Pericardial clot after open heart surgery: its specific localization and haemodynamics

Transoesophageal echocardiography disclosed a localized pericardialblood clot compressing the right atrium (RA) and/or right ventricle(RV) in 15 patients suffering from low cardiac output failuresoon after open-heart surgery. The left ventricular end-diastolicdiameter was small (38.4 ± 10.1 mm) and its fractionalshortening normal (34.9 ± 10.2%). These findings suggestedcardiac tamponade as a result of pericardial clot. However,the ‘y’ trough of the RA pressure tracing was prominent,which is not characteristic of typical cardiac tamponade, butrather of constrictive pericarditis. This implies thereforethat the pathophysiology of cardiac tamponade by pericardialclot differs from that of tamponade by fluid. Emergency open-chestremoval of the pericardial clot was performed in seven patients,with good results. Pericardial clot produces low cardiac outputsoon after open-heart surgery, but its location is specificand its haemodynamics are not characteristic of cardiac tamponade.     

An autopsied case of Williams syndrome complicated by moyamoya disease

An 18 year old girl with typical clinical features of Williams syndrome suddenly died of intracerebral hemorrhage due to moyamoya disease. Autopsy revealed vascular abnormalities, such as supravalvular aortic stenosis (SAS) and an abnormal complicated cerebrovascular network in the cerebral arteries. The arterial wall of the SAS lesion consisted of thickened medial tissue showing elastic disorganization with prominence of the smooth muscle cells. The narrowed vessels of the circle of Willis showed intimal thickening with an extremely wavy internal elastic lamina and marked thinning of the media. To our knowledge, this is the first report of moyamoya disease associated with Williams syndrome.     

Indirect hemagglutination assay for antibodies to Escherichia coli lipopolysaccharides O157, O111 and O26 in patients with hemolytic uremic syndrome

We examined sera from 10 patients with hemolytic uremic syndrome (HUS) and 51 controls, with and without diarrhea, for antibodies to Escherichia coli lipopolysaccharides (LPS) O157, O111 and O26 using the indirect hemagglutination (IHA) assay. A significant rise (to a titer of ≥ 2560) in IHA antibody to O157 LPS was detected in eight of the 10 HUS patients, to O111 in two patients, one of whom showed concomitantly an antibody rise to O157, but to O26 in no patients. The IHA titers fell rapidly after the acute phase of the illness. Of the control sera 15 (29.4%) non-specifically agglutinated uncoated sheep red blood cells (SRBC) at a titer of ≥80, six (3.9%) at ≥320 and the maximum was 640. In spite of the relatively low level of non-specific agglutination the IHA appeared to be a useful screening method to identify verotoxin-producing E. coli infections at the early stage of HUS because the titers were clearly higher than non-specific agglutination and the assay is easy to perform and gives results quickly. Artificial carriers are being considered for use in place of SRBC to diminish the non-specific hemagglutination.     

Vagal Enhancement as Evidence of Residual Ischemia After Inferior Myocardial Infarction

Background: Acute inferior myocardial infarction (MI) often induces transient sinus bradycardia through vagal enhancement, known as Bezold-Jarisch reflex, which is explained by preferential distribution of vagal nerve in the inferior wall. We examined vagal activity in relation to the occurrence of residual ischemia in patients with old inferior MI and assessed its diagnostic usefulness.
Methods: Exercise myocardial scintigraphy was performed in 15 patients with old inferior MI, 19 angina pectoris (AP) patients with inferior ischemia but no MI, and 32 control subjects who had no evidence of cardiac disease. We analyzed the connection of residual ischemia in old MI with ST-segment response to exercise and with vagal activity as determined by coefficient of component variance of high frequency (CCV_HF).
Results: Exercise-induced percentage change in CCV_HF was higher in patients with old MI and residual ischemia (18.8 ± 13.5%) and AP (5.5 ± 9.7%) than old MI but no residual ischemia (–24.1 ± 4.9%) or control (–22.8 ± 4.5%, P = 0.006). Percentage change in CCV_HF > –5% had a good diagnostic value for the detection of residual ischemia in patients with old inferior MI with sensitivity of 83%, specificity of 89%, accuracy of 87%, and positive likelihood ratio of 7.50, which was higher than that of ST-segment depression (67%, 50%, 56%, and 1.33).
Conclusions: Vagal enhancement was associated with residual ischemia in old inferior MI as well as inferior AP. Measurement of CCV_HF is useful in improving the diagnostic reliability of exercise electrocardiography in patients with old inferior MI.     

