vol 26 (3) ◽  
pp. 833-840 ◽  
Author(s):  
Alberto Bestetti ◽  
Besart Cuko ◽  
Adriano Decarli ◽  
Alessio Galli ◽  
Federico Lombardi
Keyword(s):  
Myocardial Stunning ◽  
Wall Thickening ◽  
Gated Perfusion Spect ◽  
Perfusion Spect ◽  
Additional Value ◽  
Systolic Wall Thickening

Differences in myocardial stunning following coronary artery occlusion in conscious dogs, pigs, and baboons

1996 ◽  
Vol 270 (4) ◽  
pp. H1312-H1322 ◽  
Author(s):  
Y. T. Shen ◽  
S. F. Vatner
Keyword(s):  
Blood Flow ◽  
Coronary Artery ◽  
Myocardial Stunning ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Conscious Dogs ◽  
Wall Thickening ◽  
Systolic Wall Thickening

To determine whether myocardial stunning differs among dogs, pigs, and baboons and is reproducible within species, we examined the effects of 10-min coronary artery (CA) occlusion (CAO) on 9 conscious dogs, 12 minipigs, and 6 baboons. During 10-min CAO, systolic wall thickening in the ischemic zone fell similarly in dogs (-108 +/- 5.6%), pigs (-102 +/- 1.8%), and baboons (-107 +/- 5.7%), but blood flow fell more (P < 0.05) in the subepicardium in pigs (0.07 +/- 0.01 ml.min-1.g-1) and baboons (0.07 +/- 0.02 ml.min-1.g-1) than in dogs (0.18 +/- 0.03 ml.min-1.g-1). At 1 h after CA reperfusion (CAR), wall thickening was reduced more (P < 0.05) in dogs (-40 +/- 4.2%) than in pigs (-22 +/- 2.1%) and baboons (-4 +/- 2.4%). In five dogs and five pigs, three separate 10-min CAO, each 2 days apart, were also examined. In dogs, reductions in wall thickening after CAR were significantly less following the second (-26 +/- 4.2%) or third (-30 +/- 3.2%) CAO, compared with the first CAO (-47 +/- 4.9%). In contrast, repetitive CAO did not induce differences in recovery of wall thickening in pigs. These results indicate that myocardial stunning is less severe in conscious pigs and baboons, compared with conscious dogs, despite more intense transmural ischemia. The dogs demonstrated a "preconditioning-like effect" with serial brief CAO, which was not exhibited in pigs.

12.6 Demonstration of myocardial stunning after dipyridamole stress test with gated perfusion SPECT

2001 ◽  
Vol 8 (1) ◽  
pp. S77-S77
Author(s):  
M BERETTA ◽  
A RENER ◽  
I VIDAL ◽  
O ALONSO ◽  
M NUNEZ ◽  
...  
Keyword(s):  
Myocardial Stunning ◽  
Stress Test ◽  
Gated Perfusion Spect ◽  
Perfusion Spect ◽  
Dipyridamole Stress

Differential role of KATP channels in late preconditioning against myocardial stunning and infarction in rabbits

2000 ◽  
Vol 279 (5) ◽  
pp. H2350-H2359 ◽  
Author(s):  
Hitoshi Takano ◽  
Xian-Liang Tang ◽  
Roberto Bolli
Keyword(s):  
Infarct Size ◽  
Myocardial Stunning ◽  
Late Phase ◽  
Katp Channels ◽  
Wall Thickening ◽  
Late Preconditioning ◽  
End Effectors ◽  
Sparing Effect ◽  
Systolic Wall Thickening

