scholarly journals Increasing home‐time after a first diagnosis of heart failure in Sweden, 20 years trends

2021 ◽  
Author(s):  
Sofia Ekestubbe ◽  
Michael Fu ◽  
Kok Wai Giang ◽  
Martin Lindgren ◽  
Annika Rosengren ◽  
...  
Keyword(s):  
Heart Failure ◽  
First Diagnosis

scholarly journals Survival of Patients Following First Diagnosis of Diabetic Foot Complications: A Nationwide 15-Year Longitudinal Analysis

2021 ◽  
Vol 12 ◽  
Author(s):  
Chia-Hung Lin ◽  
David G. Armstrong ◽  
Pi-Hua Liu ◽  
Cheng-Wei Lin ◽  
Chung-Huei Huang ◽  
...  
Keyword(s):  
Heart Failure ◽  
Type 2 Diabetes ◽  
Survival Rate ◽  
Diabetic Foot ◽  
Term Survival ◽  
Cardiovascular Comorbidity ◽  
Cardiovascular Comorbidities ◽  
Foot Complications ◽  
First Diagnosis

Background and AimsThe long-term survival in people with type 2 diabetes following first diagnosis of diabetic foot complications (FDDFC) is unclear. The object is to evaluate the mortality rate in subjects with type 2 diabetes following FDDFC and the impacts of the major cardiovascular comorbidities.MethodsNationwide data were analyzed for subjects with T2D and DFC between 2003 and 2017 according to ICD-9 coding. DFC was defined with the codes of ulcers, infections, or severe peripheral artery disease that required intervention (PAD) to mimic the real world diagnosis. Criteria of FDDFC were preceded by a period without any DFC for at least 5 years. Major cardiovascular comorbidities: established PAD and cardiovascular diseases (CVD: including coronary heart disease (CHD), stroke, or heart failure) before the index date as well as lower-extremity amputations (LEA) at the index episode were analyzed.ResultsAmong 300,115 subjects with DFC, a total of 103,396 patients had FDDFC. The mean 5-year survival rate of these subjects was 81.05%. Using subjects without associated major cardiovascular comorbidity as baseline, the adjusted hazard ratios (aHR) were1.43 (95% confidence interval 1.38–1.49) in group PAD-/CVD+, followed by 1.70 (1.59–1.80) in PAD+/CVD- and 1.98 (1.89–2.08) in PAD+/CVD+. The aHR was further increased in patients with PAD who additionally had heart failure (3.77, 3.50–4.05), stroke (2.06, 1.95–2.18), or CHD (1.89, 1.79–2.00). Subjects with PAD rather than other CVD were associated with LEA at FDDFC. Patients with major LEA (above the ankle) at FDDFC episode had lower 5-year survival rate (65.01%) followed by those with minor LEA (72.24%) and without LEA (81.61%).ConclusionsCardiovascular comorbidity as well as LEA status at the event of FDDFCs were both associated with patient survival outcomes. Earlier identification of this large population could lead to higher survival rates.

scholarly journals Clinical profiles and incident heart failure in cardiomyopathies: a population-based linked electronic health record cohort study

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
J Brownrigg ◽  
J Rose ◽  
E Low ◽  
S Richard ◽  
G Carr-White ◽  
...  
Keyword(s):  
Heart Failure ◽  
Clinical Characteristics ◽  
Index Date ◽  
Population Based ◽  
Clinical Practice Research Datalink ◽  
Routine Practice ◽  
Funding Source ◽  
Private Company ◽  
Electronic Health ◽  
First Diagnosis

Abstract Background Cardiomyopathies frequently cause heart failure (HF), however their prevalence in the general population and the natural history of incident HF across the spectrum of cardiomyopathy phenotypes is poorly understood. Improved understanding will help guide rational selection of diagnostic tests and accelerate the recognition of underlying causes of HF. Purpose To estimate the prevalence of cardiomyopathies using electronic health records; to compare clinical characteristics between patients with cardiomyopathy phenotypes; and to describe the temporal relationship between diagnosis of cardiomyopathy and incident HF. Methods A population-based cohort of patients with cardiomyopathy (n=4058) was provided by the UK Clinical Practice Research Datalink (CPRD) from a denominator sample of ∼9 million individuals. Patients were phenotyped into groups according to ESC criteria: hypertrophic cardiomyopathy (HCM), dilated cardiomyopathy (DCM), arrhythmogenic right ventricular cardiomyopathy (ARVC) and restrictive cardiomyopathy (RCM). An additional group of transthyretin amyloid cardiomyopathy (ATTR-CM) was reported separately. Point prevalence was estimated for each cardiomyopathy subtype and clinical characteristics defined. An index date at first diagnosis of HF was determined for each patient and the time from/to first diagnosis of cardiomyopathy calculated relative to the index date and presented graphically. Results DCM was the most common cardiomyopathy phenotype among women and men with 3.4 and 7.7 cases per 10,000 population, respectively. The 2-fold increase in prevalence among men was consistent across DCM, HCM and RCM; the reverse trend was observed for ARVC which was found in 2.3 per 10,000 women and 1.1 per 10,000 men. At the time of first diagnosis of cardiomyopathy, most patients with ATTR-CM (73.5%), DCM (71.0%) and RCM (71.3%) had pre-existing HF though this proportion fell to 41.0% in ARVC and 31.0% in HCM. In relation to incident HF, a diagnosis of HCM and DCM were recorded earliest at a mean −2.2 years (SE 0.2) and −0.6 years (SE 0.1), respectively. We observed a clustering of diagnoses of RCM (mean −0.2 years, SE 0.4) and ARVC (mean 0.1 years, SE 0.1) around the time of onset of heart failure, whereas a diagnosis of ATTR-CM was first recorded at a mean of 0.9 years (SE 0.2) following the onset of heart failure. Conclusions Most diagnoses of ATTR-CM, DCM and RCM were preceded by clinical expression of HF whereas most people with ARVC or HCM developed HF after their cardiomyopathy diagnosis. Our findings in ARVC and HCM suggest a more indolent course with respect to cardiac function or better recognition in an asymptomatic phase. The clustering of a diagnosis of heart failure around the time of diagnosis of cardiomyopathy highlights a need for greater awareness of specific aetiologies of heart failure in routine practice and suggests opportunities for presymptomatic or earlier diagnosis. Temporality of HF in cardiomyopathies Funding Acknowledgement Type of funding source: Private company. Main funding source(s): Pfizer

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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