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1
Packer, Milton. "Nonarrhythmic Sudden Cardiac Death in Chronic Heart Failure—A Preventable Event?" JAMA Cardiology 4, no. 8 (August 1, 2019): 721. http://dx.doi.org/10.1001/jamacardio.2019.2228.
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Ran, Yuqin, Jingzhou Chen, Ning Li, Weili Zhang, Li Feng, Rongrong Wang, Rutai Hui, Shu Zhang, and Jielin Pu. "Common RyR2 variants associate with ventricular arrhythmias and sudden cardiac death in chronic heart failure." Clinical Science 119, no. 5 (June 4, 2010): 215–26. http://dx.doi.org/10.1042/cs20090656.
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Ca2+ cycling plays a critical role in heart failure and lethal arrhythmias. As susceptibility to sudden cardiac death is considered to be a heritable trait in general population, we have therefore investigated whether potentially functional variants of genes encoding RyR2 (ryanodine receptor 2) and the L-type Ca2+ channel are related to the risk of ventricular arrhythmias and sudden cardiac death in CHF (chronic heart failure) in a case-control study. We found that the A allele of rs3766871 in RYR2 was associated with an increased risk of ventricular arrhythmias in patients with CHF {odds ratio, 1.66 [95% CI (confidence interval), 1.21–2.26]; P=0.002}. During a median follow-up period of 32 months in 1058 (85.0%) patients, 296 (28.0%) patients died from heart failure, of whom 141 (47.6%) had sudden cardiac death. After adjustment for age, gender and suspected risk factors, patients carrying the A allele of rs3766871 had an increased risk of cardiac death {HR (hazard ratio), 1.53 [95% CI, 1.11–2.12]; P=0.010} and sudden cardiac death [HR, 1.92 (95% CI, 1.25–2.94); P=0.003]. Patients carrying the A allele of rs790896 in RYR2 had a reduced risk of sudden cardiac death [HR, 0.65 (95% CI, 0.45–0.92); P=0.015]. In conclusion, the A allele of rs3766871 in RYR2 not only associates with ventricular arrhythmias, but also serves as an independent predictor of sudden cardiac death, and the A allele of rs790896 in RYR2 is a protective factor against sudden cardiac death in patients with CHF.
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Unic-Stojanovic, Dragana, Miroslav Milicic, Petar Vukovic, Srdjan Babic, and Miomir Jovic. "Heart surgery in patients on chronic dialysis." Medical review 66, no. 1-2 (2013): 64–69. http://dx.doi.org/10.2298/mpns1302064u.
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Introduction. Patients on dialysis for end-stage renal failure are subjected to cardiac surgery with increasing frequency. End-stage renal failure is known to be an important risk factor for complications of cardiac operations performed with cardiopulmonary bypass. The aim of this study was to determine the impact of preoperative clinical status and operative variables on perioperative morbidity and mortality in hemodialysis dependent patients subjected to a cardiac surgery. Material and Methods. The following operative variables were examined: urgency, type and duration of surgery and duration of extracorporeal circulation. The study is a retrospective analysis of consecutive patients with end-stage renal failure dependent on maintenance hemodialysis who underwent cardiac surgery during four years. Results. The study included 46 patients. Operations performed included isolated coronary artery bypass grafting (CABG, n = 24), valve surgery alone (n = 6), and combined valve surgery or coronary artery bypass grafting and valve surgery (n = 16). The perioperative mortality rate was 13% with four fatal outcomes in patients who had undergone combined cardiac surgery. We found age > 70 years, preoperative New York Heart Association class IV, preoperative anemia, combined surgery and emergent surgery to be associated with a higher relative risk for perioperative death. Conclusion. Patients on dialysis have an increased morbidity and mortality following cardiac surgery; however, we believe that end-stage renal failure should not be regarded as a contraindication to cardiac surgery or cardiopulmonary bypass.
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Verschure, Derk O., G. Aernout Somsen, Berthe L. F. van Eck-Smit, and Hein J. Verberne. "Renal Function in Relation to Cardiac 123I-MIBG Scintigraphy in Patients with Chronic Heart Failure." International Journal of Molecular Imaging 2012 (May 14, 2012): 1–8. http://dx.doi.org/10.1155/2012/434790.
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The aim of this study was to explore if estimates of renal function could explain variability of 123I-metaiodobenzylguanidine (123I-MIBG) assessed myocardial sympathetic activity. Furthermore estimates of renal function were compared to 123I-MIBG as predictors of cardiac death in chronic heart failure (CHF). Semi-quantitative parameters of 123I-MIBG myocardial uptake and washout were calculated using early heart/mediastinum ratio (H/M), late H/M and washout. Renal function was calculated as estimated Creatinine Clearance (e-CC) and as estimated Glomerular Filtration Rate (e-GFR). Thirty-nine patients with CHF (24 males; age: 64.4±10.5 years; NYHA II/III/IV: 17/20/2; LVEF: 24.0±11.5%) were studied. Variability in any of the semi-quantitative 123I-MIBG myocardial parameters could not be explained by e-CC or e-GFR. During follow-up (60±37 months) there were 6 cardiac deaths. Cox proportional hazard regression analysis showed that late H/M was the only independent predictor for cardiac death (Chi-square 3.2, regression coefficient: −4.095; standard error: 2.063; hazard ratio: 0.17 [95% CI: 0.000–0.950]). Addition of estimates of renal function did not significantly change the Chi-square of the model. Semi-quantitative 123I-MIBG myocardial parameters are independent of estimates of renal function. In addition, cardiac sympathetic innervation assessed by 123I-MIBG scintigraphy seems to be superior to renal function in the prediction of cardiac death in CHF patients.
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Walker, Andrew MN, and Richard M. Cubbon. "Sudden cardiac death in patients with diabetes mellitus and chronic heart failure." Diabetes and Vascular Disease Research 12, no. 4 (April 10, 2015): 228–33. http://dx.doi.org/10.1177/1479164115573225.
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Claydon, Susan M. "Myocardial Degeneration in Chronic Solvent Abuse." Medicine, Science and the Law 28, no. 3 (July 1988): 217–18. http://dx.doi.org/10.1177/002580248802800308.
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Chronic solvent abuse is leading to increasing reports of death from cardiac related causes. This case involves a 21-year-old man who died of acute heart failure. Histological examination of his heart showed extensive chronic damage of the myocardium. He had regularly and frequently abused solvents for five years.
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La Rovere, Maria Teresa, Gian Domenico Pinna, Roberto Maestri, Andrea Mortara, Soccorso Capomolla, Oreste Febo, Roberto Ferrari, et al. "Short-Term Heart Rate Variability Strongly Predicts Sudden Cardiac Death in Chronic Heart Failure Patients." Circulation 107, no. 4 (February 4, 2003): 565–70. http://dx.doi.org/10.1161/01.cir.0000047275.25795.17.
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Moore, Roger K. G., David G. Groves, Pauline E. Barlow, Keith A. A. Fox, Ajay Shah, James Nolan, and Mark T. Kearney. "Heart rate turbulence and death due to cardiac decompensation in patients with chronic heart failure." European Journal of Heart Failure 8, no. 6 (October 2006): 585–90. http://dx.doi.org/10.1016/j.ejheart.2005.11.012.
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Mareev, V. Yu Mareev, and Yu V. Mareev Mareev. "Methods of Prevention of Sudden Death in Chronic Heart Failure." Kardiologiia 9_2015 (September 27, 2015): 72–83. http://dx.doi.org/10.18565/cardio.2015.9.72-83.
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Lei, Li, Steve Mason, Dinggang Liu, Yan Huang, Carolyn Marks, Reed Hickey, Ion S. Jovin, Marc Pypaert, Randall S. Johnson, and Frank J. Giordano. "Hypoxia-Inducible Factor-Dependent Degeneration, Failure, and Malignant Transformation of the Heart in the Absence of the von Hippel-Lindau Protein." Molecular and Cellular Biology 28, no. 11 (February 19, 2008): 3790–803. http://dx.doi.org/10.1128/mcb.01580-07.
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ABSTRACT Hypoxia-inducible transcription factor 1 (HIF-1) and HIF-2α regulate the expression of an expansive array of genes associated with cellular responses to hypoxia. Although HIF-regulated genes mediate crucial beneficial short-term biological adaptations, we hypothesized that chronic activation of the HIF pathway in cardiac muscle, as occurs in advanced ischemic heart disease, is detrimental. We generated mice with cardiac myocyte-specific deletion of the von Hippel-Lindau protein (VHL), an essential component of an E3 ubiquitin ligase responsible for suppressing HIF levels during normoxia. These mice were born at expected frequency and thrived until after 3 months postbirth, when they developed severe progressive heart failure and premature death. VHL-null hearts developed lipid accumulation, myofibril rarefaction, altered nuclear morphology, myocyte loss, and fibrosis, features seen for various forms of human heart failure. Further, nearly 50% of VHL−/− hearts developed malignant cardiac tumors with features of rhabdomyosarcoma and the capacity to metastasize. As compelling evidence for the mechanistic contribution of HIF-1α, the concomitant deletion of VHL and HIF-1α in the heart prevented this phenotype and restored normal longevity. These findings strongly suggest that chronic activation of the HIF pathway in ischemic hearts is maladaptive and contributes to cardiac degeneration and progression to heart failure.