The role of ATP-sensitive potassium (KATP) channels in the late phase of ischemic preconditioning (PC) remains unclear. Furthermore, it is unknown whether KATP channels serve as end effectors both for late PC against infarction and against stunning. Thus, in phase I of this study, conscious rabbits underwent a 30-min coronary occlusion (O) followed by 72 h of reperfusion (R) with or without ischemic PC (6 4-min O/4-min R cycles) 24 h earlier. Late PC reduced infarct size ∼46% versus controls. The KATPchannel blocker 5-hydroxydecanoic acid (5-HD), given 5 min before the 30-min O, abrogated the infarct-sparing effect of late PC but did not alter infarct size in non-PC rabbits. In phase II, rabbits underwent six 4-min O/4-min R cycles for 3 consecutive days ( days 1, 2, and 3). In controls, the total deficit of systolic wall thickening (WTh) after the sixth reperfusion was reduced by 46% on day 2 and 54% on day 3compared with day 1, indicating a late PC effect against myocardial stunning. Neither 5-HD nor glibenclamide, given on day 2, abrogated late PC. The KATP channel opener diazoxide, given on day 1, attenuated stunning, and this effect was completely blocked by 5-HD. Thus the same dose of 5-HD that blocked the antistunning effect of diazoxide failed to block the antistunning effects of late PC. Furthermore, when diazoxide was administered in PC rabbits on day 2, myocardial stunning was further attenuated, indicating that diazoxide and late PC have additive anti-stunning effects. We conclude that KATP channels play an essential role in late PC against infarction but not in late PC against stunning, revealing an important pathogenetic difference between these two forms of cardioprotection.

Reduction in postsystolic wall thickening during late preconditioning

2007 ◽  
Vol 292 (1) ◽  
pp. H158-H164 ◽  
Author(s):  
Xavier Monnet ◽  
Laurence Lucats ◽  
Patrice Colin ◽  
Geneviève Derumeaux ◽  
Jean-Luc Dubois-Rande ◽  
...  
Keyword(s):  
Myocardial Stunning ◽  
Time Course ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Wall Thickening ◽  
Circumflex Artery ◽  
Late Preconditioning ◽  
Rapid Ventricular Pacing ◽  
Systolic Wall Thickening ◽  
Similar Decrease

Brief coronary artery occlusion (CAO) and reperfusion induce myocardial stunning and late preconditioning. Postsystolic wall thickening (PSWT) also develops with CAO and reperfusion. However, the time course of PSWT during stunning and the regional function pattern of the preconditioned myocardium remain unknown. The goal of this study was to investigate the evolution of PSWT during myocardial stunning and its modifications during late preconditioning. Dogs were chronically instrumented to measure (sonomicrometry) systolic wall thickening (SWT), PSWT, total wall thickening (TWT = SWT + PSWT), and maximal rate of thickening (dWT/d tmax). Two 10-min CAO (circumflex artery) were performed 24 h apart ( day 0 and day 1, n = 7). At day 0, CAO decreased SWT and increased PSWT. During the first hours of the subsequent stunning, evolution of PSWT was symmetrical to that of SWT. At day 1, baseline SWT was similar to day 0, but PSWT was reduced (−66%), while dWT/d tmax and SWT/TWT ratio increased (+48 and +14%, respectively). After CAO at day 1, stunning was reduced, indicating late preconditioning. Simultaneously vs. day 0, PSWT was significantly reduced, and dWT/d tmax as well as SWT/TWT ratio were increased, i.e., a greater part of TWT was devoted to ejection. Similar decrease in PSWT was observed with a nonischemic preconditioning stimulus (rapid ventricular pacing, n = 4). In conclusion, a major contractile adaptation occurs during late preconditioning, i.e., the rate of wall thickening is enhanced and PWST is almost abolished. These phenotype adaptations represent potential approaches for characterizing stunning and late preconditioning with repetitive ischemia in humans.

