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The Authors have examined the PO2 and PCO2 of peripheral arterial blood in 10 hypertensive subjects before and after 20 mg of nifedipine administered by sublingual route. A PaO2 decrease and a light increase of PaCO2 were observed; this pattern, if considered together with the increase of CO2 and the decrease of pulmonary resistance, may be attributed to a greater perfusion of those districts having a low V/Q ratio.

The haemodynamic effects of salbutamol were studied in 14 patients with chronic obstructive lung disease with a single dose of 100 and 200 gamma, administered by i.v. injection. The results of study revealed salbutamol intravenous injection significantly increases heart rate, cardiac index and decreases vascular systemic resistance. There was no significant change in blood gas tensions. This study indicates that salbutamol produces variation in preload and afterload by a direct action on vascular smooth muscle.

Background: Ivabradine (IVA) is effective in patients with coronary artery disease (CAD) or systolic heart failure in sinus rhythm. Its action consists in reducing heart rate (HR) and improving the time of left ventricular (LV) diastolic filling. The aim of this study was to evaluate the effects of IVA added to conventional therapy on patients with diastolic heart failure (DHF) and preserved ejection fraction (HFpEF). Methods: We evaluated 25 patients with DHF in the New York Heart Association (NYHA) Class II-III and sinus rhythm. In these, IVA per os (5 mg/twice a day) was added to the conventional medical therapy and given for 12 weeks. Immediately before the beginning of IVA therapy and 3 months later, patients underwent echocardiographic evaluation by two-dimensional (2D) ultrasound and tissue Doppler imaging (TDI). The patterns of diastolic mitral inflow and pulmonary venous flow were recorded using 2D echocardiography, while the diastolic phase of mitral flow was recorded by TDI, from the lateral mitral annulus. Results: Three months after the addition of IVA to conventional treatment, HR significantly decreased in comparison to the baseline values. On the contrary, the echocardiographic indexes of LV diastolic dysfunction improved. Conclusions: These results testify that the addition of IVA to conventional therapy in patients with HFpEF can improve LV diastolic function evaluated by 2D and tissue Doppler-echocardiographic patterns. These Doppler-echocardiographic results match with the clinical improvement of patients evaluated.

Resistant hypertension is defined as a blood pressure above therapeutic goals, despite the concurrent use of three or more antihypertensive drugs of different pharmacological classes, and all being administered according to an optimum dosage schedule. The prevalence of resistant hypertension in the older people has not yet been exactly quantified. The updated available estimates deriving from some clinical trials report a prevalence of approximately 20-30% of all hypertensive patients. Advanced age seems to be an important risk factor in resistant forms of high blood pressure. Therefore this clinical condition may potentially increase in the coming years. Chronic kidney disease is the most frequent comorbidity associated with resistant hypertension and often leads to poor prognosis. The article describes a case report of an older subject with such a clinical condition suggesting diagnostic and therapeutic plan based on a rational strategy to control hypertension and the most recent knowledge reported in the medical literature.

Inherited and acquired tendency to the formation of clots represents an important cause of morbidity and mortality for ischemic events in young people (aged between 40 and 50 years) that is more and more frequently identified. The haemostasis' disorders may happen on the venous or arterial side. Arterial thrombus is a 'white' thrombus, also called temporary thrombus. It consists of aggregate platelets only. On the contrary, venous thrombus is 'red' or permanent thrombus composed of platelets, red cells and fibrin. The first is the result of platelets' adhesion or aggregation. Instead, the permanent thrombus derives from the coagulant factors successively acting on 'white' thrombus. The different pathogenesis justifies both the distinction between 'hypercoagulability' and 'thrombophilia' and the different treatments employed. Antiphospholipid antibody syndrome, polycythemia vera, atrial fibrillation-acquired hyperhomocysteinemia, diabetes mellitus and myeloproliferative disease are the most frequent causes of acquired hypercoagulable state, prevalently responsible for deep venous thrombosis. Among the inherited forms, congenital hyperhomocysteinemia, factor V Leiden mutation, proteins C and S deficiency and antithrombin mutation are included. These may induce both venous and arterial acute events. Hyperhomocysteinemia can be congenital and acquired and is more correctly named as 'thrombophilia' rather than 'hypercoagulability'. That happens because it involves the platelets' aggregation rather than the coagulant cascade. The optimal treatment of thrombophilias consists of oral (warfarin) or injectable (heparins) anticoagulants. Direct thrombin inhibitors, platelet glycoprotein IIb/IIIa antagonists, and tissue factor inhibitors also appear to be some attractive approaches. For acquired forms, treatments of their aetiologies must also be carried out. For acquired hyperhomocysteinemia, both antiplatelets' therapy (aspirin + clopidogrel) and new direct thrombin inhibitors (as dabigatran) could be considered. Finally, as secondary prevention of an arterial acute event (stroke, IMA or peripheral ischemia) due to hyperhomocysteinemia, lifetime dual antiplatelets' therapy should be used.

