Vittorio Palmieri

ASL Lecco, Lecco, Lombardy, Italy

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Publications (101)411.39 Total impact

  • Article: Lytic failure in the current pharmacointensive ST-elevated acute myocardial infarction care: insights from a pilot real-world study.
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    ABSTRACT: BACKGROUND: Thrombolysis remains a very acceptable reperfusion option for ST-elevated acute myocardial infarction (STEMI); however, it fails relatively frequently and unpredictably. AIM AND METHODS: To investigate correlates of lytic failure (according to the standard ST resolution criterion) in current pharmacointensive STEMI care (dual antiplatelets with antithrombin), we analyzed retrospectively clinical data and echocardiographic left ventricular systolic function before initiation of reperfusion treatment in Killip I-III STEMI patients admitted to our 'spoke' intensive cardiac care unit between 1 January and 31 December 2010. RESULTS: Of the 53 STEMI patients enrolled, 28% failed thrombolysis. Patients who did not reperfuse were less frequently active smokers (P < 0.05, odds ratio 4.33) and had a higher prevalence of hemodynamic instability [heart rate/SBP (i.e. shock index) >0.75; P < 0.05, odds ratio 13.45) and left ventricular systolic dysfunction (ejection fraction <45%; P < 0.005, odds ratio 11.14). In an exploratory multivariable logistic regression analysis, those variables were the only discriminators independently associated with lytic failure (adjusted odds ratio 8.74, 230.10, and 18.22, respectively, all P < 0.05). Moreover, the combined variables had a high accuracy for prediction of failed thrombolysis (all discriminators positive, 99% specificity and 83% positive predictive value). CONCLUSION: Our pilot study indicates that thrombolysis still fails in about one-third of STEMI patients despite the current pharmacointensive approach and suggests that failed ST resolution might be independently associated with nonsmoking habit and pretreatment hemodynamic instability and left ventricular systolic dysfunction. Larger trials are needed to verify the potential clinical implications of our preliminary observation.
    Journal of Cardiovascular Medicine 07/2012; · 1.51 Impact Factor
  • Article: Arterial stiffness and wave reflection: sex differences and relationship with left ventricular diastolic function.
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    ABSTRACT: Increased arterial stiffness and wave reflection have been reported in heart failure with normal ejection fraction (HFNEF) and in asymptomatic left ventricular (LV) diastolic dysfunction, a precursor of HFNEF. It is unclear whether women, who have higher frequency of HFNEF, are more vulnerable than men to the deleterious effects of arterial stiffness on LV diastolic function. We investigated, in a large community-based cohort, whether sex differences exist in the relationship among arterial stiffness, wave reflection, and LV diastolic function. Arterial stiffness and wave reflection were assessed in 983 participants from the Cardiovascular Abnormalities and Brain Lesions study using applanation tonometry. The central pulse pressure/stroke volume index, total arterial compliance, pulse pressure amplification, and augmentation index were used as parameters of arterial stiffness and wave reflection. LV diastolic function was evaluated by 2-dimensional echocardiography and tissue-Doppler imaging. Arterial stiffness and wave reflection were greater in women compared with men, independent of body size and heart rate (all P<0.01), and showed inverse relationships with parameters of diastolic function in both sexes. Further adjustment for cardiovascular risk factors attenuated these relationships; however, a higher central pulse pressure/stroke volume index predicted LV diastolic dysfunction in women (odds ratio, 1.54; 95% confidence intervals, 1.03 to 2.30) and men (odds ratio, 2.09; 95% confidence interval, 1.30 to 3.39), independent of other risk factors. In conclusion, in our community-based cohort study, higher arterial stiffness was associated with worse LV diastolic function in men and women. Women's higher arterial stiffness, independent of body size, may contribute to their greater susceptibility to develop HFNEF.
    Hypertension 07/2012; 60(2):362-8. · 6.21 Impact Factor
  • Article: Contrasting hemodynamic mechanisms of losartan- vs. atenolol-based antihypertensive treatment: a LIFE study.
