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Journal articles on the topic 'Primary dilated cardiomyopathy'

Author: Grafiati
Published: 4 June 2021
Last updated: 18 February 2022

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1

YACOUB, A. "Pregnancy With Primary Dilated Cardiomyopathy." Obstetrics & Gynecology 99, no. 5 (May 2002): 928–30. http://dx.doi.org/10.1016/s0029-7844(01)01745-8.

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2

Subedi, Deepika, Diptesh Aryal, and Anil Shrestha. "Anesthetic Management of an Elderly Patient with Dilated Cardiomyopathy and Hypothyroidism for Inter-Trochanteric Fracture." Journal of Chitwan Medical College 9, no. 3 (September 25, 2019): 97–99. http://dx.doi.org/10.3126/jcmc.v9i3.25791.

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Dilated cardiomyopathy is a primary myocardial disease charac­terized by left ventricular or biventricular dilation and impaired contractility. The anesthetic management of a patient with dilat­ed cardiomyopathy undergoing a non-cardiac surgery is always challenging and may be associated with high mortality. Further­more, perioperative morbidity becomes more frequent in the el­derly with steep increases after the age of 75. We are reporting the successful anaesthetic management of a 93 years old patient with severe dilated cardiomyopathy planned for surgical repair of inter-trochanteric fracture under combined spinal anesthesia.
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3

Shin, Gil Ja. "A Clinical Study of Primary Dilated Cardiomyopathy." Ewha Medical Journal 14, no. 1 (1991): 61. http://dx.doi.org/10.12771/emj.1991.14.1.61.

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4

Pace, Charlotte. "Diet associated canine dilated cardiomyopathy." Veterinary Nurse 12, no. 4 (May 2, 2021): 170–75. http://dx.doi.org/10.12968/vetn.2021.12.4.170.

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Dilated cardiomyopathy (DCM) is a common cause of heart failure in the dog. Primary DCM is often a disease of exclusion, but inherited genetic breed dispositions have been reported. Secondary causes of DCM include toxins, nutritional deficiency, systemic and infectious disease. The number of dogs diagnosed with DCM has increased significantly in the last 20 years, and has been linked to the rise in popularity of boutique, exotic and grain-free, legume-rich diets. Veterinary cardiologists raised concerns as DCM was being reported in atypical breeds. Subsequently, the United States Food and Drug Agency released a statement in 2018 warning pet owners of the risks of grain-free and novel protein diets. It is assumed that the problem also occurs in the UK because these diets are popular here also. Contrary to primary causes of DCM, dogs have improved clinically and on echocardiograph when their diet has been changed and/or supplemented. No clear cause has yet been identified between these diets and DCM, but the potential reasons seem to be multifactorial and limited by a lack of understanding of the bioavailability, digestibility and metabolism of the novel proteins and legume-rich diets.
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5

Cheng, Zhenli, Shiv Kumar Yadav, Xiaoyan Liu, and Qijian Yi. "A reversible hypocalcemic dilated cardiomyopathy caused by primary hypoparathyroidism." Asian Journal of Medical Sciences 10, no. 2 (March 1, 2019): 65–68. http://dx.doi.org/10.3126/ajms.v10i2.22323.

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Dilated cardiomyopathy (DCM) is characterized by dilation and impaired contraction of one or both ventricles. Affected patients have impaired systolic function and may or may not develop overt heart failure (HF). Prognosis is generally poor without heart transplantation. We experienced a case of a 10-year-old child with dilated cardiomyopathy (DCM) accompanied by undiagnosed primary hypoparathyroidism. In our case,aggressive management of hypoparathyroidism significantly improved the manifestations of DCM. The case presentation highlights the importance of considering hypoparathyroidism as a cause of reversible myocardial dysfunction.
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6

Kesici, Selman, Hüseyin Demirbilek, Murat Tanyıldız, Mehmet Gumustas, Benan Bayrakci, and Mutlu Yazici. "Reversible Dilated Cardiomyopathy Due to Combination of Vitamin D–Deficient Rickets and Primary Hypomagnesemia in an 11-Month-Old Infant." Journal of Pediatric Intensive Care 07, no. 01 (May 2, 2017): 046–48. http://dx.doi.org/10.1055/s-0037-1602803.

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AbstractVitamin D–deficient rickets is still an important and common health problem in developing countries. Since calcium is an essential ion for cardiac muscle contraction, calcium deficiency caused by rickets can cause secondary dilated cardiomyopathy. This situation can be exacerbated by coexisting hypomagnesemia. Here, we report a case of dilated cardiomyopathy due to hypocalcemia induced by vitamin D–deficient rickets and accompanying primary hypomagnesemia in an infant whose cardiomyopathy was successfully treated by replacement of calcium, vitamin D, and magnesium. In addition to genetic causes, viral infections, and idiopathic factors, metabolic abnormalities are important etiologic factors in pathogenesis of dilated cardiomyopathy and since they are treatable, prompt diagnosis of these disorders is crucial.
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7

Yacoub, Ashraf, and M. Jocelyne Martel. "Pregnancy in a Patient With Primary Dilated Cardiomyopathy." Obstetrics & Gynecology 99, no. 5, Part 2 (May 2002): 928–30. http://dx.doi.org/10.1097/00006250-200205001-00022.