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Mady, Charles, and Ricardo Nacruth. "Natural history of chronic Chagas' heart disease: prognosis factors." Sao Paulo Medical Journal 113, no. 2 (April 1995): 791–96. http://dx.doi.org/10.1590/s1516-31801995000200009.
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Chronic Chagas' disease shows several progression modes. Usually, the different clinical syndromes manifest themselves together, however, isolated forms can occur. Cardiac arrhythmias, which are very frequent, are present in about 50% of patients. The cardiac damage manifests itself later, with the emergence of heart failure. Thromboembolism can occur in both pulmonary and systemic circulation. Pulmonary embolism is the most frequent, appearing in more advanced phases of heart disease. Sudden death is the fatal outcome of these patients. It predominates in males and it generally occurs in a disease stage when patients have their highest productivity. The presence of serious ventricular arrhythmias, conduction disturbances in the eletrocardiogram, and heart failure, provide an unfavorable prognosis.
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Chen, Olivia, and Li Qian. "Direct Cardiac Reprogramming: Advances in Cardiac Regeneration." BioMed Research International 2015 (2015): 1–8. http://dx.doi.org/10.1155/2015/580406.
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Heart disease is one of the lead causes of death worldwide. Many forms of heart disease, including myocardial infarction and pressure-loading cardiomyopathies, result in irreversible cardiomyocyte death. Activated fibroblasts respond to cardiac injury by forming scar tissue, but ultimately this response fails to restore cardiac function. Unfortunately, the human heart has little regenerative ability and long-term outcomes following acute coronary events often include chronic and end-stage heart failure. Building upon years of research aimed at restoring functional cardiomyocytes, recent advances have been made in the direct reprogramming of fibroblasts toward a cardiomyocyte cell fate bothin vitroandin vivo. Several experiments show functional improvements in mouse models of myocardial infarction followingin situgeneration of cardiomyocyte-like cells from endogenous fibroblasts. Though many of these studies are in an early stage, this nascent technology holds promise for future applications in regenerative medicine. In this review, we discuss the history, progress, methods, challenges, and future directions of direct cardiac reprogramming.
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Pathak, Atul, Daniel Curnier, Joëlle Fourcade, Jéme Roncalli, Phyllis K. Stein, Patricia Hermant, Marc Bousquet, et al. "QT dynamicity: a prognostic factor for sudden cardiac death in chronic heart failure." European Journal of Heart Failure 7, no. 2 (February 8, 2005): 269–75. http://dx.doi.org/10.1016/j.ejheart.2004.10.016.
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Dey, Swati, Deeptankar DeMazumder, Agnieszka Sidor, D. Brian Foster, and Brian O’Rourke. "Mitochondrial ROS Drive Sudden Cardiac Death and Chronic Proteome Remodeling in Heart Failure." Circulation Research 123, no. 3 (July 20, 2018): 356–71. http://dx.doi.org/10.1161/circresaha.118.312708.
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Pino-Marín, Antonia, Germán José Medina-Rincón, Sebastian Gallo-Bernal, Alejandro Duran-Crane, Álvaro Ignacio Arango Duque, María Juliana Rodríguez, Ramón Medina-Mur, Frida T. Manrique, Julian F. Forero, and Hector M. Medina. "Chagas Cardiomyopathy: From Romaña Sign to Heart Failure and Sudden Cardiac Death." Pathogens 10, no. 5 (April 22, 2021): 505. http://dx.doi.org/10.3390/pathogens10050505.
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Despite nearly a century of research and accounting for the highest disease burden of any parasitic disease in the Western Hemisphere, Chagas disease (CD) is still a challenging diagnosis, primarily due to its poor recognition outside of Latin America. Although initially considered endemic to Central and South America, globalization, urbanization, and increased migration have spread the disease worldwide in the last few years, making it a significant public health threat. The international medical community’s apparent lack of interest in this disease that was previously thought to be geographically restricted has delayed research on the complex host–parasite relationship that determines myocardial involvement and its differential behavior from other forms of cardiomyopathy, particularly regarding treatment strategies. Multiple cellular and molecular mechanisms that contribute to degenerative, inflammatory, and fibrotic myocardial responses have been identified and warrant further research to expand the therapeutic arsenal and impact the high burden attributed to CD. Altogether, cardiac dysautonomia, microvascular disturbances, parasite-mediated myocardial damage, and chronic immune-mediated injury are responsible for the disease’s clinical manifestations, ranging from asymptomatic disease to severe cardiac and gastrointestinal involvement. It is crucial for healthcare workers to better understand CD transmission and disease dynamics, including its behavior on both its acute and chronic phases, to make adequate and evidence-based decisions regarding the disease. This review aims to summarize the most recent information on the epidemiology, pathogenesis, clinical presentation, diagnosis, screening, and treatment of CD, emphasizing on Chagasic cardiomyopathy’s (Ch-CMP) clinical presentation and pathobiological mechanisms leading to sudden cardiac death.
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Plawecki, Maëlle, Marion Morena, Nils Kuster, Leila Chenine, Hélène Leray-Moragues, Bernard Jover, Pierre Fesler, et al. "sST2 as a New Biomarker of Chronic Kidney Disease-Induced Cardiac Remodeling: Impact on Risk Prediction." Mediators of Inflammation 2018 (October 8, 2018): 1–9. http://dx.doi.org/10.1155/2018/3952526.
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Heart failure is the most frequent cardiac complication of chronic kidney disease (CKD). Biomarkers help identify high-risk patients. Natriuretic peptides (BNP and NT-proBNP) are largely used for monitoring patients with cardiac failure but are highly dependent on glomerular filtration rate (GFR). Soluble suppression of tumorigenicity 2 (sST2) biomarker is well identified in risk stratification of cardiovascular (CV) events in heart failure. Furthermore, sST2 is included in a bioclinical score to stratify mortality risk. The aims of this study were to evaluate (i) the interest of circulating sST2 level in heart dysfunction and (ii) the bioclinical score (Barcelona Bio-Heart Failure risk calculator) to predict the risk of composite outcome (major adverse coronary events) and mortality in the CKD population. A retrospective study was carried out on 218 CKD patients enrolled from 2004 to 2015 at Montpellier University Hospital. sST2 was measured by ELISA (Presage ST2® kit). GFR was estimated by the CKD-EPI equation (eGFR). Indices of cardiac parameters were performed by cardiac echography. No patient had reduced ejection fraction. 112 patients had left ventricular hypertrophy, and 184 presented cardiac dysfunction, with structural, functional abnormalities or both. sST2 was independent of age and eGFR (ρ=0.05, p=0.44, and ρ=−0.07, p=0.3, respectively). Regarding echocardiogram data, sST2 was correlated with left ventricular mass index (ρ=0.16, p=0.02), left atrial diameter (ρ=0.14, p=0.04), and volume index (ρ=0.13, p=0.05). sST2 alone did not change risk prediction of death and/or CV events compared to natriuretic peptides. Included in the Barcelona Bio-Heart Failure (BCN Bio-HF) score, sST2 added value and better stratified the risk of CV events and/or death in CKD patients (p<0.0001). To conclude, sST2 was associated with cardiac remodeling independently of eGFR, unlike other cardiac biomarkers. Added to the BCN Bio-HF score, the risk stratification of death and/or CV events in nondialyzed CKD patients was highly improved.
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Arzilli, Chiara, Alberto Aimo, Giuseppe Vergaro, Andrea Ripoli, Michele Senni, Michele Emdin, and Claudio Passino. "N-terminal fraction of pro-B-type natriuretic peptide versus clinical risk scores for prognostic stratification in chronic systolic heart failure." European Journal of Preventive Cardiology 25, no. 8 (March 23, 2018): 889–95. http://dx.doi.org/10.1177/2047487318766580.
