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Journal articles on the topic 'Early heart failure'

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Published: 10 December 2022
Last updated: 29 January 2023

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1

Creager, Mark A. "Early Intervention in Heart Failure." Drugs 39, Supplement 4 (1990): 4–9. http://dx.doi.org/10.2165/00003495-199000394-00003.

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2

Spacie, Robin, James M. Duffell, and Megan Jones. "Heart failure." InnovAiT: Education and inspiration for general practice 12, no. 5 (March 25, 2019): 243–51. http://dx.doi.org/10.1177/1755738019829789.

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Heart failure is a progressive condition that is increasing in prevalence. Clinical findings, together with natriuretic peptide measurement and echocardiography, underpin diagnosis. Drugs can improve the prognosis (ACE-inhibitor, beta blockers) and ameliorate symptoms (diuretics). Non-pharmacological treatment includes exercise therapy, smoking cessation and nutritional care. Heart failure has a poor prognosis and early palliative input is recommended.
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3

Gustafsson, I., and P. Hildebrandt. "Early Failure of the Diabetic Heart." Diabetes Care 24, no. 1 (January 1, 2001): 3–4. http://dx.doi.org/10.2337/diacare.24.1.3.

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4

Subramaniam, Kathirvel. "Early Graft Failure After Heart Transplantation." International Anesthesiology Clinics 50, no. 3 (2012): 202–27. http://dx.doi.org/10.1097/aia.0b013e3182603ead.

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5

ERIKSSON, HENRY, KURT SVÄRDSUDD, KENNETH CAIDAHL, THORVALD BJURÖy, BO LARSSON, LENNART WELIN, LARS-OLOF OHLSON, and LARS WILHELMSEN. "Early Heart Failure in the Population." Acta Medica Scandinavica 223, no. 3 (April 24, 2009): 197–209. http://dx.doi.org/10.1111/j.0954-6820.1988.tb15788.x.

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6

Peacock, William Frank, Charles Emerman, Maria R. Costanzo, Deborah B. Diercks, Margarita Lopatin, and Gregg C. Fonarow. "Early Vasoactive Drugs Improve Heart Failure Outcomes." Congestive Heart Failure 15, no. 6 (November 2009): 256–64. http://dx.doi.org/10.1111/j.1751-7133.2009.00112.x.

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7

Kotooka, Norihiko. "Biomarkers for Early Diagnosis of Heart Failure." Journal of Cardiac Failure 18, no. 10 (October 2012): S137. http://dx.doi.org/10.1016/j.cardfail.2012.08.079.

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8

Kwak, Min Ji, Lincy S. Lal, John M. Swint, Xianglin L. Du, Wenyaw Chan, Bindu Akkanti, and Abhijeet Dhoble. "Early tracheostomy in acute heart failure exacerbation." Heart & Lung 49, no. 5 (September 2020): 646–50. http://dx.doi.org/10.1016/j.hrtlng.2020.03.024.

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9

Wang, Xiaoxia, Chun Song, Xiao Zhou, Xiaorui Han, Jun Li, Zengwu Wang, Haibao Shang, Yuli Liu, and Huiqing Cao. "Mitochondria Associated MicroRNA Expression Profiling of Heart Failure." BioMed Research International 2017 (2017): 1–10. http://dx.doi.org/10.1155/2017/4042509.

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Heart failure (HF) is associated with mitochondrial dysfunction and energy metabolism impairment. MicroRNAs are implicated in the development of heart failure. However, the mitochondria enriched microRNA during heart failure remains elusive. Here, we generated a pressure overload-induced early and late stage heart failure model at 4 weeks and 8 weeks following transverse aortic constriction (TAC) in mice. We found that expression of mitochondrion protein COX4 was highly enriched in isolated mitochondria from cardiac tissues while GAPDH could hardly be detected. Furthermore, small RNA sequencing for mitochondria RNAs from failing hearts was performed. It was found that 69 microRNAs were upregulated and 2 were downregulated in early heart failure, while 16 microRNAs were upregulated and 6 were downregulated in late heart failure. 15 microRNA candidates were measured in both mitochondria and total cardiac tissues of heart failure by real-time PCR. MiR-696, miR-532, miR-690, and miR-345-3p were enriched in mitochondria from the failing heart at early stage. Bioinformatics analysis showed that mitochondria enriched microRNAs in HF were associated with energy metabolism and oxidative stress pathway. For the first time, we demonstrated microRNAs were enriched in mitochondria during heart failure, which established a link between microRNA and mitochondrion in heart failure.
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10

Yontz, Lynn L. "Congestive Heart Failure: Early Recognition of Congestive Heart Failure in the Primary Care Setting." Journal of the American Academy of Nurse Practitioners 6, no. 6 (June 1994): 273–79. http://dx.doi.org/10.1111/j.1745-7599.1994.tb00952.x.

