Xi Su

Cardiac arrest with anaphylactic shock: a successful resuscitation using extracorporeal membrane oxygenation

Anaphylactic shock is a serious allergic reaction, setting in rapidly, which may lead to life-threatening circulatory failure and necessitates aggressive support to ensure full recovery. We report the case of a 50-year-old man who developed cardiovascular collapse and cardiac arrest to iodine contrast media, occurring during coronary angiography. He was required temporary mechanical circulatory support with an venoarterial extracorporeal membrane oxygenation system by failure of conventional therapy and intra-aortic balloon pump counterpulsation therapy. He had full recovery of cardiac function and released from the hospital 21 days after admission without a neurologic deficit.

Cardiac arrest with coronary artery spasm: does the use of epinephrine during cardiopulmonary arrest exacerbate the spasm?

Coronary artery spasm can lead to sudden cardiac death due to ventricular arrhythmias or heart block. Cardiopulmonary resuscitation guidelines recommend the use of epinephrine during cardiopulmonary arrest. However, in the event of cardiac arrest caused by coronary artery spasm, the use of epinephrine may be harmful. We report 2 cases who had witnessed cardiac arrest due to ventricular fibrillation and complete heart block. Intravenous epinephrine was administered during resuscitation.Their hemodynamics did not improve. Emergent coronary angiography revealed that the entire right and left coronary artery systems diffuse spasm. One patients coronary artery spasm was successfully reversed immediately with administration of intracoronary boluses of nitroglycerin. The other patients hemodynamic instability persisted,requiring temporary mechanical circulatory support with an intra aortic balloon pump. His hemodynamics finally improved with administration of intravenous diltiazem and nitroglycerin under the intraaortic balloon pump support. They both were discharged from the hospital without any other complications.

Continuous Mechanical Chest Compression-assisted Percutaneous Coronary Intervention in a Patient with Cardiac Arrest Complicating Acute Myocardial Infarction

