Irreversible Cardiogenic Shock Research Articles

SAT475 Levothyroxine and Liothyronine Treated Myxedema Coma with Irreversible Cardiopulmonary Failure: A Rare Phenomenon

Abstract Disclosure: T. Menon: None. Y. Xie: None. A. Wang: None. Introduction: We describe a case of myxedema coma associated with irreversible cardiogenic shock and the challenges in optimal management. Case Presentation: A previously healthy 23-year-old man with a history of untreated hypothyroidism (TSH 100 uIU/mL six months prior) presented to the hospital for abdominal pain, shortness of breath, and cough. He soon had two cardiac arrests with successful resuscitation and was stabilized via mechanical ventilation and vasopressors. Physical exam showed peripheral and facial edema with mild jaundice. Laboratory results showed elevated creatinine 1.73 (0.5-1.30 mg/dL), AST 440 (10-40 U/L), ALT 353 (10-45 U/L), and total bilirubin 3.6 (0.2-1.2 mg/dL). Thyroid function tests showed TSH 857 (0.27-4.20 uIU/mL), FT4 <0.1 (0.9-1.8 ng/dL), and TT3 < 20 (80-200 ng/dL), and negative thyroglobulin and TPO antibodies. A thyroid ultrasound showed a small thyroid gland. Echocardiogram revealed severe bi-ventricular failure, with an ejection fraction of 10-15%, dilated chambers, pulmonary hypertension, and moderate pericardial effusion. The patient was initiated on VA-ECMO and treated medically for cardiogenic shock. Myxedema coma treatment was started with IV levothyroxine (LT4) 400 mcg, IV Liothyronine (LT3) 10 mcg, and IV hydrocortisone 100 mg every eight hours. The patient subsequently received IV LT4 100 mcg daily and IV LT3 10-30 mcg daily based on levels of daily FT4 and TT3. Hydrocortisone was tapered down as free cortisol levels prior to steroid administration were elevated at 4.6 (0.2-1.8 ug/dL). Despite significant improvements in TSH values (from 857 to 67 uIU/L), FT4 (from <0.1 to 1.2 ng/dL), and TT3 (from < 20 to 60 ng/dL), the patient’s cardiac function did not improve and he underwent successful orthotopic heart transplantation two weeks after initial presentation. A cardiac biopsy demonstrated cardiomegaly with left ventricular hypertrophy, subendocardial fibrosis, and patent arteries, without other etiologies of heart failure. The patient recovered and was discharged on oral LT4 137 mcg daily, LT3 5 mcg twice daily, and prednisone per cardiac transplantation protocol. Discussion: Several cases describe myxedema coma with reversible heart failure in 4 to 5 days with appropriate hypothyroidism treatment. This case, however, describes irreversible cardiomyopathy despite optimal medical therapy, eventually requiring heart transplantation. Because the cardiac myocyte is dependent on plasma T3 due to lack of intracellular deiodinase, T3 administration may improve cardiac function in myxedema coma induced heart failure. Consensus regarding the use, optimal dose, and duration of LT3 in these situations requires further investigation. Conclusion: We report an unusual case of irreversible cardiomyopathy due to myxedema coma in a young, healthy patient, highlighting the need for rapid correction of hypothyroidism with both IV LT4 and LT3. Presentation Date: Saturday, June 17, 2023

Filamentous fungal infection in burned patients: retrospective study.

