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Pitfalls and Misinterpretations of Cardiac Findings on PET/CT Imaging: A Careful Look at the Heart in Oncology Patients.
Betancourt Cuellar, SL, Palacio, D, Benveniste, MF, Carter, BW, Gladish, G
Current problems in diagnostic radiology. 2019;(2):172-183
Abstract
Positron emission tomography (PET) computed tomography (CT) with 2-[fluorine-18] fluoro-2-deoxy-d-glucose (FDG) has been established as an effective modality for evaluation of cancer. Interpretations of patterns of physiologic 18F-FDG uptake by the heart is particularly difficult given the wide normal variations of 18F-FDG metabolic activity observed. Atypical patterns of focal or diffuse physiologic cardiac 18F-FDG uptake and post-therapeutic effects after radiation therapy, systemic diseases, or cardiomyopathy may also be confused with malignant disease on 18F-FDG PET/CT. In this article, we review the variations of normal cardiac 18F-FDG uptake observed in oncology patients and the appearances of other patterns of pathologic metabolic activity, related or not related to the malignancy being investigated, that may lead to false-negative and false-positive results.
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Cardiac Alternans: Mechanisms and Clinical Utility in Arrhythmia Prevention.
Kulkarni, K, Merchant, FM, Kassab, MB, Sana, F, Moazzami, K, Sayadi, O, Singh, JP, Heist, EK, Armoundas, AA
Journal of the American Heart Association. 2019;(21):e013750
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Intelligent Imaging: Radiomics and Artificial Neural Networks in Heart Failure.
Currie, G, Iqbal, B, Kiat, H
Journal of medical imaging and radiation sciences. 2019;(4):571-574
Abstract
BACKGROUND Our previous work with 123iodine meta-iodobenzylguanidine (123I-mIBG) radionuclide imaging among patients with cardiomyopathy reported limitations associated with the prognostic power of global parameters derived from planar imaging [1]. Employing multivariate analysis, we further showed the regional washout associated with territories adjacent to infarcted myocardium obtained from single-photon emission computed tomography imaging (SPECT) yielded superior prognostic power over the other planar and SPECT indices in predicting future cardiac events [1]. The aim of this study was to apply an artificial neural network (Neural Analyser version 2.9.5) to the original data from the same patient cohort to evaluate the most potent prognostic index for future cardiac events among patient with cardiomyopathy. METHODS The original data were reevaluated using an artificial neural network (Neural Analyser version 2.9.5). There were 84 input variables in the original 22 patients from clinical data, electrocardiogram (rest, stress, and continuous ambulatory electrocardiogram recording), transthoracic echocardiography, coronary angiogram, sestamibi myocardial perfusion SPECT, planar and SPECT 123I-mIBG, and genetic and biomarkers, detailed in the previous work. A single binary output was a cardiac event or no cardiac event in the follow-up period. RESULTS Following training and validation phases, the optimal number of inputs was determined to be two with a training loss of 0.025 and selection loss <0.001. The final architecture had inputs of a change in left ventricular ejection fraction (Δ > -10%) and 123I-mIBG planar global washout (>30%), two hidden layers of 6 and 1 node, respectively, and a binary output. Using receiver operator characteristics analysis demonstrated an area under the curve of 0.75 correlating to a sensitivity of 100% and specificity of 50%. CONCLUSION The premise that regional washout of 123I-mIBG SPECT from noninfarcted tissue is the best predictor of cardiac events was built on has a sound and logical foundation. By artificial neural network analysis; however, 123I-mIBG planar global washout of >30% was shown to be the best indicator for risk of cardiac event when accompanied by a decline in left ventricular ejection fraction of >10%. Further investigation should be undertaken assessing assimilation into big data and the potential for automated feature extraction from raw image datasets with convolutional neural networks.
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Heat, Hydration and the Human Brain, Heart and Skeletal Muscles.
