Unroofed coronary sinus associated with atrial septal defect and significant mitral regurgitation.
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Biomedical subjects
Publications and source records attributed to J M Bennett.
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Identification and modification of risk factors for cardiovascular disease can be carried out effectively in the workplace. Coronary artery disease is multifactorial. A cardiac exercise program conducted by the occupational health nurse should serve as a catalyst for modification of all coronary risk factors. Employers have begun to value and support worksite cardiac rehabilitation programs because of the benefits of health care cost avoidance, increased attendance and productivity at work, and improved employee relations. It is the responsibility of the occupational health nurse and other health care providers to see that this continues.
Numerous morphologic features have been described in bone marrow and peripheral blood in myelodysplastic syndrome (MDS). We draw attention to a high incidence of a subtle morphologic feature, internuclear bridging (INB), not previously recognized as a morphologic feature in MDS. The occurrence of INB in MDS suggests an underlying abnormality of mitotic division that could explain the impaired production of hematopoietic cells, the addition and deletion cytogenetic changes, and the stepwise disease progression and cytogenetic progression characteristic of MDS. Lack of awareness that INB occurs in MDS may cause confusion of MDS and congenital dyserythropoietic anemia type I, a congenital process also characterized by INB.
Two cases of sudden cardiac death during ambulatory ECG monitoring, each with an episode of torsade de pointes as part of the terminal dysrhythmia, are reported. In the first case, pause-dependent changes of the TU waves favour early after-depolarisations and triggered activity as the initiating mechanism of torsade. Quinidine therapy was probably an aggravating factor. Torsade was not initiated in a pause-dependent fashion in the second patient, who had ECG evidence of an episode of ischaemia as trigger for the terminal dysrhythmia. Both patients had impaired left ventricular function and underlying coronary artery disease.
Thirty-three patients with acute inferior myocardial infarction (MI), who were treated with intravenous streptokinase, were studied by serial 12-lead ECGs for 48 hours to determine the relationship between early changes in the sum of elevations above the baseline 40 ms after the end of the QRS complex in leads II, III and AFV (SumST), the sum of amplitude of R waves in leads II, III and AVF, the sum of the Q waves in leads II, III and AVF, the sum of ST-segment depression in leads V1-V4 as measured from the baseline to 80 ms after the J point (SumST (V1-V4] and the patency of the infarct-related artery at angiography after MI. Patients with patent arteries had a faster rate of decline in the SumST during the first 2.5 hours; reached the steady state earlier; had a more pronounced decrease in the SumST at 1.25 hours; a larger percentage drop in SumR at 4.5 hours and a more pronounced SumST (V1-V4) early on but resolution times similar to that of patients with closed arteries. Several ECG indices may indicate reperfusion of the infarct-related artery in patients with inferior MI.
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This case report concerns a patient who initially presented with an apparent congenital left ventricular aneurysm with successful aneurysmectomy. The patient had a recurrence of the aneurysm and, at reoperation, the diagnosis of cardiac tuberculosis was made.
A patient with exertional angina pectoris and an arterial fistula of the left anterior descending artery is reported. After successful embolization of the fistula, the anginal symptoms disappeared and the exercise stress test normalized.
Seventeen elderly patients with acute nonlymphocytic leukemia (EP-ANLL) were treated with cytarabine, either 1.5 g/m2 or 2.0 g/m2 q 12 h for 4 days [attenuated high-dose ARA-C (HDARAC)]. One complete and one partial response was seen in 15 evaluable cases. Toxicity, evaluated in all 17 patients, was severe, with 47% showing a variety of Eastern Cooperative Oncology Group grade 3, 4, or 5 toxicities. Forty-one percent of all patients died within 33 days of initiating treatment. We conclude that attenuated HDARAC is ineffective in inducing remission and is very toxic in the EP-ANLL.
We have studied aminoglutethemide (AG) combined with hydrocortisone in 28 patients with advanced and refractory prostate carcinoma. All the patients had failed at least one endocrine therapy. Six patients received only one prior hormonal treatment. Five patients were off study within 3 weeks due to early death and toxicity, 14 had progressive disease, and 9 had stable disease. No objective partial remission was observed, but the nine stable patients had therapeutic benefit, with improvement in bone pain and performance status for a median duration of 153 days. Three patients withdrew because of postural hypotension, dizziness, weakness, and lethargy. The median survival of the entire group was 186 days (range 41-606 days). Our results suggest that aminoglutethemide and hydrocortisone can be an alternative treatment for patients with advanced and refractory prostate carcinoma.
Peripheral blood, bone marrow films, and bone marrow biopsy specimens from 110 patients, well characterised by clinical and laboratory studies, including electron microscopy, were reviewed, to determine proposals for the classification of chronic (mature) B and T cell leukaemias. On the basis of cytology and membrane phenotype the following disorders were defined: (i) B cell type: chronic lymphocytic leukaemia (CLL); CLL of mixed cell type, which includes cases with more than 10% and less than 55% prolymphocytes (CLL/PL), and a less well defined form with pleomorphic lymphocytes but less than 10% prolymphocytes; prolymphocytic leukaemia (PLL); hairy cell leukaemia (HCL); HCL variant; splenic lymphoma with circulating villous lymphocytes; leukaemic phase of non-Hodgkin's lymphoma (follicular lymphoma, intermediate, or mantle zone lymphoma and others); lymphoplasmacytic lymphoma with peripheral blood disease (mostly Waldenström's macroglobulinaemia); and plasma cell leukaemia. (ii) T cell type: T/CLL, which was differentiated from reactive T/lymphocytosis; T/PLL; adult T cell leukaemia/lymphoma; and Sézary's syndrome. The recognition of distinct entities within the B and T cell leukaemias seems to have clinical and epidemiological connotations. It is hoped that these proposals may serve as the basis for further work, discussion, and improved management of patients.
