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ures highlight the importance of the subject whilst Dept. of Perinatal Cardiology emphasising the increasing demands and indication for Guy’s Hospital this relatively new technique. London, SE1 9RT. U.K.

His wide experience and undoubted skills are well

reflected in this book which has the additional ad- vantage of being produced by one author only. a rare

achievement these days. There are excellent chapters on the historical background of angioplasty decision mak- ing, technical approaches and performance. The volume is amply illustrated and the references are of the highest

standard.

Atherosclerosis Reviews vol. 17: Lipoproteins and Atherosclerosis

The cardiologist constantly involved in managing

patients with coronary arterial disease will find in this impartial book ample guidance and advice about the extraordinary ability of percutaneous transluminal coronary angioplasty to restore flow in all sorts of anatomico-pathological situations. Long-term compara-

tive results against coronary arterial bypass grafting are awaited but, in the meantime, many patients around the world have undoubtedly benefitted from angioplasty

and will continue to do so.

Editors: Robert I. Levy, Anatoli N. Klimov, Vladimir N. Smimov and Herman A. Tyroler Raven Press, New York, 1988; 311 pp.; $119.00; ISBN o-88167-402-8

Atherosclerosis Reviews vol. 18: Hypercholesterol- emia: Clinical and Therapeutic Implications Editors: Joseph Stokes II and Mario Mancini Series Editors: Antonio M. Gotto Jr. and Rodolfo Paoletti Raven Press, New York, 1988; 202 pp.; $81.50: ISBN O-88167-435-4

The author is to be congratulated on the most com- plete up-to-date publication on coronary angioplasty

that I have yet had to review and which I have done

with great satisfaction.

These volumes give a valuable summary of the latest developments in research concerning lipoproteins. An important development of the recent past is the un-

ravelling of the structure and function of the apoproteins of which lipoproteins are composed. The biggest struct-

ural apoproteins are those in the B group, Apo B-100 with a molecular weight of 550,000, and Apo B-48 with

a molecular weight of 250,000. The smallest are the Apo C-s, with molecular weights of 6-7000. The Apo A-s, D-s and E-s are of intermediate size, with molecular weights from 16,000 to 48,000. The lipid-binding func-

tion of these apoproteins is due to amphipathic helices localised in discrete regions of the protein, which pre-

sent a polar face to the aqueous exterior, and a hydro- phobic face to the lipid interior. In addition to the

binding and transport of lipids, apoproteins play a part in the activation of enzymes involved in lipid metabo- lism, and the presentation of sites of recognition to

lipoprotein receptors.

The Manor House Hospital London NW11 7HX. U.K.

Romeo J. Vecht Consultant Cardiologist

Fetal Ekhocardiography - an Atlas Kathryn L. Reed, Caroline F. Anderson and Lewis Shenker Alan R. Liss, New York, 1988; 138 pp.; $62.50; ISBN 0-8451-4250-X

This book is essentially about cardiology, but is written by obstetricians. It is presented in an extremely simple style. This is not without its merits, but it is so over-sim-

plified that it is often inaccurate. The author regurgi- tates many cliches of received wisdom on fetal cardio-

vascular physiology which recent observations in the human fetus do not support.

Some of the illustrations are nice, but the experience of the topic presented appears very limited. The book is heavily illustrated with drawings which I understand are popular, although I personally do not like them. They do make the book expensive for so little text. I feel cardiologists will find the presentation of cardiology here naive, although it may be suitable for obstetricians involved in this field.

Lindsey D. Allan

The disturbing finding of this research is a multitude of genetic defects that can occur both in apoproteins and in lipoprotein receptors. Thus a paper by Brown

and Goldstein (vol. 18) reveals that familial hyper- cholesterolaemia can be the result of several genetic mutations. In one of these, no surface receptors are produced. In another, the receptors are produced nor- mally in the endoplasmic reticulum, but fail to fold properly and cannot reach the surface of the cell. In another case, the receptors reach the surface, but their receptor mechanism is faulty, so that they are unable to bind plasma lipoproteins. In another case the receptors

411

fail in the last act of their functions, namely to move (like haemorrhagic telangiectasia), the circulatory sys- with the captured lipoproteins to a coated pit on the tem appears to be the site of a frightening number of cellular surface, where the complex would be inter- defective mutations. Serious thought might be indicated nalised by endocytosis. on the subject.

Another paper (Schaefer, McNamara and Ordovas, vol. 17) points out that familial hypercholesterolaemia is

only one out of four common and several rare disorders

affecting lipid transport in the circulation. The com- monest is familial hypo-alpha-proteinaemia, resulting in

low levels of HDL cholesterol. Familial combined hy-

perlipidaemia and familial hypertriglyceridaemia are the other two. It is now beginning to emerge that apoproteins are just as prone to genetic disorders as

surface receptors. An entire class of apolipoproteinopa- thies, named on the analogy of haemoglobinopathies, are being identified (Gotto, vol. 17).

A large part of vol. 17 is devoted to epidemiological

studies, notably comparisons between prospective stud- ies conducted collaboratively in the U.S.A. and U.S.S.R., producing puzzling results in some instances. Thus the 7-year all-causes mortality in the U.S.A. is rising while

it is falling in the U.S.S.R. despite increasing levels of total serum cholesterol. Mortality of all causes falls in both countries with increasing levels of high-density

lipoprotein, but the fall is much more pronounced in the U.S.A. than in the U.S.S.R. Science has a long way to go yet before mysteries of this nature are likely to be resolved.

If these defects are added to haemoglobinopathies

(thalassaemias), of which so many varieties exist that they probably represent the entire repertoire of nature for genetic mutations, haemophilias of two different forms (factor VIII and factor IX deficiency) and others

Dept. of Cardiology University of Manchester The Royal Infirmary Manchester Ml3 9WL, U.K. Stephen Seely