Nitric oxide alleviates cadmium- but not arsenic-induced damages in rice roots.

Nitric oxide (NO) has signalling roles in plant stress responses. Cadmium (Cd) and arsenic (As) soil pollutants alter plant development, mainly the root-system, by increasing NO-content, triggering reactive oxygen species (ROS), and forming peroxynitrite by NO-reaction with the superoxide anion. Interactions of NO with ROS and peroxynitrite seem important for plant tolerance to heavy metal(oid)s, but the mechanisms underlying this process remain unclear. Our goal was to investigate NO-involvement in rice (Oryza sativa L.) root-system after exposure to Cd or As, to highlight possible differences in NO-behaviour between the two pollutants. To the aim, morpho-histological, chemical and epifluorescence analyses were carried out on roots of different origin in the root-system, under exposure to Cd or As, combined or not with sodium nitroprusside (SNP), a NO-donor compound. Results show that increased intracellular NO levels alleviate the root-system alterations induced by Cd, i.e., inhibition of adventitious root elongation and lateral root formation, increment in lignin deposition in the sclerenchyma/endodermis cell-walls, but, even if reducing As-induced endodermis lignification, do not recover the majority of the As-damages, i.e., enhancement of AR-elongation, reduction of LR-formation, anomalous tissue-proliferation. However, NO decreases both Cd and As uptake, without affecting the pollutants translocation-capability from roots to shoots. Moreover, NO reduces the Cd-induced, but not the As-induced, ROS levels by triggering peroxynitrite production. Altogether, results highlight a different behaviour of NO in modulating rice root-system response to the toxicity of the heavy metal Cd and the metalloid As, which depends by the NO-interaction with the specific pollutant.

Indole-3-butyric acid promotes adventitious rooting in Arabidopsis thaliana thin cell layers by conversion into indole-3-acetic acid and stimulation of anthranilate synthase activity.

BACKGROUND: Indole-3-acetic acid (IAA), and its precursor indole-3-butyric acid (IBA), control adventitious root (AR) formation in planta. Adventitious roots are also crucial for propagation via cuttings. However, IBA role(s) is/are still far to be elucidated. In Arabidopsis thaliana stem cuttings, 10 µM IBA is more AR-inductive than 10 µM IAA, and, in thin cell layers (TCLs), IBA induces ARs when combined with 0.1 µM kinetin (Kin). It is unknown whether arabidopsis TCLs produce ARs under IBA alone (10 µM) or IAA alone (10 µM), and whether they contain endogenous IAA/IBA at culture onset, possibly interfering with the exogenous IBA/IAA input. Moreover, it is unknown whether an IBA-to-IAA conversion is active in TCLs, and positively affects AR formation, possibly through the activity of the nitric oxide (NO) deriving from the conversion process. RESULTS: Revealed undetectable levels of both auxins at culture onset, showing that arabidopsis TCLs were optimal for investigating AR-formation under the total control of exogenous auxins. The AR-response of TCLs from various ecotypes, transgenic lines and knockout mutants was analyzed under different treatments. It was shown that ARs are better induced by IBA than IAA and IBA + Kin. IBA induced IAA-efflux (PIN1) and IAA-influx (AUX1/LAX3) genes, IAA-influx carriers activities, and expression of ANTHRANILATE SYNTHASE -alpha1 (ASA1), a gene involved in IAA-biosynthesis. ASA1 and ANTHRANILATE SYNTHASE -beta1 (ASB1), the other subunit of the same enzyme, positively affected AR-formation in the presence of exogenous IBA, because the AR-response in the TCLs of their mutant wei2wei7 was highly reduced. The AR-response of IBA-treated TCLs from ech2ibr10 mutant, blocked into IBA-to-IAA-conversion, was also strongly reduced. Nitric oxide, an IAA downstream signal and a by-product of IBA-to-IAA conversion, was early detected in IAA- and IBA-treated TCLs, but at higher levels in the latter explants. CONCLUSIONS: Altogether, results showed that IBA induced AR-formation by conversion into IAA involving NO activity, and by a positive action on IAA-transport and ASA1/ASB1-mediated IAA-biosynthesis. Results are important for applications aimed to overcome rooting recalcitrance in species of economic value, but mainly for helping to understand IBA involvement in the natural process of adventitious rooting.

Ethylene and auxin interaction in the control of adventitious rooting in Arabidopsis thaliana.

