Vagal sensory neurons mediate the Bezold-Jarisch reflex and induce syncope.

Visceral sensory pathways mediate homeostatic reflexes, the dysfunction of which leads to many neurological disorders1. The Bezold-Jarisch reflex (BJR), first described2,3 in 1867, is a cardioinhibitory reflex that is speculated to be mediated by vagal sensory neurons (VSNs) that also triggers syncope. However, the molecular identity, anatomical organization, physiological characteristics and behavioural influence of cardiac VSNs remain mostly unknown. Here we leveraged single-cell RNA-sequencing data and HYBRiD tissue clearing4 to show that VSNs that express neuropeptide Y receptor Y2 (NPY2R) predominately connect the heart ventricular wall to the area postrema. Optogenetic activation of NPY2R VSNs elicits the classic triad of BJR responses-hypotension, bradycardia and suppressed respiration-and causes an animal to faint. Photostimulation during high-resolution echocardiography and laser Doppler flowmetry with behavioural observation revealed a range of phenotypes reflected in clinical syncope, including reduced cardiac output, cerebral hypoperfusion, pupil dilation and eye-roll. Large-scale Neuropixels brain recordings and machine-learning-based modelling showed that this manipulation causes the suppression of activity across a large distributed neuronal population that is not explained by changes in spontaneous behavioural movements. Additionally, bidirectional manipulation of the periventricular zone had a push-pull effect, with inhibition leading to longer syncope periods and activation inducing arousal. Finally, ablating NPY2R VSNs specifically abolished the BJR. Combined, these results demonstrate a genetically defined cardiac reflex that recapitulates characteristics of human syncope at physiological, behavioural and neural network levels.

Frequency of Low Cardiac Output Syndrome Following on Pump Coronary Artery Bypass Grafting Surgery and it's Association with Degree of Pre-operative Left Ventricular Dysfunction.

Background Low cardiac output syndrome (LCOS) is a serious complication after coronary artery bypass grafting (CABG) surgery. It is associated with 10 times to 17 times increase in mortality and markedly increase morbidity. Objective To find out the frequency of Low cardiac output syndrome following on pump coronary artery bypass grafting surgery, to determine the association of Low cardiac output syndrome with degree of pre-operative left ventricular dysfunction and to compare in hospital outcomes of coronary bypass surgery with and without low cardiac output syndrome. Method This prospective, descriptive study enrolled 200 patients who underwent on pump coronary artery bypass grafting surgery using antegrade St Thomas blood cardioplegia. Pre-operatively grouped into two groups consisting Group A of 100 patients with pre-operative left ventricular ejection fraction (LVEF) ≥ 40% and group B of 100 patients with pre-operative left ventricular ejection fraction (LVEF) < 40%. Post-operatively frequency of low cardiac output syndrome was compared between the groups and in-hospital outcomes were studied. Result The mean age of the patients in the study was 53.50±7.57 years. Male to female ratio was 1.8:1. Results showed overall frequency of low cardiac output syndrome was 21.5%. The frequency of LCOS was 15 vs 28% (p - 0.038) in patients with preoperative LV EF ≥ 40% and < 40% respectively. The outcomes of coronary artery bypass grafting surgery were stroke (3.82 vs. 30.23%, p - 0.001), acute kidney injury (5.09 vs. 23.25%, p - 0.001), respiratory failure (6.36 vs. 34.88%, p - 0.001), ICU stay days (4.75 ± 1.28 vs. 7.44 ± 4.66, p - 0.018), hospital stay days (9.56 ± 2.40 vs. 15.22 ± 3.89, p - 0.001) and mortality (4.45 vs. 32.55%, p - 0.001) in patients without and with low cardiac output syndrome respectively. Conclusion The frequency of low cardiac output syndrome following coronary artery bypass surgery is 21.5%. Left ventricular dysfunction pre-operatively is associated with high frequency of low cardiac output syndrome following surgery. There is significantly poor outcome of coronary artery bypass surgery with low cardiac output syndrome in terms of stroke, respiratory failure, acute kidney injury, mortality and significant ICU stay, hospital stay in compare to patients without low cardiac output syndrome.

