Pier Sergio Saba

Assessment of left ventricular function by the midwall fractional shortening/end-systolic stress relation in human hypertension☆

OBJECTIVES This study examined left ventricular performance in relatively unselected hypertensive patients by use of physiologically appropriate midwall shortening/end-systolic stress relations. BACKGROUND Supranormal left ventricular function has been reported in hypertensive patients, possibly due to an artifact of mismatching endocardial rather than midwall fractional shortening to mean left ventricular end-systolic stress. METHODS Samples of 474 hypertensive patients (150 women, 324 men) and 140 normal subjects (68 women, 72 men) were drawn from a large urban employed population. The inverse relations (p < 0.0001) of both echocardiographic endocardial and midwall fractional shortening to end-systolic stress in normal subjects were used to calculate the ratios of observed to predicted endocardial and midwall fractional shortening in hypertensive patients. Midwall shortening was calculated from an elliptic model, taking into account the epicardial migration of the midwall during systole. RESULTS Use of midwall fractional shortening in hypertensive patients reduced the proportion of patients with function above the 95th percentile of normal from 22% to 4% (p < 0.0001) and fractional shortening as a percent of predicted from 107% (p < 0.001 vs. 100% in normotensive control subjects) to 95% (p < 0.0001; p < 0.001 vs. 101% in normotensive control subjects). Midwall shortening was below the 5th percentile of normal in 16% of hypertensive patients instead of 2% with endocardial shortening (p < 0.0001): They tended to be older than other hypertensive patients and had concentric left ventricular hypertrophy. Among hypertensive patients, those with concentric left ventricular hypertrophy or remodeling had reduced midwall shortening as a percent of predicted from end-systolic stress (p < 0.0001). CONCLUSIONS Use of the physiologically more appropriate midwall shortening/end-systolic stress relation 1) markedly reduces the proportion of hypertensive subjects identified as having high endocardial left ventricular function; and 2) identifies a substantial subgroup of patients with reduced left ventricular function who have concentric geometry of the left ventricle, a pattern associated with high cardiovascular risk.

Relation of arterial pressure waveform to left ventricular and carotid anatomy in normotensive subjects.

OBJECTIVES The purpose of this study was to examine the relation of the central arterial pressure waveform to left ventricular and carotid structure. BACKGROUND The pressure waveform in the central arteries is affected by reflection of the pressure wave from the periphery. When reflected waves merge with the incident wave during systole, a late systolic peak and increment in systolic blood pressure are observed. The consequent increase in hemodynamic load may stimulate left ventricular and vascular adaptive changes. METHODS Sixty-seven normotensive adults were studied by noninvasive techniques. Anatomy and function of the left ventricle and carotid artery were investigated by ultrasonography. Pressure waveforms were recorded by an external tonometer applied to the carotid artery, and waveform shape was expressed by the augmentation index, calculated from the difference between the maximal systolic pressure and that at the inflection between early and late systolic pressure peaks divided by the pulse pressure. Subjects were assigned to groups with a dominant early (group 1, augmentation index < or = 0) or dominant late systolic peak (group 2, augmentation index > 0). RESULTS Left ventricular mass index was significantly higher in group 2 than in group 1, a difference that persisted after controlling for the confounding effects of gender, age and blood pressure. Carotid wall thickness and regional arterial stiffness were significantly increased in group 2, but differences disappeared in the analysis of covariance for age. CONCLUSIONS Left ventricular and carotid artery structure are related to the shape of the central pressure waveform. Although the increase in left ventricular mass seen in subjects with a dominant late systolic peak pressure appears to be directly related to the shape of the pressure waveform, changes in the structural and physical properties of the carotid artery appear to be more closely related to the aging process.

