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OBJECTIVES To investigate the relationship of 24-h ambulatory central blood pressure (ABP) with preclinical organ damage in youth. METHODS Individuals aged 10-25 years referred for suspected hypertension and healthy volunteers had simultaneous 24-h peripheral and central ABP monitoring (Mobil-O-Graph 24 h PWA). Central BP was calculated using two different calibration methods (c1 using oscillometric systolic/diastolic ABP; c2 using mean arterial/diastolic ABP). Their association with preclinical organ damage [left ventricular mass index (LVMI), carotid intima-media thickness (IMT), 24-h pulse wave velocity (PWV)] was investigated. RESULTS A total of 136 participants were analyzed (age 17.9 ± 4.7 years, 54% adolescents, 77% males, 34% with elevated ABP). Twenty-four-hour peripheral systolic ABP (pSBP) was higher than c1 systolic ABP (c1SBP) by 14.1 ± 3.7 mmHg, but lower than c2SBP by 6.5 ± 7.6 mmHg (all P

OBJECTIVES To compare the association of home (HBP), ambulatory (ABP) and office blood pressure (OBP) measurements with preclinical organ damage in young individuals. METHODS Individuals referred for elevated blood pressure and healthy volunteers aged 6-25 years were evaluated with OBP (2-3 visits), 7-day HBP and 24-h ABP monitoring. Organ damage was assessed by echocardiographic left ventricular mass index (LVMI), carotid ultrasonography [intima--media thickness (IMT)] and pulse wave velocity (PWV) using piezo-electronic or oscillometric technique. RESULTS Analysis included 251 individuals (mean age 14 ± 3.9 years, 70.9% men: 31.1% children, 54.6% adolescents, 14.3% young adults) of whom 189 had LVMI, 123 IMT and 198 PWV measurements. Office, ambulatory and home hypertension was diagnosed in 29.5, 27.1 and 26.3% of participants. The agreement of OBP with ABP was 74.5% (kappa 0.37) and HBP 76.1% (kappa 0.41), with closer agreement between HBP and ABP (84.9%, kappa 0.61). LVMI gave comparable correlations with systolic OBP, 24-h ABP and HBP (r = 0.31/0.31/0.30, all P

A 41-yo male with history of bicuspid aortic valve and dilatation of ascending aorta (49 mm), was transferred from a peripheral hospital with staphylococcus aureus endocarditis. On day 4 he developed fulminant pulmonary edema with a continuous murmur best heard at the left second intercostal space and impressive cardiothoracic index augmentation. TTE revealed the presence of a large aorto-pulmonary fistula (A-PF), (figure 1, left), with left to right shunt during systole and diastole (figure 1, right), between the ascending aorta and the main pulmonary artery. Despite diuretic and antibiotic therapy with cloxacillin, gentamicin and cefazolin, the patient remained in class NYHA IV, soon became inotrope dependent and he progressively developed renal dysfunction. In the ICU unit he had an episode of ventricular fibrillation and was successfully defibrillated. He underwent emergent surgery with aortic valve and ascending aorta replacement. The fistula was closed using pericardial patch. Three years postoperatively he remains well. Aortopulmonary fistula is an uncommon but highly lethal condition if untreated. The etiology of acquired A-PFs includes aneurysm rupture, trauma, aortic dissections and infective endocarditis, most commonly of a prosthetic valve. Chest pain, dyspnea and intermittent hemoptysis are frequent symptoms whereas fulminant heart failure and low cardiac output syndrome may predominate the clinical picture as in our patient. Aortopulmonary fistula is an extremely rare complication of native valve endocarditis. Abstract 92 Figure 1

Cross-sectional studies have shown that ambulatory and home blood pressure (ABP and HBP, respectively) measurements are more closely associated with preclinical organ damage than are office measurements. This study investigated the association between treatment-induced changes in BP assessed by the three methods and the corresponding changes in organ damage. Untreated hypertensives were evaluated with office, ABP and HBP measurements and indices of organ damage (echocardiographic left-ventricular mass index (LVMI), pulse wave velocity (PWV), albuminuria) before and after 12 months of treatment. A total of 116 subjects completed the study (mean age 50.7±10.5 years, 69 men (59%), mean follow-up 13.4±1.4 months). The treatment-induced change in the LVMI was correlated with changes in BP and pulse pressure (PP) assessed by all methods. The change in PWV was correlated with changes in home systolic and ABP and PP and with the change in home diastolic BP. Albuminuria showed no correlations. In linear regression models, changes in home BP and PP had the strongest predictive ability for the change in the LVMI, whereas the change in ABP was the strongest predictor of the change in PWV. The change in office BP had no predictive value. HBP and ABP measurements appear to be superior to office BP measurements and should be considered complementary rather than interchangeable methods for monitoring the effects of antihypertensive treatment on target-organ damage.

Diabet. Med. 27, 1420–1429 (2010) Abstract Aims To examine differences in the spatial QRS-T angle in patients with Type 2 diabetes mellitus with and without cardiac autonomic neuropathy. Methods Two hundred and thirty-two patients with diabetes mellitus (105 with cardiac autonomic neuropathy and 127 without cardiac autonomic neuropathy) and 232 control subjects, matched by gender and age, were studied. Diagnosis of cardiac autonomic neuropathy was based on the classic autonomic function tests. All subjects underwent a digital electrocardiographic recording. Electrocardiographic parameters were measured using the Modular Electrocardiographic Analysis (MEANS) program. Left ventricular mass index (LVMi) and global myocardial performance index (Tei index) of the left ventricle were assessed by ultrasonography. Results The spatial QRS-T angle was higher in the patients with diabetes in comparison with the control subjects (24.5 ± 10.7 vs. 9.7 ± 4.5°, P

Background Systemic sarcoidosis (Sar) is a granulomatous disorder involving multiple organs. Widespread vascular involvement and microangiopathy are common in patients with Sar. In addition, subclinical cardiac involvement is increasingly recognized in patients with Sar. However, data on the effect of Sar on the elastic properties of the arteries and myocardial performance are limited. In this study we looked for differences in aortic distensibility (AoD) which is an index of aortic elasticity, and myocardial performance of the ventricles, between patients with Sar and healthy subjects. In addition, we examined potential associations between AoD and clinical, respiratory and echocardiographic findings in patients with Sar. Materials and methods A total of 83 consecutive patients (26 male/57 female, mean age 51·1 ± 13·3 years) with Sar, without cardiac symptoms, were included. All patients underwent echocardiographic and respiratory evaluation including lung function tests. Additionally, 83 age- and sex-matched healthy subjects served as controls. AoD was determined non-invasively by ultrasonography. Results AoD was lower in the Sar compared to the control group (2·29 ± 0·26 vs. 2·45 ± 0·20 ·10−6 cm2· dyn−1, P

