Nicola De Luca

The use of a telematic connection for the follow-up of hypertensive patients improves the cardiovascular prognosis

Background Inadequate blood pressure (BP) control could be due to incorrect management of hypertensives caused by the lack of interaction between general practitioners (GP) and hypertension specialists. Objectives To test the effectiveness on BP and total cardiovascular risk (TCVR) control of an internet-based digital network connecting specialists and GPs. Methods We created a network among the Hypertension Clinic, Federico II University (Naples, Italy), 23 hospital-based hypertension clinics and 60 GPs from the area (CampaniaSalute Network, CS). Randomized GPs enrolled in CS could update online records of patients (n = 1979). As a control, we included 2045 patients referred to the specialist clinics by GPs from outside the network. All patients completed a 2-year follow-up. Results CS provided a larger reduction in BP [systolic/diastolic BP (SBP/DBP): 7.3 ± 0.4/5.4 ± 0.3 versus 4.1 ± 0.4/3.1 ± 0.26 mmHg, CS versus control; P < 0.001 for both] and percentage of patients with BP < 140/90 mmHg (CS versus control: baseline, 33 versus 34%, NS; end of follow-up, 51 versus 47%, χ2 = 13.371; P < 0.001). A European Society of Hypertension–European Society of Cardiology (ESH/ESC) TCVR score was calculated [from 1 (average) to 5 (very high TCVR)]. The CS group showed a reduction in the mean TCVR score (CS: from 3.5 ± 0.02 to 3.2 ± 0, P < 0.01, ANOVA; control group: 3.5 ± 0.03 to 3.4 ± 0.03, NS) and, accordingly, fatal and non-fatal major cardiovascular events (MACE) were less frequent (2.9 versus 4.3%; χ2 = 5.047, P < 0.02). CS predicts fewer MACE in multiple binary regression analysis (β:−7.27, P < 0.008) reducing the risk for MACE compared to control [odds ratio (OR): 0.838; 95% confidence interval (CI): 0.73–0.96]. Conclusion Our results support the idea that telemedicine can achieve better control of BP and TCVR.

Atrial fibrillation and microRNAs

Atrial fibrillation (AF) is the most common sustained arrhythmia, especially in the elderly, and has a significant genetic component. Recently, several independent investigators have demonstrated a functional role for small non-coding RNAs (microRNAs) in the pathophysiology of this cardiac arrhythmia. This report represents a systematic and updated appraisal of the main studies that established a mechanistic association between specific microRNAs and AF, focusing both on the regulation of electrical and structural remodeling of cardiac tissue.

Cardiac function in systemic hypertension before and after reversal of left ventricular hypertrophy.

In 3 age- and sex-matched groups of subjects--15 normotensives, 15 hypertensives without left ventricular (LV) hypertrophy and 15 hypertensives with LV hypertrophy--the slopes of the regression line obtained by plotting the individual values of LV fractional shortening against the corresponding values of echocardiographic end-systolic stress were compared. The first 2 groups were studied only in control conditions while the third group was restudied after a 20% reduction in LV mass index induced by a long-term antihypertensive treatment and after a 3-week washout period. A significant relation between fractional shortening and end-systolic stress was found in all instances. The slope of this correlation was higher in normotensives (-0.251) and in hypertensives without LV hypertrophy (-0.232) (both p less than 0.01) than in hypertensives with ventricular hypertrophy (-0.079). In this latter group, the slope increased after the reversal of LV hypertrophy (-0.230, p less than 0.01) and remained unchanged (-0.202) at the end of the washout period. No difference was detectable between the slopes obtained in these patients after reversal of LV hypertrophy, both with the antihypertensive treatment on and off, and those of normotensives and hypertensives without LV hypertrophy. Thus, LV hypertrophy attenuates the influence of changes in afterload on LV function. Reversal of LV hypertrophy restores a fractional shortening end-systolic stress relation quite comparable to that found both in normotensives and in hypertensives before the development of LV hypertrophy.

