scholarly journals Resistance to ventricular fibrillation predicted by the QRS/QTc - ratio in an intact rat model of hypothermia/rewarming

2020 ◽  
Author(s):  
Erik Sveberg Dietrichs ◽  
Timofey Kondratiev ◽  
Karen McGlynn ◽  
Godfrey Smith ◽  
Torkjel Tveita
Keyword(s):  
Ventricular Fibrillation ◽  
Rat Model ◽  
Ventricular Arrhythmias ◽  
Accidental Hypothermia ◽  
Moderate Hypothermia ◽  
Experimental Protocol ◽  
Cooling Period ◽  
Increased Risk ◽  
High Incidence ◽  
Lethal Hypothermia

Abstract Background Accidental hypothermia is associated with increased risk for arrhythmias, including ventricular fibrillation and cardiac arrest. Recently QRS/QTc was proposed as an ECG-marker, where decreasing QRS/QTc ratio could predict ventricular arrhythmias in such patients. If reliable it should also predict nonappearance of arrhythmias, observed in species like rat that regularly tolerate prolonged hypothermia, during sustained sinus rhythm. Methods A rat model designed for studying cardiovascular function during cooling, 4 h experimental hypothermia (15 °C core temperature) and subsequent rewarming was used, and ECG recorded throughout the experimental protocol. Results No ventricular arrhythmias occured and there was no sign of a hypothermia-induced reduction of QRS/QTc values during moderate hypothermia. The ratio steadily increased throughout the entire cooling period and remained above normothermic baseline until rewarmed. Conclusion Different from the high incidence of hypothermia-induced ventricular arrhythmias in accidental hypothermia patients, where QRS/QTc ratio is decreased in moderate hypothermia, hypothermia and rewarming of rats is not associated with increased risk for ventricular fibrillation. This resistance to lethal hypothermia-induced arrhythmias was predicted by the QRS/QTc ratio.

Awake and aware with ongoing ventricular fibrillation during LVAD treatment: is it possible?

2020 ◽  
Vol 13 (4) ◽  
pp. e234527
Author(s):  
Ingrid Hell Mott ◽  
Steen Hvitfeldt Poulsen ◽  
Brian Bridal Løgstrup
Keyword(s):  
Ventricular Fibrillation ◽  
Ventricular Arrhythmias ◽  
Left Ventricular ◽  
Ventricular Assist Devices ◽  
Left Ventricular Assist Devices ◽  
Randomised Trials ◽  
Ventricular Assist ◽  
Increased Risk ◽  
Left Ventricular Assist ◽  
Shed Light

Left ventricular assist devices (LVADs) are currently used as destination therapy or bridge to heart transplantation in patients with advanced chronic heart failure (CHF). It has been proved to reduce mortality and symptoms in these patients. Patients with advanced CHF are known to have increased risk of ventricular arrhythmias (ventricular tachycardia or ventricular fibrillation (VF)) despite the presence of LVAD. We report the case of patients with ongoing VF during LVAD treatment while being awake and aware. We discuss the challenges introduced along with the increasing use of LVAD treatment. The decision whether a patient with LVAD automatically should have an implantable cardioverter-defibrillator is challenging. Randomised trials are warranted to shed light on these challenging decisions.

scholarly journals Severe Prinzmetal’s Angina Inducing Ventricular Fibrillation Cardiac Arrest

2020 ◽  
Vol 2020 ◽  
pp. 1-8 ◽  
Author(s):  
Bashar Khiatah ◽  
David Philips ◽  
Jonathan Dukes ◽  
Amanda Frugoli
Keyword(s):  
Cardiac Arrest ◽  
Ventricular Fibrillation ◽  
Cardiac Death ◽  
Ventricular Arrhythmias ◽  
Case Vignette ◽  
Cardioverter Defibrillator ◽  
Coronary Syndrome ◽  
Increased Risk ◽  
Vascular Spasm ◽  
Normal Cardiac Function

Prinzmetal’s angina is a vascular spasm of the coronary artery that can mimic acute coronary syndrome. It is rarely responsible for ventricular arrhythmias and cardiac arrest; however, survivors with these complications are at increased risk for recurrent ventricular arrhythmias and sudden cardiac death. This is true despite the presence of normal cardiac function and optimal medical therapy. Thus, this select population should be considered for an implantable cardioverter defibrillator (ICD). In this case vignette, we describe a healthy 48-year-old female with ventricular fibrillation arrest, followed by recurrent ventricular tachyarrhythmias caused by Prinzmetal’s angina.

