scholarly journals Myocarditis and intramural coronary vasculitis in polyarteritis nodosa: an unusual treatable form of heart failure

2020 ◽  
Vol 7 (6) ◽  
pp. 4357-4360
Author(s):  
Cristina Chimenti ◽  
Maria Alfarano ◽  
Federica Toto ◽  
Francesca Fanisio ◽  
Romina Verardo ◽  
...  
Keyword(s):  
Heart Failure ◽  
Polyarteritis Nodosa ◽  
Coronary Vasculitis

Abstract 17425: Prevalence of Heart Failure in Polyarteritis Nodosa. A Descriptive Analysis From the National Inpatient Sample

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Akshaya Gopalakrishnan ◽  
Aman M Amanullah ◽  
Janani Rangaswami ◽  
Sarath Reddy ◽  
Viswanath Vasudevan
Keyword(s):  
Risk Factors ◽  
Heart Failure ◽  
Coronary Artery ◽  
Polyarteritis Nodosa ◽  
Descriptive Analysis ◽  
Artery Aneurysm ◽  
Cardiac Risk ◽  
International Classification Of Diseases ◽  
National Database ◽  
National Inpatient Sample

Introduction: Polyarteritis Nodosa (PAN) is a systemic necrotizing vasculitis of medium sized arteries. Congestive heart failure (CHF) in PAN could be due to coronary artery disease, coronary artery aneurysm or renal artery vasculitis. We utilized a national database to study the prevalence of CHF in patients with PAN. Hypothesis: We hypothesized that patients with PAN might have increased prevalence of CHF. Methods: All inpatients more than 18 years of age from the National Inpatient Sample (NIS) between 2009-10 with a diagnosis of PAN were extracted using 9th revision of International Classification of Diseases (ICD-9) code 446.0. Prevalence of CHF and other cardiac risk factors were identified using ICD-9 codes. Logistic regression analysis was performed to examine the association between PAN and CHF. Results: PAN was prevalent in 0.01% (n=3,944) of all inpatient hospitalizations. Patients with PAN were slightly older, more commonly females and had higher rates of CHF (11.3% vs 6.4%; p<0.0001) when compared to the general population. Diabetes mellitus, hypertension, atrial fibrillation, chronic renal insufficiency and chronic lung disease were more prevalent in patients with PAN (p<0.0001 for all). PAN independently predicted CHF both in unadjusted [OR 1.88 (1.49-2.38); p<0.001] and multivariable model adjusted for demographics and other risk factors for CHF [OR 1.36 (1.05-1.78); p=0.02. Conclusions: PAN was associated with increased prevalence and independent predictor of CHF. Further studies are recommended to validate this finding and consider it as a part of routine work up.

scholarly journals Heart failure in a patient with polyarteritis nodosa

2020 ◽  
Vol 4 (5) ◽  
pp. 1-2
Author(s):  
Yuta Watanabe ◽  
Kayo Sakamoto ◽  
Shoichi Matsukage ◽  
Akiyoshi Ogimoto
Keyword(s):  
Heart Failure ◽  
Polyarteritis Nodosa

scholarly journals A case report of heart transplant for ischaemic cardiomyopathy from lupus coronary vasculitis

2019 ◽  
Author(s):  
Shuktika Nandkeolyar ◽  
Hyungjin B Kim ◽  
Tanya Doctorian ◽  
Liset N Stoletniy ◽  
Vaneet K Sandhu ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Transplant ◽  
Lupus Erythematosus ◽  
Treatment Plan ◽  
Young Patients ◽  
Anterior Wall ◽  
Orthotopic Heart Transplant ◽  
Cardiac Symptoms ◽  
Triple Vessel Disease ◽  
Coronary Vasculitis

Abstract Background  Coronary vasculitis is a rare, life-threatening complication of systemic lupus erythematosus (SLE). Case summary A 23-year-old woman with SLE presented with typical angina and worsening dyspnoea on exertion. Coronary angiography revealed severe triple vessel disease with a ‘string of beads’ appearance classic for coronary vasculitis. Transthoracic echocardiogram revealed ejection fraction of 25–30% with a severely hypokinetic distal septum and distal anterior wall and an akinetic apical wall. Despite vasculitis treatment with cyclophosphamide and pulse-dose steroids, her coronary vasculitis did not improve. She was refractory to anti-anginal and guideline-directed medical therapy for heart failure and successfully underwent orthotopic heart transplant (OHT). Discussion  This is the first reported case of OHT in the case of SLE coronary vasculitis. Chronic SLE coronary vasculitis is caused by lymphocyic infiltration leading to inflammation and fibrosis of the major epicardial coronary arteries but can be successfully managed with OHT when refractory to medical SLE and heart failure therapies. It can affect patients of all ages with SLE, emphasizing the importance of thorough history taking and clinical evaluation in young patients presenting with cardiac symptoms to establish an appropriate diagnosis and treatment plan.

