Corrigendum: Regional myocardial work measured by echocardiography for the detection of myocardial ischemic segments: a comparative study with invasive fractional flow reserve.

[This corrects the article DOI: 10.3389/fcvm.2022.813710.].

Exercise training affects calcium ion transport by downregulating the CACNA2D1 protein to reduce hypertension-induced myocardial injury in mice.

Hypertension is a risk factor for cardiovascular disease, and exercise has cardioprotective effects on the heart. However, the mechanism by which exercise affects hypertension-induced myocardial injury remains unclear. Exercise response model of hypertension-induced myocardial injury in mice was analyzed using multiomics data to identify potential factors. The study found that serum Ca2+ and brain natriuretic peptide concentrations were significantly higher in the HTN (hypertension) group than in the control, HTN+MICT (moderate intensity continuous exercise), and HTN+HIIT (high intensity intermittent exercise) groups. Cardiac tissue damage and fibrosis increased in the HTN group, but exercise training reduced pathological changes, with more improvement in the HTN+HIIT group. Transcriptomic and proteomic studies showed significant differences in CACNA2D1 expression between the different treatment groups. HIIT ameliorated HTN-induced myocardial injury in mice by decreasing Ca2+ concentration and diastolizing vascular smooth muscle by downregulating CACNA2D1 via exercise.

The Role of NAD+ in Myocardial Ischemia-induced Heart Failure in Sprague-Dawley Rats and Beagles.

INTRODUCTION: Nicotinamide adenine dinucleotide (NAD+) participates in various processes that are dysregulated in cardiovascular diseases. Supplementation with NAD+ may be cardioprotective. However, whether the protective effect exerted by NAD+ in heart failure (HF) is more effective before acute myocardial infarction (MI) or after remains unclear. The left anterior descending arteries of male Sprague Dawley rats and beagles that developed HF following MI were ligated for 1 week, following which the animals were treated for 4 weeks with low, medium, and high doses of NAD+ and LCZ696. METHOD: Cardiac function, hemodynamics, and biomarkers were evaluated during the treatment period. Heart weight, myocardial fibrosis, and MI rate were measured eventually. RESULT: Compared with the HF groups, groups treated with LCZ696 and different doses of NAD+ showed increased ejection fractions, fractional shortening, cardiac output, and stroke volume and decreased end-systolic volume, end-systolic dimension, creatine kinase, and lactic dehydrogenase. LV blood pressure was lower in the HF group than in the control group, but this decrease was significantly greater in the medium and high NAD+ dose groups. CONCLUSION: The ratios of heart weight indexes, fibrotic areas, and MI rates in the CZ696 and medium and high NAD+ dose groups were lower than those in the HF group. Medium and high-dose NAD+ showed superior positive effects on myocardial hypertrophy, cardiac function, and myocardial fibrosis and reduced the MI rate.

Regulation of Sirtuins in Sepsis-Induced Myocardial Damage: The Underlying Mechanisms for Cardioprotection.

Sepsis is defined as "a life-threatening organ dysfunction caused by a dysregulated host response to infection". Although the treatment of sepsis has evolved rapidly in the last few years, the morbidity and mortality of sepsis in clinical treatment are still climbing. Sirtuins (SIRTs) are a highly conserved family of histone deacetylation involved in energy metabolism. There are many mechanisms of sepsis-induced myocardial damage, and more and more evidence show that SIRTs play a vital role in the occurrence and development of sepsis-induced myocardial damage, including the regulation of sepsis inflammation, oxidative stress and metabolic signals. This review describes our understanding of the molecular mechanisms and pathophysiology of sepsis-induced myocardial damage, with a focus on disrupted SIRTs regulation. In addition, this review also describes the research status of related therapeutic drugs, so as to provide reference for the treatment of sepsis.

NAD+-A Hub of Energy Metabolism in Heart Failure.