Genetic Evidence for Causal Association Between Atrial Fibrillation and Dementia: A Mendelian Randomization Study.

Background The knowledge gap regarding whether the correlation between atrial fibrillation (AF) and dementia in observational studies is causation or driven by other shared risk factors remains substantially unfilled. Methods and Results We performed a comprehensive 2-sample Mendelian randomization study to evaluate the causal effect of AF on overall dementia and its subtypes, including vascular dementia, Alzheimer dementia, Lewy body dementia, and frontotemporal dementia. The primary results in inverse variance-weighted analyses were further validated by various Mendelian randomization sensitivity analyses. Additionally, we conducted multivariable Mendelian randomization to examine 10 candidate mediators of the causal association of AF and dementia. Genetic predisposition to AF was modestly associated with an increased risk of overall dementia (odds ratio, 1.140 [95% CI, 1.023-1.271]; P=0.018) and strongly associated with vascular dementia (odds ratio, 1.350 [95% CI, 1.076-1.695]; P=0.010). Genetically predicted AF indicated neutral effects on Alzheimer dementia, Lewy body dementia, and frontotemporal dementia. In multivariable Mendelian randomization analysis, the total effect of AF on overall dementia was remarkably attenuated by adjusting for genetic effect for ischemic stroke (odds ratio, 1.068 [95% CI, 0.953-1.197]; P=0.259) and low cardiac output (odds ratio, 1.046 [95% CI, 0.926-1.181]; P=0.475), indicating that the causal association of genetically predicted AF with dementia was potentially mediated by ischemic stroke and low cardiac output. The causal effect of genetically predicted AF on dementia was independent of cerebral small-vessel disease and brain volume phenotypes. Conclusions Our findings provided novel evidence supporting the causal effect of genetically predicted AF on dementia mediated by ischemic stroke and low cardiac output. Future clinical trials are warranted to evaluate the potential role of appropriate AF management in dementia prevention.

Mitral Valve Surgery in Patients With an Implanted Amplatzer Septal Occluder: A Review of 2 Cases.

Surgical approaches for mitral valve exploration vary, with the preferred approach being via the interatrial groove. Data on whether the interatrial groove approach can be used for mitral valve surgery in patients with a previously implanted Amplatzer septal occluder (ASO) (St Jude Medical, an Abbott company) are extremely limited. The authors performed mitral valve surgery using the transatrial septal approach on 2 patients following explantation of an ASO, which significantly impedes the interatrial groove approach. Concomitant surgical procedures with mitral valve replacement, removal of the ASO, and closure of an atrial septal defect with a patch significantly prolonged the cross-clamp and cardiopulmonary bypass durations, which is the reason for intraoperative low cardiac output syndrome. An intra-aortic balloon pump and venoarterial extra-corporeal membrane oxygenation were used in these 2 patients because of low cardiac output syndrome. When planning mitral valve surgery in patients with a previously implanted ASO, the device precludes the interatrial groove approach and can produce an unpredictable clinical scenario.

Comprehensive and Safe Decongestion in Acutely Decompensated Heart Failure.

PURPOSE OF THE REVIEW: Progressive intravascular, interstitial, and alveolar fluid overload underlies the transition from compensated to acutely decompensated heart failure and loop diuretics are the mainstay of treatment. Adverse effects and resistance to loop diuretics received much attention while the contribution of a depressed cardiac output to diuretic resistance was downplayed. RECENT FINDINGS: Analysis of experience with positive inotropic agents, especially dobutamine, indicates that enhancement of cardiac output is not consistently associated with increased renal blood flow. However, urinary output and renal sodium excretion increase likely due to dobutamine-mediated decrease in renal and systemic reduced activation of sympathetic nervous- and renin-angiotensin-aldosterone system. Mechanical circulatory support with left ventricular assist devices ascertained the contribution of low cardiac output to diuretic resistance and the pathogenesis and progression of kidney disease in acutely decompensated heart failure. Diuretic resistance commonly occurs in acutely decompensated heart failure. However, failure to resolve fluid overload despite high doses of loop diuretics should alert to the presence of a low cardiac output state.