A condition of insulin resistance (IR) frequently occurs in the elderly. This is because of some age-related hormonal and metabolic changes, which are responsible for increased serum levels of fasting blood glucose. IR also induces an increased and prolonged serum value of post-prandial hyperglycaemia, favouring the atherosclerotic process and frequent acute cardiovascular events. This review examines how the post-prandial hyperglycaemic “spikes” play a major role in vascular damage in aged individuals with or without diabetes mellitus. This occurs through oxidative stress, endothelial dysfunction and subclinical inflammation induced by IR, as illustrated by numerous experiments and clinical reports. The evidence opposing all this is from two major trials, the STOP-NIDDM study and the recent HEART2D study. Finally, it is hypothesised that a daily dose of acarbose may prevent or mitigate this damage in aged people without overt diabetes mellitus.

Fetuin-A, or α2-Heremans–Schimd glycoprotein, is a potent inhibitor of calcium-phosphate precipitation. In end-stage renal disease (ESRD) patients, its serum levels are significantly reduced favouring ectopic calcifications, such as vascular and valvular calcifications for hyperphosphatemia and increased Ca × P product. Numerous evidences indicate that in low fetuin-A levels patients, mitral and/or aortic calcifications are often present. Coronary, carotid calcifications and/or other vascular phatological findings connected with increased calcium deposition in the lamina media of the arterial wall (Monkeberg’s calcinosis or arteriosclerosis), acute inflammation and/or endothelial dysfunction can be also found. Thus, low levels of fetuin-A in ESRD act as “non-traditional” risk factor for cardiovascular disease. Other “non-traditional” cardiovascular risk factors in dialyzed patients are: extracellular volume overload; insulin resistance; anaemia, and oxidative stress, many cross-sectional studies showed a direct associations of high fetuin-A levels with impaired glucose and lipid metabolism inducing metabolic syndrome in non-dialyzed patients. In these, high fetuin-A levels induce atherosclerotic lesions by insulin resistance. In conclusion, fetuin-A is able to induce both arteriosclerosis and atherosclerosis. Its serum levels seems to act (both in dialyzed and non-dialyzed patients) such as “non-traditional” cardiovascular risk factor, even if its action mechanism was not completely elucidated and further studies performed in wide range are requested. Therapeutically, some compounds such as Sevelamer, etidronate, calcium channel blockers and others interventions, are promising in to reduce calcium deposition in the vessel walls and acute inflammation induced by the low α2-Heremans–Schmid glycoprotein serum levels in dialyzed patients. On the contrary, extended-release niacin seems to be able to reduce cardiovascular, metabolic and inflammatory complicances dependent on high fetuin-A serum levels.

The aim of this review was to describe the different ultrasonic modalities to non-invasively evaluate right cardiac chambers and pulmonary vascular bed function. M-Mode, 2-D, conventional pulsed doppler, tissue doppler imaging (TDI), strain rate imaging (SRI) and 3D echocardiography are illustrated in order to obtain both regional and global right heart and pulmonary function. The results have a good correlation with other invasive and non-invasive diagnostic techniques, as magnetic resonance imaging (MRI). All these echocardiograpic techniques can be employed to evaluate the morphologic and functional pictures of right heart and pulmonary circulation in presence of pulmonary hypertension (PH). The hemodynamic profile obtained consent to anatomically and functionally characterize PH. But, other experiences performed on more wide range of healthy and PH patients are necessary to confirm the described results