Adventitious roots (ARs) are post-embryonic roots essential for plant survival and propagation. Indole-3-acetic acid (IAA) is the auxin that controls AR formation; however, its precursor indole-3-butyric acid (IBA) is known to enhance it. Ethylene affects many auxin-dependent processes by affecting IAA synthesis, transport and/or signaling, but its role in AR formation has not been elucidated. This research investigated the role of ethylene in AR formation in dark-grown Arabidopsis thaliana seedlings, and its interaction with IAA/IBA. A number of mutants/transgenic lines were exposed to various treatments, and mRNA in situ hybridizations were carried out and hormones were quantified In the wild-type, the ethylene precursor 1-aminocyclopropane-1-carboxylic acid (ACC) at 0.1 µM enhanced AR formation when combined with IBA (10 µM), but reduced it when applied alone; this effect did not occur in the ein3eil1 ethylene-insensitive mutant. ACC inhibited the expression of the IAA-biosynthetic genes WEI2, WEI7, and YUC6, but enhanced IBA-to-IAA conversion, as shown by the response of the ech2ibr10 mutant and an increase in the endogenous levels of IAA. The ethylene effect was independent of auxin-signaling by TIR1-AFB2 and IBA-efflux by ABCG carriers, but it was dependent on IAA-influx by AUX1/LAX3.Taken together, the results demonstrate that a crosstalk involving ethylene signaling, IAA-influx, and IBA-to-IAA conversion exists between ethylene and IAA in the control of AR formation.

Romiplostim for secondary thrombocytopenia following allogeneic stem cell transplantation in children.

The outcome of romiplostim for secondary failure of platelet recovery (SFPR) was investigated in children who had undergone hematopoietic stem cell transplantation (HSCT). Seven transfusion-dependent pediatric patients (median age 11 years), with platelet counts below 10 × 10(9)/L, received four weekly doses of subcutaneous romiplostim to treat SFPR developed after HSCT. All patients, except one (patient 4), became platelet transfusion-independent in the second week from the beginning of treatment and no patient needed to discontinue drug treatment because of adverse events. Romiplostim could represent a beneficial first-line treatment, but further studies are required.

Arabidopsis SHR and SCR transcription factors and AUX1 auxin influx carrier control the switch between adventitious rooting and xylogenesis in planta and in in vitro cultured thin cell layers.

BACKGROUND AND AIMS: Adventitious roots (ARs) are essential for vegetative propagation. The Arabidopsis thaliana transcription factors SHORT ROOT (SHR) and SCARECROW (SCR) affect primary/lateral root development, but their involvement in AR formation is uncertain. LAX3 and AUX1 auxin influx carriers contribute to primary/lateral root development. LAX3 expression is regulated by SHR, and LAX3 contributes to AR tip auxin maximum. In contrast, AUX1 involvement in AR development is unknown. Xylogenesis is induced by auxin plus cytokinin as is AR formation, but the genes involved are largely unknown. Stem thin cell layers (TCLs) form ARs and undergo xylogenesis under the same auxin plus cytokinin input. The aim of this research was to investigate SHR, SCR, AUX1 and LAX3 involvement in AR formation and xylogenesis in intact hypocotyls and stem TCLs in arabidopsis. METHODS: Hypocotyls of scr-1, shr-1, lax3, aux1-21 and lax3/aux1-21 Arabidopsis thaliana null mutant seedlings grown with or without auxin plus cytokinin were examined histologically, as were stem TCLs cultured with auxin plus cytokinin. SCR and AUX1 expression was monitored using pSCR::GFP and AUX1::GUS lines, and LAX3 expression and auxin localization during xylogenesis were monitored by using LAX3::GUS and DR5::GUS lines. KEY RESULTS: AR formation was inhibited in all mutants, except lax3. SCR was expressed in pericycle anticlinally derived AR-forming cells of intact hypocotyls, and in cell clumps forming AR meristemoids of TCLs. The apex was anomalous in shr and scr ARs. In all mutant hypocotyls, the pericycle divided periclinally to produce xylogenesis. Xylary element maturation was favoured by auxin plus cytokinin in shr and aux1-21. Xylogenesis was enhanced in TCLs, and in aux1-21 and shr in particular. AUX1 was expressed before LAX3, i.e. in the early derivatives leading to either ARs or xylogenesis. CONCLUSIONS: AR formation and xylogenesis are developmental programmes that are inversely related, but they involve fine-tuning by the same proteins, namely SHR, SCR and AUX1. Pericycle activity is central for the equilibrium between xylary development and AR formation in the hypocotyl, with a role for AUX1 in switching between, and balancing of, the two developmental programmes.