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Background The Seattle heart failure model or the cardiac and comorbid conditions (3C-HF) scores may help define patient risk in heart failure. Direct comparisons between them or versus N-terminal fraction of pro-B-type natriuretic peptide (NT-proBNP) have never been performed. Methods Data from consecutive patients with stable systolic heart failure and 3C-HF data were examined. A subgroup of patients had the Seattle heart failure model data available. The endpoints were one year all-cause or cardiovascular death. Results The population included 2023 patients, aged 68 ± 12 years, 75% were men. At the one year time-point, 198 deaths were recorded (10%), 124 of them (63%) from cardiovascular causes. While areas under the curve were not significantly different, NT-proBNP displayed better reclassification capability than the 3C-HF score for the prediction of one year all-cause and cardiovascular death. Adding NT-proBNP to the 3C-HF score resulted in a significant improvement in risk prediction. Among patients with Seattle heart failure model data available ( n = 798), the area under the curve values for all-cause and cardiovascular death were similar for the Seattle heart failure model score (0.790 and 0.820), NT-proBNP (0.783 and 0.803), and the 3C-HF score (0.770 and 0.800). The combination of the 3C-HF score and NT-proBNP displayed a similar prognostic performance to the Seattle heart failure model score for both endpoints. Adding NT-proBNP to the Seattle heart failure model score performed better than the Seattle heart failure model alone in terms of reclassification, but not discrimination. Conclusions Among systolic heart failure patients, NT-proBNP levels had better reclassification capability for all-cause and cardiovascular death than the 3C-HF score. The inclusion of NT-proBNP to the 3C-HF and Seattle heart failure model score resulted in significantly better risk stratification.
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Dadarlat-Pop, Alexandra, Dana Pop, and Anca Buzoianu. "Particularities of arrhythmias and obesity in heart failure." Romanian Journal of Cardiology 30, no. 1 (March 30, 2020): 7–11. http://dx.doi.org/10.47803/rjc.2020.30.1.7.
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Chronic heart failure and obesity are two conditions which despite all the advances made in the recent years, still represent two of the leading causes of morbidity and mortality worldwide. Moreover, a well-known fact is that the risk of sudden cardiac death, mostly related to malignant arrhythmias is higher in apparently healthy obese individuals in comparison with lean subjects. On the other hand, obese heart failure patients bring unique challenges in the diagnosis of heart failure, having a better prognosis than their normal or underweight counterparts. Taking into account the above-mentioned existing data, there are questions regarding whether cardiac arrhythmias such as atrial fibrillation or ventricular arrhythmias in this population have certain evolutive particularities. This paper describes various mechanisms of cardiac arrhythmias found in obese heart failure patients, such as myocardial architectural changes, neurohormonal and paracrine modifications.
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Liu, Haibo, Xiaofang Guo, Kang Yao, Chunming Wang, Guozhong Chen, Wei Gao, Jie Yuan, Wangjun Yu, and Junbo Ge. "Pentraxin-3 Predicts Long-Term Cardiac Events in Patients with Chronic Heart Failure." BioMed Research International 2015 (2015): 1–7. http://dx.doi.org/10.1155/2015/817615.
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The aim of this study was to investigate the long-term prognostic value of pentraxin-3 (PTX3) in patients with chronic heart failure (CHF). 377 patients were prospectively followed up for 3 years to determine cardiac events including cardiac death or rehospitalization for worsening heart failure. The plasma PTX3 levels were significantly higher in CHF patients than in healthy subjects (p<0.001), and they increased with advancing New York Heart Association (NYHA) Functional Classification (p<0.001). Plasma PTX3 levels in CHF patients with cardiac events were significantly higher than in event-free patients (p<0.001). We determined the normal upper limit of plasma PTX3 levels from the mean + 2 SD value of 64 control subjects (3.64 ng/mL). A Kaplan-Meier analysis revealed that patients with increased PTX3 (≥3.64 ng/mL) were at a higher risk for cardiac events than those without increased PTX3 (p<0.01). A multifactorial Cox proportional hazards model showed that increased PTX3 (≥3.64 ngImL) was an independent risk factor for cardiac events in CHF patients (hazard ratio (HR) = 4.224,p<0.01; 95% CI: 1.130–15.783). Plasma PTX3 levels are a long-term independent predictor of prognosis in patients with CHF.
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Ali, Md Ashraf, Dilara Alo, and Abdul Latif Molla. "Correlation Of Serum Cardiac Troponin I With Significant Left Ventricular Systolic Dysfunction In Patients With Chronic Heart Failure." KYAMC Journal 5, no. 2 (April 27, 2017): 503–8. http://dx.doi.org/10.3329/kyamcj.v5i2.32363.
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Objective: The aim of the study was to observe the relationship between elevated levels of serum cardiac Troponin I (cTnI) and in-hospital morbidity & mortality in chronic heart failure with LV systolic dysfunction.Background: Chronic heart failure is a public health problem in the United Kingdom and also in our country. Serum Cardiac troponin I (cTnI) has been validated as a sensitive and specific marker of cardiac myocyte damage and is elevated in some patients with chronic heart failure with LV systolic dysfunction and predicts adverse outcome.Materials and Methods: This study was prospective, cross sectional and observational study. The study was carried out among chronic heart failure with LV systolic dysfunction patients in the Department of Cardiology, National Institute of Cardiovascular Diseases, Sher-E-Bangla Nagar, Dhaka, during the period of April 2004 to December 2004. In this Study, total 740 patients of heart failure were evaluated Among 740 patients, initially 100 patients were selected as chronic heart failure on the basis of inclusion & exclusion criteria, history, physical examination, biochemical, X-ray, ECG & other relevant investigations. Finally, 60 patients were selected by echocardiography who had ejection fraction of 40%. Cardiac troponin I was measured in each and every studied patient. In-hospital outcome was observed in terms of morbidity & mortality. So hospitalised patients were followed up clinically and by investigation. Results: The results of this study revealed that serum cTnI was significantly elevated (cTnI 0.04 ng/ml) in serum of 29 patients (48.33%) and low or insignificant (cTnI 0.04 ng/ml) in serum of 31 patients (51.67%). Patients with significantly elevated serum cardiac troponin I (cTnI) level (group-A) had significantly higher inhospital morbidity & mortality than patients who had insignificant serum cardiac troponin I (cTnI) level (group-B). In-hospital mortality was 15% (number of death 09) out of total 60 patients. All expired patients were in NYHA class-IV. On the other hand, there was no mortality in group-B. In-hospital morbidity was 2.75 times higher among the patients who had significantly elevated serum cTnI level. A significant correlation was found between the patients who had significantly elevated serum cTnI level (cTnI level > 0.04 ng/ml) and the patients who had insignificant serum cTnI level (cTnI level < 0.04 ng/ml) in consideration to in-hospital morbidity & mortality.Conclusion: Conclusion of this study is that serum cardiac troponin I (cTnI) level is significant predictor of increased morbidity & mortality in chronic heart failure. with LV systolic dysfunction. Serum Cardiac troponin I (cTnI) level may be a useful tool for identification, selection of therapeutic strategies and assessment of prognosis in patients with chronic heart failure who are at increased risk of ventricular systolic dysfunction and death. So it is a message for the physician as well as patients.KYAMC Journal Vol. 5, No.-2, Jan 2015, Page 503-508
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Abd Alla, Joshua, Yahya F. Jamous, and Ursula Quitterer. "Stearoyl-CoA Desaturase (SCD) Induces Cardiac Dysfunction with Cardiac Lipid Overload and Angiotensin II AT1 Receptor Protein Up-Regulation." International Journal of Molecular Sciences 22, no. 18 (September 13, 2021): 9883. http://dx.doi.org/10.3390/ijms22189883.
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Heart failure is a major cause of death worldwide with insufficient treatment options. In the search for pathomechanisms, we found up-regulation of an enzyme, stearoyl-CoA desaturase 1 (Scd1), in different experimental models of heart failure induced by advanced atherosclerosis, chronic pressure overload, and/or volume overload. Because the pathophysiological role of Scd1/SCD in heart failure is not clear, we investigated the impact of cardiac SCD upregulation through the generation of C57BL/6-Tg(MHCSCD)Sjaa mice with myocardium-specific expression of SCD. Echocardiographic examination showed that 4.9-fold-increased SCD levels triggered cardiac hypertrophy and symptoms of heart failure at an age of eight months. Tg-SCD mice had a significantly reduced left ventricular cardiac ejection fraction of 25.7 ± 2.9% compared to 54.3 ± 4.5% of non-transgenic B6 control mice. Whole-genome gene expression profiling identified up-regulated heart-failure-related genes such as resistin, adiponectin, and fatty acid synthase, and type 1 and 3 collagens. Tg-SCD mice were characterized by cardiac lipid accumulation with 1.6- and 1.7-fold-increased cardiac contents of saturated lipids, palmitate, and stearate, respectively. In contrast, unsaturated lipids were not changed. Together with saturated lipids, apoptosis-enhancing p53 protein contents were elevated. Imaging by autoradiography revealed that the heart-failure-promoting and membrane-spanning angiotensin II AT1 receptor protein of Tg-SCD hearts was significantly up-regulated. In transfected HEK cells, the expression of SCD increased the number of cell-surface angiotensin II AT1 receptor binding sites. In addition, increased AT1 receptor protein levels were detected by fluorescence spectroscopy of fluorescent protein-labeled AT1 receptor-Cerulean. Taken together, we found that SCD promotes cardiac dysfunction with overload of cardiotoxic saturated lipids and up-regulation of the heart-failure-promoting AT1 receptor protein.
