The association between hypertension and chronic renal disease is well known. The pathogenesis of hypertension in patients with chronic kidney disease (CKD) is complex and multifactorial, which may explain why it is resistant to treatment. The traditional paradigm is that hypertension in CKD is due either to an excess of intravascular volume (volume dependent) or to excessive activation of the renin-angiotensin system in relation to the state of sodium/volume balance (renin-dependent hypertension). This review focuses on the importance of less established mechanisms, such as increased activity of the sympathetic nervous system, increased endothelin production, decreased availability of endothelium-derived vasodilators and structural changes of the arteries, renal ischemia, and sleep apnea.
Introduction:While the role of inflammation in acute coronary events is well established, the impact of inflammatory-mediated vulnerability of coronary plaques from the entire coronary tree, on the extension of ventricular remodeling and scaring, has not been clarified yet.Materials and methods:The present manuscript describes the procedures of the VIABILITY trial, a descriptive prospective single-center cohort study. The main purpose of this trial is to assess the link between systemic inflammation, pan-coronary plaque vulnerability (referring to the plaque vulnerability within the entire coronary tree), myocardial viability and ventricular remodeling in patients who had suffered a recent ST-segment elevation acute myocardial infarction (STEMI). One hundred patients with STEMI who underwent successful revascularization of the culprit lesion in the first 12 hours after the onset of symptoms will be enrolled in the study. The level of systemic inflammation will be evaluated based on the serum biomarker levels (hs-CRP, matrix metalloproteinases, interleukin-6) in the acute phase of the myocardial infarction (MI) and at 1 month. Pan-coronary plaque vulnerability will be assessed based on serum biomarkers known to be associated with increased plaque vulnerability (V-CAM or I-CAM) and at 1 month after infarction, based on computed tomographic angiography analysis of vulnerability features of all coronary plaques. Myocardial viability and remodeling will be assessed based on 3D speckle tracking echocardiography associated with dobutamine infusion and LGE-CMR associated with post-processing imaging methods. The study population will be categorized in 2 subgroups: subgroup 1 - subjects with STEMI and increased inflammatory response at 7 days after the acute event (hs-CRP ≥ 3 mg/dl), and subgroup 2 - subjects with STEMI and no increased inflammatory response at 7 days (hs-CRP < 3 mg/dl). Study outcomes will consist in the rate of post-infarction heart failure development and the major adverse events (MACE) rate.Conclusion:VIABILITY is the first prospective study designed to evaluate the influence of infarct-related inflammatory response on several major determinants of post-infarction outcomes, such as coronary plaque vulnerability, myocardial viability, and ventricular remodeling.
With coronary artery disease (CAD) projected to remain the leading cause of global mortality, prevention strategies seem to be the only effective approach able to reduce the burden and improve mortality and morbidity. At this moment, diagnostic strategies focus mainly on symptomatic patients, ignoring the occurrence of major cardiovascular events as the only manifestation of CAD. As two thirds of fatal myocardial infarction are resulting from plaque rupture, an approach based on the "vulnerable plaque" concept is mandatory in order to improve patient diagnosis, treatment, and, by default, prognosis. Given that the main studies focus on a plaque-centered approach, this is a prospective observational study that will perform a complex assessment of the features that characterize unstable coronary lesions, in terms of both local assessment via specific coronary computed tomography angiography markers of coronary plaque vulnerability and systemic approach based on serological markers of systemic inflammation in patients proved to be "vulnerable" by developing acute cardiovascular events.
Decades of research and experimental studies have investigated various strategies to prevent acute coronary events. However, significantly efficient preventive methods have not been developed and still remains a challenge to determine if a coronary atherosclerotic plaque will become vulnerable and unstable. This review aims to assess the significance of plaque vulnerability markers, more precisely the role of spotty calcifications in the development of major cardiac events, given that coronary calcification is a hallmark of atherosclerosis. Recent studies have suggested that microcalcifications, spotty calcifications, and the presence of the napkin-ring sign are predictive vulnerable plaque features, and their presence may cause plaque instability.
Atherosclerosis is a slow, progressive disease, its most common manifestation and most severe consequence being coronary artery disease, one of the main causes of mortality and morbidity worldwide. The vast majority of cardiovascular deaths are caused by complications of atherosclerosis, most often being represented by the rupture of an unstable coronary plaque, regularly triggered by inflammation. A vulnerable plaque is characterized by a large, lipid-rich necrotic core, a thin fibrous cap with macrophage infiltration, and the presence of multiple specific biomarkers such as positive remodeling, irregular calcifications, and low attenuation visible with coronary computed tomography angiography (CCTA). Identifying biomarkers that could predict the risk of plaque rupture with high accuracy would be a significant advance in predicting acute cardiac events in asymptomatic patients, furthermore guiding treatment of patients with this disease. The main indication of noninvasive imaging is to identify patients at risk based on the presence or absence of symptoms that can be related to myocardial ischemia. The diagnostic objective is to confirm or to exclude the presence of coronary plaques. Coronary imaging in asymptomatic individuals is used to estimate the risk of future cardiac events through the identification of non-obstructive high-risk plaques. The possibility to monitor the evolution of vulnerable plaques via noninvasive imaging techniques, prior to the occurrence of an acute clinical event, is the main goal in plaque imaging. This manuscript will be focusing on recent advances of noninvasive imaging of vulnerable coronary plaques.
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