Objective: To investigate the effect of raloxifene on atherosclerosis progression in healthy postmenopausal women. Design: In a prospective fashion, a total of 155 healthy postmenopausal women were randomly assigned to receive raloxifene 60 mg/day or a matching placebo for 18 months. Atherosclerosis progression was evaluated by B-mode ultrasonography measuring the intima-media thickness (IMT) of the carotid arteries. Plasma levels of triglycerides, low-density lipoprotein cholesterol, soluble forms of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1, E-selectin, interleukin-6, tumor necrosis factor a, adiponectin, and the degree of insulin resistance by the homeostatic model assessment method were also determined. Results: The progression slope of carotid IMT was 0.0112 mm/18 months in the raloxifene group and 0.0857 mm/18 months in the placebo group (P < 0.004). Raloxifene treatment compared with placebo produced a significant decrease in plasma triglycerides (P < 0.02), low-density lipoprotein cholesterol (P < 0.02), soluble forms of intercellular adhesion molecule-1(P < 0.005) and vascular cell adhesion molecule-1 (P < 0.04), E-selectin (P < 0.02), interleukin-6 (P < 0.005), tumor necrosis factor a (P < 0.005) levels, and homeostatic model assessment index (P < 0.005) and a significant increase in plasma adiponectin levels (P < 0.001). Logistic regression analysis indicated that women receiving raloxifene had a lower risk of IMT progression (odds ratio = 0.41; 95% CI: 0.32-0.70). Conclusion: Raloxifene treatment, possibly through an increase in plasma adiponectin levels, may slow the progression of IMT in postmenopausal women.

BACKGROUND Oxidative stress and increased inflammation have been reported to be increased in subjects with diabetes and to be involved in the pathogenesis of cardiovascular complications after myocardial infarction (MI). It is well recognized that red wine has antioxidant and anti-inflammatory activities. We examined the effects of moderate red wine intake on echocardiographic parameters of functional cardiac outcome in addition to inflammatory cytokines and nitrotyrosine (oxidative stress marker), in subjects with diabetes after a first uncomplicated MI. METHODS One hundred and fifteen subjects with diabetes who had sustained a first non-fatal MI were randomized to receive a moderate daily amount of red wine (intervention group) or not (control group). Echocardiographic parameters of ventricular dys-synchrony, circulating levels of nitrotyrosine, tumour necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), interleukin-18 (IL-18) and C-reactive protein (CRP) were investigated at baseline and 12 months after randomization. RESULTS After 1 year of diet intervention, concentrations of nitrotyrosine (P < 0.01), CRP (P < 0.01), TNF-alpha (P < 0.01), IL-6 (P < 0.01) and IL-18 (P < 0.01) were increased in the control group compared with the intervention group. In addition, myocardial performance index (P < 0.02) was higher, and transmitral Doppler flow (P < 0.05), pulmonary venous flow analysis (P < 0.02) and ejection fraction (P < 0.05) were lower in the control group, indicating ventricular dys-synchrony. The concentrations of nitrotyrosine, CRP, TNF-alpha and IL-6 were related to echocardiographic parameters of ventricular dys-synchrony. CONCLUSIONS In subjects with diabetes, red wine consumption, taken with meals, significantly reduces oxidative stress and pro-inflammatory cytokines as well as improving cardiac function after MI. Moderate red wine intake with meals may have a beneficial effect in the prevention of cardiovascular complications after MI in subjects with diabetes.

