Low Body Temperature Linked to Increased Mortality in Heart Failure

2005 ◽  
Vol 38 (16) ◽  
pp. 43
Author(s):  
Heidi Splete
2008 ◽  
Vol 14 (6) ◽  
pp. 489-496 ◽  
Author(s):  
Amany Ahmed ◽  
Ibrahim Aboshady ◽  
Shahzeb M. Munir ◽  
Sreedevi Gondi ◽  
Alan Brewer ◽  
...  

2006 ◽  
Vol 47 (12) ◽  
pp. 2563-2564 ◽  
Author(s):  
Brahmajee K. Nallamothu ◽  
Saeed Payvar ◽  
Yongfei Wang ◽  
Mikhail Kosiborod ◽  
Frederick A. Masoudi ◽  
...  

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
Y Yoshida ◽  
I Shimizu ◽  
K Walsh ◽  
T Minamino

Abstract Prognosis of severe heart failure is unacceptably high, and it is our urgent task to find therapies for this critical condition. It has been reported that low body temperature predicts poor clinical outcomes in patients with heart failure, however, underlying mechanisms and pathological implications are largely unknown. Brown adipose tissue (BAT) was initially characterized as a heat generating organ, and studies suggest that BAT has crucial roles for the maintenance of systemic metabolic health. Here we show that BAT dysfunction develops in a murine thoracic aortic constriction (TAC) model, and has a causal role for promoting pathologies in failing heart. TAC operation led to a significant reduction both in intraperitoneal and subcutaneous temperature. TUNEL-positive cells significantly increased in BAT during left ventricular (LV)-pressure overload, and in-vitro studies with differentiated brown adipocytes suggested that the chronic activation of adrenergic signaling promotes apoptosis in these cells. Gain of BAT function model, generated with BAT implantation into peritoneal cavity, improved thermogenesis and ameliorated cardiac dysfunction in TAC. In contrast, genetic model of BAT dysfunction promoted cardiac dysfunction. Metabolomic analyses showed that BAT dysfunction led to an increase of oxidized choline that promoted metabolic dysfunction in the failing heart. Electron microscope study showed that oxidized choline induced mitochondrial dysfunction in vitro as well as in vivo settings. Extracellular flux analyzerindicated that oxidized choline suppresses oxidative phosphorylation in mitochondria. We found that dilated cardiomyopathy patients have lower body temperature, and confirmed by metabolomic study that both choline and oxidized choline are increased in circulation. Maintenance of BAT homeostasis and suppression of oxidized choline would become a novel therapeutic target for heart failure.


2005 ◽  
Vol 53 (2) ◽  
pp. S400.2-S400
Author(s):  
B. K. Nallamothu ◽  
S. Payvar ◽  
Y. Wang ◽  
M. Kosiborod ◽  
J. M. Foody ◽  
...  

Author(s):  
V Batushkin ◽  
D Dakalov

Due to the COVID-19 outbreak, management of patients with severe cardiovascular disease has become much more complicated. The paper describes first-hand experience of managing a COVID-19 patient with chronic heart failure secondary to myocardial infarction who died from sudden cardiac death. Mortality risk factors in COVID-19-associated cardiac patients are discussed. The authors describe a case of a female patient B., 67 years old, who was taken to the hospital by ambulance with a preliminary diagnosis of community-acquired right lower lobe pneumonia, respiratory failure (RF) II (SpO294%). Coronary heart disease (CHD). Athero-sclerotic and postinfarction (2019) cardiosclerosis. Permanent atrial fibrillation. Hypertension, stage III, grade 3, risk 4 (stroke, 2019). Heart failure (HF) II-A (NYHA class II). Rapid tests for the diagnosis of influenza A and B and detection of COVID-19 antibodies IgG and IgM were negative. From the patient’s history it was found out that over the last 2 months she was in a private medical rehabilitation center. Nine days before her hospitalization, her relatives took her home. According to them, the patient developed fever (37.5–38.4 °C) 4 days before hospitalization, she took paracetamol in her discretion. On admission, her body temperature was 37.5 °C. The patient was hospitalized to the triage department; on the day of hospitalization, her nasopharyngeal lavage was taken for real-time PCR (polymerase chain reaction) for COVID-19. During the hospital stay the patient’s condition stabilized. The next day after hospitalization, the maximum body temperature was within 37.0 °C, shortness of breath decreased, heart rate slowed, RF disappeared, room-air SpO2increased up to 96%. According to the results of echocardiography, the left ventricle (LV) pump function remained preserved (LV ejection fraction was 50%), LV cavities were slightly enlarged, and valvular pathology was characterized by moderate mitral and tricuspid insufficiency. The area of hypokinesia due to myocardial infarction was determined only in the apical segment of the lateral wall and was compensated due to moderate left ventricular hypertensive hypertrophy (left ventricular mass index 129 g/L2). R wave amplitude on the electrocardiography was preserved, which indicated relative compensation of the central hemodynamics of the patient B. On day 2 of hospitalization, the patient’s condition remained stable. The body temperature normalized, leg swelling disappeared, cough and shortness of breath decreased, physical activity significantly improved. The patient was examined by an infectious disease specialist. After receiving the COVID-19 test result (positive PCR test), it was agreed to transfer the patient to a coronavirus hospital for further treatment in the infectious department. However, the patient died suddenly. Final diagnosis: coronavirus disease. COVID-19. Community-acquired bilateral lower lobe pneumonia (viral). Respiratory failure (RF) – 0. CHD. Atherosclerotic and postinfarction (2019) cardiosclerosis. Permanent atrial fibrillation. Hypertension, stage III, grade 3, risk 4 (stroke, 2019). HF II-B. Since dissection was not performed, the exact cause of death is unknown. The article describes important aspects of diagnosis and treatment that can prevent mortality. The authors emphasize that prevention and control of infectious diseases should be prioritized at any time. Individual measures of diagnosis and treatment should be taken considering specific local epidemic situations.


Author(s):  
George Hug ◽  
William K. Schubert

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.


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