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Biomedical subjects

V Palmieri

Publications and source records attributed to V Palmieri.

At least 19 recordsLinked to original sources
PubMed2006

Effects of different dietary protein intakes on body composition and vascular reactivity.

OBJECTIVE: To assess the effects of a diet rich in protein of animal origin in comparison to one with a protein intake of about 15% of the total daily calories on body composition and arterial function. DESIGN: Randomized prospective study with parallel groups. Body weight (BW), blood pressure (BP), main parameters of carbohydrate and lipid metabolism, body mass composition by bioelectrical impedance analysis, forearm blood flow at rest and in the postischaemic phase by strain gauge plethysmography and flow-mediated dilation of the brachial artery by echography were measured at baseline and after 6 months of the dietary intervention. SUBJECTS: In total, 15 clinically healthy male volunteers, regularly performing a mixed training three times weekly for 90 min. INTERVENTION: The participants were randomly prescribed a diet with high (1.9 g/kg BW) or normal (1.3 g/kg BW) protein content. STATISTICAL ANALYSIS: Differences between means were evaluated by the t-tests for paired or unpaired data and by one way analysis of variance. The strength of correlation between variables was investigated by bivariate Pearson correlation. RESULTS: Serum cholesterol significantly decreased with both diets in comparison to baseline values, whereas BW was slightly but significantly reduced only by the high-protein (HP) diet. No change was detected in BP and the other metabolic parameters. Body mass composition was not significantly modified by either diet. On the other hand, postischaemic flow-mediated dilation of the brachial artery was enhanced by the sole normal protein (NP) diet, whereas no change in the forearm blood flow, both at rest and in the postischaemic phase, was detected. CONCLUSIONS: These preliminary results indicate that HP diet was found to be not useful in increasing the muscle mass in comparison to a NP intake. In contrast to this, the latter diet seems to enhance the endothelial function of the arterial vessels with a more pronounced dilatation of the lumen in response to the increase in blood flow.

Adolescent↗
PubMed2005

Plasma fibrinogen level and the risk of major cardiovascular diseases and nonvascular mortality: an individual participant meta-analysis.

CONTEXT: Plasma fibrinogen levels may be associated with the risk of coronary heart disease (CHD) and stroke. OBJECTIVE: To assess the relationships of fibrinogen levels with risk of major vascular and with risk of nonvascular outcomes based on individual participant data. DATA SOURCES: Relevant studies were identified by computer-assisted searches, hand searches of reference lists, and personal communication with relevant investigators. STUDY SELECTION: All identified prospective studies were included with information available on baseline fibrinogen levels and details of subsequent major vascular morbidity and/or cause-specific mortality during at least 1 year of follow-up. Studies were excluded if they recruited participants on the basis of having had a previous history of cardiovascular disease; participants with known preexisting CHD or stroke were excluded. DATA EXTRACTION: Individual records were provided on each of 154,211 participants in 31 prospective studies. During 1.38 million person-years of follow-up, there were 6944 first nonfatal myocardial infarctions or stroke events and 13,210 deaths. Cause-specific mortality was generally available. Analyses involved proportional hazards modeling with adjustment for confounding by known cardiovascular risk factors and for regression dilution bias. DATA SYNTHESIS: Within each age group considered (40-59, 60-69, and > or =70 years), there was an approximately log-linear association with usual fibrinogen level for the risk of any CHD, any stroke, other vascular (eg, non-CHD, nonstroke) mortality, and nonvascular mortality. There was no evidence of a threshold within the range of usual fibrinogen level studied at any age. The age- and sex- adjusted hazard ratio per 1-g/L increase in usual fibrinogen level for CHD was 2.42 (95% confidence interval [CI], 2.24-2.60); stroke, 2.06 (95% CI, 1.83-2.33); other vascular mortality, 2.76 (95% CI, 2.28-3.35); and nonvascular mortality, 2.03 (95% CI, 1.90-2.18). The hazard ratios for CHD and stroke were reduced to about 1.8 after further adjustment for measured values of several established vascular risk factors. In a subset of 7011 participants with available C-reactive protein values, the findings for CHD were essentially unchanged following additional adjustment for C-reactive protein. The associations of fibrinogen level with CHD or stroke did not differ substantially according to sex, smoking, blood pressure, blood lipid levels, or several features of study design. CONCLUSIONS: In this large individual participant meta-analysis, moderately strong associations were found between usual plasma fibrinogen level and the risks of CHD, stroke, other vascular mortality, and nonvascular mortality in a wide range of circumstances in healthy middle-aged adults. Assessment of any causal relevance of elevated fibrinogen levels to disease requires additional research.

