scholarly journals Veno-occlusive unloading of the heart reduces infarct size in experimental ischemia–reperfusion

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Esben Søvsø Szocska Hansen ◽  
Tobias Lynge Madsen ◽  
Gregory Wood ◽  
Asger Granfeldt ◽  
Nikolaj Bøgh ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Ejection Fraction ◽  
Infarct Size ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Cardiac Work ◽  
Area At Risk ◽  
Lv Ejection Fraction

AbstractMechanical unloading of the left ventricle reduces infarct size after acute myocardial infarction by reducing cardiac work. Left ventricular veno-occlusive unloading reduces cardiac work and may reduce ischemia and reperfusion injury. In a porcine model of myocardial ischemia–reperfusion injury we randomized 18 pigs to either control or veno-occlusive unloading using a balloon engaged from the femoral vein into the inferior caval vein and inflated at onset of ischemia. Evans blue and 2,3,5-triphenyltetrazolium chloride were used to determine the myocardial area at risk and infarct size, respectively. Pressure–volume loops were recorded to calculate cardiac work, left ventricular (LV) volumes and ejection fraction. Veno-occlusive unloading reduced infarct size compared with controls (Unloading 13.9 ± 8.2% versus Control 22.4 ± 6.6%; p = 0.04). Unloading increased myocardial salvage (54.8 ± 23.4% vs 28.5 ± 14.0%; p = 0.02), while the area at risk was similar (28.4 ± 6.7% vs 27.4 ± 5.8%; p = 0.74). LV ejection fraction was preserved in the unloaded group, while the control group showed a reduced LV ejection fraction. Veno-occlusive unloading reduced myocardial infarct size and preserved LV ejection fraction in an experimental acute ischemia–reperfusion model. This proof-of-concept study demonstrated the potential of veno-occlusive unloading as an adjunctive cardioprotective therapy in patients undergoing revascularization for acute myocardial infarction.

scholarly journals Infarct Size and Left Ventricular Ejection Fraction in Acute Myocardial Infarction

1977 ◽  
Vol 41 (11) ◽  
pp. 1299-1306 ◽  
Author(s):  
MASATSUGU HORI ◽  
MICHITOSHI INOUE ◽  
MASAYOSHI MISHIMA ◽  
TAKASHI SHIMAZU ◽  
HIROSHI ABE ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Left Ventricular Ejection Fraction ◽  
Ejection Fraction ◽  
Infarct Size ◽  
Left Ventricular ◽  
Ventricular Ejection ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction

Abstract 3379: Feasibility Of Adrenomedullin Infusion In Patients With Acute Myocardial Infarction -a Possible Cardioprotective Therapy Against Ischemic Injury-

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Satoshi Yasuda ◽  
Shunichi Miyazaki ◽  
Noritoshi Nagaya ◽  
Yu Kataoka ◽  
Teruo Noguchi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Infarct Size ◽  
Intravenous Administration ◽  
Ischemia Reperfusion ◽  
Coronary Intervention ◽  
Reperfusion Therapy ◽  
Left Ventricular ◽  
Stress Generation

Background : Adrenomedullin (ADM) is a 52-amino-acid vasodilator peptide that was originally isolated from human pheochromocytoma. In the previous experimental study with rat ischemia/reperfusion model, ADM reduced infarct size and inhibited myocyte apoptosis. ADM also suppressed the production of oxygen-free-radicals. The present study was designed to evaluate the feasibility of intravenous administration of ADM in patients with acute myocardial infarction (AMI). Methods : We studied 10 patients with first AMI (M/F;9/1, mean age;65 years, peak CPK level; 4090 U/L[median]), who were hospitalized within 12 hours of symptom onset. ADM infusion preceded percutaneous coronary intervention (PCI) and was continued at concentration of 0.0125 − 0.025μg/kg/minute for 12 hours. We also studied 10 control AMI patients matched for age, sex and infarct size, who did not receive ADM. Results : During ADM infusion, hemodynamics kept stable except one patient with right ventricular infarction. Urinary levels of 8-iso-prostaglandine F2α, which was measured after the reperfusion therapy with ADM infusion as a marker of oxidative stress, was significantly lower in patients who received ADM than those who did not (76 ± 40 vs 174±21 pmol/mol of creatinine, P<0.01). Infarct area (IA) evaluated by magnetic resonance imaging and brain natriuretic peptide (BNP) levels were also different between the two groups (Table ). Conclusions : Intravenous administration of ADM, which possesses a variety of cardiovascular protective actions, is feasible and can be adjunctive to PCI. Suppression of oxidative stress generation may be beneficial for attenuation of left ventricular dysfunction and remodeling following AMI.

