Fibrosis in Hypertrophic Cardiomyopathy Patients With and Without Sarcomere Gene Mutations.

Background: Patients with hypertrophic cardiomyopathy (HCM) and an identified sarcomere mutation have worse outcomes than those without though the underlying mechanism is incompletely understood. The presence of replacement fibrosis measured by late gadolinium enhancement (LGE) and diffuse fibrosis measured by extracellular volume (ECV) using cardiac magnetic resonance imaging (CMR) are associated with ventricular arrhythmias and cardiac mortality. We aimed to associate these two forms of fibrosis with identified sarcomere mutations.

Investigation of Aortic Wall Thickness, Stiffness and Flow Reversal in Patients With Cryptogenic Stroke: A 4D Flow MRI Study.

Background: Stroke etiology is undetermined in approximately one-sixth to one-third of patients. The presence of aortic flow reversal and plaques in the descending aorta (DAo) has been identified as a potential retrograde embolic mechanism.

Purpose: To assess the relationships between aortic stiffness, wall thickness, and flow reversal in patients with cryptogenic stroke and healthy controls.

Renin Angiotensin System Inhibitors Reduce Aortic Stiffness and Flow Reversal After a Cryptogenic Stroke.

Background: Blood flow reversal is a possible mechanism for retrograde embolism in the setting of high-risk atherosclerotic plaques in the descending aorta (DAo). Evidence suggests that pulse wave velocity (PWV) is a determinant of blood flow reversal and can be reduced by the destiffening effect of renin-angiotensin system inhibitors (RASI).

Purpose: To evaluate the impact of antihypertensive therapy on in vivo changes in PWV and flow reversal in patients with cryptogenic stroke.

Aldosterone, inactive matrix gla-protein, and large artery stiffness in hypertension.

Vascular calcification leads to increased large artery stiffness. Matrix gla-protein (MGP) is a vitamin K-dependent protein that inhibits arterial calcification. Aldosterone promotes vascular calcification and stiffness, but the relationships between aldosterone, MGP, and arterial stiffness are unknown.

Poor Glycemic Control Is Associated With Increased Extracellular Volume Fraction in Diabetes.

Objective: We assessed whether poor glycemic control is associated with an increase in myocardial fibrosis among adults with diabetes.

Research Design And Methods: We studied 47 adults with type 2 diabetes and stratified them into three groups according to their hemoglobin A1c (HbA) level: <6.5% (group 1; = 12), 6.

Late Systolic Myocardial Loading Is Associated With Left Atrial Dysfunction in Hypertension.

Background: Late systolic load has been shown to cause diastolic dysfunction in animal models. Although the systolic loading sequence of the ventricular myocardium likely affects its coupling with the left atrium (LA), this issue has not been investigated in humans. We aimed to assess the relationship between the myocardial loading sequence and LA function in human hypertension.

Beta-Blocker Use Is Associated With Impaired Left Atrial Function in Hypertension.

Background: Impaired left atrial (LA) mechanical function is present in hypertension and likely contributes to various complications, including atrial arrhythmias, stroke, and heart failure. Various antihypertensive drug classes exert differential effects on central hemodynamics and left ventricular function. However, little is known about their effects on LA function.

Inactive Matrix Gla-Protein and Arterial Stiffness in Type 2 Diabetes Mellitus.

Background: Large artery stiffness is increased in diabetes mellitus and causes an excessive pulsatile load to the heart and to the microvasculature. The identification of pathways related to arterial stiffness may provide novel therapeutic targets to ameliorate arterial stiffness in diabetes. Matrix Gla-Protein (MGP) is an inhibitor of vascular calcification.

Heart Failure, Left Ventricular Remodeling, and Circulating Nitric Oxide Metabolites.

Background: Stable plasma nitric oxide (NO) metabolites (NO), composed predominantly of nitrate and nitrite, are attractive biomarkers of NO bioavailability. NO levels integrate the influence of NO-synthase-derived NO production/metabolism, dietary intake of inorganic nitrate/nitrite, and clearance of NO. Furthermore, nitrate and nitrite, the most abundant NO, can be reduced to NO via the nitrate-nitrite-NO pathway.