Artificial Intelligence (AI) has impacted every aspect of clinical medicine, and is predicted to revolutionise diagnosis, treatment and patient care. Through novel machine learning (ML) and deep ...learning (DL) techniques, AI has made significant grounds in cardiology and cardiac investigations, including echocardiography. Echocardiography is a ubiquitous tool that remains first-line for the evaluation of many cardiovascular diseases, with large data sets, objective parameters, widespread availability and an excellent safety profile, it represents the perfect candidate for AI advancement. As such, AI has firmly made its stamp on echocardiography, showing great promise in training, image acquisition, interpretation and analysis, diagnostics, prognostication and phenotype development. However, there remain significant barriers in real-world clinical application and uptake of AI derived algorithms in echocardiography, most importantly being the lack of clinical outcome studies. While AI has been shown to match or even best its human counterparts, an improvement in real world outcomes remains to be established. There are also legal and ethical concerns that hinder its progress. Large outcome focused trials and a collaborative multi-disciplinary effort will be necessary to push AI into the clinical workspace. Despite this, current and emerging trials suggest that these systems will undoubtedly transform echocardiography, improving clinical utility, efficiency and training.Artificial Intelligence (AI) has impacted every aspect of clinical medicine, and is predicted to revolutionise diagnosis, treatment and patient care. Through novel machine learning (ML) and deep learning (DL) techniques, AI has made significant grounds in cardiology and cardiac investigations, including echocardiography. Echocardiography is a ubiquitous tool that remains first-line for the evaluation of many cardiovascular diseases, with large data sets, objective parameters, widespread availability and an excellent safety profile, it represents the perfect candidate for AI advancement. As such, AI has firmly made its stamp on echocardiography, showing great promise in training, image acquisition, interpretation and analysis, diagnostics, prognostication and phenotype development. However, there remain significant barriers in real-world clinical application and uptake of AI derived algorithms in echocardiography, most importantly being the lack of clinical outcome studies. While AI has been shown to match or even best its human counterparts, an improvement in real world outcomes remains to be established. There are also legal and ethical concerns that hinder its progress. Large outcome focused trials and a collaborative multi-disciplinary effort will be necessary to push AI into the clinical workspace. Despite this, current and emerging trials suggest that these systems will undoubtedly transform echocardiography, improving clinical utility, efficiency and training.
Low concentrations of insulin-like growth factor (IGF) binding protein-1 (IGFBP1) are associated with insulin resistance, diabetes, and cardiovascular disease. We investigated whether increasing ...IGFBP1 levels can prevent the development of these disorders. Metabolic and vascular phenotype were examined in response to human IGFBP1 overexpression in mice with diet-induced obesity, mice heterozygous for deletion of insulin receptors (IR(+/-)), and ApoE(-/-) mice. Direct effects of human (h)IGFBP1 on nitric oxide (NO) generation and cellular signaling were studied in isolated vessels and in human endothelial cells. IGFBP1 circulating levels were markedly suppressed in dietary-induced obese mice. Overexpression of hIGFBP1 in obese mice reduced blood pressure, improved insulin sensitivity, and increased insulin-stimulated NO generation. In nonobese IR(+/-) mice, overexpression of hIGFBP1 reduced blood pressure and improved insulin-stimulated NO generation. hIGFBP1 induced vasodilatation independently of IGF and increased endothelial NO synthase (eNOS) activity in arterial segments ex vivo, while in endothelial cells, hIGFBP1 increased eNOS Ser(1177) phosphorylation via phosphatidylinositol 3-kinase signaling. Finally, in ApoE(-/-) mice, overexpression of hIGFBP1 reduced atherosclerosis. These favorable effects of hIGFBP1 on insulin sensitivity, blood pressure, NO production, and atherosclerosis suggest that increasing IGFBP1 concentration may be a novel approach to prevent cardiovascular disease in the setting of insulin resistance and diabetes.
Transoesophageal echocardiography (TOE) carries a risk of oesophageal and pharyngeal trauma, particularly in the setting of previous instrumentation or surgery. We describe the novel use of ...videolaryngoscopy to assist during the placement of a TOE probe in a patient with a difficult airway.
Early gadolinium enhancement cardiac magnetic resonance (D) and first-pass perfusion (Online Video 2) confirmed thrombosis within, and noncommunication of, the excluded left ventricular aneurysm.
Obesity and type 2 diabetes mellitus are characterized by insulin resistance, reduced bioavailability of the antiatherosclerotic signaling molecule nitric oxide (NO), and accelerated atherosclerosis. ...IGF-I, the principal growth-stimulating peptide, which shares many of the effects of insulin, may, like insulin, also be involved in metabolic and vascular homeostasis. We examined the effects of IGF-I on NO bioavailability and the effect of obesity/type 2 diabetes mellitus on IGF-I actions at a whole-body level and in the vasculature. In aortic rings IGF-I blunted phenylephrine-mediated vasoconstriction and relaxed rings preconstricted with phenylephrine, an effect blocked by NG-monomethyl l-arginine. IGF-I increased NO synthase activity to an extent similar to that seen with insulin and in-vivo IGF-I led to serine phosphorylation of endothelial NO synthase (eNOS). Mice rendered obese using a high-fat diet were less sensitive to the glucose-lowering effects of insulin and IGF-I. IGF-I increased aortic phospho-eNOS levels in lean mice, an effect that was blunted in obese mice. eNOS activity in aortae of lean mice increased 1.6-fold in response to IGF-I compared with obese mice. IGF-I-mediated vasorelaxation was blunted in obese mice. These data demonstrate that IGF-I increases eNOS phosphorylation in-vivo, increases eNOS activity, and leads to NO-dependent relaxation of conduit vessels. Obesity is associated with resistance to IGF-I at a whole-body level and in the endothelium. Vascular IGF-I resistance may represent a novel therapeutic target to prevent or slow the accelerated vasculopathy seen in humans with obesity or type 2 diabetes mellitus.
