scholarly journals Effects of Levosimendan Preconditioning on Left Ventricular Remodeling after Myocardial Reperfusion in Acute Myocardial Infarction Patients Receiving Percutaneous Coronary Intervention

2022 ◽  
Vol 25 (1) ◽  
pp. E001-E007
Author(s):  
Shengqin Yu ◽  
Jindong Zhang
Keyword(s):  
Risk Factors ◽  
Myocardial Infarction ◽  
Protective Factor ◽  
Ventricular Remodeling ◽  
Left Ventricular Remodeling ◽  
Coronary Intervention ◽  
Left Ventricular ◽  
Myocardial Reperfusion ◽  
Observation Group ◽  
Percutaneous Coronary

Objective: Levosimendan is a novel drug often used to treat heart failure. We aimed to explore the effects of levosimendan preconditioning on left ventricular remodeling (LVR) after myocardial reperfusion in acute myocardial infarction (AMI) patients receiving the percutaneous coronary intervention (PCI). Methods: A total of 258 AMI patients treated from January 2018 to September 2020 were randomly divided into control and observation groups. Based on conventional drug therapy, levosimendan was given 30 min before PCI for the observation group, and dobutamine was intravenously injected for the control group. Baseline data, thrombolysis in myocardial infarction (TIMI) blood flow grade, myocardial injury markers, and LVR indices were compared, and the influencing factors for LVR were analyzed. Results: After treatment, various degrees of blood perfusion were found, and the TIMI grade was better than that before treatment in both groups (P < .05). The levels of aspartate aminotransferase, creatine kinase-MB, cardiac troponin T, and brain natriuretic peptide (BNP) declined in both groups, more significantly in the observation group (P < .05). Left ventricular end-systolic diameter, left ventricular end-diastolic diameter and left ventricular end-diastolic volume declined, whereas left ventricular ejection fraction rose in both groups, more significantly in the observation group (P < .05). Age and BNP were risk factors for LVR, whereas levosimendan preconditioning was a protective factor (P < .05). Conclusion: Levosimendan preconditioning can protect cardiac function and promote the recovery of the left ventricular structure. Age and BNP are risk factors for LVR after myocardial reperfusion in AMI patients undergoing PCI, and levosimendan preconditioning is a protective factor.

scholarly journals Optimized Treatment of ST-Elevation Myocardial Infarction

2019 ◽  
Vol 125 (2) ◽  
pp. 245-258 ◽  
Author(s):  
Giampaolo Niccoli ◽  
Rocco A. Montone ◽  
Borja Ibanez ◽  
Holger Thiele ◽  
Filippo Crea ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Infarct Size ◽  
Ventricular Remodeling ◽  
Left Ventricular Remodeling ◽  
Coronary Intervention ◽  
Left Ventricular ◽  
Major Adverse Cardiovascular Events ◽  
St Segment Elevation ◽  
St Segment ◽  
Percutaneous Coronary

Primary percutaneous coronary intervention is nowadays the preferred reperfusion strategy for patients with acute ST-segment–elevation myocardial infarction, aiming at restoring epicardial infarct-related artery patency and achieving microvascular reperfusion as early as possible, thus limiting the extent of irreversibly injured myocardium. Yet, in a sizeable proportion of patients, primary percutaneous coronary intervention does not achieve effective myocardial reperfusion due to the occurrence of coronary microvascular obstruction (MVO). The amount of infarcted myocardium, the so-called infarct size, has long been known to be an independent predictor for major adverse cardiovascular events and adverse left ventricular remodeling after myocardial infarction. Previous cardioprotection studies were mainly aimed at protecting cardiomyocytes and reducing infarct size. However, several clinical and preclinical studies have reported that the presence and extent of MVO represent another important independent predictor of adverse left ventricular remodeling, and recent evidences support the notion that MVO may be more predictive of major adverse cardiovascular events than infarct size itself. Although timely and complete reperfusion is the most effective way of limiting myocardial injury and subsequent ventricular remodeling, the translation of effective therapeutic strategies into improved clinical outcomes has been largely disappointing. Of importance, despite the presence of a large number of studies focused on infarct size, only few cardioprotection studies addressed MVO as a therapeutic target. In this review, we provide a detailed summary of MVO including underlying causes, diagnostic techniques, and current therapeutic approaches. Furthermore, we discuss the hypothesis that simultaneously addressing infarct size and MVO may help to translate cardioprotective strategies into improved clinical outcome following ST-segment–elevation myocardial infarction.

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