Heart failure is a condition where reduced levels of adenosine triphosphate (ATP) affect energy supply in myocardial cells. Nicotinamide adenine dinucleotide (NAD+) plays a crucial role as a coenzyme for electron transfer in energy metabolism. Decreased NAD+ levels in myocardial cells lead to inadequate ATP production and increased susceptibility to heart failure. Researchers are exploring ways to increase NAD+ levels to alleviate heart failure. Targets such as sirtuin2 (sirt2), sirtuin3 (sirt3), Poly (ADP-ribose) polymerase (PARP), and diastolic regulatory proteins are being investigated. NAD+ supplementation has shown promise, even in heart failure with preserved ejection fraction (HFpEF). By focusing on NAD+ as a central component of energy metabolism, it is possible to improve myocardial activity, heart function, and address energy deficiency in heart failure.

NAD+ Protects against Hyperlipidemia-induced Kidney Injury in Apolipoprotein E-deficient Mice.

Background: Hyperlipidemia is an independent risk factor for kidney injury. Several studies have shown that nicotinamide adenine dinucleotide (NAD+) is an important coenzyme involved in normal body metabolism. Therefore, this study aimed to investigate the possible protective effects of NAD+ against hyperlipidemia-induced kidney injury in apolipoprotein Edeficient (ApoE-/-) mice.

Methods: Twenty-five eight-week-old male ApoE-/- mice were randomly assigned into four groups: normal diet (ND), ND supplemented with NAD+ (ND+NAD+), high-fat diet (HFD), and HFD supplemented with NAD+ (HFD+NAD+). The mice were subjected to their respective diets for a duration of 16 weeks. Blood samples were obtained from the inferior vena cava, collected in serum tubes, and stored at -80°C until use. Kidney tissues was fixed in 10% formalin and then embedded in paraffin for histological evaluation. The remainder of the kidney tissues was snapfrozen in liquid nitrogen for Western blot analysis.

Results: Metabolic parameters (total cholesterol, triglycerides, low-density lipoprotein-cholesterol, creatinine, and blood urea nitrogen) were significantly higher in the HFD group compared to the other groups. Histological analysis revealed prominent pathological manifestations in the kidneys of the HFD group. The HFD+NAD+ group showed increased levels of oxidative stress markers (NRF2 and SOD2) and decreased levels of NOX4 compared to the HFD group. Furthermore, the HFD group exhibited higher levels of TGF-ß, Smad3, Collagen I, Collagen III, Bax, and Bak compared to the other groups. NAD+ supplementation in the HFD+NAD+ group significantly increased the levels of SIRT3, HO-1, Bcl-2, and Bcl-xL compared to the HFD group. Additionally, NF-κB protein expression was higher in the HFD group than in the HFD+NAD+ group.

Conclusion: These findings demonstrated that NAD+ may hold potential as a clinical treatment for kidney injury caused by hyperlipidemia.

NAD+: A key metabolic regulator with great therapeutic potential for myocardial infarction via Sirtuins family.

Myocardial infarction (MI) is one of the complex phenotypes of coronary artery disease, which results from the interaction of multiple genetic and environmental factors. Nicotinamide Adenine Dinucleotide (NAD+) is an important cofactor regulating metabolic homeostasis and a rate-limiting substrate for sirtuin (SIRT) deacetylase. Numerous NAD+ studies have shown that it can be used as an anti-MI treatment. However, there have been few systematic reviews of the overall role of NAD+ in treating MI. MI, which has long been a global health problem, still lacks effective treatment till now, and the discovery of NAD+ provides a new perspective on its adjuvant treatment. This review summarizes the role of NAD+ signaling in SIRTs in alleviating MI.

Different exercise training intensities prevent type 2 diabetes mellitus-induced myocardial injury in male mice.

