Michel Telerman

The spectrum of mitral regurgitation in idiopathic mitral valve prolapse: a color Doppler study.

To characterize the spectrum of mitral regurgitation in mitral valve prolapse, one hundred patients were studied by color Doppler flow mapping. The findings were correlated with the clinical presentation and with the possible complications. Mitral regurgitation was absent in 46 patients, mild in 26 patients, moderate in 18 patients and severe in 10 patients. The jet orientation was central in 15 patients, antero-medial in 13 patients and postero-lateral in 26 patients. The regurgitation was early systolic in 7 patients, late systolic in 20 patients and holosystolic in 27 patients. A good agreement was observed between the color flow patterns and the presence, timing and radiation of a murmur. Systolic clicks were not predictors of the presence or the severity of regurgitation. The grade of mitral regurgitation was positively correlated with age, left heart enlargement and valvular redundancy. No sex difference was observed. The prevalence of serious arrhythmias or cerebral ischemic events was not significantly increased when a regurgitation was present.

Clinical usefulness of biplane transesophageal echocardiography.

The clinical usefulness of biplane color Doppler transesophageal echocardiography is illustrated by the results obtained in 300 successive examinations. The additional contribution of the newer longitudinal plane was judged significant or major in 64% of the cases. The method was useful mainly for intraoperative examinations, assessment of native valvular disease, prosthetic valve evaluation, search for tumors, and assessment of endocarditis, congenital heart disease, and aortic disease. In contrast, the longitudinal plane option was not contributory in 68% of the cases of thromboembolism. Typically, the technique aided in the evaluation of mitral valve insufficiency and the detection of paraprosthetic leaks. Lesions located at the level of the ascending aorta, the left and right ventricular outflow tracts, and the interatrial septum were also visualized best. The limitations of the method were negligible and the duration of the examination was not significantly increased in comparison to the monoplane method. When available, biplane transesophageal echocardiography seems to be preferred in most clinical settings.

Vascular Liver Disease

n Th is book deals with the vascular structures of the liver, consisting of the portal and the hepatic venous system, the arterial system and the sinusoids. A sinusoid is a terminal capillary blood vessel but with pores between adjacent endothelial cells and fenestrae in the cells to enhance vascular entry and exit of molecules. Th e sinusoids of the liver are distinct from those of the spleen and bone marrow since the latter have inter-endothelial slits that can open up to allow migration of blood cells. Th e hepatic sinusoids lack a basement membrane and make use of a specialized structure, the space of Disse, and of unique features of liver sinusoidal endothelial cells (LSEC) having fenestrae without diaphragm, and of pericytes, the hepatic stellate cells (HSC) located in the space of Disse. Th e fi rst four chapters of the book give an excellent and detailed description of these sinusoidal cells and structure. Although the HSC represent only 5-8% of all liver cells, they encircle the whole endothelial lining due to their long peri-endothelial extensions. In addition, they also have long inter-hepatocellular “fi ngers”, which may extend into nearby sinusoids. As such, an important communication network is formed, which is in close contact with autonomic nerve fi bres. Th is interaction is further strengthened by the presence of several neurotrophins in the HSC. Upon activation, HSC gain contractile properties and act as myofi broblasts. Th is becomes very important in the pathogenesis of portal hypertension. Exposure of the parenchymal cells to blood products derived from the portal (digestive) venous system is controlled by the sieving capacity of the LSEC, which also act as antigen-presenting cells, and even possess phase I and II enzymes, and by the immunological action of Kupff er and dendritic cells. Cirrhosis oft en develops in the course of most chronic liver diseases and is characterized by capillarization, with loss of fenestration and development of a basement membrane. Th is restricts the fl exibility of the intravascular sinusoidal space. Normal LSEC maintain HSC quiescence, but when altered in cirrhosis, HSC become activated and secrete i.a. pro-fi brotic proteins. Lack of vascular fl exibility and altered coagulation proteins can lead to development of small thrombotic events, all adding to the onset of hypertension in the portal tributaries. Th is portal hypertension (chapters 6 & 7) is caused by both intra-hepatic and extra-hepatic mechanisms. Structural changes (capillarization, cell enlargement, necrosis, fi brosis and nodule formation, etc.) take up two thirds of the former while one third is of a dynamic nature and amendable to drug therapy. Extrahepatic changes result in an enhanced blood infl ow into the portal system, amplifying the portal pressure. Th e large list of vascular liver diseases is discussed in part II, starting with beautifully illustrated descriptions of the histological and radiological diagnosis, followed by a detailed description of the most frequent clinical syndromes: portal vein thrombosis, BuddChiari syndrome and congenital hepatic malformations (shunts and hereditary telangiectasia). Part III deals at fi rst with the management of portal hypertension by interventional radiology and by liver transplantation, outlining indications and results in vascular tumours, Budd-Chiari syndrome and congenital vascular disorders, but also describing vascular complications following transplantation. Chapter 5 describes cellular aspects such as reperfusion injury, eff ects of ischemia and endothelial cytoprotection and regeneration aft er transplantation. A special chapter is devoted to hepatic vascular pathology that can possibly occur aft er bone marrow transplantation: sinusoidal obstruction syndrome, focal nodular hyperplasia and nodular regenerative hyperplasia. Overall, this is a nicely written and beautifully illustrated book, giving detailed information on cellular and coagulation pathology, and on the pathogenesis of portal hypertension. However, to complete the picture of vascular derangements and to elicit more interest by non-hepatologists, I would have loved to fi nd chapters on cardiac ascites (right heart failure and constrictive pericarditis), on porto-pulmonary hypertension, and on the functional disorders known as hepato-pulmonary and hepato-renal syndromes. Th e price is also somewhat high. Johan Fevery [ Book reviews ]

Perioperative Mapping of Parahisian Accessory Pathways

VERBEET, T.W., ET AL.: Perioperative Mapping of Parahisian Accessory Pathways. In 1989, two patients were operated for deep septal “parahisian” pathways in our institution. Three different mapping techniques were used. (1) Epicardial activation mapping with a belt of 21 bipolar electrodes positioned around the heart. This belt was positioned either on the atrial or on the ventricular side of the atrio‐ventricular annulus in order to localize both the atrial and the ventricular insertion of the bypass tract. (2) Right intra‐atrial activation mapping on the normothermic beating heart with a bipolar hand‐held probe. (3) Right intra‐atrial cryomapping at 0°C. The “parahisian” pathways are remote from the epicardium and the pattern of epicardial activation is different from that of the free‐wall pathways. Case 1: The electrophysiological study showed a concealed anteroseptal bypass tract. The peroperative atrial epicardial mapping during orthodromic tachycardia (OT) showed simultaneous activation of the posteroseptal area and of the basis of the right appendage. Right intra‐atrial mapping during OT showed an anteroseptal “parahisian” pathway. Case 2: The ECG and electrophysiological study showed a right posterior pathway. The first site of epicardial ventricular activation during atrial stimulation was the right posterior area, 30 ms after the onset of the delta wave. The first site of epicardial atrial activation during OT was the posteroseptal area. The right intra‐atrial mapping showed a posteroseptal “parahisian” bypass tract. This localization was confirmed with cryomapping. Conclusions: Some patterns of epicardial mapping may suggest the presence of a deep septal “parahisian” bypass tract: retrograde atrial activation at different sites (mimicking activation among multiple pathways); delay between the delta wave and the first epicardial electrogram. Right intra‐atrial activation and cryomapping are useful to confirm the diagnosis.