The Italian Society of Andrology and Sexual Medicine (SIAMS), along with ten other Italian Scientific Societies, guidelines on the diagnosis and management of erectile dysfunction.

PURPOSE: Erectile dysfunction (ED) is one of the most prevalent male sexual dysfunctions. ED has been in the past mistakenly considered a purely psycho-sexological symptom by patients and doctors. However, an ever-growing body of evidence supporting the role of several organic factors in the pathophysiological mechanisms underlying ED has been recognized. METHODS: The Italian Society of Andrology and Sexual Medicine (SIAMS) commissioned an expert task force involving several other National Societies to provide an updated guideline on the diagnosis and management of ED. Derived recommendations were based on the Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) system. RESULTS: Several evidence-based statements were released providing the necessary up-to-date guidance in the context of ED with organic and psychosexual comorbidities. Many of them were related to incorrect lifestyle habits suggesting how to associate pharmacotherapies and counseling, in a couple-centered approach. Having the oral therapy with phosphodiesterase type 5 inhibitors as the gold standard along with several other medical and surgical therapies, new therapeutic or controversial options were also discussed. CONCLUSIONS: These are the first guidelines based on a multidisciplinary approach that involves the most important Societies related to the field of sexual medicine. This fruitful discussion allowed for a general agreement on several recommendations and suggestions to be reached, which can support all stakeholders in improving couple sexual satisfaction and overall general health.

Systematic review and meta-analysis on coronary calcifications in COVID-19.

Chest CT is valuable to detect alternative diagnoses/complications of COVID-19, while its role for prognostication requires further investigation. Non-pulmonary radiological findings such as cardiovascular calcifications could increase the predictivity of clinical outcomes of COVID-19 patients beyond pulmonary involvement. Several observational studies have reported mixed results on the role of coronary calcifications in COVID-19 patients as a predictor of hospitalization, ventilatory support, and mortality. The purpose of the study is to systematically review the available evidence on the predictive role of cardiovascular calcifications in SARS-CoV2 disease. The meta-analysis confirms the prognostic significance of coronary calcifications on hospital mortality, and coronary calcifications (CAC ≠ 0) were associated with an OR for mortality of 2.19 (95% CI 1.36-3.52). CAC was neutral on respiratory outcomes, but it was associated with an increased trend of cardiovascular events. Coronary calcium appears as a promising biomarker imaging even in short-term outcomes (MACEs, hospital mortality) in a non-cardiovascular disease such as Sars-CoV2 infection. Further large studies are needed to confirm promising results of this imaging biomarker in non-cardiovascular disease.

From the abluminal biodegradable polymer stent to the polymer free stent. Clinical evidence.

The implementation of methods of the coronary angioplasty was one of the most important achievement in the field of treatment of coronary artery disease. Abluminal biodegradable polymer stents (BDS) and polymer free stent are the newest and the most promising research concerning coronary stent technology. In this article we discuss the perceived need for BDS-polymer free stents, the current clinical evidence, limits and future perspectives.

Evaluation of re-endothelization extent at mid-term follow-up after drug eluting balloon plus bare metal stent implantation during primary coronary angioplasty: insight from OCT imaging.

One quarter of patients with STEMI submitted to primary percutaneous coronary intervention (PCI) need repeated target vessel revascularization (TVR) because of stent restenosis or thrombosis. Introduction of DES has effectively reduced the incidence of these complications but the safety of this type of stent in the setting of AMI is limited due to the unpredictable risk of stent malapposition and vessel remodelling in the long term follow-up. Recently, treatment with drug eluting balloon (DEB) in association with bare metal stenting (BMS) has been reported to have an excellent efficacy and safety profile. However, little is known regarding the extent of stent coverage in BMS after DEB utilization.

Carotid plaque characterisation by IVUS-VH during carotid stenting: the "eyes wide shut" between plaque morphology and symptoms.