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    ABSTRACT: Pharmaceutical differences in central hemodynamics might influence cardiac response to antihypertensive treatment despite similar lowering of brachial blood pressure (BP). Data from all patients with at least two echocardiographic examinations in the Losartan Intervention For Endpoint Reduction in Hypertension (LIFE) echocardiographic substudy (n = 801); high-risk patients on losartan- vs. atenolol-based antihypertensive therapy. Echocardiography was performed annually for 4 years to measure stroke index (SI), heart rate, cardiac index (CI), conduit artery stiffness assessed as pulse pressure/stroke index (PP/SI) and total peripheral resistance index (TPRI). Atenolol- and losartan-based therapy reduced BP similarly (cumulative difference in mean brachial blood pressure 0.3 mm Hg, P = 0.65). After 4 years the cumulative means of SI and heart rate were 1.8 ml/m(2) higher and 5.7 beats/min lower on atenolol-based treatment, respectively (both P < 0.001). This kept CI below baseline in atenolol-treated patients, whereas in the losartan group CI was unchanged from baseline throughout the study. TPRI was decreased more and remained lower in the losartan group (cumulative difference in mean TPRI 287 dynes/sec(-5)/cm/m(2), P < 0.001). These findings partly explained univariate differences in systolic- and diastolic function indices between the two treatments; fully adjusted losartan was only associated with a smaller left atrial diameter (cumulative mean difference 0.07 cm; 95% confidence intervals, -0.13 to -0.01, P = 0.03). Contrasting hemodynamics impacted cardiac response to similar reductions in brachial BP on losartan- vs. atenolol-based therapy. The similar reduction of PP/SI suggests that the antihypertensive regimens used in the LIFE study had comparable effects on arterial stiffness (LIFE study; NCT00338260)
    American Journal of Hypertension 06/2012; 25(9):1017-23. · 3.18 Impact Factor
  • Article: [Cardiac resynchronization therapy: mortality, heart failure rehospitalization, and procedure-related complications. A three-year single-center observational study within the Italian Health System].
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    ABSTRACT: The aim of this study was to evaluate whether the benefit of cardiac resynchronization therapy with an implantable defibrillator (CRT-D) may differ among classes of indications to device therapy. All-cause mortality, first hospitalization for non-fatal heart failure, stable improvement of NYHA functional class (responders), and implant-related complications were evaluated retrospectively in 103 patients selected among those (n = 133) who received consecutively CRT-D between 2006 and 2009. Patients were divided into three groups: group IA (n = 65) included patients receiving CRT-D for a class IA indication; group IIa (n = 26) included patients with atrial fibrillation and QRS ≥ 130 ms receiving CRT-D for a class IA indication; nonconventional group (NC) (n = 12) included patients with an indication to defibrillator implantation extended to CRT-D because of NYHA class III-IV and echocardiographic evidence of electromechanical dyssynchrony. Echocardiographic examination was performed in all patients to identify wall target for left-side lead placement. Group IIa patients were slightly older than group IA patients (p<0.05); gender distribution, left ventricular ejection fraction at implantation, ischemic etiology, and heart failure treatment were comparable among groups (all p>0.5), except for a higher digitalis use in group IIa patients (p<0.05). In a mean observation period of 3 years (up to December 2010), the rates of fatal events (IA: 22%, IIa: 23%, NC: 20%), rehospitalization for worsening heart failure (IA: 30%, IIa: 33%, NC: 22%), clinical responders (IA: 78%, IIa: 78%, NC: 78%), implant-related complications requiring reintervention (IA: 15%, IIa: 19%, NC: 25%), including pocket or catheter infections (IA: 5%, IIa: 11%, NC: 8%) were comparable among groups (all p>0.5). In the "real world", the benefit of CRT-D in advanced heart failure patients might be comparable among class IA, IIa or NC indication.
    Giornale italiano di cardiologia (2006) 05/2012; 13(5):369-76.
  • Article: [Home-based telemonitoring of simple vital signs to reduce hospitalization in heart failure patients: real-world data from a community-based hospital].
