 MI. In this section, we introduce a new therapeutic option of LVAD in the management of acute MI and discuss the physiological and mechanical impact of LVAD in terms of cardiac energetics.

Development of left ventricular assist device
In 1966, DeBakey [98] first implanted an LVAD for the treatment of postoperative cardiogenic shock. The LVAD improved cardiac function and was successfully removed after a week. LVADs were initially developed as a bridge to heart transplantation for patients with end-stage heart failure. However, they have been increasingly used as a destination therapy or bridge to recovery. The REMATCH trial demonstrated a significant survival advantage and improvement of quality of life in patients with end-stage heart failure treated with first-generation, implantable, pulsatile flow LVAD compared with optimal medical management [99]. Second-generation implantable LVADs that circulate blood in a continuous flow fashion using an internal rotor are smaller and have proven to be more durable than pulsatile first-generation LVADs. Clinical trial of HeartMate II, a second-generation implantable axial continuous flow pump, concluded that the device provides effective hemodynamic support for at least 18 months in patients awaiting transplantation, with improved functional status and quality of life [100]. Recently, temporary LVADs that can be placed percutaneously by cardiologists in the catheterization room are also available ( Fig. 9) [101]. Percutaneous LVADs such as Impella Ò (Abiomed, Inc.; Danvers, MA, USA; Fig. 9a) and TandemHeart TM (Cardiac Assist, Inc.; Pittsburgh, PA, USA; Fig. 9b), have become essential tools in the treatment of cardiogenic shock [102] and high-risk percutaneous coronary intervention [103].

Left ventricular assist device for the treatment of myocardial infarction
Despite advances in early reperfusion therapy for patients with MI, 10% of patients die in the acute phase and about 30% develop heart failure in the long term [104]. Since the Fig. 9 Schematic representation of two percutaneous LVADs. Impella Ò (a) pulls blood from the left ventricle into the ascending aorta. TandemHeart TM (b) pumps blood from the left atrium into one or both femoral arteries presence of residual myocardial damage leads to heart failure, there exists an unmet need to develop better cardioprotective strategies that improve the long-term outcome after MI. LVAD supports hemodynamics and unloads the left ventricle. In addition, the development of percutaneous LVADs allows application of the device to acute clinical setting.
The concept of left ventricular unloading using percutaneous LVAD to protect the ischemic left ventricle has been proposed and several animal and clinical studies have been conducted. Meyns and colleagues [105] reported that left ventricular unloading using Impella Ò significantly reduced the infarct size in a sheep model of myocardial ischemia-reperfusion. Using an ischemia-reperfusion model, Kapur and colleagues [106] showed that left ventricular unloading by TandemHeart TM activated the RISK (reperfusion-injury salvage kinase) pathway that protects the myocardium from apoptosis, and significantly reduced infarct size despite longer ischemic exposure. In clinical trials, Engström and colleagues [107] reported the longterm effects of 3-day support with Impella 2.5 Ò on left ventricular ejection fraction (LVEF). They concluded that Impella 2.5 Ò significantly improved the recovery of LVEF. In addition, the USpella registry showed that initiation of LVAD support using Impella 2.5 Ò prior to reperfusion was associated with more complete revascularization and improved survival in the setting of refractory cardiogenic shock complicating acute MI [108]. Based on these findings, Kapur and colleagues [106] proposed a novel concept of initial mechanical unloading of the ischemic left ventricle before coronary reperfusion, so-called ''door to unloading'', and emphasized its importance.