Stroke is the third most common cause of death in North America and ever year approximately 700,000 new strokes are reported in the United States. Seventy-five percent of these occur in the distribution of the carotid arteries. Among strokes of a thromboembolic etiology, carotid occlusive disease is the most common cause. As many as 150,300 stroke-related fatalities are documented annually, with a total cost for the health-care system of approximately $ 18 billion per year. This review will focus on the different pathomorphologic aspects of carotid plaque, outlining the similarities and differences with the coronary plaque, with particular attention on how intravascular imaging may contribute to a better stratification of the patient treatment.

High plasma levels of the soluble receptor for advanced glycation endproducts in patients with symptomatic carotid atherosclerosis.

BACKGROUND: Advanced glycation endproducts (AGEs), particularly carboxymethyl(lysine)-adducts (CML), exert part of their cellular effects by binding to a receptor, named receptor for AGEs (RAGE). The soluble form of this receptor (sRAGE) has been shown to have an athero-protective role. We hypothesized the existence of a relationship between the AGE-RAGE axis and the occurrence of symptoms related to carotid atherosclerosis in nondiabetic conditions. MATERIALS AND METHODS: We evaluated plasma levels of CML and sRAGE (by ELISA), and tissue levels (tAGEs and tRAGE, semiquantitatively, by immunohistochemistry) in endarterectomy carotid plaque tissue in 29 nondiabetic patients. At the time of surgery, 10 patients were asymptomatic and 19 were symptomatic. RESULTS: Plasma levels of sRAGE were higher in symptomatic patients than in asymptomatic patients [median (interquartile range): 676 (394-858) pg mL(-1) vs. 347 (284-479) pg mL(-1), P = 0.009]. In symptomatic patients, plasma levels of sRAGE correlated positively with CML (r = 0.60, P < 0.01), C-reactive protein (CRP) (r = 0.618, P < 0.01) and fibrinogen (r = 0.522, P<0.005), while in asymptomatic patients, no correlation was observed. Although tissue and plasma levels of AGEs and RAGE did not correlate between each other, tAGEs and tRAGE were also positively correlated only in symptomatic patients (chi(2) = 8.93, P = 0.003). CONCLUSIONS: Plasma levels of sRAGE are higher in symptomatic than asymptomatic carotid atherosclerosis. Higher levels of sRAGE in symptomatic patients may be markers of a higher degree of vascular inflammation in such patients.

Paclitaxel eluting balloon: from bench to bedside.

Despite the impressive progress of percutaneous treatment modalities, restenosis remains the major Achilles heel of interventional cardiology. Approximately 25% of the general population treated for coronary diseases with a bare-metal stent and about 10% of patients treated with a drug-eluting stent develop an overgrowth of vascular tissue and renarrowing inside the stent, or in-stent restenosis. These rates are even greater in diabetics and patients at higher risk of restenosis both for clinical presentation (patients in dialysis, low ejection fraction) or anatomical characteristics (ostial, bifurcation, long lesions). Non-stent based local drug delivery and particularly the use of paclitaxel eluting balloon (PEB) could be one promising strategy to reduce restenosis. This review will briefly explore the different characteristics of PEB devices currently present in the market and summarize the results obtained both in animal models and clinical practice, giving an indication of the potential field of application of this new technology.

Deferred urgency carotid artery stenting in symptomatic patients: clinical lessons and biomarker patterns from a prospective registry.