Does Information on Systolic and Diastolic Function Improve Prediction of a Cardiovascular Event by Left Ventricular Hypertrophy in Arterial Hypertension

Left ventricular (LV) mass (LVM) is the most important information requested in hypertensive patients referred for echocardiography. However, LV function also predicts cardiovascular (CV) risk independent of LVM. There is no evidence that addition of LV function significantly improves model prediction of CV risk compared with LVM alone. Thus, composite fatal and nonfatal CV or cerebrovascular events were evaluated in 5380 hypertensive outpatients (2336 women, 298 diabetics, and 1315 obese subjects) without prevalent CV disease (follow-up: 3.5±2.8 years). We compared 5 risk models using Cox regression and adjusting for age and sex: (1) LV mass normalized for height in meters2.7 (LVMi); (2) LVMi, concentric LV geometry, by relative wall thickness (>0.43), ejection fraction, and transmitral diastolic pattern (by thirtiles of mitral deceleration index); (3) LVMi, LV geometry, midwall shortening, and mitral deceleration index thirtiles; (4) as No. 2 with the addition of left atrial dilatation (>23 mm); and (5) as No. 3 with the addition of left atrial dilatation. Individual hazard functions were compared using receiving operating characteristic curves and z statistics. Areas under the curves increased from 0.60 in the model with the sole LVMi to 0.62 in the others (all P values for differences were not significant). The additional information on systolic and diastolic function decreased the contribution (Wald statistics) of LVMi in the Cox model without improving the model ability to predict CV risk. We conclude that risk models with inclusion of information on LV geometry and systolic and diastolic function, in addition to LVMi, do not improve the prediction of CV events but rather redistribute the impact of individual predictors within the risk variance.

Insufficient control of blood pressure and incident diabetes

OBJECTIVE Incidence of type 2 diabetes might be associated with preexisting hypertension. There is no information on whether incident diabetes is predicted by blood pressure control. We evaluated the hazard of diabetes in relation to blood pressure control in treated hypertensive patients. RESEARCH DESIGN AND METHODS Nondiabetic, otherwise healthy, hypertensive patients (N = 1,754, mean ± SD age 52 ± 11 years, 43% women) participated in a network over 3.4 ± 1 years of follow-up. Blood pressure was considered uncontrolled if systolic was ≥140 mmHg and/or diastolic was ≥90 mmHg at the last outpatient visit. Diabetes was defined according to American Diabetes Association guidelines. RESULTS Uncontrolled blood pressure despite antihypertensive treatment was found in 712 patients (41%). At baseline, patients with uncontrolled blood pressure were slightly younger than patients with controlled blood pressure (51 ± 11 vs. 53 ± 12 years, P < 0.001), with no differences in sex distribution, BMI, duration of hypertension, baseline blood pressure, fasting glucose, serum creatinine and potassium, lipid profile, or prevalence of metabolic syndrome. During follow-up, 109 subjects developed diabetes. Incidence of diabetes was significantly higher in patients with uncontrolled (8%) than in those with controlled blood pressure (4%, odds ratio 2.08, P < 0.0001). In Cox regression analysis controlling for baseline systolic blood pressure and BMI, family history of diabetes, and physical activity, uncontrolled blood pressure doubled the risk of incident diabetes (hazard ratio [HR] 2.10, P < 0.001), independently of significant effects of age (HR 1.02 per year, P = 0.03) and baseline fasting glucose (HR 1.10 per mg/dl, P < 0.001). CONCLUSIONS In a large sample of treated nondiabetic hypertensive subjects, uncontrolled blood pressure is associated with twofold increased risk of incident diabetes independently of age, BMI, baseline blood pressure, or fasting glucose.