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11

Modesti, P. A. "Impairment of cardiopulmonary receptor sensitivity in the early phase of heart failure." Heart 90, no. 1 (January 1, 2004): 30–36. http://dx.doi.org/10.1136/heart.90.1.30.

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12

Lin, Li, S. C. Kim, Yin Wang, S. Gupta, B. Davis, S. I. Simon, G. Torre-Amione, and A. A. Knowlton. "HSP60 in heart failure: abnormal distribution and role in cardiac myocyte apoptosis." American Journal of Physiology-Heart and Circulatory Physiology 293, no. 4 (October 2007): H2238—H2247. http://dx.doi.org/10.1152/ajpheart.00740.2007.

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Heat shock protein (HSP) 60 is a mitochondrial and cytosolic protein. Previously, we reported that HSP60 doubled in end-stage heart failure, even though levels of the protective HSP72 were unchanged. Furthermore, we observed that acute injury in adult cardiac myocytes resulted in movement of HSP60 to the plasma membrane. We hypothesized that the inflammatory state of heart failure would cause translocation of HSP60 to the plasma membrane and that this would provide a pathway for cardiac injury. Two models were used to test this hypothesis: 1) a rat model of heart failure and 2) human explanted failing hearts. We found that HSP60 localized to the plasma membrane and was also found in the plasma early in heart failure. Plasma membrane HSP60 localized to lipid rafts and was detectable on the cell surface with the use of both flow cytometry and confocal microscopy. Localization of HSP60 to the cell surface correlated with increased apoptosis. In heart failure, HSP60 is in the plasma membrane fraction, on the cell surface, and in the plasma. Membrane HSP60 correlated with increased apoptosis. Release of HSP60 may activate the innate immune system, promoting a proinflammatory state, including an increase in TNF-α. Thus abnormal trafficking of HSP60 to the cell surface may be an early trigger for myocyte loss and the progression of heart failure.
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13

Larosa, Giulia, Paul W. Armstrong, and Christine Forster. "Endothelium-dependent relaxations in canine coronary arteries are enhanced in early heart failure and persist in recovery." Canadian Journal of Physiology and Pharmacology 72, no. 10 (October 1, 1994): 1148–54. http://dx.doi.org/10.1139/y94-162.

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In vitro coronary artery responsiveness to noradrenaline, phenylephrine, and BHT-920 together with functional relaxation to acetylcholine was assessed in dogs at the early onset of pacing-induced heart failure (1 week) and in dogs recovered from heart failure (3 weeks paced, followed by 4 weeks discontinued pacing). α-Adrenoceptor stimulation produced contractile responses that were unaltered in early congestive heart failure and recovery. Contractions to noradrenaline and BHT-920 were always less than those produced by phenylephrine. Endothelium-intact arteries demonstrated relaxations in response to noradrenaline and BHT-920, but not phenylephrine. Relaxations to noradrenaline were enhanced 24% in early heart failure and 47% following recovery from heart failure, compared with control. BHT-920 produced relaxations that were augmented 21 and 76% in early heart failure and recovery, respectively. Contractile sensitivity to noradrenaline increased 5-fold in early heart failure and was not different in recovery, compared with control. Contractile sensitivity to BHT-920 and phenylephrine was unaltered throughout. Acetylcholine produced relaxations that were increased 21% in early heart failure and 13% after recovery from congestive heart failure. Furthermore, acetylcholine sensitivity was significantly enhanced in early heart failure and recovery. The current study reveals a progressive adaptation of the coronary endothelium in congestive heart failure, possibly directed towards protection against excessive vasoconstriction due to circulating catecholamines.Key words: endothelium, congestive heart failure, coronary arteries, α-adrenoceptors, noradrenaline, acetylcholine.
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14

Salivonchyk, D. P., E. F. Semenyago, and V. A. Shilova. "CHRONIC HEART FAILURE: MODERN DIAGNOSTICS." Health and Ecology Issues, no. 2 (June 28, 2016): 4–10. http://dx.doi.org/10.51523/2708-6011.2016-13-2-1.