Infections are the most frequent complications in burn patients. Filamentous fungi have an uncertain place within the statistics, since in our media data regarding their prevalence, causal agents and outcome of those who suffer them remain scarce. The aim of this study was to evaluate the prevalence of fungal infection by filamentous fungi (IHF) in patients hospitalized in burn intensive care unit (BICU), and to review clinical, epidemiological, microbiological and evolutionary characteristics of these patients and to know the frequency and distribution of the isolated fungi. Retrospective and descriptive study. It includes all individuals admitted in burns intensive care unit (2012-2015), with positive culture for filamentous fungi in skin biopsies and bedsores. A total of 168 patients were admitted in the BICU in a period of 3 years. 90% were major burned and 17% of them developed IHF (29/168). Aspergillus spp (24%), Fusarium sp (14%), Mucor spp (3%) and various black fungus genera (58%) were the main genera found in cultives. About 24% of the patients with IHF died and Fusarium spp was found in 50% of the cases. The cause of death was irreversible cardiogenic shock with multiorgan failure. Filamentous fungal infection was present in 17% of burned patients. The main isolatte fungi in samples were dematiaceous mould. Mortality among patients was 24%, with Fusarium being the fungus found in the highest number of deaths (50%).

Takotsubo cardiomyopathy after severe emotional stress: a case report and a brief literature review

The goal: Takotsubo cardiomyopathy is recognized as an important differential diagnosis of acute myocardial infarction. It is characterized by a transient systolic dysfunction of apical, mid or basal segments of the left ventricle with an absence of obstructive coronary artery disease. Despite a rapid onset and severity of symptoms, it is considered to be a relatively benign condition with swift resolution of symptoms and wall motion abnormalities, even though it may have complicated clinical course and lead to mortal outcome. Our aim was to present a patient under severe emotional stress in which the clinical course was complicated with an irreversible cardiogenic shock. Results: A 78-year-old woman was presented with signs and symptoms of acute heart failure. The ECG and laboratory findings lead to suspect on ST elevation myocardial infarction. Coronarography excluded the acute myocardial infarction and left ventriculography indicated takotsubo cardiomyopathy as a cause of the existing symptoms. Despite the intensive treatment, respiratory insufficiency and irreversible cardiogenic shock developed and in five days the patient succumbed to the illness. Conclusion: Takotsubo cardiomyopathy has a benign clinical course in the most of the cases, which leads to a total recuperation of the systolic function and resolution of symptoms. Complications such as cardiogenic shock are rare. In this case we present a patient with irreversible cardiogenic shock as a rare complication of Takotsubo cardiomyopathy.

Editorial Comment: Acute myocardial infarction and refractory cardiogenic shock: the simpler, the better?