INTRODUCTION: The aim of this prospective observational registry was to study the outcome of symptomatic patients presenting with recent TIA or minor stroke and severe carotid stenosis, submitted to early percutaneous treatment by stenting. A secondary aim was to evaluate the biological activity of the symptomatic carotid plaques by serial serum and urinary markers (PAPP-A, hs-CRP, MMP-2/MMP-9, IL-6/IL-8, TNF alpha, CD40L) measured by enzyme-linked immunosorbent assay before and after treatment. METHODS: From May 2005 to June 2006, 57 patients were enrolled in this prospective registry. All patients underwent carotid stenting using a concentric filter for cerebral protection. The procedure was performed within 24-48hrs of the last attack in patients with TIA (n=24, 42%) and between 14 and 30 days in patients with stroke (n=33, 58%). RESULTS: Successful stent implantation was achieved in all cases (100%). Adverse events at 1 month were 1 death (1.7%) and 2 TIAs (3.5%). Some of the vulnerability markers, in particular those reflecting an active systemic inflammatory process of the plaque (PAPP-A, hs-CR, and IL-6), were significantly elevated at the time of enrolment, increased after stenting and decreased after 30 days. CONCLUSION: Deferred CAS is feasible and safe in selected patients with symptomatic carotid stenosis. This preliminary study in a limited series of patients with unstable carotid plaques revealed that endovascular treatment has a satisfactory outcome considering the very high risk profile of the patient population. The evaluation of some biomarkers suggested an inflammatory role in the process of an unstable carotid plaque generating an acute cerebral event.

Enhanced coronary vasa vasorum neovascularization in experimental hypercholesterolemia.

Coronary arteries contain a network of vasa vasorum in the adventitia. The three-dimensional anatomy of the vasa vasorum in early coronary atherosclerosis is unknown. This study was designed to visualize and quantitate the three-dimensional spatial pattern of vasa vasorum in normal and experimental hypercholesterolemic porcine coronary arteries, using a novel computed tomography technique. Animals were killed after being fed either a high cholesterol diet (n = 4) or a control diet (n = 4) for 12 wk. The proximal left anterior descending coronary artery was removed from the heart, scanned, and reconstructed, and quantitation of vasa vasorum density was performed. Two different types of vasa vasorum were defined: first-order vasa vasorum ran longitudinally parallel to the vessel and second-order originated from first-order vasa circumferentially around the vessel wall. Compared with controls in hypercholesterolemic coronary arteries, there was a significant increase in the area of the vessel wall (3.86+/-0.22 vs. 8.07+/-0.45 mm2, respectively, P < 0.01) and in the density of vasa vasorum (1. 84+/-0.05/mm2 vs. 4.73+/-0.24/mm2; respectively, P = 0.0001). This occurred especially by an increase of second-order vasa vasorum and disorientation of normal vasa vasorum spatial pattern. This study suggests that adventitial neovascularization of vasa vasorum occurs in experimental hypercholesterolemic coronary arteries and may be a part of the early atherosclerotic remodeling process.

From carotid plaque biology to serologic markers of vulnerability to predict the risk of cerebrovascular events.

Stroke is the second cause of mortality in industrialized countries. Atherosclerotic plaque rupture with atheromatous debris distal embolization is the pathogenetic mechanism responsible for cerebrovascular events due to atherosclerotic carotid disease. Plaque composition rather than lesion burden seems to be the determinant factor producing rupture and subsequent thrombosis. Histologic features of vulnerability are : a large lipid core, a thin fibrous cap, and an inflammatory infiltrate rich of monocytes and macrophages. In the clinical practice, it is difficult to predict the risk of experiencing a major cerebrovascular events especially in asymptomatic patients. New invasive techniques such as intravascular ultrasound with termography, optical coherence tomography, fotons spectroscopy and elastography have been developed to detect atherosclerotic lesion tissue composition. However, such techniques are difficult to apply on a large scale basis in primary prevention. On the contrary, new serologic biomarkers such as Pregnancy Associated Plasma Protein-A, Lp-PLA2, Interleukin-6, Interleukin-12, metalloproteinases, lipoprotein-(a), and plaque oxidative products have been recently proposed for screening general and high risk population. The present paper will briefly review the current histologic characteristics of vulnerable plaque and the new imaging tools proposed for its detection, focusing on the most recent serologic biomarkers evaluated in the clinical practice to increase our accuracy in predicting not only the plaque but moreover the patient at risk for an acute cerebrovascular event.

Plasma levels of metalloproteinases-3 and -9 as markers of successful abdominal aortic aneurysm exclusion after endovascular graft treatment.