Adult↗
PubMed2005

Relations of left ventricular mass and systolic function to endothelial function and coronary flow reserve in healthy, new discovered hypertensive subjects.

Left ventricular hypertrophy (LVH) is prognostically relevant, associated with major cardiovascular risk factors and with atherosclerosis. However, whether LVH is independently associated with impaired coronary flow reserve (CFR) and with endothelial dysfunction is disputed. We assessed the relationship of LV mass and systolic function to CFR and endothelial function in new discovered never treated subjects with essential arterial hypertension, but without coronary artery disease or microalbuminuria. LVH, ejection fraction (EF) and stress-corrected midwall shortening (MWS, a measure of myocardial contractility) were assessed by echocardiography. CFR was assessed by single-photon emission computed tomography and dipyridamole infusion. Endothelial function was evaluated by assessing 1-min postischaemic flow-mediated dilatation of the brachial artery (FMD); nitroglycerine-mediated dilatation (NMD) of the same brachial artery was used as measure of nonendothelium-dependent vasodilatation. In approximately 1 year, we enrolled 21 subjects who met stringent inclusion criteria (47+/-10 years old, 26.6+/-2.8 kg/m2, 78% men). Five patients showed LVH. Multivariate analyses showed a significant negative correlation of LV mass index with FMD (beta=-0.61, P<0.05) but not with NMD, neither with CFR. Stress-corrected MWS showed independent correlation with CFR (beta=0.51, P<0.05). Thus, in clinically healthy, new discovered hypertensive subjects, never treated and mostly in the early stage of arterial hypertension, LVH can be associated with endothelial dysfunction while maximal dipyridamole- dependent CFR may be preserved; nevertheless, a cardiac phenotype presenting with tendency to impaired myocardial contractility, assessed by stress-corrected MWS, showed association with lower CFR in the early stage of arterial hypertension.

Coronary Circulation↗
PubMed2005

Boxing and "commotio cordis": ECG and humoral study.

The objective of the study was to analyze the presence of myocardial damage in relation to official boxing matches. Low-energy chest wall impact could be responsible for sudden cardiac death, i.e. commotio cordis. As boxing is a traumatic sport in which thoracic hits usually occur, it seems interesting to know if there are any significant cardiac changes during official bouts. Fifteen amateur boxers, participating in the semifinals of the Italian Championship were investigated. A standard ECG before, immediately after, 1 hour and 12 hours after the match were obtained from each athlete to analyze atrio-ventricular conduction, QRS axis and duration, and ventricular repolarization. A blood sample was also obtained before and 12 hours after the match for analysis of total-creatin-phosphokinase, myoglobin, and T-troponin. After the fight, the following significant changes were encountered: higher QRS voltages, lowering of J-point and ST segment in lateral leads, higher ST-slope, lower T-wave amplitude, shorter T-wave peak time, and shorter QT interval. When the last 2 parameters were corrected for heart rate, no differences were observed for QTc, while T-wave peak time significantly increased. All these changes persisted until one hour after the match. Moreover, 3/15 boxers (20 %) showed marked ventricular repolarization anomalies in lateral leads after the contest, persisting for 12 hours in one case. However, no athlete had clinical and humoral signs of myocardial damage following the match. It was concluded that no clinical and humoral signs of myocardial damage were found after amateur boxing matches, although ventricular repolarization abnormalities can be found on ECG in 20 % of boxers, probably due to sympathetic hyper-activity related to the agonistic event.

Adult↗
PubMed2005

Ocular complications of boxing.

