Nonuniform transmural recovery of contractile function in stunned myocardium

1989 ◽  
Vol 257 (2) ◽  
pp. H375-H385 ◽  
Author(s):  
R. Bolli ◽  
B. S. Patel ◽  
C. J. Hartley ◽  
J. I. Thornby ◽  
M. O. Jeroudi ◽  
...  

With the use of an epicardial Doppler probe, systolic wall thickening was selectively measured in the inner, mid, and outer layers of the left ventricular (LV) wall in 16 conscious dogs undergoing a 15-min left anterior descending artery (LAD) occlusion followed by 7 days of reperfusion (REP). Under control conditions, percent thickening fraction (ThF) was significantly greater (P less than 0.01) in the inner layer [36.0 +/- 2.3% (mean +/- SE)] than in the mid (28.6 +/- 2.1%) or outer (21.3 +/- 2.2%) layers. During LAD occlusion, 11 dogs exhibited transmural dyskinesis (group 1), whereas 5 had transmural hypokinesis (group 2). In group 1, all layers exhibited comparable degrees of paradoxical systolic thinning during LAD occlusion. After REP, however, recovery was delayed in the inner compared with the mid and outer layers. At 2 h, ThF averaged 34.2 +/- 11.9% of base line in the endocardium vs. 61.7 +/- 16.2% in the midmyocardium and 51.0 +/- 12.3% in the epicardium (F = 4.29, P less than 0.002); similar differences were noted at 3 and 4 h. In the mid and outer layers, ThF returned to base-line values by 24 h, whereas in the inner layer it was still significantly depressed (P less than 0.05) at 24 h (77.3 +/- 5.1% of base line) and recovered by 48 h. The inner-to-outer ThF ratio was decreased (P less than 0.01) for 24 h after REP, indicating maldistribution of thickening in the "stunned" myocardium. In group 2, all layers exhibited hypokinesis during LAD occlusion. Again, recovery of function after REP was delayed in the endocardium compared with the other layers. This study demonstrates that after both severe ischemia resulting in dyskinesis and mild ischemia resulting in hypokinesis, REP is associated with slower recovery of function in the inner than in the outer layers. Thus myocardial "stunning" is a nonuniform phenomenon with maximal severity in the subendocardium.

2000 ◽  
Vol 279 (3) ◽  
pp. H1106-H1110 ◽  
Author(s):  
Rainer Schulz ◽  
Jochen Rose ◽  
Heiner Post ◽  
Andreas Skyschally ◽  
Gerd Heusch

Short-term hibernating myocardium is characterized by reduced contractile function during persistent moderate ischemia, the recovery of metabolic parameters, and the absence of necrosis. To study the afterload dependence of regional wall excursion in short-term hibernating myocardium, in 11 enflurane-anesthetized swine the left anterior descending coronary artery was cannulated and hypoperfused for 90 min to reduce anterior systolic wall thickening (WT, sonomicrometry) by 60%. Under control conditions, at 5 and 90 min ischemia the descending thoracic aorta was acutely constricted to increase left ventricular (LV) pressure by 30 mmHg. Under control conditions, increased LV pressure resulted in decreased WT [i.e., a negative slope of the relationship between WT and LV end-systolic pressure: −11.2 ± 4.2 (SD) μm/mmHg]. This slope was further significantly decreased at 5 min ischemia (−26.5 ± 8.8 μm/mmHg) but returned toward control values in short-term hibernating myocardium at 90 min ischemia (−17.2 ± 6.6 μm/mmHg). At 30 min reperfusion, the slope was once more significantly decreased (−27.8 ± 8.1 μm/mmHg). In conclusion, WT in short-term hibernating myocardium is less afterload dependent than in acutely ischemic and reperfused myocardium.


1996 ◽  
Vol 35 (05) ◽  
pp. 146-152 ◽  
Author(s):  
A. Kögler ◽  
H.-A. Schmitt ◽  
D. Emrich ◽  
H. Kreuzer ◽  
D. L. Munz ◽  
...  