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Modern diagnostics is aimed at detecting heart failure with preserved ejection fraction (HF-SPI) at early stages. The most informative technique to diagnose CH-SPI is echocardiography (echocardiography) using tissue Doppler imaging.
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15

Ezzaher, A., N. el Houda Bouanani, and B. Crozatier. "Force-frequency relations and response to ryanodine in failing rabbit hearts." American Journal of Physiology-Heart and Circulatory Physiology 263, no. 6 (December 1, 1992): H1710—H1715. http://dx.doi.org/10.1152/ajpheart.1992.263.6.h1710.

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Force-frequency relations were studied in an isolated-perfused rabbit heart model. Heart failure was induced by a double volume plus pressure overload. Studies were performed at the early stage of heart failure when basal ventricular function was not decreased. The normal positive staircase induced by pacing in control hearts (CH) was replaced by a negative staircase in failing hearts (FH) with an increase in end-diastolic pressure for increased heart rates in FH. Postpacing potentiation and postextrasystolic potentiation (PESP) were significantly reduced in FH as compared with CH. Ventricular function decreased by 60% in both CH and FH under ryanodine with similar dose-response curves. Postpacing and PESP disappeared under ryanodine in CH and in FH with a reversal of the negative staircase in FH. The abnormal force-frequency relations observed in heart failure are thus attributed to sarcoplasmic reticulum dysfunction. Basal ventricular function during spontaneous heart rate may be normal in the early stage of heart failure, but sarcoplasmic reticulum dysfunction produces abnormalities in ventricular function when heart rate is abruptly modified, particularly during tachycardia.
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16

Ventura-Clapier, Renée, Elvira De Sousa, and Vladimir Veksler. "Metabolic Myopathy in Heart Failure." Physiology 17, no. 5 (October 2002): 191–96. http://dx.doi.org/10.1152/nips.01392.2002.

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Heart failure is a syndrome that also affects the periphery. Exercise intolerance and early fatigue seem to be linked in part to intrinsic alterations of skeletal muscle with decreases in both the production of ATP by mitochondria and the transfer of energy through the phosphotransfer kinases.
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17

Yilmaz, Mehmet Birhan. "Very early management of acute heart failure syndromes." Turk Kardiyoloji Dernegi Arsivi-Archives of the Turkish Society of Cardiology 39, no. 5 (July 1, 2011): 427–32. http://dx.doi.org/10.5543/tkda.2011.01599.

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18

Suzuki, Shoya, Ryo Momosaki, Tomomi Watanabe, and Masahiro Abo. "Effectiveness of Early Rehabilitation for Acute Heart Failure." Journal of Cardiopulmonary Rehabilitation and Prevention 39, no. 4 (July 2019): E23—E25. http://dx.doi.org/10.1097/hcr.0000000000000422.

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19

Summers, Richard L., and Sarah Sterling. "Early emergency management of acute decompensated heart failure." Current Opinion in Critical Care 18, no. 4 (August 2012): 301–7. http://dx.doi.org/10.1097/mcc.0b013e328354f05a.

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20

BATES, BETSY. "Obese Children Likely to Face Early Heart Failure." Pediatric News 41, no. 2 (February 2007): 35. http://dx.doi.org/10.1016/s0031-398x(07)70096-6.

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21

Leeson, Paul, and Adam J. Lewandowski. "A New Risk Factor for Early Heart Failure." Journal of the American College of Cardiology 69, no. 21 (May 2017): 2643–45. http://dx.doi.org/10.1016/j.jacc.2017.03.574.

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22

Gheorghiade, Mihai, and Robert O. Bonow. "Early follow-up after hospitalization for heart failure." Nature Reviews Cardiology 7, no. 8 (August 2010): 422–24. http://dx.doi.org/10.1038/nrcardio.2010.102.