Auxin and cytokinin control formation of the quiescent centre in the adventitious root apex of Arabidopsis.

BACKGROUND AND AIMS: Adventitious roots (ARs) are part of the root system in numerous plants, and are required for successful micropropagation. In the Arabidopsis thaliana primary root (PR) and lateral roots (LRs), the quiescent centre (QC) in the stem cell niche of the meristem controls apical growth with the involvement of auxin and cytokinin. In arabidopsis, ARs emerge in planta from the hypocotyl pericycle, and from different tissues in in vitro cultured explants, e.g. from the stem endodermis in thin cell layer (TCL) explants. The aim of this study was to investigate the establishment and maintenance of the QC in arabidopsis ARs, in planta and in TCL explants, because information about this process is still lacking, and it has potential use for biotechnological applications. METHODS: Expression of PR/LR QC markers and auxin influx (LAX3)/efflux (PIN1) genes was investigated in the presence/absence of exogenous auxin and cytokinin. Auxin was monitored by the DR5::GUS system and cytokinin by immunolocalization. The expression of the auxin-biosynthetic YUCCA6 gene was also investigated by in situ hybridization in planta and in AR-forming TCLs from the indole acetic acid (IAA)-overproducing superroot2-1 mutant and its wild type. KEY RESULTS: The accumulation of auxin and the expression of the QC marker WOX5 characterized the early derivatives of the AR founder cells, in planta and in in vitro cultured TCLs. By determination of PIN1 auxin efflux carrier and LAX3 auxin influx carrier activities, an auxin maximum was determined to occur at the AR tip, to which WOX5 expression was restricted, establishing the positioning of the QC. Cytokinin caused a restriction of LAX3 and PIN1 expression domains, and concomitantly the auxin biosynthesis YUCCA6 gene was expressed in the apex. CONCLUSIONS: In ARs formed in planta and TCLs, the QC is established in a similar way, and auxin transport and biosynthesis are involved through cytokinin tuning.

Two SERK genes are markers of pluripotency in Cyclamen persicum Mill.

The genetic basis of stem cell specification in somatic embryogenesis and organogenesis is still obscure. SOMATIC EMBRYOGENESIS RECEPTOR-LIKE KINASE (SERK) genes are involved in embryogenesis and organogenesis in numerous species. In vitro culture of Cyclamen persicum immature ovules provides a system for investigating stem cell formation and maintenance, because lines forming either organs or embryos or callus without organs/embryos are available for the same cultivar and plant growth regulator conditions. The present aim was to exploit this property of cyclamen cultures to understand the role of SERK(s) in stem cell formation and maintenance in somatic embryogenesis and organogenesis in vitro, in comparison with expression in planta. CpSERK1 and CpSERK2 were isolated from embryogenic callus. CpSERK1 and CpSERK2 levels by RT-PCR showed that expression is high in embryogenic, moderate in organogenic, and null in recalcitrant calli. in situ hybridizations showed that the expression of both genes started in clumps of pluripotent stem cells, from which both pre-embryogenic aggregates and organ meristemoids derived, and continued in their trans-amplifying, meristem-like, derivatives. Expression declined in organ meristemoids, in parallel with a partial loss of meristematization. In mature somatic embryos, and in shoot and root primordia, CpSERK1 and CpSERK2 were expressed in meristems, and similar patterns occurred in zygotic embryo and primary meristems in planta. The results point to SERK1 and SERK2 as markers of pluripotency in cyclamen. It is proposed that the high expression of these genes in the trans-amplifying derivatives of the stem cells maintains a pluripotent condition leading to totipotency and, consequently, somatic embryogenesis.

Treatment of hyperhomocysteinaemia in haemodialysis patients at high cardiovascular risk.

