[Pulmonary embolectomy for acute massive pulmonary thromboembolism after failure of thrombolytic therapy].

Acute massive pulmonary thromboembolism (PTE) is associated with an exceptionally high mortality rate and results in death if not diagnosed early and treated properly. We observed 3 cases of acute massive PTE. One of the patients had undergone a surgery for femoral neck fracture. Ten days postoperatively, she developed severe dyspnea with hypoxia, and computed tomography (CT) pulmonary angiography confirmed the PTE diagnosis. She then had cardiac arrest when catheter examination. Although emergency surgical thrombectomy was successful with good postoperative hemodynamic stability and oxygenation, the patient did not recover from the unconsciousness caused by preoperative ischemic brain damage. Subsequently, she died 6 months after surgery. Of the 3 patients, 2 suffered from right ventricular dysfunction without hemodynamic instability. They underwent open thrombectomy after the failure of conservative treatment with a systemic injection of urokinase. Both patients demonstrated a good clinical course and were discharged from hospital in a good general condition 22 and 28 days postoperatively. Herein, we review the current literature on PTE treatment. We concluded that an aggressive surgical intervention might be preferred to thrombolytic therapy for PTE patients with massive thrombosis and progressive right ventricular dysfunction.

Coronary flow reserve after coronary intervention in similar in patients with preserved viability in previous myocardial infarction and in those with angina pectoris.

The relationship between coronary flow reserve (CFR) and viability in the infarcted myocardium has not been fully clarified. We measured coronary blood flow velocity immediately after coronary intervention (with percutaneous transluminal coronary angioplasty [PTCA] or stenting) in 38 patients with previous myocardial infarction and preserved viability and 48 with angina pectoris. CFR was calculated and was similar between the two patient groups. No differences in the incidence of post-intervention CFR > 2.0 were detected; there were no differences in post-intervention CFR between patients with preserved myocardial viability and those with angina pectoris who underwent PTCA. Coronary stenting reduced the percentage diameter stenosis in both groups compared with PTCA and slightly increased the post-intervention CFR. No differences were, however, detected in post-intervention CFR between patients with preserved myocardial viability and those with angina pectoris who underwent additional stenting. These results reveal that in patients with preserved myocardial viability, post-intervention CFR was restored to values similar to those in patients with angina pectoris.

Removal of indigenous coliphages and fecal coliforms by a novel sewage treatment system consisting of UASB and DHS units.

A novel sewage treatment system, which consists of an upflow anaerobic sludge blanket (UASB) pre-treatment unit and the following downflow hanging sponge (DHS) unit for polishing up the UASB effluent, was developed as a cost-effective and easy-maintenance sewage treatment system for developing countries. A long-term experiment with actual sewage was conducted in order to evaluate its treatment efficiency of organic substances, nutrients, and pathogen indicator microorganisms such as total coliphages, F+-specific RNA coliphages (RNA coliphages), and fecal coliforms. The main objective of this paper is to investigate the removal efficiency of those indicator microorganisms by the UASB-DHS combined system. The results obtained from the continuous flow experiment indicated a fairly promising removal of the indicator microorganisms, i.e., the log10 reductions of total coliphages, RNA coliphages, and fecal coliforms (based on sewage and DHS effluent) achieved were 2.01 log, 2.02 log, and 2.57 log, respectively. The UASB-DHS combined system was superior to the conventional activated sludge process in the reduction of fecal coliforms, but in the reductions of total and RNA coliphages, the system showed somewhat less removal efficiency. The vertical reducing patterns of the indicator microorganisms along the DHS reactor were also discussed.

Use of serum creatine kinase MM isoforms for predicting the progression of left ventricular dilation in patients with hypertrophic cardiomyopathy.

