scholarly journals Possible mechanism by which renal sympathetic denervation improves left ventricular remodelling after myocardial infarction

2015 ◽  
Vol 101 (2) ◽  
pp. 260-271 ◽  
Author(s):  
Xiao-Xin Zheng ◽  
Xiao-Yan Li ◽  
Yong-Nan Lyu ◽  
Yi-Yu He ◽  
Wei-Guo Wan ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Left Ventricular ◽  
Sympathetic Denervation ◽  
Renal Sympathetic Denervation ◽  
Ventricular Remodelling ◽  
Left Ventricular Remodelling ◽  
Renal Sympathetic

Abstract 15493: Renal Sympathetic Denervation Reduces Ventricular Arrhythmias Inducibility in Dogs With Healed Myocardial Infarction

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Bing Huang ◽  
Lilei Yu ◽  
Zhibing Lu ◽  
Bo He ◽  
Zhuo Wang ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Rate ◽  
Ventricular Arrhythmias ◽  
Canine Model ◽  
Left Ventricular ◽  
Sympathetic Denervation ◽  
Left Ventricular Ejection ◽  
Renal Sympathetic Denervation ◽  
Protein Levels ◽  
Renal Sympathetic

Introduction: Previous studies have suggested that renal sympathetic denervation (RSD) could suppress acute myocardial ischemia-induced ventricular arrhythmias (VAs), but the long-term effects of RSD in a post-infarction canine model is not fully established. Methods: Thirty dogs underwent embolization of the left anterior descending artery. After a 14-days of recovery period, all the dogs were equally randomized to the RSD, medicine (MED; carvedilol 12.5mg PO BID), or control (CTRL; no therapy) group. Animals were monitored for 3 months after interventions. The serum norepinephrine (NE), echocardiographic indices, heart rate variability (HRV), and VAs inducibility were measured at the end of 90-day follow-up. Tyrosine hydroxylase (TH) and growth-associated protein 43 (GAP43) expressions in the peri-infarcted zone were also determined immunohistochemically. The protein levels of metrix metalloproteinases (MMP-2 and MMP-9) and tissue inhibitor of matalloproteinases (TIMP-1) were also determined. Results: When compared with CTRL group, RSD significantly (1) decreased heart rate, serum NE, sympathetic nerve indices of HRV, and the density of both TH- and GAP43-positive nerves in the peri-infarcted zone; (2) increased left ventricular ejection fraction and reduced left ventricular dilatation; (3) decreased the protein levels of MMP-2, MMP-9 and TIMP-1 in left ventricular tissues; (4) decreased the inducibility of ventricular tachyarrhythmias. Beta-receptor blockade by carvedilol showed comparable effects. Conclusions: RSD could reduce VAs inducibility in a canine model of healed myocardial infarction. Inhibition of autonomic and structural remodeling by RSD may be responsible for this salutary result.

scholarly journals Roles of ghrelin in left-ventricular remodelling after acute myocardial infarction

Heart Asia ◽  
2010 ◽  
Vol 2 (1) ◽  
pp. 1-4 ◽  
Author(s):  
H. Kondo ◽  
Y. Hojo ◽  
N. Takahashi ◽  
T. Ikemoto ◽  
H. Aoki ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Left Ventricular ◽  
Ventricular Remodelling ◽  
Left Ventricular Remodelling

Novel role of platelet reactivity in adverse left ventricular remodelling after ST-segment elevation myocardial infarction: The REMODELING Trial

2017 ◽  
Vol 117 (05) ◽  
pp. 911-922 ◽  
Author(s):  
Yongwhi Park ◽  
Udaya Tantry ◽  
Jin-Sin Koh ◽  
Jong-Hwa Ahn ◽  
Min Kang ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Platelet Reactivity ◽  
Left Ventricular ◽  
Ventricular Remodelling ◽  
Left Ventricular Remodelling ◽  
St Segment Elevation ◽  
Segment Elevation Myocardial Infarction ◽  
St Segment ◽  
Hs Crp

SummaryThe role of platelet-leukocyte interaction in the infarct myocardium still remains unveiled. We aimed to determine the linkage of platelet activation to post-infarct left ventricular remodelling (LVR) process. REMODELING was a prospective, observational, cohort trial including patients (n = 150) with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention. Patients were given aspirin plus clopidogrel therapy (600 mg loading and 75 mg daily). Platelet reactivity (PRU: P2Y12 Reaction Units) was assessed with VerifyNow P2Y12 assay on admission. Transthoracic echocardiography was performed on admission and at one-month follow-up. The primary endpoint was the incidence of LVR according to PRU-based quartile distribution. LVR was defined as a relative ≥ 20 % increase in LV end-diastolic volume (LVEDV) between measurements. Adverse LVR was observed in 36 patients (24.0 %). According to PRU quartile, LVR rate was 10.8 % in the first, 23.1 % in the second, 27.0 % in the third, and 35.1 % in the fourth (p = 0.015): the optimal cut-off of PRU was ≥ 248 (area under curve: 0.643; 95 % confidence interval: 0.543 to 0.744; p = 0.010). LVR rate also increased proportionally according to the level of high sensitivity-C reactive protein (hs-CRP) (p = 0.012). In multivariate analysis, the combination of PRU (≥ 248) and hs-CRP (≥ 1.4 mg/l) significantly increased the predictive value for LVR occurrence by about 21-fold. In conclusion, enhanced levels of platelet activation and inflammation determined the incidence of adverse LVR after STEMI. Combining the measurements of these risk factors increased risk discrimination of LVR. The role of intensified antiplatelet or anti-inflammatory therapy in post-infarct LVR process deserves further study.

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