Woman's or baby's rights? Genes make the difference.
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Biomedical subjects
Publications and source records attributed to C Del Campo.
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Arrhythmogenic right ventricular dysplasia is a myopathy that affects the right ventricular free wall (RVFW) and gives rise to recurrent reentrant ventricular tachycardia (VT). Because the entire right ventricle is potentially arrhythmogenic, ablating a single site of VT may not eliminate the arrhythmia. We developed an operation to confine any arrhythmic activity arising from the right ventricle to that chamber: total disconnection of the RVFW from the left ventricle. We performed RVFW disconnection in two patients with refractory VT associated with arrhythmogenic right ventricular dysplasia. At least two sites or origin of morphologically distinct VT were identified in the RVFW in each patient. RVFW disconnection was carried out under normothermic cardiopulmonary bypass. An encircling incision was made along the attachment of the RVFW to the aortoventricular unit and the tricuspid annulus; the right coronary artery and its RVFW branches were left intact. Electrical activity of the two chambers became dissociated, and VT arising from the RVFW was confined to that chamber. Postoperatively, there was no clinical evidence of hemodynamic impairment (follow-up 4 months and 3 months). Left ventricular function was unchanged and right ventricular flow was maintained by atrial contraction and motion of the septum toward the RVFW during left ventricular systole. One patient had incessant right ventricular tachycardia confined to the RVFW for 3 weeks. We conclude that RVFW disconnection is feasible and applicable to patients with refractory VT originating in the diffusely diseased RVFW.
In situations where severe femoropopliteal disease is present and profundoplasty is deemed unreliable, successful revascularization is not usually possible. A technique is presented that increases the accessibility for repair and may improve the limb salvage rate in those patients considered nonoperable by other techniques.
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In spite of the efficacy of tricuspid annuloplasty, there remain occasional cases in which tricuspid valve replacement (TVR) is indicated. There is to date no late follow-up data on the Carpentier-Edwards porcine bioprosthesis (CEPB) in the tricuspid position. We present a series of twelve consecutive cases of TVR with the CEPB. Ten patients had multiple valve replacements. The duration of follow-up was 5 to 50 months (mean 27.7 months) on all patients. The operative mortality was 18% (2/12), with 82% (10/12) actuarial 5-year survival. The mean valve follow-up was 2.3 years per prosthesis. Ten patients were in the New York Heart Association (NYHA) Class IV preoperatively. Postoperatively, eight patients moved to Class II, one to Class III and one remained unchanged. There was no valve replacement necessary. Subclinical pulmonary emboli were detected by lung scan in one patient for 4.3% events per year. Echocardiography revealed no evidence of orifice thrombus or leaflet calcification. In our opinion, the Carpentier-Edwards bioprosthesis can be used safely in the tricuspid position with satisfactory functional results.
The most recent statistics clearly show that the incidence of amebiasis in Canada has increased progressively over the past 10 years. The authors review the incidence, pathophysiology and management of thoracic complications of amebiasis, including the experience from endemic countries. Complications include amebic liver abscess, best treated with metronidazole, and the resulting thoracic complications of pleural and pericardial effusion, atelectasis and rupture into the thoracic cavity. Since amebic liver abscess always precedes the thoracic complications, its early diagnosis and treatment will prevent these complications in most cases of amebiasis.
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The natural history of patients with coronary artery disease associated with poor left ventricular (LV) function is dismal. This report analyzes the efficacy of myocardial revascularization in this subset of patients with coronary artery disease manifesting severe LV dysfunction on the basis of LV angiography, LV ejection fraction (LVEF), and left ventricular end-diastolic pressure (LVEDP). For the 2 1/2 year period ending November, 1977, 59 consecutive patients with coronary artery disease complicated by severe LV dysfunction underwent aorta-coronary bypass at the University of Western Ontario. All patients had angina refractory to medical therapy. Objective criteria for compromised LV function included the presence of three or more dysfunctional (hypokinetic of akinetic) segments on biplane LV angiography. Eighty-three percent (49/59) of patients had triple-vessel coronary artery disease. The mean LVEF for the series was 0.28 and the mean LVEDP was 18 mm Hg. The duration of follow-up was 24 to 60 months (mean 37 months), with follow-up survival data available on 100% of patients. The hospital mortality was 1.7% (1/59), and there were nine late deaths. The 5 year actuarial survival rate (+/- SEM) was 80% +/- 6%. Of the 44 long-term survivors available for direct assessment, 98% (43/44) report improvement with respect to angina and 66% (29/44) are totally asymptomatic. Eighty percent (28/35) of the long-term survivors under the age of 65 years are currently employed. These results indicate that myocardial revascularization can be performed in patients with severe ischemic LV dysfunction at very low risk and, further, that operation results in a dramatic improvement in survival expectations compared with optimal medical therapy.