Cardiac arrest with ventricular tachycardia or ventricular fibrillation in the catheterization laboratory is not uncommon, but patients who suffered cardiac arrest requiring prolonged cardiopulmonary resuscitation is not infrequent and still a major problem, because it is essentially impossible to perform effective manual chest compressions during percutaneous coronary interventions (PCIs).[1] Recently, the use of a novel mechanical chest compression device, Lund University Cardiopulmonary Assist System (LUCAS, Jolife AB, Lund, Sweden), has been shown to sustain both coronary and cerebral circulation despite cardiac arrest and it may be possible to allow for continued PCI despite ongoing cardiac or circulatory arrest with artificially sustained circulation.[2] We here report a case who presented with acute myocardial infarction complicated by cardiac arrest undergoing successful PCI while continuous mechanical chest compression with LUCAS device. A 47-year-old male was admitted to our hospital with a 5 h history of chest pain. His initial vital signs included temperature 36.4°C, heart rate 108 beats/min, blood pressure 74/42 mmHg, respiratory rate 22 breaths/min. The initial electrocardiogram revealed sinus tachycardia with ST-segment elevation in leads V1 through V5. Bedside transthoracic echocardiography showed that hypokinesia of the anterior wall motion and left ventricular ejection fraction was 35%. The blood tests revealed a leukocyte level of 15.91 × 109/L and the serum levels of troponin I of 0.115 ng/ml (normal range 0–0.04 ng/ml). Since the patient was diagnosed as acute ST-segment elevation myocardial infarction complicated by cardiogenic shock, we decided to emergency PCI. Initial treatment was managed on intravenous dopamine, oral aspirin, clopidogrel, and intravenous unfractionated heparin. About 20 min after admission, while the patient was transferred from the emergency room to the catheterization laboratory, he had a witnessed cardiac arrest with ventricular fibrillation in the elevator [Figure 1]. Continuous chest compression and electrical defibrillation were preformed immediately. The ventricular fibrillation was terminated with defibrillation at first, but in a while he developed repetitive prolonged phases of incessant ventricular tachycardia and ventricular fibrillation. In the catheterization laboratory, repeat defibrillation and intravenous epinephrine, antiarrhythmic drugs such as lidocaine, amiodarone, and magnesium sulfate also could not control the ventricular tachyarrhythmias. His hemodynamic status continued to worsen and required continuous chest compressions and tracheal intubation. Because implantation of extracorporeal membrane oxygenation (ECMO) required surgeons and perfusionists, and they couldn’t quickly arrive at the catheterization laboratory, the ECMO could not be performed in the first. LUCAS device was first used for continuous mechanical chest compression to maintain blood pressure about 104/50 mmHg, While continuous automatic mechanical chest compression with the LUCAS device, emergency coronary angiography was performed via the right femoral artery about 42 min after admission (Door to Balloon time), which revealed right coronary artery (RCA) dominance and mild stenosis in the middle portion of the RCA, total occlusion in the proximal left anterior descending artery (LAD), and no stenosis of the left circumflex coronary artery [Figure ​[Figure2a2a and ​and2b].2b]. We performed PCI in the LAD and a stent was deployed to the LAD [Figure ​[Figure2c2c and ​and2d].2d]. An intra-aortic balloon pump (IABP) was inserted via the right femoral artery sheath after PCI. The whole procedure took about 13 min. Although the PCI was successful performed, his spontaneous circulation was still not recovered. So, while continuous mechanical chest compression, ECMO was inserted to provide hemodynamic support in a veno-arterial configuration by cannulation on left femoral vessels following cardiac arrest occurred about 75 min [Figure 3]. With the ECMO support for the circulation, the LUCAS device was withdrawn. The patient was transferred to the cardiac care unit to continue to rescue. Figure 1 This patient suffered sudden cardiac arrest with ventricular fibrillation following arrival in the catheterization laboratory. Electrocardiograph monitoring showed incessant ventricular tachycardia/ventricular fibrillation which could not controlled by ... Figure 2 Emergency coronary angiography and PCI while continuous mechanical chest compression with LUCAS device. (a) Coronary angiography revealed mild stenosis in the middle portion of the RCA; (b) Total occlusion in the proximal LAD, and no significant stenosis ... Figure 3 Timeline of events after the patient was admitted to the ED. ED: Emergency department; CPR: Cardiopulmonary resuscitation; PCI: Percutaneous coronary intervention; ECMO: Extracorporeal membrane oxygenation; IABP: Intra-aortic balloon pump; ROSC: Return ... About more than 30 min with the ECMO and IABP support, the patients rhythm converted to sinus rhythm and his spontaneous circulation was also recovered. His left ventricular function and hemodynamics obviously improved under the ECMO and IABP assist. The ECMO was removed on the 4th day and the IABP weaned off on the 7th day after admission. Although the recovery of cardiac function was very well, his consciousness had never recovered. The patient had incurred a serious hypoxic brain injury and later died in the hospital. Cardiac arrest in the cardiac catheterization laboratory during PCI, although an uncommon event, is associated with high mortality.[1] Immediate chest compression and defibrillation are the most important strategies to improve the outcome in sudden cardiac arrest. However, PCI in the setting of cardiac arrest requiring prolonged resuscitation is a significant challenge to the interventional cardiologists because it may be difficult to perform efficacious cardiopulmonary resuscitation while continuing the coronary angiography or interventions.[2] Mechanical cardiopulmonary resuscitation devices provide chest compressions more reliably at a set rate and depth and thus generate better hemodynamic characteristics than manual chest compressions.[3] These devices clearly offer new opportunities for in-hospital cardiac arrest resuscitation as they help to sustain circulation with consistent compressions according to the guidelines during prolonged resuscitation efforts, transportation, and during diagnostics. Mechanical cardiopulmonary resuscitation device, such as the LUCAS has been shown to sustain both coronary and cerebral circulation despite cardiac arrest. The LUCAS device due to its design, which is mostly plastic, not fully radiopaque, and from acceptable size, assures a reliable continuous chest compression during angiography/angioplasty, without significant interferences.[4] Utility of the LUCAS device for continuous mechanical chest compressions during PCI has been confirmed to be feasible, safe and highly effective.[3] In recent years, ECMO can provide oxygenation and circulatory support and may be the other mean to solve restoration of blood flow in the setting of refractory cardiac arrest in the catheterization laboratory. Several small studies using ECMO in acute coronary syndrome complicated by intractable cardiac arrest have been reported with good results.[5] Compared with continuous mechanical chest compression-assisted PCI, ECMO seems to provide more effective circulatory support than continuous mechanical chest compressions with LUCAS device in cardiac arrest, but implantation of the ECMO usually takes longer and often requires extra staff with special skills, such as a cardiovascular surgeon and a perfusionist. In addition, it may delay revascularization of the occluded infarct-related artery. LUCAS, on the other hand, may be applied quickly (<1 min).[1] In the crisis situations, such as in our case, when the refractory cardiac arrest with ventricular tachyarrhythmias could not be controlled by defibrillation and antiarrhythmic drugs, emergency PCI while continuous mechanical chest compressions may be as the preferred option at that time. Although the patient was treated by successful PCI during continuous mechanical chest compressions and the heart fully recovered under the ECMO and IABP support, serious hypoxic brain injury had caused a poor outcome. There are several potential limitations in our case. First, as the patient was admitted with acute myocardial infarction complicated by cardiogenic shock, IABP should be immediately inserted in the emergency department. Second, guidelines are somewhat cautious in recommending intravenous β-blockers use in acute myocardial infarction, but in the setting of the electrical storm, whether intravenous β-blockers should be used? Third, therapeutic hypothermia had not be performed as soon as possible in the catheterization laboratory. Finally, also the most important, the ECMO should be immediately used to provide effective circulation perfusion and then to perform PCI under the ECMO support. However, in our institution, implantation of the ECMO usually requires surgeons and perfusionists and could not be performed immediately at that time. In conclusion, in the setting of acute myocardial infarction complicated by cardiac arrest requiring prolonged resuscitation, it is a significant challenge for the interventional cardiologists to perform PCI. This case, although the finally outcome was poor, illustrates the use of LUCAS device for mechanical chest compressions had made it possible to the continued uninterrupted PCI procedure during ongoing cardiac arrest, especially under the condition of EMCO could not be applied immediately.