Purpose We evaluated the prevalence and progression of Libman-Sacks endocarditis in patients with systemic lupus erythematosus and any association between this valvulopathy and their clinical and laboratory characteristics. Methods Doppler echocardiography was performed in 342 consecutive patients with systemic lupus erythematosus (297 females and 45 males). The clinical and laboratory data were recorded. Patients were reevaluated after a follow-up period of 4 years. Results Libman-Sacks endocarditis was found in 38 patients (11%). In 24 of 38 patients, mitral valve involvement was found, resulting in regurgitation in all (mild in 18, moderate in 4, and severe in 2), whereas stenosis co-occurred with regurgitation in 9 patients (mild in 6 and moderate in 3). Thirteen (34%) of 38 patients had aortic valve involvement; 11 had regurgitation (mild) and 8 had stenosis (mild), coexistent with regurgitation in 6 of them. One patient had mild tricuspid regurgitation. A significant association was found between Libman-Sacks endocarditis and disease duration and activity, thromboses, stroke, thrombocytopenia, anticardiolipin antibodies, and antiphospholipid syndrome. During the follow-up period, 252 of 342 patients were reevaluated echocardiographically. Among the 38 patients with Libman-Sacks vegetations, 5 with mild mitral regurgitation at the beginning developed moderate (n=4) and severe mitral regurgitation (n=1), 2 patients with mitral stenosis (mild in 1 and moderate in 1) developed severe mitral regurgitation, and 2 patients with mild aortic regurgitation developed moderate and severe mitral regurgitation, whereas a significant deterioration of aortic stenosis was found. Two patients who were candidates for surgery died. Among the 213 patients without vegetations at the beginning, 8 developed new Libman-Sacks lesions. Conclusions Libman-Sacks vegetations can be found in approximately 1 of 10 patients with systemic lupus erythematosus, and they are associated with lupus duration, disease activity, anticardiolipin antibodies, and antiphospholipid syndrome manifestations. A progression of valve lesions may occur during long-term follow-up.

Objective To assess the prevalence and pattern of myocardial fibrosis as detected by delayed enhanced magnetic resonance imaging (DE-MRI) in patients with systemic sclerosis (SSc), and to evaluate a possible association between myocardial fibrosis and cardiac arrhythmias. Methods Forty-one patients with SSc underwent 24-hour Holter monitoring, Doppler echocardiography, and DE-MRI following gadolinium administration. Results Technically acceptable DE-MRIs were obtained in 36 patients with SSc. Enhancement on DE-MRI, consistent with myocardial fibrosis, was observed in 24 of these patients (66%), and it was invariably midwall with a linear pattern, mostly involving basal and midcavity segments of the left ventricle. The volume of enhancement (total volume percentage index [TVPI]) did not differ between patients with diffuse SSc and those with limited SSc (mean ± SD 1.46 ± 1.73% versus 1.44 ± 1.77%; P = 0.98). Patients with a long duration (≥15 years) of Raynaud's phenomenon had a greater number of enhancing segments (mean ± SD 6.55 ± 4.93 versus 2.96 ± 3.46; P = 0.017) and a greater TVPI (mean ± SD 2.44 ± 1.97% versus 1.02 ± 1.43%; P = 0.02) than those with a duration of Raynaud's phenomenon

PURPOSE: There are studies indicating more pronounced left atrial (LA) systolic dysfunction at rest in idiopathic (IDDC) than in ischaemic-dilated cardiomyopathy (ISDC). It was hypothesized that the findings would be similar with regards LA systolic reserve. METHODS: Twenty-six patients with IDDC, 28 with ISDC and 25 normal controls underwent low-dose dobutamine stress echocardiography (5-10 microg kg(-1) min(-1) IV). Left atrial volumes were echocardiographically determined at rest and during stress at the mitral valve opening (maximal, Vmax), electrocardiographic P wave (onset of atrial systole, Vp) and mitral valve closure (minimal, Vmin) from the apical 4- and 2-chamber views (biplane area-length method). Left atrial systolic function was assessed with the LA-active emptying volume (ACTEV) = Vp-Vmin and fraction (ACTEF) = ACTEV/Vp. RESULTS: Vmax at rest was similar in IDDC and ISDC and greater than in the controls (54.2 +/- 12 vs. 48.5 +/- 18 vs. 27.1 +/- 6.3 cm(3) m(-2), respectively, P < 0.001) and did not change with stress (53.9 +/- 13.8 vs. 46.9 +/- 16.2 vs. 25.8 +/- 5.9 cm(3) m(-2), P < 0.001). The ACTEV at rest was similar in IDDC and ISDC and greater than in the controls (8.6 +/- 3.5 vs. 9.7 +/- 2.9 vs. 6.1 +/- 2.2 cm(3) m(-2) P < 0.01), whereas during the dobutamine infusion it remained unaltered in IDDC (10.8 +/- 4.6 cm(3) m(-2), P = NS vs. rest) and increased in ISDC (11.8 +/- 3.3 cm(3) m(-2), P < 0.05) and the controls (13.1 +/- 3.2 cm(3) m(-2), P < 0.01). The ACTEF was lower in IDDC than ISDC and the controls at rest (20 +/- 10% vs. 33 +/- 8% vs. 36 +/- 10%, P < 0.01). Dobutamine infusion was associated with no significant increase in ACTEF in IDDC (25 +/- 12%, P = NS vs. rest), and with an increase in this variable in ISDC (39 +/- 10%, P < 0.05) and the controls (49 +/- 12%, P < 0.01). CONCLUSIONS: Dobutamine infusion is associated with an increase in LA ACTEV and fraction in ISDC and no significant change in these indices in IDDC. These findings indicate a reduced LA systolic reserve in IDDC.

AIMS To compare plasma adiponectin levels between healthy controls and patients with chronic renal failure and to examine for a relationship between plasma adiponectin levels and ischemic heart disease as well as aortic distensibility which is an early marker of atherosclerosis. METHODS We included 89 patients with CRF (45 on and 44 not on hemodialysis) and 70 controls in a cross-sectional study. Plasma adiponectin levels were measured by radioimmunoassay. Aortic distensibility was assessed by high-resolution ultrasonography. RESULTS Plasma adiponectin levels were significantly almost twice as high in patients with renal failure compared to controls (9.7 +/- 1.1 vs. 5.4 +/- 0.6 microg/ml, p < 0.0001). No significant differences were found between renal patients on hemodialysis and not on hemodialysis (p = 0.71). Multivariate linear regression analysis in the renal patient group demonstrated a significant negative relationship between plasma adiponectin levels and ischemic heart disease (p = 0.02). The same analysis in the control subjects group showed a significant, negative relationship between plasma adiponectin levels and body mass index (p = 0.02) and a highly significant positive relationship with the high density lipoprotein cholesterol (p < 0.0001). In the total study population, glomerular filtration rate was the only independent predictor of plasma adiponectin concentrations. Aortic distensibility was lower in renal patients than in controls at a high level of significance (p < 0.0001). However, no significant relationship could be found between plasma adiponectin and aortic distensibility in either the controls or the renal patients. CONCLUSIONS Plasma adiponectin levels are almost twice as high in patients with chronic renal failure in comparison with healthy controls, but not different between renal patients on and those not on hemodialysis. In addition, low plasma adiponectin levels are strongly associated with ischemic heart disease, but not with aortic distensibility in chronic renal failure.

