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MYOCARDIAL STUNNING AND HIBERNATION. Dr Binjo J Vazhappilly . SR , Cardiology Dept. Calicut Medical College. Stunning. Definition : Prolonged and fully reversible dysfunction of the ischemic heart that persists despite the normalization of blood flow.

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myocardial stunning and hibernation

MYOCARDIAL STUNNING AND HIBERNATION

Dr Binjo J Vazhappilly.

SR , Cardiology Dept.

Calicut Medical College

stunning
Stunning
  • Definition :

Prolonged and fully reversible dysfunction of the ischemic heart that persists despite the normalization of blood flow.

slide3

1stdescribed by Heyndrickx et al in 1975 in conscious dogs undergoing brief coronary occlusions.

  • In that study regional contractile dysfunction lasted for 6 hrs following 5 min and > 24 hrs following 15 min of ischemia.
features of stunning
Features of stunning
  • Normal perfusion.
  • Depressed myocardial function.
  • Dissociation of usual relationship between subendocardial flow and function.
  • Reversible .
  • Function improves with inotropic agents.
slide7

Stunning occurs in a wide variety of settings that differ from one another in several aspects

  • At experimental level it can occur during

1. Single , completely reversible episode of

regional ischemia (< 20 min )

2. Multiple, completely reversible episodes of

regional ischemia

3. Partly reversible plus partly irreversible

ischemia in vivo ( > 20 min & < 3 hrs)

slide8

After global ischemia in vitro (isolated heart

preparations)

5. After global ischemia in vivo (cardioplegic arrest)

6. After exercise-induced ischemia

clinical relevance
Clinical Relevance
  • In the clinical setting stunning can occur

1. Brief period of total coronary occlusion:

pts with angina due to spasm

2. Global ischemia after cardiopulmonary bypass.

3. In combination : Subendocardium is infarcted and

overlying subepicardium reversibly injured in MI

4. Following exercise in presence of a flow limiting

stenosis

5. Ischemic bout that is induced by PCI

mechanisms of stunning
Mechanisms of Stunning
  • There is no unified view of pathogenesis of stunning
  • Most plausible hypotheses are

Oxyradical hypothesis : oxidant stress secondary

to the generation of ROS.

Calcium hypothesis : results from disturbance of

cellular calcium homeostasis.

oxyradical hypothesis
Oxyradical Hypothesis
  • Role of ROS in pathogenesis of stunning is proven
  • Its role in all settings of stunning is unclear
  • ROS-mediated injury responsible for stunning occurs in initial moments of reperfusion
  • Antioxidant therapies alleviate stunning whether begun before ischemia or just prior to reperfusion
  • But ineffective when begun after reperfusion
  • None of the antioxidant therapies completely prevented myocardial stunning
calcium hypothesis
Calcium hypothesis
  • Transient Ca2+ overload activates Ca2+-dependent proteases which degrades and induces covalent modifications of myofilaments.
  • It results in ↓ responsiveness to Ca2+, manifested by a decrease in maximal force of contraction.
slide15

Term hibernation is borrowed from zoology and implies an adaptive reduction of energy expenditure through reduced activity in situation of reduced energy supply.

  • In CAD myocardial hibernation refers to adaptive reduction of myocardial contractile function in response to reduction of myocardial blood flow.
slide16

Diamond et al. in 1978 1st used the word hibernation in ischemic dog myocardium.

  • Its importance was recognized by Rahimtoola in early 1980s.
mechanisms of hibernation
Mechanisms of hibernation
  • Smart heart hypothesis :

Myocardial metabolism and function are reduced to match concomitant reduction in coronary blood flow which prevents necrosis.

  • Repetitive stunning hypothesis:

Repetitive episodes of ischemia results in

sustained depression of contractile function.

slide18

Genomics of Survival

Maintained viability in hibernation suggests possibility of genomic adaptation.

Major survival genes (antiapoptotic, cytoprotective & growth-promoting genes) and their corresponding proteins are up regulated in hibernating myocardium.

histological features
Histological Features
  • Myolysis
  • Glycogen accumulation
  • Increased interstitial fibrosis
clinical relevance1
Clinical Relevance
  • 20 to 50 % of pts with chronic ischemic LV dysfunction have significant amount of viable hibernating myocardium.
  • They improve with revascularization.
assessment of myocardial viability
ASSESSMENT OF MYOCARDIAL VIABILITY
  • ECG : gives little information.
  • Dobutamine stress echocardiography.
  • SPECT with thallium-201 or technetium-99 m.
  • PET
  • MRI
slide26

ECG

No clear correlation between Q waves on ECG and presence of viability.