SummaryThis prospective study assessed myocardial viability in 30 patients with coronary heart disease and persistent defects despite reinjection on TI-201 single-photon computed tomography (SPECT). In each patient, three observers graded TI-201 uptake in 7 left ventricular wall segments. Gradient-echo magnetic resonance imaging in the region of the persistent defect generated 12 to 16 short axis views representing a cardiac cycle. A total of 120 segments were analyzed. Mean end-diastolic wall thickness and systolic wall thickening (± SD) was 11.5 ± 2.7 mm and 5.8 ± 3.9 mm in 48 segments with normal TI-201 uptake, 10.1 ± 3.4 mm and 3.7 ± 3.1 mm in 31 with reversible lesions, 11.3 ± 2.8 mm and 3.3 ± 1.9 mm in 10 with mild persistent defects, 9.2 ± 2.9 mm and 3.2 ±2.2 mm in 15 with moderate persistent defects, 5.8 ± 1.7 mm and 1.3 ± 1.4 mm in 16 with severe persistent defects, respectively. Significant differences in mean end-diastolic wall thickness (p <0.0005) and systolic wall thickening (p <0.005) were found only between segments with severe persistent defects and all other groups, but not among the other groups. On follow-up in 11 patients after revascularization, 6 segments with mild-to-moderate persistent defects showed improvement in mean systolic wall thickening that was not seen in 6 other segments with severe persistent defects. These data indicate that most myocardial segments with mild and moderate persistent TI-201 defects after reinjection still contain viable tissue. Segments with severe persistent defects, however, represent predominantly nonviable myocardium without contractile function.


1996 ◽  
Vol 271 (4) ◽  
pp. H1384-H1393 ◽  
Author(s):  
Y. Ishibashi ◽  
J. Zhang ◽  
D. J. Duncker ◽  
C. Klassen ◽  
T. Pavek ◽  
...  

This study was performed to test the hypothesis that increases in myocardial oxygen consumption (MVo2) and myocardial contractile function during exercise are flow limited. Studies were performed in 15 chronically instrumented normal dogs. MVo2 and regional percent systolic wall thickening were measured during control conditions and during maximal vasodilation produced by infusion of adenosine (20-75 micrograms.kg-1.min-1) or adenosine combined with nitroglycerin (0.4 micrograms.kg-1.min-1; TNG) into the left anterior descending coronary artery during a three-stage graded treadmill exercise protocol. Adenosine and adenosine plus TNG significantly increased coronary blood flow by 298 +/- 26 and 306 +/- 24%, respectively, at rest and by 134 +/- 7 and 145 +/- 9%, respectively, during the heaviest level of exercise (each P < 0.01). Adenosine and adenosine plus TNG increased MVo2 at rest, but this was associated with a parallel increase in heart rate, so that MVo2 per beat was not significantly changed. Systolic wall thickening was also not changed by hyperperfusion during resting conditions. However, MVo2 per beat was increased by 12 +/- 4% with adenosine and by 13 +/- 5% with adenosine plus TNG during moderate exercise and by 23 +/- 5% with adenosine and by 27 +/- 4% with adenosine plus TNG during the heaviest level of exercise (each P < 0.05). Systolic thickening of the full left ventricular wall did not change during hyperperfusion, but thickening in the subepicardial layer was increased by 14 +/- 3% with adenosine and 18 +/- 3% with adenosine plus TNG during the heaviest level of exercise (each P < 0.05). There was no difference in wall thickening between adenosine and adenosine plus TNG. These findings imply that the increases in MVo2 which occur during exercise are limited by coronary blood flow.


1988 ◽  
Vol 254 (1) ◽  
pp. H102-H114 ◽  
Author(s):  
R. Bolli ◽  
W. X. Zhu ◽  
J. I. Thornby ◽  
P. G. O'Neill ◽  
R. Roberts