BACKGROUND: Structural alterations of aortic wall resulting from degradation of matrix proteins by matrix metalloproteinases (MMPs) characterize abdominal aortic aneurysms (AAAs). No studies have compared circulating levels of MMPs after endovascular graft (EVG) exclusion in comparison with open surgical repair (OSR) in patients affected by AAA. METHODS AND RESULTS: An abdominal angiography and CT scan were performed in all patients at the time of enrollment. A spiral CT scan was performed at 6 months to detect presence of endoleaks. MMP-3 and MMP-9 levels were measured before EVG (n=30) and OSR (n=15) treatments and at 1, 3, and 6 months of follow-up by a sandwich ELISA technique. Healthy volunteers (n=10) were used as control subjects. Immunohistochemical staining for MMP-9 and MMP-3 was performed on tissue samples from surgical cases. Both MMP-9 and MMP-3 mean basal levels were significantly higher in patients affected by AAA than in control subjects (32.3+/-20.7 ng/mL for EVG and 28+/-9.9 ng/mL for OSR versus 8.9+/-2.5 ng/mL, 2P<0.05; 18.3+/-9.7 ng/mL and 26.7+/-10.8 ng/mL versus 8.2+/-5.3 ng/mL, 2P<0.001). In the OSR group, both MMP-9 and MMP-3 mean levels decreased after surgery (28+/-9.9 ng/mL at basal versus 14.7+/-6.6 ng/mL at 6 months, 2P<0.001; 26.7+/-10.8 versus 12+/-5.3 ng/mL; 2P<0.001). In the EVG group, a statistically significant difference at 6-month follow-up in MMP-9 and MMP-3 mean plasma values was detected in patients who had endoleakage in comparison with patients without endoleakage (44.3+/-20.7 versus 14.6+/-7.0 ng/mL, 2P<0.005; 25+/-11.5 versus 10.3+/-5.4 ng/mL, 2P<0.005). CONCLUSIONS: After EVG exclusion, MMP-9 and MMP-3 levels decreased to a level similar to that of patients undergoing OSR. In addition, a lack of decrease in MMP levels after EVG exclusion may help in identifying patients who will have endoleakage and consequent aneurysm expansion caused by continuous sac pressurization during follow-up.

Hyperfibrinogenemia is associated with specific histocytological composition and complications of atherosclerotic carotid plaques in patients affected by transient ischemic attacks.

BACKGROUND: Epidemiological studies have demonstrated that hyperfibrinogenemia is an independent risk factor for cerebrovascular atherosclerosis. However, the underlying mechanisms are poorly understood. We studied whether hyperfibrinogenemia could modify the histological composition of atherosclerotic plaque and precipitate carotid thrombosis resulting from rupture of the plaque. METHODS AND RESULTS: We studied the histological composition of 71 carotid atherosclerotic plaques from patients who had undergone surgical endarterectomy after a first episode of transient ischemic attack. Patients were divided into 3 groups corresponding to the tertiles of plasma fibrinogen values. Hypercholesterolemia, hypertriglyceridemia, hypertension, diabetes, and smoking habit were also assessed. At the histological analysis, plaques of patients in the highest tertile of fibrinogen (>407 mg/dL) were characterized by a high incidence of thrombosis (66.7% of cases) compared with plaques of subjects in the lower (21.7%) (P=0.002) and middle (29. 2%) (P=0.009) tertiles. Plaque rupture was significantly associated with high fibrinogen levels (54.2%, P=0.003). Multivariate logistic regression indicated that hyperfibrinogenemia was an independent risk factor for a decrease in cap thickness (P=0.0005), macrophage foam cell infiltration of the cap (P=0.003), and thrombosis (P=0. 003). When the presence of other risk factors was accounted for, hyperfibrinogenemia remained an independent predictor of carotid thrombosis with an odds ratio of 5.83, compared with other risk factors. CONCLUSIONS: The results of the present study add to the evidence that hyperfibrinogenemia, independently of other risk factors, is associated with a specific histological composition of carotid atherosclerotic plaques that predisposes them to rupture and thrombosis.