OBJECTIVES: Cardiovascular disease (CVD) is the main cause of death among haemodialysis (HD) patients. Emerging cardiovascular risk factors such as oxidative stress and chronic inflammation are involved in these patients together with traditional risk factors. Here we investigate the effects of a short-term folate treatment on some markers of chronic inflammation in two groups of HD patients with and without vascular occlusive disease (VOD). PATIENTS AND METHODS: Homocysteine (HCy), C-reactive protein (CRP), Folate, fibrinogen and alpha1 acid glycoprotein (alpha1AGP) were dosed before and after a 3-month course of high-dose folate (25 mg intravenous calcium laevofolinate pentahydride once weekly) and again after a one-month washout in 15 HD patients with established VOD (group A) and in 15 comparable HD patients with no diagnosis of VOD (group B). RESULTS: Baseline HCy and CRP were significantly elevated in patients of both groups A and B compared to normal values. Folate treatment significantly reduced HCy in patients of both groups A and B and alpha1AGP only in patients of group A, while the other markers were not modified. After the one-month washout a significant raise of CRP could be observed in patients of group A; again, the other markers were not modified. CONCLUSIONS: Our results suggest that significant reduction of serum HCy can be achieved in both patients with or without VOD after administration of high-dose folic acid. Hence, folic acid supply is useful in the treatment of hyperhomocysteinemia in HD patients, although it is not sufficient to modify their chronic inflammatory status.

-SH groups and glutathione in cancer patient's blood.

As reported in previous investigations, erythrocytes are the elements of peripheral blood most affected by free radical activity in the pathogenesis of cancer. In these studies, the level of sulphydrilic groups and reduced glutathione were assayed in the erythrocytes and plasma, while their successful scavenger activity against cell membrane oxidation and peroxidation has already been established. In subjects with cancer, the levels of -SH groups (p < 0.002) and reduced glutathione in both plasma and erythrocytes (p < 0.0001) were shown be a statistically significantly decreased compared to healthy controls. These differences were related to the defence of the hematic tissue against free radical activity. A similar pattern has also been reported when studying vitamin A and E content in the peripheral blood of cancer patients. The role of oxido-reduction phenomena in this disease is discussed, as well as the importance of reducing the oxido-peroxidation involvement of tissues and cell elements. The study of the GSH/GSSG ratio in order to determine the stage of the disease would be useful and might represent a systemic marker for cancerous lesions.

Free radical erythrocyte damage in tumoral disease assessed by He-Ne laser and optical microscope through "Heinz Bodies" method.

Results obtained from blood sample readings by optical microscopy and He-Ne laser (lambda = 630.1 mW), have confirmed the reduction in Heinz Bodies (HB) formation time and the Transmittance Reduction Degree (TRD), in malignancies. The results of spectrometric readings in colorectum polyposis, (TRD = 0.07) and fibrocystic mastopathy (TRD = 0.08) gave results overlapping with controls (TRD = 0.08). In neoplasias, the early HB formation in erythrocytes observed by optical microscope corresponded to TRD increase = 0.17 (P < 0.01). TRD increase was statistically significant (P < 0.01), as well as the reduction in the time of HB appearance (< 0.01). The relationship between optical and laser readings was exponential in tumors, while it was linear in controls, in polyposis and mastopathies. The values of the correlation coefficients obtained by both methods were significant (P < 0.01) for all the studied groups. Moreover, these research data further support the existence, even in the earlier stages of the disease, of the labile state of the red cell membrane due to strong lipid peroxidation by FRs.

Anti free radical action of calcium antagonists and H1 and H2 receptors antagonists in neoplastic disease.

The blood of the subjects suffering from Neoplastic Disease (ND) shows phenomena of membrane peroxidation due to the presence of Free Radicals (FRs), in a quantity much greater than the one observed in the blood of healthy subjects. This can be detected either by calculating the time necessary for the formation of "Heinz bodies" (Hbs), (p < 0.00001) after oxidative stress of the blood in vitro with acetylphenylidrazine (APH), or by calculating the methemoglobin (metHb) quantity that forms after the same treatment (P < 0.00001). The statistical analyses we carried out showed that metHb formation was not affected by age, sex, smoking habits, red blood cell number, Hb, Ht or tumor staging. In this study, by using equal parameters of investigation, we noted that the blood of the subjects with ND who were previously treated with calcium-antagonists drugs and with antagonists of H1 and H2 receptors, gave results completely superimposable on the results obtained from healthy subjects, implying that the treatment had avoided the increase of FRs. Therefore we concluded that calcium-antagonists and the antagonists of the H1 and H2 receptors behave as antioxidant substances, having decreased the FRs damaging activity on the cellular membranes, thus controlling, although to a limited degree, the pejorative evolution of the disease. It is also important to remember that investigations into the ND, even possible screenings, must take into account the above said data, submitting the subjects under investigation to a pharmacological wash out, particularly with those substances which, are considered to be scavengers of FRs. Some of these substances are investigated in this work.