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23

de Couto, Geoffrey, Maral Ouzounian, and Peter P. Liu. "Early detection of myocardial dysfunction and heart failure." Nature Reviews Cardiology 7, no. 6 (May 11, 2010): 334–44. http://dx.doi.org/10.1038/nrcardio.2010.51.

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24

Hauptman, Paul J., Sary Aranki, Gilbert H. Mudge, Gregory S. Couper, and Evan Loh. "Early cardiac allograft failure after orthotopic heart transplantation." American Heart Journal 127, no. 1 (January 1994): 179–86. http://dx.doi.org/10.1016/0002-8703(94)90523-1.

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25

Devlin, G. P., R. Troughton, M. Lund, and R. Doughty. "The New Zealand Heart Failure Registry: Early observations." Heart, Lung and Circulation 16 (January 2007): S23. http://dx.doi.org/10.1016/j.hlc.2007.06.059.

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26

Devlin, GP, R. Troughton, M. Lund, and R. Doughty. "THE NEW ZEALAND HEART FAILURE REGISTRY: EARLY OBSERVATIONS." Heart, Lung and Circulation 17 (January 2008): S13. http://dx.doi.org/10.1016/j.hlc.2008.03.028.

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27

Altice, Nancy, and Renee Gerow. "Early Cardiac Rehab to Reduce Heart Failure Readmissions." Heart & Lung 49, no. 2 (March 2020): 211. http://dx.doi.org/10.1016/j.hrtlng.2020.02.013.

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28

ZIMMER, ETAN Z., AVIHAI REICHLER, and MOSHE BRONSHTEIN. "ULTRASONOGRAPHY OF FETAL HEART FAILURE IN EARLY GESTATION." Prenatal Diagnosis 17, no. 5 (May 1997): 461–65. http://dx.doi.org/10.1002/(sici)1097-0223(199705)17:5<461::aid-pd87>3.0.co;2-s.

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29

Ikram, H. "Identifying the Patient with Heart Failure." Journal of International Medical Research 23, no. 3 (May 1995): 139–53. http://dx.doi.org/10.1177/030006059502300301.

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Heart failure is becoming an increasing concern to healthcare worldwide, and of particular concern in the Western world where the age of the population continues to rise. Furthermore, it has now become clear that, if heart failure is identified and treated in the earliest stages of ventricular dysfunction, the possibility of recovery from or substantial delay in progression to complete heart failure is extremely good and will give the patient a considerably improved quality of life. Certain signs and symptoms found on routine examination, coupled with knowledge of patient history, can indicate early heart failure. Patients will normally present to their family practitioner, who is likely to have long term, firsthand knowledge of the patient's medical and family history. Consequently, the general practitioner has a key role in identifying individuals with early heart failure. It is essential that the general practitioner is aware of the signs and symptoms of early heart failure, can interpret them correctly and knows what follow-up tests are necessary to confirm the diagnosis. Guidelines are presented here to assist the general practitioner in this task.
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30

Mentz, Robert J., Marco Metra, Gad Cotter, Olga Milo, Colleen McKendry, Karen Chiswell, Beth A. Davison, et al. "Early vs. late worsening heart failure during acute heart failure hospitalization: insights from the PROTECT trial." European Journal of Heart Failure 17, no. 7 (June 17, 2015): 697–706. http://dx.doi.org/10.1002/ejhf.308.

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31

Kaimoto, Satoshi, Atsushi Hoshino, Makoto Ariyoshi, Yoshifumi Okawa, Shuhei Tateishi, Kazunori Ono, Motoki Uchihashi, Kuniyoshi Fukai, Eri Iwai-Kanai, and Satoaki Matoba. "Activation of PPAR-α in the early stage of heart failure maintained myocardial function and energetics in pressure-overload heart failure." American Journal of Physiology-Heart and Circulatory Physiology 312, no. 2 (February 1, 2017): H305—H313. http://dx.doi.org/10.1152/ajpheart.00553.2016.

