PATHOPHYSIOLOGIC MECHANISMS OF OBESITY-ASSOCIATED CARDIOVASCULAR DISEASE: RFA-HL-02-016

2002 ◽  
Vol 50 (3) ◽  
pp. 226-227
2020 ◽  
Vol 8 ◽  
pp. 205031212093546
Author(s):  
Theresa J Barnes ◽  
Maxwell A Hockstein ◽  
Craig S Jabaley

Cardiovascular disease remains the leading cause of death in the United States, and cardiopulmonary bypass is a cornerstone in the surgical management of many related disease states. Pathophysiologic changes associated both with extracorporeal circulation and shock can beget a syndrome of low systemic vascular resistance paired with relatively preserved cardiac output, termed vasoplegia. While increased vasopressor requirements accompany vasoplegia, related pathophysiologic mechanisms may also lead to true catecholamine resistance, which is associated with further heightened mortality. The introduction of a second non-catecholamine vasopressor, angiotensin II, and non-specific nitric oxide scavengers offers potential means by which to manage this challenging phenomenon. This narrative review addresses both the definition, risk factors, and pathophysiology of vasoplegia and potential therapeutic interventions.


Biomedicines ◽  
2021 ◽  
Vol 9 (11) ◽  
pp. 1579
Author(s):  
Ali A. Rizvi ◽  
Anca Pantea Stoian ◽  
Andrej Janez ◽  
Manfredi Rizzo

Dyslipidemia is a potent risk factor for the genesis and progression of cardiovascular disease (CVD), and both the concentration and type of low-density lipoproteins (LDL) augment this association. The small, dense LDL (sdLDL) subfraction is the subtype which is most strongly predictive of atherosclerosis and cardiovascular events. In addition to the traditionally available lipid-lowering treatment options, certain novel therapies have been shown to favorably impact sdLDL, among them the antidiabetic class of agents known as glucagon-like peptide 1 receptor agonists (GLP1-RAs). These drugs seem to alter the pathophysiologic mechanisms responsible for the formation and accumulation of atherogenic lipoprotein particles, thus potentially reducing cardiovascular outcomes. They represent a uniquely targeted therapeutic approach to reduce cardiometabolic risk and warrant further study for their beneficial nonglycemic actions.


2021 ◽  
Vol 22 (13) ◽  
pp. 6864
Author(s):  
Elena Barbu ◽  
Mihaela-Roxana Popescu ◽  
Andreea-Catarina Popescu ◽  
Serban-Mihai Balanescu

Even though the new thresholds for defining prediabetes have been around for more than ten years, there is still controversy surrounding the precise characterization of this intermediate glucose metabolism status. The risk of developing diabetes and macro and microvascular disease linked to prediabetes is well known. Still, the prediabetic population is far from being homogenous, and phenotyping it into less heterogeneous groups might prove useful for long-term risk assessment, follow-up, and primary prevention. Unfortunately, the current definition of prediabetes is quite rigid and disregards the underlying pathophysiologic mechanisms and their potential metabolic progression towards overt disease. In addition, prediabetes is commonly associated with a cluster of risk factors that worsen the prognosis. These risk factors all revolve around a common denominator: inflammation. This review focuses on identifying the population that needs to be screened for prediabetes and the already declared prediabetic patients who are at a higher risk of cardiovascular disease and require closer monitoring.


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