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    ABSTRACT: Whether home telemonitoring after acute episodes of heart failure (HF) may reduce de-novo cardiac decompensation is disputed. We tested home telemonitoring of blood pressure (BP), heart rate (HR), and blood oxygen saturation (SO2) to reduce rehospitalization in patients with recent admission for acute HF. METHODS; We screened patients hospitalized in Cardiology due to prominent cardiac cause of acute dyspnea, and pulmonary/peripheral congestion, and with one admission or more for similar symptoms/signs in the previous year. Patients with acute coronary syndrome, poor prognosis due to extracardiac causes, and reduced self-sufficiency and cognitive ability were excluded. Of the selected patients, 63% accepted and received a device for BP, HR and SO2 measurement connected to an analogical modem for data transmission to a hospital server. Patients were educated to measure vital signs 3 times/week. A dedicated doctor-nurse unit monitored the patients' data twice weekly to manage therapeutic adjustments of diuretic dosage or in-hospital visits if necessary. HF treatment was standardized based on current guidelines. Unplanned hospitalizations for HF or all-cause death were primary endpoints; unplanned hospitalizations (total) for any cause, and all-cause death were the composite endpoints. Twenty-three patients (mean age 70 years, range 44-80 years) were recruited: 26% were women, 61% had coronary heart disease, 52% chronic lung disease, 57% renal insufficiency, 30% anemia; 17% had moderate or severe mitral regurgitation. At a mean follow-up of 302 days (range 55-622 days), 12 patients experienced the composite endpoints (52%, p=0.1), with the primary endpoint occurring in 8 patients (35%, 1 sudden death, p=0.058), the secondary endpoints occurring in 2 patients, and hospitalization not for HF occurring in 2 patients. The total number of hospitalizations/patient/year decreased from 2.2 ± 1.3 in the previous year to 0.9 ± 1.2 during the study period (p<0.01). On average, systolic BP tended to decrease, but BP, HR and SO 2 values prior to the index event (1-7 days) did not significantly differ from those recorded at the beginning of telemonitoring. In HF, home telemonitoring of simple variables had no significant impact on all-cause hospitalization/mortality, but was associated with a higher patient compliance and achievement of therapeutic targets, which may translate into a reduction in hospitalization rates for HF.
    Giornale italiano di cardiologia (2006) 12/2011; 12(12):829-36.
  • Article: Relation of flow-mediated dilation to global arterial load: impact of hypertension and additional cardiovascular risk factors.
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    ABSTRACT: Endothelial dysfunction may be related to increased left ventricular (LV) mass due to an association between endothelial dysfunction with increased arterial load. Therefore, we evaluated whether brachial artery flow-mediated dilation (FMD) is related to global arterial load. Pulse pressure/stroke index (PP/SVi, global arterial stiffness, prognostically validated), stroke volume/PP (SV/PP, global arterial compliance), and % of the predicted SV/PP by heart rate, age and body weight (confounder-adjusted global compliance, prognostically validated) were used as LV geometry-related indices of global arterial load. Compared to normotensive participants (NT, n = 50), those with hypertension (HTN, n = 51) had lower FMD (8.3% ± 5.4 vs. 12.8% ± 6.5), higher PP/SVi (1.24 ± 0.34 vs. 1.04 ± 0.28 mmHg m(2)/ml), higher LV mass and higher relative wall thickness (all p < 0.01); in contrast, SV/PP and % of predicted SV/PP did not differ between NT and HTN (all p>0.1). Impaired FMD was 3-4-fold more prevalent than LV hypertrophy or increased arterial load both in NT and in HTN. Within NT and HTN separately, PP/SVi, SV/PP and % of predicted SV/PP were comparable among tertiles of FMD. Only in NT, lower FMD was associated with higher peak exercise systolic BP (p < 0.05). In multivariable regression models, FMD was not associated with indices of arterial load independently (all p > 0.1). In young-to-middle-age subjects with cardiovascular risk factors, impaired FMD is more prevalent than traditional preclinical manifestation of cardiovascular disease, and may exist independent to increased arterial load. Thus, endothelial dysfunction assessment may refine cardiovascular risk profile and risk-reduction strategies based on detection of traditional target organ damage.
    International journal of cardiology 10/2011; 152(2):225-30. · 7.08 Impact Factor
  • Article: Genotype-independent in vivo oxidative stress following a methionine loading test: maximal platelet activation in subjects with early-onset thrombosis.