Incomplete Pericardial Dissection, Fluid Overload, Delayed Diagnosis And Treatment, And Tuberculosis Pericarditis Are Associated With Low Cardiac Output Syndrome Following Pericardiectomy.

BACKGROUND: We aimed to investigate risk factors of LCOS following pericardiectomy. METHODS: This was a retrospective study of patients undergoing pericardiectomy at three hospitals between January 1994 and May 2021. RESULTS: A total of 826 patients were divided into two groups: group with LCOS (N = 126) and group without LCOS (N = 700). The incidence of postoperative LCOS was 15.3%. There were 66 operative deaths (8.0%). Univariable and multivariable analyses showed that factors are associated with LCOS, including postoperative LVEDD (P < 0.001), preoperative LVEDD (P < 0.001), time between symptoms and surgery (P < 0.001), thickness of pericardium (P < 0.001), intubation time (P = 0.002), hospitalized time postoperative (P < 0.001), preoperative central venous pressure (P = 0.016), postoperative central venous pressure (P = 0.034), D0 fluid balance (P = 0.019), D2 fluid balance (P = 0.017), postoperative chest drainage (P < 0.001), surgical duration (P < 0.001), bleeding during operation (P = 0.001), serum creatinine 24h after surgery (P < 0.001), serum creatinine 48h after surgery (P = 0.017), fresh-frozen plasma (P = 0.005), packed red cells (P = 0.006), and tuberculosis pericarditis (P = 0.026). CONCLUSION: In our study, incomplete pericardial dissection, fluid overload, delayed diagnosis and treatment, and tuberculosis pericarditis are associated with LCOS following pericardiectomy.

Preoperative Pericardial Effusion is Associated with Low Cardiac Output Syndrome After Pericardiectomy for Constrictive Pericarditis.

BACKGROUND: Low cardiac output syndrome is the main cause of death after pericardiectomy. METHODS: Patients who underwent pericardiectomy for constrictive pericarditis from January 2009 to October 2020 at our hospital were included in the study. Histopathologic studies of pericardium tissue from every patient were performed. All survivors were followed up. RESULTS: Ninety-two consecutive patients underdoing pericardiectomy were included in the study. The incidence of postoperative low cardiac output syndrome was 10.7% (10/92). There were five operative deaths. Mortality and incidence of LCOS in the group with pericardial effusion were significantly higher than those in the group without pericardial effusion. Tuberculosis of the pericardium (60/92, 65.2%) was the most common histopathologic finding in this study. Both univariate and multivariate analyses showed that preoperative pericardial effusion is associated with increased rate of low cardiac output syndrome. Eighty-five survivors were in NYHA class I (85/87, 97.7%), and two were in class II (2/87, 2.3%) at the latest follow up. CONCLUSIONS: Preoperative pericardial effusion is associated with low cardiac output syndrome after pericardiectomy. Tuberculosis of the pericardium was the most common histopathologic finding in this study. For constrictive pericarditis caused by tuberculous bacteria, systematic antituberculosis drugs should be given. Preoperative pericardial effusion is associated with increased rate of low cardiac output syndrome. Perfect preoperative preparation is very important to reduce the incidence of postoperative low cardiac output syndrome and mortality. It is very important to use a large dose of diuretics with cardiotonic or vasopressor in a short time after the operation.

Isquemia mesentérica por bajo gasto secundaria a hemodiálisis / Mesenteric ischemia due to low cardiac output secondary to hemodialysis

No disponible

Semi-urgent pulmonary vein isolation using cryoballoon for haemodynamically unstable atrial fibrillation storm in a patient with low cardiac output syndrome: a case report.

