scholarly journals Myocardial Cell Death and Regeneration during Progression of Cardiac Hypertrophy to Heart Failure

2004 ◽  
Vol 279 (50) ◽  
pp. 52630-52642 ◽  
Author(s):  
Sagartirtha Sarkar ◽  
Mamta Chawla-Sarkar ◽  
David Young ◽  
Kazutoshi Nishiyama ◽  
Mary E. Rayborn ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cell Death ◽  
Cardiac Hypertrophy ◽  
Disease Process ◽  
Myocardial Damage ◽  
Myocardial Cell ◽  
Mouse Heart ◽  
Ki 67 ◽  
End Stage Heart Failure ◽  
End Stage

Cardiac hypertrophy and ensuing heart failure are among the most common causes of mortality worldwide, yet the triggering mechanisms for progression of hypertrophy to failure are not fully understood. Tissue homeostasis depends on proper relationships between cell proliferation, differentiation, and death and any imbalance between them results in compromised cardiac function. Recently, we developed a transgenic (Tg) mouse model that overexpress myotrophin (a 12-kDa protein that stimulates myocyte growth) in heart resulting in hypertrophy that progresses to heart failure. This provided us an appropriate model to study the disease process at any point from initiation of hypertrophy end-stage heart failure. We studied detailed apoptotic signaling and regenerative pathways and found that the Tg mouse heart undergoes myocyte loss and regeneration, but only at a late stage (during transition to heart failure). Several apoptotic genes were up-regulated in 9-month-old Tg hearts compared with age-matched wild type or 4-week-old Tg hearts. Cardiac cell death during heart failure involved activation of Fas, tumor necrosis factor-α, and caspases 9, 8, and 3 and poly(ADP-ribose) polymerase cleavage. Tg mice with hypertrophy associated with compromised functionshowedsignificantup-regulationofcyclins,cyclin-dependent kinases (Cdks), and cell regeneration markers in myocytes. Furthermore, in human failing and nonfailing hearts, similar observations were documented including induction of active caspase 3 and Ki-67 proteins in dilated cardiomyopathic myocytes. Taken together, our data suggest that the stress of extensive myocardial damage from longstanding hypertrophy may cause myocytes to reenter the cell cycle. We demonstrate, for the first time in an animal model, that cell death and regeneration occur simultaneously in myocytes during end-stage heart failure, a phenomenon not observed at the onset of the disease process.

Nutrition Management in Mechanical Circulatory Support

2019 ◽  
Author(s):  
Dane A Coyne ◽  
Mitali P Shah ◽  
Kris M Mogensen ◽  
John C Klick
Keyword(s):  
Heart Failure ◽  
Cardiogenic Shock ◽  
Nutritional Support ◽  
Mechanical Circulatory Support ◽  
Disease Process ◽  
Circulatory Support ◽  
Mechanical Support ◽  
Number Of Patients ◽  
End Stage Heart Failure ◽  
End Stage

Heart failure is a devastating progressive disease process that is rising in incidence throughout the world. For patients with end-stage heart failure, orthotopic heart transplantation had been the only therapeutic option. Unfortunately, the number of patients requiring such therapy far exceeds the number of available organs. Recent advancements in technology have made implantable cardiac assist devices a reality. Outcomes with these devices are superior to maximal medical therapy and may serve either as a bridge to the availability of a donor organ or as “destination” therapy for the patient with end-stage heart failure. In addition, new technology can also provide temporary mechanical support for patients with acute decompensated cardiogenic shock, allowing preservation of end-organ function until more definitive long-term mechanical support can be coordinated. Patients with end-stage heart failure experience unique nutritional challenges. Mechanical circulatory support adds yet another unique dimension to the nutritional support challenges of this patient population. This review contains 2 figures, 5 tables, and 29 references. Key words: cardiogenic shock, enteral nutrition, extracorporeal membrane oxygenation, heart failure, mechanical circulatory support, nutritional support, parenteral nutrition, ventricular assist device

scholarly journals Expression of Concern: Myocardial cell death and regeneration during progression of cardiac hypertrophy to heart failure.