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Failing heart loses its metabolic flexibility, relying increasingly on glucose as its preferential substrate and decreasing fatty acid oxidation (FAO). Peroxisome proliferator-activated receptor α (PPAR-α) is a key regulator of this substrate shift. However, its role during heart failure is complex and remains unclear. Recent studies reported that heart failure develops in the heart of myosin heavy chain-PPAR-α transgenic mice in a manner similar to that of diabetic cardiomyopathy, whereas cardiac dysfunction is enhanced in PPAR-α knockout mice in response to chronic pressure overload. We created a pressure-overload heart failure model in mice through transverse aortic constriction (TAC) and activated PPAR-α during heart failure using an inducible transgenic model. After 8 wk of TAC, left ventricular (LV) function had decreased with the reduction of PPAR-α expression in wild-type mice. We examined the effect of PPAR-α induction during heart failure using the Tet-Off system. Eight weeks after the TAC operation, LV construction was preserved significantly by PPAR-α induction with an increase in PPAR-α-targeted genes related to fatty acid metabolism. The increase of expression of fibrosis-related genes was significantly attenuated by PPAR-α induction. Metabolic rates measured by isolated heart perfusions showed a reduction in FAO and glucose oxidation in TAC hearts, but the rate of FAO preserved significantly owing to the induction of PPAR-α. Myocardial high-energy phosphates were significantly preserved by PPAR-α induction. These results suggest that PPAR-α activation during pressure-overloaded heart failure improved myocardial function and energetics. Thus activating PPAR-α and modulation of FAO could be a promising therapeutic strategy for heart failure. NEW & NOTEWORTHY The present study demonstrates the role of PPAR-α activation in the early stage of heart failure using an inducible transgenic mouse model. Induction of PPAR-α preserved heart function, and myocardial energetics. Activating PPAR-α and modulation of fatty acid oxidation could be a promising therapeutic strategy for heart failure.
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32

Rillig, Andreas, Christina Magnussen, Ann-Kathrin Ozga, Anna Suling, Axel Brandes, Günter Breithardt, A. John Camm, et al. "Early Rhythm Control Therapy in Patients With Atrial Fibrillation and Heart Failure." Circulation 144, no. 11 (September 14, 2021): 845–58. http://dx.doi.org/10.1161/circulationaha.121.056323.

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Background: Even on optimal therapy, many patients with heart failure and atrial fibrillation experience cardiovascular complications. Additional treatments are needed to reduce these events, especially in patients with heart failure and preserved left ventricular ejection fraction. Methods: This prespecified subanalysis of the randomized EAST-AFNET4 trial (Early Treatment of Atrial Fibrillation for Stroke Prevention Trial) assessed the effect of systematic, early rhythm control therapy (ERC; using antiarrhythmic drugs or catheter ablation) compared with usual care (allowing rhythm control therapy to improve symptoms) on the 2 primary outcomes of the trial and on selected secondary outcomes in patients with heart failure, defined as heart failure symptoms New York Heart Association II to III or left ventricular ejection fraction [LVEF] <50%. Results: This analysis included 798 patients (300 [37.6%] female, median age 71.0 [64.0, 76.0] years, 785 with known LVEF). The majority of patients (n=442) had heart failure and preserved LVEF (LVEF≥50%; mean LVEF 61±6.3%), the others had heart failure with midrange ejection fraction (n=211; LVEF 40%–49%; mean LVEF 44 ± 2.9%) or heart failure with reduced ejection fraction (n=132; LVEF<40%; mean LVEF 31±5.5%). Over the 5.1-year median follow-up, the composite primary outcome of cardiovascular death, stroke, or hospitalization for worsening of heart failure or for acute coronary syndrome occurred less often in patients randomly assigned to ERC (94/396; 5.7 per 100 patient-years) compared with patients randomly assigned to usual care (130/402; 7.9 per 100 patient-years; hazard ratio, 0.74 [0.56–0.97]; P =0.03), not altered by heart failure status (interaction P value=0.63). The primary safety outcome (death, stroke, or serious adverse events related to rhythm control therapy) occurred in 71 of 396 (17.9%) patients with heart failure randomly assigned to ERC and in 87 of 402 (21.6%) patients with heart failure randomly assigned to usual care (hazard ratio, 0.85 [0.62–1.17]; P =0.33). LVEF improved in both groups (LVEF change at 2 years: ERC 5.3±11.6%, usual care 4.9±11.6%, P =0.43). ERC also improved the composite outcome of death or hospitalization for worsening of heart failure. Conclusions: Rhythm control therapy conveys clinical benefit when initiated within 1 year of diagnosing atrial fibrillation in patients with signs or symptoms of heart failure. Registration: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT01288352. URL: http://www.controlled-trials.com ; Unique identifier: ISRCTN04708680. URL: https://www.clinicaltrialsregister.eu ; Unique identifier: 2010-021258-20.
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33