Objectives The aim of this study was to evaluate the significance of the development of a restrictive response to an acute saline load, defined as an increase in the ratio of peak early to peak late diastolic transmitral flow velocity (E/A ratio) associated with a decrease in the deceleration time, in patients with mild to moderate untreated hypertension. Background Recognised abnormal patterns of transmitral diastolic flow include, from ‘best’ to ‘worst’: prolonged relaxation, pseudonormalisation, and restrictive physiology. The common denominator of these transitions is the constellation of an increase in the E/A ratio associated with a decrease in deceleration time. Patients and Methods Sixteen normal control subjects (6 males, 10 females, age 51·6 ± 6·9 years) and 24 patients with mild to moderate untreated hypertension (12 males, 12 females, age 46·8 ± 7·5 years) underwent supine blood pressure measurement with sphygmomanometry, biochemical studies, and transthoracic M-mode, 2D, and Doppler echocardiography before and after an acute saline load (7 mL kg−1, maximum 500 mL, NaCl 0·9% within 15 min IV). Results The baseline E/A ratio was lower (0·90 ± 0·14 vs. 1·04 ± 0·18; P

OBJECTIVE—To evaluate the prevalence of diastolic dysfunction in patients with anticardiolipin antibodies (aCL) and to examine whether the antiphospholipid syndrome (APS) is associated with diastolic dysfunction independently of valvular abnormalities and systolic dysfunction. METHODS—Pulsed, continuous, colour Doppler echocardiography was performed in 179 subjects, of whom 15 were excluded from the analysis because of systolic dysfunction or severe valvular disease. The remaining 164 subjects included 29 patients with primary APS, 26 patients with secondary APS (APS in the presence of systemic lupus erythematosus (SLE)), and 30 patients with SLE and aCL but without APS; 43 patients with SLE without aCL and 36 normal volunteers served as control groups. RESULTS—The groups compared differed significantly in all measures of right ventricular function. There was a gradation of increasing diastolic function impairment as manifested by prolonged deceleration time (DT) and isovolumic relaxation time (IVRT) across the groups of patients with SLE without aCL, SLE with aCL, secondary APS, and primary APS. Differences in left ventricular diastolic function measures were less prominent. In regression analysis, DT increased by 19.6 ms (p=0.002) in the presence of primary APS and by 20.1 ms (p=0.038) in the presence of pulmonary hypertension. The titre of IgG aCL was the strongest predictor of a prolonged IVRT. CONCLUSION—Diastolic dysfunction, in particular of the right ventricle—that is, independent of valvular disease and systolic dysfunction, is a prominent feature of APS and may be related to the pathogenesis of the syndrome.

BACKGROUND: Left atrial systolic dysfunction, unexplained by altered loading conditions, has been reported in idiopathic dilated cardiomyopathy suggesting left atrial involvement in the myopathic process. MATERIALS AND METHODS: Seventeen patients with idiopathic dilated cardiomyopathy, 16 with ischemic dilated cardiomyopathy and 18 normal controls were studied with transthoracic echocardiography and cardiac catheterization. Transmitral diastolic flow was evaluated with pulsed Doppler. Left atrial volume (cm3/m2) at mitral valve opening (maximal, Vmax.), onset of atrial systole (P wave of the electrocardiogram, Vp), and mitral valve closure (minimal, Vmin. ) was determined with two-dimensional echocardiography using the biplane area-length method. The left atrial active emptying fraction (ACTEF = [Vp-Vmin.] x 100/Vp) served as an index of systolic function. RESULTS: The peak early diastolic transmitral flow velocity (cm/sec) was similar in the three groups (idiopathic: 60 +/- 16, ischemic: 58 +/- 20, control: 56 +/- 22; P = NS), whereas the late diastolic transmitral flow velocity was lower but not significantly different in idiopathic compared to ischemic cardiomyopathy, and in both was lower than control (26 +/- 12 vs. 34 +/- 13 vs. 44 +/- 14, respectively; P < 0.05). Vmax. and Vp were similar in idiopathic and ischemic cardiomyopathy and greater than control (44.6 +/- 13.6 vs. 48.2 +/- 18.3 vs. 26.9 +/- 6.2; P < 0.05, and 34.6 +/- 13.4 vs. 30.8 +/- 10.9 vs. 16.7 +/- 3.7, respectively; P < 0.05). ACTEF was lower in idiopathic than in ischemic cardiomyopathy and in the latter it was similar to control (18 +/- 10% vs. 32 +/- 10% vs. 36 +/- 10%, respectively; P < 0.05). Moreover, ACTEF was inversely related to left atrial tension at end-of atrial systole both in idiopathic and in ischemic cardiomyopathy (r2 = 0.52, P = 0.001 and r2 = 0.57, P = 0.0007, respectively). However, at any given level of left atrial tension at end of atrial systole, ACTEF was lower in idiopathic than ischemic cardiomyopathy. CONCLUSION: Left atrial systolic function is depressed in idiopathic and preserved in ischemic dilated cardiomyopathy despite similar left atrial loading conditions. This finding suggests left atrial myopathy in the former, and may be related to the differences in the response to medical treatment and clinical outcome observed between the two conditions.

Objectives To assess the incidence and natural course of paravalvular leaks detected early after aortic valve replacement. Background Although the use of echocardiography has simplified the postoperative assessment of patients with aortic valve replacement, there are no data regarding the natural history of early detected paravalvular aortic leaks. Methods Eighty-four consecutive patients with aortic valve replacement were prospectively followed clinically every 6 months and by echocardiography early (11 ± 7 days), at midterm (27 ± 3 months), and late (63 ± 4 months) after aortic valve replacement. The competence of artificial valves was assessed by Doppler color flow mapping. Results Paraprosthetic leaks were detected in 40 (47.6%) aortic prostheses during the early study; the majority (90%) were small. All leaks remained unchanged during the follow-up period. Left ventricular dimensions and function did not differ between patients with or without paravalvular leak during the follow-up. Left ventricular fractional shortening, however, increased during the intermediate study in both subgroups, indicating improved left ventricular function overall. Three patients had severe paravalvular regurgitation suddenly develop from late infective endocarditis, and 1 patient had a degenerative tissue valve failure 4 years after implantation. Conclusions Paraprosthetic aortic leaks detected early after surgery, in the absence of valve infection, are common, are usually small, and have a benign course. However, the development of new, usually severe, regurgitation should raise the suspicion of prosthetic valve endocarditis or bioprosthetic valve failure. (Am Heart J 1999;138:351-7.)