Association of suboptimal blood pressure control with body size and metabolic abnormalities

Background Blood pressure control is disappointingly suboptimal in populations. Whether metabolic abnormalities influence blood pressure control is unclear. We evaluated the relationship between metabolic risk factors and blood pressure control in a large population of patients with hypertension. Methods From our Hypertension Centre, 4551 subjects (43.4% women; age 51 ± 12 years) were selected with available data for metabolic and cardiovascular evaluation (no prevalent cardiovascular disease), at the last control visit. A modified Adult Treatment Panel III definition of metabolic syndrome was adopted changing waist girth for body mass index (≥ 30 kg/m2). Blood pressure was considered controlled when supine office blood pressure was below 140/90 mmHg, or uncontrolled if this target was not achieved. Blood pressure control has been evaluated in relation to metabolic risk factors, adjusting for age, sex, and the number of antihypertensive medications. Results The metabolic syndrome phenotype was found in 1444 individuals (31.72%). The probability of uncontrolled blood pressure was 43% higher in patients with the metabolic syndrome than in those without, independently of covariates. This probability was also confirmed in 728 untreated patients. The probability of uncontrolled blood pressure significantly and independently increased with the increasing number of metabolic risk factors. Uncontrolled blood pressure was also independently associated with the prescription of more medications. Conclusion Insufficient control of blood pressure is independently associated with the presence of the metabolic syndrome. Blood pressure control worsens with the increasing number of metabolic risk factors associated with hypertension, despite the use of a greater number of medications.

Improvement of diastolic function after reversal of left ventricular hypertrophy induced by long-term antihypertensive treatment with tertatolol

In 15 previously untreated hypertensive subjects with left ventricular (LV) hypertrophy who responded favorably (supine blood pressure less than or equal to 140/90 mm Hg) to antihypertensive treatment with a nonselective beta-blocking agent, tertatolol, the effects of reversal of LV hypertrophy on systolic and diastolic function were assessed. Patients underwent echocardiographic and radionuclide studies in control conditions (phase 1), after 1 month of blood pressure normalization (phase 2), after reversal of LV hypertrophy or at least a 20% reduction of LV mass compared to basal value (phase 3) and finally, after a 1-month washout (phase 4). In phase 2, blood pressure (130 +/- 2/85 +/- 1 vs 148 +/- 4/104 +/- 1 mm Hg) and heart rate (59 +/- 1 vs 76 +/- 2 beats/min) decreased (both p less than 0.01); LV mass remained unchanged. There were improvements in peak filling rate (end-diastolic volume/s) (2.4 +/- 0.1 vs 2.0 +/- 0.1), ejection fraction (65 +/- 1 vs 61 +/- 1%) and their ratio (stroke counts/s) (3.7 +/- 0.2 vs 3.2 +/- 0.1) (all p less than 0.05). In phase 3, blood pressure and heart rate were unchanged and reversal of LV hypertrophy was accompanied by a further increase in peak filling rate (2.9 +/- 0.1), ejection fraction (69 +/- 1%) and their ratio (4.1 +/- 0.1) compared to phase 2 (all p less than 0.01). Finally, in phase 4 blood pressure and heart rate returned to the basal value, but peak filling rate (2.7 +/- 0.1) and ejection fraction (65 +/- 1%), although reduced compared to phase 3, were still higher than phase 1.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of acebutolol on left ventricular hemodynamics and anatomy in systemic hypertension

In 18 patients with mild or moderate essential hypertension who responded favorably to acebutolol antihypertensive therapy, echocardiography (echo) was performed in the basal condition and after 6 and 12 months of follow-up. Acebutolol induced a significant decrease in blood pressure (BP), from a basal value of 167 +/- 3/105 +/- 2 mm Hg to 138 +/- 5/90 +/- 2 mm Hg after 6 months (p less than 0.01) and to 134 +/- 3/91 +/- 3 mm Hg after 1 year (p less than 0.01), and in heart rate, from 75 +/- 3 to 63 +/- 2 beats/min after 6 months (p less than 0.01) and to 63 +/- 2 beats/min after 1 year (p less than 0.01). The decrease in BP was achieved through a decrease in cardiac output from 6.3 +/- 0.28 to 5.3 +/- 0.25 liters/min after 6 months (p less than 0.05) and to 5.32 +/- 0.2 liters/min after 1 year (p less than 0.05), which resulted from a reduction in heart rate; stroke volume did not show significant change during the treatment and left ventricular (LV) performance was improved. There was a parallel decrease in LV posterior wall and ventricular septal thicknesses and estimated LV mass. In patients with LV hypertrophy, the change in mass was significantly correlated with the change in heart rate both after 6 and 12 months of therapy (r = 0.6234, p less than 0.05 and r = 0.7121, p less than 0.05 after 6 and 12 months, respectively).

