Pentti Siltanen

Subclinical cytomegalovirus infections and cytomegalovirus mononucleosis after open heart surgery

Abstract In a series of 63 patients submitted to open heart operations in which fresh blood was used for perfusion, a significant (i.e., at least eight-fold) postoperative rise in the titer of complement-fixing antibodies to the cytomegalovirus was established in 19 cases (30 per cent). After the operation, 1 patient had a febrile syndrome with hematologic features of infectious mononucleosis but without positive findings on a heterophil agglutination test. The cytomegalovirus was isolated from the urine. The illness was considered to be a clinical manifestation of acquired cytomegalovirus infection, cytomegalovirus mononucleosis. In 18 other patients with a postoperative rise of cytomegalovirus antibody titer, no clinical disease was observed. The frequency of significant postoperative rises in the antibody titer was clearly correlated to the preoperative level of antibody titer. A significant rise was established in 10 of 17 patients (59 per cent) who had no demonstrable antibodies preoperatively, in 9 of 36 patients (25 per cent) whose preoperative titer was relatively low and in none of those with higher preoperative titers. In a control series of 60 patients submitted to other kinds of heart operations, without extra-corporeal circulation and with the use of citrated bank blood only, no significant rise of cytomegalovirus antibody titer was established in any patient. The transfer of the infection via fresh or relatively fresh blood, transfused in large quantities, offers the best explanation for the common occurrence of cytomegalovirus infection after open heart operations. Extracorporeal circulation may be of importance in the transmission of a new infection or reactivation of a latent infection.

Atrial myxoma in a family.

A family is described in which the mother and three of seven children had atrial myxoma. The mother had biatrial myxoma; surgical treatment resulted in massive intraoperative embolization and death. Surgery was sucessful in two sons with left atrial myxoma and systemic arterial embolization. A third son had calcified right atrial myxoma with destruction of the tricuspid valve and episodes of syncope and pulmonary embolism; surgery including valve replacement, was successful. The mothers father and a brother had died suddenly without a definite diagnosis. The family data are consistent with dominant transmission. The possibility of finding affected relatives should be borne in mind when studying patients with atrial myxoma.

Studies of auricular catecholamines by fluorescence histochemistry in various heart diseases of man

A comparative histochemical and clinical study concerning the state of the intrinsic adrenergic innervation of the human atrial myocardium was carried out, using the glyoxylic acid-induced fluorescence histochemical method. Specimens from the right auricular appendage were obtained during open-heart surgery from patients suffering from 1. ischaemic heart disease (IHD), 2. atrial septal defect of the secundum type (ASD), and 3. left-sided univalvular or multivalvular heart disease (VHD) with or without congestive heart failure (CHF) experienced prior to surgery. In the IHD group the densities of both the perivascular and the “free” myocardial adrenergic nerve net were greater than in the ASD group and especially in the VHD/ CHF group. Secondly, the intensity of fluorescence of the adrenergic structures was generally higher in the IHD group than that in the VHD/CHF group. Further, the average size of the varicosities, the number of varicosities per given length of axon, and the proportional share of the large varicosities were greater in the IHD group than in the ASD and VHD/CHF groups. The difference between the IHD and ASD groups was not great but was obvious in any case. In some patients with VHD/CHF fluorescing axons were observed only occasionally, and the tiny varicosities exhibited a hardly discernible fluorescence. Thus the amount of noradrenaline (NA) in the adrenergic fibres in the IHD group seems to be higher than in the ASD and especially VHD/CHF groups. The high level of NA in the IHD group is assumed to constitute a contributory factor in both intracellular metabolic changes and the systemic changes typical of myocardial ischaemia and infarction. In one patient with IHD and in six patients with VHD/CHF with significantly higher heart volume (mean±SD) compared with the rest of the patients (P<0.001), huge local axonal accumulations of NA in the form of “droplet fibres” were found. These enlarged, bulging adrenergic axons are assumed to be a consequence of mechanical trauma with stretching or disruption of the axons due to myodegenerative processes. It is further assumed that these “droplet fibres” are relatively common in those patients with diseased myocardium. They may constitute an extra contributory factor to the tendency to arrhythmias so typical of patients of this kind, by increasing the excitability of non-automatic tissue.

Effect of cold ischaemic arrest and subsequent coronary reperfusion on the intrinsic adrenergic innervation and neural noradrenaline of the atrial myocardium during aortic valve replacement.

The effect of cold ischaemic arrest (aortic cross-clamping for 50-70 min during general hypothermia of +30 degrees C, associated with local cardiac cooling with +4 degrees C saline solution) and subsequent coronary reperfusion (20-30 min) on the intrinsic adrenergic innervation of the right atrial myocardium, was studied in 10 patients in the course of prosthetic aortic valve replacement using the glyoxylic acid-induced fluorescence histochemical method. No clear changes were observed: (a) the morphological integrity of the intrinsic adrenergic nerve net remained intact, (b) no obvious depletion occurred in the neural noradrenaline level, (c) the procedure did not affect the droplet fibres (i.e. huge axonal accumulations of noradrenaline). Thus, the common need for catecholamine support during and after weaning off from cardiopulmonary bypass does not seem to be explained by damage to the adrenergic axons or depletion of the adrenergic neurotransmitter noradrenaline.

Atrial Acetylcholinesterase Activity in Various Heart Diseases of Man

Distribution and activity of the acetylcholinesterase enzyme in the human atrial myocardium was studied histochemically in a clinical series of patients subjected to cardiac surgery for (1) uncomplicated atrial septal defect (ASD), (2) ischaemic heart disease (IHD), (3) mitral and/or aortic valvular disease (VHD) necessitating replacement with a prosthetic valve, without major symptoms or signs of myocardial incompensation, or (4) clinically overt congestive heart failure (CHF) due to VHD prior to cardiac surgery. In all specimens, a rich distribution of acetylcholinesterase-positive single axons and small fascicles, constituting a three-dimensional nerve net, was observed within the myocardial tissue. This nerve net was obviously mainly parenchymatous, i.e. unrelated to the blood vessels. Small groups of acetylcholinesterase-positive small nerve cells were observed in some specimens, with loosely woven fascicles of axons emerging from one pole of the ganglia. No differences in the distribution of the acetylcholinesterase activity or in the pattern of the inbuilt intrinsic nervous apparatus were observed in the various groups of patients. All specimens were completely devoid of non-specific cholinesterase activity. It was concluded that (I) the human atrial myocardium is richly supplied with cholinergic intrinsic (post-ganglionic vagal) axons and (II) the acetylcholinesterase activity is not a major determinant of the parasympathetic abnormalities associated with cardiac diseases, especially with myocardial pump failure.

Histochemically demonstrable monoamine oxidase activity in the adult human heart in various cardiac diseases

The present work was undertaken in order to study the role of monoamine oxidase (MAO) enzyme in the genesis of altered cardiac noradrenalin level in the human heart in various underlying pathologic conditions. The histochemical localization and the activity of MAO were studied in the right atrial appendage of man in ischemic heart disease, in valvular heart disease without or with congestive myocardial failure, and in hearts with an uncomplicated atrial septal defect. MAO was found to be localized mainly extraneuronally in the muscle cells, a little activity was detected in the connective tissue spaces, and nerves reacting positively were tentatively identified. There were no significant differences in MAO activity measured photometrically between the various heart disease groups. It seems that MAO enzyme plays only a small or no role in the genesis of the altered noradrenalin level in the human heart observed in ischemic heart disease or congestive cardiac failure.