The postischemic recovery of contractile function [measured as systolic wall thickening (WT)] was analyzed in 21 conscious dogs undergoing a 15-min coronary occlusion followed by 7 days of reperfusion (REP). Average WT was still depressed 24 h after REP (85% of base line, P less than 0.001) and returned to base line by 48 h. Analysis of individual dogs, however, revealed marked variability, whereby some recovered completely by 1 h of REP and others required up to 48 h. WT recovered completely within 30 min in dogs with collateral blood flow (CBF) greater than 50% of nonischemic zone flow (NZF) but was still impaired at 24 h (P less than 0.05) in those with CBF less than 25% of NZF. There was a close, curvilinear relation between WT during the first 4 h of REP and transmural CBF, which was described best by an exponential equation WT (as percent of base line) = P0-P1e-P2.CBF(as % of NZF) (r2 = 0.92 at 1 h, 0.76 at 2 h, 0.71 at 3 h, and 0.72 at 4 h), where P0, P1, and P2 are regression coefficients. Importantly, the slope of the regression line was very steep at low CBF, implying that even small differences in CBF produce large differences in postischemic function. Heart rate, systolic pressure, and rate-pressure product during ischemia were also related to WT after REP, but when the effect of CBF was taken into account, the influence of these variables became insignificant. The size of the occluded vascular bed did not correlate with postischemic WT. The presence of hypokinesis or akinesis during ischemia was associated with rapid recovery after REP, but there was no relation between ischemic and postischemic dysfunction when dyskinesis was present during occlusion. Thus, on the average, regional function remains depressed for 24 h after a 15-min ischemic episode, but there is considerable individual variability. This variable rate of recovery is determined primarily by the severity of blood flow reduction during ischemia. Systemic hemodynamics may modulate recovery of function indirectly via their effects on ischemic blood flow.


2001 ◽  
Vol 281 (4) ◽  
pp. H1575-H1582 ◽  
Author(s):  
J. David Symons ◽  
Saul Schaefer

Myocardial ischemia and reperfusion cause myocyte and vascular dysfunction, frequently termed “stunning.” We hypothesized that inhibiting the Na+/H+ exchanger subtype 1 isoform (NHE1) during ischemia and reperfusion limits myocardial and coronary microvascular stunning. Anesthetized rats completed 2 × 10-min coronary artery occlusions separated by 5-min of reperfusion, followed by 15 or 60 min of reperfusion. Vehicle (saline) or the NHE1 inhibitor cariporide (HOE-642) was administered 15 min before ischemia and was continued throughout each protocol. After reperfusion, hearts were excised, and the reactivity of resistance arteries (internal diameter, ∼120 μm) was assessed. The first derivative of left ventricular (LV) pressure, LV developed pressure, and LV systolic wall thickening were depressed ( P < 0.05) similarly in vehicle- and cariporide-treated rats during ischemia and after 15 or 60 min of reperfusion compared with sham-operated animals that were not exposed to ischemia (i.e., controls). In vessels obtained after 15 min of reperfusion, the maximal response to acetylcholine-induced relaxation (10−8–10−4 M) was blunted ( P < 0.05) in vessels from vehicle- (∼35%) and cariporide-treated rats (∼55%) compared with controls (∼85%). However, the percent relaxation to acetylcholine was greater ( P < 0.05) in cariporide-treated rats compared with vehicle-treated rats. Maximal contractile responses to endothelin-1 (10−11–10−7 M) were increased ( P < 0.05) similarly in vehicle- and cariporide-treated rats compared with controls. Relaxation to sodium nitroprusside (10−4 M) was not different among groups. Results were similar in vessels obtained from animals after 60 min of reperfusion. These findings suggest that NHE1inhibition before coronary occlusion lessens ischemia-induced microvascular dysfunction for 15–60 min after reperfusion but does not alter myocardial contractile function in the area at risk.


1987 ◽  
Vol 253 (6) ◽  
pp. H1372-H1380 ◽  
Author(s):  
R. Bolli ◽  
B. S. Patel ◽  
W. X. Zhu ◽  
P. G. O'Neill ◽  
C. J. Hartley ◽  
...  

Recent evidence suggests that postischemic myocardial dysfunction ("stunning") may be mediated by oxygen free radicals, but the mechanism by which they produce myocellular damage remains unknown. Since iron catalyzes formation of hydroxyl radicals (HO.) as well as HO.-initiated lipid peroxidation, we explored the potential role of this metal in the pathogenesis of myocardial stunning. Open-chest dogs undergoing a 15-min occlusion of the left anterior descending coronary artery (LAD) followed by 4 h of reperfusion (REP) received the iron chelator desferrioxamine intravenously (10 mg/kg over 45 min beginning 30 min before occlusion, then 1.7 mg.kg-1.h-1 throughout REP, n = 19) or normal saline (n = 17). Regional myocardial function was assessed by measuring systolic wall thickening with an epicardial Doppler probe. The two groups exhibited comparable systolic thickening under base-line conditions and similar degrees of dyskinesis during ischemia. After REP, however, recovery of contractile function (expressed as percent systolic thickening) as considerably greater in desferrioxamine-treated compared with control dogs: 5 +/- 3 (mean +/- SE) vs. -3 +/- 2% (P less than 0.05) at 1 h, 6 +/- 3 vs. -2 +/- 3% (P less than 0.05) at 2 h, 5 +/- 3 vs. -6 +/- 2% (P less than 0.005) at 3 h, and 6 +/- 3 vs. -6 +/- 2% (P less than 0.002) at 4 h. These differences could not be ascribed to hemodynamic factors. The results suggest that iron-catalyzed reactions (possibly HO. generation) play a significant role in myocardial stunning after a brief episode of reversible regional ischemia.