Artery size, neointima, and remodeling: time for some standards.

Controversy continues regarding the mechanism of coronary restenosis. While neointimal thickening was initially considered the major cause, recent studies suggest that changes in arterial size, or remodeling, plays an important or even dominant role in late lumen loss. Moreover, neointimal thickness and remodeling may be interrelated. The field has been complicated by the fact that remodeling analyses have not used consistent definitions or methods. In this editorial we thus describe a quantitative paradigm for remodeling analyses: as arterial plaque or neointima forms in an artery, it is accompanied by luminal encroachment, artery expansion or gradations of either. In this manner, remodeling is generally defined as any arterial size change (enlargement or contraction), independent or dependent of neointimal thickening. Standardization of definitions and quantitative methods may improve understanding of the components of restenosis resulting from artery size changes, neointimal thickening and their impact on lumen size.

Fibrin-film stenting in a porcine coronary injury model: efficacy and safety compared with uncoated stents.

OBJECTIVES: This study was designed to test the efficacy and safety of a fibrin-film-covered stent compared with that of a bare metal stent in the porcine coronary injury model. BACKGROUND: Biodegradable stents are a potential method of achieving total lesion coverage and delivering local, lesion-specific drug therapy. METHODS: Two coronary arteries in each pig were randomly assigned to deployment of either a fibrin-film or a bare tantalum wire-coil stent. An oversized balloon injury, 1.15 to 1.30 times the reference vessel diameter, was induced in each coronary segment before stenting to simulate angioplasty injury. Thirty pigs were studied: group 1 for 28 days (15 pigs); group 2 for 90 days (5 pigs); group 3 for 6 months (5 pigs); group 4 for 1 year (5 pigs). RESULTS: Two pigs died of occlusion of the bare stent and one of occlusion of the fibrin stent (p > 0.99). There were no significant differences between the fibrin-stented and bare-stented coronary segments with regard to arterial injury. In group 1 (28 days, 14 pigs), the mean neointimal thicknesses in the fibrin-stented and bare-stented groups were 0.57+/-0.31 and 0.57+/-0.27 mm, respectively (p=0.89). In groups 2 to 4 (90 days, four pigs; 6 months, four pigs; 1 year, five pigs), the mean neointimal thicknesses for fibrin- and bare-stented coronary segments at the times studied were 0.48+/-0.26 versus 0.50+/-0.22 mm at 90 days; 035+/-0.04 versus 0.35+/-0.16 mm at 6 months; and 0.33+/-0.14 versus 0.30+/-0.14 mm at 1 year (p=0.98). CONCLUSIONS: Fibrin-film stents appear to be an excellent candidate for local drug delivery because they can completely and safely cover the stented coronary segment while degrading slowly over 1 to 3 months. This result is important when compared with the poor results of previous studies of synthetic polymer stents.

Histologic correlates of angiographic chronic total coronary artery occlusions: influence of occlusion duration on neovascular channel patterns and intimal plaque composition.

OBJECTIVES: Age-related changes in histologic composition and neovascular channel (NC) pattern of angiographic chronic total coronary artery occlusions (CTOs) were studied to define histologic correlates of age-related revascularization profiles and neovascular channel formation. BACKGROUND: Revascularization of CTOs is frequently characterized by inability to cross or dilate the lesion and a high incidence of reocclusion or restenosis but low periprocedural ischemic complication rates. Little is known about the histopathologic basis of these observations. METHODS: Ninety-six angiographic CTOs from autopsy studies in 61 patients who had undergone coronary angiography within 3 months of death were studied. Abrupt plaque rupture was excluded. Occlusion segments were analyzed for 1) histologic composition as a function of lesion age; and 2) NC pattern as a function of lesion age and intimal plaque (IP) composition. RESULTS: Cholesterol and foam cell-laden IP was more frequent in younger lesions (p = 0.0007), whereas fibrocalcific IP increased with CTO age (p = 0.008). IP NCs arose directly from adventitial vasa vasorum and were anatomically and quantitatively related in terms of number and size (p = 0.0001) to the extent of IP cellular inflammation. IP cellular inflammation exceeded that found in the adventitia (p < 0.001) or media (p = 0.0001) across all CTO ages. In CTOs < 1 year old, the adventitia was associated with a larger number and size of NCs relative to the IP (p = 0.0006 and p = 0.009), media (p = 0.0001 and p = 0.002) and recanalized lumen (p = 0.0001 and p = 0.001). In CTOs >1 year old, the adventitia and IP NC numbers were similar and exceeded NC numbers found in the media (p = 0.0001) and recanalized lumen (p = 0.0001 and p = 0.003). CONCLUSIONS: Angiographic CTO frequently corresponds to less than complete occlusion by histologic criteria. Age-related changes in IP composition from cholesterol laden to fibrocalcific may explain the adverse revascularization profile of older CTOs. IP NC growth derived from the adventitia increases with age and is strongly associated with IP cellular inflammation. IP NC formation may protect against the flow-limiting effects of IP growth.