Suppressive Effects of Eviprostat,a Phytotherapeutic Agent,on Lower Urinary Tract Symptoms in Prostate Cancer Patients Treated with Brachytherapy

Objectives: Eviprostat is an anti‐oxidant, anti‐inflammatory phytotherapeutic agent that is commonly used to treat lower urinary tract symptoms (LUTS) in benign prostatic hyperplasia in Japan and Germany. Prostate cancer patients treated with brachytherapy generally have complaints of LUTS for several months postoperatively. Methods: We investigated the protective effects of Eviprostat against the development of LUTS in 37 patients, who had received ¹²⁵I prostate brachytherapy as monotherapy. These patients were divided into two groups, an Eviprostat‐treated group (n = 18) and an untreated control (n = 19), whose background had no significant difference. The group treated with Eviprostat was prophylactically medicated from 3 weeks preoperatively until 3 months postoperatively. Symptom scores and quality of life for urination were evaluated according to the International Prostate Symptom Score (IPSS) and Expanded Prostate Cancer Index Composite (EPIC) on preoperative day 1, and postoperative months 1, 3 and 6. Results: Both the scores of IPSS and the levels of quality of life in EPIC were significantly worse at 1 month postoperatively compared to the pretreatment baseline, and thereafter progressively improved in both groups. Eviprostat‐treated patients showed significantly better recovery compared to Eviprostat‐untreated control at 6 months postoperatively, with respect to urinary summary score, urinary function and urinary irritation/obstruction subscales in EPIC. Moreover, the feeling of incomplete emptying in IPSS and the urinary irritation/obstruction subscale in EPIC were significantly improved at 3 months postoperatively compared to the peak impairment at 1 month in the Eviprostat‐treated group. Conclusions: It is possible that Eviprostat has the potential to ameliorate postoperative LUTS caused by brachytherapy.     

Xanthine Oxidase Inhibition Prevents Atrial Fibrillation in a Canine Model of Atrial Pacing‐Induced left Ventricular Dysfunction

Allopurinol and Atrial Fibrillation . Aims: Oxidative stress could be a possible mechanism and a therapeutic target of atrial fibrillation (AF). Xanthine oxidase (XO) inhibition reduces oxidative stress, but the effects of XO inhibitor on AF have not been evaluated. Hence, we assessed the effects of XO inhibitor, allopurinol, on progression of atrial vulnerability in dogs associated with tachycardia‐induced cardiomyopathy. Methods and Results: The dogs were subjected to atrial tachypacing (ATP, 400 bpm) without atrioventricular block for 4 weeks. The dynamics of atrial‐tachycardia remodeling were evaluated in allopurinol‐treated dogs (ALO, n = 5), placebo‐treated controls (CTL, n = 6), and sham‐operated dogs (n = 6). In CTL dogs, 4 weeks of ATP significantly increased AF duration (DAF; from 0.2 ± 0.2 seconds to 173 ± 67 seconds, P < 0.05) and decreased atrial effective refractory period (ERP; from 152 ± 9 milliseconds to 80 ± 4 milliseconds at a cycle length of 350 milliseconds, P < 0.01). Allopurinol attenuated the ATP effects on ERP (118 ± 6 milliseconds, P < 0.01) or DAF (0.6 ± 0.3 seconds, P < 0.05). In CTL dogs, ATP‐induced rapid ventricular responses decreased left ventricular ejection fraction (LVEF; from 58.6 ± 0.1 to 23.5 ± 2.4%, P < 0.01), and increased left atrial diameter (LAD; from 17 ± 1 mm to 24 ± 1 mm, P < 0.01). ATP increased atrial fibrosis when compared with sham‐operated dogs (CTL 10.7 ± 0.8% vs Sham 1.1 ± 0.3%, P < 0.01). Allopurinol suppressed atrial fibrosis (2.3 ± 0.6%, P < 0.01 vs CTL) and eNOS reduction without affecting LVEF (20.6 ± 2.2%, ns) and LAD (23 ± 1 mm, ns). Conclusion: Allopurinol suppresses AF promotion by preventing both electrical and structural remodeling. These results suggest that XO may play an important role in enhancement of atrial vulnerability, and might be a novel target of AF therapy. (J Cardiovasc Electrophysiol, Vol. 23 pp. 1130‐1135, October 2012)