OBJECTIVES: To investigate the prevalence of ocular injuries in a large population of boxers over a period of 16 years, in particular, the most severe lesions that may be vision threatening. METHODS: Clinical records of the medical archive of the Italian Boxing Federation were analysed. A total of 1032 boxers were examined from February 1982 to October 1998. A complete ophthalmological history was available for 956, who formed the study population (a total of 10 697 examinations). The following data were collected: age when started boxing; duration of competitive boxing career (from the date of the first bout); weight category; a thorough ocular history. The following investigations were carried out: measurement of visual acuity and visual fields, anterior segment inspection, applanation tonometry, gonioscopy, and examination of ocular fundus. Eighty age matched healthy subjects, who had never boxed, formed the control group. RESULTS: Of the 956 boxers examined, 428 were amateur (44.8%) and 528 professional (55.2%). The median age at first examination was 23.1 (4.3) years (range 15-36). The prevalence of conjunctival, corneal, lenticular, vitreal, ocular papilla, and retinal alterations in the study population was 40.9% compared with 3.1% in the control group (p< or =0.0001). The prevalence of serious ocular findings (angle, lens, macula, and peripheral retina alterations) was 5.6% in boxers and 3.1% in controls (NS). CONCLUSIONS: Boxing does not result in a higher prevalence of severe ocular lesions than in the general population. However, the prevalence of milder lesions (in particular with regard to the conjunctiva and cornea) is noteworthy, justifying the need for adequate ophthalmological surveillance.

Adolescent↗
PubMed2005

Medical survey of female boxing in Italy in 2002-2003.

BACKGROUND: Female boxing has been permitted in Italy since 2001. According to the latest Italian laws, athletes applying to become boxers have to pass a pre-participation medical examination. OBJECTIVE: To collect novel medical information from the pre-participation visits and mandatory pre-competition and post-competition examinations for all fights involving Italian female boxers in 2002-2003. METHODS: A retrospective study on all official female boxing competitions in Italy from January 2002 to October 2003 was conducted. A prospective study on 28 amateur female boxers was also carried out. RESULTS: Retrospective study: data from 664 examinations were collected. Pre-match examinations were negative. After competitions, 19/645 visits showed some injuries, with mild, soft tissue facial lesions, epistaxis, and hand-wrist problems being the most common. Prospective study: no major lesions were found during the study. One fibroadenoma, one ovarian cyst, and one intramural uterine myoma were found. One boxer was referred to a neurologist because of non-specific electroencephalographic (EEG) abnormalities, which persisted six months later. On a re-admission examination, which was needed because of a contest that was stopped because the referee judged that she was receiving blows to the head that were dangerous, one boxer showed non-specific EEG alterations and nystagmus. A cerebral magnetic resonance imaging scan was normal. She was allowed to participate in competitions again when her EEG returned to normal and clinical signs disappeared. Deviation of the nasal septum was quite common (68%). No major eye injuries were reported. CONCLUSION: Probably because of the correct preventive medical approach, female boxing is much safer than expected, and no major lesions (requiring hospital admission) were reported. Any lesions to the breast and reproductive system could not be considered to be boxing related.

Adult↗
PubMed2004

Sex-related difference in regression of left ventricular hypertrophy with antihypertensive treatment: the LIFE study.

While left ventricular (LV) structure and function differ between hypertensive women and men, it remains unclear whether sex affects regression of LV hypertrophy with antihypertensive treatment. We analysed paired echocardiograms in 500 men and 347 women enrolled in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study at baseline and after 12 months of antihypertensive treatment with either losartan or atenolol. At enrollment, 177 women and 242 men were randomized to losartan-based treatment and 161 women and 247 men were randomized to atenolol-based treatment (sex difference=NS). After 12 months of antihypertensive treatment, blood pressure was lowered similarly in women (152/83 from 174/97 mmHg) and men (149/85 from 173/99 mmHg; both P<0.001, sex difference=NS), without significant change in body weight in either sex. Cardiac output and pulse pressure/stroke volume were equivalently reduced in both sexes (-0.2 vs -0.1 l/min and both -0.20 mmHg/ml/m(2), respectively; both P=NS). Absolute LV mass change after 12 months of antihypertensive treatment was greater in men than in women (-30 vs -24 g, P=0.01). However, after adjusting for baseline LV mass and randomized study treatment, LV mass reduction was greater in women than in men (-33 vs -23 g, P=0.001). LV mass regression was greater in women, by 8.0+/-2.8 g, after adjusting for baseline LV mass and randomized study treatment. After consideration of baseline LV mass and randomized study treatment, antihypertensive treatment regressed LV hypertrophy more in women. Further studies are needed to identify the mechanisms and prognostic implications of this sex-related difference.

