scholarly journals Epidemiological Aspects of Cardiac Decompensation Factors Renaissance Hospital N’Djamena Chad

2019 ◽  
Vol 2 (3) ◽  
Author(s):  
Adam Ahamat Ali
Author(s):  
Fabio A. Recchia ◽  
Robert D. Bernstein ◽  
Pravin B. Sehgal ◽  
Nicholas R. Ferreri ◽  
Thomas H. Hintze

Toxins ◽  
2020 ◽  
Vol 13 (1) ◽  
pp. 19
Author(s):  
Mark Little ◽  
Peter Pereira ◽  
Jamie Seymour

Carukia barnesi was the first in an expanding list of cubozoan jellyfish whose sting was identified as causing Irukandji syndrome. Nematocysts present on both the bell and tentacles are known to produce localised stings, though their individual roles in Irukandji syndrome have remained speculative. This research examines differences through venom profiling and pulse wave Doppler in a murine model. The latter demonstrates marked measurable differences in cardiac parameters. The venom from tentacles (CBVt) resulted in cardiac decompensation and death in all mice at a mean of 40 min (95% CL: ± 11 min), whereas the venom from the bell (CBVb) did not produce any cardiac dysfunction nor death in mice at 60 min post-exposure. This difference is pronounced, and we propose that bell exposure is unlikely to be causative in severe Irukandji syndrome. To date, all previously published cubozoan venom research utilised parenterally administered venom in their animal models, with many acknowledging their questionable applicability to real-world envenomation. Our model used live cubozoans on anaesthetised mice to simulate normal envenomation mechanics and actual expressed venoms. Consequently, we provide validity to the parenteral methodology used by previous cubozoan venom research.


2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Feyza Bora ◽  
Emine Asar ◽  
Fatih Yılmaz ◽  
Ümit Çakmak ◽  
Fevzi F Ersoy ◽  
...  

Abstract Background and Aims It is evident that Chronic Kidney Disease (CKD) influences the risk of developing AKI (Acute Kidney Injury) and recent studies suggest that CKD patients who experienced an episode of AKI are more likely to progress to end stage renal disease (ESRD) than patients without CKD. AKI-CKD association might originate from common comorbidities associated with both AKI and CKD, such as diabetes and/or hypertension, and concurrent increase in interventions leading to frequent exposure to various nephrotoxins. AKI in the elderly has been shown to increase the risk of progression to CKD to ESRD. AKI is common in critically ill patients, and those patients with the most severe form of AKI, requiring RRT, have a mortality rate of 50–80 %. Patients with an eGFR <45 ml/min per 1.73m2 who experienced an episode of dialysis-requiring AKI were at very high risk for impaired recovery of renal function. Our aim was to determine the reasons that initiate hemodialysis (renal decompensation) in patients with regular follow-up in the low clearance polyclinic without renal replacement treatment (RRT). Method The retrospective study included predialysis CKD patients who had followed up regularly and had undergone RRT in recent 4 years. Data on baseline characteristics and medical history were obtained from patient hospital records. Results Of the 228 patients, 155 (68%) were male and 73 (32%) were female. The mean age was 58 years (45-66). Diabetes Mellitus was the first in the etiology of CKD (26,3 %), the second was unknown (12,7 %), the third was hypertension (11,8 %). 145 patients (63,6%) underwent regular hemodialysis (HD) (62 years, 55-69), 25 patients (11%) began peritoneal dialysis (PD), 58 patients (25%) had renal transplantation. 52 patients underwent HD with renal decompensation, 22 (%42,3) had working arteriovenous fistula (AVF). There was no decompensation in patients with PD or transplantation plan. 34 patients started HD because of infections (65%), 8 patients (15%) after operations (4 was Coronary Artery Bypass Grafting-CABG), 6 patients (%11,5) after coronary angiography, 4 patients (7,5%) with cardiac decompensation. 2 patients died during the hospitalisation for infections. Of 145 HD patients, 89 (%61,4) had AVF. The patients who had renal decompensation were more older 63 (58-70), have lower Hgb 9,7 g/L (9,1-10,7) and albumin 3,5 g/L (3,2-3,9) level (p<0,05). There was no difference in eGFR at the beginning of HD between renal decompensation and other HD patients. 42 patients did not undergo HD at the time we suggested during visits. Of them 9 patients (%21) had renal decompensation (6 infections,3 CABG), 17 patients (%40) had AVF. 3 of them died. The others underwent HD for uremic complications. Conclusion We have shown that infections are as the leading cause of renal decompensation. Most of our patients who started to RRT from our low clearance outpatient clinic have chosen HD for RRT. Prevention of infections via vaccination programs or early diagnosis at regular policlinic or telephone visits, and informing patients adequately about nephrotoxic drugs or the conditions that may cause renal decompensation are among the first tasks of the predialysis outpatient clinic. Transition of CKD patients to RRTs, with proper preparation, neither late nor early- at the most appropriate time- should be among in our goals. This may reduce the cost of ESRD patients.


