Cardiovascular events, diabetes and guidelines: the virtue of simplicity

Abstract

Cardiovascular (CV) events or their minor syndromes, as various forms of ischemia, are medical emergencies that do not allow enough time for a guiding anamnesis or proper clinical examination, and lead to relying on Treatment Guidelines, but in many situations it is appropriate to deviate from them. Pathological studies have associated 75% of coronary artery events with atherosclerotic plaque rupture; it is now known that rupture alone is not enough for obstruction or occlusion of the vessel lumen. Concomitant conditions are required for the clinical manifestation of cardiovascular disease, including prothrombogenic and dysfunctional endothelium, less fibrinolytic capacity to protect it, increased platelet activation, increased adrenergic tone, microcirculation vasoconstriction, and other countless factors that contribute to thrombus formation, causing ischemia or infarction. But in most cases, repair of plaque rupture and re endothelization of the lesion are asymptomatic and silent. Atherosclerotic process is a chronic and progressive immune inflammation. Most of the therapeutic indications include statins, which cause side effects in 10% of patients, with a range varying between 7 and 21%, according to different authors. Many investigators have proved that statin use contribute to the genesis of diabetes, reports vary between 1 and 46%, where marked elevation of blood glucose fasting levels and glycosylated hemoglobin have been observed, be it by increased tissue resistance to insulin or by reduced β-cell insulin secretion. Physicians should base their indications on the recommendations provided by Guidelines, but they should not forget that every patient is different, and they should not get confused due to lack of time in an emergency nor be influenced by the latest publications or techniques until they have been properly tested.

Hyperglycemia, inflammatory response and infarct size in obstructive acute myocardial infarction and MINOCA

“…This subgroup of hyperglycemic subjects exhibited an “inflammatory status” as expressed by increased levels of all measured inflammatory markers. High values of NLR, NPR, PLR and CRP had been previously described in this setting, and our results are in line with the existing literature, confirming the relationship between glycemic disorders and inflammation in the context of obs-AMI [ 22 , 23 ]. Indeed, the activation of inflammatory mediators and pathways is vastly described as a cornerstone of atherosclerosis [ 24 ], not only in terms of chronic arterial remodelling but also favouring plaque instability and rupture [ 25 ].…”

“…In fact, not only does hyperglycemia amplify the inflammatory cascade, but it is also promoted by the inflammatory process itself throughout the generation of insulin-resistance and gluconeogenesis [ 30 – 32 ]. As a result, the interplay between hyperglycemia and inflammation triggers a vicious circle, ultimately leading to a heightened atherosclerotic burden and plaque rupture [ 33 ] with an increased mortality risk [ 1 , 23 , 34 ].…”

Shenlian Extract Against Myocardial Injury Induced by Ischemia Through the Regulation of NF-κB/IκB Signaling Axis

“…Previous pathological studies have shown that IHD and acute myocardial infarction, as main clinical manifestations, have increasingly become a major cause of death (Zhao et al, 2019). IHD and acute myocardial infarctions are associated with atherosclerosis (Esper and Nordaby, 2019), a chronic inflammatory disease that is characterized by the development of cholesterol-rich arterial plaques (Stary et al, 1994) due to several factors, such as hyperlipidaemia, inflammation, oxidative stress, and immune cell infiltration (Viola and Soehnlein, 2015;Libby et al, 2016). Ischemia and necrotic cardiomyocytes would trigger early inflammation through IL-1b signaling and the NF-kB pathway (Latet et al, 2015;Sager et al, 2017;Michels et al, 2019).…”

Peripheral arterial endothelial dysfunction predicts future cardiovascular events in diabetic patients with albuminuria: a prospective cohort study

“…PED was defined as RHI < 1.67. Primary outcome was composed of 3-point major adverse cardiovascular events (MACE); secondary outcome was a composite of 3-point MACE, hospitalization for heart failure, or chronic kidney disease (CKD) Model 1: adjusted for age, sex, hypertension, HbA1c, LDL cholesterol, triglyceride, proteinuria, duration of diabetes, and premedical history of ischemic events Model 2: adjusted for systolic blood pressure, baseline e-GFR, anti-platelet agents, and smoking history in addition to Model 1 1 CKD progression defined as decrease from baseline in eGFR by 30% or more to an eGFR of less than 60 mL/min per 1.73 m 2 , or an eGFR of less than 30 mL/min per 1.73 m 2 during the follow-up period * Comparison the number of events between those with and without PED factors, [31,32], the determination of ASCVD risk by PED in addition to CAC should be further investigated [33][34][35]. Low RHI was reported not only in diabetes [13,[36][37][38] but also in metabolic syndrome [39] and nonalcoholic fatty liver disease [40].…”