Trangmar, SJ, González-Alonso, J
Sports medicine (Auckland, N.Z.). 2019;(Suppl 1):69-85
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Abstract
People undertaking prolonged vigorous exercise experience substantial bodily fluid losses due to thermoregulatory sweating. If these fluid losses are not replaced, endurance capacity may be impaired in association with a myriad of alterations in physiological function, including hyperthermia, hyperventilation, cardiovascular strain with reductions in brain, skeletal muscle and skin blood perfusion, greater reliance on muscle glycogen and cellular metabolism, alterations in neural activity and, in some conditions, compromised muscle metabolism and aerobic capacity. The physiological strain accompanying progressive exercise-induced dehydration to a level of ~ 4% of body mass loss can be attenuated or even prevented by: (1) ingesting fluids during exercise, (2) exercising in cold environments, and/or (3) working at intensities that require a small fraction of the overall body functional capacity. The impact of dehydration upon physiological function therefore depends on the functional demand evoked by exercise and environmental stress, as cardiac output, limb blood perfusion and muscle metabolism are stable or increase during small muscle mass exercise or resting conditions, but are impaired during whole-body moderate to intense exercise. Progressive dehydration is also associated with an accelerated drop in perfusion and oxygen supply to the human brain during submaximal and maximal endurance exercise. Yet their consequences on aerobic metabolism are greater in the exercising muscles because of the much smaller functional oxygen extraction reserve. This review describes how dehydration differentially impacts physiological function during exercise requiring low compared to high functional demand, with an emphasis on the responses of the human brain, heart and skeletal muscles.
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Possible Mechanism of Hematocrit Elevation by Sodium Glucose Cotransporter 2 Inhibitors and Associated Beneficial Renal and Cardiovascular Effects.
Sano, M, Goto, S
Circulation. 2019;(17):1985-1987
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Bioprinting Approaches to Engineering Vascularized 3D Cardiac Tissues.
Puluca, N, Lee, S, Doppler, S, Münsterer, A, Dreßen, M, Krane, M, Wu, SM
Current cardiology reports. 2019;(9):90
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Abstract
PURPOSE OF REVIEW 3D bioprinting technologies hold significant promise for the generation of engineered cardiac tissue and translational applications in medicine. To generate a clinically relevant sized tissue, the provisioning of a perfusable vascular network that provides nutrients to cells in the tissue is a major challenge. This review summarizes the recent vascularization strategies for engineering 3D cardiac tissues. RECENT FINDINGS Considerable steps towards the generation of macroscopic sizes for engineered cardiac tissue with efficient vascular networks have been made within the past few years. Achieving a compact tissue with enough cardiomyocytes to provide functionality remains a challenging task. Achieving perfusion in engineered constructs with media that contain oxygen and nutrients at a clinically relevant tissue sizes remains the next frontier in tissue engineering. The provisioning of a functional vasculature is necessary for maintaining a high cell viability and functionality in engineered cardiac tissues. Several recent studies have shown the ability to generate tissues up to a centimeter scale with a perfusable vascular network. Future challenges include improving cell density and tissue size. This requires the close collaboration of a multidisciplinary teams of investigators to overcome complex challenges in order to achieve success.
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Uric acid and the cardio-renal effects of SGLT2 inhibitors.
Bailey, CJ
Diabetes, obesity & metabolism. 2019;(6):1291-1298
Abstract
Sodium/glucose co-transporter-2 (SGLT2) inhibitors, which lower blood glucose by increasing renal glucose elimination, have been shown to reduce the risk of adverse cardiovascular (CV) and renal events in type 2 diabetes. This has been ascribed, in part, to haemodynamic changes, body weight reduction and several possible effects on myocardial, endothelial and tubulo-glomerular functions, as well as to reduced glucotoxicity. This review evaluates evidence that an effect of SGLT2 inhibitors to lower uric acid may also contribute to reduced cardio-renal risk. Chronically elevated circulating uric acid concentrations are associated with increased risk of hypertension, CV disease and chronic kidney disease (CKD). The extent to which uric acid contributes to these conditions, either as a cause or an aggravating factor, remains unclear, but interventions that reduce urate production or increase urate excretion in hyperuricaemic patients have consistently improved cardio-renal prognoses. Uric acid concentrations are often elevated in type 2 diabetes, contributing to the "metabolic syndrome" of CV risk. Treating type 2 diabetes with an SGLT2 inhibitor increases uric acid excretion, reduces circulating uric acid and improves parameters of CV and renal function. This raises the possibility that the lowering of uric acid by SGLT2 inhibition may assist in reducing adverse CV events and slowing progression of CKD in type 2 diabetes. SGLT2 inhibition might also be useful in the treatment of gout and gouty arthritis, especially when co-existent with diabetes.
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Potential Mechanisms of Sodium-Glucose Co-Transporter 2 Inhibitor-Related Cardiovascular Benefits.