Hemoglobin oxidative stress in cancer.

The role played by free radicals in carcinogenesis and their relationships with antioxidant pool and cancer have already been shown. Free radicals induce increased membrane permeability through membrane lipid peroxidation, protein oxidation and histamine release from mast cells. Free radicals also cause oxyhemoglobin oxidative stress which increases methemoglobin and hemichromes. For this reason, we studied the in vitro formation of methemoglobin at 0' and 90', dosed following the HPLC method, after oxidative stress of blood by means of acetylphenylhydrazine in 40 subjects with cancer and 40 healthy donors. The results showed that methemoglobin formation was highly significant in tumors as compared to controls (P < 0.0001). The statistical analyses we carried out showed that metHb formation is not affected by age, sex, smoking habit, red blood cell number, Hb, Ht or tumor staging. This makes us believe that free radicals alter erythrocyte membrane permeability and predenaturate oxyhemoglobin so that erythrocyte membrane becomes more susceptible to new oxidative stress. This caused the abnormal response we found. Our results clearly underline the role played by free radicals in tumorous disease and provide a successful and easy method to detect early, even in a pre-clinical stage, the presence of tumorous alterations in the human body.

Relation between ECG strain pattern and left ventricular morphology, left ventricular function, and DPTI/SPTI ratio in patients with aortic regurgitation.

The relative contributions of left ventricular structural changes, dysfunction, and subendocardial ischemia in determining electrocardiographic repolarization abnormalities were assessed in 53 patients with chronic, pure aortic regurgitation and no evidence of coronary artery disease. Thirty-six patients with an abnormal electrocardiographic pattern of repolarization showed larger end-diastolic (154 +/- 46 vs 120 +/- 32 mL/m2; P < .001) and end-systolic (80 +/- 40 vs 52 +/- 30 mL/m2; P = .016) volumes, higher end-diastolic pressure (22 +/- 11 vs 15 +/- 10 mmHg; P = .021), lower ejection fraction (52 +/- 12 vs 59 +/- 13%; P < .05) and greater mass (168 +/- 48 vs 140 +/- 44 g/m2; P < .05) of the left ventricle compared to 17 patients with normal repolarization. Furthermore, patients with repolarization abnormalities also showed higher peak meridian (217 +/- 68 vs 153 +/- 92 Kdyne/cm2; P < .001) and circumferential (358 +/- 110 vs 259 +/- 153 Kdyne/cm2; P < .001) stress and a more spherical shape (end-diastolic shape: 1.4 +/- 0.1 vs 1.5 +/- 0.2, P = .046; end-systolic shape: 1.7 +/- 0.3 vs 1.9 +/- 0.3, P = .026) of the left ventricle. Patients with secondary repolarization abnormalities were also older than patients with normal repolarization (56 +/- 10 vs 40 +/- 11 years; P < .001). However, the diastolic pressure-time index/systolic pressure-time index, which is an estimate of the myocardial oxygen supply-to-demand ratio, was similar in both groups of patients (0.74 +/- 0.3 vs 0.8 +/- 0.2; P = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Emergency surgical treatment for total left main coronary artery occlusion. A report of 2 cases.

Treatment of total left main coronary artery occlusion is rarely reported (84 chronic and acute cases in the world literature), due to the high mortality rate from massive myocardial infarction. Acute occlusions have been treated with intracoronary streptokinase, with percutaneous transluminal coronary angioplasty, or with both. To date, there has been no report of successful surgical revascularization in an acute case. We present 2 cases of surgically treated patients who survived total left main coronary artery occlusion that appears to have been acute, or acutely evolving. Both patients had an 80% or greater stenosis of the right coronary artery, yet have remained in New York Heart Association functional class I or II postoperatively. We attribute this not only to the aggressive surgical approach, which enabled reperfusion to be achieved within 2 hours of total occlusion, but to the protective effect in these patients of right coronary-to-left anterior descending collaterals.

Coronary occlusion secondary to blunt chest trauma: a first attempt at balloon angioplasty.