Background Currently recognized types of amyloidosis include primary, familial and secondary, each of which may affect the heart. There may be differences in the heart response to the deposition of amyloid fibrils in these three forms of the disease. Materials and methods Over a period of 10 years (1985–95), 28 consecutive patients with primary, 11 with secondary and 17 with familial amyloidosis were studied at the Departments of Cardiology of Laiko and Hammersmith Hospitals. The diagnosis of amyloidosis was confirmed by biopsies of subcutaneous fat, rectum, kidney, bone marrow, gum or sural nerve. Diagnosis of cardiac involvement was based on typical electrocardiographic and echocardiographic findings. Results The left ventricular fractional shortening (%) was reduced in primary compared with familial or secondary amyloidosis (29.8 ± 10.2 vs. 36.2 ± 6.5 vs. 36 ± 5.9, P

Background: Hypotensive response during dobutamine stress echocardiography (DSE) is a common complication, lacking the prognostic significance of hypotension during exercise treadmill test. Hypothesis: The present study aimed to assess the possible mechanisms of hypotensive response during DSE and to compare it with exercise treadmill test. Methods: In all, 91 patients with known coronary artery disease (CAD) underwent both DSE and exercise treadmill test. Dobutamine-induced hypotension was defined as a systolic blood pressure drop ≥20 mmHg from baseline or from the previous level of infusion. Results: Twenty-one (23%) patients, 10 of whom also had bradycardia, developed hypotension during dobutamine infusion. Five (5.5%) patients were severely symptomatic and the infusion was stopped prematurely, while in the remaining 16 the addition of atropine allowed the continuation of the test. Patients prone to hypotension were predominantly female (p = 0.0004). had smaller (p = 0.01) and better functioning left ventricles (p = 0.0004), were unlikely to have rest wall motion abnormalities (p = 0.0008) or multivessel CAD (p = 0.02), and had less ischemia (wall motion score difference) (p = 0.03). Hypotension during exercise treadmill test was observed in only one (1%) patient with left main disease. Conclusions: Hypotension during DSE is unrelated to the anatomical or functional extent of CAD and is frequent in the setting of a well-functioning left ventricle. We suppose that vigorous contraction of a small chamber during dobutamine infusion results in an excessive stimulation of cardiac mechanoreceptors that mediate reflex hypotension and bradycardia.

A 71-year-old man with von Recklinghausen’s disease presented with NYHA class II exertional dyspnea and easy fatigability since about 20 days. Echocardiography and angiography demonstrated dilatation of aortic root, ascending aorta, and left ventricle, together with severe aortic regurgitation. Because of very few cases of cardiovascular abnormalities having been reported with von Recklinghausen’s disease, it is logical to concur that this is simply co-existence, whereas other possible mechanisms are endothelial dysfunction or sympathetic denervation.

BACKGROUND: Out-of-office blood pressure (BP) measurement using home BP (HBP) or ambulatory BP (ABP) monitoring is often necessary for the accurate evaluation of hypertension. These methods have several similarities but also have major differences. Therefore, they are regarded as complementary, and there is uncertainty on how they should be applied in clinical practice. This study compared hypertension management based on clinic and ABP measurements or on HBP measurements alone. METHODS: Untreated subjects with elevated BP were randomized to treatment initiation and titration based on clinic and ABP measurements or on HBP measurements alone. Target organ damage was assessed at baseline and after 1 year of treatment with echocardiographic left ventricular mass index (primary endpoint), pulse wave velocity, and urinary albumin excretion. RESULTS: A total of 145 subjects were randomized, and 116 completed the study (mean age = 50.7±10.5 years; 69 men (59%); mean follow-up = 13.4±1.4 months). There was no difference between the 2 arms in treatment-induced change in left ventricular mass index (mean difference = 0.50±1.11 g/m2; 95% confidence interval (CI) = -1.70 to 2.70). Moreover, there was no difference between the 2 arms in treatment-induced changes in pulse wave velocity (mean difference = -0.16±0.42 m/s; 95% CI = -0.99 to 0.66), urinary albumin excretion (mean difference = -0.85±4.28 mg/dl; 95% CI = -9.37 to 7.66), HBP and ABP levels, and hypertension control rates. CONCLUSIONS: These data suggest that HBP monitoring alone is as reliable as combined clinic and ABP measurements in monitoring the effects of antihypertensive drug treatment on BP and preclinical target organ damage.

To describe the evolution of valve involvement and myocardial dysfunction over time in patients with systemic lupus erythematosus (SLE) with or without antiphospholipid antibodies (aPL) and/or antiphospholipid syndrome (APS).From an initial cohort of 150 patients assessed by transthoracic echocardiography 10 years ago, 17 patients with primary APS (PAPS), 23 with SLE-associated APS (SLE/APS), 19 with SLE positive for aPL without APS, and 23 with SLE negative for aPL were re-evaluated in the present echocardiography study.Valvulopathy was detected in 65% of PAPS and 62% of SLE patients with or without aPL. Disease duration [odds ratio (OR), 1.63; 95% confidence interval (CI), 1.13-2.36; p = 0.009 for every 5 years of increase] and presence of SLE/APS (OR, 3.51; 95% CI, 1.27-9.67; p = 0.015) were the only factors associated with the progression of valvular disease in univariate and multivariate analyses. Left ventricular diastolic dysfunction similarly progressed over time, with deceleration time (DT) and isovolumic relaxation time (IVRT) being equally prolonged in each of the four groups (p0.05). Right ventricular DT was significantly prolonged in each of the three SLE patient groups (p0.001), whereas IVRT increased only in SLE/APS patients (p = 0.040).Among patients with APS and SLE (with or without aPL), SLE/APS and disease duration were independent factors for valvular disease progression in the present 10-year follow-up echocardiography study. Anticoagulation did not arrest valvular disease progression. Ventricular diastolic dysfunction, primarily of the left ventricle, also progressed over the 10-year period.

Cirrhosis is associated with several extrahepatic manifestations including portopulmonary hypertension (PPHT). Recent data suggest that endothelins (ETs) are related to the pathophysiology of PPHT. The study aimed to measure serum ET levels in hospitalized cirrhotic patients and to determine their association with PPHT and patient outcome.Fifty-seven cirrhotic patients [43 males; median age 58 (28-87) years] underwent Doppler echocardiography. Patients with systolic pulmonary arterial pressure ≥40 mmHg and pulmonary acceleration time100 ms were deemed to have PPHT. ET-1, 2, and 3 serum levels were measured with an ELISA assay. All-cause mortality was recorded over a median period of 24 months.Nine out of 57 patients (15.8%) had PPHT. Among various clinical variables, only autoimmune hepatitis was associated with PPHT (OR=11.5; 95% CI, 1.58-83.4; P=0.01). ET-1 levels [9.1 (1.6-20.7) vs 2.5 (1.4-9.2) pg/mL, P=0.02] and the ET-1/ET-3 ratio [4.73 (0.9-22.4) vs 1.6 (0.3-10.7), P=0.02] were significantly higher in patients with PPHT than in those without. ET-2 and ET-3 levels did not differ between the two groups. There was no difference in survival between the two groups, although ET-1 levels were associated with an adverse outcome in Cox regression analysis (HR=1.11; 95% CI, 1.02-1.22; P=0.02 per unit increase in ET-1).Our data suggest that ET-1 and the ET-1/ET-3 ratio are elevated in patients with PPHT and that ET-1 is associated with a poor outcome irrespective of PPHT.