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De Marco, Teresa, and Kanu Chatterjee. "Refractory Heart Failure: A Therapeutic Approach." Journal of Intensive Care Medicine 11, no. 3 (May 1996): 121–48. http://dx.doi.org/10.1177/088506669601100301.
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Optimal “triple therapy” for patients with chronic congestive heart failure (CHF) includes diuretics, digoxin, and either angiotensin-converting enzyme inhibitors or hydralazine plus nitrates. Refractory CHF is defined as symptoms of CHF at rest or repeated exacerbations of CHF despite “optimal” triple-drug therapy. Most patients with refractory CHF require hemodynamic monitoring and treatment in the intensive care unit. If easily reversible causes of refractory CHF cannot be identified, then more aggressive medical and surgical interventions are necessary. The primary goal of intervention is to improve hemodynamics to palliate CHF symptoms and signs (i.e., dyspnea, fatigue, edema). Secondary goals include improved vital organ and tissue perfusion, discharge from the intensive care unit, and, in appropriate patients, bridge to cardiac transplantation. Medical interventions include inotropic resuscitation (e.g., adrenergic agents, phosphodiesterase inhibitors, allied nonglycoside inodilators), load resuscitation (e.g., afterload and preload reduction with nitroprusside or nitroglycerin; preload reduction with diuretics and diuretic facilitators, such as dopaminergic agents or ultrafiltration), and electrical resuscitation (e.g., prevention of sudden death, correction of new or rapid atrial fibrillation, or dual chamber pacing in the setting of relative prolongation of the PR interval and diastolic mitral/tricuspid regurgitation). Surgical interventions are temporizing (e.g., intra-aortic balloon pump and other mechanical assist devices) or definitive (e.g., coronary artery revascularization, valvular surgery, and cardiac transplantation). Although these interventions may improve immediate survival in the short term, only coronary artery revascularization and cardiac transplantation have been shown to improve long-term survival.
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Tanner, Miles A., Charles A. Maitz, and Laurel A. Grisanti. "Immune cell β2-adrenergic receptors contribute to the development of heart failure." American Journal of Physiology-Heart and Circulatory Physiology 321, no. 4 (October 1, 2021): H633—H649. http://dx.doi.org/10.1152/ajpheart.00243.2021.
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Immune cell β2-adrenergic receptors (β2ARs) are important for proinflammatory macrophage infiltration to the heart in a chronic isoproterenol administration model of heart failure. Mice lacking immune cell β2AR have decreased immune cell infiltration to their heart, primarily proinflammatory macrophage populations. This decrease culminated to decreased cardiac injury with lessened cardiomyocyte death, decreased interstitial fibrosis and hypertrophy, and improved function demonstrating that β2AR regulation of immune responses plays an important role in the heart’s response to persistent βAR stimulation.
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Güler, Niyazi, Mehmet Bilge, Beyhan Eryonucu, Kürcat Uzun, Mehmet Emin Avci, and Haluk Dülger. "Cardiac Troponin I Levels in Patients with Left Heart Failure and Cor Pulmonale." Angiology 52, no. 5 (May 2001): 317–22. http://dx.doi.org/10.1177/000331970105200504.
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Cardiac troponin levels are regarded as the most specific of currently available biochemical markers of myocardial damage. Elevated levels of troponin have been previously reported in patients with left heart failure, reflecting small areas of undetected myocardial cell death. The aim of this study was to compare the levels of the cardiac troponin I (cTnl) in patients with left- and right-sided heart failure. Cardiac troponin I levels were studied with immunochemical methods in patients with right heart failure (n = 17) resulting from chronic obstructive pulmonary disease, ischemic left heart failure (n = 23), and nonischemic left heart failure (n = 18) who were admitted to departments of cardiology and chest diseases. Also, cTnl levels were measured in 32 healthy subjects as control group. Protein markers of myocardial injury (cTnl and myoglobin) in patients with left and right heart failure were collected approximately 12 to 36 hours after onset of obvious symptoms. Serum creatine kinase MB band was determined on admission and thereafter twice a day during the first 3 days. Elevated levels of serum cTnl were found in patients with nonischemic (0.83 ±0.6 ng/mL, p<0.01) and ischemic left heart failure (0.9 ±0.5 ng/mL, p<0.01) when compared to healthy subjects, whereas serum cTnl levels in patients with right heart failure due to chronic obstruc tive pulmonary disease were not significantly different from those of control subjects (0.22 ±0.1 vs 0.16 ±0.1 ng/mL, p> 0.05). In addition, creatine kinase MB band and myoglobin levels were not significantly different between patient and healthy groups. The mean of cTnl levels in ischemic and even nonischemic left heart failure were increased compared to the mean of values in healthy individuals but without significant creatine kinase MB band and myoglobin elevations. But cTnl levels were not increased in patients with right heart failure due to chronic obstructive pulmonary disease. These data indicate that the cTnl levels are abnormal in left heart failure but not in cor pulmonale.
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Packer, Milton. "What causes sudden death in patients with chronic heart failure and a reduced ejection fraction?" European Heart Journal 41, no. 18 (August 7, 2019): 1757–63. http://dx.doi.org/10.1093/eurheartj/ehz553.
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Abstract Sudden death characterizes the mode of demise in 30–50% of patients with chronic heart failure and a reduced ejection fraction. Occasionally, these events have an identifiable pathophysiological trigger, e.g. myocardial infarction, catecholamine surges, or electrolyte imbalances, but in most circumstances, there is no acute precipitating mechanism. Instead, adverse left ventricular remodelling and fibrosis creates an exceptionally fragile and highly vulnerable substrate, which can be characterized using the model developed in theoretical physics of ‘self-organizing criticality’. This framework has been applied to describe the genesis of avalanches, nodes of traffic congestion unrelated to an accident, the abrupt system-wide failure of electrical grids, and the initiation of cancer and neurodegenerative diseases. Self-organizing criticality within the ventricular myocardium relies on complex adaptations to progressive stress and stretch, which evolve inevitably to an abrupt end (termed ‘cascading failure’), even though the rate of deterioration of the underlying disease process has not changed. The result is acute circulatory collapse (i.e. sudden death) in the absence of an identifiable triggering event. Cascading failure in a severely remodelled or fibrotic heart can become manifest electrically as a first-time ventricular tachyarrhythmia that is responsive to the shock delivered by an implantable cardioverter-defibrillator (ICD). Alternatively, it may present as an acute mechanical failure, which is manifest as (i) asystole, bradyarrhythmia, or electromechanical dissociation; or (ii) incessant ventricular fibrillation that persists despite repetitive ICD discharges; in both instances, the sudden deaths cannot be prevented by an ICD. This conceptual framework explains why anti-remodelling and antifibrotic interventions (i.e. neurohormonal antagonists and cardiac resynchronization) reduce the risk of sudden death in patients with heart failure in the absence of an ICD and provide incremental benefits in those with an ICD. The adoption of anti-remodelling and antifibrotic treatments may explain why the incidence of sudden death in clinical trials of heart failure has declined dramatically over the past 10–15 years, independent of the use of ICDs.
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Shiba, Nobuyuki, Kotaro Nochioka, Jun Watanabe, Tomohiro Tada, Haruka Kohno, Masanobu Miura, and Hiroaki Shimokawa. "Sudden Cardiac Death in Patients with Chronic Heart Failure-Epidemiological Findings From the CHART Study." Journal of Cardiac Failure 15, no. 7 (September 2009): S141. http://dx.doi.org/10.1016/j.cardfail.2009.07.207.
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Izadi, Neda, and Siamak Sabour. "Sudden cardiac death in patients with chronic heart failure: Rule of thumb in prediction studies." Journal of Nuclear Cardiology 24, no. 5 (June 23, 2017): 1829–30. http://dx.doi.org/10.1007/s12350-017-0936-6.
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Guarracino, Fabio, Endre Zima, Piero Pollesello, and Josep Masip. "Short-term treatments for acute cardiac care: inotropes and inodilators." European Heart Journal Supplements 22, Supplement_D (May 1, 2020): D3—D11. http://dx.doi.org/10.1093/eurheartj/suaa090.
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Abstract Acute heart failure (AHF) continues to be a substantial cause of illness and death, with in-hospital and 3-month mortality rates of 5% and 10%, respectively, and 6-month re-admission rates in excess of 50% in a range of clinical trials and registry studies; the European Society of Cardiology (ESC) Heart Failure Long-Term Registry recorded a 1-year death or rehospitalization rate of 36%. As regards the short-term treatment of AHF patients, evidence was collected in the ESC Heart Failure Long-Term Registry that intravenous (i.v.) treatments are administered heterogeneously in the critical phase, with limited reference to guideline recommendations. Moreover, recent decades have been characterized by a prolonged lack of successful innovation in this field, with a plethora of clinical trials generating neutral or inconclusive findings on long-term mortality effects from a multiplicity of short-term interventions in AHF. One of the few exceptions has been the calcium sensitizer and inodilator levosimendan, introduced 20 years ago for the treatment of acutely decompensated chronic heart failure. In the present review, we will focus on the utility of this agent in the wider context of i.v. inotropic and inodilating therapies for AHF and related pathologies.
