Changes In Myocardial Uptake Research Articles

Cardiac metabolism in HFpEF: from fuel to signalling.

Heart failure (HF) is marked by distinctive changes in myocardial uptake and utilization of energy substrates. Among the different types of HF, HF with preserved ejection fraction (HFpEF) is a highly prevalent, complex, and heterogeneous condition for which metabolic derangements seem to dictate disease progression. Changes in intermediate metabolism in cardiometabolic HFpEF-among the most prevalent forms of HFpEF-have a large impact both on energy provision and on a number of signalling pathways in the heart. This dual, metabolic vs. signalling, role is played in particular by long-chain fatty acids (LCFAs) and short-chain carbon sources [namely, short-chain fatty acids (SCFAs) and ketone bodies (KBs)]. LCFAs are key fuels for the heart, but their excess can be harmful, as in the case of toxic accumulation of lipid by-products (i.e. lipotoxicity). SCFAs and KBs have been proposed as a potential major, alternative source of energy in HFpEF. At the same time, both LCFAs and short-chain carbon sources are substrate for protein post-translational modifications and other forms of direct and indirect signalling of pivotal importance in HFpEF pathogenesis. An in-depth molecular understanding of the biological functions of energy substrates and their signalling role will be instrumental in the development of novel therapeutic approaches to HFpEF. Here, we summarize the current evidence on changes in energy metabolism in HFpEF, discuss the signalling role of intermediate metabolites through, at least in part, their fate as substrates for post-translational modifications, and highlight clinical and translational challenges around metabolic therapy in HFpEF.

Association Between Changes in Myocardial F-18 Fluorodeoxyglucose Uptake and Cardiac Toxicity or Overall Survival for Inoperable NSCLC Patients Receiving Chemoradiation

<h3>Purpose/Objective(s)</h3> Previous studies have shown that increased cardiac uptake of 18F-fluorodeoxyglucose (FDG) on positron emission tomography (PET) may be an indicator of myocardial injury after radiotherapy. Our study aimed to investigate the predictive value of changes in myocardial ¹⁸F-FDG uptake for cardiotoxicity and overall survival (OS) in patients with inoperable NSCLC receiving definitive chemoradiation. <h3>Materials/Methods</h3> One hundred and fifty unresectable locally advanced NSCLC patients enrolled in a retrospective study who had undergone pre- and post-chemoradiation FDG-PET imaging were evaluated. Our primary endpoint was grade ≥ 3 cardiac toxicity. Patient clinicopathologic factors, dosimetric parameters for the whole heart and cardiac substructures, and myocardial changes within the irradiated fields on 18F-FDG PET were utilized to seek the best predictive model for cardiotoxicity. Competing risk analysis and Cox regressions analysis were performed. <h3>Results</h3> At a median follow-up interval of 35 months, twenty-six patients (17.3%) developed grade ≥ 3 cardiac everts. Twenty-nine patients (19.3%) showed increased myocardial FDG uptake within the irradiated fields associated with the heart dosimetric parameters. The best multivariable model based on the lowest Akaike information criterion for predicting grade ≥ 3 cardiotoxicity included the following covariates: pre-existing cardiac disease, changes in pre- and post-chemoradiation myocardial SUV_mean (∆SUV_mean), and mean heart dose. Subanalysis showed that pre-existing cardiac disease, ∆SUV_mean, and mean left anterior descending dose were significantly associated with grade ≥ 3 acute coronary syndrome/congestive heart failure events. ∆SUV_mean and grade ≥ 3 cardiac toxicity were independent indicators of OS. <h3>Conclusion</h3> ∆SUV_mean was an independent indicator of grade ≥ 3 cardiac toxicity and OS in unresectable locally advanced NSCLC patients receiving definitive chemoradiation. Changes in myocardial uptake of FDG is a promising biomaker for predicting radiation-induced cardiotoxicity.

Association between FDG uptake in the right ventricular myocardium and cancer therapy-induced cardiotoxicity

BackgroundThe aim of this study was to investigate changes in myocardial uptake evaluated by oncologic 18F-fluorodeoxyglucose (FDG) PET/CT scans and to determine the relationship between myocardial FDG uptake and cancer therapy-induced cardiotoxicity in breast cancer patients who underwent anthracycline or trastuzumab. MethodsWe reviewed 121 consecutive patients who underwent oncologic FDG PET/CT and echocardiography at baseline and post-therapy with anthracyclines or trastuzumab for breast cancer. Grade in LV wall, uptake pattern in LV wall, and the presence of RV wall uptake were assessed by visual analysis, and the mean SUV in the LV and RV walls and the change of SUV (ΔSUV) between baseline and post-therapy PET/CT were measured by quantitative analysis. Multiple logistic regression analyses were performed to evaluate the association between PET parameters and cardiotoxicity. ResultsFifteen patients (12%) showed cardiotoxicity after therapy. The cardiotoxic group tended to show more diffuse LV uptake, higher SUV, and ΔSUV of RV wall than the non-cardiotoxic group following therapy with anthracyclines or trastuzumab. Logistic regression analysis showed that the presence of RV wall uptake, SUV of RV wall (> 1.8), and ΔSUV of RV wall (> 0.4) were significantly associated with cardiotoxicity after controlling for age, radiotherapy, and treatment. ConclusionsThe presence of RV wall uptake and the increase of SUV of RV wall on post-therapy PET/CT were associated with cardiotoxicity in breast cancer patients who underwent anthracycline or trastuzumab. Oncologic FDG PET/CT scans can provide information regarding cancer therapy-induced cardiotoxicity as well as tumor response.

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Left ventricular myocardial perfusion and function in systemic sclerosis before and after diltiazem treatment.

To examine left ventricular (LV) myocardial perfusion and function, in systemic sclerosis. Myocardial perfusion was assessed at rest, during cold exposure, and at peak exercise in 10 patients with systemic sclerosis. Seven of the 10 patients were examined with Doppler echocardiography; before and after long-term diltiazem treatment. Compared with average resting values, isotope uptake was increased by 48% after exercise, compared with cold exposure the exercise value was increased by 35%. After 11 months of diltiazem treatment there was no change in myocardial uptake, compared with respective values before treatment. Doppler echocardiography showed an increase in LV end-diastolic diameter, fractional shortening, and left ventricular outflow tract velocity, after treatment. This indicates that long-term diltiazem treatment does not increase myocardial perfusion at rest, post-exercise, or during cold exposure. On the other hand diltiazem treatment may improve left ventricular performance.

Effects of Secretin Infusion on Myocardial Performance and Metabolism in the Dog

The effects of pharmacological doses of secretin were studied in closed-chest, pentobarbital anesthetized dogs. Infusion of secretin 16 clinical units (CU)/kg-h caused a rise in cardiac output (p less than 0.01), peak first derivative of the left ventricular pressure (p less than 0.01), and heart rate (p less than 0.01) and a fall in systemic arteriolar resistance (p less than 0.01) and left ventricular end-diastolic pressure (p less than 0.01). Stroke volume did not change significantly. Myocardial blood flow and oxygen consumption were unchanged. Secretin caused reductions in arterial lactate (p less than 0.01) and glucose (p less than 0.05) concentrations, and arterial concentrations of free fatty acids and insulin were unaltered. There was no change in myocardial uptake of lactate, glucose, or FFA. Secretin 64 CU/kg-h infused in two dogs caused further changes of the hemodynamic variables. Thus, secretin enhances left ventricular function in intact anesthetized dog by combined vasodilating, inotropic, and chronotropic effects, without changing myocardial oxygen or substrate uptake.