2018 ◽  
Vol 129 (3) ◽  
pp. 576-579 ◽  
Author(s):  
David C. Warltier

Abstract Recovery of Contractile Function of Stunned Myocardium in Chronically Instrumented Dogs Is Enhanced by Halothane or Isoflurane. By Warltier DC, al-Wathiqui MH, Kampine JP, and Schmeling WT. Anesthesiology 1988; 69:552–65. Reprinted with permission. Following brief periods (5–15 min) of total coronary artery occlusion and subsequent reperfusion, despite an absence of tissue necrosis, a decrement in contractile function of the postischemic myocardium may nevertheless be present for prolonged periods. This has been termed “stunned” myocardium to differentiate the condition from ischemia or infarction. Because the influence of volatile anesthetics on the recovery of postischemic, reperfused myocardium has yet to be studied, the purpose of this investigation was to compare the effects of halothane and isoflurane on systemic and regional hemodynamics following a brief coronary artery occlusion and reperfusion. Nine groups comprising 79 experiments were completed in 42 chronically instrumented dogs. In awake, unsedated dogs a 15-min coronary artery occlusion resulted in paradoxical systolic lengthening in the ischemic zone. Following reperfusion active systolic shortening slowly returned toward control levels but remained approximately 50% depressed from control at 5 h. In contrast, dogs anesthetized with halothane or isoflurane (2% inspired concentration) demonstrated complete recovery of function 3–5 h following reperfusion. Because the anesthetics directly depressed contractile function, additional experiments were conducted in which a 15-minute coronary artery occlusion was produced during volatile anesthesia; however, each animal was allowed to emerge from the anesthetized state at the onset of reperfusion. Similar results were obtained in these experiments, demonstrating total recovery of contractile function within 3–5 h following reperfusion. Thus, despite comparable degrees of contractile dysfunction during coronary artery occlusion in awake and anesthetized dogs, the present results demonstrate that halothane and isoflurane produce marked improvement in the recovery of segment function following a transient ischemic episode. Therefore, volatile anesthetics may attenuate postischemic left ventricular dysfunction occurring intraoperatively and enhance recovery of regional wall motion abnormalities during reperfusion.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Matevž Jan ◽  
David Žižek ◽  
Tine Prolič Kalinšek ◽  
Dimitrij Kuhelj ◽  
Primož Trunk ◽  
...  

Abstract Background Conventional fluoroscopy guided catheter ablation (CA) is an established treatment option for ventricular arrhythmias (VAs). However, with the complex nature of most procedures, patients and staff bare an increased radiation exposure. Near-zero or zero-fluoroscopy CA is an alternative method which could substantially reduce or even eliminate the radiation dose. Our aim was to analyse procedural outcomes with fluoroscopy minimising approach for treatment of VAs in patients with structurally normal hearts (SNH) and structural heart disease (SHD). Methods Fifty-two (age 53.4 ± 17.8 years, 38 male, 14 female) consecutive patients who underwent CA of VAs in our institution between May 2018 and December 2019 were included. Procedures were performed primarily with the aid of the three-dimensional electro-anatomical mapping system and intra-cardiac echocardiography. Fluoroscopy was considered only in left ventricular (LV) summit mapping for coronary angiography and when epicardial approach was planned. Acute and long-term procedural outcomes were analysed. Results Sixty CA procedures were performed. Twenty-five patients had SHD-related VAs (Group 1) and 27 patients had SNH (Group 2). While Group 1 had significantly higher total procedural time (256.9 ± 71.7 vs 123.6 ± 42.2 min; p < 0.001) compared to Group 2, overall procedural success rate [77.4% (24/31) vs 89.7% (26/29); p = 0.20)] and recurrence rate after the first procedure [8/25, (32%) vs 8/27, (29.6%); p = 0.85] were similar in both groups. Fluoroscopy was used in 3 procedures in Group 1 where epicardial approach was needed and in 4 procedures in Group 2 where LV summit VAs were ablated. Overall procedure-related major complication rate was 5%. Conclusions Fluoroscopy minimising approach for CA of VAs is feasible and safe in patients with SHD and SNH. Fluoroscopy could not be completely abolished in VAs with epicardial and LV summit substrate location.