Mitochondria in Cardiomyopathy: Alterations in Size, Number and Internal Structures

1968 ◽  
Vol 26 ◽  
pp. 126-127
Author(s):  
George Hug ◽  
William K. Schubert
Keyword(s):  
Heart Failure ◽  
Biochemical Analysis ◽  
Left Ventricular ◽  
Size Number ◽  
Internal Structures ◽  
Left Ventricular Outflow ◽  
Chest X Ray ◽  
Myocardial Fibers ◽  
Muscle Biopsies ◽  
Needle Liver Biopsy

A white boy six months of age was hospitalized with respiratory distress and congestive heart failure. Control of the heart failure was achieved but marked cardiomegaly, moderate hepatomegaly, and minimal muscular weakness persisted.At birth a chest x-ray had been taken because of rapid breathing and jaundice and showed the heart to be of normal size. Clinical studies included: EKG which showed biventricular hypertrophy, needle liver biopsy which showed toxic hepatitis, and cardiac catheterization which showed no obstruction to left ventricular outflow. Liver and muscle biopsies revealed no biochemical or histological evidence of type II glycogexiosis (Pompe's disease). At thoracotomy, 14 milligrams of left ventricular muscle were removed. Total phosphorylase activity in the biopsy specimen was normal by biochemical analysis as was the degree of phosphorylase activation. By light microscopy, vacuoles and fine granules were seen in practically all myocardial fibers. The fibers were not hypertrophic. The endocardium was not thickened excluding endocardial fibroelastosis. Based on these findings, the diagnosis of idiopathic non-obstructive cardiomyopathy was made.

Localization of endothelial nitric oxide synthase in the normal and failing human atrial myocardium

1996 ◽  
Vol 54 ◽  
pp. 786-787
Author(s):  
Chi-Ming Wei ◽  
Margarita Bracamonte ◽  
Shi-Wen Jiang ◽  
Richard C. Daly ◽  
Christopher G.A. McGregor ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Cardiac Tissues ◽  
Mammalian Tissues ◽  
End Stage Heart Failure ◽  
End Stage ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Nitric oxide (NO) is a potent endothelium-derived relaxing factor which also may modulate cardiomyocyte inotropism and growth via increasing cGMP. While endothelial nitric oxide synthase (eNOS) isoforms have been detected in non-human mammalian tissues, expression and localization of eNOS in the normal and failing human myocardium are poorly defined. Therefore, the present study was designed to investigate eNOS in human cardiac tissues in the presence and absence of congestive heart failure (CHF).Normal and failing atrial tissue were obtained from six cardiac donors and six end-stage heart failure patients undergoing primary cardiac transplantation. ENOS protein expression and localization was investigated utilizing Western blot analysis and immunohistochemical staining with the polyclonal rabbit antibody to eNOS (Transduction Laboratories, Lexington, Kentucky).

Protective role of peroxiredoxin-4 in heart failure

2020 ◽  
Vol 134 (1) ◽  
pp. 71-72
Author(s):  
Naseer Ahmed ◽  
Masooma Naseem ◽  
Javeria Farooq
Keyword(s):  
Heart Failure ◽  
Cardiac Fibroblasts ◽  
Protective Role ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
Total Antioxidant ◽  
Galectin 3 ◽  
Consequent Increase ◽  
And Oxidative Stress

Abstract Recently, we have read with great interest the article published by Ibarrola et al. (Clin. Sci. (Lond.) (2018) 132, 1471–1485), which used proteomics and immunodetection methods to show that Galectin-3 (Gal-3) down-regulated the antioxidant peroxiredoxin-4 (Prx-4) in cardiac fibroblasts. Authors concluded that ‘antioxidant activity of Prx-4 had been identified as a protein down-regulated by Gal-3. Moreover, Gal-3 induced a decrease in total antioxidant capacity which resulted in a consequent increase in peroxide levels and oxidative stress markers in cardiac fibroblasts.’ We would like to point out some results stated in the article that need further investigation and more detailed discussion to clarify certain factors involved in the protective role of Prx-4 in heart failure.

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