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Ventricular Unloading (ventricular + unloading)
Selected AbstractsMyocardial Perfusion As Assessed by Positron Emission Tomography During Long-Term Mechanical Circulatory SupportCONGESTIVE HEART FAILURE, Issue 2 2006George V. Letsou MD Although mechanical circulatory support (MCS) can improve myocardial function in patients with advanced heart failure, its effects on relative myocardial perfusion are unclear. Using positron emission tomographic imaging techniques, the authors assessed relative myocardial perfusion in patients with ischemic or idiopathic cardiomyopathy who were receiving chronic MCS with a left ventricular assist device (pulsatile HeartMate [n=2] [Thoratec Corporation, Pleasanton, CA] or nonpulsatile Jarvik 2000 [n=4] [Jarvik Heart, Inc., New York, NY]). Relative myocardial perfusion was compared at lower and higher levels of MCS (50 vs. 100,110 ejections/min for the HeartMate and 8000 vs. 12,000 rpm for the Jarvik 2000). The size and severity of perfusion defects at rest and after dipyridamole stress were measured objectively and subjectively by computer algorithms and visual inspection, respectively. Relative myocardial perfusion increased >5% from baseline in only one of six patients when MCS was increased. No change in relative myocardial perfusion of >5% was seen in any of the other five patients, even after subsequent dipyridamole stress positron emission tomographic imaging. These pilot study findings suggest that the decreased metabolic requirements induced by ventricular unloading correspondingly decreased blood flow requirements to physiologically inactive myocardium. [source] A Mathematical Model to Evaluate Control Strategies for Mechanical Circulatory SupportARTIFICIAL ORGANS, Issue 8 2009Lieke G.E. Cox Abstract Continuous flow ventricular assist devices (VADs) for mechanical circulatory support (MCS) are generally smaller and believed to be more reliable than pulsatile VADs. However, regarding continuous flow, there are concerns about the decreased pulsatility and ventricular unloading. Moreover, pulsatile VADs offer a wider range in control strategies. For this reason, we used a computer model to evaluate whether pulsatile operation of a continuous flow VAD would be more beneficial than the standard constant pump speed. The computer model describes the left and right ventricle with one-fiber heart contraction models, and the systemic, pulmonary, and coronary circulation with lumped parameter hemodynamical models, while the heart rate is regulated with a baroreflex model. With this computer model, both normal and heart failure hemodynamics were simulated. A HeartMate II left ventricular assist device model was connected to this model, and both constant speed and pulsatile support were simulated. Pulsatile support did not solve the decreased pulsatility issue, but it did improve perfusion (cardiac index and coronary flow) and unloading (stroke work and heart rate) compared with constant speed. Also, pulsatile support would be beneficial for developing control strategies, as it offers more options to adjust assist device settings to the patient's needs. Because the mathematical model used in this study can simulate different assist device settings, it can play a valuable role in developing mechanical circulatory support control strategies. [source] Use of mechanical assist during high-risk PCI and STEMI with cardiogenic shock,CATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS, Issue S1 2010Tillmann Cyrus MB Abstract Infarct size may be reduced by left ventricular unloading after ST-segment elevation MI (STEMI) in addition to reperfusion therapy. Likewise, high-risk percutaneous coronary intervention (PCI) may benefit from periprocedural support especially in patients with low cardiac output at baseline or when periprocedural hemodynamic deterioration is anticipated. Traditionally, intraaortic balloon-pumps have been used in acute MI with cardiogenic shock. As this modality has limited hemodynamic benefits, new developments have focused on active hemodynamic assist devices. These devices actively unload the left ventricle increasing cardiac output by 2.5,5 L/min and are increasingly easier to implant and monitor. Thus, interventional cardiologists will be able to offer a safer more effective alternative to an increasing patient population with complex cardiac conditions and high-risk PCI. © 2010 Wiley-Liss, Inc. [source] Effects of left ventricular unloading by Impella recover LP2.5 on coronary hemodynamicsCATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS, Issue 4 2007Maurice Remmelink MD Abstract Objectives: We studied the effects of LV unloading by the Impella on coronary hemodynamics by simultaneously measuring intracoronary pressure and flow and the derived parameters fractional flow reserve (FFR), coronary flow velocity reserve (CFVR), and coronary microvascular resistance (MR). Background: Patients with compromised left ventricular (LV) function undergoing high-risk percutaneous coronary intervention (PCI) may benefit from LV unloading. Limited information is available on the effects of LV unloading on coronary hemodynamics. Methods: Eleven patients (mean LV ejection fraction of 35 ± 11%) underwent PCI during LV support by the LV unloading device (Impella Recover® LP2.5). Intracoronary measurements were performed in a nonstenotic coronary artery after the PCI, before and after adenosine-induced hyperemia at four different