Anatomically specific reactive oxygen species production participates in Marfan syndrome aneurysm formation.

Marfan syndrome (MFS) is a connective tissue disorder that results in aortic root aneurysm formation. Reactive oxygen species (ROS) seem to play a role in aortic wall remodelling in MFS, although the mechanism remains unknown. MFS Fbn1 mouse root/ascending (AS) and descending (DES) aortic samples were examined using DHE staining, lucigenin-enhanced chemiluminescence (LGCL), Verhoeff's elastin-Van Gieson staining (elastin breakdown) and in situ zymography for protease activity.

Effects of Endurance Training on Detrimental Structural, Cellular, and Functional Alterations in Skeletal Muscles of Heart Failure With Preserved Ejection Fraction.

Background: Heart failure with preserved ejection fraction (HFpEF) is underpinned by detrimental skeletal muscle alterations that contribute to disease severity, yet underlying mechanisms and therapeutic treatments remain poorly established. This study used a nonhuman animal model of HFpEF to better understand whether skeletal muscle abnormalities were (1) fiber-type specific and (2) reversible by various exercise training regimes.

Methods And Results: Lean control rats were compared with obese ZSF1 rats at 20 weeks and then 8 weeks after sedentary, high-intensity interval training, or moderate continuous treadmill exercise.

Exercise Training Reveals Inflexibility of the Diaphragm in an Animal Model of Patients With Obesity-Driven Heart Failure With a Preserved Ejection Fraction.

Background: Respiratory muscle weakness contributes to exercise intolerance in patients with heart failure with a preserved ejection fraction (HFpEF)-a condition characterized by multiple comorbidities with few proven treatments. We aimed, therefore, to provide novel insight into the underlying diaphragmatic alterations that occur in HFpEF by using an obese cardiometabolic rat model and further assessed whether exercise training performed only after the development of overt HFpEF could reverse impairments.

Methods And Results: Obese ZSF1 rats (n=12) were compared with their lean controls (n=8) at 20 weeks, with 3 additional groups of obese ZSF1 rats compared at 28 weeks following 8 weeks of either sedentary behavior (n=13), high-intensity interval training (n=11), or moderate-continuous training (n=11).

Small-molecule inhibition of MuRF1 attenuates skeletal muscle atrophy and dysfunction in cardiac cachexia.

Background: Muscle ring finger 1 (MuRF1) is a muscle-specific ubiquitin E3 ligase activated during clinical conditions associated with skeletal muscle wasting. Yet, there remains a paucity of therapeutic interventions that directly inhibit MuRF1 function, particularly in vivo. The current study, therefore, developed a novel compound targeting the central coiled coil domain of MuRF1 to inhibit muscle wasting in cardiac cachexia.

Exercise Training Reverses Extrapulmonary Impairments in Smoke-exposed Mice.

Purpose: Cigarette smoking is the main risk factor for chronic obstructive pulmonary disease and emphysema. However, evidence on the extrapulmonary effects of smoke exposure that precede lung impairments remains unclear at present, as are data on nonpharmacological treatments such as exercise training.

Methods: Three groups of mice, including control (n = 10), smoking (n = 10), and smoking with 6 wk of high-intensity interval treadmill running (n = 11), were exposed to 20 wk of fresh air or whole-body cigarette smoke.

Exercise Training Prevents Diaphragm Contractile Dysfunction in Heart Failure.

Purpose: Patient studies have demonstrated the efficacy of exercise training in attenuating respiratory muscle weakness in chronic heart failure (HF), yet direct assessment of muscle fiber contractile function together with data on the underlying intracellular mechanisms remains elusive. The present study, therefore, used a mouse model of HF to assess whether exercise training could prevent diaphragm contractile fiber dysfunction by potentially mediating the complex interplay between intracellular oxidative stress and proteolysis.

Methods: Mice underwent sham operation (n = 10) or a ligation of the left coronary artery and were randomized to sedentary HF (n = 10) or HF with aerobic exercise training (HF + AET; n = 10).

High-intensity interval training prevents oxidant-mediated diaphragm muscle weakness in hypertensive mice.

Hypertension is a key risk factor for heart failure, with the latter characterized by diaphragm muscle weakness that is mediated in part by increased oxidative stress. In the present study, we used a deoxycorticosterone acetate (DOCA)-salt mouse model to determine whether hypertension could independently induce diaphragm dysfunction and further investigated the effects of high-intensity interval training (HIIT). Sham-treated (n = 11), DOCA-salt-treated (n = 11), and DOCA-salt+HIIT-treated (n = 15) mice were studied over 4 wk.

Presence and extent of coronary artery disease as predictor for AF recurrences after catheter ablation: The Leipzig Heart Center AF Ablation Registry.

Background: Occlusion of the right coronary artery (RCA) may promote atrial fibrillation (AF) by creating a right atrial substrate. However, the presence and extent of coronary artery disease (CAD) is usually not considered to tailor AF ablation strategies. This study was aimed to analyze the possible association between the presence and extent of CAD and rhythm outcomes of left-atrial AF catheter ablation.

Diaphragm muscle weakness in mice is early-onset post-myocardial infarction and associated with elevated protein oxidation.

Heart failure induced by myocardial infarction (MI) causes diaphragm muscle weakness, with elevated oxidants implicated. We aimed to determine whether diaphragm muscle weakness is 1) early-onset post-MI (i.e.

Septic vegetation at the left atrial appendage entrance after pulmonary vein ablation for atrial fibrillation.

Pulmonary vein (PV) ablation is increasingly used to treat highly symptomatic atrial fibrillation. Here, we present a case of infective endocarditis (IE) after PV ablation at the uncommon position of the left atrial appendage entrance. We conclude that iatrogenic intracardial manipulation may create predisposing lesions for IE.

Free-hand four-dimensional echocardiography: a diagnostic tool in coronary artery disease.

Direct echocardiographic visualization of coronary arteries has been difficult due to the inherent problems involved in obtaining ultrasound access. We used freehand four-dimensional echocardiography in a 79-year-old patient with a trifurcational stenosis. We were able to identify a 6 x 11 mm possibly subintimal atheromathous plaque and to measure the diameters of the left descending coronary artery before, in, and behind the stenosis.

Atypical Bland-White-Garland syndrome: a 58-year-old woman with stenosis of the pulmonary origin of the left coronary artery.

Unlabelled: The anomalous origin of the left coronary artery from the main pulmonary trunk (also known as Bland-White-Garland syndrome) is a rare congenital malformation that occurs in 0.4% of patients with cardiac anomalies. We present an adult case (a 58-year-old woman) of atypical Bland-White-Garland syndrome.

Spontaneous echo contrast caused by platelet and leukocyte aggregates?

Background And Purpose: Spontaneous echocardiographic contrast (SEC) is correlated to clinical thromboembolic events. We sought to determine the origin of SEC by utilizing direct analysis of left atrial blood.

Methods: We examined the blood of 13 patients with and 19 without SEC.