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Futterman, LG, and L. Lemberg. "Heart failure: update on treatment and prognosis." American Journal of Critical Care 10, no. 4 (July 1, 2001): 285–93. http://dx.doi.org/10.4037/ajcc2001.10.4.285.
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HF is a prevalent and debilitating disease, affecting nearly 5 million patients and perhaps an equal number with asymptomatic left ventricular dysfunction who are at high risk of atrial fibrillation developing. An estimated 550,000 new cases occur every year. HF is the most common diagnosis in hospitalized patients aged 65 and over and is a major cause of death. The median survival after onset is 1.7 years in men and 3.2 years in women. The majority of cardiac deaths in patients with HF are sudden and arrhythmogenic: the rest are due to progressive hemodynamic deterioration. A significant advance in the past decade has been the recognition of the importance of inhibiting the neurohormonal action in HF with the use of beta-blockers, angiotensin receptor, and aldosterone antagonists. In addition, a new concept in HF therapy has evolved. The view that chronic HF is an irreversible, end-stage process is being supplanted by the fact that it is possible to effect biological improvement in the intrinsic defects of function and structure in hearts afflicted with chronic HF. Reversibility of HF has been reported by (1) unloading the failing heart using an LVAD, (2) the sophisticated use of diuretic combinations and neurohormonal blocking drugs, or (3) employing continuous arteriovenous hemofiltration. Thus it is now possible to reverse a process that has long been considered irreversible. Exercise programs designed for patients with HF that have been advocated recently can be difficult to apply. Fine tuning of an exercise regimen is required because a reduction in cardiac work is mandatory when treating HF, where the concern is that the heart may not be capable of supplying the metabolic needs of the body, even in resting states. Finally, although not emphasized in the recent literature on HF, the use of diuretics and sodium restriction continue to be the mainstays of therapy without which compensation of HF is not possible.
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Kaesler, Nadine, Anne Babler, Jürgen Floege, and Rafael Kramann. "Cardiac Remodeling in Chronic Kidney Disease." Toxins 12, no. 3 (March 5, 2020): 161. http://dx.doi.org/10.3390/toxins12030161.
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Cardiac remodeling occurs frequently in chronic kidney disease patients and affects quality of life and survival. Current treatment options are highly inadequate. As kidney function declines, numerous metabolic pathways are disturbed. Kidney and heart functions are highly connected by organ crosstalk. Among others, altered volume and pressure status, ischemia, accelerated atherosclerosis and arteriosclerosis, disturbed mineral metabolism, renal anemia, activation of the renin-angiotensin system, uremic toxins, oxidative stress and upregulation of cytokines stress the sensitive interplay between different cardiac cell types. The fatal consequences are left-ventricular hypertrophy, fibrosis and capillary rarefaction, which lead to systolic and/or diastolic left-ventricular failure. Furthermore, fibrosis triggers electric instability and sudden cardiac death. This review focuses on established and potential pathophysiological cardiorenal crosstalk mechanisms that drive uremia-induced senescence and disease progression, including potential known targets and animal models that might help us to better understand the disease and to identify novel therapeutics.
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Terekhina, N. A., and O. G. Goryacheva. "The Role of Oxidative Stress and Antioxidants in Occurrence of Myocardial Infarction and Chronic Heart Failure." Medical University 3, no. 4 (December 1, 2020): 155–64. http://dx.doi.org/10.2478/medu-2020-0019.
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Abstract Oxidative stress is one of the most important mechanisms of cardiovascular diseases, especially in heart failure. Mitochondrial dysfunction and inflammation play a major role in formation of free radicals and antioxidants. The association between oxidative stress, telomere biology and cell senescence plays the key role in cardiovascular pathology development. The paper considers role of pro-oxidant and antioxidant enzymes in heart pathology development. Specifically, the role of such antioxidant enzymes as glutathione peroxidase 3, catalase, and superoxide dismutase is described. The role of gamma-glutamyl transferase is emphasized as its activity increases significantly in cases of heart failure, coronary heart disease, stroke, arterial hypertensions, and arrhythmias. This article is a literature review of the effect of such antioxidants as alpha-tocopherol, ubiquinone, uric acid, and triiodothyronine on development of heart failure and myocardial infarction. A decrease in triiodothyronine concentration is a risk factor for coronary heart disease. High uric acid values in patients with myocardial infarction upon admission to the hospital are associated with a high risk of sudden death. The influence of such minerals such as zinc, copper, magnesium, selenium, potassium, sodium, calcium, and iron on heart failure development has been analyzed. The role of ceruloplasmin as an independent predictor of acute and chronic cardiac disorders cardiac events, mortality, and bad prognosis in patients with heart failure and myocardial infarction is examined. The authors demonstrate the influence of inflammation on heart failure development as well as association of inflammation with oxidative stress.
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Kurlianskaya, E. K., A. G. Mrochek, T. L. Denisevich, M. G. Kaliadka, and I. I. Russkich. "The Prognostic Role of Biomarkers in Patients With Chronic Heart Failure." Kardiologiia 60, no. 1 (February 6, 2020): 16–22. http://dx.doi.org/10.18087/cardio.2020.1.n882.
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Objective Investigate the role of biomarkers in the prognosis of the clinical course of the disease in patients with chronic heart failure (CHF) of different NYHA functional classes (FC).Material and Methods The study included 132 patients with CHF: Group 1 was composed of 70 patients with NYHA FC II CHF, and Group 2 included 62 patients with FC III-IV CHF. The patients underwent clinical, instrumental, functional, and laboratory measurements, which included serum concentrations of NT-proBNP, ST-2, galectin-3, and C-reactive protein. Patients were examined at baseline and at 3, 6, and 12 mos of follow-up. The following cardiac complications were used as endpoints: urgent hospitalization due to decompensated CHF, heart transplantation, cardiovascular death. Endpoints were registered during the 12-mo follow-up period.Results Endpoints were recorded for 58 patients (44%) of the total sample of patients with CHF: 38 patients were urgently hospitalized, 10 patients underwent heart transplantation, 10 patients died. Cardiac complications were recorded at a higher rate in patients with FC III-IV CHF (63% vs. 27% of patients with FC II; p<0.001). In FC II CHF patients, the incidence of cardiac complications was significantly correlated with NT-proBNP blood concentrations (Rpb=0.53; p=0.023), left ventricular end-diastolic volume (LVEDV) (Rpb=0.50; p=0.044), and mitral regurgitation (Rpb=0.53; p=0.038). Cardiac complications in patients with FC III-IV CHF were associated with ST-2 (Rpb=0.52; p=0.004) and galectin-3 (Rpb=0.46; p=0.009) blood concentrations, and with systolic pulmonary artery pressure (PAP) (Rpb=0.41; p=0.014). Unlike other laboratory measurements, galectin-3 concentrations were significantly correlated with type 2 diabetes mellitus (DM2) (Rpb=0.40; p=0.003). In this study, correlation analysis and evidence of significant differences in the concentrations of biomarkers provided a rationale for identifying potential predictors of severe cardiac complications during medium- and long-term follow-up periods in patients with CHF of different severity: NT-proBNP concentrations in FC II patients; ST-2 and galectin-3 serum concentrations in FC III-IV patients; galectin-3 concentrations in patients with CHF and DM2.Conclusion NT-proBNP blood concentrations are associated with CHF severity and serious cardiac complications in patients with FC II CHF within the following 12 mos. The poor prognosis of FC III-IV CHF is associated with the concentration of the ST-2 biomarker. The blood concentration of galectin-3 is a significant predictor of poor prognosis in patients with CHF and DM2. Predictors of the adverse course of CHF of varying severity were differentiated. For FC II CHF, NT-proBNP > 1723 pg/ml or, if NT-proBNP < 1723 pg/mL, then EDV > 311 ml. For FC III-IV CHF, ST-2 > 67 ng/mL or, if ST-2 < 67 ng/mL, then PAP > 61 mm Hg. Galectin-3 has a prognostic value for the clinical course of the disease at different follow-up periods in patients with CHF and DM2: galectin-3 concentrations > 16 ng/mL and 13-16 ng/mL are risk factors for mid- and long-term cardiac complications, respectively.
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Taneva, Borjanka, and Daniela Caparoska. "The Impact of Treatment with Beta-Blockers upon Mortality in Chronic Heart Failure Patients." Open Access Macedonian Journal of Medical Sciences 4, no. 1 (February 8, 2016): 94–97. http://dx.doi.org/10.3889/oamjms.2016.022.