The excellent report by the Mount Sinai Medical Center Group [1] supports the concept of an immediate primary implantation of a long-term ventricular assist device (VAD), in patients in refractory cardiogenic shock because of an acute myocardial infarction (AMI). This primary implantation is probably preferable to more complex strategies, including the ‘bridge-to-bridge’ approach. It may be quite surprising that, after more than 30 years of experience, we are still wondering about the best option in these patients. The probable reason is that few papers focus on the specific issues of these AMI patients. There is actually still a wide variety of options. The most appealing option is the use of very small intraventricular devices (Tamdem, Impella ... ). They may be implanted with a non-invasive technique, under local anaesthesia, and even by the cardiologists who see the patients first and who try to apply some effective treatment such as percutaneous interventions. The device, ideally, should achieve full left ventricular decompression and deliver a pump output meeting the patient’s needs, so as to allow the recovery of peripheral organ function. The return to an adequate arterial pressure improves the coronary circulation, permitting some improvement of left ventricular function. Good left ventricular decompression enables the limitation of the acute myocardial infarct, by recovery of the borderline ischaemic myocardium. However, we currently lack this tiny pump that permits full left ventricular decompression and a return to normal aortic pressure. The available systems do not meet the requirements, in terms of ventricular decompression and pump flow. Moreover, they are also beset by other problems: difficulty in inserting the pump head into the left ventricle either from a peripheral artery, which is often atherosclerotic, or from a peripheral vein, since trans-septal catheterization may be hazardous in these unstable patients. Few papers have reported good results of this elegant approach. However, good results are usually seen in patients with less severe disease [2]. Finally, until now, we may say that great expectations have not been met. A second approach, totally different in its concept, is the use of extracorporeal membrane oxygenation (ECMO). The main advantages of this option are well known: it may be used almost everywhere, even outside a specialized centre, quite rapidly, without any surgical intervention, and is inexpensive. ECMO can therefore be instituted very early in the course of severe AMI. However, experience has shown that ECMO in AMI patients in cardiogenic shock does not fulfil the objectives as well as expected: the death rate during ECMO is quite high, whereas a low rate is quite seen in patients who can be stabilized or improved and receive a long-term VAD. The cost of ECMO also rises rapidly as the time spent in the intensive care unit increases. These less than satisfactory results are actually not that surprising: during ECMO, left ventricular unloading is less than optimal, making pulmonary recovery very unlikely, and right ventricular unloading is most often less than optimal, leading to persistent high venous pressure, which is unfavourable for the recovery of hepatic and renal function. In addition, activation of the inflammatory cascade, which is already stimulated by AMI, does not facilitate the recovery of pulmonary function. Finally, the lack of pulsatility does not help to improve renal and peripheral function. It is interesting to emphasize that the best results using ECMO support in irreversible cardiogenic shock are obtained in patients in whom cardiogenic shock is linked to reversible myocardial damage related, for example, to a toxic aetiology or acute myocarditis [3]. Results in AMI patients are less favourable: 5 of 16 AMI patients receiving urgent ECMO are discharged from the hospital, compared with a 56% overall success rate. Because of its simplicity and apparent low cost, ECMO is nevertheless still performed routinely, almost as a routine first treatment in patients in cardiogenic shock. However, in AMI patients, ECMO actually minimizes the chances of the patients getting a long-term VAD or a transplant. Our personal findings even show that replacement of ECMO by a pulsatile bi-VAD may reverse a situation, which is deteriorating on ECMO. A third approach is the use of pulsatile, paracorporeal VADs. The advantages of this technique are the quality of ventricular decompression, which is almost always complete and the rapid return to normal pulsatile perfusion. The versatility of the system permits either a left VAD or, in the case of additional right ventricular dysfunction, which is frequent in major AMI, temporary right ventricular support. This right ventricular support may be as short as a few days, permitting the recovery of right ventricular function and, in the meantime, avoiding the pulmonary embolic complications of long-term use. The limitation of this approach is obviously the discomfort of a long-term period of

Advanced treatment strategies for acute pulmonary embolism, including thrombolysis and embolectomy.

The optimal treatment strategy for acute pulmonary embolism relies upon a multidisciplinary team that rapidly assesses available data, performs additional testing if necessary, weighs treatment options, and recommends an appropriate therapeutic plan to the patient and family. Round-the-clock availability is imperative. Centers that specialize in pulmonary embolism management offer a wide range of therapeutic options. Hospitals with more limited facilities should establish pulmonary embolism patient referral and transfer contingency plans that can be activated at a moment's notice. Management options include anticoagulation alone, thrombolysis plus anticoagulation, insertion of an inferior vena caval filter, catheter embolectomy, or surgical embolectomy. The decision-making process requires accurate risk stratification, which is comprised of several crucial components: clinical evaluation that includes history and physical examination, biomarker measurement especially of troponin, as well as assessment of right ventricular size and function based upon chest CT scanning and echocardiography. The 'old school' approach of declaring a benign prognosis based solely upon the presence of normal systemic arterial pressure can delay advanced therapy until after the onset of irreversible cardiogenic shock. We have now formulated a more contemporary, comprehensive, and multifaceted strategy to prognosticate. Our 'new approach' uses advanced treatment strategies in addition to anticoagulation for those pulmonary embolism patients deemed to be at high risk for a poor outcome.