Waleed, Madeeha. "Prevalence of different type of valvular heart disease and other cardiac pathologies of the heart in high risk patients with suspicion of heart failure. A retrospective cohort study." Clinical Cardiology and Cardiovascular Interventions 3, no. 9 (October 16, 2020): 01–07. http://dx.doi.org/10.31579/2641-0419/088.

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Background: Valvular heart disease and other cardiac pathologies are associated with impending heart failure. An early diagnosis of these can help prevent the disabling ad disastrous effects and improve the prognosis. Aim: The prevalence of various pathologies associated with heart failure is not known. This study helps in recognizing various pathologies that can lead to heart failure, which if diagnosed early can improve the patient’s outcome. Materials and Methods: A total of 4560 patients were included in the study. All the patients were aged greater than 15 years. Patients with suspicion of heart failure on symptoms were ordered echocardiography. Transthoracic echo was done using echocardiography ultrasound machine using the British Society of Echocardiography guidelines. Echocardiography was done by registered sonologists. Echocardiograph were later read by cardiologists. Data was collected on Excel sheet. Echocardiographic results Of 9 690 patients, were admitted to the hospital during the year 2013 to year 2017 with the suspicion of heart failure based on symptoms echocardiogram was ordered. Among these 2448 patients had normal echocardiographic findings were as 4560 had valvular disease. Among the valvular disease patients 2951(64.71%) were females and 1609(35.2%) were males. Among these 2950(64.6%) had mild valvular disease 959(21.0%) had moderate valvular disease and 651(14.2) patients had severe valvular disease. Mitral stenosis occurred in 1200(26.3%) patients, mitral regurgitation in 2953(64.7%) patients, tricuspid stenosis in 40 (0.008%)patients ,tricuspid regurgitation in 1592(34.8%) patients, aortic stenosis in 81 (0.017%) patients and aortic regurgitation in 1957(42.9%) patients. Ischemic cardiomyopathy was present in 24 patients, dilated cardiomyopathy in 14 patients, rheumatic heart disease in 23 patients, ventricular septum defect in 5 patients ,Atrial septum defect in 2 patients , Apical aneurysm formation in 4 patients, Uremic cardiomyopathy on 3 patients, Grade 1 diastolic dysfunction in 2200 patients, Grade 3 diastolic dysfunction in 400 patients, Bicuspid aortic valve in 5 patients and restrictive cardiomyopathy in two patients, 1100 patients had a thin rim of pericardial effusion and were ordered Thyroid function tests. Conclusion: In the community heart failure is a common cause of death. Various pathologies of the heart are predictors of the outcome and hence early diagnosis can help in proper treatment and increased survival
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34

Vuckovic, Karen M., Rebecca (Schuetz) Bierle, and Catherine J. Ryan. "Navigating Symptom Management in Heart Failure: The Crucial Role of the Critical Care Nurse." Critical Care Nurse 40, no. 2 (April 1, 2020): 55–63. http://dx.doi.org/10.4037/ccn2020685.

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High-acuity, progressive care, and critical care nurses often provide care for patients with heart failure during an exacerbation of acute disease or at the end of life. Identifying and managing heart failure symptoms is complex and requires early recognition and early intervention. Because symptoms of heart failure are not disease specific, patients may not respond to them appropriately, resulting in treatment delays. This article reviews the complexities and issues surrounding the patient’s ability to recognize heart failure symptoms and the critical care nurse’s role in facilitating early intervention. It outlines the many barriers to symptom recognition and response, including multimorbidities, age, symptom intensity, symptom escalation, and health literacy. The influence of self-care on heart failure management is also described. The critical care nurse plays a crucial role in teaching heart failure patients to identify and respond appropriately to their symptoms, thus promoting early intervention.
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35

Essay, Patrick, Baran Balkan, and Vignesh Subbian. "Decompensation in Critical Care: Early Prediction of Acute Heart Failure Onset." JMIR Medical Informatics 8, no. 8 (August 7, 2020): e19892. http://dx.doi.org/10.2196/19892.