Type 2 diabetes mellitus (T2DM) usually develop myocardial injury and that exercise may have a positive effect on cardiac function. However, the effect of exercise intensity on cardiac function has not yet been fully examined. This study aimed to explore different exercise intensities on T2DM-induced myocardial injury. 18-week-old male mice were randomly divided into four groups: a control group, the T2DM, T2DM + medium-intensity continuous training (T2DM + MICT), and T2DM + high-intensity interval training (T2DM + HIIT) groups. In the experimental group, mice were given high-fat foods and streptozotocin for six weeks and then divided into two exercise training groups, in which mice were subjected to exercise five days per week for 24 consecutive weeks. Finally, metabolic characteristics, cardiac function, myocardial remodeling, myocardial fibrosis, oxidative stress, and apoptosis were analyzed. HIIT treatment improved cardiac function and improved myocardial injury. In conclusion, HIIT may be an effective means to guard against T2DM-induced myocardial injury.

Luteolin reduces cardiac damage caused by hyperlipidemia in Sprague-Dawley rats.

Objective: Hyperlipidemia is a risk factor for cardiac damage that can lead to many cardiovascular diseases. A recent study reported the cardioprotective effects of luteolin in vitro and in vivo. In this study, we aimed to investigate the possible protective effects of luteolin against hyperlipidemia-induced cardiac damage in Sprague-Dawley (SD) rats. Methods: Six-week-old male SD rats were randomly divided into five groups: a normal diet (ND) group; a high-fat diet (HFD) group; and three high-fat diet mixed with luteolin (HFD + LUT) groups, where in a luteolin dosage 50, 100, or 200 mg/kg/day was administered. All groups were fed their respective diets for 12 weeks. Results: Left ventricular ejection fraction and fractional shortening (parameters of cardiac function) were lower in the HFD + LUT (100 mg/kg/day) group than in the HFD group. Metabolic parameters were lower in the HFD + LUT (100 mg/kg/day) group than in the HFD group. Collagen I, collagen III, and TGF-ß expression levels were lower in the cardiac tissues of the HFD + LUT (100 mg/kg/day) group, compared to those of the HFD group. Expression of the profibrotic genes MMP2 and MMP9 was suppressed in the cardiac tissues of the HFD + LUT (100 mg/kg/day) group, compared to those of the HFD group. Furthermore, CD36 and lectin-like oxidized low-density lipoprotein receptor-1 protein levels were lower in the cardiac tissues of the HFD + LUT (100 mg/kg/day) group, compared to those of the HFD group. Conclusion: These findings would provide new insights into the role of luteolin in hyperlipidemia-induced cardiac damage and contribute to the development of novel therapeutic interventions to treat cardiovascular disease progression.

Exercise reduces hyperlipidemia-induced cardiac damage in apolipoprotein E-deficient mice via its effects against inflammation and oxidative stress.

Cardiovascular disease is a high incidence and mortality rate disease worldwide. Exercise training has become an established evidence-based treatment strategy that is beneficial for many cardiovascular diseases. This study aimed to investigate the effects of exercise on hyperlipidemia-induced cardiac damage in apolipoprotein E-deficient (ApoE-/-) mice. Male ApoE-/- mice were randomly divided into the following four groups: normal diet (ND), normal diet + exercise training (ND + E), high-fat diet (HFD), and high-fat diet + exercise training (HFD + E). Exercise training consisted of swimming for 40 min, 5 days/week for 12 weeks. After 12 weeks, histopathological alterations in cardiac tissue and the serum were measured. Furthermore, the NOX4, NRF2, SIRT1, TGF-ß, HO-1, collagen III, Smad3, Bax, Bak, Bcl-2, Bcl-xl, IL-1ß, IL-6, and IL-18 expression levels were evaluated using immunohistochemistry and western blotting; Results: the serum levels of SIRT1, GSH-Px, and SOD were lower in ApoE-/- HFD mice compared with those in ApoE-/- HFD + E mice. Significant pathological changes were observed in the ApoE-/- HFD + E group compared with those in the ApoE-/- HFD group. Increased levels of oxidative stress, fibrosis, and apoptosis, and decreased antioxidant expression in the ApoE-/- HFD group compared with those in ApoE-/- HFD + E mice. Exercise exerts protective effects against cardiac damage caused by hyperlipidemia.