Cardiac involvement may be under-diagnosed in asymptomatic patients with systemic sclerosis (SSc). Standard electrocardiography-derived spatial QRS-T angle (spQRS-Ta) is an established marker of ventricular repolarisation heterogeneity, and a strong independent predictor of cardiac morbidity and mortality, including sudden death, in the general population. We examined whether spQRS-Ta is abnormal in asymptomatic SSc patients and assessed its predictive value for possibly concurrent, serious ventricular arrhythmia.SpQRS-Ta and 24-hour Holter recordings were obtained from 69 SSc patients (aged 51±13 years, 63 women) without clinically evident cardiac involvement and having left ventricular ejection fraction at least 50% by echocardiography. 'Healthy' subjects matched 1:1 with patients for age, gender and body mass index served as controls.SpQRS-Ta was wider in SSc (median value 15.6°, interquartile range 10.6-24.3°) than controls (10.5°, 7.3-13.5°, p=0.0001) and not associated with skin fibrosis extent or specific clinical manifestations and autoantibodies. Twenty-four-hour Holter recordings revealed couplets of ventricular beats in six (Lown class IVa) and non-sustained ventricular tachycardia in five patients (Lown class IVb); spQRS-Ta was wider in those eleven patients with serious ventricular arrhythmia than the remaining patients (24.9°, 14.9-31.3° vs. 14.4°, 9.6-22.3°; p=0.02). A spQRS-Ta19.3° demonstrated 80% sensitivity and 68% specificity (area under the curve 0.81, p=0.02) to predict the presence of non-sustained ventricular tachycardia in Holter monitoring.Ventricular repolarisation heterogeneity, as reflected by wider spQRS-Ta, is common in SSc. Increased spQRS-Ta could serve as a simple screening test for further investigation to identify patients at risk or prone to develop life-threatening ventricular arrhythmia.

To examine differences in the spatial QRS-T angle in patients with Type 2 diabetes mellitus with and without cardiac autonomic neuropathy.Two hundred and thirty-two patients with diabetes mellitus (105 with cardiac autonomic neuropathy and 127 without cardiac autonomic neuropathy) and 232 control subjects, matched by gender and age, were studied. Diagnosis of cardiac autonomic neuropathy was based on the classic autonomic function tests. All subjects underwent a digital electrocardiographic recording. Electrocardiographic parameters were measured using the Modular Electrocardiographic Analysis (MEANS) program. Left ventricular mass index (LVMi) and global myocardial performance index (Tei index) of the left ventricle were assessed by ultrasonography.The spatial QRS-T angle was higher in the patients with diabetes in comparison with the control subjects (24.5 ± 10.7 vs. 9.7 ± 4.5°, P0.001) and in the patients with diabetes and cardiac autonomic neuropathy than in those without cardiac autonomic neuropathy (30.1 ± 11.3 vs. 19.5 ± 7.1, P0.001). No differences were found in the QT interval between the studied groups. Multivariate linear regression analysis in subjects with diabetes after controlling for age, gender, BMI, blood pressure, diabetes duration, HbA(1c) , lipids, microalbuminuria and insulin resistance, demonstrated significant and independent associations between the spatial QRS-T angle with presence and severity of cardiac autonomic neuropathy, all parameters of heart rate variability, LVMi and Tei index.The spatial QRS-T angle is increased in patients with Type 2 diabetes who have cardiac autonomic neuropathy, suggesting increased ventricular arrhythmogenicity, and is associated with the structural and functional properties of the myocardium. Further research is warranted to evaluate its role in cardiovascular risk stratification of patients with diabetes.

To measure aortic stiffness and global left ventricular (LV) function in patients with ankylosing spondylitis (AS) and no clinical evidence of heart disease.Fifty-seven consecutive patients with AS (54 males, three females, mean age 41.78+/-10.02 years) without clinical evidence of cardiac involvement and 78 healthy subjects (73 males, five females, mean age 39.92+/-9.11 years) underwent complete echocardiographic study. Aortic stiffness was determined non-invasively by aortic distensibility (AoD) and the global LV function was evaluated by the myocardial performance index (the Tei index).AoD in patients with AS [(2.21+/-0.24)x10(-6) cm(2) dyn(-1)] was decreased compared to controls [(2.58+/-0.19) )x10(-6) cm(2) dyn(-1), p0.01], confirming that aortic stiffness is increased in AS. The LV Tei index was significantly increased in the patient group compared to the control group (0.392+/-0.031 vs. 0.370+/-0.034, p0.01). The ejection fraction (EF) did not differ between the two groups (p0.05). In multivariate linear regression analysis, AoD was significantly associated with the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) and LV isovolumic relaxation time (IVRT) whereas the LV Tei index was associated with BASDAI and the LV mass index.Patients with AS and no clinical evidence of cardiac disease have increased stiffness of the aorta and decreased global myocardial performance and both of these abnormal measurements correlate with disease activity. The abnormal Tei index may reflect an early manifestation of cardiac dysfunction in these patients.

To define the risk factors associated with a relatively rapid increase in estimated pulmonary arterial systolic pressure (PASP) in patients with systemic sclerosis (SSc).SSc patients undergoing screening for pulmonary arterial hypertension (PAH) by echocardiography were identified and their charts were retrospectively reviewed. In all patients, we recorded PASP, pulmonary function, and clinical and laboratory data. PAH was defined as an estimated PASPor =40 mmHg. In each patient, the PASP values with their corresponding time intervals were fitted to a linear function and the slope of the line was calculated.Seventy-one patients with at least two echocardiographic studies each were analysed. In 16 (23%) patients, the rate of PASP progression wasor =2.5 mmHg/year whereas in the remaining 55 (77%) patients the rate of progression was2.5 mmHg/year. In multiple logistic regression analysis, anti-centromere antibodies (ACA) (OR 8.75, CI 1.12-68.38, p = 0.039) and ageor =50 years at diagnosis (OR 8.76, CI 1.28-60.14, p = 0.027) were independently associated with a rise of PASP byor =2.5 mmHg/year. Baseline forced vital capacity (FVC)70% (predicted), Raynaud's duration preceding skin manifestations byor =5 years, and fibrosis on lung computed tomography (CT) were not associated with a rapid rise of PASP (p0.05).Old age at diagnosis and ACA are associated with a relatively rapid rise of PASP estimated by echocardiography in SSc. Screening for PAH in these patients may, if followed by right heart catheterization, detect PAH at an earlier stage and guide therapeutic decisions.