Prognostic Value of Plasma Long Noncoding RNA ANRIL for In-Stent Restenosis

Background In-stent restenosis (ISR) remains a major cause of failure of contemporary percutaneous revascularization therapies. Invasive biomarkers to improve the prognosis of ISR should be considered. This study aimed to investigate the association between plasma ANRIL expression and ISR. Material/Methods A total of 444 patients were included in this research. Serial coronary angiography was performed at baseline (before and after intervention) and within 36 months’ follow-up. ISR was defined as >50% diameter stenosis at follow-up. ANRIL expression was quantified using reverse transcription-PCR. An area under the ROC curve (auROC) was generated to assess the diagnostic values of ANRIL. Logistic regression models were used to assess the independent risk factors for ISR. Results Plasma ANRIL expression was significantly increased in patients with ISR, as compared with that in patients without ISR (1.6 [1.1–2.5] vs. 0.9 [0.6–1.3], P<0.001). The auROC (95% confidence interval [CI]) of plasma ANRIL in diagnosing ISR was 0.745 (0.687–0.811). Multiple logistic regression models indicated that drinking (odds ratio [OR]=2.09, 95% CI: 1.08–4.04, P=0.028), hypertension (OR=2.01, 95% CI: 1.14–3.57, P=0.017), diabetes (OR=3.15, 95% CI: 1.63–3.57, P<0.001), low-density lipoprotein (OR=3.14, 95% CI: 1.57–6.31, P=0.001), and ANRIL (OR=2.21, 95% CI: 1.68–2.92, P<0.001) were the independent risk factors for ISR. Conclusions We found that higher ANRIL expression is associated with ISR, indicating that ANRIL may be an optimal prognostic factor for ISR.

