Abstract 13813: Intravascular Vagal Nerve Stimulation in Acute Myocardial Infarction Markedly Reduced Infarct Size and Improved Cardiac Function in the Long Term

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Takahiro Arimura ◽  
Keita Saku ◽  
Takamori Kakino ◽  
Takuya Nishikawa ◽  
Takeshi Tohyama ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Acute Myocardial Infarction ◽  
Infarct Size ◽  
Nerve Stimulation ◽  
Myocardial Damage ◽  
Vagal Nerve ◽  
Vagal Nerve Stimulation ◽  
Lv Function

Backgrounds: In acute myocardial infarction (AMI), the extent of myocardial damage governs the progression to heart failure in the long-term. Therefore, reducing the myocardial damage is prerequisite to prevent chronic heart failure. Although vagal nerve stimulation (VNS) has been repeatedly demonstrated to have the powerful anti-infarct effect, technical difficulties preclude its clinical applications. Recently we developed an new percutaneous, intravascular VNS (iVNS). In this study, we investigated whether iVNS reduces the infarct size and prevents heart failure one month after ischemia reperfusion (IR). Methods: In mongrel dogs, we ligated the left anterior descending coronary artery for 3 hours and reperfused. We transvascularly stimulated the right vagal nerve with a pacing catheter in the superior vena cava. We maximized the intensity of iVNS that did not deteriorate hemodynamics (amplitude; 5.1±2.1 V, pulse width; 0.2ms, frequency; 10 Hz). We started iVNS at the onset of ischemia (iVNS0, n=7) or 90 min after the onset of ischemia (iVNS90, n=7) and continued to 60 min after reperfusion. One month after IR, we compared the infarct size, left ventricular (LV) function and hormonal responses among 3 groups including the no treatment group (IR, n=10). Results: Both iVNS0 and iVNS90 significantly reduced the infarct size (IR: 11.6±3.1, iVNS0: 2.4±2.1, iVNS90: 4.5±1.9%, p<0.05, Figure), improved LV ejection fraction (IR: 50±7, iVNS0: 61±6, iVNS90: 60±5.1%, p<0.05) and decreased LV end-diastolic pressure (IR: 14.6±1.9, iVNS0: 4.2±1.0, iVNS90: 5.0±2.8mmHg, P<0.05). The benefits were larger in iVNS0 than iVNS90. Conclusion: Short term iVNS delivered prior to coronary reperfusion markedly reduced the infarct size and preserved LV function one month after ischemia. Since we can transvascularly deliver iVNS, it may serve as a new non-pharmacological therapeutic strategy and contribute to improve the long term survival in patients with AMI.

The Neuro-Mechanical Unloading for Acute Myocardial Infarction Markedly Reduces the Infarct Size and Prevents Heart Failure in the Long Term

2015 ◽  
Vol 21 (10) ◽  
pp. S167-S168
Author(s):  
Keita Saku ◽  
Takahiro Arimura ◽  
Takamori Kakino ◽  
Takafumi Sakamoto ◽  
Takeshi Tohyama ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Acute Myocardial Infarction ◽  
Infarct Size ◽  
Mechanical Unloading

scholarly journals Vagal Nerve Stimulation Markedly Improves Long-Term Survival After Chronic Heart Failure in Rats

Circulation ◽  
2004 ◽  
Vol 109 (1) ◽  
pp. 120-124 ◽  
Author(s):  
Meihua Li ◽  
Can Zheng ◽  
Takayuki Sato ◽  
Toru Kawada ◽  
Masaru Sugimachi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Nerve Stimulation ◽  
Vagal Nerve ◽  
Vagal Nerve Stimulation ◽  
Term Survival ◽  
Long Term Survival

Abstract 14058: Transvascular Total Left Ventricular Unloading for Acute Myocardial Infarction Strikingly Reduced Myocardial Oxygen Consumption, Limited the Infarct Size and Prevented Heart Failure in the long term

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Takahiro Arimura ◽  
Keita Saku ◽  
Takamori Kakino ◽  
Takuya Akashi ◽  
Yoshinori Murayama ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Acute Myocardial Infarction ◽  
Oxygen Consumption ◽  
Infarct Size ◽  
Myocardial Oxygen Consumption ◽  
Left Ventricular ◽  
Early Reperfusion ◽  
The Impact

Backgrounds: Despite the latest progresses of early reperfusion, myocardial infarction (MI) remains a leading cause of chronic heart failure (CHF). Left ventricular (LV) assist device (VAD) mechanically unloads LV, thus myocardial oxygen consumption (MVO2). Theoretical analysis indicates that the partial VAD (p-VAD) where LV remains ejecting decreases preload (EDV) while increases afterload (ESV), thereby marginally decreases MVO2. In contrast, total LVAD (t-VAD) where LV no longer ejects, markedly decreases ESV as well as EDV, thus markedly reduces MVO2. We examined whether t-VAD in ischemia reperfusion (IR) could reduce the infarct size and prevent heart failure in the long term. Methods: First, in normal dogs, we examined the impact of p-VAD and t-VAD on MVO2 by Fick principle (coronary flow and arterial venous O2 difference). Second, we occluded the left anterior descending coronary artery for 3 hours and reperfused. We started transvascular LVAD (Impella®) from 1 hour after ischemia to 1 hour after reperfusion. We compared cardiac function, infarct size and hormones 1 month after ischemia among 3 groups, control group (IR, n=8), p-VAD (n=6), and t-VAD (n=6). Results: t-VAD markedly decreased MVO2 (p<0.05, Figure 1). 1 month after ischemia, t-VAD normalized LV end-systolic elastance (IR: 6.5±3.2, p-VAD: 9.7±1.3, t-VAD: 12.8±5.1 mmHg/ml, p<0.05) and reduced LV end-diastolic pressure (16.5±2.7, 6.4±2.9, 4.4±1.5 mmHg, p<0.05), and NT proBNP (3391±1364, 2084±348, 1632±228 pg/ml, p<0.05) indicating the successful prevention of heart failure. t-VAD markedly reduced the infarct size by more than 80% relative to IR (p<0.05, Figure 2) despite the fact that it started 1 hour after the onset of ischemia. Conclusions: Transvascular total left ventricular unloading for acute myocardial infarction strikingly reduces the MI size and prevents heart failure in the chronic phase. It might serve as a new therapeutic strategy in the management of patients with acute MI.

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