Aged↗
PubMed2004

Albuminuria predicts cardiovascular events independently of left ventricular mass in hypertension: a LIFE substudy.

We wanted to investigate whether urine albumin/creatinine ratio (UACR) and left ventricular (LV) mass, both being associated with diabetes and increased blood pressure, predicted cardiovascular events in patients with hypertension independently. After 2 weeks of placebo treatment, clinical, laboratory and echocardiographic variables were assessed in 960 hypertensive patients from the LIFE Echo substudy with electrocardiographic LV hypertrophy. Morning urine albumin and creatinine were measured to calculate UACR. The patients were followed for 60+/-4 months and the composite end point (CEP) of cardiovascular (CV) death, nonfatal stroke or nonfatal myocardial infarction was recorded. The incidence of CEP increased with increasing LV mass (below the lower quartile of 194 g to above the upper quartile of 263 g) in patients with UACR below (6.7, 5.0, 9.1%) and above the median value of 1.406 mg/mmol (9.7, 17.0, 19.0%(***)). Also the incidence of CV death increased with LV mass in patients with UACR below (0, 1.4, 1.3%) and above 1.406 mg/mmol (2.2, 6.4, 8.0%(**)). The incidence of CEP was predicted by logUACR (hazard ratio (HR)=1.44(**) for every 10-fold increase in UACR) after adjustment for Framingham risk score (HR=1.05(***)), history of peripheral vascular disease (HR=2.3(*)) and cerebrovascular disease (HR=2.1(*)). LV mass did not enter the model. LogUACR predicted CV death (HR=2.4(**)) independently of LV mass (HR=1.01(*) per gram) after adjustment for Framingham risk score (HR=1.05(*)), history of diabetes mellitus (HR=2.4(*)) and cerebrovascular disease (HR=3.2(*)). (*)P<0.05, (**)P<0.01, (***)P<0.001. In conclusion, UACR predicted CEP and CV death independently of LV mass. CV death was predicted by UACR and LV mass in an additive manner after adjustment for Framingham risk score and history of CV disease.

Aged↗
PubMed2004

Impact of valvular regurgitation on left ventricular geometry and function in hypertensive patients with left ventricular hypertrophy: the LIFE study.

Mild-to-moderate aortic and mitral regurgitation are frequently detected by echocardiogram in asymptomatic hypertensive patients. Our goal was to assess the prevalence and impact of mild-to-moderate mitral and/or aortic regurgitation on left ventricular (LV) structure and function in patients with hypertension and LV hypertrophy (LVH). Hypertensive patients with ECG LVH enrolled in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) echocardiography substudy were evaluated. Among 939 patients with needed LV measurements and Doppler data, 242 had mild (1+) valvular regurgitation, and 51 patients had moderate (2+ or 3+) regurgitation of one or both valves. In analyses adjusting for gender, patients with mild mitral and/or aortic regurgitation had larger LV internal dimensions (5.25 vs 5.33 cm, P<0.05), higher LV mass indexed for body surface area (122 vs 125 g/m(2), P<0.05) or height(2.7) (55.4 vs 57.3, P<0.05), and larger left atrial diameter. Patients with moderate regurgitation of one or both valves had larger LV chambers (5.25 vs 5.9 cm, P<0.001), greater mean LV mass (232 vs 248 g, P<0.001) and LV mass indexed for body surface area or height(2.7), and higher Doppler stroke volume. Patients with moderate valvular regurgitation also had a higher prevalence of LVH due to an increased prevalence of eccentric LVH. There were no differences among groups defined by the presence and severity of valvular regurgitation in cardiac output, total peripheral resistance, or pulse pressure/stroke volume, indicating that the observed inter-group differences in LV geometry were not due to differences in the haemodynamic severity of hypertension. Hypertensive patients with mild-to-moderate mitral or aortic valvular insufficiency have additional LV structural and functional changes that may affect prognosis.