Author(s):  
Malgorzata Zalewska-Adamiec ◽  
Jolanta Malyszko ◽  
Ewelina Grodzka ◽  
Lukasz Kuzma ◽  
Slawomir Dobrzycki ◽  
...  

Abstract Background Myocardial infarction with nonobstructive coronary arteries (MINOCA) constitutes about 10% of the cases of acute coronary syndromes (ACS). It is a working diagnosis and requires further diagnostics to determine the cause of ACS. Methods In this study, 178 patients were initially diagnosed with MINOCA over a period of 3 years at the Department of Invasive Cardiology of the University Clinical Hospital in Białystok. The value of estimated glomerular filtration rate (eGFR) was calculated for all patients. The patients were divided into 2 groups depending on the value of eGFR: group 1—53 patients with impaired kidney function (eGFR < 60 mL/min/1.73 m2; 29.8%) and group 2—125 patients with normal kidney function (eGFR ≥ 60 mL/min/1.73 m2; 70.2%). Results In group 1, the mean age of patients was significantly higher than that of group 2 patients (77.40 vs 59.27; p < 0.0001). Group had more women than group 2 (73.58% vs 49.60%; p = 0.003). Group 1 patients had higher incidence rate of arterial hypertension (92.45% vs 60.80%; p < 0.0001) and diabetes (32.08% vs 9.60%; p = 0.0002) and smoked cigarettes (22.64% vs 40.80%; p = 0.020). Group 1 patients had higher incidence rate of pulmonary edema, cardiogenic shock, sudden cardiac arrest (13.21% vs 4.00%; p = 0.025), and pneumonia (22.64% vs 6.40%; p = 0.001). After the 37-month observation, the mortality rate of the patients with MINOCA was 16.85%. Among group two patients, more of them became deceased during hospitalization (7.55% vs 0.80%; p = 0.012), followed by after 1 year (26.42% vs 7.20%; p = 0.0004) and after 3 years (33.96% vs 9.6%; p < 0.0001). Multivariate analysis revealed that the factors increasing the risk of death in MINOCA are as follows: older age, low eGFR, higher creatinine concentration, low left ventricular ejection fraction, and ST elevation in ECG. Conclusion Impaired kidney function is diagnosed in every third patient with MINOCA. Early and late prognosis of patents with MINOCA and renal dysfunction is poor, and their 3-year mortality is comparable to patients with myocardial infarction with significant stenosis of the coronary arteries and impaired kidney function.


2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Cristina Chimenti ◽  
Romina Verardo ◽  
Andrea Frustaci

Abstract Aim To investigate the contribution of unaffected cardiomyocytes in Fabry disease cardiomyopathy. Findings Left ventricular (LV) endomyocardial biopsies from twenty-four females (mean age 53 ± 11 ys) with Fabry disease cardiomyopathy were studied. Diagnosis of FD was based on the presence of pathogenic GLA mutation, Patients were divided in four groups according with LV maximal wall thickness (MWT): group 1 MWT ≤ 10.5 mm, group 2 MWT 10.5–15 mm, group 3 MWT 16–20 mm, group 4 MWT > 20 mm. At histology mosaic of affected and unaffected cardiomyocytes was documented. Unaffected myocytes’ size ranged from normal to severe hypertrophy. Hypertrophy of unaffected cardiomyocytes correlated with severity of MWT (p < 0.0001, Sperman r 0,95). Hypertrophy of unaffected myocytes appear to concur to progression and severity of FDCM. It is likely a paracrine role from neighboring affected myocytes.


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