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8

Kroumpouzou, E., I. P. Gomatos, A. Kataki, M. Karayannis, G. D. Dangas, and P. Toutouzas. "Common Pathways for Primary Hypertrophic and Dilated Cardiomyopathy." Hybridoma and Hybridomics 22, no. 1 (February 2003): 41–45. http://dx.doi.org/10.1089/153685903321538071.

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9

Agnetti, Aldo, Lee Bitton, Bertrand Tchana, Akamin Raymond, and Nicola Carano. "Primary carnitine deficiency dilated cardiomyopathy: 28years follow-up." International Journal of Cardiology 162, no. 2 (January 2013): e34-e35. http://dx.doi.org/10.1016/j.ijcard.2012.05.038.

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10

ALFONSO, F., A. L. P. CAFOALO, J. DEL TORO, E. TORRECILLA, M. REY, and P. DE RABAGO. "Right ventricular dilated cardiomyopathy associated with primary biliary cirrhosis." European Heart Journal 12, no. 11 (November 1, 1991): 1240–43. http://dx.doi.org/10.1093/eurheartj/12.11.1240.

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11

Arora, Aanchal, Y. C. Porwal, Pushpa Kumari, and Dilip Kumar. "Reversible dilated cardiomyopathy in a case of primary hypothyroidism." Indian Journal of Medical Specialities 7, no. 4 (October 2016): 171–73. http://dx.doi.org/10.1016/j.injms.2016.09.001.

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12

Arbustini, Eloisa, Marcello Disertori, and Jagat Narula. "Primary Prevention of Sudden Arrhythmic Death in Dilated Cardiomyopathy." JACC: Heart Failure 5, no. 1 (January 2017): 39–43. http://dx.doi.org/10.1016/j.jchf.2016.11.009.

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13

KLEIN, GEORGE J., ANDREW D. KRAHN, ALLAN C. SKANES, RAYMOND YEE, and LORNE J. GULA. "Primary Prophylaxis of Sudden Death in Hypertrophic Cardiomyopathy, Arrhythmogenic Right Ventricular Cardiomyopathy, and Dilated Cardiomyopathy." Journal of Cardiovascular Electrophysiology 16, s1 (September 2005): S28—S34. http://dx.doi.org/10.1111/j.1540-8167.2005.50116.x.

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14

Iskandrian, Abdulmassih S., Hope Helfeld, Joseph Lemlek, Jaetae Lee, Basil Iskandrian, and Jaekyeong Heo. "Differentiation between primary dilated cardiomyopathy and ischemic cardiomyopathy based on right ventricular performance." American Heart Journal 123, no. 3 (March 1992): 768–73. http://dx.doi.org/10.1016/0002-8703(92)90518-z.

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15

Lin, Kimberly Y., Basavaraj Kerur, Char M. Witmer, Lauren A. Beslow, Daniel J. Licht, Rebecca N. Ichord, and Beth D. Kaufman. "Thrombotic events in critically ill children with myocarditis." Cardiology in the Young 24, no. 5 (September 9, 2013): 840–47. http://dx.doi.org/10.1017/s1047951113001145.

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AbstractBackground: Children with myocarditis have multiple risk factors for thrombotic events, yet the role of antithrombotic therapy is unclear in this population. We hypothesised that thrombotic events in critically ill children with myocarditis are common and that children with myocarditis are at higher risk for thrombotic events than children with non-inflammatory dilated cardiomyopathy. Methods: This is a retrospective chart review of all children presenting to a single centre cardiac intensive care unit with myocarditis from 1995 to 2008. A comparison group of children with dilated cardiomyopathy was also examined. Antithrombotic regimens were recorded. The primary outcome of thrombotic events included intracardiac clots and any thromboembolic events. Results: Out of 45 cases with myocarditis, 40% were biopsy-proven, 24% viral polymerase chain reaction-supported, and 36% diagnosed based on high clinical suspicion. There were two (4.4%) thrombotic events in the myocarditis group and three (6.7%) in the dilated cardiomyopathy group (p = 1.0). Neither the use of any antiplatelet or anticoagulation therapy, use of intravenous immune globulin, presence of any arrhythmia, nor need for mechanical circulatory support were predictive of thrombotic events in the myocarditis, dilated cardiomyopathy, or combined groups. Conclusions: Thrombotic events in critically ill children with myocarditis and dilated cardiomyopathy occurred in 6% of the combined cohort. There was no difference in thrombotic events between inflammatory and non-inflammatory cardiomyopathy groups, suggesting that the decision to use antithrombotic prophylaxis should be based on factors other than the underlying aetiology of a child's acute decompensated heart failure.
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16

He, Quan, Miao Wang, Nicole Harris, and Xianlin Han. "Tafazzin knockdown interrupts cell cycle progression in cultured neonatal ventricular fibroblasts." American Journal of Physiology-Heart and Circulatory Physiology 305, no. 9 (November 1, 2013): H1332—H1343. http://dx.doi.org/10.1152/ajpheart.00084.2013.