Aged↗
PubMed2004

Association between vascular dysfunction and reduced myocardial flow reserve in patients with hypertension: a LIFE substudy.

Impaired myocardial flow reserve (MFR) has been demonstrated in hypertension, and has been associated with peripheral vascular changes. We investigated whether MFR was impaired and associated with structural and/or functional vascular changes in hypertensive patients without evidence of coronary artery disease (CAD). We measured left ventricular (LV) mass index by echocardiography and MFR by positron emission tomography in 33 unmedicated, hypertensive patients with electrocardiographic LV hypertrophy without CAD, and 15 age- and gender-matched normotensive subjects. We also measured 24-h ambulatory blood pressure, minimal forearm vascular resistance (MFVR) by plethysmography, media:lumen ratio in isolated, subcutaneous resistance arteries by myography, intima-media cross-sectional area of the common carotid artery, and flow-mediated (FMD) and nitroglycerin-induced dilatation (NID) of the brachial artery by ultrasound. Compared to the controls, the patients had impaired MFR (2.4 (95% CI 1.95-2.8) vs 3.4 (2.7-4.2), P<0.01) due to increased resting myocardial blood flow (MBF) (0.82 (0.73-0.91) vs 0.65 (0.56-0.75) ml/g min), and decreased dipyridamole-stimulated MBF (1.80 (1.55-2.1) vs 2.3 (1.80-2.8) ml/g min, both P<0.05). The difference in resting MBF disappeared (80 (74-87) vs 86 (74-97) microl/kg mmHg, NS) when normalized for blood pressure and heart rate. MFR correlated negatively to median 24-h systolic blood pressure (r=-0.50, P<0.01) as well as to LV mass index (r=-0.45, P<0.05) and MFVR in men (r=-0.47, P<0.05), and positively to FMD (r=0.44, P<0.05) and NID (r=0.40, P<0.05). Hypertensive patients with electrocardiographic LV hypertrophy without CAD had impaired MFR associated with cardiovascular hypertrophy and vasodilatory dysfunction. This suggests that MFR is impaired by LV hypertrophy and structural/functional vascular damage in the coronary and noncoronary circulation.

Aged↗
PubMed2004

Impact of age on left ventricular hypertrophy regression during antihypertensive treatment with losartan or atenolol (the LIFE study).

To assess the influence of age on changes in left ventricular (LV) mass and geometry during antihypertensive treatment, we related age to clinical and echocardiographic findings before and after 4 years of antihypertensive treatment in a subset of 560 hypertensive patients without known concurrent disease in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study, which randomized patients to blinded losartan- or atenolol-based treatment. Patients >/=65 years (older group) included more women and patients with isolated systolic hypertension or albuminuria (all P<0.05). Compared to patients <65 years, older patients had higher pulse pressure, LV mass, and prevalence of concentric hypertrophy at baseline (78 vs 69 mmHg, 234 vs 224 g, and 28 vs 16%, respectively, all P<0.01), while the mean blood pressure did not differ. Over 4 years, reductions in LV mass and the mean blood pressure were similar in both groups, but older patients more often had residual hypertrophy (31 vs 15%, P<0.001) with a preponderance of eccentric geometry. In multivariate analysis of 4-year change in LV mass controlling for baseline mass, larger hypertrophy reduction was associated with losartan treatment, while age, gender, body mass index, and 4-year change in pulse pressure and albuminuria did not enter (Multiple R (2)=0.40, P<0.001). Thus, in up-to-80-year-old hypertensive patients with left ventricular hypertrophy, age did not significantly attenuate hypertrophy reduction during antihypertensive treatment, although residual hypertrophy was more prevalent in older patients as a consequence of higher initial LV mass.