Dietary-induced obesity leads to whole body and vascular IGF-1 resistance.
Introduction:
Myocardial infarction with non-obstructive coronary arteries (MINOCA) occurs in ~10% of all patients with acute myocardial infarction (AMI), with an over-representation amongst women. ...Remarkably, it is estimated that as many as 1 in 4 patients with MINOCA experience ongoing angina at 12 months despite having no flow-restricting stenoses in their epicardial arteries. This manuscript presents the rationale behind Randomized Evaluation of Beta Blocker and Angiotensin-converting enzyme inhibitors/Angiotensin Receptor Blocker Treatment (ACEI/ARB) for Post Infarct Angina in MINOCA patients—The MINOCA BAT post infarct angina sub study.
Methods:
This trial is a registry-based, randomized, parallel, open-label, multicenter trial with 2 × 2 factorial design. The primary aim is to determine whether oral beta blockade compared with no oral beta blockade, and ACEI/ARB compared with no ACEI/ARB, reduce post infarct angina in patients discharged after MINOCA without clinical signs of heart failure and with left ventricular ejection fraction ≥40%. A total of 664 patients will be randomized into four groups; (i) ACEI/ARB with beta blocker, (ii) beta blocker only, (iii) ACEI/ARB only, or (iv) neither ACEI/ARB nor beta blocker and followed for 12 months.
Results:
The trial is currently recruiting in Australia and Sweden. Fifty six patients have been recruited thus far. Both sexes were equally distributed (52% women and 48% men) and the mean age was 56.3 ± 9.9 years.
Conclusions:
It remains unclear whether conventional secondary preventive therapies are beneficial to MINOCA patients in regard to post infarct angina. Existing registry-based literature suggest cardioprotective agents are less likely to be used in MINOCA patients. Thus, results from this trial will provide insights for future treatment strategies and guidelines specific to MINOCA patients.
We sought to compare mortality reduction associated with secondary prevention in patients with and without diabetes after acute coronary syndrome (ACS).
We conducted a cohort study involving 2,499 ...patients with ACS recruited from 11 U.K. hospitals. Multivariable analysis comparing all-cause mortality risk reduction associated with pharmacologic agents in patients with and without diabetes.
Aspirin was not associated with significant mortality benefit in diabetes sufferers (95% CI 0.50-1.08); nondiabetic patients derived a 48% mortality reduction (P < 0.001). The interaction between diabetes and aspirin use was statistically significant (P = 0.037), indicating that patients with diabetes experience less effective mortality reduction from aspirin use.
Aspirin, but not other secondary prevention agents, is associated with less effective mortality reduction in patients with diabetes and unstable coronary artery disease.
The structural and functional integrity of the vascular endothelium plays a critical role in vascular homeo-stasis. Insulin resistance, an important risk factor for cardiovascular disease, is thought ...to promote atherosclerosis through a reciprocal relationship with endothelial dysfunction. In health, cumulative damage to endothelial cells incurred by exposure to risk factors is mitigated by endogenous reparative processes. Disruption of the balance between endothelial damage and repair may mediate atherosclerotic progression. Bone marrow-derived ‘endothelial progenitor cells' (EPC) have been identified as significant contributors to endogenous vascular repair. Insulin resistance is associated with a spectrum of biochemical abnormalities which have the potential to reduce the availability of EPCs and diminish their capacity for vascular repair. Many lifestyle and pharmacological interventions which improve insulin resistance also increase the numbers and functionality of EPCs. Cell-based therapies may also hold promise for the prevention and treatment of cardiovascular disease.
Abstract Objectives Predictors of residual leak following percutaneous LAA closure were evaluated. Background Left atrial appendage (LAA) closure aims to exclude this structure from the circulation, ...typically using a circular occluder. A noncircular orifice is frequently encountered however, and fibrous remodeling of the LAA in atrial fibrillation may restrict orifice deformation. Noncircularity may thus be implicated in the occurrence of residual leak despite an appropriately oversized device. Methods Pre-procedural multislice computerized tomography was used to quantify LAA orifice eccentricity and irregularity. Univariate predictors of residual leak were identified with respect to the orifice, device, and relevant clinical variables, with the nature of any correlations then further evaluated. Results Eccentricity and irregularity indexes of the orifice in 31 individuals were correlated with residual leak even where the device was appropriately oversized. An eccentricity index of 0.15 predicted a residual leak with 85% sensitivity and 59% specificity. An irregularity index of 0.05 predicted a significant residual leak ≥3 mm with 100% sensitivity and 86% specificity. Orifice size, device size, degree of device oversize, left atrial volume, and pulmonary artery pressure were not predictors of residual leak. Conclusions Eccentricity and irregularity of the LAA orifice are implicated in residual leak after percutaneous closure even where there is appropriate device over-size. Irregularity index in particular is a novel predictor of residual leak, supporting a closer consideration of orifice morphology before closure.
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