Effects of adenosine and acadesine on interstitial nucleosides and myocardial stunning in the pig

1999 ◽  
Vol 77 (4) ◽  
pp. 259-267 ◽  
Author(s):  
Robert D Lasley ◽  
Mohinder PS Randhawa, Jr. ◽  
Julia O Hegge ◽  
Robert M Mentzer, Jr.
Keyword(s):  
Myocardial Stunning ◽  
Interstitial Fluid ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Ischemic Myocardium ◽  
Wall Thickening ◽  
Control Value ◽  
Cardioprotective Effects ◽  
Systolic Wall Thickening ◽  
Regional Ventricular Function

5-Amino-4-imidazolecarboxamide riboside (AICAr) or acadesine has been proposed to exert cardioprotection by enhancing adenosine production in ischemic myocardium. However, there are conflicting reports on acadesine's effects in ischemic myocardium and few studies in which myocardial adenosine levels have been measured. The purpose of this study was to determine whether acadesine increases interstitial fluid adenosine levels and attenuates myocardial stunning or potentiates the effects of adenosine in the intact pig. In pentobarbital-anesthetized pigs, myocardial stunning was induced by 10 min left anterior descending coronary artery occlusion and 90 min reperfusion. Regional ventricular function was assessed by measuring systolic wall thickening, and interstitial nucleosides were estimated by cardiac microdialysis. Control hearts were compared with hearts treated with acadesine, adenosine, and adenosine plus acadesine. Adenosine pretreatment (100 µg·kg-1·min-1, intracoronary) immediately prior to ischemia increased interstitial adenosine levels 9-fold and improved postischemic functional recovery from a control value of 17.6 ± 4.1% to 43.6 ± 3.4% of preischemic systolic wall thickening. In contrast, acadesine (20 mg/kg i.v. bolus 10 min prior to ischemia + 0.5 mg·kg-1·min-1, i.v. infusion through 60 min reperfusion) had no effect on interstitial fluid adenosine levels or the recovery of regional function (21.5 ± 5.9% recovery), nor were the functional effects of adenosine potentiated by acadesine. These findings indicate that acadesine does not enhance myocardial adenosine levels, attenuate myocardial stunning, or potentiate the cardioprotective effects of adenosine in the pig.Key words: adenosine, acadesine, interstitial fluid, microdialysis, myocardial stunning.

Characteristics of regional myocardial stunning after exercise in dogs with chronic coronary stenosis

1989 ◽  
Vol 257 (1) ◽  
pp. H113-H119 ◽  
Author(s):  
E. Thaulow ◽  
B. D. Guth ◽  
G. Heusch ◽  
E. Gilpin ◽  
R. Schulz ◽  
...  
Keyword(s):  
Blood Flow ◽  
Coronary Stenosis ◽  
Myocardial Stunning ◽  
Wall Thickening ◽  
Regional Ischemia ◽  
Ischemic Region ◽  
Regional Dysfunction ◽  
Exercise Induced ◽  
Systolic Wall Thickening ◽  
Chronically Instrumented Dogs

Persistent impairment of regional contraction of the left ventricle after restoration of blood flow following transient coronary occlusion has been termed “stunning,” and reversible regional dysfunction has also been observed during recovery from exercise-induced regional ischemia. To determine whether limitation of subendocardial blood flow after exercise is a determinant of such dysfunction in the presence of chronic coronary stenosis, nine conscious chronically instrumented dogs having an Ameroid constrictor were studied before, during, and after treadmill runs that induced regional ischemia. During exercise, systolic wall thickening (%WTh, sonomicrometers) in the ischemic region decreased from a normal level of 22.1 +/- 9.1% at rest to 8.8 +/- 5.2% (+/- SD, P less than 0.01), whereas subendocardial blood flow (microspheres) in the ischemic region decreased from 0.75 +/- 0.25 to 0.45 +/- 0.27 ml.min-1.g-1 (P less than 0.05). %WTh in the ischemic region gradually improved after exercise but remained depressed (75% of control) at 30 min after the run (P less than 0.05). Postexercise dysfunction was not related to simultaneous regional hypoperfusion, since at 5 and 10 min after running there was a tendency toward subendocardial hyperemia (control 0.75 vs. 1.33 and 1.30 ml.min-1.g-1, NS) with a return to control by 30 min. Thus persistent regional dysfunction after exercise-induced regional ischemia in the conscious dog is not due to sustained subendocardial ischemia in the presence of chronic coronary stenosis and represents an example of myocardial stunning.

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