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Mutation of the mitochondrial protein tafazzin causes dilated cardiomyopathy in Barth syndrome. Previous studies have shown that tafazzin knockdown promotes hypertrophy of neonatal cardiac myocytes. The current investigation was designed to show whether tafazzin knockdown affects cardiac fibroblast proliferation and collagen secretion, which contribute to fibrosis in dilated cardiomyopathy. In primary cultures of neonatal ventricular fibroblasts (NVFs) transduced with a tafazzin short hairpin RNA adenovirus, tafazzin knockdown increased production of reactive oxygen species and activation of mitogen-activated protein kinases and induced protein and DNA synthesis via cell cycle regulators. It also reduced intracellular ATP, activated AMPK, and caused multinucleation, hypertrophy, and enhanced collagen secretion. We concluded that tafazzin knockdown interrupts the NVF cell cycle and this in turn may contribute to fibrosis and dilated cardiomyopathy in Barth syndrome.
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17

Meyer, Christian, Per Schueller, Astrid Rodenbeck, Marcus Hennersdorf, Marc Merx, Joachim Winter, Tienush Rassaf, Malte Kelm, and Patrick Schauerte. "Primary and Secondary Prevention of Ventricular Arrhythmias in Dilated Cardiomyopathy." International Heart Journal 50, no. 6 (2009): 741–51. http://dx.doi.org/10.1536/ihj.50.741.

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18

Perin, Francesca, María del Mar Rodríguez-Vázquez del Rey, Carmen Carreras-Blesa, Luisa Arrabal-Fernández, Juan Jiménez-Jáimez, and Luis Tercedor. "Dilated Cardiomyopathy With Short QT Interval Suggests Primary Carnitine Deficiency." Revista Española de Cardiología (English Edition) 71, no. 12 (December 2018): 1074–75. http://dx.doi.org/10.1016/j.rec.2017.09.004.

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19

Tziomalos, Konstantinos, Nikitas Kakavas, Evangelia Kountana, Faidon Harsoulis, and Elias Basayannis. "Reversible dilated hypocalcaemic cardiomyopathy in a patient with primary hypoparathyroidism." Clinical Endocrinology 64, no. 6 (June 2006): 717–18. http://dx.doi.org/10.1111/j.1365-2265.2006.02538.x.

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20

Yamamoto, Hidenori, Yoshie Fukasawa, Naoki Ohashi, Takehiko Yokoyama, Kazutaka Suzuki, Takaya Ota, Kazushi Yasuda, Kentaro Omoya, Yoshiyuki Takahashi, and Taichi Kato. "Prediction of postnatal clinical course in primary congenital dilated cardiomyopathy." Pediatrics International 61, no. 12 (December 2019): 1196–201. http://dx.doi.org/10.1111/ped.14029.

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21

Bänsch, Dietmar, Matthias Antz, Sigrid Boczor, Marius Volkmer, Jürgen Tebbenjohanns, Karlheinz Seidl, Michael Block, Frank Gietzen, Jürgen Berger, and Karl Heinz Kuck. "Primary Prevention of Sudden Cardiac Death in Idiopathic Dilated Cardiomyopathy." Circulation 105, no. 12 (March 26, 2002): 1453–58. http://dx.doi.org/10.1161/01.cir.0000012350.99718.ad.

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22

Bansch, D., M. Antz, and S. Boczor. "Primary prevention of sudden cardiac death in idiopathic dilated cardiomyopathy. the cardiomyopathy trial (CAT)." ACC Current Journal Review 11, no. 5 (September 2002): 73. http://dx.doi.org/10.1016/s1062-1458(02)00817-6.

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23

Markovic, Natasa, Snezana Djurica, Milan Brajovic, and Dragoslav Milosevic. "Dilated cardiomyopathy associated with autoimmune disease of thyroid gland." Srpski arhiv za celokupno lekarstvo 133, Suppl. 1 (2005): 46–51. http://dx.doi.org/10.2298/sarh05s1046m.

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Congestive heart failure is the main cause of cardiovascular morbidity and mortality with more than one million hospitalizations per year. Dilated cardiomyopathy is one of the main causes of congestive heart failure characterized by diminished function of the left, right or both ventricles and ejection fraction less than 40%. Numerous studies reported that the diseases of thyroid gland among the patients with dilated cardiomiopathy were very frequent: with prevalence from 18% to 49%. The impaired thyroid gland function was found as primary cause of cardiomyopathy in 1% of patients. At the same time, among patients with terminal dilated cardiomyopathy, euthyroid sick syndrome was very frequent with low values of T3. According to our results, 29.4% of patients with dilated cardiomyopathy also had autoimmunity disorder of thyroid gland with present antithyroglobin and antimicrosomal antibodies. These patients had lower ejection fraction and worse prognosis. In American College of Cardiology/American Heart Association guidelines for the evaluation and treatment of the congestive heart failure, evaluation of thyroid gland function was recommended; but the evaluation of antitireoglobulin antibodies and free T3 and free T4 was also essential, as was calculation of their ratio. This is the way to discover the autoimmunity disorder of thyroid gland and/ or ??euthyroid sick syndrome??. In patients with dilated cardiomyopathy and low-T3 syndrome, short-term administration of thyroid hormones resulted in improvement of ejection fraction, diminishing of symptoms and better survival.
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24

Barman, Rabindra Nath, Shakil Ghafur, Haripada Sarkar, Md Abu Zahid, Md Abdullah Al Mahmud, Md Mahbubur Rahman, and Md Hasanul Islam. "Electrocardiographic and Echocardiographic Profile of Dilated Cardiomyopathy Patients." Cardiovascular Journal 12, no. 2 (July 3, 2020): 109–12. http://dx.doi.org/10.3329/cardio.v12i2.47987.