The TandemHeart®, percutaneous transseptal left ventricular assist device: a safeguard in high-risk percutaneous coronary interventions. The six-year Rotterdam experience

Percutaneous coronary interventions (PCI) in high-risk cardiac patients are preferentially referred to specialised myocardial intervention centres (MIC). Included in this group are patients with a haemodynamic collapse or high likelihood of haemodynamic collapse, either during balloon inflation or with acute vessel closure. The TandemHeart, a percutaneous transseptal left ventricular assist (PTVA) that can be introduced using standard catheterisation laboratory techniques, offers interesting perspectives to reduce procedural risks. Between September 2000 to July 2006, The TandemHeart, supported the circulation of 23 patients (age: range 46-74, mean 59) admitted to our centre for high risk, either emergency or elective, PCI. Successful implantation was achieved in 100% of patients. The mean time for implementation of circulatory support was 35 minutes (range 16-62). The index PCI was successful in all patients except two. A pump flow up to 4L/min was achieved with significant reduction of left ventricular filling pressures, pulmonary capillary wedge pressure and with significant increase of systemic arterial pressures. Duration of support ranged from 1-222 hours (mean 31+/-49.8 hours). Five patients died with the TandemHeart in place, four of whom were in irreversible cardiogenic shock at admission. Mild to moderate access site bleeding was seen in 27% of patients. One patient experienced a loge syndrome of the leg. Core temperature (Ct) decreased to <36.5 degrees C in six patients, profound hypothermia (Ct <35 degrees C) was observed in two patients. There was no technical device failure. The TandemHeart - PTVA provides effective, total left ventricular support in very high risk PCI settings. The rate of device related cardiac and vascular complications was acceptable.

Tako-tsubo-like left ventricular dysfunction: transient left ventricular apical ballooning syndrome

This review examines the 'tako-tsubo-like' syndrome or transient left ventricular apical ballooning. The aim of this review is a complete evaluation of epidemiology, clinical and instrumental features, pathophysiological mechanisms, therapy and prognosis of this syndrome. We have evaluated the data from literature for a comprehensive consideration of multiple aspects of this syndrome. Transient left ventricular apical ballooning typically affects women, and the clinical presentation is comparable to acute coronary syndrome with chest pain or sudden dyspnoea, changes in ECG and elevated cardiac enzymes in the absence of significant coronary stenosis, with complete resolution of wall-motion abnormalities in a period of days or weeks. This syndrome is triggered by marked psychological or physiological stress. Several pathophysiological mechanisms have been proposed, such as cathecolamine-mediated cardiotoxicity, abnormalities in coronary microvascular function and multivessel coronary vasospasm. The highest incidence of transient left ventricular apical ballooning is in the Japanese population, but it has been recently identified also in the USA and Europe. Treatment is empirical and supportive. The prognosis is generally favourable, although some deaths have been reported, usually the result of irreversible cardiogenic shock, refractory ventricular arrhythmias, or other catastrophic cardiovascular event. We conclude by emphasising the importance of a more deeper knowledge of this syndrome for general physicians and cardiologists and it should be often considered as a possible diagnosis occurring in emergency department and in patients admitted in the Chest Pain Units with a diagnosis of coronary acute syndrome.

Implantation of Cardio West Total Artificial Heart for Irreversible Acute Myocardial Infarction Shock

Patients who develop cardiogenic shock after acute myocardial infarction have a very high mortality rate despite early reperfusion therapy. Hemodynamic stabilization can often only be achieved by implanting a mechanical circulatory support system. When, in cases representing expansive myocardial impairment without any chance of recovery, pharmacological therapy and the use of percutaneous assist devices have failed, the implantation of a total artificial heart is indicated. We report our first experiences with this extensive and innovative method of managing irreversible cardiogenic shock patients. The CardioWest total artificial heart was implanted in 5 patients (male; mean age, 50 years). All patients were in irreversible cardiogenic shock despite maximum dosages of catecholamines, an intra-aortic balloon pump and/or a femoro-femoral bypass. In all patients early reperfusion therapy was performed. After implantation of the Cardio West system, all dysfunctional organ systems rapidly recovered in all patients. Four of 5 patients underwent successful heart transplantation after a mean support time of 156 days. One patient died because of enterocolic necroses caused by an embolic event after termination of dicumarol therapy. In summary, our first experiences justify this extensive management in young patients who would otherwise have died within a few hours.

