Acute Hemodynamic Decompensation Research Articles

EaRly-start ExerciSe training afTer acute hemodynAmic decompensation in patients with chRonic hearT failure (RE-START). A multicenter, randomized, controlled trial on short-term feasibility and impact on functional capacity, symptoms and neurohumoral activation .

RE-START is a multicenter, randomized, prospective, open, controlled trial aiming to evaluate the feasibility and the short- and medium-term effects of an early-start AET program on functional capacity, symptoms and neurohormonal activation in chronic heart failure (CHF) patients with recent acute hemodynamic decompensation. Study endpoints will be: 1) safety of and compliance to AET; 2) effects of AET on i) functional capacity, ii) patient-reported symptoms and iii) AET-induced changes in beta-adrenergic receptor signaling and circulating angiogenetic and inflammatory markers. Two-hundred patients, randomized 1:1 to training (TR) or control (C), will be enrolled. Inclusion criteria: 1) history of systolic CHF for at least 6 months, with ongoing acute decompensation with need of intravenous diuretic and/or vasodilator therapy; 2) proBNP > 1000 pg/mI at admission. Exclusion criteria: 1) ongoing cardiogenic shock; 2) need of intravenous inotropic therapy; 3) creatinine > 2.5 mg/dl at admission. After a 72-hour run-in period, TR will undergo the following 12-day early-start AET protocol: days 1-2: active/passive mobilization (2 sessions/day, each 30 minutes duration); days 3-4: as days 1-2 + unloaded bedside cycle ergometer (3 sessions/day, each 5-10 minutes duration); days 5-8: as days 1-2 + unloaded bedside cycle ergometer (3 sessions/day, each 15-20 minutes duration); days 9-12: as days 1-2 + bedside cycle ergometer at 10-20 W (3 sessions/day, each 15-20 minutes duration). During the same period, C will undergo the same activity protocol as in days 1-2 for TR. All patients will undergo a 6-min WT at day 1, 6, 12 and 30 and echocardiogram, patient-reported symptoms on 7-point Likert scale and measurement of lymphocyte G protein coupled receptor kinase, VEGF, angiopoietin, TNF alfa, IL-1, IL-6 and eNOS levels at day 1, 12 and 30.

Near-Fatal Pneumopericardium During Tracheal Stent Exchange

PATIENTS WITH BRONCHIAL FISTULAS, including bronchopleural, bronchomediastinal, bronchopericardial, or bronchoesophageal, may present with significant difficulties in airway and ventilatory management. Fistulas are an infrequent, but well-described complication, of metal airway stents, and in the setting of advanced malignancy, communication with the mediastinal or pericardial space may occur. 1 Lund M.E. Force S. Airway stenting for patients with benign airway disease and the Food and Drug Administration advisory: A call for restraint. Chest. 2007; 132: 1107-1108 Crossref PubMed Scopus (61) Google Scholar , 2 Alazemi S. Lunn W. Majid A. et al. Outcomes, health-care resources use, and costs of endoscopic removal of metallic airway stents. Chest. 2010; 138: 350-356 Crossref PubMed Scopus (45) Google Scholar When these fistulas are present, positive-pressure ventilation has a high likelihood of developing cardiac tamponade, which may be catastrophic if diagnosis and management are delayed. 3 Xu Y. Xu Z. Wang Y. Cardiac tamponade due to pneumopericardium. Pak J Med Sci. 2014; 30: 924-926 Google Scholar The authors present a rare case of stent migration and fistula formation into the pericardial space that presented with acute intraoperative hemodynamic and respiratory decompensation, which never has been described in the literature.

Acute hemodynamic decompensation during catheter ablation of scar-related ventricular tachycardia: incidence, predictors, and impact on mortality.