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Background Heart failure is a leading cause of mortality and morbidity worldwide. Acute heart failure, broadly defined as rapid onset of new or worsening signs and symptoms of heart failure, often requires hospitalization and admission to the intensive care unit (ICU). This acute condition is highly heterogeneous and less well-understood as compared to chronic heart failure. The ICU, through detailed and continuously monitored patient data, provides an opportunity to retrospectively analyze decompensation and heart failure to evaluate physiological states and patient outcomes. Objective The goal of this study is to examine the prevalence of cardiovascular risk factors among those admitted to ICUs and to evaluate combinations of clinical features that are predictive of decompensation events, such as the onset of acute heart failure, using machine learning techniques. To accomplish this objective, we leveraged tele-ICU data from over 200 hospitals across the United States. Methods We evaluated the feasibility of predicting decompensation soon after ICU admission for 26,534 patients admitted without a history of heart failure with specific heart failure risk factors (ie, coronary artery disease, hypertension, and myocardial infarction) and 96,350 patients admitted without risk factors using remotely monitored laboratory, vital signs, and discrete physiological measurements. Multivariate logistic regression and random forest models were applied to predict decompensation and highlight important features from combinations of model inputs from dissimilar data. Results The most prevalent risk factor in our data set was hypertension, although most patients diagnosed with heart failure were admitted to the ICU without a risk factor. The highest heart failure prediction accuracy was 0.951, and the highest area under the receiver operating characteristic curve was 0.9503 with random forest and combined vital signs, laboratory values, and discrete physiological measurements. Random forest feature importance also highlighted combinations of several discrete physiological features and laboratory measures as most indicative of decompensation. Timeline analysis of aggregate vital signs revealed a point of diminishing returns where additional vital signs data did not continue to improve results. Conclusions Heart failure risk factors are common in tele-ICU data, although most patients that are diagnosed with heart failure later in an ICU stay presented without risk factors making a prediction of decompensation critical. Decompensation was predicted with reasonable accuracy using tele-ICU data, and optimal data extraction for time series vital signs data was identified near a 200-minute window size. Overall, results suggest combinations of laboratory measurements and vital signs are viable for early and continuous prediction of patient decompensation.
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36

Subramani, Sudhakar, Aric Aldrich, Sanjay Dwarakanath, Ami Sugawara, and Satoshi Hanada. "Early Graft Dysfunction Following Heart Transplant: Prevention and Management." Seminars in Cardiothoracic and Vascular Anesthesia 24, no. 1 (August 5, 2019): 24–33. http://dx.doi.org/10.1177/1089253219867694.

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Heart transplant can be considered as the “gold standard” treatment for end-stage heart failure, with nearly 5.7 million adults in the United States carrying a diagnosis of heart failure. According to the International Society for Heart and Lung Transplantation registry, nearly 3300 orthotopic heart transplants were performed in 2016 in North America. In spite of significant improvements in overall perioperative care of heart transplant recipients for the past few decades, the risk of 30-day mortality remains 5% to 10%, primarily related to early failure of the allograft. Early graft dysfunction (EGD) occurs within 24 hours after transplant, manifesting as left ventricular dysfunction, right ventricular dysfunction, or biventricular dysfunction. EGD is further classified into primary and secondary graft dysfunction. This review focus on describing overall incidences of EGD, potential risk factors associated with EGD, perioperative preventive measures, and various management options.
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37

Brown, Allen K. "Drug treatment of heart failure." Morecambe Bay Medical Journal 1, no. 10 (January 4, 1993): 267–69. http://dx.doi.org/10.48037/mbmj.v1i10.1202.

