Mechanically supported PCI for ischemic cardiomyopathy reawakening of hibernating myocardium

2020 ◽  
Vol 96 (4) ◽  
pp. 771-772
Author(s):  
James A. Goldstein ◽  
Simon R. Dixon
Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Ken Matsuoka ◽  
Masami Nishino ◽  
Daisuke Nakamura ◽  
Takahiro Yoshimura ◽  
Yasuharu Ri ◽  
...  

Backgrounds: In medically treated patients with ischemic cardiomyopathy, myocardial viability is associated with a worse prognosis than scar. Hibernating myocardium (chronic regional dysfunction with reduced resting flow) assessed with nuclear imaging is a major risk factor for cardiac death when left ventricular function is depressed. End-diastolic wall thickness (EDWT) is an important and easy marker of myocardial viability in patients with suspected hibernation, as well as Tl-201 scintigraphy. Thus, in this study, we assessed whether hibernating myocardium evaluated by echocardiography could identify patients with ischemic cardiomyopathy who are at high risk for sudden cardiac death (SCD) and mortality. Methods: Patients with ischemic cardiomyopathy who showed low-grade cardiac function (ejection fraction (EF) < or =50%) and had no plans for coronary revascularization were enrolled. All patients underwent coronary angiography and echocardiography. Hibernating myocardium was defined as the area with major epicardial artery stenosis > or =75%, wall motion abnormality, and EDWT >6mm. The onset of SCD or mortality was determined by outpatient or telephone follow-up. Results: The study patients consisted of 60 consecutive patients (47 men, EF: 35 ± 8%, follow-up duration: 38 ± 16 months). Results were shown in a figure . Hibernating myocardium significantly increased the risk of SCD and mortality. Conclusion: Hibernating myocardium evaluated by echocardiography can predict SCD and mortality in medically treated patients with ischemic cardiomyopathy. Figure Kalpan-Meler Estimates of the Time to SCD or Mortality


2014 ◽  
Vol 2014 ◽  
pp. 1-15 ◽  
Author(s):  
Georg D. Duerr ◽  
Bettina Mesenholl ◽  
Jan C. Heinemann ◽  
Martin Zoerlein ◽  
Peter Huebener ◽  
...  

Repetitive brief ischemia and reperfusion (I/R) is associated with ventricular dysfunction in pathogenesis of murine ischemic cardiomyopathy and human hibernating myocardium. We investigated the role of matricellular protein osteopontin-1 (OPN) in murine model of repetitive I/R. One 15-min LAD-occlusion followed by reperfusion was performed daily over 3, 5, and 7 consecutive days in C57/Bl6 wildtype- (WT-) and OPN−/−-mice (n=8/group). After echocardiography hearts were processed for histological and mRNA-studies. Cardiac fibroblasts were isolated, cultured, and stimulated with TGF-β1. WT-mice showed an early, strong, and cardiomyocyte-specific osteopontin-expression leading to interstitial macrophage infiltration and consecutive fibrosis after 7 days I/R in absence of myocardial infarction. In contrast, OPN−/−-mice showed small, nontransmural infarctions after 3 days I/R associated with significantly worse ventricular dysfunction. OPN−/−-mice had different expression of myocardial contractile elements and antioxidative mediators and a lower expression of chemokines during I/R. OPN−/−-mice showed predominant collagen deposition in macrophage-rich small infarctions. We found lower induction of tenascin-C, MMP-9, MMP-12, and TIMP-1, whereas MMP-13-expression was higher in OPN−/−-mice. Cultured OPN−/−-myofibroblasts confirmed these findings. In conclusion, osteopontin seems to modulate expression of contractile elements, antioxidative mediators, and inflammatory response and subsequently remodel in order to protect cardiomyocytes in murine ischemic cardiomyopathy.