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    ABSTRACT: Methionine ingestion (100mg/kg) identifies subjects in whom fasting total homocysteine (tHcy) may be normal but the post-methionine load (PML) tHcy is abnormally high. In 96 subjects [54 M/42 F, 40.4 ± 12.3 yrs old; 28 with the 68 bp844 ins of the cystathionine-β-synthase gene (CBSins+); 20 homozygotes for the C677T mutation of the methylene-tetrahydrofolate reductase gene (MTHFR++); 13 with the combination of the two, and 35 without any of them], we have evaluated in vivo oxidative stress and platelet activation, as reflected by urinary excretions of 8-iso-PGF(2α) and of 11-dehydro-TXB(2) respectively, before and after a methionine load test (PML). A history of early-onset thrombosis (18 arterial, 32 venous, 2 both) was present in 52/96 of them. Baseline; tHcy was highest in MTHFR++ carriers (p < 0,05); 8-iso-PGF(2α) and 11-dehydro-TXB(2) levels were independent of sex, MTHFR++ and/or CBSins + (p > 0.05). PML; The ~3-fold increase (p < 0.01 vs baseline) in tHcy reached a plateau within 6-8 hrs. Mean PML tHcy was maximal in MTHFR++ carriers (p = 0.000). 8-iso-PGF(2α) and 11-dehydro-TXB(2) increase reached a maximum within 4 hrs. 11-dehydro-TXB(2) increase was highest (p = 0.023 vs baseline) in subjects with a history of thrombosis. Baseline 11-dehydro-TXB(2) and a history of thrombosis independently predicted PML 11-dehydro-TXB(2) (β = 0.287, p = 0.000 and β = 0.308, p = 0.026, respectively).The PML increase in 8-iso-PGF(2α) or in 11-dehydro-TXB(2) were comparable in the different genotypes (p > 0.05). Regardless genotypes associated with moderate hyperhomocysteinemia, following a methionine loading test, in vivo oxidative stress and platelet activation occur, being the latter maximal in subjects with a history of early-onset thrombosis.
    Thrombosis Research 06/2011; 128(4):e43-8. · 2.44 Impact Factor
  • Article: Arterial wave reflection and subclinical left ventricular systolic dysfunction.
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    ABSTRACT: Increased arterial wave reflection is a predictor of cardiovascular events and has been hypothesized to be a cofactor in the pathophysiology of heart failure. Whether increased wave reflection is inversely associated with left-ventricular (LV) systolic function in individuals without heart failure is not clear. Arterial wave reflection and LV systolic function were assessed in 301 participants from the Cardiovascular Abnormalities and Brain Lesions (CABL) study using two-dimensional echocardiography and applanation tonometry of the radial artery to derive central arterial waveform by a validated transfer function. Aortic augmentation index (AIx) and wasted energy index (WEi) were used as indices of wave reflection. LV systolic function was measured by LV ejection fraction (LVEF) and tissue Doppler imaging (TDI). Mitral annulus peak systolic velocity (Sm), peak longitudinal strain and strain rate were measured. Participants with history of coronary artery disease, atrial fibrillation, LVEF less than 50% or wall motion abnormalities were excluded. Mean age of the study population was 68.3 ± 10.2 years (64.1% women, 65% hypertensive). LV systolic function by TDI was lower with increasing wave reflection, whereas LVEF was not. In multivariate analysis, TDI parameters of LV longitudinal systolic function were significantly and inversely correlated to AIx and WEi (P values from 0.05 to 0.002). In a community cohort without heart failure and with normal LVEF, an increased arterial wave reflection was associated with subclinical reduction in LV systolic function assessed by novel TDI techniques. Further studies are needed to investigate the prognostic implications of this relationship.
    Journal of hypertension 03/2011; 29(3):574-82. · 4.02 Impact Factor
  • Article: Test-re-test reproducibility of Doppler echocardiography for assessment of electromechanical dyssynchrony: implications for heart failure clinic.
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    ABSTRACT: Reproducibility of Doppler echocardiography for assessment of inter-ventricular and intra-left ventricular (LV) dyssynchrony, and its clinical implications, have not been established. Twenty-eight subjects (heart failure stages A-C, 61% with QRS ≥ 120 ms, ejection fraction (EF) ≤ 35%) underwent two consecutive echo-studies within 24h to evaluate test-re-test reproducibility of inter-ventricular electromechanical delay (VV delay, by traditional pulsed-Doppler), and intra-LV electromechanical delay between opposite LV walls by color-coded Doppler tissue-velocity (COLOR-DTI), and by pulsed-Doppler tissue spectrum (PW-DTI). Reproducibility of LV internal diastolic diameter (LVIDD) and of EF (by Simpson's method) assessments was evaluated contextually for reference. Intra-study and inter-study reproducibility of inter-ventricular and intra-LV electromechanical dyssynchrony was in general good, and comparable to the reproducibility of LVIDD and EF assessments. Between-study reproducibility of PW-TDI method was fair, but showed poor agreement with COLOR-TDI method. In repeated studies, agreement of significant electromechanical delay by COLOR-TDI was comparable to the agreement of EF ≤ 35%. In the 5 patients who had simultaneously large QRS, EF ≤ 35%, and significant inter- and intra-ventricular dyssynchrony at study #1, 3 had EF 36-40% and 1 showed no significant dyssynchrony by study #2. In serial echocardiographic studies, Doppler echocardiography showed a good test-re-test reproducibility for the identification of significant electromechanical delay. Planimetry for EF assessment was a source of variability as relevant as Doppler echocardiography, but COLOR-DTI may add meaningful and reproducible information to QRS duration for cardiac-resynchronization therapy.