Mechanism of CD38 via NAD+ in the Development of Non-alcoholic Fatty Liver Disease.

Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease globally, and it can proceed to cirrhosis and hepatocellular carcinoma, as well as cardiovascular disease, chronic renal disease, and other complications, resulting in a massive economic burden. At the moment, nicotinamide adenine dinucleotide (NAD+) is thought to be a possible treatment target for NAFLD, besides Cluster of differentiation 38(CD38) is the primary NAD+ degrading enzyme in mammals and may play a role in the pathophysiology of NAFLD. For example, CD38 regulates Sirtuin 1 activity and hence affects inflammatory responses. CD38 inhibitors enhance glucose intolerance and insulin resistance in mice and lipid accumulation in the liver is greatly decreased in CD38-deficient mice. This review describes the role of CD38 in the development of NAFLD in terms of Macrophage-1, insulin resistance, and abnormal lipid accumulation in order to offer recommendations for future NAFLD pharmacological trials.

Nomogram for Predicting Intraoperative Hemodynamic Instability in Patients With Normotensive Pheochromocytoma.

CONTEXT: Intraoperative hemodynamic instability (HI) deteriorates surgical outcomes of patients with normotensive pheochromocytoma (NP). OBJECTIVE: To characterize the hemodynamics of NP and develop and externally validate a prediction model for intraoperative HI. METHODS: Data on 117 patients with NP (derivation cohort) and 40 patients with normotensive adrenal myelolipoma (NAM) who underwent laparoscopic adrenalectomy from January 2011 to November 2021 were retrospectively collected. Data on 22 patients with NP (independent validation cohort) were collected from another hospital during the same period. The hemodynamic characteristics of patients with NP and NAM were compared. Machine learning models were used to identify risk factors associated with HI. The final model was visualized via a nomogram. RESULTS: Forty-eight (41%) out of 117 patients experienced HI, which was significantly more than that for NAM. A multivariate logistic regression including age, tumor size, fasting plasma glucose, and preoperative systolic blood pressure showed good discrimination measured by area under curve (0.8286; 95% CI 0.6875-0.9696 and 0.7667; 95% CI 0.5386-0.9947) for predicting HI in internal and independent validation cohorts, respectively. The sensitivities and positive predictive values were 0.6667 and 0.7692 for the internal and 0.9167 and 0.6111 for the independent validations, respectively. The final model was visualized via a nomogram and yielded net benefits across a wide range of risk thresholds in decision curve analysis. CONCLUSION: Patients with NP experienced HI during laparoscopic adrenalectomy. The nomogram can be used for individualized prediction of intraoperative HI in patients with NP.

Advances in Exercise Therapy in Hemodialysis: A Systematic Review.

BACKGROUND: The main and common treatment of renal replacement therapy (RRT) for chronic kidney disease (CKD), especially in end-stage kidney disease (ESKD) patients, is hemodialysis (HD). Many reports have shown that exercise therapy is good for HD patients. This review aims to describe recent advances in exercise therapy in HD patients. OBJECTIVE: Our key opinions have focused on varied types of exercise therapy and identified barriers to exercise therapy among HD patients. Exercise implementation includes aerobic exercise training, resistance exercise training, combined exercise training, and novel exercise interventions. Barriers include internal and external distress, such as HD patients' restrictions and environmental problems. METHODS: This review is based on the novel/ most findings in PubMed, Web of Science, Google Scholar, and MEDLINE from the inception of every database until August 2022. RESULTS: The systematic search strategy identified 6 articles that met the inclusion criteria. Four were specific to exercise therapy in HD, and three were to exercise barriers in HD. Massive evidence has demonstrated exercise therapy for HD has specific benefits and neglectful causes of exercise barriers. CONCLUSION: In this review, we aimed to summarize recent advances in individual exercise therapy recommendations (type, intensity, time, and frequency) and exercise barriers in HD patients. In conclusion, Low/moderate-intensity exercise trained for at least thirty minutes five times per week, including aerobic exercise (Walking, Jogging, Swimming, and Health Exercises), resistance training (Dumbbells, Band training, and Knee extension), and combination exercise (both) during the first 2 hours of dialysis treatment or non-dialysis days is advisable treatment recommendation.