Arterial calcification and not lumen stenosis is highly correlated with atherosclerotic plaque burden in humans: a histologic study of 723 coronary artery segments using nondecalcifying methodology.

OBJECTIVES: This study was designed to evaluate whether calcium deposition in the coronary arteries is related to atherosclerotic plaque burden and narrowing of the arterial lumen. BACKGROUND: Many studies have recently documented the feasibility of electron beam computed tomography to detect and quantify coronary artery calcification in patients. Although these studies suggest a general relation between calcification and severity of coronary artery disease, the value of coronary calcium in defining atherosclerotic plaque and coronary lumen narrowing is unclear. Previous pathologic comparisons have failed to detail such a relation in identical histologic sections. This finding may be due to atherosclerotic remodeling. METHODS: A total of 37 nondecalcified coronary arteries were processed, sectioned at 3-mm intervals (723 sections) and evaluated by computer planimetry and densitometry. RESULTS: A significant relation between calcium area and plaque area was found on a per-heart basis (n = 13, r = 0.87, p < 0.0001), per-artery basis (left anterior descending coronary artery [LAD]: n = 13, r = 0.89, p < 0.0001; left circumflex coronary artery [LCx]: n = 11, r = 0.7, p < 0.001; right coronary artery [RCA]: n = 13, r = 0.89, p < 0.0001) and per-segment basis (n = 723, r = 0.52, p < 0.0001). In contrast, a poor relation existed between residual histologic lumen area and calcium area for individual hearts (r = 0.48, p = NS), individual coronary arteries (LAD: r = 0.59, p = NS; LCx: r = 0.10, p = NS; RCA: r = 0.59, p = NS) and coronary segments (r = 0.07, p = NS). Longitudinal changes in external elastic lamina areas were highly correlated with changes in plaque area values (r = 0.60, p < 0.0001), whereas lumen area did not correlate with plaque size change (r = 0.01, p = NS). CONCLUSIONS: Coronary calcium quantification is an excellent method of assessing atherosclerotic plaque presence at individual artery sites. Moreover, the amount of calcium correlates with the overall magnitude of atherosclerotic plaque burden. This study suggests that the remodeling phenomenon is the likely explanation for the lack of a good predictive value between lumen narrowing and quantification of mural calcification.

Adventitial vasa vasorum in balloon-injured coronary arteries: visualization and quantitation by a microscopic three-dimensional computed tomography technique.

