Bridge Experience With Long-term Implantable Left Ventricular Assist Devices

Öz, Mehmet C.; Argenziano, Michael; Catanese, Katharine A.; Gardocki, Michael; Goldstein, Daniel J.; Ashton, Robert C.; Gelijns, Annetine C.; Rose, Eric A.; Levin, Howard R.

doi:10.1161/01.cir.95.7.1844

Cited by 194 publications

(88 citation statements)

References 20 publications

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“…Indeed, a small subgroup of patients can be successfully weaned from LVAD after recovery of ventricular function. 6,[11][12][13][14] Although it has been suggested that these beneficial changes are attributed to chronic unloading of the ventricular myocardium, the molecular mechanisms that play a role in LVAD-induced myocardial plasticity and LV remodeling remain undefined. …”

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confidence: 99%

Downregulation of Matrix Metalloproteinases and Reduction in Collagen Damage in the Failing Human Heart After Support With Left Ventricular Assist Devices

et al. 2001

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Background-Left ventricular assist device (LVAD) support of the failing heart induces salutary changes in myocardial structure and function. Matrix metalloproteinases (MMPs) are increased in the failing heart and are induced by stretch in cardiac cells in vitro. We hypothesized that mechanical unloading may affect LV plasticity by regulating MMPs and their substrates. Methods and Results-LV samples were collected from patients with dilated cardiomyopathy (DCM, nϭ14) or ischemic cardiomyopathy (ICM, nϭ16) at the time of implantation of the LVAD and again during cardiac transplantation. MMP-1, -3, and -9 were measured by ELISA, MMP-2 and -9 gelatinolytic activity by gelatin zymography, and tissue inhibitors of metalloproteinases (TIMPs) by Western blot. Total soluble and insoluble collagens were separated by pepsin solubilization, and the contents were determined by quantification of hydroxyproline. The undenatured soluble collagen was measured by Sircol collagen assay. The results showed that MMP-1 and -9 were decreased, whereas TIMP-1 and -3 were increased, but there was no change in MMP-2 and -3 and TIMP-2 and -4 after LVAD support. The undenatured collagen was increased, with the ratio of undenatured to total soluble collagens increased in ICM and that of insoluble to total soluble collagens increased in DCM after LVAD support. Conclusions-The reduced MMPs and increased TIMPs and ratios of undenatured to total soluble collagens and insolubleto total soluble collagens after LVAD support suggest that reduced MMP activity diminished damage to the matrix. These changes may contribute to the functional recovery and LV plasticity after LVAD support. Key Words: collagen Ⅲ metalloproteinases Ⅲ remodeling Ⅲ heart-assist device Ⅲ heart failure L eft ventricular assist devices (LVADs) provide mechanical support for the failing heart and serve as a bridge to cardiac transplantation, with the potential to be a destiny therapy for heart failure. [1][2][3] Recent reports demonstrate that LVAD support may be associated with adaptive remodeling of the ventricular myocardium, including reduced LV mass, wall thickness, and myocyte diameter; changes in LV pressure-volume relationships; and reversal of LV chamber dilation and molecular remodeling of proteins involved in Ca 2ϩ cycling. [3][4][5][6][7][8][9][10] In addition, LVAD support has been associated with salutary changes in cardiomyocyte function. Indeed, a small subgroup of patients can be successfully weaned from LVAD after recovery of ventricular function. 6,[11][12][13][14] Although it has been suggested that these beneficial changes are attributed to chronic unloading of the ventricular myocardium, the molecular mechanisms that play a role in LVAD-induced myocardial plasticity and LV remodeling remain undefined. See p 1089We hypothesized that the myocardial remodeling that occurs with LVAD unloading might be attributable to alterations in the components of the extracellular matrix, and specifically in the activity of matrix metalloproteinases (MMPs) and the physical pr...

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confidence: 99%

Downregulation of Matrix Metalloproteinases and Reduction in Collagen Damage in the Failing Human Heart After Support With Left Ventricular Assist Devices

et al. 2001

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“…13,14 The LVAD used in the present study obtains oxygenated blood from the native left ventricle and sends it to the arterial circulation. Thus, patients are dependent on the output of the prosthetic heart, which is tightly regulated by the programming mode, for maintenance of blood pressure.…”

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confidence: 99%

Evidence for a Central Origin of the Low-Frequency Oscillation in RR-Interval Variability

et al. 1998

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Background-Short-term variability of RR interval and blood pressure occurs predominantly at low frequency (LF; Ϸ0.1 Hz) and high frequency (Ϸ0.25 Hz). The arterial baroreflex is thought to be the predominant determinant of the LF component of RR variability. Patients with severe congestive heart failure (CHF) have an attenuated or absent LF oscillation in RR variability. The left ventricular assist device (LVAD) offers a unique possibility for analysis of spectral oscillations in RR interval independent of any effects of blood pressure that influence these oscillations via the baroreflex. Methods and Results-We performed spectral analysis of RR, blood pressure, and respiration in 2 patients with CHF before and after LVAD implantation. LF components of the RR-interval and blood pressure variability were absent in both CHF patients before LVAD implantation. After LVAD implantation, spectral analysis of the RR interval showed restoration of a clear and predominant LF oscillation in the native hearts of both patients, with no such oscillation evident in the blood pressure profile. Conclusions-During total circulatory support with the LVAD, the LF oscillation in RR interval of the native heart, absent in CHF, is restored. This LF oscillation in RR interval occurs in the absence of LF oscillations in blood pressure and thus is unlikely to be explained by baroreflex mechanisms. Hence, the absence of LF oscillation in the RR interval in CHF is functional and is reversible by LVAD circulation. The presence of a predominant LF oscillation in RR interval independent of any oscillation in blood pressure suggests that the LF oscillation is a fundamental property of central autonomic outflow. (Circulation. 1998;98:556-561.)

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“…Endocarditis in patients with LVAD has a 50% mortality rate (7). LVAD-associated endocarditis is defined as clinical evidence of pump and/or cannula infection along with the presence of vegetation on echocardiography or a vascular phenomenon as defined by modified Duke's criteria (15).…”

Section: Endocarditis In Lvadmentioning

confidence: 99%

“…But it's strongly emphasized that eradication of fungemia with drugs alone without LVAD removal is an impossible task (15). In summary, the effective treatment methodologies for positive outcomes in patients with LVAD endocarditis were documented to be treating a patient with systemic antibiotic suppression therapy alone, LVAD replacement, LVAD transplantation and LVAD explantation without transplantation (7). More clinical data is required for a specific treatment approach for LVAD endocarditis regarding the use of just antibiotics versus device exchange and explantation.…”

Section: Managementmentioning

confidence: 99%