PEDIATRICS ◽  
1959 ◽  
Vol 24 (4) ◽  
pp. 522-522
Author(s):  
S. G.

Cardiovascular lesions are known to be frequently associated with arachnodactyly. The most common pathologic finding is cystic medionecrosis, particularly affecting the aorta, which often gives rise to aneurysm formation. Congenital cardiac malformations have also been described in patients with arachnodactyly; the more common lesions encountered are coarctation of the aorta and septal defects. From his experience at the Gronigen Clinic, Netherlands, the author reports another, but less frequently observed, finding of myocardial hypertrophy and fibrosis, in the absence of other cardiovascular pathology; this lesion leads eventually to cardiac decompensation and demise. The term "arachnodactyly heart" is proposed to designate the primary myocardial pathology in this hereditary disease.


PEDIATRICS ◽  
1949 ◽  
Vol 3 (2) ◽  
pp. 201-207
Author(s):  
JAMES G. HUGHES ◽  
HERMAN ROSENBLUM ◽  
LACY G. HORN

A case of Wilms' tumor of the right kidney is presented, in which the dominant clinical features were extreme elevation of blood pressure and hypertensive encephalopathy, associated with cardiac decompensation and death. Generalized convulsions and right hemiplegia developed, believed to have been due to cerebral anoxia incident to angiospasm. No metastases were found, and no other cause for arterial hypertension was discovered. This patient is thought to be the first case reported where death from Wilms' tumor was due to the hypertensive factor. The literature with reference to the association of hypertension with Wilms' tumor is reviewed. The mechanisms by which Wilms' tumors may produce unilateral renal ischemia with arterial hypertension are discussed. The presence of clearcut hypertension in a child with a kidney area mass points toward the probability of a Wilms' tumor.


2000 ◽  
Vol 278 (2) ◽  
pp. H461-H468 ◽  
Author(s):  
Dong Sun ◽  
An Huang ◽  
Gong Zhao ◽  
Robert Bernstein ◽  
Paul Forfia ◽  
...  

Our previous studies have suggested that there is reduced nitric oxide (NO) production in canine coronary blood vessels after the development of pacing-induced heart failure. The goal of these studies was to determine whether flow-induced NO-mediated dilation is altered in coronary arterioles during the development of heart failure. Subepicardial coronary arterioles (basal diameter 80 μm) were isolated from normal canine hearts, from hearts with dysfunction but no heart failure, and from hearts with severe cardiac decompensation. Arterioles were perfused at increasing flow or administered agonists with no flow in vitro. In arterioles from normal hearts, flow increased arteriolar diameter, with one-half of the response being NO dependent and one-half prostaglandin dependent. Shear stress-induced dilation was eliminated by removing the endothelium. Arterioles from normal hearts and hearts with dysfunction but no failure responded to increasing shear stress with dilation that reached a maximum at a shear stress of 20 dyn/cm2. In contrast, arterioles from failing hearts showed a reduced dilation, reaching only 55% of the dilation seen in vessels of normal hearts at a shear stress of 100 dyn/cm2. This remaining dilation was eliminated by indomethacin, suggesting that the NO-dependent component was absent in coronary microvessels after the development of heart failure. Similarly, agonist-induced NO-dependent coronary arteriolar dilation was markedly attenuated after the development of heart failure. After the development of severe dilated cardiomyopathy and heart failure, the NO-dependent component of both shear stress- and agonist-induced arteriolar dilation is reduced or entirely absent.


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