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Background: Cardiomyopathy is a primary disorder of heart muscle with abnormal myocardial performance. It is an important cause of heart failure and accounts for upto 25% of causes of heart failure. In view of the high prevalence of chronic heart failure due to underlying dilated cardiomyopathy and the lack of data on DCM, the study was undertaken. Methods: A total of 100 patients (71 males and 29 females) of dilated cardiomyopathy were taken who was undergone Echocardiography at popular Diagnostic centre, Rangpur. ECG and echocardiography was done among all these patients using standard techniques. Results: Majority of the patient was above the age 50 years with male to female ratio is 2.4 :1. Sinus tachycardia, non specific ST-T change, LVH, non progression of R in v1-v5 were common ECG abnormalities. Conclusion: ECG may be normal in patients with DCM though sinus tachycardia and non specific ST-T abnormalities were common. Cardiovasc. j. 2020; 12(2): 109-112
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25

Blazsó, Péter, Kornél Kákonyi, Tamás Forster, and Róbert Sepp. "Cardiomyopathiás és ioncsatorna-betegek regisztere: a Szegedi CardioGen Regiszter." Orvosi Hetilap 158, no. 3 (January 2017): 101–5. http://dx.doi.org/10.1556/650.2017.30659.

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Abstract: The Szeged cardiomyopathy and ion channel diseases registry aims to establish a representative disease-specific registry based on the recruitment of patients with different cardiomyopathies and ion channel diseases followed at the Cardiology Center, University of Szeged. The registry collects patient data on the main forms of primary cardiomyopathies (hypertrophic, dilated, restrictive, arrhythmogenic right ventricular, left ventricular non-compact, tako-tsubo cardiomyopathy) and ion channel diseases (long QT syndrome, short QT syndrome, Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia). Patients with hypertrophic cardiomyopathy (388 patients) make up the largest group of patients in the registry. Patients with dilated cardiomyopathy (310 patients) and patients with the long QT syndrome (111 patients) form two other sizable groups. Analyzed data of the group of patients with hypertrophic cardiomyopathy indicate similar figures with regard to disease related mortality and morbidity and clinical parameters. Orv. Hetil., 2017, 158(3), 101–105.
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Gramley, Felix, and Andreas Goette. "Implantable Cardioverter–Defibrillators for Primary Prevention of Sudden Cardiac Death." European Cardiology Review 6, no. 3 (2010): 92. http://dx.doi.org/10.15420/ecr.2010.6.3.92.

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Sudden cardiac death (SCD) remains a major cause of death in the industrialised world. Implantable cardioverter–defibrillators (ICDs) have been shown to be an effective therapy option for the primary prevention of SCD in patients at high risk of SCD. This review will discuss adequate risk stratification in various disease states, such as coronary artery disease, ischaemic and non-ischaemic cardiomyopathies (dilated cardiomyopathy, hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy), channelopathies (Brugada syndrome, long- QT syndrome, short-QT syndrome, catecholaminergic polymorphic ventricular tachycardia) and congenital heart diseases, to identify patients at high risk of SCD and selection criteria for ICD therapy. The most important clinical primary prevention trials will be highlighted. Finally, complications of device therapy and quality of life issues will be addressed.
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27

Nishinarita, M., M. Nakagawa, and E. Tanaka. "Dilated cardiomyopathy (DCM) associated with SSA antibody in primary Sjögren syndrome." Modern Rheumatology 10, no. 2 (June 2000): 114–16. http://dx.doi.org/10.3109/s101650050009.

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28

Calore, Chiara, Luisa Cacciavillani, Giovanni Maria Boffa, Caterina Silva, Enrico Tiso, Martina Perazzolo Marra, Enrico Bacchiega, Francesco Corbetti, and Sabino Iliceto. "Contrast-enhanced cardiovascular magnetic resonance in primary and ischemic dilated cardiomyopathy." Journal of Cardiovascular Medicine 8, no. 10 (October 2007): 821–29. http://dx.doi.org/10.2459/jcm.0b013e3280101e3c.

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29

Radovanović, Ninoslav, Bogoljub Mihajlović, Jan Seletianskyštianskỳ, Vladimir Torbica, Milan Mijatov, Miroslava Popov, and Z̆ivojin S. Jonjev. "Reductive annuloplasty of double orifices in patients with primary dilated cardiomyopathy." Annals of Thoracic Surgery 73, no. 3 (March 2002): 751–55. http://dx.doi.org/10.1016/s0003-4975(01)03433-6.

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30

Groner, Abraham, Jen Yau, Irene D. Lytrivi, H. Helen Ko, James C. Nielsen, Ira A. Parness, and Shubhika Srivastava. "The role of right ventricular function in paediatric idiopathic dilated cardiomyopathy." Cardiology in the Young 23, no. 3 (August 23, 2012): 409–15. http://dx.doi.org/10.1017/s104795111200114x.

