Ilija Srdanovic

Therapeutic hypothermia and neurological outcome after cardiac arrest.

INTRODUCTION/AIMnThe most important clinically relevant cause of global cerebral ischemia is cardiac arrest. Clinical studies showed a marked neuroprotective effect of mild hypothermia in resuscitation. The aim of this study was to evaluate the impact of mild hypothermia on neurological outcome and survival of the patients in coma, after cardiac arrest and return of spontaneous circulation.nnnMETHODSnThe prospective study was conducted on consecutive comatose patients admitted to our clinic after cardiac arrest and return of spontaneous circulation, between February 2005 and May 2009. The patients were divided into two groups: the patients treated with mild hypothermia and the patients treated conservatively. The intravascular in combination with external method of cooling or only external cooling was used during the first 24 hours, after which spontaneous rewarming started. The endpoints were survival rate and neurological outcome. The neurological outcome was observed with Cerebral Performance Category Scale (CPC). Follow-up was 30 days.nnnRESULTSnThe study was conducted on 82 patients: 45 patients (age 57.93 +/- 14.08 years, 77.8% male) were treated with hypothermia, and 37 patients (age 62.00 +/- 9.60 years, 67.6% male) were treated conservatively. In the group treated with therapeutic hypothermia protocol, 21 (46.7%) patients had full neurological restitution (CPC 1), 3 (6.7%) patients had good neurologic outcome (CPC 2), 1 (2.2%) patient remained in coma and 20 (44.4%) patients finally died (CPC 5). In the normothermic group 7 (18.9%) patients had full neurological restitution (CPC 1), and 30 (81.1%) patients remained in coma and finally died (CPC 5). Between the two therapeutic groups there was statistically significant difference in frequencies of different neurologic outcome (p = 0.006), specially between the patients with CPC 1 and CPC 5 outcome (p = 0.003). In the group treated with mild hypothermia 23 (51.1%) patients survived, and in the normothermic group 30 (81.1%) patients died, while in the group of survived patients 23 (76.7%) were treated with mild hypothermia (p = 0.003).nnnCONCLUSIONnMild therapeutic hypothermia applied after cardiac arrest improved neurological outcome and reduced mortality in the studied group of comatose survivors.

Ventriculoatrial synchrony induced heart failure

Abstract Objective and importance: Endless loop tachycardia or pacemaker-mediated tachycardia, and atrioventricular desynchronization arrhythmia or repetitive non-reentrant ventriculoatrial synchrony (RNRVAS) are two forms of reverse impulse conduction – ventriculoatrial (VA) synchrony. Although VA synchrony can theoretically cause aggravation of heart failure, clinical cases describing severe consequential heart failure are lacking. Clinical presentation and intervention: We describe a case of a 60-year-old patient who underwent primary percutaneous coronary intervention and mitral valve surgery. Implantation of a two-chamber pacemaker was also performed during the same hospitalization due to development of third-degree atrioventricular block. Ten months later, he presented with a severe form of heart failure with a significant reduction of left ventricular ejection fraction (LVEF). The atrial lead was displaced and VA synchrony was registered (RNRVAS-like condition). The pacemaker was reprogrammed and VA synchrony induced heart failure was successfully resolved. Echocardiographic follow-up showed improvement in LVEF. Conclusion: Ventriculoatrial conduction can be present even when the patient has a complete atrioventricular block. Atrial lead displacement and consequently loss of atrial capture with preserved sensing can be a predisposing factor for initiation of ventriculoatrial synchrony. Permanent ventriculoatrial synchrony may provoke aggravation of heart failure.

Association of coronary ischemia estimated by fractional flow reserve and psychological characteristics of patients

Introduction Psychological characteristics of patients, depression, stress and anxiety are recognized as important confounding risk factors for ischemic heart disease. However, the impact of psychological characteristics on coronary ischemia and vice versa remain poorly understood. Aim To demonstrate the interplay of psychological characteristics, depression, stress and anxiety with coronary ischemia estimated with fractional flow reserve (FFR). Material and methods From 2014 to 2016, 147 patients who were planned for FFR measurement were included in this study. Psychological characteristics of patients were evaluated using the Depression, Anxiety and Stress Scale 21 items (DASS 21) self-report questionnaire. Results Comparing the FFR ischemic vs. FFR non-ischemic groups, a significant difference was observed regarding results achieved for the depression, anxiety and stress scales. Multivariate logistic regression analysis was used to model the correlation between FFR and the DAS scale. It was clear, when controlling for previous myocardial infarction, that FFR was significant in all analyses. However, when the Canadian Cardiovascular Society grading of angina pectoris (CCS) class was entered in the model, FFR was not a significant predictor of anxiety, but was significant in other analysis. Conclusions Higher degrees of the psychological characteristics depression, stress and anxiety were observed in the group of patients with coronary ischemia, corresponding to lower fractional flow values.

Late complications of transcatheter atrial septal defect closure requiring urgent surgery

A 21-year-old female patient was transferred to our hospital after being diagnosed with massive pulmonary thromboembolism (PTE). Three years prior to admission, she underwent transcatheter closure of the secundum ASD with a 33 mm CardioSEAL-StarFLEX occluder (NMT Medical, Boston, MA, USA). A year ago, she was involved in a car accident and sustained significant blunt chest trauma. Transthoracic echocardiography confirmed the presence of thrombi in the right atrium and the pulmonary artery, with massive dilatation of the right ventricle and the pulmonary artery, along with severe pulmonary hypertension. Also, protrusion or dislodgement of the occluder was suspected. Her deteriorated clinical conditions warranted immediate surgery. The patient was put on a cardiopulmonary bypass (CPB) and the right atrium and the pulmonary artery were opened. Several thrombi were removed, the largest being 2 × 3 cm. The ASD occluder was identified with a thrombus attached to it and evident device-arm fracture (Figure 1). The occluder underwent almost complete healing with full endocardium covering except in the rim area. The device was removed and the ASD was repaired with a patch. Unfortunately, due to right heart failure, the patient could not be successfully weaned from the CPB, not even after an artificially created interatrial shunt, and she expired. Although one cannot say with absolute certainty that massive PTE developed because of device-related thrombosis, it seems intuitive that blood turbulence around the protruded umbrella and device-arm fracture could have acted as a nidus for repeated thrombus formation with subsequent embolization. The occluder malfunction (fracture) was most likely the result of sustained blunt chest trauma a year prior to admission. We hypothesize that the sudden increase in intrathoracic pressure during trauma as well as direct compression on the heart generated a point of high wall stress around the occluder’s septal insertion, which may have led to device fracture and dislodgment.