Hypertensive target organ damage predicts incident diabetes mellitus

Aims Whether patients with hypertensive preclinical cardiovascular disease (CVD) are at higher risk of incident diabetes has never been studied. Methods and results We assessed incident diabetes in 4176 hypertensive non-diabetic patients (age 58.7 ± 8.9 years, 58% male) with ≥1 year follow-up (median: 3.57 years; inter-quartile range: 2.04–7.25). Left ventricular (LV) hypertrophy (LVH) was defined as LV mass index (LVMi) ≥51 g/m2.7. Carotid atherosclerosis (CA) was defined as intima-media thickness >1.5 mm. During follow-up, diabetes developed in 393 patients (9.4%), more frequently in those with than without initial LVH or CA (odds ratio = 1.97 and 1.67, respectively; both P < 0.0001). In the Cox regression, the presence of either initial LVH or CA was associated with higher hazard of diabetes [hazards ratio (HR) = 1.30 and 1.38, respectively; both P = 0.03], independently of the type and number of anti-hypertensive medications, initial systolic blood pressure (P < 0.001), body mass index, fasting glucose, family history of diabetes (all P < 0.0001), and therapy with β-blockers. The presence of one of the, or both, markers of preclinical CVD increased the chance of incident diabetes by 63 or 64%, respectively (both P < 0.002), independently of significant confounders, a result that was confirmed (HR = 1.70 or 1.93, respectively; both P < 0.0001) using ATPIII metabolic syndrome (HR = 2.73; P < 0.0001) in the Cox model. Conclusion Initial LVH and CA are significant predictors of new onset diabetes in a large population of treated hypertensive patients, independently of initial metabolic profile, anti-hypertensive therapy, and other significant covariates. This sequence may be attributable to risk factors common to preclinical CVD and diabetes, but a vascular origin of diabetes cannot be excluded.

Power spectral analysis of heart period variability in hypertensive patients with left ventricular hypertrophy.

This study aimed to characterize sympathovagal balance by heart period power spectrum analysis in hypertensive patients with echocardiographic evidence of left ventricular hypertrophy. Twenty ambulatory patients (11 men and 9 women), aged 50 +/- 10 years, with established essential hypertension and echocardiographic left ventricular hypertrophy, performed 24-h blood pressure monitoring and electrocardiogram Holter recording on 2 consecutive days. Twenty age- and sex-matched normal subjects comprised the control group. Power spectrum analysis, performed using the fast Fourier transform algorithm, demonstrated lower values of low and high frequency power in hypertensives than in controls, while ultralow and very low frequency power were similar in the two groups. Very low frequency, low frequency, and high frequency power increased during the night in both groups, showing a similar circadian pattern. We found a direct correlation between daytime systolic (r = 0.51; P < .05) and diastolic (r = 0.52; P < .05) blood pressure and left ventricular mass index. Moreover, negative correlations were found between left ventricular mass index and low frequency (r = -0.47; P < .05) and high frequency power (r = -0.47; P < .05). There was a direct correlation between nighttime decrease in systolic blood pressure and nighttime increase in high frequency power (r = 0.45; P < .05). As 24-h low frequency and high frequency power, obtained using the Fourier transform algorithm, both reflect the parasympathetic modulation of heart rate, our results demonstrate that hypertensive patients with left ventricular hypertrophy are characterized by a sympathovagal imbalance with a reduction of vagal tone that is more evident with increasing severity of hypertension.