Mechanical impact of left ventricular assist device on left ventricle
Understanding the underlying pathophysiology is a prerequisite to optimal use of LVAD treatment in MI patients. Systolic PVA, a specific area circumscribed by the endsystolic and end-diastolic pressure-volume relation curves and the PV loop (Fig. 10a), represents the total mechanical work of each ventricular contraction. Since PVA tightly couples with myocardial oxygen consumption (MVO 2 ) [109], the impact of LVAD support on MVO 2 can be revealed by examining PVA under the fixed heart rate (HR) condition. In this framework, LVAD decreases preload by withdrawing blood from the left ventricle and increases afterload by infusing blood into the aorta. Therefore, the impact of LVAD on PVA depends on the balance between the decreased preload and increased afterload. A theoretical analysis indicates that partial LVAD support, where the left ventricle remains ejecting, does not significantly decrease PVA [110]. In this setting, the impact on PVA is almost the same as that of extracorporeal membrane oxygenation [111,112]. In contrast, total LVAD support, where the left ventricle no longer ejects, markedly reduces left ventricular pressure and volume, thereby significantly decreases PVA (Fig. 10b). Although some drugs such as b-blockers [113] and angiotensin-converting enzyme (ACE) inhibitors [114] have been known to reduce MVO 2 and decrease the infarct size in MI or ischemia-reperfusion, these drugs do not stabilize the hemodynamics in an acute MI setting. LVAD is the only modality that markedly reduces PVA while stabilizing systemic hemodynamics. Thus, total LVAD support minimizes PVA and MVO 2 of the left ventricle, and maximally reduces infarct size in MI patients without compromising systemic hemodynamics [110]. Considering these physiological and mechanical effects of LVAD on the left ventricle, LVAD has promising potential in MI treatment. In addition, heart rate is also the major component of MVO 2 [115]. Therefore, the combination of bradycardic agent, e.g., If channel inhibitor, and LVAD will attribute to the further reduction of MVO 2 and infarct size in MI. Appropriate left ventricular unloading will maximize the beneficial impact of LVAD in the clinical setting of acute MI.

Conclusions
We reviewed four selected topics of cardiovascular physiology. This review may leave several messages for clinicians. First, a noninvasive monitoring method of arterial stiffness may be useful in evaluating the left ventricular arterial coupling (Ees/Ea) in the clinical setting. Second, careful consideration of the unique physiological characteristics of pulmonary circulation may be essential in optimizing medical care for pulmonary hypertension. Third, accurate evaluation of wall shear stress may be helpful in predicting graft patency after CABG. Lastly, mechanical ventricular unloading using LVAD may be useful in improving the outcome of patients with acute MI.
Diagnostic and therapeutic methods for cardiovascular diseases will continue to be developed in the 21st century. Insight into the physiological characteristics of the cardiovascular system is necessary for optimal uses of newly developed drugs and devices in patients with cardiovascular diseases. Clinical development of diagnostic and therapeutic modalities for cardiovascular diseases should be based on physiological insights of the cardiovascular system.Q:Title: This 3D bluray is defective. Product review: I purchased this from amazon and it would not play on both a sony and samsung 3d bluray player. It would either eject and say disc error or load forever, or occasionally make it to the menu, but the movie would only play for a few seconds then lock up. Even though I've never had a bad dvd or bluray before I thought that particular disc must of been bad. I sent it back to amazon and they sent me another brand new one. Guess what? Same exact problem.Sony also makes the swimsuit sports illustrated 3d bluray and it plays fine along with all my other 3D and 2D blurays and dvds.The few seconds I saw of the film between it locking up did show great 3D and was really pretty to look at, I wish I could watch the whole thing. Would you say this review depicts the product in a flattering or unflattering light?
A:
unflatteringA… I can’t really speak for all other online trainers as there are some good trainers/coaches and then there are poor ones too. What I can do is tell you about my service. Being an online coach is not only a test of a skilled coach to get the best out of his/her client, but it is also a test of how much a client really wants to achieve the goal set before them.
Communication is key to building a good and lasting client/coach relationship I always try my up most to return emails in good time as there is nothing worse than asking a question and never getting an answer or even a response.
I have also tried to make the program as easy and straight forward for my clients to use by going the extra mile and providing things that I would expect if I were using the service.
I have provided a library of exercise demonstration videos for my clients to use. I remember a client once told me that she had used an online coach in the past who was only interested in taking her money every month and only going on his reputation. He would provide a daily workout, she would get the email in the morning and then spend the next hour goggling each and every exercise.
We save you time and even provide the link for you to arrive at the body part, then you just choose the exercise you want to watch and within 30 seconds you’ve watch that video.
A…Motivation or lack of it is one of the key reasons why clients stop attending the gym or completing their program. I am a firm believer that motivation and gym work go hand in hand. Results are a direct link to motivations.
At the consultation stage, I ask clients