Respiratory Complications in Outpatient Endoscopy with Endoscopist-Directed Sedation

2014 ◽  
Vol 23 (3) ◽  
pp. 255-259 ◽  
Author(s):  
Kilian Friedrich ◽  
Sabine G. Scholl ◽  
Sebastian Beck ◽  
Daniel Gotthardt ◽  
Wolfgang Stremmel ◽  
...  
Keyword(s):  
Antibiotic Treatment ◽  
Respiratory Infection ◽  
Endoscopic Procedure ◽  
Shortness Of Breath ◽  
Respiratory Complications ◽  
Endoscopic Procedures ◽  
Increased Risk ◽  
High Incidence ◽  
Respiratory Complaints

Background & Aims: Respiratory complications represent an important adverse event of endoscopic procedures. We screened for respiratory complications after endoscopic procedures using a questionnaire and followed-up patients suggestive of respiratory infection.Method: In this prospective observational, multicenter study performed in Outpatient practices of gastroenterology we investigated 15,690 patients by questionnaires administered 24 hours after the endoscopic procedure.Results: 832 of the 15,690 patients stated at least one respiratory symptom after the endoscopic procedure: 829 patients reported coughing (5.28%), 23 fever (0.15%) and 116 shortness of breath (SOB, 0.74%); 130 of the 832 patients showed at least two concomitant respiratory symptoms (107 coughing + SOB, 17 coughing + fever, 6 coughing + coexisting fever + SOB) and 126 patients were followed-up to assess their respiratory complaints. Twenty-nine patients (follow-up: 22.31%, whole sample: 0.18%) reported signs of clinically evident respiratory infection and 15 patients (follow-up: 11.54%; whole sample: 0.1%) received therefore antibiotic treatment. Coughing or vomiting during the endoscopic procedure resulted in a 156.12-fold increased risk of respiratory complications (95% CI: 67.44 - 361.40) and 520.87-fold increased risk of requiring antibiotic treatment (95% CI: 178.01 - 1524.05). All patients of the follow-up sample who coughed or vomited during endoscopy developed clinically evident signs of respiratory infection and required antibiotic treatment while this occurred in a significantly lower proportion of patients without these symptoms (17.1% and 5.1%, respectively).Conclusions: We demonstrated that respiratory complications following endoscopic sedation are of comparably high incidence and we identified major predictors of aspiration pneumonia which could influence future surveillance strategies after endoscopic procedures.

Myocardial Noncompaction

2018 ◽  
Vol 69 (8) ◽  
pp. 2209-2212
Author(s):  
Alexandru Radu Mihailovici ◽  
Vlad Padureanu ◽  
Carmen Valeria Albu ◽  
Venera Cristina Dinescu ◽  
Mihai Cristian Pirlog ◽  
...  
Keyword(s):  
Ventricular Arrhythmias ◽  
Specific Treatment ◽  
Left Ventricular ◽  
Left Ventricular Noncompaction ◽  
Ventricular Noncompaction ◽  
Genetic Transmission ◽  
Asymptomatic Patients ◽  
Increased Risk ◽  
Patients With Heart Failure

Left ventricular noncompaction is a primary cardiomyopathy with genetic transmission in the vast majority of autosomal dominant cases. It is characterized by the presence of excessive myocardial trabecularities that generally affect the left ventricle. In diagnosing this condition, echocardiography is the gold standard, although this method involves an increased risk of overdiagnosis and underdiagnosis. There are also uncertain cases where echocardiography is inconclusive, a multimodal approach is needed, correlating echocardiographic results with those obtained by magnetic resonance imaging. The clinical picture may range from asymptomatic patients to patients with heart failure, supraventricular or ventricular arrhythmias, thromboembolic events and even sudden cardiac death. There is no specific treatment of left ventricular noncompaction, but the treatment is aimed at preventing and treating the complications of the disease. We will present the case of a young patient with left ventricular noncompactioncardiomyopathy and highlight the essential role of transthoracic echocardiography in diagnosing this rare heart disease.

scholarly journals Kidney Injury Caused by Preeclamptic Pregnancy Recovers Postpartum in a Transgenic Rat Model

2021 ◽  
Vol 22 (7) ◽  
pp. 3762
Author(s):  
Sarah M. Kedziora ◽  
Kristin Kräker ◽  
Lajos Markó ◽  
Julia Binder ◽  
Meryam Sugulle ◽  
...  
Keyword(s):  
Rat Model ◽  
Renal Damage ◽  
Kidney Injury ◽  
Tissue Growth ◽  
Female Rats ◽  
Male Rats ◽  
Renal Diseases ◽  
Transgenic Rat ◽  
Increased Risk ◽  
Before And After