    Journal of Cardiology 11/2010; 56(3):271-9. · 1.28 Impact Factor
  • Article: Prognostic significance of left ventricular diastolic dysfunction in patients with left ventricular hypertrophy and systemic hypertension (the LIFE Study).
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    ABSTRACT: Patients with hypertension and left ventricular (LV) hypertrophy commonly have impaired diastolic filling. However, it remains unknown whether changes in LV diastolic filling variables are associated with cardiovascular morbidity and mortality. In this study, 778 patients with hypertension with electrocardiographic LV hypertrophy who underwent echocardiography at baseline and annually thereafter during randomized losartan- or atenolol-based antihypertensive treatment were followed for a mean of 4.6 years. The composite cardiovascular end point was the first occurrence of fatal or nonfatal myocardial infarction, fatal or nonfatal stroke, and cardiovascular mortality. Antihypertensive therapy resulted in an increase in the prevalence of normal transmitral flow pattern from 28% to 46% of patients. Although antihypertensive treatment often resulted in a marked increase in the prevalence of normal mitral valve flow pattern, this was not associated with reduced cardiovascular morbidity and mortality when adjusting for blood pressure, left atrial diameter, LV mass index, and treatment in time-varying Cox analyses. In contrast, lower in-treatment E/A ratios and shorter mitral valve deceleration times were associated with less risk for heart failure. Similarly, normal in-treatment transmitral flow pattern was strongly associated with less risk for heart failure (hazard ratio 0.22, 95% confidence interval 0.05 to 0.98, p = 0.048), even when taking in-treatment left atrial diameter and blood pressure into account. In conclusion, antihypertensive treatment in patients with hypertension with electrocardiographic LV hypertrophy resulted in significant improvement in transmitral flow patterns; this was not associated with reduced cardiovascular morbidity and mortality. However, normal in-treatment LV filling was strongly associated with a reduced risk for hospitalization for heart failure.
    The American journal of cardiology 10/2010; 106(7):999-1005. · 3.58 Impact Factor
  • Article: Protein C and protein S changes in GH-deficient adults on r-HGH replacement therapy: correlations with PAI-1 and t-PA plasma levels.
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    ABSTRACT: In the rat liver, growth hormone (GH) affects the synthesis of vitamin-K-dependent factors, including Protein C (prot.C) and protein S (prot.S), two natural anticoagulants that prevent hypercoagulable states. Adults with GH deficiency (GHD) are at risk of thrombotic events. High circulating levels of PAI-1 and t-PA, that reflect hypercoagulable states, may contribute to such risk. In GHD adults on replacement therapy with recombinant human GH (r-HGH), %Δ PAI-1 and %Δ t-PA are related to %Δ insulin changes. To evaluate changes in vitamin-K-dependent factors in GHD on r-HGH replacement. In 60 GHD adults, to relate plasma levels of vitamin-K-dependent factors with those of PAI-1, t-PA and insulin before and after 6-month (6-mo) replacement therapy with r-HGH. After 6-mo r-HGH replacement, %Δ insulin enhancements occurred in 36/60 subjects. PAI-1, t-PA, Prot.C, Prot.S and FVIIact did not change in them. In the 24/40 subjects that experienced %Δ insulin reductions, Prot.C (p=0.025), Prot.S (p=0.031) and FVIIact (p=0.049) decreased significantly. PAI-1 (p=0.019) and t-PA antigen (p=0.009) behaved similarly. In a multivariate analysis, %∆ PAI-1 (β=0.436, p<0.01) was the strongest predictor of %∆ prot.S, wheras %∆ t-PA (β=0.385, p<0.008) and %∆ insulin (β=0.429, p<0.004) were the strongest predictors of %∆ prot.C. In all cases, regardless of %Δ insulin changes, FII, FVII Ag and FIX levels did not change from baseline. In GHD adults on r-HGH replacement, changes in vitamin-K-dependent factors reflect a subtle adaptation of the natural anticoagulant system to PAI-1 and t-PA changes, via the response of insulin to r-HGH.