BACKGROUND: Atrial fibrillation and heart failure are common coexisting conditions requiring hospitalisation for heart failure and death. Pulmonary vein isolation is a well-established option for symptomatic atrial fibrillation and for atrial fibrillation concomitant with heart failure with reduced left ventricular ejection fraction. Recently, pulmonary vein isolation using cryoballoon showed non-inferiority to radiofrequency ablation with respect to the treatment of patients with drug-refractory paroxysmal atrial fibrillation. However, the effectiveness of acute-phase rhythm control by semi-urgent pulmonary vein isolation using cryoballoon in patients with haemodynamically unstable atrial fibrillation storm accompanied with low cardiac output syndrome is unclear. Herein, we present a case in which semi-urgent pulmonary vein isolation using cryoballoon was effective for acute-phase rhythm control against drug-resistant and haemodynamically unstable repetitive atrial fibrillation tachycardia accompanied with low cardiac output syndrome. CASE PRESENTATION: A 57-year-old man was hospitalised for New York Heart Association functional class 4 heart failure with atrial fibrillation tachycardia and reduced left ventricular ejection fraction of 20% accompanied with low cardiac output syndrome-induced liver damage. The haemodynamics collapsed during atrial fibrillation tachycardia, which had become resistant to intravenous amiodarone and repeated electrical cardioversions. In addition to atrial fibrillation, atrial tachycardia and common-type atrial flutter appeared on day 3. Multiple organ failure progressed gradually due to haemodynamically unstable atrial fibrillation tachycardia storm accompanied with low cardiac output syndrome. On day 4, to focus on treatment of heart failure and multiple organ failure, semi-urgent rescue pulmonary vein isolation using cryoballoon to atrial fibrillation and cavotricuspid isthmus ablation to common-type atrial flutter were performed for acute-phase rhythm control. Soon after the ablation procedure, atrial fibrillation and common-type atrial flutter were lessened, and sinus rhythm was restored. A stable haemodynamics was successfully achieved with the improvement of hepatorenal function. The patient was discharged on day 77 without complications. CONCLUSIONS: This case demonstrates that acute-phase rhythm control by semi-urgent pulmonary vein isolation using cryoballoon could be a treatment option in patients with haemodynamically unstable atrial fibrillation tachycardia storm accompanied with low cardiac output syndrome, which is refractory to cardioversion and drug therapy.

Volume-associated hemodynamic variables for prediction of cardiac surgery-associated acute kidney injury.

BACKGROUND: Delayed diagnosis of acute kidney injury (AKI) is common because the changes in renal function markers often lag injury. We aimed to find optimal non-invasive hemodynamic variables for the prediction of postoperative AKI and AKI renal replacement therapy (RRT). METHODS: The data were collected from 1,180 patients who underwent cardiac surgery in our hospital between March 2015 and Feb 2016. Postoperative central venous pressure (CVP), mean arterial pressure (MAP), heart rate, PaO2, and PaCO2 on ICU admission and daily fluid input and output (calculated as 24 h PFO) were monitored and compared between AKI vs. non-AKI and RRT vs non-RRT cases. RESULTS: The AKI and AKI-RRT incidences were 36.7% (n = 433) and 1.2% (n = 14). Low cardiac output syndromes (LCOSs) occurred significantly more in AKI and RRT than in non-AKI or non-RRT groups (13.2% vs. 3.9%, P < 0.01; 42.9% vs. 7.1%, P < 0.01). CVP on ICU admission was significantly higher in AKI and RRT than in non-AKI and non-RRT groups (11.5 vs. 9.0 mmHg, P < 0.01; 13.3 vs. 9.9 mmHg, P < 0.01). 24 h PFO in AKI and RRT cases were significantly higher than in non-AKI or non-RRT patients (1.6% vs. 0.9%, P < 0.01; 3.9% vs. 0.8%, P < 0.01). The areas under the ROC curves to predict postoperative AKI by CVP on ICU admission (> 11 mmHg) + LCOS + 24 h PFO (> 5%) and to predict AKI-RRT by CVP on ICU admission (> 13 mmHg) + LCOS + 24 h PFO (> 5%) were 0.763 and 0.886, respectively. CONCLUSION: The volume-associated hemodynamic variables, including CVP on ICU admission, LCOS, and 24 h PFO after surgery could predict postoperative AKI and AKI-RRT.