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BACKGROUND: Besides the conventional therapy for heart failure, the diuretics, cardiac glycosides and ACE-inhibitors, current pharmacotherapy includes beta-blockers, mainly because of their pathophysiological mechanisms upon heart remodeling.AIM: The study objective was to assess the cardiovascular mortality in the beta-blocker therapy group and to correlate it with the mortality in the control group as well as to correlate the combined outcome of death and/or hospitalization for cardiovascular reason between the two groups. MATERIALS AND METHODS: The study included 113 chronic heart failure patients followed up for a period of 18 months. The therapy group received conventional therapy plus the target dose of beta blockers, and the control group received the conventional therapy only. The therapy group was divided in three separate subgroups in terms of the type of beta-blocker (Metoprolol subgroup, Bisoprolol and Carvedilol subgroup). To compare the mortality and the combined outcome, the RRR (relative risk reduction) and NNT (number needed to treat) were used, as well as the survival analysis by Kaplan-Meier.RESULTS: The results showed the following: in regards of the cardiovascular mortality, the relative risk for death in the therapy group was 34%, which, though statistically not significant, is of great clinical significance. In regards of the combined outcome (death and/or number of hospitalizations) the results showed a RRR of 40% in the therapy group compared to the control group, which is statistically highly significant.CONCLUSION: The study confirmed that patients with stable chronic heart failure, treated with optimal doses of beta-blockers, show a significant reduction of the risk from death as well as combined outcome (death and/or number of hospitalizations).
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Wehbe, Nadine, Suzanne Nasser, Gianfranco Pintus, Adnan Badran, Ali Eid, and Elias Baydoun. "MicroRNAs in Cardiac Hypertrophy." International Journal of Molecular Sciences 20, no. 19 (September 23, 2019): 4714. http://dx.doi.org/10.3390/ijms20194714.
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Like other organs, the heart undergoes normal adaptive remodeling, such as cardiac hypertrophy, with age. This remodeling, however, is intensified under stress and pathological conditions. Cardiac remodeling could be beneficial for a short period of time, to maintain a normal cardiac output in times of need; however, chronic cardiac hypertrophy may lead to heart failure and death. MicroRNAs (miRNAs) are known to have a role in the regulation of cardiac hypertrophy. This paper reviews recent advances in the field of miRNAs and cardiac hypertrophy, highlighting the latest findings for targeted genes and involved signaling pathways. By targeting pro-hypertrophic genes and signaling pathways, some of these miRNAs alleviate cardiac hypertrophy, while others enhance it. Therefore, miRNAs represent very promising potential pharmacotherapeutic targets for the management and treatment of cardiac hypertrophy.
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Poskurica, Mileta, and Dejan Petrovic. "Congestive heart failure in patients with chronic kidney disease." Srpski arhiv za celokupno lekarstvo 142, no. 11-12 (2014): 747–55. http://dx.doi.org/10.2298/sarh1412747p.
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Cardiovascular disorders are the most frequent cause of death (46-60%) among patients with advanced chronic renal failure (CRF), and on dialysis treatment. Uremic cardiomyopathy is the basic pathophysiologic substrate, whereas ischemic heart disease (IHD) and anemia are the most important contributing factors. Associated with well-know risk factors and specific disorders for terminal kidney failure and dialysis, the aforementioned factors instigate congestive heart failure (CHF). Suspected CHF is based on the anamnesis, clinical examination and ECG, while it is confirmed and defined more precisely on the basis of echocardiography and radiology examination. Biohumoral data (BNP, NT-proBNP) are not sufficiently reliable because of specific volemic fluctuation and reduced natural clearance. Therapy approach is similar to the one for the general population: ACEI, ARBs, ?-blockers, inotropic drugs and diuretics. Hypervolemia and most of the related symptoms can be kept under control effectively by the isolated or ultrafiltation, in conjunction with dialysis, during the standard bicarbonate hemodialysis or hemodiafiltration. In the same respect peritoneal dialysis is efficient for the control of hypervolemia symptoms, mainly during the first years of its application and in case of the lower NYHA class (II?/III?). In general, heart support therapy, surgical interventions of the myocardium and valve replacement are rarely used in patients on dialysis, whereas revascularization procedures are beneficial for associated IHD. In selected cases the application of cardiac resynchronization and/or implantation of a cardioverter defibrillator are advisable.
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Jankowski, Joachim, Jürgen Floege, Danilo Fliser, Michael Böhm, and Nikolaus Marx. "Cardiovascular Disease in Chronic Kidney Disease." Circulation 143, no. 11 (March 16, 2021): 1157–72. http://dx.doi.org/10.1161/circulationaha.120.050686.
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Patients with chronic kidney disease (CKD) exhibit an elevated cardiovascular risk manifesting as coronary artery disease, heart failure, arrhythmias, and sudden cardiac death. Although the incidence and prevalence of cardiovascular events is already significantly higher in patients with early CKD stages (CKD stages 1–3) compared with the general population, patients with advanced CKD stages (CKD stages 4–5) exhibit a markedly elevated risk. Cardiovascular rather than end-stage kidney disease (CKD stage 5) is the leading cause of death in this high-risk population. CKD causes a systemic, chronic proinflammatory state contributing to vascular and myocardial remodeling processes resulting in atherosclerotic lesions, vascular calcification, and vascular senescence as well as myocardial fibrosis and calcification of cardiac valves. In this respect, CKD mimics an accelerated aging of the cardiovascular system. This overview article summarizes the current understanding and clinical consequences of cardiovascular disease in CKD.
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Alejandro Lerman, Daniel, Nasri Alotti, Kiddy Levente Ume, and Bruno Péault. "Cardiac Repair and Regeneration: The Value of Cell Therapies." European Cardiology Review 11, no. 1 (2016): 43. http://dx.doi.org/10.15420/ecr.2016:8:1.
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Ischaemic heart disease is the predominant contributor to cardiovascular morbidity and mortality; one million myocardial infarctions occur per year in the USA, while more than five million patients suffer from chronic heart failure. Recently, heart failure has been singled out as an epidemic and is a staggering clinical and public health problem associated with significant mortality, morbidity and healthcare expenditures, particularly among those aged ≥ 65 years. Death rates have improved dramatically over the last four decades, but new approaches are nevertheless urgently needed for those patients who go on to develop ventricular dysfunction and chronic heart failure. Over the past decade, stem cell transplantation has emerged as a promising therapeutic strategy for acute or chronic ischaemic cardiomyopathy. Multiple candidate cell types have been used in preclinical animal models and in humans to repair or regenerate the injured heart, either directly or indirectly (through paracrine effects), including: embryonic stem cells (ESCs), induced pluripotent stem cells (iPSCs), neonatal cardiomyocytes, skeletal myoblasts (SKMs), endothelial progenitor cells, bone marrow mononuclear cells (BMMNCs), mesenchymal stem cells (MSCs) and, most recently, cardiac stem cells (CSCs). Although no consensus has emerged yet, the ideal cell type for the treatment of heart disease should: (a) improve heart function; (b) create healthy and functional cardiac muscle and vasculature, integrated into the host tissue; (c) be amenable to delivery by minimally invasive clinical methods; (d) be available ‘off the shelf’ as a standardised reagent; (e) be tolerated by the immune system; (f) be safe oncologically, i.e. not create tumours; and (g) circumvent societal ethical concerns. At present, it is not clear whether such a ‘perfect’ stem cell exists; what is apparent, however, is that some cell types are more promising than others. In this brief review, we provide ongoing data on agreement and controversy arising from clinical trials and touch upon the future directions of cell therapy for heart disease.
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Karam, Sarah, Jean Piero Margaria, Aurélia Bourcier, Delphine Mika, Audrey Varin, Ibrahim Bedioune, Marta Lindner, et al. "Cardiac Overexpression of PDE4B Blunts β-Adrenergic Response and Maladaptive Remodeling in Heart Failure." Circulation 142, no. 2 (July 14, 2020): 161–74. http://dx.doi.org/10.1161/circulationaha.119.042573.