Serum creatine kinase (CK) isoforms were examined to detect the progression of left ventricular (LV) enlargement with reduced motion, resembling dilated cardiomyopathy (DCM), in hypertrophic cardiomyopathy (HCM). Changes in LV indices were determined annually by echocardiography in 51 patients until serum measurements (first follow-up period, 6.5 +/- 2.2 years). Serum creatine isoforms (CKMM1, CKMM2 and CKMM3) were measured with high-voltage electrophoresis in 35 of these patients from 1991 to 1992, and the data for these latter patients are reported here. Serum total CK, CKMB, lactate dehydrogenase and its isoenzyme LDH1 were also measured. The changes in LV indices were further monitored until January, 1995 (second follow-up). During the 2 follow-up periods, the patients in the on-going group showed a reduction in the LV ejection fraction (LVEF) to < 55% with LV end-diastolic dimension (LVDd) < 55 mm, and those in the DCM-like group showed a reduction in LVEF to < 55% and an increase in LVDd to > 55 mm. During the first follow-up period, LVEF and LVDd remained at > or = 55% and < 55 mm, respectively, in 26 patients (nonprogressive-disease group), while 3 patients entered the on-going group and 6 entered the DCM-like group. The CKMM3/CKMM1 ratios in the on-going and DCM-like groups were significantly higher than those in the control and nonprogressive-disease groups. The CKMM3/CKMM1 ratio was significantly correlated with the annual rate of change for the LV end-systolic dimension (LVDs), LVDd, and LVEF, with the closest correlation observed for the annual change in LVDs. Moreover, 5 patients in the nonprogressive-disease group with elevation of the CKMM3/CKMM1 ratio to > + 2SD above the mean for the controls had an elevated annual change in LVDs within +/- 1SD of the mean in the DCM-like group. These results indicate that the ratio of CKMM3 to CKMM1 can be used to predict the progression of LV enlargement in HCM.

Effects of adenosine triphosphate on wide QRS tachycardia. Analysis in 18 patients.

A few studies have indicated that adenosine terminated triggered-activity idiopathic ventricular tachycardia, but all involved a small number of cases. The effects of adenosine triphosphate (ATP) on wide QRS tachycardia have thus not yet been completely clarified. This retrospective study was performed to evaluate the therapeutic and diagnostic utility of ATP in wide QRS tachycardia. A total of 18 patients with wide QRS tachycardia (QRS width > 120 msec, rate > or = 150 beats/min) were evaluated. ATP, 20-40 mg, was administered intravenously. An electrophysiological study and treadmill stress test were performed in all patients to elucidate the mechanism of the tachycardia. ATP terminated tachycardia or induced atrio-ventricular block in all 6 patients who had supraventricular tachycardia, but it had no effect on preexcited atrial fibrillation or pre-excited atrial flutter. Ventricular tachycardia was terminated by ATP in 5 of the 10 patients. In 4 of these 5 patients, the focus of the tachycardia was the right ventricular outflow tract. No entrainment phenomenon was demonstrated by electrophysiological study with induction of the tachycardia by stress test or isoproterenol infusion, suggesting the contribution of triggered activity to the tachycardia. In the remaining patient with complete right bundle branch block type tachycardia with right axis deviation, the mechanism of ventricular tachycardia could not be determined. In the 5 patients in whom ATP failed to terminate ventricular tachycardia, the reentry mechanism was suggested by the presence of entrainment phenomenon depicted on electrophysiological study. In summary, this study suggests that ATP terminates supraventricular wide QRS tachycardia and ventricular tachycardia due to triggered-activity, but that it has no effect on pre-excited atrial fibrillation or flutter or on ventricular tachycardia due to a reentry mechanism. These findings add to the mounting evidence regarding the therapeutic and diagnostic utility of ATP in wide QRS tachycardia.

[Preventive effect of pravastatin on restenosis following coronary angioplasty: prospective randomized trial].

This study investigated the preventive effect of pravastatin on restenosis following successful transluminal coronary angiography (PTCA) in 109 consecutive patients. Patients were randomly and prospectively assigned to the pravastatin group (group P, n = 57) or the control group (group C, n = 52). The former received 10 mg/day pravastatin from the day of PTCA for 3 months. Restenosis was defined as a > or = 50% diameter stenosis at follow-up angiography with a > or = 15% reduction in luminal diameter compared to post-PTCA. The effect of pravastatin was analyzed in association with 7 clinical and 15 angiographic factors. Follow-up rate, serum lipid levels (total cholesterol, triglyceride, and HDL-cholesterol), and clinical and angiographic backgrounds except age and angularity of the lesions were not significantly different between the two groups at PTCA. Three months later, total cholesterol decreased from 222.3 +/- 35.1 to 179.2 +/- 31.2 mg/dl in group P, but was unchanged in group C (from 226.0 +/- 33.7 to 211.7 +/- 30.9 mg/dl). The restenosis rate was not different between the two groups (35.6 vs 35.7% per patient, 32.0 vs 33.3% per lesion). Moreover, no relationship between restenosis rate and serum total cholesterol level at follow-up angiography was observed. Multivariate analysis, including 7 clinical and 15 angiographic factors, found neither pravastatin administration nor serum lipid levels were significantly correlated with decreased luminal diameter. Pravastatin (10 mg/day) did not reduce the incidence of restenosis after PTCA when administered from the day of PTCA for 3 months.