Atherosclerosis is a major cause of death in elderly individuals. Endothelial dysfunction is recognized as a key early event in atherogenesis. In the present study, we evaluated the possible beneficial effect of amino acid administration on endothelial regulation in elderly subjects.A total of 25 healthy elderly subjects were administered essential amino acids (EAA) for 4 months. Before and after EAA administration, each subject underwent brachial reactivity investigation with and without an intra-arterial infusion of 4 micromol/min of N(G)-monomethyl-l-arginine (L-NMMA), an inhibitor of nitric oxide (NO) synthase.At baseline, age correlated with free plasma insulin growth factor-1 IGF-1 (r = -0.48; P.01), plasma Trolox equivalent antioxidant capacity (TEAC) (r = -0.40; P.04), and thiobarbituric acid-reactive substances (TBARS) (r = 0.42, P.04), and homeostasis model assessment (HOMA) index (r = 0.45, P.03), as well as with changes in diameter (r = -0.49, P.01) and flow (r = -0.43, P.03). Administration of EAA was associated with a significant increase in plasma TEAC (P.001) and decline in plasma TBARS (P.001) and with improvement in changes in diameter (7.15 +/-1.10 v 8.98 +/-1.80, P.001) and flow (5.6 +/-1.2 v 6.4 +/- 1.2, P.03). These latter two associations were independent of changes in HOMA index (P.04 for both correlations). The beneficial effects of EAA administration on brachial reactivity were partly attenuated by L-NMMA.Administration of EAA may improve brachial reactivity in elderly persons and may also protect against the development of atherosclerosis via the rise in plasma-free IGF-1 levels.

Carcinoid heart disease is a rare cause of heart failure with or without right valvular heart impairments. In this study, we showed a case of carcinoid tumour with hepatic metastases inducing carcinoid heart disease. Neuroendocrine heart involvement happens for severe tricuspid valve insufficiency and plaques on right ventricular (RV) walls produced by a release of serotonin (5-HT). A patient affected by primitive ileal tumour with 5-HT-secernent hepatic metastases inducing tricuspid insufficiency is showed. Transthoracic 2-D echocardiography showed tricuspid valve regurgitation and both right atrium, RV-walls plaques and RV dilation. Continue-wave Doppler showed a characteristic "dagger shaped" spectrum of tricuspid systolic flow. RV function was evaluated with 3-D transthoracic echocardiography. In particular, RV volumes, RV ejection fraction and stroke volume were defined by this technique. 2, 3-D echocardiography and Doppler method are useful techniques to show heart valves' derangements and RV function to non-invasively detect RV impairments in carcinoid heart disease.

This perspective study was performed to demonstrate the prevention of left ventricular hypertrophy by ACE-inhibitor, ramipril, in hypertensives of recent onset. Thirty-four hypertensive patients, treated with ramipril (group I), and 32 controls who received another frequently employed drug (the calcium channel-antagonist, felodipine (group II), were evaluated. Neither of two groups received any anti-hypertensive drug and did not suffer from left ventricular hypertrophy. All selected patients underwent M-mode echocardiography for measuring the following parameters: diastolic diameter of left ventricle, (DDLV); systolic diameter of left ventricle (SDLV); inter-ventricular septum (IVS); thickness of the posterior wall (PW); and left ventricular mass index (LVMI). Two anti-hypertensive drugs reduce systemic hypertension the same way. But, in hypertensives receiving ramipril (group I), the echocardiographic parameters of the left ventricle increased non-significantly. On the other hand, in those treated with felodipine (II group), these parameters significantly changed. The mechanisms of non-increase in cardiac and non-cardiac proteins, due to the ACE-inhibitors, are illustrated.

vascular disease with hyperglicemia as a late manifestation [1]. It’s known that T2DM causes coronary morbility and mortality from two to six times more than in individuals without diabetes [2]. Mortality from stroke rised almost 3-fold when diabetics are matched to the persons without diabetes [3]. Peripheral arterial and retinal diseases are some common complications of diabetes mellitus [4]. Patients having diabetes have an enhanced myocardial dysfunction, often evolving in chronic heart failure [5–7]. Premature atherosclerosis, hyperglycemia, increased insulin resistance and glycosilation of some proteins are undelay all these cardiovascular occurrences. In addition, these impairments often are clouped with elevated blood pressure and hyperhomocisteine, obesity, rised levels of triglycerides and low HDL-cholesterol. These conditions further favour the atherosclerotic processes