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Background: The cyclic AMP (adenosine monophosphate; cAMP)-hydrolyzing protein PDE4B (phosphodiesterase 4B) is a key negative regulator of cardiac β-adrenergic receptor stimulation. PDE4B deficiency leads to abnormal Ca 2+ handling and PDE4B is decreased in pressure overload hypertrophy, suggesting that increasing PDE4B in the heart is beneficial in heart failure. Methods: We measured PDE4B expression in human cardiac tissues and developed 2 transgenic mouse lines with cardiomyocyte-specific overexpression of PDE4B and an adeno-associated virus serotype 9 encoding PDE4B. Myocardial structure and function were evaluated by echocardiography, ECG, and in Langendorff-perfused hearts. Also, cAMP and PKA (cAMP dependent protein kinase) activity were monitored by Förster resonance energy transfer, L-type Ca 2+ current by whole-cell patch-clamp, and cardiomyocyte shortening and Ca 2+ transients with an Ionoptix system. Heart failure was induced by 2 weeks infusion of isoproterenol or transverse aortic constriction. Cardiac remodeling was evaluated by serial echocardiography, morphometric analysis, and histology. Results: PDE4B protein was decreased in human failing hearts. The first PDE4B-transgenic mouse line (TG15) had a ≈15-fold increase in cardiac cAMP-PDE activity and a ≈30% decrease in cAMP content and fractional shortening associated with a mild cardiac hypertrophy that resorbed with age. Basal ex vivo myocardial function was unchanged, but β-adrenergic receptor stimulation of cardiac inotropy, cAMP, PKA, L-type Ca 2+ current, Ca 2+ transients, and cell contraction were blunted. Endurance capacity and life expectancy were normal. Moreover, these mice were protected from systolic dysfunction, hypertrophy, lung congestion, and fibrosis induced by chronic isoproterenol treatment. In the second PDE4B-transgenic mouse line (TG50), markedly higher PDE4B overexpression, resulting in a ≈50-fold increase in cardiac cAMP-PDE activity caused a ≈50% decrease in fractional shortening, hypertrophy, dilatation, and premature death. In contrast, mice injected with adeno-associated virus serotype 9 encoding PDE4B (10 12 viral particles/mouse) had a ≈50% increase in cardiac cAMP-PDE activity, which did not modify basal cardiac function but efficiently prevented systolic dysfunction, apoptosis, and fibrosis, while attenuating hypertrophy induced by chronic isoproterenol infusion. Similarly, adeno-associated virus serotype 9 encoding PDE4B slowed contractile deterioration, attenuated hypertrophy and lung congestion, and prevented apoptosis and fibrotic remodeling in transverse aortic constriction. Conclusions: Our results indicate that a moderate increase in PDE4B is cardioprotective and suggest that cardiac gene therapy with PDE4B might constitute a new promising approach to treat heart failure.
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Hitosugi, Masahito, Akio Shigeta, and Akihiro Takatsu. "1. An Autopsy Case of Sudden Death in a Patient with Idiopathic Scoliosis." Medicine, Science and the Law 40, no. 2 (April 2000): 175–78. http://dx.doi.org/10.1177/002580240004000216.
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A 38-year-old woman with idiopathic scoliosis (right convex thoracic scoliosis, 78°; left convex lumbar curvature, 75°) died suddenly. Forensic autopsy and histopathologic examination revealed chronic congestive oedema, numerous cavities and atrophic changes of heart. These changes, including both respiratory changes and biventricular failure caused by hypoplastic cardiac changes, were due to a deformed thoracic cage. This case illustrates that not only abnormalities of respiratory function and cor pulmonare, but also hypoplastic cardiac changes, may cause sudden death in a patient with untreated scoliosis.
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Kadesjö, Erik, Andreas Roos, Anwar Siddiqui, Liyew Desta, Magnus Lundbäck, and Martin J. Holzmann. "Acute versus chronic myocardial injury and long-term outcomes." Heart 105, no. 24 (July 23, 2019): 1905–12. http://dx.doi.org/10.1136/heartjnl-2019-315036.
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ObjectiveThere is a paucity of data regarding prognosis in patients with acute versus chronic myocardial injury for long-term outcomes. We hypothesised that patients with chronic myocardial injury have a similar long-term prognosis as patients with acute myocardial injury.MethodsIn an observational cohort study of 22 589 patients who had high-sensitivity cardiac troponin T (hs-cTnT) measured in the emergency department during 2011–2014, we identified all patients with level >14 ng/L and categorised them as acute myocardial injury, type 1 myocardial infarction (T1MI), type 2 myocardial infarction (T2MI) or chronic myocardial injury through adjudication. We estimated adjusted HRs with 95% CIs for the primary outcome all-cause mortality and secondary outcomes MI, and heart failure in patients with acute myocardial injury, T1MI and T2MI compared with chronic myocardial injury.ResultsIn total, 3853 patients were included. During 3.9 (±2) years of follow-up, 48%, 24%, 44% and 49% of patients with acute myocardial injury, T1MI, T2MI and chronic myocardial injury died, respectively. Patients with acute myocardial injury had higher adjusted risks of death (1.21, 95% CI 1.08 to 1.36) and heart failure (1.24, 95% CI 1.07 to 1.43), but a similar risk for myocardial infarction (MI) compared with the reference group. Patients with T1MI had a lower adjusted risk of death (0.86, 95% CI 0.74 to 1.00) and higher risk of MI (2.09, 95% CI 1.62 to 2.68), but a similar risk of heart failure. Patients with T2MI had a higher adjusted risk of death (1.46, 95% CI 1.18 to 1.80) and heart failure (1.30, 95% CI 1.00 to 1.69) compared with patients with chronic myocardial injury.ConclusionsAbsolute long-term risks for death are similar, and adjusted risks are slightly higher, among patients with acute myocardial injury and T2MI, respectively, compared with chronic myocardial injury. The lowest risk of long-term mortality was found in patients with T1MI. Both acute and chronic myocardial injury are associated with very high risks of adverse outcomes.
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Nicolini, G., L. Pitto, C. Kusmic, S. Balzan, L. Sabatino, G. Iervasi, and F. Forini. "New Insights into Mechanisms of Cardioprotection Mediated by Thyroid Hormones." Journal of Thyroid Research 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/264387.
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Heart failure represents the final common outcome in cardiovascular diseases. Despite significant therapeutic advances, morbidity and mortality of heart failure remain unacceptably high. Heart failure is preceded and sustained by a process of structural remodeling of the entire cardiac tissue architecture. Prevention or limitation of cardiac remodeling in the early stages of the process is a crucial step in order to ameliorate patient prognosis. Acquisition of novel pathophysiological mechanisms of cardiac remodeling is therefore required to develop more efficacious therapeutic strategies. Among all neuroendocrine systems, thyroid hormone seems to play a major homeostatic role in cardiovascular system. In these years, accumulating evidence shows that the “low triiodothyronine” syndrome is a strong prognostic, independent predictor of death in patients affected by both acute and chronic heart disease. In experimental models of cardiac hypertrophy or myocardial infarction, alterations in the thyroid hormone signaling, concerning cardiac mitochondrion, cardiac interstitium, and vasculature, have been suggested to be related to heart dysfunction. The aim of this brief paper is to highlight new developments in understanding the cardioprotective role of thyroid hormone in reverting regulatory networks involved in adverse cardiac remodeling. Furthermore, new recent advances on the role of specific miRNAs in thyroid hormone regulation at mitochondrion and interstitial level are also discussed.
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Ramírez, Julia, Michele Orini, Ana Mincholé, Violeta Monasterio, Iwona Cygankiewicz, Antonio Bayés de Luna, Juan Pablo Martínez, Pablo Laguna, and Esther Pueyo. "Sudden cardiac death and pump failure death prediction in chronic heart failure by combining ECG and clinical markers in an integrated risk model." PLOS ONE 12, no. 10 (October 11, 2017): e0186152. http://dx.doi.org/10.1371/journal.pone.0186152.
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Taneva, B., J. Davceva, M. Vavlukis, V. Andova, and N. Kostova. "Bisoprolol reduces episodes of ventricular tachycardia and sudden cardiac death in subjects with chronic heart failure." European Journal of Heart Failure 2 (June 2000): 98. http://dx.doi.org/10.1016/s1388-9842(00)80348-7.
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Juanhui, Pei, Pu Jielin, Chen Jingzhou, and Zhang Yinhui. "J Wave Inferior Leads-A New ECG Predictor of Sudden Cardiac Death in Chronic Heart Failure." Journal of Arrhythmia 27, Supplement (2011): OP67_2. http://dx.doi.org/10.4020/jhrs.27.op67_2.
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Đerić, Mirjana, and Velibor Čabarkapa. "Cardiovascular Biomarkers in Chronic Kidney Disease." Journal of Medical Biochemistry 29, no. 4 (October 1, 2010): 298–303. http://dx.doi.org/10.2478/v10011-010-0033-8.
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Cardiovascular Biomarkers in Chronic Kidney DiseaseCardiovascular morbidity and mortality are markedly increased in chronic renal failure patients. Although it cannot be regarded as a cardiovascular disease risk equivalent, kidney dysfunction is considered an independent predictor of increased cardiovascular risk that increases with deteriorating kidney function. The association is a very complex one, and the term cardiorenal syndrome is now widely used. Cardiovascular disease in chronic kidney disease patients usually manifests as ischemic heart disease (in the form of angina, acute coronary syndrome or sudden cardiac death), cerebrovascular disease, peripheral vascular disease, and congestive heart failure. Vascular disease includes atherosclerosis and vascular calcifications, and cardiomyopathy comprises left ventricular hypertrophy, cardiac fibrosis and left ventricular systolic and diastolic dysfunction. In addition to the well-established traditional risk factors such as hypertension, hyperlipidemia, insulin resistance and diabetes mellitus, the association is supported by synergistic action of non-traditional risk factors such as excessive calcium-phosphorus load, hyperparathyroidism, anemia, hemodynamic overload, malnutrition, inflammation, hyperhomocysteinemia, altered nitric oxide synthase and increased oxidative stress. This paper summarizes the current understanding of the significance of specific uremic retention solutes, natriuretic peptides, biochemical markers of disorders in calcium-phosphorus homeostasis, systemic inflammation, oxidative stress, and dyslipidemia.
