The role of systolic–diastolic coupling in distinguishing impaired diastolic recoil in healthy aging and heart failure with preserved ejection fraction

2021 ◽  
Author(s):  
James P. MacNamara ◽  
Vivek Koshti ◽  
I‐Jou Cheng ◽  
Katrin A. Dias ◽  
Christopher M. Hearon ◽  
...  
2010 ◽  
Vol 6 (2) ◽  
pp. 33 ◽  
Author(s):  
Christopher R deFilippi ◽  
G Michael Felker ◽  
◽  

For many with heart failure, including the elderly and those with a preserved ejection fraction, both risk stratification and treatment are challenging. For these large populations and others there is increasing recognition of the role of cardiac fibrosis in the pathophysiology of heart failure. Galectin-3 is a novel biomarker of fibrosis and cardiac remodelling that represents an intriguing link between inflammation and fibrosis. In this article we review the biology of galectin-3, recent clinical research and its application in the management of heart failure patients.


Author(s):  
Monil Majmundar ◽  
Rajkumar Doshi ◽  
Harshvardhan Zala ◽  
Palak Shah ◽  
Devina Adalja ◽  
...  

2021 ◽  
pp. postgradmedj-2021-139933
Author(s):  
Akash Batta ◽  
Ganesh Kasinadhuni ◽  
Manphool Singhal ◽  
Pankaj Malhotra ◽  
Rajesh Vijayvergiya

2018 ◽  
Vol 131 (12) ◽  
pp. 1473-1481 ◽  
Author(s):  
Phillip H. Lam ◽  
Neha Gupta ◽  
Daniel J. Dooley ◽  
Steven Singh ◽  
Prakash Deedwania ◽  
...  

Author(s):  
Gabriele G Schiattarella ◽  
Daniele Rodolico ◽  
Joseph A Hill

Abstract One in 10 persons in the world aged 40 years and older will develop the syndrome of HFpEF (heart failure with preserved ejection fraction), the most common form of chronic cardiovascular disease for which no effective therapies are currently available. Metabolic disturbance and inflammatory burden contribute importantly to HFpEF pathogenesis. The interplay within these two biological processes is complex; indeed, it is now becoming clear that the notion of metabolic inflammation—metainflammation—must be considered central to HFpEF pathophysiology. Inflammation and metabolism interact over the course of syndrome progression, and likely impact HFpEF treatment and prevention. Here, we discuss evidence in support of a causal, mechanistic role of metainflammation in shaping HFpEF, proposing a framework in which metabolic comorbidities profoundly impact cardiac metabolism and inflammatory pathways in the syndrome.


2019 ◽  
Vol 40 (16) ◽  
pp. 1287-1293 ◽  
Author(s):  
Maarten P van den Berg ◽  
Bart A Mulder ◽  
Sebastiaan H C Klaassen ◽  
Alexander H Maass ◽  
Dirk J van Veldhuisen ◽  
...  

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