Verma, S
The American journal of cardiology. 2019;:S36-S44
Abstract
The findings of recent clinical trials have shown that sodium-glucose co-transporter 2 (SGLT2) inhibitors produce effects beyond glucose lowering and have demonstrated beneficial cardiovascular effects that have been observed across a broad range of patients with type 2 diabetes mellitus. In particular, the cardiovascular benefit results largely from substantial and early effects of SGLT2 inhibition on cardiovascular death and hospitalization for heart failure. Recent cardiovascular outcomes trials (CVOTs) have also shown that relative risk reductions in cardiovascular outcomes were observed with SGLT2 inhibition both in patients with current and prior heart failure. Since the observed reductions of cardiovascular outcomes with SGLT2 inhibitor therapy were observed much earlier than would be expected by an anti-atherosclerotic effect, these results have led to speculation about the potential underlying pathways. Suggested mechanisms include natriuresis and osmotic diuresis; reductions in inflammation, oxidative stress, and arterial stiffness; reductions in blood pressure and body weight; and possible renoprotective effects. These effects could produce cardiovascular benefits through a range of cardiac effects, including reduction in left ventricular load, attenuation of cardiac fibrosis and inflammation, and improved myocardial energy production. Other possible mechanisms include inhibition of sodium-hydrogen exchange, increases in erythropoietin levels, and reduction in myocardial ischemia or reperfusion injury. It is likely that a range of mechanisms underlie the observed cardiovascular benefits of SGLT2 inhibitors; further elucidation of these mechanisms will be answered by ongoing research.
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Cardiac cachexia: the mandate to increase clinician awareness.
Lena, A, Ebner, N, Coats, AJS, Anker, MS
Current opinion in supportive and palliative care. 2019;(4):298-304
Abstract
PURPOSE OF REVIEW Heart failure is a frequent problem in an ageing population, associated with high rates of morbidity and mortality. Today, it is important to not only treat heart failure itself but also the related comorbidities. Among them, cardiac cachexia is one of the major challenges. It is a complex multifactorial disease with a negative impact on quality of life and prognosis. Therefore, prevention, early recognition and treatment of cardiac cachexia is essential. RECENT FINDINGS Cardiac cachexia frequently presents with skeletal as well as heart muscle depletion. Imaging-based diagnostic techniques can help to identify patients with cardiac cachexia and muscle wasting. Several blood biomarkers are available to detect metabolic changes in cardiac cachexia. SUMMARY Several studies are currently ongoing to better comprehend the underlying pathophysiological mechanisms of cardiac cachexia and to find new treatments. It is essential to diagnose it as early as possible to initiate therapy.
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Effect of S-equol and Soy Isoflavones on Heart and Brain.
Sekikawa, A, Ihara, M, Lopez, O, Kakuta, C, Lopresti, B, Higashiyama, A, Aizenstein, H, Chang, YF, Mathis, C, Miyamoto, Y, et al
Current cardiology reviews. 2019;(2):114-135
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Abstract
BACKGROUND Observational studies in Asia show that dietary intake of soy isoflavones had a significant inverse association with coronary heart disease (CHD). A recent randomized controlled trial (RCT) of soy isoflavones on atherosclerosis in the US, however, failed to show their benefit. The discrepancy may be due to the much lower prevalence of S-equol producers in Westerners: Only 20-30% of Westerners produce S-equol in contrast to 50-70% in Asians. S-equol is a metabolite of dietary soy isoflavone daidzein by gut microbiome and possesses the most antiatherogenic properties among all isoflavones. Several short-duration RCTs documented that soy isoflavones improves arterial stiffness. Accumulating evidence shows that both atherosclerosis and arterial stiffness are positively associated with cognitive decline/dementia. Therefore, potentially, soy isoflavones, especially S-equol, are protective against cognitive decline/dementia. METHODS/RESULTS This narrative review of clinical and epidemiological studies provides an overview of the health benefits of soy isoflavones and introduces S-equol. Second, we review recent evidence on the association of soy isoflavones and S-equol with CHD, atherosclerosis, and arterial stiffness as well as the association of atherosclerosis and arterial stiffness with cognitive decline/ dementia. Third, we highlight recent studies that report the association of soy isoflavones and S-equol with cognitive decline/dementia. Lastly, we discuss the future directions of clinical and epidemiological research on the relationship of S-equol and CHD and dementia. CONCLUSIONS Evidence from observational studies and short-term RCTs suggests that S-equol is anti-atherogenic and improves arterial stiffness and may prevent CHD and cognitive impairment/ dementia. Well-designed long-term (≥ 2years) RCTs should be pursued.