There have been only 58 angiographically documented reports of transmural myocardial infarction due to closed-chest trauma. None of these cases has been treated by percutaneous transluminal coronary angioplasty. We report the case of a 40-year-old man who developed an anterior-wall myocardial infarction secondary to blunt chest trauma suffered in an automobile accident. Angiographic study performed 2 months after the injury revealed an isolated total obstruction of the left anterior descending coronary artery. The patient was judged a good candidate for balloon angioplasty, but total reocclusion occurred within 24 hours of the procedure and a 2nd attempt did not restore patency. Surgical revascularization was performed a week later. A year after his injury, the patient remains asymptomatic and is back at work. Despite the failure of percutaneous transluminal coronary angioplasty in its 1st application to coronary artery repair after blunt chest trauma, we believe it to be the treatment of choice in young patients and in single-vessel disease.

[Anatomo-functional correlations of changes in electrocardiographic repolarization in aortic and mitral valve insufficiency. Comparison of indices based on QRS voltages]. / Corrispettivo anatomo-funzionale delle alterazioni della ripolarizzazione all'elettrocardiogramma nelle insufficienze valvolari aortica e mitralica. Confronto con gli indici basati sul voltaggio del QRS.

Electrocardiographic repolarization changes and voltage criteria for left ventricular hypertrophy were examined, in relation to hemodynamic, echocardiographic and angiographic data. This was done to evaluate their association with abnormalities in cardiac function and structure in 53 patients with chronic aortic regurgitation and 36 patients with chronic mitral regurgitation. No patient showed evidence of coronary artery disease. Of the patients with aortic regurgitation, the 27 patients with an abnormal repolarization pattern at ECG had worse NYHA functional class when compared to the 24 patients with normal repolarization (2.4 +/- 1 vs 1.6 +/- 0.9; p less than .01). They also had greater left ventricular dimensions (end-diastolic volume: 162 +/- 57 ml/m2 vs 109 +/- 15 ml/m2, p less than .01; end-systolic volume: 85 +/- 46 ml/m2 vs 44 +/- 31 ml/m2, p less than .01), lower left ventricular ejection fraction (.50 +/- .12 vs .63 +/- .14; p less than .01), greater left ventricular mass (170 +/- 56 gr/m2 vs 119 +/- 29 gr/m2; p less than .01) and higher end-diastolic left ventricular pressure (21 +/- 11 mmHg vs 11 +/- 8 mmHg; p less than .01). QRS voltage was less closely related to cardiac function and structure and thus, did not modify the conclusions based on repolarization findings alone. Furthermore, repolarization patterns identified patient subgroups with high or low prevalences of previously described predictors of poor surgical outcome. The presence or absence of the "strain" pattern was not related to differences in cardiac structure and function, in patients with mitral regurgitation.(ABSTRACT TRUNCATED AT 250 WORDS)

[Surgical results in mitral insufficiency: prognostic value of the indices of left ventricular function]. / Risultato operatorio nell'insufficienza mitralica: valore prognostico degli indici di funzione ventricolare sinistra.

Left ventricular function is a major prognostic factor in patients with mitral regurgitation, but the ability of echocardiographic and hemodynamic parameters to predict the surgical result is controversial. We investigated the prognostic role of various pre-operative indices of left ventricular function in 23 consecutive patients who underwent successful surgical correction of chronic mitral regurgitation. At a mean follow-up of 20 +/- 16 months, patients underwent echocardiography and radio-nuclide angiography and were grouped according to the post-operative left ventricular ejection fraction. Group A was made up of 16 patients with a left ventricular ejection fraction greater than or equal to .45: they showed post-operative reduction of the left ventricular end-diastolic diameter (from 36.3 +/- 3.2 to 30.5 +/- 4.5 mm/m2; p less than .001) and of the radius/thickness ratio (from 3.5 +/- 0.6 to 2.9 +/- 0.6; p less than .01). In 7 patients (group B), post-operative left ventricular ejection fraction was less than .45 and no significant changes in the left ventricular end-diastolic diameter (from 41.5 +/- 2.7 to 36.9 +/- 6.1 mm/m2; NS) or the radius/thickness ratio (from 3.9 +/- 0.9 to 3.4 +/- 1.0; NS) were observed. During the follow-up all group A patients remained asymptomatic or minimally symptomatic, whereas 2 group B patients died of refractory left ventricular failure. Pre-operative left ventricular volumes and diameters, both at end-diastole and end-systole, were significantly greater in group B patients.(ABSTRACT TRUNCATED AT 250 WORDS)