OBJECTIVES: The objective of this study was to examine the quantitative response of the adventitial vasa vasorum to balloon-induced coronary injury. BACKGROUND: Recent attention has focused on the role of vasa vasorum in atherosclerotic and restenotic coronary artery disease. However, the three-dimensional anatomy of these complex vessels is largely unknown, especially after angioplasty injury. The purpose of this study was to visualize and quantitate three-dimensional spatial patterns of vasa vasorum in normal and balloon injured porcine coronary arteries. We also studied the spatial growth of vasa vasorum in regions of neointimal formation. A novel imaging technique, microscopic computed tomography, was used for these studies. METHODS: Four pigs were killed 28 d after coronary balloon injury, and four pigs with uninjured coronary arteries served as normal controls. The coronary arteries were injected with a low-viscosity, radiopaque liquid polymer compound. Normal and injured coronary segments were scanned using a microscopic computed tomography technique. Three-dimensional reconstructed maximum intensity projection and voxel gradient shading images were displayed at different angles and voxel threshold values, using image analysis software. For quantitation, seven to 10 cross-sectional images (40 normal and 32 balloon injured cross-sections) were captured from each specimen at a voxel size of 21 microm. RESULTS: Normal vasa vasorum originated from the coronary artery lumen, principally at large branch points. Two different types of vasa were found and classified as first-order or second-order according to location and direction. In balloon-injured coronary arteries, adventitial vasa vasorum density was increased (3.16+/-0.17/mm2 vs. 1.90+/-0.06/mm2, p = 0.0001; respectively), suggesting neovascularization by 28 d after vessel injury. Also, in these injured arteries, the vasa spatial distribution was disrupted compared with normal vessels, with proportionally more second-order vasa vasorum. The diameters of first-order and second-order vasa were smaller in normal compared with balloon-treated coronary arteries (p = 0.012 first-order; p < 0.001, second-order; respectively). The density of newly formed vasa vasorum was proportional to vessel stenosis (r = 0.81, p = 0.0001). Although the total number of vasa was increased after injury, the total vascular area comprised of vasa was significantly reduced in injured vessels compared with normals (3.83+/-0.20% to 5.42+/-0.56%, p = 0.0185). CONCLUSIONS: Adventitial neovascularization occurs after balloon injury. The number of new vessels is proportional to vessel stenosis. These findings may hold substantial implications for the therapy of vascular disease and restenosis.

Intensive care complications in liver and multivisceral transplantation.

The complications concerning liver and intestinal transplant surgery have relevance for the field of intensive care because they share some characteristics with those following complex long-term surgery. Thus, in this article we shall try to describe complications that are specific to liver and multivisceral transplants. A review of the existing literature on this topic reveals a large number of studies dedicated to early as well as late surgical complications, and immunosuppressive treatment, while there are far fewer contributions describing complications exclusively concerning intensive care. We shall thus attempt to focus on certain aspects where, besides the literature data, we have personal experience. In particular we want to underline the implications of failure in the functional recovery of the graft; alterations in water, electrolyte, and glycemic balance; as well as neurological, respiratory, renal, nutritional, and infective complications.

Effect of long-term treatment with propionyl-L-carnitine on smooth muscle cell polyploidy in spontaneously hypertensive rats.

Experimental studies suggest that DNA content is increased in the smooth muscle cells of the arteries of hypertensive animals. It is unclear whether an increase in DNA content occurring in the smooth muscle cells of hypertensive rats represents a pressure-dependent effect. To evaluate the antihypertensive effect of long-term treatment with propionyl-L-carnitine and the possible morphological changes in thoracic smooth muscle cells correlated with this effect, we studied 4-month-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) randomly divided into five groups. One group of SHR was treated with propionyl-L-carnitine for 12 months; the other four groups of SHR and WKY received no treatment and were controls. We used static and flow cytometry to evaluate the polyploid cell content in thoracic aorta smooth muscle cells. Systolic pressure in untreated SHR progressively increased during the experiment. Treatment did not significantly influence pressure values in SHR. In WKY, blood pressure was significantly lower than that in treated and untreated age-matched SHR (2P < .02). The number of polyploid smooth muscle cells was significantly lower in the propionyl-L-carnitine-treated SHR than in the untreated rats (2P < .04) and similar to values for WKY. The reduction of polyploid cells in treated SHR was paralleled by a significant decrease of the aortic total DNA content, whereas no modifications occurred in smooth muscle cell mass. Long-term treatment with propionyl-L-carnitine may interfere with cellular mechanisms regulating the secondary responses involved in DNA synthesis.