Preeclampsia (PE) is characterized by the onset of hypertension (≥140/90 mmHg) and presence of proteinuria (>300 mg/L/24 h urine) or other maternal organ dysfunctions. During human PE, renal injuries have been observed. Some studies suggest that women with PE diagnosis have an increased risk to develop renal diseases later in life. However, in human studies PE as a single cause of this development cannot be investigated. Here, we aimed to investigate the effect of PE on postpartum renal damage in an established transgenic PE rat model. Female rats harboring the human-angiotensinogen gene develop a preeclamptic phenotype after mating with male rats harboring the human-renin gene, but are normotensive before and after pregnancy. During pregnancy PE rats developed mild tubular and glomerular changes assessed by histologic analysis, increased gene expression of renal damage markers such as kidney injury marker 1 and connective-tissue growth factor, and albuminuria compared to female wild-type rats (WT). However, four weeks postpartum, most PE-related renal pathologies were absent, including albuminuria and elevated biomarker expression. Only mild enlargement of the glomerular tuft could be detected. Overall, the glomerular and tubular function were affected during pregnancy in the transgenic PE rat. However, almost all these pathologies observed during PE recovered postpartum.

scholarly journals Does deeper hypothermia reduce the risk of acute kidney injury after circulatory arrest for aortic arch surgery?

2021 ◽  
Author(s):  
Andrew M Vekstein ◽  
Babtunde A Yerokun ◽  
Oliver K Jawitz ◽  
Julie W Doberne ◽  
Jatin Anand ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Circulatory Arrest ◽  
Aortic Surgery ◽  
Multivariable Analysis ◽  
Kidney Injury ◽  
Deep Hypothermia ◽  
Moderate Hypothermia ◽  
Bladder Temperature ◽  
Increased Risk ◽  
The Impact

Abstract OBJECTIVES The impact of hypothermic circulatory arrest (HCA) temperature on postoperative acute kidney injury (AKI) has not been evaluated. This study examined the association between circulatory arrest temperatures and AKI in patients undergoing proximal aortic surgery with HCA. METHODS A total of 759 consecutive patients who underwent proximal aortic surgery (ascending ± valve ± root) including arch replacement requiring HCA between July 2005 and December 2016 were identified from a prospectively maintained institutional aortic surgery database. The primary outcome was AKI as defined by Risk, Injury, Failure, Loss, End Stage Renal Disease (ESRD) criteria. The association between minimum nasopharyngeal (NP) and bladder temperatures during HCA and postoperative AKI was assessed, adjusting for patient-level factors using multivariable logistic regression. RESULTS A total of 85% (n = 645) of patients underwent deep hypothermia (14.1–20.0°C), 11% (n = 83) low-moderate hypothermia (20.1–24.0°C) and 4% (n = 31) high-moderate hypothermia (24.1–28.0°C) as classified by NP temperature. When analysed by bladder temperature, 59% (n = 447) underwent deep hypothermia, 22% (n = 170) low-moderate, 16% (n = 118) high-moderate and 3% mild (n = 24) (28.1–34.0°C) hypothermia. The median systemic circulatory arrest time was 17 min. The incidence of AKI did not differ between hypothermia groups, whether analysed using minimum NP or bladder temperature. In the multivariable analysis, the association between degree of hypothermia and AKI remained non-significant whether analysed as a categorical variable (hypothermia group) or as a continuous variable (minimum NP or bladder temperature) (all P > 0.05). CONCLUSIONS In patients undergoing proximal aortic surgery including arch replacement requiring HCA, degree of systemic hypothermia was not associated with the risk of AKI. These data suggest that moderate hypothermia does not confer increased risk of AKI for patients requiring circulatory arrest, although additional prospective data are needed.

The Association Between Immunodeficiency and the Development of Autoimmune Disease

1996 ◽  
Vol 10 (1) ◽  
pp. 57-61 ◽  
Author(s):  
J.W. Sleasman
Keyword(s):  
Immune System ◽  
Autoimmune Disease ◽  
Lupus Erythematosus ◽  
Iga Deficiency ◽  
Selective Iga Deficiency ◽  
Increased Risk ◽  
High Incidence ◽  
Autoimmune Cytopenias ◽  
The Complement System ◽  
Common Variable