Pts with preserved QT dispersion are likely to have viable myocardium.

Pts with high QT dispersion have predominantly non-viable scar tissue.

dobutamine stress echocardiography
Dobutamine Stress Echocardiography
  • Hypokinetic or akinetic regions improving during low dose dobutamine infusion (5–10 µg/kg/min) is indicative of viable tissue.
  • At higher doses (upto 40 µg/kg/min plus atropine) wall motion may improve or diminish, reflecting inducible ischemia.
  • Biphasic response is highly predictive of recovery of function after revascularization.
slide30

Advantage of Echo based techniques

Safety , low cost , widespread availability of equipment .

  • Disadvantage

Spatial resolution is relatively low.

High interobserver variability.

Diagnostic accuracy is reduced in pts with poor

acoustic window.

spect
SPECT
  • Thallium-201

Early uptake is proportional to regional blood flow & delayed uptake indicates preserved Na+ K+ pump and an intact cell membrane.

Defects on initial images that improve later are viable.

slide32

Technetium 99

lipophilic molecules and their intracellular retention requires intact mitochondrial function.

Gating allow simultaneous assessment of myocardial perfusion & contractile function.

  • SPECT has higher sensitivity & lower specificity than techniques based on contractile reserve.
slide33
PET
  • Glucose utilization is evaluated with FDG and regional perfusion assessed with N13-ammonia, rubidium-82, or O15- labeled water.
  • A normal perfusion and FDG uptake or reduced perfusion with enhanced FDG uptake indicates viable myocardium.
  • Concordant reduction in FDG uptake and myocardial perfusion is indicative of scar tissue.
  • PET is regarded as gold standard for viability assessment.
magnetic resonance imaging
Magnetic resonance imaging
  • Three techniques are being used:

1.Resting MRI to measure end diastolic wall thickness.

2. Dobutamine MRI to evaluate contractile reserve

3. Contrast enhanced MRI to detect extent

and transmurality of scar tissue.

slide38

Resting MRI

End diastolic wall thickness < 6 mm represent

transmural scar.

  • Dobutamine MRI

Evaluate contractile reserve.

Increased resolution of MRI avoid subjective

variation of echo.

Has sensitivity of 89% & specificity of 94% to predict improvement after revascularization.

slide39

Contrast enhanced MRI

Allows precise detection of scar tissue.

Extent & transmurality of scar can be assessed.

Can detect subendocardial scar.

Similar to FDG PET in detecting scar.

impact of revascularization on lv function
Impact of Revascularization on LV Function
  • Studies shows LV ejection fraction improves significantly (ie ≥ 5%) after revascularization in 60% of patients (range 38% to 88%).
  • To predict 5% improvement in LVEF, at least 25% of LV should be viable using DSE and ≈38% using conventional nuclear medicine and PET.
slide42

In dyskinetic and akinetic segments, absence of scar or a transmural extension of scar of <25% have PPV of 88% and NPV 89% for functional recovery.

treatment and survival rates
Treatment and Survival Rates
  • Meta-analysis that pooled data of 3,088 pts from 24 studies demonstrated improved survival after revascularization in pts with hibernation.
  • Revascularization resulted in 79.6% reduction in mortality (16% vs 3.2%)
  • In absence of hibernation, no significant difference in mortality with revascularization (7.7% vs 6.2%).
summary
Summary
  • Stunning and hibernation are 2 causes for LV dysfunction.
  • Both conditions imply presence of viable myocardium and are reversible.
references
References
  • HURST’S THE HEART 13TH EDITION
  • BRAUNWALD’S HEART DISEASE NINTH EDITION
  • Medical and Cellular Implications of Stunning, Hibernation, and Preconditioning :Circulation. 1998;97:1848-1867
  • Stunning, Hibernation and Assessment of Myocardial Viability : Circulation.2008;117:103-114
  • Molecular and Cellular Mechanisms of Myocardial Stunning :PHYSIOLOGICAL REVIEWS Vol. 79, No. 2, April 1999
slide47

Hibernating Myocardium : PHYSIOLOGICAL REVIEWS Vol. 78, No. 4, October 1998

  • Clinical assessment of myocardial hibernation Heart 2005;91;111-117