CoQ10 Improves Myocardial Damage in Doxorubicin-Induced Heart Failure in C57BL/6 Mice.

BACKGROUND: Cardiovascular disease is associated with high morbidity and mortality. Doxorubicin (DOX) is an effective adjunct to cancer chemotherapy but leads to cardiovascular-related side effects. Because coenzyme Q10 (CoQ10) has been shown to protect against cardiac damage, this study was conducted to investigate the protective effects of CoQ10 against cardiac damage in mice. METHODS: We randomly divided six-week-old male C57BL/6 mice into four groups: control (n = 7), CoQ10 (n = 7), heart failure (HF) (n = 7), and HF+CoQ10 (n = 6) groups. HF group was induced via intraperitoneal injections with DOX (5 mg/kg) once weekly for 4 weeks. CoQ10 was solube in corn oil. The mice of CoQ10 and HF+CoQ10 group were given CoQ10 (100 mg/kg) once a day for 8 weeks. All mice were subjected to different treatment regimens for eight weeks. Metabolic characteristics, cardiac damage, oxidative stress markers (SIRT1, SIRT3, eNOS, TE, P53, SIRT5, CAT, HO-1, and SOD), energy metabolism markers (PARP-1 and PPAR-γ), myocardial fibrosis markers (Smad3 and TGF-ß), and apoptosis markers (BAK, BCL-XL, and caspase-8) were analyzed at eight weeks after the different treatments. RESULTS: CoQ10 reduced the levels of molecules related to cardiac damage, oxidative stress, energy metabolism, and myocardial fibrosis in mice with doxorubicin-induced HF. CoQ10 also exerted anti-apoptotic effects in HF mice. CONCLUSIONS: CoQ10 may be useful for preventing cardiac damage in DOX-induced HF.

Regional Myocardial Work Measured by Echocardiography for the Detection of Myocardial Ischemic Segments: A Comparative Study With Invasive Fractional Flow Reserve.

Purpose: This study is to assess the diagnostic value of noninvasive regional myocardial work (MW) by echocardiography for detecting the functional status of coronary stenosis using fractional flow reserve (FFR) as a standard criterion. Methods: A total of 84 consecutive patients were included in this study, among which 92 vessels were identified with ≥50% stenosis confirmed by invasive coronary angiography. Patients were investigated by invasive FFR and transthoracic echocardiography. Regional MW indices including myocardial work index (MWI), myocardial constructive work (MCW), myocardial wasted work, and myocardial work efficiency were calculated. Results: MWI and MCW were significantly impaired in the FFR ≤ 0.75 group compared with the FFR > 0.75 group (both p < 0.01). There were significant positive associations between MWI and MCW with FFR. In total group, MWI <1,623.7 mmHg% [sensitivity, 78.4%; specificity, 72.2%; area under the curve value, 0.768 (0.653-0.883)] and MCW <1,962.4 mmHg% [77.0%; 72.2%; 0.767 (0.661-0.872)], and in single-vessel subgroup, MWI <1,412.1 mmHg% [93.5%; 63.6%; 0.808 (0.652-0.965)] and MCW <1,943.3 mmHg% [(84.8%; 72.7%; 0.800 (0.657-0.943)] were optimal to detect left ventricular segments with an FFR ≤ 0.75. MWI and MCW significantly increased after percutaneous coronary intervention in 13 cases. Conclusion: In patients with coronary artery disease, especially those with single-vessel stenosis, the regional MW measured by echocardiography exhibited a good diagnostic value in detecting significant myocardial ischemia compared to the standard FFR approach.