Extracorporeal Membrane Oxygenation Support for Incessant Tachyarrhythmia-Induced Severe Cardiogenic Shock

To the Editor: Junctional ectopic tachycardia is uncommon; however, it is one of the most serious incessant supraventricular tachycardia. This tachyarrhythmia has a high association with tachycardia‐induced cardiomyopathy or myocardial depressant. It is often refractory to conventional medical therapy and is not usually responsive to direct current cardioversion. Due to the fact that antiarrhythmic medications are associated with the adverse effects of proarrhythmic or refractory hypotension, the use of these agents may further deteriorate the condition of patients with tachyarrhythmias. In such instances, it often requires other alternatives to conventional therapy to prevent hemodynamic deterioration. Extracorporeal life support such as extracorporeal membrane oxygenation (ECMO) can be used in such cases and may be lifesaving. It may allow time for satisfactory control of dysrhythmias while awaiting recovery of myocardial and other organ functions. Herein, we described the use of venoarterial ECMO in a patient with severe cardiogenic shock because of incessant junctional ectopic tachycardia with no response to conventional therapy.

Role of Soluble ST2 Levels and Beta-Blockers Dosage on Cardiovascular Events of Patients with Unselected ST-Segment Elevation Myocardial Infarction

Background: Serum soluble ST2 (sST2) levels are elevated early after acute myocardial infarction and are related to adverse left ventricular (LV) remodeling and cardiovascular outcomes in ST-segment elevation myocardial infarction (STEMI). Beta-blockers (BB) have been shown to improve LV remodeling and survival. However, the relationship between sST2, final therapeutic BB dose, and cardiovascular outcomes in STEMI patients remains unknown. Methods: A total of 186 STEMI patients were enrolled at the Wuhan Asia Heart Hospital between January 2015 and June 2015. All patients received standard treatment and were followed up for 1 year. Serum sST2 was measured at baseline. Patients were divided into four groups according to their baseline sST2 values (high >56 ng/ml vs. low ⩽56 ng/ml) and final therapeutic BB dose (high ≥47.5 mg/d vs. low <47.5 mg/d). Cox regression analyses were performed to determine whether sST2 and BB were independent risk factors for cardiovascular events in STEMI. Results: Baseline sST2 levels were positively correlated with heart rate (r = 0.327, P = 0.002), Killip class (r = 0.408, P = 0.000), lg N-terminal prohormone B-type natriuretic peptide (r = 0.467, P = 0.000), lg troponin I (r = 0.331, P = 0.000), and lg C-reactive protein (r = 0.307, P = 0.000) and negatively correlated to systolic blood pressure (r = −0.243, P = 0.009) and LV ejection fraction (r = −0.402, P = 0.000). Patients with higher baseline sST2 concentrations who were not titrated to high-dose BB therapy (P < 0.0001) had worse outcomes. Baseline high sST2 (hazard ratio [HR]: 2.653; 95% confidence interval [CI]: 1.201–8.929; P = 0.041) and final low BB dosage (HR: 1.904; 95% CI, 1.084–3.053; P = 0.035) were independent predictors of cardiovascular events in STEMI. Conclusions: High baseline sST2 levels and final low BB dosage predicted cardiovascular events in STEMI. Hence, sST2 may be a useful biomarker in cardiac pathophysiology.

Effect of atorvastatin and trimetazidine combination treatment in patients with NSTE-ACS undergoing PCI

Background: Our study sought to assess the effect of atorvastatin (ATV) and trimetazidine (TMZ) combination treatment in patients with non-ST elevation acute coronary syndromes (NSTE-ACS) undergoing percutaneous coronary intervention (PCI). Materials and Methods: Two hundred and fifty patients with NSTE-ACS who were undergoing PCI were enrolled in this study. Standard secondary prevention of coronary heart disease drug treatment was administered to both the groups (the ATV + TMZ group and the ATV group). In the ATV + TMZ group, patients were given 80mg of the combination medical orally 12h before PCI, 60mg 30min before PCI, and a further 20mg every day for 30t days after PCI, and. In the ATV group, patients were given only 80mg orally 12h before PCI, with a further 20mg every day for 30t days after PCI. Echocardiography was executed and plasma N-terminal pro brain natriuretic peptide (NT-pro-BNP) levels were measured just prior to the PCI and at 30 days after PCI. The major cardiovascular events (MACE) were also evaluated in both groups 30 days after PCI. Results: MACE occurred in 14.17% of patients in the ATV group and 6.50% of those in the ATV + TMZ group (P = 0.047). NT-pro-BNP levels were decreased 30 days after PCI for both groups; however, NT-pro-BNP levels in the ATV + TMZ group were significantly lower than those in the ATV group (P < .05). Cardiac function in NSTE-ACS patients, as reflected by the increased left ventricular ejection fraction, fractional shortening as well as decreased left ventricular end-diastolic dimension (P < .05) increased in all groups at 30 days after intervention, but cardiac function parameters were more significantly improved in the group administered with ATV + TMZ (P < .05). Conclusions: Our study suggests that short-term pretreatment with the combination of ATV and TMZ administration before PCI could reduce the incidence of MACE, further decrease NT-pro-BNP levels and improve cardiac function compared to a single administration of the ATV.