    Thrombosis Research 10/2010; 126(6):e434-8. · 2.44 Impact Factor
  • Article: In-treatment midwall and endocardial fractional shortening predict cardiovascular outcome in hypertensive patients with preserved baseline systolic ventricular function: the Losartan Intervention For Endpoint reduction study.
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    ABSTRACT: Endocardial fractional shortening (EFS) and midwall shortening (MWS) are impaired in patients with left ventricular hypertrophy. However, it remains unknown whether improvement of left ventricular systolic function during treatment reduces cardiovascular morbidity and mortality in hypertensive patients with preserved left ventricular function. Echocardiograms were performed yearly in 840 hypertensive patients with electrocardiographic left ventricular hypertrophy and baseline left ventricular ejection fraction more and equal to 50%. Baseline and annual in-treatment levels of EFS, MWS and blood pressure (BP) were related to occurrence of a composite endpoint (cardiovascular death, myocardial infarction or stroke) and the component endpoints during 3914 patient-years of follow-up. Adjusting for in-treatment BP, left ventricular mass, relative wall thickness and randomized treatments, higher in-treatment EFS was associated with lower risk of myocardial infarction (by 35% per standard deviation [4.5%], P = 0.004) and heart failure (49%, P < 0.001), but in-treatment stress-corrected EFS predicted only incident heart failure (41%, P = 0.014) but not other endpoints. Higher in-treatment MWS tended to be associated with lower risk of composite endpoints (16% per standard deviation [1.8%], P = 0.07) and was significantly associated with myocardial infarction (33%, P = 0.004) and heart failure (43%, P < 0.001). Higher in-treatment stress-corrected MWS was associated with lower rates of myocardial infarction (35%, P = 0.021) and heart failure (50%, P = 0.001). These results support a prognostic role for left ventricular myocardial function, as estimated by stress-corrected MWS, during aggressive BP lowering in hypertensive patients with preserved ejection fraction at baseline evaluation.
    Journal of hypertension 07/2010; 28(7):1541-6. · 4.02 Impact Factor
  • Article: In-treatment reduced left atrial diameter during antihypertensive treatment is associated with reduced new-onset atrial fibrillation in hypertensive patients with left ventricular hypertrophy: The LIFE Study.
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    ABSTRACT: It is unclear whether improvement of left atrial (LA) and ventricular (LV) structure results in reduction in new-onset atrial fibrillation (AF). The aim of the present study was to examine whether changes in-treatment LA diameter were related to changes in risk of new-onset AF. We followed 939 hypertensive patients with electrocardiographic LV hypertrophy randomized to atenolol or losartan-based regimens in the LIFE Study for a mean of 4.8 years with echocardiograms at enrolment and annually during treatment. New-onset AF occurred in 46 patients (10.2/1000 patient-years of follow-up). At baseline, patients with new-onset AF were older, had higher systolic blood pressure and heart rate as well as higher prevalence of LA dilatation, but had similar prevalences of LV hypertrophy and mitral or aortic valve disease. In univariate Cox analysis baseline LA diameter (HR=4.67 per cm increase [95% CI 2.86-7.65], p<0.001) and LV mass index (HR=1.11 per 10 g/m(2) increase [95% CI 1.02-1.22], p<0.05) both predicted new-onset AF. In multivariate analysis, increased baseline LA diameter increased the risk of new-onset AF (HR=5.16 per cm [95% CI 2.85-9.35], p<0.001) whereas reduction of in-treatment LA diameter reduced the risk (HR=0.21 per cm lower LA diameter during treatment [95% CI 0.14-0.32], p<0.001) with adjustment for in-treatment LV mass in-treatment systolic blood pressure, age and Framingham risk score. LA diameter at baseline and during antihypertensive treatment were equally strong predictors of new-onset AF independent of the level of arterial pressure, LV mass and other covariates. Prevention of AF during antihypertensive treatment may be improved by antihypertensive therapy that reduces LA size in addition to controlling blood pressure.
    Blood pressure 06/2010; 19(3):169-75. · 1.26 Impact Factor
  • Article: Treatment of isolated left ventricular diastolic dysfunction in hypertension: reaching blood pressure target matters.