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AbstractIntroductionThe prevalence of right ventricular dysfunction in idiopathic dilated cardiomyopathy is incompletely studied in children. Furthermore, right ventricular function may signal worse outcomes. We evaluated recently published right ventricular function echocardiographic indices in identifying dysfunction in children with idiopathic dilated cardiomyopathy and the impact of right ventricular dysfunction on long-term prognosis.MethodsA retrospective database review of right ventricular function indices in 30 patients with idiopathic dilated cardiomyopathy was compared with 60 age- and sex-matched controls from January, 2001 until December, 2010. Right ventricular function was assessed by Doppler tissue peak systolic S′, early and late diastolic E′ and A′ waves and isovolumic acceleration at the tricuspid valve annulus; pulsed wave Doppler tricuspid valve inflow E and A waves; right ventricular myocardial performance index; tricuspid annular plane systolic excursion; right ventricular fractional area change.ResultsRight ventricular systolic and diastolic function in idiopathic dilated cardiomyopathy was significantly impaired. All measured indices except for isovolumic acceleration and fractional area change were significantly reduced, with a p-value less than 0.05. There was no right ventricular index predictive of death or transplantation. Patients with poor outcome were significantly more likely to need inotropic support (p-value equal to 0.018), be placed on a ventricular assist device (p equal to 0.005), and have a worse left ventricular ejection fraction z-score (p-value equal to 0.002).ConclusionRight ventricular dysfunction is under-recognised in children presenting with idiopathic dilated cardiomyopathy. The need for clinical circulatory support and left ventricular ejection fraction z-score less than minus 8 were primary determinants of outcome, independent of the degree of derangement in right ventricular function.
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31

Ciarambino, Tiziana, Giovanni Menna, Gennaro Sansone, and Mauro Giordano. "Cardiomyopathies: An Overview." International Journal of Molecular Sciences 22, no. 14 (July 19, 2021): 7722. http://dx.doi.org/10.3390/ijms22147722.

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Background: Cardiomyopathies are a heterogeneous group of pathologies characterized by structural and functional alterations of the heart. Aims: The purpose of this narrative review is to focus on the most important cardiomyopathies and their epidemiology, diagnosis, and management. Methods: Clinical trials were identified by Pubmed until 30 March 2021. The search keywords were “cardiomyopathies, sudden cardiac arrest, dilated cardiomyopathy (DCM), hypertrophic cardiomyopathy (HCM), restrictive cardiomyopathy, arrhythmogenic cardiomyopathy (ARCV), takotsubo syndrome”. Results: Hypertrophic cardiomyopathy (HCM) is the most common primary cardiomyopathy, with a prevalence of 1:500 persons. Dilated cardiomyopathy (DCM) has a prevalence of 1:2500 and is the leading indication for heart transplantation. Restrictive cardiomyopathy (RCM) is the least common of the major cardiomyopathies, representing 2% to 5% of cases. Arrhythmogenic cardiomyopathy (ARCV) is a pathology characterized by the substitution of the myocardium by fibrofatty tissue. Takotsubo cardiomyopathy is defined as an abrupt onset of left ventricular dysfunction in response to severe emotional or physiologic stress. Conclusion: In particular, it has been reported that HCM is the most important cause of sudden death on the athletic field in the United States. It is needless to say how important it is to know which changes in the heart due to physical activity are normal, and when they are pathological.
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Goyal, Abhishek, Bishav Mohan, Kavita Saggar, and Gurpreet Singh Wander. "Primary haemochromatosis resulting in dilated cardiomyopathy arising out of mutation in HJV gene in Indian patients: a rare scenario." BMJ Case Reports 13, no. 9 (September 2020): e235650. http://dx.doi.org/10.1136/bcr-2020-235650.

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Primary haemochromatosis (PH) is a genetic disorder of iron metabolism with multiorgan involvement due to mutations in HFE or more rarely haemojuvelin (HJV) gene. Cardiac involvement results in dilated cardiomyopathy with reduced ejection fraction and progressive heart failure. PH is rarely reported from India and cardiomyopathy due to PH from HJV mutations is thought to be uncommon. We report two families with cardiomyopathy resulting from PH. Diagnosis was suspected on the basis of skin pigmentation, markedly elevated serum ferritin and transferring saturation. Genetic testing revealed a rare mutation in HJV gene in one family. Being a treatable condition, PH should be suspected and investigated in cardiomyopathy patients in Indian subcontinent. If HFE is negative, analysis of non-HFE mutation should always be considered.
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33

Kota, Sunil Kumar, Prabhas Ranjan Tripathy, Siva Krishna Kota, Sruti Jammula, Lalit Kumar Meher, and Kirtikumar Dharmshibhai Modi. "Primary hypothyroidism: uncommon presentation with reversible dilated cardiomyopathy in a young subject." International Journal of Endocrinology & Metabolism 10, no. 1 (March 1, 2012): 440–43. http://dx.doi.org/10.5812/ijem.2382.

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34

&NA;. "Labour Analgesia Guided by Echocardiography in a Parturient with Primary Dilated Cardiomyopathy." Obstetric Anesthesia Digest 25, no. 4 (December 2005): 212. http://dx.doi.org/10.1097/00132582-200512000-00042.

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35

Gatzoulis, Konstantinos A., Apostolos-Ilias Vouliotis, Dimitris Tsiachris, Maria Salourou, Stefanos Archontakis, Polychronis Dilaveris, Theodoros Gialernios, et al. "Primary Prevention of Sudden Cardiac Death in a Nonischemic Dilated Cardiomyopathy Population." Circulation: Arrhythmia and Electrophysiology 6, no. 3 (June 2013): 504–12. http://dx.doi.org/10.1161/circep.113.000216.