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Capin, Ivana, Christine A. Capone, and Matthew D. Taylor. "Acute on Chronic Heart Failure Secondary to Left Ventricular Noncompaction." Case Reports in Pediatrics 2020 (October 26, 2020): 1–5. http://dx.doi.org/10.1155/2020/6369806.
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Left ventricular noncompaction (LVNC) is a rare cardiomyopathy characterized by hypertrabeculations and intertrabecular recesses most often seen in the left ventricle (LV). The patient may be asymptomatic or present with heart failure, arrhythmia, and sudden death. We discuss a previously healthy 7-year-old male who presented to the Emergency Department (ED) multiple times over a three-week period. His complaints evolved over the course of his illness, initially presenting with fatigue and suicidal ideation, followed by diffuse abdominal pain. Prior to his ICU admission, he had been discharged from the ED twice, due to well appearance and reassuring lab findings. He returned to the ED a final time with severe venous congestion and cardiogenic shock with acute hepatic injury. Echocardiogram revealed LV apical hypertrabeculation with a severe dilated cardiomyopathy and biventricular failure along with a large thrombus in the left ventricular cavity. Congestive heart failure and anticoagulation therapy was initiated, and the patient went on to biventricular assist device (BiVAD) placement and cardiac transplant. Although LVNC is rare, pediatric heart failure does present to the general pediatrician and has high morbidity and mortality. The presenting symptoms can be obscure and pose a challenge to pediatricians. This case report and review will assist in familiarizing the general pediatrician with pediatric heart failure presentation, treatment, and course.
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Omar, Sabry, and Ahmed Zedan. "Cardiorenal syndrome." Southwest Respiratory and Critical Care Chronicles 1, no. 1 (January 30, 2013): 11. http://dx.doi.org/10.12746/swrccc.v1i1.24.
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Cardiovascular disease is the leading cause of death in patients with chronic kidney disease. Heart failure may lead to acute kidney injury and vice versa. Chronic kidney disease may affect the clinical outcomes in patients with cardiovascular disorders. Renal impairment with any degree of albuminuria has been increasingly recognized as an independent risk factor for cardiovascular events and heart failure hospitalizations, while chronic heart failure may cause chronic kidney disease. The bidirectional nature of these disorders contributes to the complexity and the composite definitions of cardiorenal syndromes. However, the most important clinical trials in heart failure tend to exclude patients with significant renal dysfunction. The mechanisms whereby renal insufficiency worsens the outcome in heart failure are not known, and several pathways could contribute to the ‘‘vicious heart/kidney circle.’’ Traditionally, renal impairment has been attributed to the renal hypoperfusion due to reduced cardiac output and decreased systemic pressure. The hypovolemia leads to sympathetic activity, increased renin-angiotensin aldosterone pathway, and arginine-vasopressin release. These mechanisms cause fluid and sodium retention, peripheral vasoconstriction, and volume overload. Therapy to improve renal dysfunction, reduce neurohormonal activation and ameliorate renal blood flow could lead to a reduction in mortality and hospitalization in patients with cardiorenal syndrome.
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Cognet, Thomas, Olivier Lairez, Pauline Marchal, Jérôme Roncalli, and Michel Galinier. "A Family History of Dilated Cardiomyopathy Induced by Viral Myocarditis." Case Reports in Cardiology 2012 (2012): 1–3. http://dx.doi.org/10.1155/2012/204371.
Full textAbstract:
Myocarditis can lead to acute heart failure, cardiogenic shock, or sudden death and later, dilated cardiomyopathy (DCM) with chronic heart failure. We report the cases of two DCM induced by acute and past myocarditis in the same family and expressed by its two main complications within few weeks: an hemodynamic presentation as a fulminant myocarditis rapidly leading to cardiac tranplantation and a rythmologic presentation as an electrical storm leading to catheter ablation of ventricular tachycardia. These cases ask the question of the family predisposition to viral myocarditis leading to DCM.
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Chen, Si, Yishuai Zhang, Janet K. Lighthouse, Deanne M. Mickelsen, Jiangbin Wu, Peng Yao, Eric M. Small, and Chen Yan. "A Novel Role of Cyclic Nucleotide Phosphodiesterase 10A in Pathological Cardiac Remodeling and Dysfunction." Circulation 141, no. 3 (January 21, 2020): 217–33. http://dx.doi.org/10.1161/circulationaha.119.042178.
Full textAbstract:
Background: Heart failure is a leading cause of death worldwide. Cyclic nucleotide phosphodiesterases (PDEs), through degradation of cyclic nucleotides, play critical roles in cardiovascular biology and disease. Our preliminary screening studies have revealed PDE10A upregulation in the diseased heart. However, the roles of PDE10A in cardiovascular biology and disease are largely uncharacterized. The current study is aimed to investigate the regulation and function of PDE10A in cardiac cells and in the progression of cardiac remodeling and dysfunction. Methods: We used isolated adult mouse cardiac myocytes and fibroblasts, as well as preclinical mouse models of hypertrophy and heart failure. The PDE10A selective inhibitor TP-10, and global PDE10A knock out mice were used. Results: We found that PDE10A expression remains relatively low in normal and exercised heart tissues. However, PDE10A is significantly upregulated in mouse and human failing hearts. In vitro, PDE10A deficiency or inhibiting PDE10A with selective inhibitor TP-10, attenuated cardiac myocyte pathological hypertrophy induced by Angiotensin II, phenylephrine, and isoproterenol, but did not affect cardiac myocyte physiological hypertrophy induced by IGF-1 (insulin-like growth factor 1). TP-10 also reduced TGF-β (transforming growth factor-β)–stimulated cardiac fibroblast activation, proliferation, migration and extracellular matrix synthesis. TP-10 treatment elevated both cAMP and cGMP levels in cardiac myocytes and cardiac fibroblasts, consistent with PDE10A as a cAMP/cGMP dual-specific PDE. In vivo, global PDE10A deficiency significantly attenuated myocardial hypertrophy, cardiac fibrosis, and dysfunction induced by chronic pressure overload via transverse aorta constriction or chronic neurohormonal stimulation via Angiotensin II infusion. Importantly, we demonstrated that the pharmacological effect of TP-10 is specifically through PDE10A inhibition. In addition, TP-10 is able to reverse pre-established cardiac hypertrophy and dysfunction. RNA-Sequencing and bioinformatics analysis further identified a PDE10A-regualted transcriptome involved in cardiac hypertrophy, fibrosis, and cardiomyopathy. Conclusions: Taken together, our study elucidates a novel role for PDE10A in the regulation of pathological cardiac remodeling and development of heart failure. Given that PDE10A has been proven to be a safe drug target, PDE10A inhibition may represent a novel therapeutic strategy for preventing and treating cardiac diseases associated with cardiac remodeling.
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Stelter, Zachary, Jana Strakova, Amritha Yellamilli, Kaleb Fischer, Katharine Sharpe, and DeWayne Townsend. "Hypoxia-induced cardiac injury in dystrophic mice." American Journal of Physiology-Heart and Circulatory Physiology 310, no. 7 (April 1, 2016): H938—H948. http://dx.doi.org/10.1152/ajpheart.00917.2015.
Full textAbstract:
Duchenne muscular dystrophy (DMD) is a disease of progressive destruction of striated muscle, resulting in muscle weakness with progressive respiratory and cardiac failure. Respiratory and cardiac disease are the leading causes of death in DMD patients. Previous studies have suggested an important link between cardiac dysfunction and hypoxia in the dystrophic heart; these studies aim to understand the mechanism underlying this connection. Here we demonstrate that anesthetized dystrophic mice display significant mortality following acute exposure to hypoxia. This increased mortality is associated with a significant metabolic acidosis, despite having significantly higher levels of arterial Po2. Chronic hypoxia does not result in mortality, but rather is characterized by marked cardiac fibrosis. Studies in isolated hearts reveal that the contractile function of dystrophic hearts is highly susceptible to short bouts of ischemia, but these hearts tolerate prolonged acidosis better than wild-type hearts, indicating an increased sensitivity of the dystrophic heart to hypoxia. Dystrophic hearts display decreased cardiac efficiency and oxygen extraction. Isolated dystrophic cardiomyocytes and hearts have normal levels of FCCP-induced oxygen consumption, and mitochondrial morphology and content are normal in the dystrophic heart. These studies demonstrate reductions in cardiac efficiency and oxygen extraction of the dystrophic heart. The underlying cause of this reduced oxygen extraction is not clear; however, the current studies suggest that large disruptions of mitochondrial respiratory function or coronary flow regulation are not responsible. This finding is significant, as hypoxia is a common and largely preventable component of DMD that may contribute to the progression of the cardiac disease in DMD patients.