There is a paradoxical relationship between immunodeficiency diseases and autoimmunity. While not all individuals with immunodeficiency develop autoimmunity, nor are all individuals with autoimmunity immunodeficient, defects within certain components of the immune system carry a high risk for the development of autoimmune disease. Inherited deficiencies of the complement system have a high incidence of systemic lupus erythematosus (SLE), glomerulonephritis, and vasculitis. Carrier mothers of children with chronic granulomatous disease, an X-linked defect of phagocytosis, often develop discoid lupus. Several antibody deficiencies are associated with autoimmune disease. Autoimmune cytopenias are commonly observed in individuals with selective IgA deficiency and common variable immune deficiency. Polyarticular arthritis can be seen in children with X-linked agammaglobulinemia. Combined cellular and antibody deficiencies, such as Wiskott-Aldrich syndrome, carry an increased risk for juvenile rheumatoid arthritis and autoimmune hemolytic anemia. Several hypothetical mechanisms have been proposed to explain the associations between autoimmunity and immunodeficiency. Immunologic defects may result in a failure to exclude microbial antigens, resulting in chronic immunologic activation and autoimmune symptoms. There may be shared genetic factors, such as common HLA alleles, which predispose an individual to both autoimmunity and immunodeficiency. Defects within one component of the immune system may alter the way a pathogen induces an immune response and lead to an inflammatory response directed at self-antigens. An understanding of the immunologic defects that contribute to the development of autoimmunity will provide an insight into the pathogenesis of the autoimmune process.

Relation of autonomic and cardiac abnormalities to ventricular fibrillation in a rat model of epilepsy

2014 ◽  
Vol 108 (1) ◽  
pp. 44-56 ◽  
Author(s):  
Isaac Naggar ◽  
Jason Lazar ◽  
Haroon Kamran ◽  
Rena Orman ◽  
Mark Stewart
Keyword(s):  
Ventricular Fibrillation ◽  
Rat Model ◽  
Cardiac Abnormalities

Abstract 2415: Long-Term Baroreflex Activation Therapy Increases the Threshold for the Induction of Lethal Ventricular Arrhythmias in Dogs with Chronic Advanced Heart Failure

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Mengjun Wang ◽  
Valerio Zaca ◽  
Alice Jiang ◽  
Itamar Ilsar ◽  
Matthew Ebinger ◽  
...  
Keyword(s):  
Heart Failure ◽  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Ventricular Arrhythmias ◽  
Lv Function ◽  
Baroreflex Activation Therapy ◽  
Increased Risk ◽  
Lv Remodeling ◽  
Activation Therapy

Heart failure (HF) is associated with a high incidence of ventricular tachycardia (VT) and fibrillation (VF). Patients with HF in whom these lethal arrhythmias can be induced by electrophysiological (EP) testing carry a high risk of sudden cardiac death. We showed that chronic electrical carotid baroreflex activation therapy (BAT) with the Rheos® System (CVRx, Inc.) improves LV function, attenuates LV remodeling and restores autonomic sympathetic-parasympathetic balance in dogs with HF. This study examined the effects of long-term therapy with BAT on the induction of VT or VF in dogs with coronary microembolization-induced HF (LV ejection fraction ~20%). Eleven dogs with HF underwent EP testing at baseline prior to therapy and after 3 and 6 months of therapy with BAT and again 6 weeks after withdrawal of BAT therapy (n = 7) or no therapy at all (Control, n = 4). Programmed ventricular stimulation was performed from the right ventricular apex and included delivery of up to 4 extrastimuli at progressively shorter coupling intervals (in steps of 10 msec). The extrastimuli were delivered following 8 ventricular paced beats with a drive cycle length between 600 and 200 msec. If a sustained monomorphic VT or VF could not be induced, isoproterenol infusion was initiated to increase the sinus rate by ~30% and the EP stimulation protocol was repeated. At baseline, a sustained VT or VF was induced in all 11 dogs (100%). After 3 and 6 months of follow-up, all Control dogs (100%) were induced into sustained VT or VF. After 3 months of BAT, only 3 of 7 dogs (43%) were induced into sustained VT or VF. After 6 months of BAT, only 2 of 7 dogs (29%) were induced into sustained VT or VF. Finally after withdrawal of BAT therapy, all dogs (100%) were again induced into systained VT or VF. In addition to improving LV function and attenuating LV remodeling, long-term monotherapy with BAT markedly increases the threshold for lethal ventricular arrhythmias in dogs with chronic HF. This is a marked improvement over inducibility of lethal arrhythmias seen in historical untreated controls. This benefit of BAT supports the continued exploration of this device as a therapeutic modality for treating patients with chronic HF and increased risk of sudden cardiac death.

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