To evaluate whether patients with primary Sjögren's syndrome without overt cardiac disease have echocardiographic abnormalities and their relation with clinical and laboratory data.One hundred and seven consecutive patients with primary Sjögren's syndrome and 112 healthy controls, matched for age and gender, underwent complete echocardiographic study.Thirty-two patients had mitral valve regurgitation (p0.001) whereas tricuspid and aortic valve regurgitation were, also, more frequent in the patient group (p=0.022 and p=0.007 respectively). In multivariate analyses, low C4 levels of complement and age were strong predictors of mitral valve regurgitation whereas age was predictor of aortic valve regurgitation. Tricuspid valve regurgitation was associated with pulmonary hypertension. Clinically silent pericardial effusion, found in 9 patients (p=0.008), was associated with cryoglobulinemia and primary biliary cirrhosis. Twenty-four patients had pulmonary hypertension (p0.001) whereas hypocomplementemia and cryoglobulinemia were strong predictors of pulmonary artery systolic pressure. The analyses reveal that easy fatigability was associated with pulmonary hypertension and low C4 levels. The patients' left ventricular mass index differed significantly from the controls (108.9+/-17.21 gm(-2) vs. 85.8+/-6.73 gm(-2), p0.001) and was associated with palpaple purpura and anti-Ro/SSA. From the diastolic function indices only the left ventricular isovolumic relaxation time differed significantly among patients and controls.Valvular regurgitation, pericardial effusion, pulmonary hypertension and increased left ventricular mass index occur with disproportionately high frequency in patients with primary Sjögren's syndrome and no clinically apparent heart disease. Thus echocardiographic studies may need to be performed in these patients especially when palpable purpura, antibody reactivity and low C4 levels are present.

Systemic sarcoidosis (Sar) is a granulomatous disorder involving multiple organs. Widespread vascular involvement and microangiopathy are common in patients with Sar. In addition, subclinical cardiac involvement is increasingly recognized in patients with Sar. However, data on the effect of Sar on the elastic properties of the arteries and myocardial performance are limited. In this study we looked for differences in aortic distensibility (AoD) which is an index of aortic elasticity, and myocardial performance of the ventricles, between patients with Sar and healthy subjects. In addition, we examined potential associations between AoD and clinical, respiratory and echocardiographic findings in patients with Sar.A total of 83 consecutive patients (26 male/57 female, mean age 51.1 +/- 13.3 years) with Sar, without cardiac symptoms, were included. All patients underwent echocardiographic and respiratory evaluation including lung function tests. Additionally, 83 age- and sex-matched healthy subjects served as controls. AoD was determined non-invasively by ultrasonography.AoD was lower in the Sar compared to the control group (2.29 +/- 0.26 vs. 2.45 +/- 0.20 .10(-) (6) cm2 x dyn(-1), P0.01), while left ventricular mass (LVM) was higher in the Sar group (221.3 +/- 50.2 vs. 195.6 +/- 31.3 g, P = 0.007). Furthermore, myocardial performance of both ventricles was impaired in the Sar group. Multivariate linear regression analysis in the total sample population demonstrated a significant and independent inverse relationship between AoD and the presence of Sar (P0.001). The same analysis in the Sar patients showed that AoD was associated significantly and independently with the stage of Sar, age, systolic blood pressure, LVM and myocardial performance of both ventricles. No significant relationship was found between AoD and disease duration, pulmonary artery pressure or lung function tests.Presence and severity of Sar are associated with reduced aortic distensibility, irrespective of the disease duration, pulmonary artery pressure and lung function. In addition, patients with Sar have increased LVM and impaired myocardial performance.

Our objective was to assess the value of home blood pressure (BP) monitoring in comparison to office BP measurements and ambulatory monitoring in predicting hypertension-induced target-organ damage.Sixty-eight untreated patients with hypertension with at least two routine prestudy office visits were included (mean age, 48.6 +/- 9.1 [SD] years; 50 men). Office BP was measured in two study visits, home BP was measured for 6 workdays, and ambulatory BP was monitored for 24 h. All BP measurements were obtained using validated electronic devices. Target-organ damage was assessed by measuring the echocardiographic left-ventricular mass index (LVMI), urinary albumin excretion rate (AER) in two overnight urine collections, and carotid-femoral pulse-wave velocity (PWV) (Complior device; Colson, Garges-les-Gonesse, Paris, France).The correlation coefficients of LVMI with office BP were 0.24/0.15 (systolic/diastolic), with home BP 0.35/0.21 (systolic, P.01), and with 24-h ambulatory BP 0.23/0.19, awake 0.21/0.16, and asleep 0.28/0.26 (asleep, both P.05). The correlation coefficients of AER with office BP were 0.24/0.31 (diastolic, P.05), with home BP 0.28/0.26 (both P.05), and with 24-h ambulatory BP 0.25/0.24, awake 0.24/0.25 (diastolic, P.05), and asleep 0.26/0.18 (systolic, P.05). There was a trend for negative correlations between PWV and diastolic BP measurements (not significant). In multiple-regression models assessing independent predictors of each of the three indices of target-organ damage, systolic home BP and age were the only independent predictors of increased LVMI that reached borderline statistical significance.These data suggest that home BP is as reliable as ambulatory monitoring in predicting hypertension-induced target-organ damage, and is superior to carefully taken office measurements.

The spatial QRS-T angle obtained by vectorcardiography is a combined measurement of the electrical activity of the heart and predicts cardiovascular morbidity and mortality. Disturbances in repolarization and depolarization are common in diabetes. No data, however, exist on the effect of diabetes on QRS-T angle. In this study we examined differences in QRS-T angle between type 2 diabetic and non-diabetic subjects; in addition, the potential relationship between QRS-T angle and left ventricular performance as well as glycaemic control were also examined. A total of 74 subjects with type 2 diabetes and 74 non-diabetic individuals, matched for age and sex with the diabetic subjects were examined. All subjects were free of clinically apparent macrovascular complications. Spatial vectorcardiogaphic descriptors of ventricular depolarization and repolarization were reconstructed from the 12-electrocardiographic leads using a computer-based electrocardiogram. Left ventricular mass and performance were measured using M-mode and Doppler echocardiography. QRS-T angle values were higher (by almost 2-fold) in the diabetic in comparison with the non-diabetic subjects (P < 0.001). After multivariate adjustment, QRS-T angle was independently associated with age (P = 0.01), HbA(1c) (P = 0.003), and low-density lipoprotein cholesterol levels (P = 0.04) in the non-diabetic, and with HbA(1c) (P = 0.03) as well as Tei index (P = 0.003) in the diabetic subjects. The spatial QRS-T angle is high in subjects with type 2 diabetes and is associated with glycaemic control and left ventricular performance. The prognostic importance of the higher spQRS-T angle values in subjects with diabetes remains to be evaluated in prospective studies.