Acute Pulmonary Embolism: Risk Stratification

The death rate from acute pulmonary embolism (PE) exceeds the mortality rate for acute myocardial infarction. Risk stratification helps optimize the selection of those patients who will benefit from more aggressive therapy, such as thrombolysis or embolectomy, in addition to anticoagulation. The classic paradigm was to observe patients deteriorate and to attempt to maintain acceptable hemodynamics by starting vasopressors. If hemodynamics failed to improve or if cardiogenic shock persisted, thrombolysis or surgical embolectomy was considered. Sadly, this "watch and wait" approach often resulted in irreversible cardiogenic shock and multisystem organ failure. The new approach hinges upon rapid and accurate risk stratification. There are four features of this strategy: 1) clinical evaluation, 2) bedside nonimaging tests-electrocardiography and pulse oximetry, 3) imaging tests-echocardiography and chest computed tomography,and 4) cardiac biomarkers-such as the troponin level. When high-risk patients are identified,they can be triaged for urgent or emergent therapy, usually prior to developing overt hypotension and cardiogenic shock.

Triple Bridge-to-Transplant in a Case of Giant Cell Myocarditis Complicated by Human Leukocyte Antigen Sensitization and Heparin-Induced Thrombocytopenia Type II

Bridge-to-bridge experience has documented the feasibility of a switch from short-term to long-term mechanical circulatory support until heart transplant. We describe a case of irreversible cardiogenic shock due to giant cell myocarditis treated consecutively with extracorporal membrane oxygenation, bi-ventricular assist device, and total artificial heart. The postoperative course was complicated by human leukocyte antigen sensitization and heparin-induced thrombocytopenia type II. Our patient successfully underwent heart transplant after 10 months of support and was discharged in good condition. This case illustrates suitable device selection for myocarditis and represents two treatable immunological complications.

Imminent Pulmonary Embolism: A Fatal Mobile Right Atrial Thrombus

Right sided heart thrombi are infrequent and if they are mobile they may cause serious morbidity and mortality due to massive pulmonary embolism or paradoxical embolism. Malignancies are one of the important etiological factors for right heart thrombi. A patient with operated but recurrent ovarian carcinoma, presented with symptoms of heart failure was admitted to oncology department. Rapidly progressing dyspnea and a pre-syncope attack required consultation of a cardiologist and echocardiography revealed a mobile thrombus in the right atrium. Urgent open heart surgery was decided but imminent massive pulmonary embolism complicated the case leading to irreversible cardiogenic shock. By means of the presented case this paper overviews etiological factors and treatment options for right sided heart thrombi.

Spontaneous coronary artery dissection mimicking aortic dissection

A 51-year-old woman suffered rapidly irreversible cardiogenic shock with left hemiparesis. Transesophageal echocardiography, which represents an essential imaging tool in the emergency room, ruled out aortic dissection involving branch vessels but did not allow an in vivo diagnosis of spontaneous coronary dissection. The in vivo diagnosis of spontaneous coronary dissection is rather difficult because of the dramatic clinical presentation and selective coronary angiography requirement.

Acute myocardial infarction with cardiogenic shock: treatment with mechanical circulatory assistance and heart transplantation

Summary The mortality of cardiogenic shock (CS) after an acute myocardial infarction (AMI) still remains high. Thrombolysis, PTCA or CABG, when possible, can improve the results, but when all the treatments fail death is almost certain. Objective We investigate the use of the mechanical circulatory assistance (MCA) and heart transplantation (HT) to improve the adverse results in this irreversible situation. Methods Among 11 patients with irreversible CS after an AMI we used a MCA (Abiomed BVS-5000). After improvement and hemodynamic stabilization, we performed heart transplantation in 7 patients of mean age 52 years (35–60) including two women. The MCA was univentricular in 7 patients and biventricular in 4. Mean duration of the MCA was 5 days (1–12). Results Three patients died during the MCA: two due to cerebrovascular accidents and one multiorgan failure. Weaning was possible in one patient. Among Seven transplanted patients one died due to sepsis. Seven (64%) patients are long-term survivors. Conclusion When all the treatments have failed for CS after an AMI, MCA may be used as a bridge to heart transplantation in a select group of patients where the procedure is not contraindicated. The long-term results of 64% survivors in our experience is satisfactory.