Impact of Arterial Stiffening on Left Ventricular Structure

Aging of the vasculature results in arterial stiffening and an increase in systolic and pulse pressures. Although pressure load is a stimulus for left ventricular hypertrophy, the extent to which vascular stiffening per se, independent of blood pressure, influences left ventricular structure is uncertain. Two hundred seventy-six subjects (79 normotensive and 197 otherwise healthy hypertensive individuals) underwent echocardiography to assess left ventricular structure. Arterial stiffness was estimated by the pressure-independent stiffness index, &bgr;, and the pressure-dependent elastic modulus derived from simultaneous carotid ultrasound and applanation tonometry. Systemic arterial compliance (the inverse of stiffness) was estimated by the arterial compliance index. In multivariate analysis, &bgr; was related to age (P <0.001) and smoking history (P <0.01) but not mean pressure, whereas elastic modulus was related to age and mean pressure (both P <0.001). The arterial compliance index was only related to age. Whereas systolic and diastolic pressures and the elastic modulus were positively associated with left ventricular mass (all P <0.001), primarily because of increases in wall thicknesses, &bgr; and the arterial compliance index bore no relation to left ventricular mass. &bgr; was inversely related to chamber diameter and directly related to left ventricular relative wall thickness, the ratio of wall thickness to chamber radius. Younger and older hypertensive subjects had comparable left ventricular mass, despite higher systolic and pulse pressures in the older group, whereas older hypertensives had higher mean relative wall thickness, associated with a significant increase in arterial stiffness (&bgr;, 7.06 versus 5.17; elastic modulus, 595 versus 437 dyne/cm2 ×10−6) and reduction in the arterial compliance index (0.87 versus 1.05 mL/mm Hg per square meter) (all P <0.001). Thus, the extent to which arterial stiffness relates to left ventricular hypertrophy is dependent on the method by which arterial stiffness is estimated. Pressure-dependent methods show an association with left ventricular hypertrophy, whereas the pressure-independent stiffness index, &bgr;, and the arterial compliance index are most strongly associated with aging and left ventricular concentric remodeling but not hypertrophy.

Relation of age to left ventricular function in clinically normal adults

The extent to which age, independent of cardiovascular diseases, influences left ventricular (LV) function in adults is uncertain. Echocardiograms and simultaneous arterial pressure in 464 clinically normal adults aged 16 to 88 years were used to measure LV dimensions, endocardial and midwall LV fractional shortening, stroke volume, cardiac output, and circumferential end-systolic stress. The ratios of observed endocardial and midwall shortening to values predicted for observed end-systolic stress were used as measures of chamber and myocardial function. LV endocardial shortening increased slightly with age, as did an index of LV chamber performance, the end-systolic stress/volume index ratio (r = 0.11, p = 0.019, and r = 0.20, p <0.001). However, when age-related increases in LV wall thickness and blood pressure were controlled for by examining afterload-corrected endocardial shortening, no age relation was detected. Weak age-related declines were observed in midwall shortening (r = -0.09, p = 0.043) and afterload-corrected midwall shortening (r = -0.12, p <0.01). Cardiac index decreased slightly with advancing age (r = -0.14, mean -6.7 ml/min/m2/ year, p = 0.003). Total peripheral resistance and the pulse pressure/stroke volume ratio, a measure of arterial stiffness, increased more strongly with age (r = 0.27 and 0.38, both p <0.001). Thus, LV pump performance at rest measured by cardiac index is slightly lower in older than in younger clinically normal adults. Endocardial fractional shortening was slightly higher in older subjects, but the physiologically more appropriate midwall measures of myocardial function decreased slightly. The observed change in LV pump performance was related to smaller LV chamber size and higher total peripheral resistance in older subjects.

Impact of arterial elastance as a measure of vascular load on left ventricular geometry in hypertension.