2020 ◽  
Vol 295 (10) ◽  
pp. 3386-3386
Author(s):  
Sagartirtha Sarkar ◽  
Mamta Chawla-Sarkar ◽  
David Young ◽  
Kazutoshi Nishiyama ◽  
Mary E. Rayborn ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cell Death ◽  
Cardiac Hypertrophy ◽  
Myocardial Cell

Increased expression of poly(ADP-ribose) polymerase-1 contributes to caspase-independent myocyte cell death during heart failure

2005 ◽  
Vol 288 (2) ◽  
pp. H486-H496 ◽  
Author(s):  
Jyothish B. Pillai ◽  
Hyde M. Russell ◽  
Jai Raman ◽  
Valluvan Jeevanandam ◽  
Mahesh P. Gupta
Keyword(s):  
Heart Failure ◽  
Cell Death ◽  
Cardiac Hypertrophy ◽  
Genome Stability ◽  
Cell Cycle Progression ◽  
Primary Cultures ◽  
Parp Cleavage ◽  
Aortic Banding ◽  
Hypertrophic Response ◽  
End Stage

Poly(ADP-ribose) polymerase-1 (PARP-1) plays a pivotal role in regulating genome stability, cell cycle progression, and cell survival. However, overactivation of PARP has been shown to contribute to cell death and organ failure in various stress-related disease conditions. In this study, we examined the role of PARP in the development and progression of cardiac hypertrophy. We measured the expression of PARP in mouse hearts with physiological (swimming exercise) and pathological (aortic banding) cardiac hypertrophy as well as in human heart samples taken at the time of transplantation. PARP levels were elevated both in swimming and banded mice hearts and demonstrated a linear positive correlation with the degree of cardiac hypertrophy. A dramatic increase (4-fold) of PARP occurred in 6-wk banded mice, accompanied by apparent signs of ventricular dilation and myocyte cell death. PARP levels were also elevated (2- to 3-fold) in human hearts with end-stage heart failure compared with controls. However, we found no evidence of caspase-mediated PARP cleavage in either mouse or human failing hearts. Overexpression of PARP in primary cultures of cardiac myocytes led to suppression of gene expression and robust myocyte cell death. Furthermore, data obtained from the analysis of PARP knockout mice revealed that these hearts produce an attenuated hypertrophic response to aortic banding compared with controls. Together, these results demonstrate a role for PARP in the onset and progression of cardiac hypertrophy and suggest that some events related to cardiac hypertrophy growth and progression to heart failure are mediated by a PARP-dependent mechanism.

Surgical Therapy of End-Stage Heart Failure: Understanding Cell-Mediated Mechanisms Interacting with Myocardial Damage

2011 ◽  
Vol 34 (7) ◽  
pp. 529-545
Author(s):  
Ali Ghodsizad ◽  
Mathias Loebe ◽  
Christoph Piechaczek ◽  
Viktor Bordel ◽  
Matthias N. Ungerer ◽  
...  
Keyword(s):  
Heart Failure ◽  
Surgical Therapy ◽  
Myocardial Damage ◽  
End Stage Heart Failure ◽  
End Stage

Nutrition Management in Mechanical Circulatory Support

2019 ◽  
Author(s):  
Dane A Coyne ◽  
Mitali P Shah ◽  
Kris M Mogensen ◽  
John C Klick
Keyword(s):  
Heart Failure ◽  
Cardiogenic Shock ◽  
Nutritional Support ◽  
Mechanical Circulatory Support ◽  
Disease Process ◽  
Circulatory Support ◽  
Mechanical Support ◽  
Number Of Patients ◽  
End Stage Heart Failure ◽  
End Stage

