Left ventricular perforation following percutaneous balloon mitral valvuloplasty.
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Biomedical subjects
Publications and source records attributed to T O Cheng.
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Mitral valve prolapse can best be diagnosed with careful clinical evaluation, including dynamic auscultation. Treatment consists of reassurance, pharmacotherapy for troublesome symptoms, and careful monitoring for signs of complications. Most complications can be either prevented or treated.
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The first 71 patients with rheumatic mitral stenosis who successfully underwent single rubber-nylon balloon (Inoue balloon) percutaneous mitral valvuloplasty (PMV) from November 1985 to August 1988 had a mean follow-up period of 27.1 +/- 11.6 months (range, 14 to 48 months). Functional status before PMV was New York Heart Association (NYHA) functional class IV in two, class III in 38, and class II in 31. Pre and post PMV and follow-up mean diastolic mitral gradient by catheter method was 17.5 +/- 6.9, 2.7 +/- 3.5, and 3.3 +/- 3.4 mm Hg (p less than 0.001 pre versus post PMV and pre PMV versus follow-up; and p greater than 0.005 post PMV versus follow-up). By Doppler method the mean diastolic gradient was 17.4 +/- 5.5, 8.5 +/- 4.7, and 9.2 +/- 4.1 mm Hg, respectively (p less than 0.001 pre versus post PMV and pre PMV versus follow-up; and p greater than 0.05 post PMV versus follow-up). Mitral valve area was 1.12 +/- 0.26, 2.04 +/- 0.41, and 1.92 +/- 0.45 cm2, respectively (p greater than 0.001 pre versus post PMV and pre PMV versus follow-up; and p less than 0.05 post PMV versus follow-up). The phonocardiographic and vectorcardiographic studies and cardiopulmonary exercise testing showed significant improvement after PMV and at follow-up. At follow-up the NYHA functional class was 1 in 57 patients, class II in 13, and class III in one patient with severe mitral valve calcification and subvalvular fusion, in whom restenosis occurred 18 months after PMV.(ABSTRACT TRUNCATED AT 250 WORDS)
Cardiac failure, which used to be rare in coronary heart disease, is now its most common complication. Coronary heart disease can cause or appear as cardiac failure through one or more of 12 mechanisms: acute myocardial infarction, acute reversible ischemia, right ventricular dysfunction, cardiogenic shock, acute mitral regurgitation, ventricular septal perforation, cardiac free wall rupture, ischemic cardiomyopathy, ventricular aneurysm, coexisting diseases, iatrogenesis, and pseudoheart failure. An understanding of the responsible mechanism or mechanisms is essential not only for appropriate treatment but also for prognostication. Various therapeutic modalities, both medical and surgical, should be able to improve not only symptoms but also survival. Current efforts in the management of patients with cardiac failure as a result of coronary heart disease should be aimed at prevention, both primary and secondary.
This is a collective review of 564 patients with Marfan syndrome among 98 pedigrees reported from 18 provinces and cities in China over a 37-year period from 1951 to 1987. A positive family history of Marfan syndrome was found in 74.3% of the patients: the mode of inheritance was dominant in 73.8% and recessive in 0.5%. Sporadic cases occurred in 25.7%. A screening of 29,067 children found five children with Marfan syndrome, giving a prevalence of 17.2 per 100,000 of the population, a gene frequency of 8.61 per 100,000 genes, and a penetrance of 71.69%. Pleiotropy was clear in these cases: arachnodactyly in 77%, ectopia lentis in 86.8%, and dilated aortic root in 80.1%. Chromosome examination showed no regular aberrations except in a family of five in whom a giant-satellited chromosome 14 was found in three afflicted members but not in the two unaffected relatives. The high prevalence of aortic root dilation in Marfan syndrome makes echocardiography the most useful and practical means of diagnosis. Close follow-up and regular echocardiographic evaluation are indicated not only in patients with Marfan syndrome but also in their families, for both diagnostic and therapeutic purposes.
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