Abstract 16525: Left Ventricular Unloading Before, Not After, Reperfusion Limits Infarct Size and Improves Survival in Acute Myocardial Infarction: A Bench to Bedside Study

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Navin K Kapur ◽  
Vikram Paruchuri ◽  
Xiaoying Qiao ◽  
Kevin Morine ◽  
Lyanne Buiten ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Infarct Size ◽  
Clinical Utility ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Coronary Reperfusion ◽  
Infarct Zone ◽  
Mitochondrial Integrity ◽  
Phosphorylated Akt

Ischemia-reperfusion injury (IRI) is a major determinant of myocardial damage in acute myocardial infarction (AMI). We explored the hypothesis that reducing left ventricular wall stress (LV unloading) with an axial flow catheter (Impella) before, not after, coronary reperfusion reduces infarct size and improves survival. Methods: We first employed a model of AMI. After 90 minutes of LAD occlusion, adult, male swine (n=4/group) were randomized to: 1) 120 minutes of reperfusion alone (IRI), 2) 30 minutes of LV unloading before 120 minutes of reperfusion (Impella to Balloon Group; ITB) or 3) 30 minutes of reperfusion followed by LV unloading and an additional 120 minutes of reperfusion (Balloon to Impella Group; BTI). Infarct size, myocardial kinase activity, and mitochondrial integrity were quantified. To explore the clinical utility of LV unloading before reperfusion we retrospectively studied all patients in the USPella registry presenting with ST-segmentc elevation AMI and cardiogenic shock who received an Impella within 120 minutes before (n=41; STEMI-ITB) or within 120 minutes after (n=76; STEMI-BTI) percutaneous reperfusion between 2009 and 2014. Results: Compared to IRI alone, infarct size was reduced in the ITB group, not the BTI group (62±2% vs 33±6% vs 58±15%, IRI vs ITB vs BTI, p<0.01 for IRI vs ITB; p<0.05 for ITB vs BTI). Levels of phosphorylated Akt, Erk-1/2, and GSK3b were increased within the infarct zone in the ITB, not BTI group. Mitochondrial numbers and markers of integrity were higher within the infarct zone in the ITB, compared to IRI or BTI. In the registry, in-hospital (51% vs 28%, p=0.02) and 30-day survival (42% vs 20%, p=0.03) were higher in the STEMI-ITB than the STEMI-BTI group. A STEMI-ITB time of less than 60 minutes (n=38) was associated with higher in-hospital survival than a STEMI-BTI time of less than 60 minutes (n=40) (50% vs 25%, p=0.02). Conclusion: Primary LV unloading before, not after, coronary reperfusion reduces infarct size, increases cardioprotective signaling, and improves mitochondrial integrity. These findings are supported by improved survival among patients treated with an Impella before, not after reperfusion in AMI. Future studies are required to explore the clinical utility of primary LV unloading in AMI.

scholarly journals Inhibition of Type 2 Sodium-Glucose Transporters and Na+/H+ Exchanger-1 produces similar cardioprotective effects in response to ischemiareperfusion injury

2019 ◽  
Vol 2 (1) ◽  
Author(s):  
Bianca S. Blaettner ◽  
Hana E. Baker ◽  
Adam G. Goodwill ◽  
Hannah E. Clark ◽  
Michael C. Kozlowski ◽  
...  
Keyword(s):  
At Risk ◽  
Infarct Size ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Glucose Transporters ◽  
Left Ventricular ◽  
Area At Risk ◽  
Cardioprotective Effects

Background and Hypothesis: Recent studies indicate that inhibition of Type 2 Sodium-Glucose Transporters (SGLT2i) augments diastolic filling volume and mitigates myocardial ischemic injury. This study tested the hypothesis that inhibition of the Na+/H+ Exchanger-1 (NHE-1) mimics the cardioprotective effects of SGLT2i in response to ischemia-reperfusion injury. Experimental Design or Project Methods: Lean swine (~50 kg) were anesthetized, a thoracotomy performed, and perivascular flow transducers placed around the left anterior descending (LAD) and circumflex coronary (LCX) arteries. A pressure-volume (PV) catheter was then inserted into the left ventricle. Swine received a 15 min infusion of vehicle (DMSO; n = 3), the SGLT2i Canagliflozin (30 µM; n = 3), or the NHE-1 inhibitor Cariporide (1µM; n = 3) prior to a 60 min total occlusion of the LCX and 2-hour reperfusion period. Following reperfusion, the LCX was re-occluded and a 2.5% Patent Blue 5 solution was administered to identify area at risk. The heart was excised, sectioned, and incubated in a 2,3,5-triphenyltetrazolium chloride (TTC) solution. Images were collected and analyzed for area at risk and infarct size. Results: In the vehicle treated group, 2 of the 3 swine studied died prematurely before the completion of the protocol; one at baseline and one during ischemia. Our initial findings support that left ventricular end diastolic volume increases in response to regional myocardial ischemia in swine that received either Canagliflozin or Cariporide. This increase in diastolic volume was associated with an increase in stroke volume (i.e. Frank-Starling effect) and a reduction in myocardial infarct size in both treatment groups. Blood pressure tended to decrease to a similar extent in all groups. Conclusion and Potential Impact: These pilot studies suggest that inhibition of SGLT2 and NHE-1 produces similar functional and protective effects in response to regional ischemia-reperfusion injury. Further experiments are needed to corroborate these findings and examine the extent to which SGLT2i directly modulates NHE-1 activity.

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