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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 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.

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 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.

Introduction: Carotid body denervation (CBD) abolishes the carotid body hypersensitivity induced sympathoexcitatory hypertension. Since the carotid body hypersensitivity is a salient feature and predicts poor outcome of chronic heart failure (CHF), we hypothesized that CBD restores normal autonomic balance, thus improves CHF in rats after large myocardial infarction (MI). Methods: We created MI in 8 weeks Sprague-Dawley rats. Surviving rats at 2 weeks after MI were randomized into CBD (n=11) and sham-operated (Sham; n=13) groups. We removed the tissues around the carotid bifurcation and established CBD. In some rats (Sham; n=5, CBD; n=5), we telemetrically recorded heart rate (HR). One month after CBD, we compared physiological, histological and immunochemical findings between CBD and Sham. Results: CBD significantly reduced HR (337±15 vs. 364±12 bpm, p Conclusions: CBD restores normal autonomic balance and prevents the worsening of heart failure in rats after large myocardial infarction. CBD may serve as a novel neuro-modulatory therapy for CHF patients.