Inheired or acquired hyperhomocysteinemia (HHcy) is associated with several impairments, as certain tumors, deep venous thrombosis, tube neural defects, osteoporosis, early atherosclerosis and vascular acute events (IMA, stroke, PVD), mild cognitive impairments till Alzheimer’s disease (AD). But, vascular and neuronal derangements are the most frequent HHcy-manifestations. As far as early atherosclerosis, some clinical trials demonstrated that folates and B6–12 vitamins supplementation is unable to reduce atherosclerotic lesions and cardiovascular events, even if it lowers HHcy levels. Thus, for atherosclerosis and its acute events (IMA, stroke, PVD) HHcy acts as a powerful biomarker rather than a risk factor. For that, the supplementation with folates and B vitamins to lower atherosclerotic lesions-events in hyperhomocysteinemic patients is not recommended. On the contrary, several clinical investigations demonstrated that folates and vitamins administration is able to reduce Hcy serum levels and antagonize some mechanisms favouring neurodegenerative impairments, as mild cognitive impairment, AD and dementia. Thus, contrarily to the atherosclerotic manifestations in hyperhomocysteinemic patients, preventive treatment with folates and B6–12 vitamins reduces Hcy concentration and could prevent or delay cognitive decline and AD.

Homocysteine (Hcy) is metabolized through two pathways, requiring folates and B6-12 vitamins as cofactors. Increased Hcy concentration is responsible for early atherosclerosis with possible acute cardiovascular events. Ample evidence has demonstrated that Hcy lowering with folic acid and B vitamin supplementation, even if reduces Hcy serum levels, is unable to lower cardiovascular risk. On the contrary, omega-3 fatty acids and some nutraceuticals, such as N-acetyl cysteine, taurine, or S-adenosyl-methionine, reduce both Hcy serum concentration and cardiovascular risk. Instead, antiplatelet drugs, such as aspirin and clopidogrel or ticlopidine and statins only antagonize vascular derangements. Finally, metformin, some lipid-lowering drugs, and some diuretics should be avoided because they can increase Hcy levels.

Twenty elderly (77 +/- 0.4 y), nonobese [body mass index (in kg/m2) 26.4 +/- 0.5] subjects with normal glucose tolerance were submitted to a euglycemic hyperinsulinemic (3.5 pmol.min/kg) glucose clamp in a double-blind, crossover, randomized procedure after 4 mo treatment with either vitamin E (900 mg d-alpha-tocopherol/d, Ephynal; Roche, Milan, Italy) or placebo. Body mass index was practically unchanged throughout the study. After the glucose clamp, insulin-mediated stimulation 2 of whole-body glucose disposal (18.4 +/- 0.5 vs 26.1 +/- 0.6 mumol.min/kg lean body mass P < 0.02) was significantly potentiated by vitamin E rather than placebo administration. Furthermore, net changes in plasma vitamin E concentrations correlated with net changes in insulin-stimulated whole-body glucose disposal (r = 0.60 P < 0.003). Plasma vitamin E concentrations seem to play an important role in the modulation of insulin action in elderly people.

Left ventricular hypertrophy (LVH) induced by systemic hypertension (SH) represents a maladaptive response to the increased overload. It is known that the LV pathological remodeling is associated with an increased risk of cardiovascular morbidity and mortality. Secretion and production of vasoactive peptides, such as angiotensin II, endothelin-1, norepinephrine, and Rho and Ras proteins, are increased during the process and play critical roles in the hypertrophic response to systemic hypertension. Oxidative stress, heat shock proteins, calcineurin, and some kinases are also involved in the hypertrophic process. Usually, antihypertensive treatments are able to reduce elevated blood pressure levels, but are not always useful to slow or prevent LVH. Experimental studies performed in animal models demonstrate that some humoral factors, by suppressing the biochemical hypertrophic responses, could prevent their cardiac complications independently of their possible anti-hypertensive effects. Cyclosporine-A, scutellarin, and spironolactone are also included among these antihypertrophic substances. Thus, new drugs deriving from these molecules and humoral factors could be employed to antagonize LVH.