Myocardial adenine nucleotides, glycogen, and Na,K-ATPase in patients with idiopathic dilated cardiomyopathy requiring mechanical circulatory support

Acute decompensation leading to progressive pump failure is a main cause of death in patients with congestive heart failure. To find possible metabolic defects associated with the onset of this fatal occurrence, we measured myocardial adenine nucleotides, glycogen, and Na,K-ATPase in patients with end-stage idiopathic dilated cardiomyopathy. The biopsy specimens were obtained from the right ventricle of beating hearts during implantation of a biventricular assistance device in 23 patients (group I) suffering from irreversible cardiogenic shock and during heart transplantation in 20 patients (group II) in compensated heart failure. Left ventricular ejection fraction (LVEF) was determined preoperatively by echocardiography. Left ventricular function in group I was more severely impaired than in group II (LVEF 16.8% ± 4.6% vs 22.1% ± 5.1%; p <0.01). Myocardial adenosine triphosphate (ATP) in group I was significantly reduced in comparison with group II (19.4 ± 10.2 vs 27.7 ± 7.4 nmol/mg noncollagen protein; p <0.01). There was no difference in glycogen levels. Na,K-ATPase concentration in group I (n = 8) was lower than that of group II (n = 20) (425 ± 80 vs 498 ± 75 pmol/g wet weight; p <0.05). Linear regression analyses showed a significant correlation between adenosine triphosphate (ATP) and LVEF (r = 0.41, p <0.01) and between Na,K-ATPase and LVEF (r = 0.55, p <0.01). These results indicate that loss of myocardial ATP and Na,K-ATPase could partially contribute to the development of spontaneous deterioration of the chronically overloaded heart.

Inhaled Nitric Oxide Is Unlikely to Have Contributed to the Death of a Young Woman Suffering From Primary Pulmonary Hypertension-Reply

Morris is partly right. We do not have definite direct evidence that our patient's death was caused by the effects of inhaled nitric oxide therapy. 1 Therefore, we wrote: It is suggested that this [decrease of blood pressure probably due to nitric oxide] provoked an irreversible cardiogenic shock. Thus, inhaled nitric oxide may be dangerous.... The severely disturbed hemodynamics of our patient remained stable before nitric oxide was administered during the first 15 hours after insertion of the pulmonary and radial artery catheters. Then, after institution of the inhaled nitric oxide therapy, her circulation deteriorated progressively with clear peripheral vasodilatation until she died 11 hours later. In the study of Wessel et al 2 cited by Morris and us, inhaled nitric oxide increased the plasma levels of vasodilatatory systemic cyclic guanosine monophosphate. In that investigation, nitric oxide also decreased mean blood pressure significantly by 7% (from 65.8 to 60.9 mm

Hemofiltration as treatment for patients with refractory heart failure.

Hemofiltration was performed in 15 patients with refractory congestive heart failure. All of these patients had oliguria, although intensive treatment with diuretics, digitalis, vasodilators, and catecholamines was prescribed. Hemofiltration was performed under hemodynamic monitoring in 14 patients. The water removal by hemofiltration decreased pulmonary arterial pressure, pulmonary capillary wedge pressure and right atrial pressure. Despite these hemodynamic improvements, nine patients (60%) died within one month after the start of hemofiltration; the causes were fatal arrhythmia in three, renal failure in two, sepsis in one and irreversible cardiogenic shock in three. Oliguria for over 15 h or a serum creatinine concentration of more than 4.0 mg/dl at the start of hemofiltration related to poor prognosis. In view of these results, hemofiltration for refractory heart failure should be started earlier and performed carefully in order to avoid arrhythmia, cardiogenic shock, and other complications.

Will emergency coronary bypass grafting after failed elective percutaneous transluminal coronary angioplasty prevent myocardial infarction?