Age Factors↗
PubMed2004

Usefulness of the assessment of the appropriateness of left ventricular mass to detect left ventricular systolic and diastolic abnormalities in absence of echocardiographic left ventricular hypertrophy: the LIFE study.

Conventional definitions of left ventricular (LV) hypertrophy do not account for interindividual differences in loading conditions. We may define LV mass as inappropriately high when exceeding 128% of theoretical values predicted by gender, height(2.7), and stroke work, which explain up to 82% of the variability of LV mass in normal reference subjects. In 652 participants in the Losartan Intervention For Endpoint reduction in hypertension study without clinically overt cardiovascular disease or diabetes, we investigated whether inappropriately high LV mass is associated with relevant LV abnormalities independent of traditional definition of LV hypertrophy (ie, LV mass index >116 g/m(2) in men and >104 g/m(2) in women). The study sample was divided into three groups: patients with inappropriately high LV mass but without LV hypertrophy were compared to patients with LV hypertrophy and to patients with appropriate LV mass and without LV hypertrophy. Patients with inappropriately high but nonhypertrophic LV mass had higher body mass index and relative wall thickness, and lower LV myocardial systolic function, than patients with appropriate LV mass or patients with LV hypertrophy. In multivariate analyses, inappropriately high LV mass was independently associated with lower myocardial systolic function independent of LV hypertrophy and other covariates. Inappropriately high LV mass was also associated with prolonged isovolumic relaxation time and lower mitral E/A ratio independent of covariates. In conclusion, inappropriately high LV mass was associated with relevant, often preclinical, manifestations of cardiac disease in the absence of traditionally defined echocardiographic LV hypertrophy and concentric geometry.

Aged↗
PubMed2004

Is inappropriate left ventricular mass related to neurohormonal factors and/or arterial changes in hypertension? A LIFE substudy.

We investigated whether inappropriately high left ventricular (LV) mass, defined as observed LV mass exceeding the level of individual LV mass predicted from gender, height, and stroke work, may be associated with an imbalance between growth-promoting and growth-inhibitory factors and/or structural vascular changes. In 53 patients with hypertension and electrocardiographic LV hypertrophy, 24-h ambulatory blood pressure (BP); echocardiographic LV mass, stroke volume and stroke work; minimal forearm vascular resistance (MFVR); and intima-media cross-sectional area in common carotid arteries (IMA) were evaluated after 2 weeks of placebo treatment. Serum insulin, plasma epinephrine, norepinephrine, endothelin, angiotensin II, aldosterone, and brain natriuretic peptide (BNP) were also measured. High observed LV mass was related to high IMA (r=0.46, P<0.001), MFVR (in men: r=0.36, P<0.05), 24-h ambulatory systolic BP (r=0.30, P=0.06), and lower plasma angiotensin II (r=-0.33, P<0.05), but not to other circulating growth factors. Stroke work was similarly related to IMA (r=0.42, P<0.01), MFVR (in men: r=0.41, P<0.05), and plasma angiotensin II (r=-0.32, P<0.05). Inappropriate LV mass, identified by the ratio between observed LV mass and the value predicted for gender, height, and stroke work, was not significantly related to any of the arterial or neurohormonal variables. In this small series of older hypertensive patients, inappropriate LV mass was not significantly related to arterial changes or to measured circulating growth factors, although weak relations cannot be excluded. Alternatively, inappropriately high LV mass might be related to unmeasured factors such as local myocardial alterations in growth factors and/or genetic predisposition to develop excessive LV hypertrophy.

Aged↗
PubMed2004

Prolonged asystolia in a young athlete: a case of sinus arrest during REM sleep.