Nicotinamide Adenine Dinucleotide in the Development and Treatment of Cardiac Remodeling and Aging.

BACKGROUND: Recently, the beneficial effects of nicotinamide adenine dinucleotide (NAD+) as an antiaging and antioxidant molecule have become a focus of research. However, the mechanisms by which NAD+ supplementation affects the associated metabolites under physiological conditions remain unclear. Specifically, although NAD+ is involved in several processes that are dysregulated in cardiovascular diseases, some effects of NAD+ precursors and NAD+ on cardiac diseases have started to gain recognition only recently. OBJECTIVE: To discuss the influence of NAD+ supplementation on adverse cardiac remodeling and aging. RESULTS: Supplementation with NAD+ precursors or nicotinamide riboside, which enhances or supplements the NAD+metabolome, might have a protective effect on the heart. NAD+ can alleviate chronic heart failure via mitochondrial oxidation-reduction (redox) state mechanism. Furthermore, NAD+ replenishment can improve the life span of mice. CONCLUSION: NAD+ exerts considerable antiaging and antioxidant effects with promising therapeutic effects. However, its effect on humans and its use as a dietary supplement need to be studied further.

Effects of thymoquinone against angiotensin II­induced cardiac damage in apolipoprotein E­deficient mice.

Herbal medicines have attracted much attention in recent years and are increasingly being used as alternatives to pharmaceutical medicines. Thymoquinone (TQ) is one of the most active ingredients in Nigella sativa seeds, which has several beneficial properties, including anti­inflammatory, anti­oxidative stress, anti­hypertensive, anti­apoptotic and free radical­scavenging effects. Angiotensin II (Ang II) is involved in cardiovascular diseases. The present study aimed to investigate the potential protective effects of TQ against Ang II­induced cardiac damage in apolipoprotein E­deficient (ApoE­/­) mice. Briefly, 8­week­old male ApoE­/­ mice were randomly divided into four groups: Control, TQ, Ang II and Ang II + TQ groups. Osmotic minipumps, filled with either a saline vehicle or an Ang II solution (1,000 ng/kg/min), were implanted in ApoE­/­ mice for up to 4 weeks. The serum levels of high­sensitivity C­reactive protein (hs­CRP) and histopathological alterations in heart tissue were assessed. In addition, the mRNA and protein expression levels of molecules associated with fibrosis (collagen I and III), oxidative stress and apoptosis (Nox4 and p53), and inflammation [tumor necrosis factor (TNF)­α, interleukin (IL)­1ß and IL­6] were analyzed by reverse transcription­quantitative PCR (RT­qPCR) and western blotting. In the in vitro study, H9c2 cells were incubated with different concentrations of Ang II, and the expression levels of pro­inflammatory cytokines were evaluated using RT­qPCR, whereas the protein expression levels of phosphorylated­extracellular signal­regulated kinase (p­ERK) were determined using western blotting. Western blotting was also performed to detect the expression levels of collagen I, collagen III, Nox4 and p53 in H9c2 cells. The results revealed that TQ inhibited the Ang II­induced increases in serum hs­CRP levels. TQ also significantly inhibited the high levels of TNF­α, IL­1ß, IL­6, collagen I, collagen III, Nox4 and p53 in Ang II­treated mice. Furthermore, TQ protected against Ang II­induced cardiac damage by inhibiting inflammatory cell infiltration, proinflammatory cytokine expression, fibrosis, oxidative stress and apoptosis by suppressing activation of the p­ERK signaling pathway. In conclusion, TQ could be considered a potential therapeutic agent for Ang II­induced cardiac damage.

Joint efficacy of the three biomarkers SNCA, GYPB and HBG1 for atrial fibrillation and stroke: Analysis via the support vector machine neural network.