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36

Alexander, Danny, Raffaella Lombardi, Gabriela Rodriguez, Matthew M. Mitchell, and Ali J. Marian. "Metabolomic distinction and insights into the pathogenesis of human primary dilated cardiomyopathy." European Journal of Clinical Investigation 41, no. 5 (December 14, 2010): 527–38. http://dx.doi.org/10.1111/j.1365-2362.2010.02441.x.

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37

Okutomi, Toshiyuki, Miwako Saito, Kan Amano, Keiko Fukuoka, and Sumio Hoka. "Labour analgesia guided by echocardiography in a parturient with primary dilated cardiomyopathy." Canadian Journal of Anesthesia/Journal canadien d'anesthésie 52, no. 6 (June 2005): 622–25. http://dx.doi.org/10.1007/bf03015773.

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38

Dadson, Keith, Ludger Hauck, and Filio Billia. "Molecular mechanisms in cardiomyopathy." Clinical Science 131, no. 13 (June 23, 2017): 1375–92. http://dx.doi.org/10.1042/cs20160170.

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Cardiomyopathies represent a heterogeneous group of diseases that negatively affect heart function. Primary cardiomyopathies specifically target the myocardium, and may arise from genetic [hypertrophic cardiomyopathy (HCM), arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D), mitochondrial cardiomyopathy] or genetic and acquired [dilated cardiomyopathy (DCM), restrictive cardiomyopathy (RCM)] etiology. Modern genomics has identified mutations that are common in these populations, while in vitro and in vivo experimentation with these mutations have provided invaluable insight into the molecular mechanisms native to these diseases. For example, increased myosin heavy chain (MHC) binding and ATP utilization lead to the hypercontractile sarcomere in HCM, while abnormal protein–protein interaction and impaired Ca2+ flux underlie the relaxed sarcomere of DCM. Furthermore, expanded access to genetic testing has facilitated identification of potential risk factors that appear through inheritance and manifest sometimes only in the advanced stages of the disease. In this review, we discuss the genetic and molecular abnormalities unique to and shared between these primary cardiomyopathies and discuss some of the important advances made using more traditional basic science experimentation.
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39

Mandal, Anirban, and Amitabh Singh. "Hypopituitarism: A Very Rare Cause of Dilated Cardiomyopathy in a Child." Journal of Nepal Paediatric Society 37, no. 2 (February 24, 2018): 197–200. http://dx.doi.org/10.3126/jnps.v37i2.17278.

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Dilated cardiomyopathy (DCMP), the leading type of cardiomyopathy in children, can be either a primary disease or secondary to a host of pathologies. Endocrine diseases are an extremely rare cause of DCMP in children. Hypopituitarism (congenital or acquired), a rare condition in children, may present in a variety of phenotypes depending on the hormonal deficiency (partial vs. pan hypopituitarism) and associated developmental defects. We describe a 10 year old boy with short stature, severely retarded bone age and congestive cardiac failure (CCF). He was diagnosed to have DCMP with hypopituitarism. Review of literature reveal possible mechanisms of DCMP and CCF in hypopituitarism and probably also indicate favorable response to hormonal replacement therapy.
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Yang, Jian, Wei-wei Xu, and Shen-jiang Hu. "Heart Failure: Advanced Development in Genetics and Epigenetics." BioMed Research International 2015 (2015): 1–11. http://dx.doi.org/10.1155/2015/352734.

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Heart failure (HF) is a complex pathophysiological syndrome that arises from a primary defect in the ability of the heart to take in and/or eject sufficient blood. Genetic mutations associated with familial dilated cardiomyopathy, hypertrophic cardiomyopathy, and arrhythmogenic right ventricular cardiomyopathy can contribute to the various pathologies of HF. Therefore, genetic screening could be an approach for guiding individualized therapies and surveillance. In addition, epigenetic regulation occurs via key mechanisms, including ATP-dependent chromatin remodeling, DNA methylation, histone modification, and RNA-based mechanisms. MicroRNA is also a hot spot in HF research. This review gives an overview of genetic mutations associated with cardiomyopathy and the roles of some epigenetic mechanisms in HF.
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Miksiunas, Rokas, Kestutis Rucinskas, Vilius Janusauskas, Siegfried Labeit, and Daiva Bironaite. "Histone Deacetylase Inhibitor Suberoylanilide Hydroxamic Acid Improves Energetic Status and Cardiomyogenic Differentiation of Human Dilated Myocardium-Derived Primary Mesenchymal Cells." International Journal of Molecular Sciences 21, no. 14 (July 8, 2020): 4845. http://dx.doi.org/10.3390/ijms21144845.