Effect of Intensive Atorvastatin Therapy on Periprocedural PTEN Expression in CD4+T Lymphocytes of Patients with Unstable Angina Undergoing Percutaneous Coronary Intervention

Objectives: To investigate the effects of intensive atorvastatin therapy on PTEN expression by CD4+ T lymphocytes in patients with unstable angina (UA) that received PCI. Methods: All patients with UA were randomly divided into the pretreatment with an intensive atorvastatin (ATV) group (80mg 12h before PCI, with a further 20mg every day after PCI, n = 56) or a conventional (control) group (only 20 mg/day, n = 56). Circulating CD4+ T cells were subsequently obtained prior to PCI and 18–24 h after successful PCI, using a magnetic cell sorting system. Plasma cTnI, CK-MB, hsCRP, IL-10 and TNF-a levels were measured just prior to the PCI and 18–24 h after PCI. PTEN mRNA and protein were determined by Real-time PCR and western blots, respectively. Results: PTEN mRNA and protein were dramatically decreased in ATV group (p 0.05). Conclusion: Intensive atorvastatin treatment reduced the post-PCI myocardial inflammatory response in patients with UA, possibly by enhancing PTEN expression in CD4+ T lymphocytes.

Thrombolysis during continuous chest compression in a patient with cardiac arrest due to pulmonary embolism: prolonged CPR–induced spinal cord injury

Pulmonary embolism (PE) is a life-threatening condition, and cardiac arrest is the most serious clinical circumstance. Clinical practice guidelines recommend systemic thrombolysis for high-risk or massive PE patients as the primary treatment. However, there are insufficient data to argue for or against the routine use of thrombolytic therapy during cardiac arrest. We report a 47-year-old man with acute PE complicated by cardiac arrest with pulseless electrical activity. Intravenous thrombolytic therapy with 1.5 million U of urokinase was performed by a constant infusion pumpwithin 30 minutes during continuous mechanical chest compression with LUCAS (Jolife AB, Lund, Sweden). After 46minutes of cardiopulmonary resuscitation, return of spontaneous circulationwas achieved, and the patient eventually survived to discharge. Unfortunately, he had an irreversible spinal cord injury due to prolonged cardiopulmonary resuscitation and traumatic injury.

Use of intra-aortic balloon pump support for oozing-type cardiac rupture after acute myocardial infarction

Left ventricular free wall rupture usually leads to acute hemopericardium and sudden cardiac death resulting in cardiac tamponade. Rarely, only a few patients with subacute free wall rupture such as oozing-type ventricular rupture or left ventricular false aneurysm may permit time for pericardiocentesis and surgery. We report a 63-year-old man with ST-elevation myocardial infarction who underwent primary percutaneous coronary intervention about 12 hours from the onset, and cardiac tamponade occurred on the second day. An intra-aortic balloon pump (IABP) was immediately inserted for hemodynamic support. After 100 mL of pericardial fresh blood was drained from the percardial cavity, his hemodynamic collapse was promptly improved with IABP support. In the following 24 hours, about 600 mL of hemorrhagic pericardial fluid was drained. The most likely diagnosis was concerning for oozing-type ventricular rupture, and a conservative approach was decided. The patient survived to the acute phase under IABP support and was discharged with complete recovery.