Atrial fibrillation (AF) is the most common type of persistent arrhythmia. Although its incidence has been increasing, the pathogenesis of AF in stroke remains unclear. In this study, a total of 30 participants were recruited, including 10 controls, 10 patients with AF and 10 patients with AF and stroke (AF + STROKE). Differentially expressed genes (DEGs) were identified, and functional annotation of DEGs, comparative toxicogenomic database analysis associated with cardiovascular diseases, and predictions of miRNAs of hub genes were performed. Using RT-qPCR, biological process and support vector machine neural networks, numerous DEGs were found to be related to AF. HBG1, SNCA and GYPB were found to be upregulated in the AF group. Higher expression of hub genes in AF and AF + STROKE groups was detected via RT-PCR. Upon training the biological process neural network of SNCA and GYPB for HBG1, only small differences were detected. Based on the support vector machine, the predicted value of SNCA and GYPB for HBG1 was 0.9893. Expression of the hub genes of HBG1, SNCA and GYPB might therefore be significantly correlated to AF. These genes are involved in the incidence of AF complicated by stroke, and may serve as targets for early diagnosis and treatment.

Recombinant Human Growth Hormone Inhibits Lipotoxicity, Oxidative Stress, and Apoptosis in a Mouse Model of Diabetic Cardiomyopathy.

Recombinant human growth hormone (rhGH), widely used in clinical studies, exerts protective effects against cardiac damage. Here, we investigated the effects and mechanisms underlying the effects of rhGH on cardiac functions in db/db mice. C57BL/6J and db/db mice were subjected to rhGH treatment. Metabolic parameters, cardiac function and morphology, oxidative stress, lipid metabolism, and apoptosis were evaluated 16 weeks after rhGH treatment. Although rhGH did not significantly affect fasting blood glucose levels in db/db mice, it protected against diabetic cardiomyopathy, by improving cardiac function and reducing oxidative stress in the heart. In addition, rhGH treatment exhibited anti-apoptotic effects in the heart of db/db mice. The rhGH treatment, besides inhibiting oxidative stress and apoptosis, ameliorated cardiac dysfunction by inhibiting lipotoxicity in mice with type 2 diabetes. These findings suggest that rhGH is a promising therapeutic agent for diabetic cardiomyopathy.

Myocardial Work by Speckle Tracking Echocardiography Accurately Assesses Left Ventricular Function of Coronary Artery Disease Patients.

Objective: Myocardial work (MW) is a novel non-invasive method that uses speckle tracking echocardiography (STE) to assess left ventricular (LV) function. MW incorporates the global longitudinal strain and afterload conditions. Here we aimed to use MW to assess the LV function of patients with coronary artery disease (CAD) with or without heart failure (HF). Methods: We enrolled a total of 150 individuals (50 each) with CAD and a normal LV ejection fraction (LVEF), CAD with HF, and healthy controls. Patients were divided into the hypertension (HTN) and normal blood pressure (no HTN) subgroups. MW was determined from the pressure-strain loop using STE. The relationships between MW indices and conventional echocardiographic parameters were evaluated, and the MW indices were compared among groups. Results: Univariate and multivariate analyses showed that MW indices were strongly correlated with LVEF. The global work index (GWI) was increased in the CAD with normal LVEF subgroup with HTN vs. controls (1,922.3 ± 393.1 vs. 1,639.7 ± 204.6 mmHg%, p < 0.05) and decreased in CAD patients with HF (no HTN: 940.9 ± 380.6 vs. 1,639.7 ± 204.6 mmHg%, p < 0.05; HTN: 857.3 ± 369.3 vs. 1,639.7 ± 204.6 mmHg%, p < 0.05). Global waste work was increased in all CAD subgroups vs. controls. Global constructive work had the same tendency as GWI in patients with CAD. Global MW efficiency was decreased in all patients with CAD. Conclusion: MW using STE accurately quantifies LV function in patients with CAD. It offers additional information about LV function with respect to disease progression, particularly in CAD patients with a normal LVEF.