Heart failure is a devastating progressive disease process that is rising in incidence throughout the world. For patients with end-stage heart failure, orthotopic heart transplantation had been the only therapeutic option. Unfortunately, the number of patients requiring such therapy far exceeds the number of available organs. Recent advancements in technology have made implantable cardiac assist devices a reality. Outcomes with these devices are superior to maximal medical therapy and may serve either as a bridge to the availability of a donor organ or as “destination” therapy for the patient with end-stage heart failure. In addition, new technology can also provide temporary mechanical support for patients with acute decompensated cardiogenic shock, allowing preservation of end-organ function until more definitive long-term mechanical support can be coordinated. Patients with end-stage heart failure experience unique nutritional challenges. Mechanical circulatory support adds yet another unique dimension to the nutritional support challenges of this patient population. This review contains 2 figures, 5 tables, and 29 references. Key words: cardiogenic shock, enteral nutrition, extracorporeal membrane oxygenation, heart failure, mechanical circulatory support, nutritional support, parenteral nutrition, ventricular assist device

scholarly journals Withdrawal: Myocardial cell death and regeneration during progression of cardiac hypertrophy to heart failure.

2020 ◽  
Vol 295 (45) ◽  
pp. 15425-15425
Author(s):  
Sagartirtha Sarkar ◽  
Mamta Chawla-Sarkar ◽  
David Young ◽  
Kazutoshi Nishiyama ◽  
Mary E. Rayborn ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cell Death ◽  
Cardiac Hypertrophy ◽  
Myocardial Cell

Programmed Cell Death (Apoptosis) in the Myocardium with Acute Myocarditis.

1997 ◽  
Vol 3 (S2) ◽  
pp. 63-64
Author(s):  
T. Nishikawa ◽  
S. Ishiyama ◽  
K. Takeda ◽  
T. Kasajima ◽  
S. Abe ◽  
...  
Keyword(s):  
Cell Death ◽  
Acute Myocarditis ◽  
Cytotoxic T Cells ◽  
Viral Myocarditis ◽  
Myocardial Damage ◽  
Myocardial Cell ◽  
Heart Tissue ◽  
Autoimmune Myocarditis ◽  
Tissue Specimens ◽  
End Stage

Acute myocarditis is a potentially lethal disease. However, the precise mechanism of myocardial damage in myocarditis is still unknown, although its pathogenesis seems to be involved in the result of natural killer cells, cytotoxic T cells and autoantibodies. Recently, it has been reported that programmed death of cardiac myocytes can be induced by several pathological conditions including infarction and end-stage cardiac failure. However, little is known about the myocardial cell death in myocarditis. In this study, we investigated whether myocardial cell death via apoptosis occurs in the heart tissue with myocarditis.Since it has been reported that the pathogenesis of the tissue damage in viral myocarditis resembles that in experimental autoimmune myocarditis induced by myosin, we used an experimental model for autoimmune myocarditis induced in Lewis rat with the use of myosin as the antigen. Rats were sacrificed on days 14, 17 and 21 after myosin injection. The tissue specimens were taken from ventricle of the heart.

Localization of endothelial nitric oxide synthase in the normal and failing human atrial myocardium

1996 ◽  
Vol 54 ◽  
pp. 786-787
Author(s):  
Chi-Ming Wei ◽  
Margarita Bracamonte ◽  
Shi-Wen Jiang ◽  
Richard C. Daly ◽  
Christopher G.A. McGregor ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Cardiac Tissues ◽  
Mammalian Tissues ◽  
End Stage Heart Failure ◽  
End Stage ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Nitric oxide (NO) is a potent endothelium-derived relaxing factor which also may modulate cardiomyocyte inotropism and growth via increasing cGMP. While endothelial nitric oxide synthase (eNOS) isoforms have been detected in non-human mammalian tissues, expression and localization of eNOS in the normal and failing human myocardium are poorly defined. Therefore, the present study was designed to investigate eNOS in human cardiac tissues in the presence and absence of congestive heart failure (CHF).Normal and failing atrial tissue were obtained from six cardiac donors and six end-stage heart failure patients undergoing primary cardiac transplantation. ENOS protein expression and localization was investigated utilizing Western blot analysis and immunohistochemical staining with the polyclonal rabbit antibody to eNOS (Transduction Laboratories, Lexington, Kentucky).

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