support levels (0,2.5 L/min). Results: Aortic and coronary pressure increased with increasing support levels, whereas FFR remained unchanged. Baseline flow velocity remained unchanged, while hyperemic flow velocity and CFVR increased significantly with increasing support levels (61 ± 24 to 72 ± 27 cm/sec, P = 0.001 and 1.88 ± 0.52 to 2.34 ± 0.63, P < 0.001 respectively). The difference between baseline MR and hyperemic MR significantly increased with increasing support levels (1.28 ± 1.32 to 1.89 ± 1.43 mm Hg cm,1 sec, P = 0.005). Conclusions: Unloading of the LV by the Impella increased aortic and intracoronary pressure, hyperemic flow velocity and CFVR, and decreased MR. The Impella-induced increase in coronary flow, probably results from both an increased perfusion pressure and a decreased LV volume-related intramyocardial resistance. © 2007 Wiley-Liss, Inc. [source] Left ventricular unloading and concomitant total cardiac output increase by the use of percutaneous impella recover LP 2.5 assist device during high-risk coronary interventionCATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS, Issue 2 2005Marco Valgimigli Abstract A number of techniques have been proposed for circulatory support during high-risk percutaneous coronary interventions (PCI), but no single approach has achieved wide acceptance so far. We report on a patient with severe left ventricular (LV) impairment who underwent a PCI with the use of a new left ventricular assist device, the Impella Recover LP 2.5 system. The effects on global cardiac output were determined by thermodilution (TD) and LV pressure-volume loops obtained by conductance catheter. The activation of the pump resulted in a rapid and sustained unloading effect of the LV. At the same time, the continuous expulsion of blood into ascending aorta throughout the cardiac cycle produced by the pump resulted in an increase of systemic overall CO, measured by the TD technique, of 1.43 L/min. The procedure was uncomplicated and the patient remained uneventful at follow-up. Our single experience gives new input for future trials to assess the effect of the Impella Recover LP 2.5 assist device on outcome in this subset of patients. © 2005 Wiley-Liss, Inc. [source] Growth hormone, acromegaly, and heart failure: an intricate triangulationCLINICAL ENDOCRINOLOGY, Issue 6 2003Luigi Saccą Summary Short-term GH or IGF-I excess provides a model of physiological cardiac growth associated with functional advantage. The physiological nature of cardiac growth is accounted for by the following: (i) the increment in cardiomyocyte size occurs prevalently at expense of the short axis. This is the basis for the concentric pattern of left ventricular (LV) hypertrophy, with consequent fall in LV wall stress and functional improvement; (ii) cardiomyocyte growth is associated with improved contractility and relaxation, and a favourable energetic setting; (iii) the capillary density of the myocardial tissue is not affected; (iv) there is a balanced growth of cardiomyocytes and nonmyocyte elements, which accounts for the lack of interstitial fibrosis; (v) myocardial energetics and mechanics are not perturbed; and (vi) the growth response is not associated with the gene re-programming that characterizes pathologic cardiac hypertrophy and heart failure. Overall, the mechanisms activated by GH or IGF-I appear to be entirely different from those of chronic heart failure. Not to be neglected is also the fact that GH, through its nitric oxide (NO)-releasing action, contributes to the maintenance of normal vascular reactivity and peripheral vascular resistance. This particular kind of interaction of GH with the cardiovascular system accounts for: (i) the lack of cardiac impairment in short-term acromegaly; (ii) the beneficial effects of GH and IGF-I in various models of heart failure; (iii) the protective effect of GH and IGF-I against post-infarction ventricular remodelling; (iv) the reversal of endothelial dysfunction in patients with heart failure treated with GH; and (v) the cardiac abnormalities associated with GH deficiency and their correction after GH therapy. If it is clear that GH and IGF-I exert favourable effects on the heart in the short term, it is equally undeniable that GH excess with time causes pathologic cardiac hypertrophy and, if it is not corrected, eventually leads to cardiac failure. Why then, at one point in time in the natural history of acromegaly, does physiological cardiac growth become maladaptive and translate into heart failure? Before this transition takes places, the acromegalic heart shares very few features with other models of chronic heart failure. None of the mechanisms involved in the progression of heart failure is clearly operative in acromegaly, save for the presence of insulin-resistance and mild alterations of lipoproteins and clot factors. Is this enough to account for the development of heart failure? Probably not. On the other hand, it must be stressed that GH and IGF-I activate several mechanisms that play a protective role against the development of heart failure. These include ventricular unloading, deactivation of neurohormonal components, antiapoptotic effect and enhanced vascular reactivity. Ultimately, all data available concur to hypothesize that acromegalic cardiomyopathy represents a progressive model of cardiac hypertrophy in which the cardiotoxic and pro-remodelling effect is intrinsic to the excessive and unrestrained myocardial growth. [source] | ||||||||||