Symmetrical Peripheral Gangrene Associated with Low Output Cardiac Failure.

Symmetrical peripheral gangrene (SPG) is a rare entity characterized by ischemic changes of the distal extremities with maintained vascular integrity. We present the case of a 64-year-old man with bilateral necrotic toes and deranged liver function tests. This was thought to be related to severely depressed ejection fraction from non-ischemic etiology, presumably chronic alcohol ingestion. We hope that awareness of SPG and association with a low output state will aid in early detection and prevention.

Risk of stroke early after implantation of a left ventricular assist device.

OBJECTIVE: Stroke is one of the major adverse events after left ventricular assist device implantation. Risk of stroke is the highest immediately after left ventricular assist device implantation and then increases again in chronic periods. There is no study that has analyzed risk factors for stroke in acute phase. We investigated the risk factors for stroke in the acute phase after left ventricular assist device implantation in the present study. METHODS: Between October 2005 and December 2016, 158 consecutive patients (mean age, 43 ± 14 years; 34% were women) underwent continuous-flow left ventricular assist device (50 HeartMate II [Abbott Medical, Abbott Park, Ill], 38 DuraHeart [Terumo Heart, Ann Arbor, Mich], 33 Jarvik2000 [Jarvik Heart, New York, NY], 23 EVAHEART [Sun Medical, Moriyama City, Japan], 14 HeartWare [Framingham, Mass]) implantation in our institution. We analyzed the risk factors for a symptomatic stroke within 90 days after left ventricular assist device implantation. RESULTS: Stroke occurred in 28 patients in the acute phase after left ventricular assist device implantation. Multivariate analysis revealed that low cardiac output (odds ratio, 0.25; 0.07-0.92; P = .024) during postoperative 12 to 24 hours was the only independent risk factor for stroke in the acute phase. Patients with stroke in the acute phase had higher serum lactate dehydrogenase levels at any point until postoperative 14 days. Patients with the HeartMate II device particularly showed a statistically significant negative relationship between cardiac output during postoperative 12 to 24 hours and serum lactate dehydrogenase levels at postoperative 14 days (r = -0.313, P = .03). CONCLUSIONS: Our study demonstrated that patients with perioperative lower cardiac output and higher lactate dehydrogenase level developed stroke in the acute phase after left ventricular assist device implantation. These results suggested that maintenance of sufficient left ventricular assist device flow is important in prevention of stroke, which may be related to subclinical pump thrombosis.

Subclinical Hypothyroidism Is Associated With Adverse Prognosis in Heart Failure Patients.

BACKGROUND: It is widely recognized that overt hyper- as well as hypothyroidism are potential causes of heart failure (HF). Additionally it has been recently reported that subclinical hypothyroidism (sub-hypo) is associated with atherosclerosis, development of HF, and cardiovascular death. We aimed to clarify the effect of sub-hypo on prognosis of HF, and underlying hemodynamics and exercise capacity. METHODS: We measured the serum levels of thyroid stimulating hormone (TSH) and free thyroxine (FT4) in 1100 consecutive HF patients. We divided these patients into 5 groups on the basis of plasma levels of TSH and FT4, and focused on euthyroidism (0.4 ≤ TSH ≤ 4 µIU/mL and 0.7 ≤ FT4 ≤ 1.9 ng/dL; n = 911; 82.8%) and sub-hypo groups (TSH > 4 µIU/mL and 0.7 ≤ FT4 ≤ 1.9 ng/dL; n = 132; 12.0%). We compared parameters of echocardiography, cardiopulmonary exercise testing, and cardiac catheterization, and followed up for cardiac event rate and all-cause mortality between the 2 groups. RESULTS: Although left ventricular ejection fraction did not differ between the 2 groups, the sub-hypo group had lower peak breath-by-breath oxygen consumption and higher mean pulmonary arterial pressure than the euthyroidism group (peak breath-by-breath oxygen consumption, 14.0 vs 15.9 mL/min/kg; P = 0.012; mean pulmonary arterial pressure, 26.8 vs 23.5 mm Hg, P = 0.020). In Kaplan-Meier analysis (mean 1098 days), the cardiac event rate and all-cause mortality were significantly higher in the sub-hypo group than those in the euthyroidism group (log rank, P < 0.01, respectively). In Cox proportional hazard analysis, sub-hypo was a predictor of cardiac event rate and all-cause mortality in HF patients (P < 0.05, respectively). CONCLUSIONS: Sub-hypo might be associated with adverse prognosis, accompanied by impaired exercise capacity and higher pulmonary arterial pressure, in HF patients.