    Vittorio Palmieri, Cesare Russo, Jonathan N Bella
    Hypertension 12/2009; 55(2):224-5. · 6.21 Impact Factor
  • Article: Novel wall motion score-based method for estimating global left ventricular ejection fraction: validation by real-time 3D echocardiography and global longitudinal strain.
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    ABSTRACT: To evaluate the reliability of a regional wall motion score index (WMSI)-based method for assessment of left ventricular (LV) ejection fraction (EF). Two-dimensional (2D) echocardiography was used to assess a LV 16-segment-based regional wall motion. Each segment received a score based on contractility status: 4, normal kinesis; 3, mild; 2.5, moderate; and 1.5, severe hypo-kinesis; 0, akinesis; -1, dyskinesis; 3.5 and 4.5 were used for low-normal and high-normal kinesis; 5 for hyper-kinesis. Hence, WMSI-based EF was derived by summing the score assigned to each segment. Contextually, EF was evaluated by real-time three-dimensional (3D) echocardiography and by traditional Simpson's method (2D). Global longitudinal strain (GLS) by speckle-tracking method was derived as a volume-independent indicator of LV chamber contractility sensitive to regional wall motion abnormalities. In 40 subjects with 3D-EF ranging from 14 to 80%, including clinically healthy hypertensive and patients with Stage B-D congestive heart failure with global or segmental wall motion abnormalities, on average, WMSI-EF did not differ from EF measured by 3D or 2D (all P > 0.5). By intraclass correlation coefficients, reliability of WMSI-EF vs. 3D method was as good as the reliability of 2D method vs. 3D method. GLS correlated with WMSI-EF as strongly as with 3D-EF (both r(2) = 0.90). Moderate-severe mitral regurgitation was associated with increased difference between WMSI-EF and 3D-EF, independent to potential confounders. Intra-observer and inter-observer reproducibility of WMSI-EF was comparable to the reproducibility of EF estimated by 3D echocardiography. Feasibility (WMSI, 3D, 2D, and GLS all available) was 78%; however, feasibility of WMSI per se was approximately 92% in clinical series. Trained readers may rapidly estimate EF by a novel WMSI system, which was found to be accurate compared with 3D method and GLS.
    European Heart Journal – Cardiovascular Imaging 11/2009; 11(2):125-30. · 2.32 Impact Factor
  • Article: Preclinical cardiovascular abnormalities in patients in early stages of renal disease without nephrotic syndrome.
    Hypertension Research 10/2009; 32(12):1155-6. · 2.58 Impact Factor
  • Article: Lack of change in insulin levels as a biological marker of PAI-1 lowering in GH-deficient adults on r-HGH replacement therapy.
    Thrombosis Research 09/2009; 124(6):711-3. · 2.44 Impact Factor
  • Article: Changes in insulin levels following 6-month treatment with recombinant human growth hormone in growth hormone-deficient adults.
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    ABSTRACT: Eighty-six adult patients with GH deficiency (GHD) of adult or childhood onset were treated for 6 months, with recombinant human growth hormone (rhGH) at a low (LD) or conventional dose (CD). The treatment effect on insulin levels was investigated. This manuscript refers to the Italian addendum to an International Study (B9R-EW-GDED) in which patients with GHD were randomized to receive r-hGH replacement therapy at a dose of either 3 microg/kg/day or 6 microg/kg/day for the 3 months. The dose was then doubled for the next 3 months. After 6 months of r-hGH treatment, insulin levels increased with both GH dosages, with a greater increase achieved in the low-dose subgroup. Insulin levels also increased significantly in the childhood-onset, while even decreased in the adult-onset subgroup. On the whole, in more than 50% of patients, insulin values rose by >13%. Moreover, mean levels of IGF-I increased 2-3 fold (p<0.001 vs baseline) in both the LD and CD groups. Significant and similar increases in IGF binding protein-3 levels were seen in both the LD and CD groups over the treatment period, regardless the time of onset of GHD. Insulin increased with both GH dosages and more than half of patients presented an important increase in insulin plasma levels. It would be of interest to assess if there is a correlation between the changes in insulin levels and other cardiovascular risk factors such as hemostatic parameters.
    Journal of endocrinological investigation 07/2009; 32(11):908-12. · 1.57 Impact Factor
  • Article: Changes in components of left ventricular mechanics under selective beta-1 blockade: insight from traditional and new technologies in echocardiography.