Mitral annular calcium (MAC) is a condition that often occurs in patients with systemic hypertension. To evaluate the effectiveness of nifedipine in preventing MAC, 223 patients with systemic hypertension of recent onset and without MAC were selected and randomly enrolled in 3 groups: group 1 (76 patients) received nifedipine; group 2 (72 patients) received enalapril; and group 3 (75 patients) received atenolol. After 5 years, these treatments significantly reduced systolic (p0.001) and diastolic (p0.05) blood pressure (BP) in 3 treated groups. M-mode echocardiography revealed MAC only in 2 patients in the nifedipine group (2.6%), in 13 in the enalapril group (18%) and in 15 in the atenolol group (20%). The degree of MAC was mild (5 mm) in the 2 patients in group 1, in 5 of the 13 in group 2, and in 6 of the 15 in the group 3, whereas it was severe (5 mm) in the remaining 8 in the enalapril group and in the other 9 in the atenolol group. There was also a significant correlation in the degree of MAC, left atrial enlargement and mitral regurgitation. In addition, atrial fibrillation and atrioventricular conduction defects were associated with severe MAC. These results indicate that nifedipine is an effective drug both in the long-term management of systemic hypertension and in preventing or delaying MAC.

OBJECTIVE Studies have suggested that insulin resistance plays a role in cognitive impairment in individuals with type 2 diabetes. We aimed to determine whether an improvement in insulin resistance could explain cognitive performance variations over 36 weeks in older individuals with mild cognitive impairment (MCI) and type 2 diabetes. RESEARCH DESIGN AND METHODS A total of 97 older individuals (mean ± SD age 76 ± 6 years) who had recently ( RESULTS At baseline, no significant differences were found between groups in clinical or neuropsychological parameters. Mean ± SD values in the entire population were as follows: A1C 7.5 ± 0.5%, fasting plasma glucose (FPG) 8.6 ± 1.3 mmol/l, fasting plasma insulin (FPI) 148 ± 74 pmol/l, MMSE 24.9 ± 2.4, TMT-A 61.6 ± 42.0, TMT-B 162.8 ± 78.7, the difference between TMT-B and TMT-A [DIFFBA] 101.2 ± 58.1, and RAVLT 24.3 ± 2.1. At follow-up, ANOVA models tested changes in metabolic control parameters (FPI, FPG, and A1C). Such parameters improved in the metformin and metformin/rosiglitazone groups (Ptrend < 0.05 in both groups). ANCOVA repeated models showed that results for the metformin/rosiglitazone group remained stable for all neuropsychological tests, and results for the diet group remained stable for the MMSE and TMT-A and declined for the TMT-B (Ptrend = 0.024), executive efficiency (DIFFBA) (Ptrend = 0.026), and RAVLT memory test (Ptrend = 0.011). Results for the metformin group remained stable for the MMSE and TMTs but declined for the RAVLT (Ptrend = 0.011). With use of linear mixed-effects models, the interaction term, FPI × time, correlated with cognitive stability on the RAVLT in the metformin/rosiglitazone group (β = −1.899; P = 0.009). CONCLUSIONS Rosiglitazone may protect against cognitive decline in older individuals with type 2 diabetes and MCI.

Objective To identify the sequence and significance of left ventricular filling abnormalities associated with progressive aging in humans. Design Cross-sectional study comparing three age groups. Setting: Department of Geriatrics at University of Naples. Participants Seventy-five healthy subjects in three age groups: 25 subjects from 25 to 45 years (Group I), 25 subjects from 46 to 65 years (Group II), and 25 subjects from 66 to 85 years (Group III). Intervention None. Main Outcome Measures All underwent pulsed-doppler echocardiography under color guide to measure the following parameters: peak velocity flow for early (E wave) and late (A wave) mitral flow; A/E wave ratio; deceleration time of mitral flow (MDt); isovolumic relaxation time (IRT); ratio of velocity time integrals of the A wave to the velocity time integrals of the entire mitral spectrum (VTIA/VTIM). Results Peak velocity of the E wave was slightly lower in Group II and III compared to Group I; in contrast, peak velocity of the A wave was greater (P < 0.005) in aged individuals. Also A/E wave ratio, MDt, and IRT were significantly greater with advancing age (P < 0.01; P < 0.05 and P < 0.001, respectively). Finally, VTIA/VTIM tended to be greater in the oldest group, but not significantly so. Conclusions Left ventricular relaxation is progressively impaired in late middle age and old age, presumably an early marker of cardiac aging. Increased left atrial pressure is compromised only in the oldest group, presumably representing a compensation for impaired left ventricular relaxation.