The occurrence of periprocedural acute hemodynamic decompensation (AHD) in patients undergoing radiofrequency catheter ablation of scar-related ventricular tachycardia (VT) has not been previously investigated. We identified univariate predictors of periprocedural AHD in 193 consecutive patients undergoing radiofrequency catheter ablation of scar-related VT. AHD was defined as persistent hypotension despite vasopressors and requiring mechanical support or procedure discontinuation. AHD occurred in 22 (11%) patients. Compared with the rest of the population, patients with AHD were older (68.5±10.7 versus 61.6±15.0 years; P=0.037); had a higher prevalence of diabetes mellitus (36% versus 18%; P=0.045), ischemic cardiomyopathy (86% versus 52%; P=0.002), chronic obstructive pulmonary disease (41% versus 13%; P=0.001), and VT storm (77% versus 43%; P=0.002); had more severe heart failure (New York Heart Association class III/IV: 55% versus 15%, P<0.001; left ventricular ejection fraction: 26±10% versus 36±16%, P=0.003); and more often received periprocedural general anesthesia (59% versus 29%; P=0.004). At 21±7 months follow-up, the mortality rate was higher in the AHD group compared with the rest of the population (50% versus 11%, log-rank P<0.001). AHD occurs in 11% of patients undergoing radiofrequency catheter ablation of scar-related VT and is associated with increased risk of mortality over follow-up. AHD may be predicted by clinical factors, including advanced age, ischemic cardiomyopathy, more severe heart failure status (New York Heart Association class III/IV, lower ejection fraction), associated comorbidities (diabetes mellitus and chronic obstructive pulmonary disease), presentation with VT storm, and use of general anesthesia.

Ventriculo-arterial decoupling in acutely altered hemodynamic states

The dynamic interaction between the heart and the systemic circulation allows the cardiovascular system to be efficient in providing adequate cardiac output and arterial pressures necessary for sufficient organ perfusion [1]. The cardiovascular system provides adequate pressure and flow to the peripheral organs in different physiological (rest and exercise) and pathological conditions because of the continuous modulation of the arterial system compliance, stiffness and resistance with respect to left ventricular (LV) systolic performance [2]. Cardiac output is the final result of this dynamic modulation. Because LV stroke volume depends on myocardial contractility and loading conditions (preload and afterload), both cardiac and arterial dysfunction can lead to acute hemodynamic decompensation and shock.