Risk Factors for Delayed Extubation after Ventricular Septal Defect Closure: a Prospective Observational Study.

OBJECTIVE: The objective of our study was to determine the feasibility of early extubation and to identify the risk factors for delayed extubation in pediatric patients operated for ventricular septal defect closure. METHODS: A prospective, observational study was carried out at our Institute. This study involved consecutive 135 patients undergoing ventricular septal defect closure. Patients were extubated if feasible within six hours after surgery. Based on duration of extubation, patients were divided two groups: Group 1= extubation time ≤ 6 hours, Group 2= extubation time >6 hours. RESULTS: A total of 99 patients were in Group 1 and 36 patients in Group 2. Duration of ventilation was 4.4±0.9 hours in Group 1 and 25.9±24.9 hours in Group 2 (P<0.001). Univariate analysis showed that young age, low weight, low partial pressure of oxygen, trisomy 21, multiple ventricular septal defect, high vasoactive inotropic score, transient heart block and low cardiac output syndrome were associated with delayed extubation. However, regression analysis revealed that only trisomy 21 (OR: 0.248; 95%CI: 0.176-0.701; P=0.001), low cardiac output syndrome (OR: 0.291; 95%CI: 0.267-0.979; P=0.001), multiple ventricular septal defect (OR: 0.243; 95%CI: 0.147-0.606; P=0.002) and vasoactive inotropic score (OR: 0.174 95%CI: 0.002-0.062; P=0.039) are strongest predictors for delayed extubation. CONCLUSION: Trisomy 21, low cardiac output syndrome, multiple ventricular septal defect and high vasoactive inotropic score are significant risk factors for delay in extubation. Age, weight, pulmonary artery hypertension, size of ventricular septal defect, aortic cross-clamp and cardiopulmonary bypass time did not affect early extubation.

Risk factors for delayed extubation after ventricular septal defect closure: a prospective observational study

Objective: The objective of our study was to determine the feasibility of early extubation and to identify the risk factors for delayed extubation in pediatric patients operated for ventricular septal defect closure. Methods: A prospective, observational study was carried out at our Institute. This study involved consecutive 135 patients undergoing ventricular septal defect closure. Patients were extubated if feasible within six hours after surgery. Based on duration of extubation, patients were divided two groups: Group 1= extubation time ≤ 6 hours, Group 2= extubation time >6 hours. Results: A total of 99 patients were in Group 1 and 36 patients in Group 2. Duration of ventilation was 4.4±0.9 hours in Group 1 and 25.9±24.9 hours in Group 2 (P<0.001). Univariate analysis showed that young age, low weight, low partial pressure of oxygen, trisomy 21, multiple ventricular septal defect, high vasoactive inotropic score, transient heart block and low cardiac output syndrome were associated with delayed extubation. However, regression analysis revealed that only trisomy 21 (OR: 0.248; 95%CI: 0.176-0.701; P=0.001), low cardiac output syndrome (OR: 0.291; 95%CI: 0.267-0.979; P=0.001), multiple ventricular septal defect (OR: 0.243; 95%CI: 0.147-0.606; P=0.002) and vasoactive inotropic score (OR: 0.174 95%CI: 0.002-0.062; P=0.039) are strongest predictors for delayed extubation. Conclusion: Trisomy 21, low cardiac output syndrome, multiple ventricular septal defect and high vasoactive inotropic score are significant risk factors for delay in extubation. Age, weight, pulmonary artery hypertension, size of ventricular septal defect, aortic cross-clamp and cardiopulmonary bypass time did not affect early extubation.