The role of surgically removing subcutaneous fat by abdominoplasty on circulating inflammatory markers and myocardial dysfunction, evaluated by myocardial performance index (MPI), were investigated. Twenty volunteers submitted to the abdominoplasty (abdominoplasty group), and other 28 women treated by hypocaloric diet (diet group) were evaluated. Echocardiographic parameters of MPI, circulating levels of tumor necrosis factor (TNF)-alpha and interleukin (IL)-6, were performed at baseline and 2 months later. Compared with nonobese women, obese women had increased concentrations of TNF-alpha (P < 0.01), IL-6 (P < 0.01), and higher MPI (P < 0.02), indicating ventricular dysfunction. Subcutaneous fat concentrations of TNF-alpha and IL-6 were related to MPI impairment. After 60 days, waist-to hip ratio was significantly reduced in the abdominoplasty group. Anthropometric changes were accompanied by a significant decline in plasma concentrations of TNF-alpha and IL-6 levels as well as by significant improvements of MPI in abdominoplasty group compared with diet group. Abdominoplasty may represent a safe method for ameliorating cardiac function in obese women.

We evaluated the role of sterol-regulatory element binding protein (SREBP)-1c/peroxisome proliferator activated receptor-gamma (PPARgamma) pathway on heart lipotoxicity in patients with metabolic syndrome (MS) and aortic stenosis (AS). Echocardiographic parameters of heart function and structural alterations of LV specimens were studied in patients with (n = 56) and without (n = 61) MS undergoing aortic valve replacement. Tissues were stained with hematoxylin-eosin (H and E) and oil red O for evidence of intramyocyte lipid accumulation. The specimens were also analyzed with PCR, Western blot, and immunohistochemical analysis for SREBP-1c and PPARgamma. Ejection fraction (EF) was lower in MS compared with patients without MS (P < 0.001); no difference was found in aortic orifice surface among the groups. H and E and oil red O staining of specimens from MS patients revealed several myocytes with intracellular accumulation of lipid, whereas these alterations were not detected in biopsies from patients without MS. Patients without MS have low levels and weak immunostaining of SREBP-1c and PPARgamma in heart specimens. In contrast, strong immunostaining and higher levels of SREBP-1c and PPARgamma were seen in biopsies from the MS patients. Moreover, we evidenced a significative correlation between both SREBP-1c and PPARgamma and EF and intramyocyte lipid accumulation (P < 0.001). SREBP-1c may contribute to heart dysfunction by promoting lipid accumulation within myocytes in MS patients with AS; SREBP-1c may do it by increasing the levels of PPARgamma protein.

Glibenclamide, a hypoglycemic sulfonylurea, is a blocker of the adenosine triphosphatase-modulated potassium ion channels. The opening of these channels in the myocardial cells, induced by acute myocardial hypoxia, can be responsible for ischemic ventricular arrhythmias. To evaluate the antiarrhythmic effects of this drug 19 non-insulin-dependent diabetic patients were selected. They had coronary artery disease and evidence on Holter monitoring of ventricular premature complexes or nonsustained ventricular tachycardia, or both, induced by transient myocardial ischemia. In all patients, 24-hour electrocardiographic monitoring was performed to evaluate the number and duration of myocardial ischemic events, the frequency of ventricular premature complexes and nonsustained ventricular tachycardia per minute of ischemia and the percentage of ventricular premature complexes versus total ischemic beats. Selected patients were classified in 2 groups: group A (9 patients) received metformin (placebo) and group B (10 patients) was treated with glibenclamide. On the fourteenth day patients underwent 24-hour control monitoring. Then a crossover between the 2 groups was made and a new Holter monitoring sequence was performed at the end of the second phase. Results indicate that glibenclamide significantly (p less than 0.001) reduced both the frequency of ventricular premature complexes and the episodes of nonsustained ventricular tachycardia during transient myocardial ischemia, but did not change the number and duration of acute myocardial ischemic attacks and did not reduce the spontaneous ventricular arrhythmias. Thus, glibenclamide appears to have an antiarrhythmic effect in preventing ventricular arrhythmias induced by transient myocardial ischemia.