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Background. In this study the effect of histone deacetylase (HDAC) inhibitor suberoylanilide hydroxamic acid (SAHA) on the energetic status and cardiomyogenic differentiation of human healthy and dilated myocardium-derived mesenchymal stromal cells (hmMSC) have been investigated. Methods. The hmMSC were isolated from the healthy and dilated post-operation heart biopsies by explant outgrowth method. Cell proliferation, HDAC activity, mitochondrial membrane potential, and level of adenosine triphosphate (ATP) were evaluated. The effect of SAHA on mitochondrial parameters has been investigated also by Seahorse XF analyzer and cardiomyogenic differentiation was confirmed by the expression of transcription factor NK2 Homeobox 5 (Nkx2.5), cardiac troponin T and alpha cardiac actin at gene and protein levels. Results. Dilated myocardium-derived hmMSC had almost 1.5 folds higher HDAC activity compared to the healthy cells and significantly lower mitochondrial membrane potential and ATP level. HDAC class I and II inhibitor SAHA improved energetic status of mitochondria in dilated myocardium-isolated hmMSC and increased expression of cardiac specific proteins during 14 days of exposure of cells to SAHA. Conclusions. HDAC inhibitor SAHA can be a promising therapeutic for dilated cardiomyopathy (DCM). Dilated hmMSC exposed to SAHA improved energetic status and, subsequently, cardiomyogenic differentiation. Data suggest that human dilated myocardium-derived MSC still have cardio tissue regenerative potential, which might be stimulated by HDAC inhibitors.
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Janus, Izabela, Marcin Nowak, and Janusz A. Madej. "Pathomorphological Changes of the Myocardium in Canine Dilated Cardiomyopathy (DCM)." Bulletin of the Veterinary Institute in Pulawy 59, no. 1 (April 1, 2015): 135–42. http://dx.doi.org/10.1515/bvip-2015-0020.

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Abstract The study was conducted on ventricular and atrial wall preparations from 11 dogs with clinically diagnosed dilated cardiomyopathy. After fixation, the specimens were stained with haematoxylin and eosin and Masson-Goldner trichrome technique. Parenchymal changes (fibrosis and fatty infiltration), vascular changes (congestion and coronary vessel wall hypertrophy), degenerative changes (loss of striation, changes in cardiomycyte and nuclei structure), and presence of inflammatory infiltrates (mononuclear and polynuclear) were estimated. Complex histological changes in both ventricular and atrial muscles were shown. It was not determined whether the processes occurring in the myocardium have a primary character, or are a consequence of developing heart failure. Such issues will be put under further and more detailed examination.
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43

Gonik, M. I., M. S. Zharkova, O. Yu Kiseleva, E. V. Berezina, Sh A. Ondos, Yu V. Lerner, E. A. Kogan, and V. T. Ivashkin. "Primary Terminal Haemochromatosis in a 50 Year-Old Patient." Russian Journal of Gastroenterology, Hepatology, Coloproctology 31, no. 1 (April 1, 2021): 64–73. http://dx.doi.org/10.22416/1382-4376-2021-31-1-64-73.

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Aim. A clinical description of end-stage hereditary haemochromatosis manifested with chronic alcohol abuse.Key points. A 50-yo patient referred with marked general weakness as a major complaint. The patient had a history of long-term alcohol consumption at toxic doses, putative cirrhosis, paroxysmal atrial fibrillation, type 2 diabetes mellitus. The patient's severity on admission was conditioned by marked hypotension. Further examination aimed at excluding occult gastrointestinal bleeding, adrenal insufficiency, decompensated heart failure. Bronze skin and icteric sclerae were positive. Blood tests revealed severe macrocytic hyperchromic anaemia, thrombocytopae-nia, hyperbilirubinaemia, hypoalbuminaemia, hypocoagulation, elevated transaminases, hyponatraemia, elevated creatinine (CKD DPI 63 mL/min), severe hyperferritinaemia. Faecal occult blood test and EGDS for bleeding were negative. Abdominal ultrasound exposed signs of liver cirrhosis and portal hypertension (ascites, splenomegaly). Echocardiographic evidence of dilated cardiomyopathy of all chambers, a reduced 24% ejection fraction at absent acute myocardial infarction. Primary haemochromatosis was suspected upon high ferritin, transferrin iron saturation and multiple organ dysfunction. Genotyping revealed the HFE 845G > A variant diagnostic of haemochromatosis type 1. Clinical diagnosis: Primary disease: haemochromatosis (homozygous variant HFE 845G > A (A/A)): liver cirrhosis, Child-Pugh class C. Portal hypertension: splenomegaly, ascites. Dilated cardiomyopathy. Diabetes mellitus. Complications: multiple organ dysfunction (SOFA 16). Liver failure: jaundice, hypoalbuminaemia, hypocoagulation. Cardiac rhythm and conduction disorder: paroxysmal atrial fibrillation. Acute cardiac failure with underlying CHF IIb, NYHA class 3. Acute renal failure (anuria) with underlying CKD stage 3 (CKD DPI 63 mL/min). Moderate macrocytic hyperchromic anaemia. Acute and chronic adrenal failure. Despite a cardiovascular and renal failure compensation therapy and albumin transfusion, the patient died. Autopsy revealed a marked organ infiltration with haemosiderin (heart, stomach, liver, pancreas, lungs, kidneys, adrenal glands).Conclusion. The case describes a classical clinical manifestation of haemochromatosis: bronze skin hyperpigmentation, liver cirrhosis, diabetes mellitus, cardiomyopathy, adrenal insufficiency. Terminal haemochromatosis, severe cardiac and renal failure decompensation precluded phlebotomy and chelation therapy. A lethal outcome was conditioned by multiple organ dysfunction with underlying massive haemosiderin deposition in most organs.
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44

Vanderniet, Joel A., Paul Z. Benitez-Aguirre, Carolyn R. Broderick, Richard I. Kelley, and Shanti Balasubramaniam. "Barth syndrome with severe dilated cardiomyopathy and growth hormone resistance: a case report." Journal of Pediatric Endocrinology and Metabolism 34, no. 7 (April 13, 2021): 951–55. http://dx.doi.org/10.1515/jpem-2020-0666.