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In my early years in Lancaster I remember my senior colleague Dr W J Hay asking whether or not digoxin and diuretics remained routine treatment for congestive cardiac failure; in fact there had been little change, in that digoxin was being used less often. Recently there have been three important alterations in management. These are:-( 1) improved diagnostic capabilities,(2) the introduction of new drugs, particularly ACE inhibitors, and(3) the reappraisal of older drugs including hydralazine, nitrates and digitalis. Finally we have seen the establishment of cardiac transplantation, various attempts at mechanical cardiac assistance and cardiomyoplasty which are out ide the scope of this article but which need to be borne in mind when drugs fail.
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38

Lockwood, S., C. Bowman, and J. Cameron. "Early intervention in systolic heart failure = early recovery in LV ejection fraction." Heart, Lung and Circulation 24 (2015): S204. http://dx.doi.org/10.1016/j.hlc.2015.06.220.

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39

Takagi, Koji, Antoine Kimmoun, Naoki Sato, and Alexandre Mebazaa. "Management of Acute Heart Failure during an Early Phase." International Journal of Heart Failure 2, no. 2 (2020): 91. http://dx.doi.org/10.36628/ijhf.2019.0014.

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40

Slomski, Anita. "Early Rehabilitation Leads to Better Function in Heart Failure." JAMA 326, no. 12 (September 28, 2021): 1139. http://dx.doi.org/10.1001/jama.2021.15004.

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41

Piazza, Vito. "‘Door-to-furosemide’ timing: early treatment of heart failure." European Heart Journal Supplements 21, Supplement_B (March 1, 2019): B69—B70. http://dx.doi.org/10.1093/eurheartj/suz001.

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42

Vinson, Janice M., Michael W. Rich, Jane C. Sperry, Atul S. Shah, and Timothy McNamara. "Early Readmission of Elderly Patients With Congestive Heart Failure." Journal of the American Geriatrics Society 38, no. 12 (December 1990): 1290–95. http://dx.doi.org/10.1111/j.1532-5415.1990.tb03450.x.

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43

Kruse, Wolfgang. "Early Readmission of Elderly Patients with Congestive Heart Failure." Journal of the American Geriatrics Society 39, no. 10 (October 1991): 1045. http://dx.doi.org/10.1111/j.1532-5415.1991.tb04059.x.

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44

Ng, Kenney, Steven R. Steinhubl, Christopher deFilippi, Sanjoy Dey, and Walter F. Stewart. "Early Detection of Heart Failure Using Electronic Health Records." Circulation: Cardiovascular Quality and Outcomes 9, no. 6 (November 2016): 649–58. http://dx.doi.org/10.1161/circoutcomes.116.002797.

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45

Vistarini, Nicola, Carlo Pellegrini, Marco Aiello, Alessia Alloni, Cristian Monterosso, Barbara Cattadori, Carmine Tinelli, Andrea M. D’Armini, and Mario Vigano. "Should we perform heart retransplantation in early graft failure?" Transplant International 23, no. 1 (January 2010): 47–53. http://dx.doi.org/10.1111/j.1432-2277.2009.00945.x.

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46

Wang, Shu-Yi, Shang-Ren Hsu, Shih-Li Su, and Shih-Te Tu. "Sheehan's Syndrome Presenting with Early Postpartum Congestive Heart Failure." Journal of the Chinese Medical Association 68, no. 8 (August 2005): 386–91. http://dx.doi.org/10.1016/s1726-4901(09)70181-9.

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47

Sweeney, Joey. "After ED visits for heart failure, follow up early." Pharmacy Today 25, no. 3 (March 2019): 2. http://dx.doi.org/10.1016/j.ptdy.2019.02.029.

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48

ANDERSON, JANE. "Early Follow-Up May Lower Readmission in Heart Failure." Hospitalist News 3, no. 7 (July 2010): 16. http://dx.doi.org/10.1016/s1875-9122(10)70181-4.

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49

Pereira, N. L., M. R. Zile, R. A. Harley, and A. B. Van Bakel. "Myocardial Mechanisms Causing Heart Failure Early After Cardiac Transplantation." Transplantation Proceedings 38, no. 9 (November 2006): 2999–3003. http://dx.doi.org/10.1016/j.transproceed.2006.08.117.

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50

SHIRANI, J., J. NARULA, W. ECKELMAN, N. NARULA, and V. DILSIZIAN. "Early imaging in heart failure: Exploring novel molecular targets." Journal of Nuclear Cardiology 14, no. 1 (January 2007): 100–110. http://dx.doi.org/10.1016/j.nuclcard.2006.12.318.

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