Long-Term Outcome of Treatment with Ruxolitinib in Myelofibrosis

Abstract 1752▪▪This icon denotes a clinically relevant abstract Background:Patients with primary (PMF) or post-polycythemia vera/essential thrombocythemia (post-PV/ET MF) myelofibrosis often harbor a JAK2 mutation and also display abnormally increased inflammatory cytokines (J Clin Oncol. 2011;29:1356). Therefore, JAK-STAT is an appealing drug target in such patients. Ruxolitinib (INCB018424) is a small molecule ATP mimetic that inhibits both JAK1 and JAK2 and has been evaluated for its therapeutic activity in MF, in the setting of phases 1, 2, and 3 clinical trials. Methods:The first phase-1/2 MF study using ruxolitinib was conducted at the MD Anderson Cancer Center and Mayo Clinic. A total of 153 patients were included in the study whose first line results were published in September, 2010 (NEJM 2010;363:1117). The current report constitutes a sponsor-independent analysis of long-term outcome in the 51 Mayo Clinic patients who participated in the particular clinical trial. Results I: Baseline characteristics:The 51 patients (37 males) from the Mayo Clinic were enrolled between October, 2007 and February 2009. The median time from treatment initiation is now 3.5 years. MF subtype distributions were PMF 60%, post-PV MF 32% and post-ET MF 10%. Median (range) values were age 61 years (39–79), hemoglobin 10.6 g/dL (7.4-15.3), leukocyte count 15.8 (2.0–136), and palpable spleen size 19 cm (0–32). The proportion of patients with red cell transfusion dependency was 24%, hemoglobin <10 g/dL 38%, unfavorable karyotype 18%, pruritus 24%, night sweats 26%, and JAK2V617F 84%. DIPSS-plus risk distributions were high 18%, intermediate-2 48%, intermediate-1 22% and low 14%. Results II: Response and treatment duration:According to the International Working Group for Myeloproliferative Neoplasms Research and Treatment (IWG-MRT) criteria, spleen response rate was 29% and anemia response rate 21%. Responses were also seen in constitutional symptoms (63%) and pruritus (92%). To date, treatment has been discontinued in 47 (92%) patients. The treatment discontinuation rates at 1, 2 and 3 years were 51%, 72% and 89%, respectively. For the 47 patients who were taken off study, median duration of treatment was 9.2 months (range 1.3–42 months). Reasons for treatment discontinuation included loss or lack of response/disease progression (∼40%), toxicity with and without lack of response/disease progression (∼34%), patient/physician choice often associated with lack of response (13%), and death on study (∼4%). Results III: Toxicity:Grade ≥2 thrombocytopenia and anemia occurred in 26% and 33% of patients and persisted in the majority of afflicted patients after drug discontinuation. To date, 18 deaths (36%) and 5 (10%) leukemic transformations have been recorded. Serious adverse events occurred upon drug discontinuation in 6 cases (13%) and were characterized by immediate relapse of symptoms, rapid and painful enlargement of spleen sometimes associated to splenic infarct, and acute hemodynamic decompensation occasionally leading to a septic shock-like syndrome. Results IV: Survival:There was no significant difference in the survival of the 51 ruxolitinib-treated patients compared to that of a cohort of 410 cases of PMF seen at the Mayo Clinic in the most recent 10-year period: unadjusted (Figure 1; p=0.43) and adjusted for DIPSS-plus (Figure 2; p=0.58). [Display omitted] [Display omitted] Conclusions:Ruxolitinib is effective in alleviating constitutional symptoms in the majority of patients with MF. Its activity in reducing spleen size is modest and not always durable. It is imperative that patients be alerted about important drug adverse events including potentially irreversible thrombocytopenia, worsening of anemia, and potentially catastrophic withdrawal symptoms. Ruxolitinib therapy does not appear to affect survival in MF. Disclosures:No relevant conflicts of interest to declare.

Acute Hemodynamic Decompensation Following Patent Ductus Arteriosus Ligation in Premature Infants

Introduction: Patent ductus arteriosus (PDA) ligation can lead to postoperative hemodynamic instability requiring inotropic support, termed hemodynamic decompensation. The purpose of this study was to prospectively determine the incidence, predictors, and clinical impact of hemodynamic decompensation after PDA ligation in preterm infants. Methods: All infants undergoing PDA ligation were eligible for this prospective cohort study. After undergoing ligation, patients were followed until 30 days after successful extubation, discharge from the NICU, or death. Data collection included perinatal and preoperative clinical information, operative details, postoperative course, and outcome. Results: Ninety-six preterm infants were enrolled and underwent PDA ligation. Hemodynamic decompensation occurred in 27 patients (28%). Overall in-hospital mortality rate was 18%. Mortality was significantly higher among infants that developed hemodynamic decompensation (33% vs 11%, p =. 012). Hemodynamic decompensation was associated with an adjusted odds ratio (OR) for death of 3.1 (95% confidence interval: 1.0–9.5, p =. 05). Lower estimated gestational age, lower corrected age, and higher rate of preoperative mechanical ventilation were significant predictors of hemodynamic decompensation. Conclusion: Hemodynamic decompensation occurred in 28% of patients after PDA ligation, resulting in a significantly higher mortality. Younger patients requiring higher ventilator support are most likely to develop hemodynamic decompensation.