We report the case of a 70-year-old patient who presented with fever of unknown origin. The initial diagnosis was infective endocarditis as a mitral valve vegetation was found in a transesophageal echocardiogram. Lack of response to empiric antibiotic treatment and further diagnostic work-up established the correct diagnosis of marantic endocarditis due to temporal arteritis. Treatment with steroids and aspirin led to rapid clinical improvement and disappearance of the vegetation. Apropos of this case, we reviewed the records of 25 patients with a new diagnosis of temporal arteritis and analyzed the echocardiographic findings in comparison to those of 40 age- and sex-matched controls. Abnormal echocardiographic findings were present in 13 (52%) out of 25 patients with temporal arteritis and in 5 (12.5 %) out of 40 controls (p0.001, chi-square test).

Background/Aims: Hardly anything is known about the effect of renal function on plasma ghrelin levels. Ghrelin is an orexigenic hormone with important hemodynamic effects. We examined differences in plasma ghrelin levels between chronic renal failure (CRF) patients and healthy subjects, and ghrelin's relationship with indices of left ventricular (LV) function. Methods: Fasting total plasma ghrelin levels were measured in 122 CRF patients (57 on, 65 not on hemodialysis) and 57 control subjects. Indices of LV function were evaluated using echocardiography. Results: Total plasma ghrelin levels were higher in patients with CRF compared to controls, but were not different between patients on and those not on hemodialysis. In a multivariate linear regression model, presence of kidney dysfunction explained 41 % of the variability of ghrelin values. The etiology of renal failure (diabetic nephropathy or not) had no influence on ghrelin levels in the renal patients. Ghrelin levels were not associated with indices of LV systolic function or blood pressure in these patients. Conclusion: Fasting plasma ghrelin concentrations are higher in CRF patients regardless of their need for hemodialysis compared to controls. The etiology of renal failure does not have any effect on plasma ghrelin levels. In addition, ghrelin levels are not associated with hemodynamic parameters in patients with CRF.

Matrix metalloproteinases (MMP) degrade myocardial fibrillar collagen in acute myocardial infarction (MI) patients. Their activity is tightly controlled in normal myocardium by a family of closely related tissue inhibitors known as TIMP. An imbalance in their activity might contribute to post-MI remodeling. Plasma levels of MMP-1, TIMP-1 and MMP-1/TIMP-1 complex were measured, using relevant ELISA kits, in 24 (22 males-2 females), acute MI patients with a mean age 59 +/- 14 years. Blood samples were taken on admission (0 h), and 3 h, 6 h, 9 h, 18 h, 24 h, 36 h, 48 h, 3rd, 4th, 5th, 7th, 15th, 30th days after MI. All patients underwent coronary arteriography with ventriculography for estimation of left ventricular ejection fraction (LVEF) and extent of coronary artery diseases, and echocardiographic study for measuring end-diastolic diameter (EDD). Ten patients with an LVEF45%, an EDD47.5 mm, and heart failure symptoms were included in group A and compared against 12 patients with an LVEF45% an EDD47.5 mm in group B. Mean plasma concentrations of MMP-1 were higher by 21% in group A (1.3 +/- 0.2 ng/mL) compared to group B (1 +/- 0.1 ng/mL) over the total study period. TIMP-1 plasma concentrations showed very little difference between the 2 groups, (704 +/- 213 ng/mL versus 691 +/- 165 ng/mL, (6%)). Finally, plasma concentrations of MMP-1/TIMP-1 complex were lower by -36% in group A with a mean value of 2.7 +/- 0.6 ng/mL versus 3.7 +/- 0.5 ng/mL in group B. Mean values for the differences were significant at time points 0, 6, 18, 24 and 48 hours for MMP-1 (p0.036), and on 48 h and the 4th day for MMP-1/TIMP-1 complex (p0.031). Moreover, a good correlation was found between plasma concentrations of creatine kinase (CK) and MMP-1 at 18 h (r = 0.422, p = 0.041) and on the 4th day (r = 0.67, p = 0.046), and TIMP-1 on the 4th day (r = 0.67, p = 0.047). Additionally, mean values for LVEF were 35.8 +/- 8.8% in group A versus 51.2 +/- 1.8% (p = 0.00014) in group B. Also, the EDD in-group A was 52.1 +/- 6.9 mm versus 42.9 +/- 3.2 mm in group B (p = 0.00013). In acute MI patients, increased MMP-1, with no change in TIMP-1, is associated with left ventricular dysfunction and dilatation, suggesting that increased collagenolytic activity contributes to loss of LV function.

To study the stiffness of large arteries in relation to the extent of skin and lung fibrosis, aortic distensibility was examined in patients with diffuse and limited systemic sclerosis (SSc).Consecutive patients (55 with diffuse and 51 with limited SSc) without signs and symptoms of heart failure or a previous history of arterial hypertension underwent echocardiography and lung function tests. Aortic stiffness was determined non-invasively by aortic distensibility and aortic strain measurements in all patients and in 50 healthy subjects, matched for age and gender.Aortic distensibility in patients with either diffuse (2.03 +/- 0.26 x 10(-6) cm(2) dyn(-1)) or limited SSc (2.12 +/- 0.33) was similarly decreased compared with controls (2.49 +/- 0.36, P0.001). Moreover, aortic strain was significantly reduced in both patient groups compared with controls, confirming that aortic stiffness is increased in SSc independently of the extent of skin involvement. Left ventricular performance was similar between patients and controls, while left ventricular mass and tricuspid systolic gradient were significantly increased in both SSc groups, the latter being associated with aortic stiffness in multivariate analysis. No association with serum levels of C-reactive protein or lung function abnormalities indicative of pulmonary fibrosis were found.Stiffness of the aorta is increased in patients with established SSc regardless of the extent of the inflammatory fibrotic process in the skin and lungs, suggesting that additional pathogenetic mechanisms contribute to the compromise of large arteries.

Matrix metalloproteinases and their tissue inhibitors are key enzymes degrading myocardial collagen in acute myocardial infarction (AMI). The aim of the present study was to determine whether angiotensin-converting enzyme inhibitors (ACEI) influence collagenase-1 (MMP-1) and their tissue inhibitor (TIMP-1) activity in AMI patients. Plasma levels of MMP-1, TIMP-1 and MMP-1/TIMP-1 complex were measured in 24 patients (aged 58.4 +/- 13.9 years) with AMI. Thirteen patients received perindopril 4 mg/day (group A) and 11 did not (group B). Plasma samples collected on admission and at 0, 3, 6, 9, 12, 18, 24, 36 and 48 hours and on days 3, 4, 5, 7, 15 and 30 thereafter were analyzed by relevant ELISA kits. Ejection fraction (EF) was assessed by ventriculography and end-diastolic diameter (EDD) echo-study on days 6 and 30. Values of collagenolytic enzymes of group A compared with those in group B were on average lower by 34%, 18.3% and 40%, respectively. The difference in values between groups at 0 h, 3 h and 9 h was significant (p0.048). ANOVA repeated measurement analysis showed significance within subjects for MMP-1 alone (p0.043) and for MMP-1 and ACEI (p0.046), while for TIMP-1 and MMP-1/TIMP-1 complex significance was only p0.0009. Regarding EDD changes, patients in group A showed minimal or no changes (51.23 +/- 1.8 mm to 51.6 +/- 2.13 mm), their EF was 38.8% and infarct size was medium to large. In contrast, group B showed a trend to increase EDD (41 +/- 0.78 mm to 42.33 +/- 0.59 mm), their EF was 50.5% and infarct size was small to medium. In conclusion, early initiation of ACEI treatment reduces collagenolytic activity. This effect may be considered an alternative mechanism for beneficial effects on postinfarction remodeling.