A young asymptomatic male athlete came to our laboratory to be enrolled in a research protocol on physical fatigue. Routine clinical and cardiological evaluations including echocardiogram were in the normal range. Several consecutive cardiopulmonary tests showed a fairly good tolerance to exercise, with no symptoms even when the effort was abruptly arrested. On the other hand, Holter ECG recordings showed long nocturnal sinus pauses. As he was absolutely asymptomatic and free from any structural heart disease, he underwent a follow-up with repeated Holter monitorings for one year. During this period he decided on his own to stop practising sports; in spite of this sharp reduction in his overall physical activity, consecutive Holter monitorings showed that the sinus pauses were progressively increasing in duration (up to 9.2 seconds). With the hypothesis of a malignant vagotonia, he underwent a tilt test; however, we could not elicit any pauses or symptoms. The pauses grew longer over time; a endocavitary electrophysiologic test was performed, which showed no evidence of disease. To rule out the hypothesis of a sleep apnoea syndrome, he also underwent a polysomnography, including EEG, eye movement electromyography, arterial blood oxygen saturation and thoracic impedance: no alterations were detected with the exception of the sinus pauses, which appeared to be strictly linked to REM sleep, as suggested by the concurrent increase in rapid eye movements and desynchronized EEG. We hence made a diagnosis of sinus arrest during REM sleep (SAdRS), a very uncommon disease belonging to the parasomnias. Pauses were then quantified for one month by implanting a ECG loop recorder. As the patient became more and more upset and worried, and the pauses increased to nearly 12 seconds, we decided to implant a pacemaker, which is the only therapeutic option established in the literature for patients with SAdRS.

Adult↗
PubMed2004

Myocardial contractility and total arterial stiffness in patients with overt hyperthyroidism: acute effects of beta1-adrenergic blockade.

OBJECTIVES: To ascertain whether myocardial contractility and total arterial stiffness are significantly altered in human thyrotoxicosis, and to what extent they are affected by acute beta(1)-adrenergic blockade. METHODS: Doppler-echocardiography was used to assess left ventricular (LV) structure and function, hemodynamics and total arterial stiffness in untreated overt hyperthyroid patients before and 2 h after 5 mg bisoprolol given orally compared with age- and sex-matched healthy euthyroid controls. RESULTS: Compared with controls, untreated patients (n=20) had a higher heart rate (HR) and LV stroke index (SI), which were associated with higher pulse pressure (PP), larger LV end-diastolic volume index (EDVI, an index of preload,+11%, P<0.05), marginally increased stress-corrected LV midwall fractional shortening (MWS, an index of myocardial contractility,+5%; P=0.066), and shorter isovolumic relaxation time (IVRT). These changes resulted in a higher cardiac index (CI) and a lower systemic vascular resistance (SVR), which were associated with fairly normal mean blood pressure (BP) but higher PP/stroke volume (an index of total arterial stiffness,+29%; P<0.01). After bisoprolol, compared with controls, the randomly treated patients (n=10) had comparable HR but additionally increased SI; PP remained enhanced, EDVI was further enlarged (+26%, P<0.001), stress-corrected MWS was substantially unchanged, and IVRT remained shorter. Overall, these effects attenuated the high-output state, which was associated with normalization of PP/stroke volume without changes of mean BP. CONCLUSIONS: In human overt hyperthyroidism, myocardial contractility does not play a major role in increasing LV performance, which is instead predominantly sustained by increased preload with enhanced LV diastolic function. In addition, human thyrotoxicosis is associated with increased total arterial stiffness despite fairly normal mean BP. In this scenario, acute beta(1)-adrenergic blockade blunts the cardiovascular hyperkinesia predominantly by slowing HR - a process that is associated with normalization of total arterial stiffness.

Adrenergic beta-1 Receptor Antagonists↗
PubMed2003

Citizens and family doctors facing awareness and management of traditional cardiovascular risk factors: results from the Global Cardiovascular Risk Reduction Project (Help Your Heart Stay Young Study).

