Results 141 to 150 of about 553,316 (296)

Increased calcification by erythrophagocytosis in aortic valvular interstitial cells

open access: yesESC Heart Failure, Volume 12, Issue 2, Page 1469-1473, April 2025.
Abstract Background Calcific aortic valve disease (CAVD) progresses over time to severe aortic stenosis and eventually heart failure. Recent evidence indicates that intraleaflet haemorrhage (ILH) strongly promotes CAVD progression. However, it remains poorly understood how it mechanistically contributes to valvular calcification.
Zihan Qin   +3 more
wiley   +1 more source

Incidence and long-term outcomes of dextro-transposition of the great arteries (d-TGA) in the Kingdom of Bahrain

open access: yesFrontiers in Cardiovascular Medicine
BackgroundDextro-Transposition of the Great Arteries (d-TGA) is a rare cyanotic congenital heart defect requiring surgical correction for survival. The arterial switch operation (ASO) is the preferred approach, offering favorable long-term outcomes ...
Ahmed J. AlAraibi   +5 more
doaj   +1 more source

Surgical Treatment of Biventricular Outflow Tract Obstruction in Hypertrophic Cardiomyopathy

open access: yes, 2019
ObjectivesHypertrophic cardiomyopathy is usually associated with left ventricular outflow tract obstruction. It is rare to have a concomitant obstruction of the right ventricular outflow tract requiring resection.
Rodrigo Zea-Vera (6797252)   +4 more
core   +1 more source

Myocardial inflammation is associated with impaired mitochondrial oxidative capacity in ischaemic cardiomyopathy

open access: yesESC Heart Failure, Volume 12, Issue 2, Page 1246-1255, April 2025.
Abstract Aims Myocardial inflammation and impaired mitochondrial oxidative capacity are hallmarks of heart failure (HF) pathophysiology. The extent of myocardial inflammation in patients suffering from ischaemic cardiomyopathy (ICM) or dilated cardiomyopathy (DCM) and its association with mitochondrial energy metabolism are unknown.
Julius Borger   +15 more
wiley   +1 more source

Metabolic abnormalities and reprogramming in cats with naturally occurring hypertrophic cardiomyopathy

open access: yesESC Heart Failure, Volume 12, Issue 2, Page 1256-1270, April 2025.
Abstract Background and aims The heart is a metabolic organ rich in mitochondria. The failing heart reprograms to utilize different energy substrates, which increase its oxygen consumption. These adaptive changes contribute to increased oxidative stress.
Qinghong Li   +12 more
wiley   +1 more source

Considerations for drug trials in hypertrophic cardiomyopathy

open access: yesESC Heart Failure, Volume 12, Issue 2, Page 1095-1112, April 2025.
Abstract Hypertrophic cardiomyopathy (HCM) is a heterogeneous condition with potentially serious manifestations. Management has traditionally comprised therapies to palliate symptoms and implantable cardioverter‐defibrillators to prevent sudden cardiac death. The need for disease‐modifying therapies has been recognized for decades.
John P. Farrant   +17 more
wiley   +1 more source

Left ventricular outflow obstruction in rhabdomyoma of infancy: meta-analysis of the literature

open access: yes, 2003
Primary heart tumors are exceptional in infants and children. Most common is the rhabdomyoma, often associated with tuberous sclerosis (Bourneville's disease).
Matthys, Dirk   +6 more
core   +1 more source

A phenomap of TTR amyloidosis to aid diagnostic screening

open access: yesESC Heart Failure, Volume 12, Issue 2, Page 1113-1118, April 2025.
Abstract Cardiac amyloidosis due to transthyretin (ATTR) remains an underdiagnosed cause of cardiomyopathy. As awareness of the disease grows and referrals for ATTR increase, clinicians are likely to encounter more atypical forms of the condition in clinical practice.
Alexios S. Antonopoulos   +4 more
wiley   +1 more source

Ventricular diastolic filling indices in pulmonary stenosis

open access: yesThe Turkish Journal of Pediatrics, 2000
Children with valvar pulmonary stenosis have right ventricular diastolic filling abnormalities that may be due to either right ventricular hypertrophy or right ventricular outflow obstruction.
F A Paç   +3 more
doaj  

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