Reduced aortic distensibility predicts cardiovascular mortality in patients with type 2 diabetes and impaired glucose tolerance. Cardiac autonomic neuropathy is common in subjects with diabetes. However, the relationship between the elastic properties of the aorta and autonomic neuropathy has not been studied to date in subjects with type 2 diabetes.In this cross-sectional study, a total of 87 subjects with type 2 diabetes (27 with and 60 without cardiac autonomic neuropathy) as well as 60 healthy individuals, matched for age and sex with the diabetic subjects, were examined. Cardiac autonomic neuropathy was diagnosed on the basis of the battery of the classic cardiovascular autonomic function tests. Aortic distensibility was assessed by high-resolution ultrasonography.Diabetic patients had reduced aortic distensibility in comparison with the control subjects: 1.81 +/- 0.58 vs. 2.53 +/- 0.34 10-6 cm2 dyn-1, respectively (P0.0001). In addition, diabetic individuals with cardiac autonomic neuropathy had reduced aortic distensibility as compared with patients without this complication: 1.60 +/- 0.72 vs. 1.90 +/- 0.48 10-6 cm2 dyn-1, respectively (P = 0.02). Multivariate linear regression analysis in the diabetic group, after controlling for a number of confounding factors such as age, systolic and diastolic blood pressure, duration of diabetes and presence as well as severity of cardiac autonomic neuropathy, demonstrated a significant and independent association between duration of diabetes [B = -0.02, SE(B) = 0.01, P = 0.01] and presence of cardiac autonomic neuropathy [B = -0.29, SE(B) = 0.14, P = 0.03] with aortic distensibility.Type 2 diabetes is associated with a significant reduction in the elastic properties of the aorta. In addition, known duration of diabetes and presence of cardiac autonomic neuropathy are the main predictors of aortic distensibility in subjects with type 2 diabetes.

The aim of this study was to evaluate the significance of the development of a restrictive response to an acute saline load, defined as an increase in the ratio of peak early to peak late diastolic transmitral flow velocity (E/A ratio) associated with a decrease in the deceleration time, in patients with mild to moderate untreated hypertension.Recognised abnormal patterns of transmitral diastolic flow include, from 'best' to 'worst': prolonged relaxation, pseudonormalisation, and restrictive physiology. The common denominator of these transitions is the constellation of an increase in the E/A ratio associated with a decrease in deceleration time.Sixteen normal control subjects (6 males, 10 females, age 51.6 +/- 6.9 years) and 24 patients with mild to moderate untreated hypertension (12 males, 12 females, age 46.8 +/- 7.5 years) underwent supine blood pressure measurement with sphygmomanometry, biochemical studies, and transthoracic M-mode, 2D, and Doppler echocardiography before and after an acute saline load (7 mL kg(-1), maximum 500 mL, NaCl 0.9% within 15 min IV).The baseline E/A ratio was lower (0.90 +/- 0.14 vs. 1.04 +/- 0.18; P0.01) and the deceleration time was longer (158.8 +/- 19.4 vs. 135 +/- 8.9 ms; P0.01) in patients with hypertension compared with normotensive controls. However, no patient with hypertension exhibited a transmitral flow velocity pattern compatible with typical prolonged relaxation. A restrictive response to the acute saline load was observed in 12 (50%) of the hypertensive and none of the control subjects. Hypertensive patients with a restrictive response to the acute saline load had a lower baseline E velocity (54.8 +/- 8.7 cm s(-1) vs. 66 +/- 6.4 cm s(-1); P = 0.003), a lower baseline E/A ratio (0.83 +/- 0.13 vs. 0.97 +/- 0.12; P = 0.015), and a longer deceleration time (167.5 +/- 15.4 ms vs. 150 +/- 19.5; P = 0.03) than hypertensive patients without such a response.A restrictive response to an acute saline load is indicative of a limited diastolic reserve in patients with mild to moderate untreated hypertension. Further studies are required in order to evaluate the significance of such a response with regards to risk stratification and efficacy of medical treatment in this patient population.

Background Cardiac involvement and clinically silent cardiac changes are reported rarely in patients with primary Sjogren’s Syndrome (pSS) whereas: a. increased rate of pericarditis (usually silent with echocardiographic findings) and mitral valve regurgitation, b. myocardiac involvement (autoimmune – asymptomatic myocarditis), and c. left ventricular diastolic dysfunction have been presented in case reports and controlled studies. Objectives The echocardiographic evaluation of the anatomic and functional heart disorders in patients with pSS (without risk factors for coronary heart disease or other symptoms of heart disease), the comparison of these findings with that of the control group, and the correlation with clinical and laboratory data (ANA, anti-Ro (SSA), anti-La (SSB), anti-CL, anti-b2GPI, RF). Methods Pulsed, colour Doppler echocardiography was performed in seventy eight (78) patients (pts) with pSS (european criteria) (75 women and 3 men), mean age 51 ± 11.6(years) and mean disease duration 7.7 ± 4.26(years) and 80 healthy controls (78 women and 2 men) mean age 51 ± 9.5(years). Left-ventricular (LV) dimensions and interventricular septum and posterior wall thickness at end-diastole were measured for the calculation of the fractional shortening (FS) and left ventricular mass with the Penn convention formula. Measurements of left ventricular mass were divided by body surface area to obtain left ventricular mass index (LVmass index). We also evaluated parameters of RV and LV diastolic function including early and late atrioventricular (AV) flow velocities (E and A wave respectively), E/A ratio, deceleration time (DT) and isovolumic relaxation time (IVRT). Pulmonary artery systolic pressure (PASP) was estimated by the peak regurgitation velocity from the tricuspid valve plus the estimated right atrial pressure, while valve lessions by continuous and colour Doppler. Results Twenty-three (29.5%) pts had mild mitral valve regurgitation versus 7 controls (p 35 mmHg) (p Conclusion Patients with pSS and no clinically apparent heart disease had, more often than healthy controls, mild mitral and tricuspid valve regurgitation, pulmonary hypertension, and had increased left ventricular mass index. The LV mass index is correlated with purpura, lung disease and the presence of rheumatoid factor.