One thousand four hundred sixty patients with 2,590 patient-years of follow-up were treated on 15 protocols for metastatic breast cancer with dibromodulcitol (mitolactol; DBD)-containing regimens since 1976. Twenty-three patients developed myelodysplastic syndrome (MDS) and/or acute nonlymphocytic leukemia (ANLL). The overall risk of developing MDS or ANLL per person is 1.6%. In patients who had received more than 16,000 mg of DBD the risk per person is 6%, and in the high-dose subsets of patients who received no prior radiation or alkylator therapy, it is 7.9%. The risk per person increases to a maximum by 30 to 36 months (5.3%). The high risk was seen despite a study population of metastatic breast cancer patients with a median survival of 16 months. This analysis strongly suggests that DBD is one of the most potent of the reported leukemogenic-inducing agents. Further use of this drug in both the adjuvant and metastatic situation should be reconsidered.
The relationship between cell features by light microscopy and therapeutic outcome of 72 patients with acute myeloblastic leukemia (FAB M1) were investigated. The patients were divided into two groups according to myeloperoxidase-(MPO) positive percentage of blast cells, namely a low (less than 50%) and high (greater than 50%) MPO group. No remarkable morphological difference of blast cells between these two groups was observed. The 38 patients with low MPO showed a significantly lower complete response rate (CR) (52.6%) than the 34 patients with high MPO (85.3%) (p = 0.003) that included 10 CAE-positive patients and 2 ANAE-positive CAE-negative patients. The low MPO group included 5 CAE-positive patients with granulocyte dysplasia and 7 additional patients with alpha naphthyl acetate esterase (ANAE) positivity who were chloroacetate esterase (CAE) negative. Low positivity of blast cells may be due to a defective enzyme expression in the former but also may be a reflection of 'monocytic' aberrant expression in the latter. The low MPO group in M1 with this heterogeneous population is less likely to achieve CR with chemotherapy, while the high MPO group with a higher CR rate suggests a more pure entity within the myeloblastic leukemias referred to as M1. After further refinement by eliminating 24 cases that were 'esterase positive' (ANAE and/or CAE), the results were still the same, suggesting that the more immature blast populations were in the low MPO group.
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A 20-week double-blind randomised study of 50 black hypertensive patients was designed to compare the efficacy and safety of indoramin (Baratol; Wyeth/Ayerst) and propranolol in patients who did not respond to diuretic therapy alone. Indoramin (initial dose 50 mg/d) or propranolol (initial dose 80 mg/d) was added to the regimen of patients whose supine diastolic blood pressure (SDBP) remained elevated at 100- 200 mmHg after 2 weeks' treatment with a combination diuretic tablet (hydrochlorothiazide 50 mg plus amiloride HCl 5 mg). Supine systolic blood pressure (SSBP) and SDBP of all patients was successfully controlled (SDBP lowered to less than 95 mmHg) by daily doses that did not exceed 100 mg of indoramin or 160 mg of propranolol; over 90% of patients in each group achieved control with lower doses, i.e. 50-75 mg of indoramin or 80-120 mg of propranolol. Although heart rate decreased from baseline values by approximately 9/min with both agents, the decreases were not significantly different between the treatment groups, and neither agent caused orthostatic hypotension. There were no statistically significant differences between the groups in the types or frequency of side-effects. Indoramin is well tolerated and is as effective as propranolol in black patients with essential hypertension who are not controlled by a thiazide diuretic alone.
Diethyldithiocarbamate (DDTC) has been shown to provide protection against most clinically significant toxic effects from cisplatin (DDP) without inhibiting tumor response in a variety of murine animal models. We conducted a phase I clinical and pharmacokinetic study of DDTC in combination with DDP to establish the types and severity of toxic effects and to determine whether protection of normal tissues and tumors occurs. Twenty-two courses of DDP plus DDTC were given to 10 patients. No nephrotoxic effects were seen at DDP doses of 50-120 mg/m2, and three patients had amelioration of nausea and vomiting. Objective antitumor responses were observed. Dose-limiting toxic effects from DDTC occurred at 150 mg/kg; these consisted of numbness in the infusion arm often accompanied by severe diaphoresis, chest discomfort, and agitation during DDTC infusion. These toxic effects resolved spontaneously, however, after termination of the infusion. The preliminary results suggest that plasma levels of DDTC that provide excellent protection in rodents were exceeded at the doses used in our clinical study without compromising antitumor response.
The safety and efficacy of streptokinase (STK) (Kabikinase; Keatings) in restoring vessel patency in 70 patients with acute myocardial infarction are reported. Return of vessel patency occurred more frequently (76%) in patients receiving STK than in patients in a control group (12%) (P = 0.001). The main complication was bleeding, which invariably resulted from invasive procedures. Dangerous dysrhythmias were uncommon and no fatalities were caused by STK administration. It is recommended that thrombolytic therapy be started as early as possible in patients with acute myocardial infarction, who can then be referred to centres equipped for coronary angiography for further management. Unnecessary invasive procedures should be avoided.
A case of spontaneous multivessel coronary artery spasm documented by coronary arteriography is reported. The patient was also resistant to sublingual nitrates and nifedipine and required intracoronary nitroglycerine to alleviate the spasm.