An emergency aorto-coronary bypass grafting operation was performed within 12 hours after the development of acute myocardial ischemia due to partial or complete vascular occlusion in 34 of 950 (3.6%) patients who had received elective percutaneous transluminal coronary angioplasty (PTCA). Of the 34 patients, three (= 8.8%) died postoperatively in irreversible cardiogenic shock. Half of the surviving patients developed a Q-wave infarction after the operation, whereas the other half remained without transmural infarct. With comparable clinical data and times of operation up to placement of the aorto-coronary bypass vessel, an adequate residual perfusion must still have been present in the cases with non Q-wave infarction. Since in many cases a myocardial necrosis is unavoidable despite relatively early operative revascularization, the decisive role will be played by the remaining perfusion of the vessel concerned and any collaterals. It follows that treatment of an early PTCA complication, occurring in the catheter laboratory, ought to be the earliest possible aorto-coronary bypass operation unless available cardiological methods can reliably assure reperfusion. Treatment of a PTCA complication occurring later, however, e.g. after hours in the intensive-care unit, should be a repeat PTCA attempt: surgery at this stage will not prevent the transmural infarction but will increase risk of lethal complications.

Acute reocclusion during percutaneous transluminal coronary angioplasty: Immediate and long‐term outcome

Acute total occlusion of a coronary artery during percutaneous transluminal coronary angioplasty (PTCA) has previously resulted in emergency surgical intervention (CABG). We retrospectively surveyed 211 elective procedures and 65 procedures for acute myocardial infarction (AMI). There were 42 patients (pts) [29 elective (14%) and 13 AMI (20%)] in whom total occlusion occurred after initial dilation had been achieved. In 30 of 42 pts reangioplasty successfully reperfused the vessel. Ten patients (24%) required CABG and two (5%) were treated medically for AMI. Death occurred in 2 pts due to irreversible cardiogenic shock despite successful angioplasty. After 6 months follow-up 22 pts remained asymptomatic. It is concluded that aggressive redilation of total occlusions which develop during PTCA will frequently result in a successful angioplasty with a long-term restenosis rate comparable to uncomplicated angioplasty.

Fatal cardiac arrhythmias and shock following yew leaves ingestion

A 40-year-old woman presented with vomiting and abdominal pain following voluntary ingestion of 150 yew leaves. She developed ventricular conduction defects and arrhythmias unresponsive to medical treatment after admission. She expired five hours after yew ingestion from irreversible cardiogenic shock. More attention should be given to this rare but severe intoxication for which no effective therapy is known.

Effect of thiopental therapy on cerebral blood flow after total cerebral ischemia.

The effect of barbiturate coma upon regional cerebral blood flow (RCBF) and ultimate neurologic outcome was examined after total cerebral ischemia (TCI). TCI was induced in dogs using a relatively noninvasive double-occlusion balloon technique; cardiopulmonary protection was provided during the period of ischemia. RCBF was measured using 15-mu radioactively labeled microspheres. A reproducible pattern of impaired reperfusion of the central nervous system (CNS) was observed in control animals after the restoration of cerebral perfusion pressure after TCI. This pattern was accentuated by the administration of pentothal to induce barbiturate coma. The additional depression in RCBF in those animals receiving pentothal was most prominent in cortical gray matter and brainstem structures at 3 and 6 h after TCI. It was also observed in cortical white matter. No untreated animal surviving TCI achieved a neurologic functional level better than persistent vegetative (decerebrate) survival over 1 wk of observation. Animals receiving 90 mg/kg body weight of pentothal post-TCI demonstrated irreversible cardiogenic shock related to the myocardial depressant effect of the drug. Animals receiving 40 to 60 mg/kg of pentothal post-TCI demonstrated a survival rate similar to that of untreated animals. Although this study did not establish the possible effectiveness of barbiturate coma in improving residual neurologic damage after TCI, the data do demonstrate that any possible effectiveness in this model is not associated with any improvement in the markedly decreased cerebral perfusion after TCI.