BACKGROUND AND AIM: The numerous guidelines and multiple approaches to managing cardiovascular risk factors have reduced the number of fatal events but not the incidence of cardiovascular disease (CVD). One rarely explored aspect is the extent to which individuals perceive their own risk in relation to their education and history of CVD. Furthermore, Italy has a State-based Health System, in which family doctors (FDs) may be an extremely useful and relatively low cost resource for risk management, but the degree of their involvement in individual CVD risk management has not been previously assessed. METHODS AND RESULTS: The Department of Clinical and Experimental Medicine of Federico II University, Naples, Italy, and the Neapolitan Section of the Italian Society of Family Doctors (SIMG), developed an epidemiological survey to evaluate the level and awareness of CVD risk in subjects in the urban area of Naples, and the degree of involvement of FDs in CVD risk management. During a period of a few months, the subjects who visited their FDs were invited to respond to a standard self-explanatory questionnaire, and the FDs were required to provide quantitative information concerning the CVD risk factors of each enrolled subject from their databases in order to assess global CVD risk. The data included cholesterol and blood pressure (BP) levels, and had to be collected within six months of the visit; if the date were missing, the fact was recorded. The present analysis was based on data concerning the 5,687 subjects who had entered the study by January 2002, 7.6% of whom reported CVD (myocardial infarction (MI), stroke, angina, cerebral transient ischemic attack: CD+) and 92.4% did not (CVD-). MI was the most frequent CVD, and 18% of the CVD+ cases reported more than one non-fatal cardiovascular event. On average, the CVD+ subjects were older and more often men. After adjusting for age and FD, they also had a higher body mass index (BMI) and prevalence of obesity, higher self-reported BP, a lower education level, and more often referred high cholesterol levels, hypertension and diabetes. On the contrary, the proportion of smokers was higher in the CVD- group. Among the subjects who declared that they did not have a high cholesterol level, 11% reported recent values of > 200 mg/dL. The FDs of 36% of the cases were unable to assess the individual global CV risk level using quantitative data from their electronic databases. The most frequently missing information was the level of total cholesterol. Missing data were more frequent in the CVD- than the CVD+ subjects, regardless of age and FD. CONCLUSIONS: The results of our study suggest that the awareness of CVD risk among subjects is somewhat vague. The FDs were generally able to provide a quantitative assessment of CVD risk in their patients. CVD risk prevention programmes may be more successful if they stress knowledge and awareness in the population, and stimulate FDs to undertake more stringent quantitative assessments of CVD risk factors.

Adult↗
PubMed2003

Relation of insulin resistance to markers of preclinical cardiovascular disease: the Strong Heart Study.

BACKGROUND AND AIMS: To investigate whether insulin-resistance influences echocardiographic markers of preclinical disease, independent of significant confounders. METHODS AND RESULTS: We examined 1,471 (59 +/- 8 years) non-diabetic individuals (WHO criteria) with available echocardiograms from the Strong Heart Study cohort. Among them, 530 subjects had arterial hypertension (62% on medications), 152 had impaired glucose tolerance (GT) and 460 were normotensive, non-obese with normal GT. Insulin resistance was estimated by the Homeostasis Model Assessment (HOMA). LV mass, systolic function measured at the endocardium and the midwall (also correcting for circumferential wall stress) and arterial compliance (stroke volume/pulse pressure as a percent of predicted from body weight, age and heart rate [delta %SV/PP]) were measured by echocardiography, as prognostically validated markers of preclinical disease. HOMA-index was related positively to body mass index (BMI), waist/hip ratio (WHR), blood pressure, left ventricular (LV) mass, and negatively to arterial compliance (all p < 0.005) in the whole population, as well as in separate normotensive or hypertensive groups. In multiple regression models, relation of HOMA-index with the markers of risk was adjusted for age, sex, WHR, body mass index, presence of hypertension and number of antihypertensive medications. In this analysis, neither LV mass nor indices of systolic function were independently related to HOMA-index. In contrast, HOMA-index maintained a significant negative association with delta %SV/PP, independent of demographics, hypertension, treatment and body fat distribution. Also, HOMA-index maintained an independent relation with LV mass, when WHR and BMI were not included in the regression model. CONCLUSIONS: After accounting for relevant biological covariates, including body mass and fat distribution, insulin-resistance measured by HOMA is not an independent correlate of LV mass and function, but negatively influences arterial compliance.

Aged↗