Author(s):  
Vasken Dilsizian ◽  
Ines Valenta ◽  
Thomas H. Schindler

Heart failure may be a consequence of ischemic or non-ischemic cardiomyopathy. Etiologies for LV systolic dysfunction in ischemic cardiomyopathy include; 1) transmural scar, 2) nontransmural scar, 3) repetitive myocardial stunning, 4) hibernating myocardium, and 5) remodeled myocardium. The LV remodeling process, which is activated by the renin-angiotensin system (RAS), stimulates toxic catecholamine actions and matrix metalloproteinases, resulting in maladaptive cellular and molecular alterations5, with a final pathway to interstitial fibrosis. These responses to LV dysfunction and interstitial fibrosis lead to progressive worsening of LV function. Established treatment options for ischemic cardiomyopathy include medical therapy, revascularization, and cardiac transplantation. While there has been continuous progress in the medical treatment of heart failure with beta-blockers, angiotensin-converting enzyme (ACE) inhibition, angiotensin II type 1 receptor (AT1R) blockers, and aldosterone to beneficially influence morbidity and mortality, the 5-years mortality rate for heart failure patients remains as high as 50%. Revascularization procedures include percutaneous transluminal coronary artery interventions (PCI) including angioplasty and endovascular stent placement and coronary artery bypass grafting (CABG). Whereas patents with heart failure due to non-coronary etiologies may best benefit from medical therapy or heart transplantation, coronary revascularization has the potential to improve ventricular function, symptoms, and long term survival, in patients with heart failure symptoms due to CAD and ischemic cardiomyopathy.


Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Andrew J Luisi ◽  
Brendan M Heavey ◽  
John M Canty ◽  
Robert A deKemp ◽  
James A Fallavollita

Background: Viable dysfunctional myocardium can be classified as chronically stunned (normal resting perfusion) or hibernating (reduced resting flow). While 13 N-ammonia (NH 3 ) retention (late uptake) is typically used to estimate perfusion, the frequency and extent of hibernating myocardium (HM) may differ when quantification of dynamically-acquired absolute myocardial blood flow (MBF) is performed. Methods: Patients with stable ischemic cardiomyopathy (n = 25, EF 32 ± 2%, NYHA Class 2.1 ± 0.7) who were candidates for an ICD for the primary prevention of sudden death underwent imaging with NH 3 and insulin-clamp 18 F-2-deoxyglucose (FDG). Segmental perfusion (17 segment LV model, % peak segment) was assessed by both retention (20 minute summed image) and absolute MBF using a 3-compartment model (ml/min/g). Normal segments were defined as perfusion ≤ 80% peak segment. Segments with <50% peak segment FDG uptake were defined as scar. The remaining segments were considered HM if FDG/perfusion ratio was ≥ 1.2. Results: Of the 425 total segments, only 15 (3.5%) were considered HM when NH 3 retention was used to assess perfusion. In contrast, the number of HM segments increased markedly with quantification of absolute MBF (159 or 37%, p<0.001 vs. retention), with a commensurate reduction in the number of normally-perfused segments. Conclusions: The estimation of perfusion with NH 3 retention significantly overestimates MBF (Figure ) and hence underestimates the frequency and extent of HM. While the differentiation of chronically stunned from HM may not influence the decision for revascularization, the distinction may be important if HM is an independent risk factor for sudden death.


2011 ◽  
Vol 301 (2) ◽  
pp. H530-H537 ◽  
Author(s):  
Kiyotake Ishikawa ◽  
Dennis Ladage ◽  
Yoshiaki Takewa ◽  
Elisa Yaniz ◽  
Jiqiu Chen ◽  
...  

A number of promising therapies for ischemic cardiomyopathy are emerging, and the role of translational research in testing the efficacy and safety of these agents in relevant clinical models has become important. The goal of this study was to develop a chronic model of ischemic cardiomyopathy in a large animal model. In this study, 40 consecutive pigs were initially enrolled. To induce progressive stenosis, a plastic occluder with a fixed diameter of 1.0 mm fitted with an 18-gauge copper wire was placed around the proximal left anterior descending (LAD) coronary artery. Coronary angiography, hemodynamic measurements, and echocardiography were performed at 2 wk and 1, 2, and 3 mo. Overall mortality was 26% at 3 mo, and up to 80% of the pigs showed total occlusion of LAD at 1 mo. A significant depression of peak LV pressure rate of rise (+dP/d tmax) was observed in the animals showing total artery occlusion throughout the study. Left ventricular ejection fraction was also impaired, and the left ventricular volumes tended to be larger in the pigs with occlusion. Approximately 10% of scar tissue was found in the LAD occluded pigs, whereas the coronary flow pattern in the rest of the area took the pattern of hibernating myocardium. At the same time, histological and protein analysis established the presence of fibrosis and ongoing apoptosis in the ischemic area. In this model, the timing and incidence of total occlusion and low mortality offer significant advantages over other ischemic cardiomyopathy models in conducting preclinical studies.


2019 ◽  
Vol 46 (11) ◽  
pp. 2322-2328 ◽  
Author(s):  
Dominik C. Benz ◽  
Anita P. von Dahlen ◽  
Wenjie Huang ◽  
Michael Messerli ◽  
Elia von Felten ◽  
...  

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