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    ABSTRACT: Myocardial inotropism is considered to be reduced under beta-1 adrenoreceptor blockage (beta1-block). However, relationships between components of left ventricular (LV) systolic mechanics under beta1-block accounting for physiological correlates are only partially explored. Hypertensive outpatient without previous cardiovascular events and with normal LV ejection fraction (EF) at rest underwent echocardiographic evaluations of LV size and systolic function by standard, tissue-Doppler, and speckle-tracking methods before and after 2 weeks of treatment with bisoprolol to obtain change in LV systolic mechanics at a stable heart rate reduction (-20 +/- 10% from baseline) without significant change in LV mass. In the study sample (n = 26, 62% women, mean age 52 +/- 10 years), under bisoprolol, afterload [i.e. circumferential (CESS) and meridional (MESS) end-systolic stress], LV mass, left atrial volume, and EF did not change significantly; LV chamber contractility [i.e. CESS/LV end-systolic volume index (CESS/ESVi) as well as MESS/ESVi] and relative wall thickness (RWT) decreased; stroke volume increased (all P < 0.05). Circumferential LV contractility (i.e. stress-corrected midwall shortening) increased, whereas regional longitudinal strain and strain rate, and global longitudinal strain decreased (all P < 0.05). Peak velocities of the systolic displacement of the lateral and medial mitral anulus did not change under bisoprolol. Parameters of longitudinal LV systolic function did not correlate with preload, afterload, RWT, or with stoke volume. In hypertensive subjects with preserved LV EF, parameters of longitudinal LV systolic mechanics may not reflect the LV myocardial contractility status in steady-state conditions under short-term treatment with beta1-block.
    European Heart Journal – Cardiovascular Imaging 05/2009; 10(6):745-52. · 2.32 Impact Factor
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    Article: Genetic and other factors determining mannose-binding lectin levels in American Indians: the Strong Heart Study.
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    ABSTRACT: Mannose-binding lectin (MBL) forms an integral part of the innate immune system. Persistent, subclinical infections and chronic inflammatory states are hypothesized to contribute to the pathogenesis of atherosclerosis. MBL gene (MBL2) variants with between 12 to 25% allele frequency in Caucasian and other populations, result in markedly reduced expression of functional protein. Prospective epidemiologic studies, including a nested, case-control study from the present population, have demonstrated the ability of MBL2 genotypes to predict complications of atherosclerosis,. The genetic control of MBL2 expression is complex and genetic background effects in specific populations are largely unknown. The Strong Heart Study is a longitudinal, cohort study of cardiovascular disease among American Indians. A subset of individuals genotyped for the above mentioned case-control study were selected for analysis of circulating MBL levels by double sandwich ELISA method. Mean MBL levels were compared between genotypic groups and multivariate regression was used to determine other independent factors influencing MBL2 expression. Our results confirm the effects of variant structural (B, C, and D) and promoter (H and Y) alleles that have been seen in other populations. In addition, MBL levels were found to be positively associated with male gender and hemoglobin A1c levels, but inversely related to triglyceride levels. Correlation was not found between MBL and other markers of inflammation. New data is presented concerning the effects of known genetic variants on MBL levels in an American Indian population, as well as the relationship of MBL2 expression to clinical and environmental factors, including inflammatory markers.
    BMC Medical Genetics 02/2009; 10:5. · 2.33 Impact Factor

Institutions

  • 2012
    • ASL Lecco
      Lecco, Lombardy, Italy
  • 2000–2011
    • Università degli Studi di Napoli Federico II
      • Department of Clinical and Experimental Medicine
      Napoli, Campania, Italy
  • 2005–2010
    • Glostrup Hospital
      • Department of Clinical Physiology and Nuclear Medicine
      Glostrup, Capital Region, Denmark
  • 2009
    • Albert Einstein College of Medicine
      New York City, NY, USA
  • 2002–2009
    • Cornell University
      • Department of Medicine
      New York City, NY, USA
    • Haukeland University Hospital
      • Department of Heart Disease
      Bergen, Hordaland Fylke, Norway
  • 2006
    • Bronx-Lebanon Hospital
      Bronxville, NY, USA
  • 1999–2005
    • Weill Cornell Medical College
      • • Division of Cardiology
      • • Division of Hospital Medicine
      New York City, NY, USA
  • 2003
    • Gracie Square Hospital, New York, NY
      New York City, NY, USA
  • 2002–2003
    • New York Presbyterian Hospital
      • • Department of Cardiology
      • • Department of Pain Medicine
      New York City, NY, USA