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Abstract Objectives To describe the metabolic and endocrine features of a patient with Barth syndrome who showed evidence of growth hormone resistance. Case presentation A male proband deteriorated rapidly with lactic acidosis after a circumcision at age three weeks and was found to have severe dilated cardiomyopathy. A cardiomyopathy gene panel led to the diagnosis of TAZ-deficiency Barth syndrome. He subsequently experienced hypotonia and gross motor delay, feeding difficulties for the first four years, constitutional growth delay and one episode of ketotic hypoglycaemia. Cardiomyopathy resolved on oral anti-failure therapy by age three years. He had a hormonal pattern of growth hormone resistance, and growth hormone treatment was considered, however height velocity improved spontaneously after age 3½ years. He also had biochemical primary hypothyroidism. Conclusions With careful metabolic management with l-arginine supplementation, overnight corn starch, and a prescribed exercise program, our patient’s strength, endurance, level of physical activity and body composition improved significantly by age six years.
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Gudenschwager, Erwin K., Jonathan A. Abbott, and Tanya LeRoith. "Dilated cardiomyopathy with endocardial fibroelastosis in a juvenile Pallas cat." Journal of Veterinary Diagnostic Investigation 31, no. 2 (January 29, 2019): 289–93. http://dx.doi.org/10.1177/1040638719827061.

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Dilated cardiomyopathy (DCM) is a myocardial disease characterized by ventricular chamber dilation associated with systolic myocardial dysfunction in the absence of other cardiac lesions. DCM occasionally develops in conjunction with proliferation of fibroelastic fibers in the endocardium, producing endocardial fibroelastosis (EFE). Although early reports describe EFE as a primary disease, evidence now suggests that EFE may develop as a response to myocardial dysfunction. Echocardiographic evaluation of a 4-wk-old Pallas cat ( Otocolobus manul) with respiratory distress revealed enlargement of both atria, enlarged end-systolic left ventricular dimension, and left ventricular dilation. DCM was diagnosed, and the cat was euthanized, given the poor prognosis. Postmortem examination revealed pericardial effusion and biventricular and biatrial enlargement. The interventricular septum and free walls of ventricles were thin. Histologically, the endocardium of the left and right ventricles was diffusely thickened; Verhoeff–Van Gieson staining of the left ventricular endocardium revealed a moderate amount of endocardial accumulation of elastin and collagen. These fibers were more prominent in papillary muscles and around coronary blood vessels. Based on these findings, we diagnosed DCM with EFE. Cardiac diseases are rarely diagnosed in wild felids.
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Yu, Sung Keun, Ji Young Park, Jong Hae Pack, Hye Jung Park, Kyeong Cheol Shin, Jin Hong Chung, and Kwan Ho Lee. "A Case of Obstructive Sleep Apnea Syndrome Associated with Primary Hypothyroidism and Dilated Cardiomyopathy." Tuberculosis and Respiratory Diseases 51, no. 6 (2001): 590. http://dx.doi.org/10.4046/trd.2001.51.6.590.

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47

ZECCHIN, M., A. DILENARDA, G. FAGANELLO, E. PETZ, D. FACCHIN, A. PROCLEMER, G. SABBADINI, and G. SINAGRA. "302 Implantable defibrillator for primary and secondary prevention of sudden death in dilated cardiomyopathy." European Journal of Heart Failure Supplements 2, no. 1 (June 2003): 54. http://dx.doi.org/10.1016/s1567-4215(03)90165-2.

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48

Quaife, Robert A., David Lynch, David B. Badesch, Norbert F. Voelkel, Brian D. Lowes, Alastair D. Robertson, and Michael R. Bristow. "Right ventricular phenotypic characteristics in subjects with primary pulmonary hypertension or idiopathic dilated cardiomyopathy." Journal of Cardiac Failure 5, no. 1 (March 1999): 46–54. http://dx.doi.org/10.1016/s1071-9164(99)90024-6.

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49

Kolb, Christof, Günter Lehmann, Jürgen Schreieck, Gjin Ndrepepa, and Claus Schmitt. "Storms of ventricular tachyarrhythmias associated with primary hyperparathyroidism in a patient with dilated cardiomyopathy." International Journal of Cardiology 87, no. 1 (January 2003): 115–16. http://dx.doi.org/10.1016/s0167-5273(02)00314-5.

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50

Kinali, M., S. E. Olpin, P. T. Clayton, P. E. F. Daubeney, E. Mercuri, A. Y. Manzur, I. Tein, J. Leonard, and F. Muntoni. "Diagnostic difficulties in a case of primary systemic carnitine deficiency with idiopathic dilated cardiomyopathy." European Journal of Paediatric Neurology 8, no. 4 (July 2004): 217–19. http://dx.doi.org/10.1016/j.ejpn.2004.03.007.

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