Coronavirus disease 2019 (COVID-19) has been reported to cause cardiovascular complications such as myocardial injury, thromboembolic events, arrhythmia, and heart failure. Multiple mechanisms—some overlapping, notably the role of inflammation and IL-6—potentially underlie these complications. The reported cardiac injury may be a result of direct viral invasion of cardiomyocytes with consequent unopposed effects of angiotensin II, increased metabolic demand, immune activation, or microvascular dysfunction. Thromboembolic events have been widely reported in both the venous and arterial systems that have attracted intense interest in the underlying mechanisms. These could potentially be due to endothelial dysfunction secondary to direct viral invasion or inflammation. Additionally, thromboembolic events may also be a consequence of an attempt by the immune system to contain the infection through immunothrombosis and neutrophil extracellular traps. Cardiac arrhythmias have also been reported with a wide range of implicated contributory factors, ranging from direct viral myocardial injury, as well as other factors, including at-risk individuals with underlying inherited arrhythmia syndromes. Heart failure may also occur as a progression from cardiac injury, precipitation secondary to the initiation or withdrawal of certain drugs, or the accumulation of des-Arg9-bradykinin (DABK) with excessive induction of pro-inflammatory G protein coupled receptor B1 (BK1). The presenting cardiovascular symptoms include chest pain, dyspnoea, and palpitations. There is currently intense interest in vaccine-induced thrombosis and in the treatment of Long COVID since many patients who have survived COVID-19 describe persisting health problems. This review will summarise the proposed physiological mechanisms of COVID-19-associated cardiovascular complications.
Background
Matched hydration and forced diuresis (MHFD) using the RenalGuard device has been shown to reduce contrast induced nephropathy (CIN) following coronary interventions.
Aim
To evaluate the potential benefits of a non-automated MHFD protocol compared to current hydration protocol in prevention of CIN in patients with CKD.
Methods
A total of 1,205 patients were randomized to either non-automated MHFD group (n = 799) or intravenous hydration control group (n = 406). The MHFD group received 250 ml IV normal saline over 30 min before the coronary procedure followed by 0.5 mg/kg IV furosemide. Hydration infusion rate was manually adjusted to replace the patient's urine output. When urine output rate reached > 300 ml/h, patients underwent coronary procedure. Matched fluid replacement was maintained during the procedure and for 4-hour post-treatment. CIN was defined conventionally as ≥ 25% or ≥ 0.5 mg/dl rise in serum creatinine over baseline.
Results
CIN occurred in 121 of 1,205 (10.0%) patients in our study. With respect to the primary outcome, 64 (8.01%) of the MHFD patients developed CIN compared with 57 (14.04%) of the control group (p < 0.001).
Conclusions
A non-automated MHFD protocol is an effective and safe method for the prevention of CIN in patients with CKD.
In this work, we have proposed a new relationship among rough set, soft set and quantales with the help of soft compatible relation. This typical relationship is used to approximate the fuzzy substructures in quantales in association with soft compatible relations by using aftersets and foresets. This type of approximation is extended notation of rough quantales, rough fuzzy subquantales and soft subquantales. We have corroborated this work by considering some test examples containing soft compatible relations over quantales. Moreover, by using soft compatible relations, we will describe the relationship between upper (lower) generalized rough fuzzy soft substructures of quantale and the upper (lower) approximations of their homomorphic images with the help of weak quantale homomorphism. The comparison of this type approximations and their results affirms the superiority of our new approximation method over current methods on the topic.
Atherosclerosis is the main cause of arterial thrombosis, causing acute occlusive cardiovascular syndromes. Numerous risk prediction models have been developed, which mathematically combine multiple predictors, to estimate the risk of developing cardiovascular events. Current risk models typically do not include information from biomarkers that can potentially improve these existing prediction models especially if they are pathophysiologically relevant. Numerous cardiovascular disease biomarkers have been investigated that have focused on known pathophysiological pathways including those related to cardiac stress, inflammation, matrix remodelling, and endothelial dysfunction. Imaging biomarkers have also been studied that have yielded promising results with a potential higher degree of clinical applicability in detection of atherosclerosis and cardiovascular event prediction. To further improve therapy decision-making and guidance, there is continuing intense research on emerging biologically relevant biomarkers. As the pathogenesis of cardiovascular disease is multifactorial, improvements in discrimination and reclassification in risk prediction models will likely involve multiple biomarkers. This article will provide an overview of the literature on potential blood-based and imaging biomarkers of atherosclerosis studied so far, as well as potential future directions.
Cardiac disease after mediastinal radiotherapy can result in progressive valvular thickening and dystrophic calcification with ensuing leaflet restriction and dysfunction. This can ultimately manifest as valvular stenosis and/or regurgitation. We report a case of a 61-year-old woman with symptomatic severe aortic stenosis and severe mitral stenosis due to severe dystrophic calcification postmediastinal radiotherapy for lymphoma. She was deemed surgically inoperable due to dense, continuous calcification throughout the leaflets and annuli of both valves, aortomitral continuity, proximal coronary arteries and proximal porcelain aorta. She underwent simultaneous transcatheter aortic valve replacement and transcatheter mitral valve replacement with an excellent technical and clinical result at 7-month follow-up. We also describe the central role of multimodality three-dimensional transoesophageal echocardiography and multidetector cardiac CT imaging in assessing the severity of valve disease, characterising the nature of cardiac calcification and guiding decisions on surgical operability and transcatheter intervention.
BackgroundElastin degradation is implicated in the pathology of vulnerable plaque. Recent studies show promising results for plasma desmosine (pDES), an elastin-specific degradation product, as a marker of cardiovascular disease (CVD) outcomes. The aim of this study was to investigate the potential role of pDES as a marker of clinical outcome in patients with acute myocardial infarction (AMI).Materials and methodsIn this case-control study, we studied 236 AMI patients: 79 patients who had death and/or myocardial infarction (MI) at 2 years, and 157 patients who did not have an event at 2 years. pDES was measured using a validated liquid chromatography-tandem mass spectrometry method. Association of pDES with adverse outcomes, and the incremental value of pDES to global registry of acute coronary events (GRACE) score for risk stratification was assessed.ResultspDES levels were elevated in patients with the composite outcome of death/MI at 2 years (p = 0.002). Logistic regression analyses showed pDES to be associated with death/MI at 2 years [Odds ratio (OR) 5.99 (95% CI 1.81–19.86) p = 0.003]. pDES remained a significant predictor of death/MI at 2 years even after adjustment for age, sex, history of CVD, revascularisation, blood pressure, medications on discharge, Troponin I, and NT-proBNP levels.[OR 5.60 (95% CI 1.04–30.04) p = 0.044]. In another multivariable model including adjustment for eGFR, pDES was significantly associated with the composite outcome at 6 months, but not at 2 years follow up. DES was also able to reclassify risk stratification for death/MI at 6 months, when added to the GRACE risk model [Net Reclassification Index (NRI) 41.2 (95% CI 12.0–70.4) p = 0.006].ConclusionpDES concentrations predict clinical outcomes in patients with AMI, demonstrating its potential role as a prognostic marker in AMI.
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