Mechanisms and Use of Calcium-Sensitizing Agents in the Failing Heart

Depressed cardiac contractility is central to many forms of cardiac disease and reflects the heart’s inability to generate adequate force despite being provided physiological activator calcium and chamber load. Yet, successful methods to enhance cardiac contractility have remained elusive. Agents such as dobutamine or milrinone that work through the β-receptor-cAMP-protein kinase A pathway are used to manage acute hemodynamic decompensation, but short-term and, particularly, long-term use can increase risks of arrhythmia and worsen outcome. These and other data have led to the conclusion that successful heart failure management should probably avoid the targeting of contractility improvement. Leading hypotheses for the failure of existing inotropic therapies is that they increase activator calcium, worsen arrhythmia, activate maladaptive Ca2+-dependent signaling cascades, and increase myocardial oxygen consumption, making hearts less efficient. An alternative approach to avoid such complications would be to directly influence the manner by which intracellular calcium is transduced into muscle force. The class of molecules that achieve this are often termed “calcium sensitizers” and have attracted growing clinical interest for more than 20 years.1 The mechanisms by which such effects are achieved vary widely and include direct activators of motor proteins such as myosin, enhancers of force generated by a cross-bridge, and agents that augment Ca2+–troponin C (TnC) binding and its consequences. To date, many such drugs have had additional effects, such as inhibiting cAMP phosphodiesterase (PDE3a), that likely contributed to their vasodilation/venodilation and Ca2+-dependent increases in heart rate and contractility. Other agents, such as levosimendan, also inhibit ATP-sensitive potassium channels, which can induce further effects. This review discusses basic molecular mechanisms for drugs that alter the myofilament response to calcium, how such agents affect muscle and whole-organ physiology, and what their clinical testing has revealed. In doing so, we attempted to bridge the …

Perioperative considerations in the patient with a left ventricular assist device.

Perioperative considerations in the patient with a left ventricular assist device.

Paroxysmal postural dyspnea related to a left atrial ball thrombus

We report herein an uncommon clinical observation of a 82-year-old woman with paroxysmal postural dyspnea related to a giant ball-thrombus located in the left atrium and partly protruding through the mitral orifice. No mitral stenosis was otherwise disclosed. The patient had a previous medical history of chronic atrial fibrillation without any anticoagulant therapy. The atrial mass was easily removed and the postoperative course was uneventful. Disclosure of such a free-floating ball-thrombus in the left atrial cavity requires prompt surgical treatment because of high risks of acute hemodynamic decompensation due to obstruction of the left ventricular inflow or, more rarely, systemic embolic events.

Concomitant traumatic coronary artery and tricuspid valve injury: a heterogeneous presentation.

Blunt thoracic trauma resulting in both tricuspid valve rupture and coronary artery injury is uncommon, encompasses a large spectrum of presentations and, therefore, can be difficult to diagnose. This report illustrates the heterogeneous presentation and clinical course of two patients with such a combination of cardiac injuries. The patient with associated right coronary artery dissection developed progressive right ventricular failure over a 12-year period before successful surgical repair, whereas another patient with left anterior descending coronary artery thrombosis required urgent operation for acute right ventricular dysfunction and hemodynamic decompensation.

Marcadores de hipercoagulabilidad y daño endotelial en pacientes con disfunción sistólica de origen isquémico

Anticoagulation is rarely indicated in patients with left ventricular dysfunction who show an increased risk for thromboembolism. In theory, the three arms of the Virchow' triad may be present: abnormal blood flow, endothelial damage and prothrombotic markers. The aim of this study was to identify the last two arms. We studied 82 consecutive patients with demonstrated ischaemic heart disease and sinus rhythm, and compared them with a control group comprised of 32 healthy subjects matched for age and sex. None or the patients had had an acute coronary event or hemodynamic decompensation within the 3 months prior to inclusion in the study. The plasma concentration or von Willebrand factor and fibrin d-dimer and fibrinogen were determined as endothelial damage and prothrombotic markers, respectively. A fractional shortening less than 29% by echography was defined as ventricular systolic dysfunction. The patients showed significantly higher levels of von Willebrand factor with respect to the control group (109.2 31.9 vs 85.5 32.6%, p < 0.01), with no differences in fibrinogen and fibrin d-dimer values. Twenty-six patients fulfilled criteria of left ventricular systolic dysfunction. Patients with left ventricular dysfunction showed higher fibrinogen (386 118 vs 322 102 mg/dl, p = 0.03) and fibrin d-dimer (0.36 0.22 vs 0.26 0.10 g/ml; p = 0.04) levels, with no differences in von Willebrand factor levels. After acute coronary events, patients with ischaemic heart disease show markers of endothelial damage. However, patients with left ventricular dysfunction show a hypercoagulable state.

Inotropic support for hemodynamic decompensation during acute myocardial transplant rejection

A LLOGENEIC orthotopic heart transplant rejection is common; however, associated acute hemodynamic decompensation at the time of rejection is rare. Improved immunosuppression and increased surveillance by serial endomyocardial biopsies are responsible for decreased mortality rates secondary to rejection.‘,’ However, those patients who do develop hemodynamic instability with rejection require immediate support until reversal of rejection (ie, immunologic rescue) can occur. This report reviews the technique used at the University of Michigan for support of patients with acute hemodynamic decompensation following cardiac rejection.

Effect of acute hemodynamic decompensation on electrical inducibility of ventricular arrhythmias in patients with dilated cardiomyopathy and complex nonsustained ventricular arrhythmias

In patients with dilated cardiomyopathy, hemodynamic decompensation has been postulated to increase vulnerability to reentrant ventricular arrhythmias. To test this hypothesis, we performed programmed ventricular stimulation with three extrastimuli on nine patients with dilated cardiomyopathy and asymptomatic complex ventricular arrhythmias during a period of acute hemodynamic decompensation; programmed ventricular stimulation was then repeated following hemodynamic improvement with nitroprusside. These patients did not have a history of documented or suspected sustained ventricular tachycardia or fibrillation. The mean left ventricular ejection fraction was 0.21 +/- 0.04 (range 0.15 to 0.26). In the baseline state, mean right atrial pressure was 8 +/- 4 mm Hg, pulmonary artery wedge pressure was 20 +/- 3 mm Hg, and cardiac index was 3.2 +/- 0.5 L/min/m2. Following acute hemodynamic decompensation, mean right atrial pressure increased to 16 +/- 5 mm Hg and pulmonary artery wedge pressure to 33 +/- 8 mm Hg; cardiac index decreased to 2.1 +/- 0.5 L/min/m2. In this decompensated state, programmed ventricular stimulation failed to induce sustained or nonsustained ventricular arrhythmias in any patient. Following nitroprusside administration (mean dose 1.5 +/- 1.1 micrograms/kg/min), there were significant decreases in mean right atrial pressure (11 +/- 3 mm Hg) and pulmonary artery wedge pressure (16 +/- 3 mm Hg), and a significant increase in cardiac index (3.1 +/- 1.1 L/min/m2) (p less than 0.05 for all values versus the decompensated state). In the improved hemodynamic state, programmed ventricular stimulation induced nonsustained ventricular tachycardia (six beats) in only one patient, and sustained arrhythmias in none.(ABSTRACT TRUNCATED AT 250 WORDS)

Use of emergency balloon dilation to reverse acute hemodynamic decompensation developing during diagnostic catheterization for aortic stenosis (bailout valvuloplasty)

Balloon aortic valvuloplasty has been shown to be an effective means of acutely reducing outflow tract obstruction in children 1 and adults 2,3 with aortic stenosis. In the present study we describe 3 patients with aortic stenosis who entered the hospital and catheterization laboratory in a stable hemodynamic state, but deteriorated acutely during routine diagnostic catheterization. In all 3 patients, balloon valvuloplasty was successfully performed as a bailout procedure after conventional measures failed to restore adequate systemic perfusion.

Embolectomy for Acute Pulmonary Artery Occlusion Following Fontan Procedure

A 5-year-old child experienced acute hemodynamic decompensation and hypoxia four weeks following an uneventful Fontan procedure for univentricular heart. Cardiac catheterization revealed complete occlusion of the left pulmonary artery, and emergent pulmonary artery embolectomy was performed. The source of the embolus was the atrial septal patch. Because of the altered hemodynamics following the Fontan procedure, stasis of right atrial blood and thrombus formation may occur. Routine anticoagulation immediately following operation is recommended. Prompt diagnosis and treatment with embolectomy may be lifesaving.