OBJECTIVE Effective arterial elastance (Ea), integrating the pulsatile component of left ventricular (LV) afterload, is an estimate of aortic input impedance. We evaluated relationships of Ea with left ventricular anatomy and function in essential hypertension. DESIGN A cross-sectional analysis in 81 normotensive and 174 untreated hypertensive individuals enrolled in a referral hypertension centre. METHODS Using echocardiography we determined left ventricular mass index (LVMI), relative wall thickness (RWT), stroke volume (SV), endocardial (FSe) and midwall (FSm) fractional shortening and total peripheral resistance (TPR). Carotid pressure waveforms were obtained by arterial tonometry, and end-systolic pressure (Pes) was measured at the dicrotic notch. Ea index (EaI) was calculated as Pes/(SV index); LV elastance (Ees) was estimated as Pes/LV end-systolic volume, and ventriculo-arterial coupling was evaluated by the Ea/Ees ratio. RESULTS EaI was higher in hypertensives than in normotensives (3.02 +/- 0.63 versus 2.40 +/- 0.52 mmHg/l per m2; P< 0.0001). Using the 95% upper confidence limit in normotensives, hypertensives were divided in two groups with normal or elevated EaI. The 38 hypertensives with elevated EaI had higher RWT (0.41 +/- 0.06 versus 0.37 +/- 0.05), lower LVMI (87.5 +/- 18.5 versus 96.8 +/- 19.3 g/m2), higher TPR (2247 +/- 408 versus 1658 +/- 371 dynes/cm s(-5)) and lower FSe and FSm (35 +/- 5 versus 39 +/- 5 and 16 +/- 2 versus 18 +/- 2%; all P< 0.05) than patients with normal EaI. Ea/Ees ratio was increased and cardiac output was reduced in hypertensives with elevated EaI. CONCLUSIONS High values of EaI identify a minority of hypertensive patients characterized by elevated TPR, left ventricular concentric remodelling, depressed left ventricular systolic function and impaired ventriculo-arterial coupling.

Endothelial Function in Pre-diabetes, Diabetes and Diabetic Cardiomyopathy: A Review

Diabetes mellitus worsens cardiovascular risk profile of affected individuals. Its worldwide increasing prevalence and its negative influences on vascular walls morphology and function are able to induce the expression of several morbidities which worsen the clinical conditions of the patients getting them running towards a reduced survival curve. Although overt diabetes increases the mortality rate of individuals due to its pathogenesis, poor information are in literature about the role of pre-diabetes and family history of diabetes mellitus in the outcome of general population. This emphasizes the importance of early detection of vascular impairment in subjects at risk of developing diabetes. The identification of early stages of atherosclerotic diseases in diabetic persons is a fundamental step in the risk stratification protocols followed-up by physicians in order to have a complete overview about the clinical status of such individuals. Common carotid intima-media thickness, flow-mediated vasodilatation, pulse wave velocity are instrumental tools able to detect the early impairment in cardiovascular system and stratify cardiovascular risk of individuals. The aim of this review is to get a general perspective on the complex relationship between cardiovascular diseases onset, pre-diabetes and family history of diabetes. Furthermore, it points out the influence of diabetes on heart function till the expression of the so-called diabetic cardiomyopathy.

Carotid Intimal-Medial Thickness and Stiffness Are Not Affected by Hypercholesterolemia in Uncomplicated Essential Hypertension

The combined effects of hypertension and hypercholesterolemia on carotid anatomy and stiffness were studied in 62 normotensives, 141 uncomplicated essential hypertensives with a total cholesterol level <240 mg/dL, and 60 essential hypertensives with a total cholesterol level >/=240 mg/dL. Carotid ultrasonography was performed to evaluate intimal-medial thickness (IMT), relative wall thickness, and the presence of plaque. Carotid pressure waveforms were recorded by applanation tonometry to measure carotid stiffness (beta) and pressure wave reflection (ie, augmentation index). After adjusting for age, body mass index, and smoking habit by analysis of covariance, no significant differences were found between normocholesterolemic hypertensives and hypercholesterolemic hypertensives in terms of IMT (0.79+/-0.19 versus 0.81+/-0.19 mm), relative wall thickness (0.27+/-0.07 versus 0.28+/-0.07), carotid stiffness (6.1+/-3.2 versus 5.6+/-2.7), augmentation index (18. 7+/-12.9% versus 17.3+/-12.8%), and prevalence of plaque (30.8% versus 30.7%). In the whole population, carotid IMT was significantly related to age (r=0.43), systolic (r=0.35) and diastolic (r=0.35) blood pressures, body surface area (r=0.22), and cholesterol levels (r=0.22) (all P<0.05). Carotid stiffness was significantly related to age, blood pressure, body mass index, and body surface area but not to cholesterol levels. In multivariate analyses, age, body surface area, and systolic blood pressure, but not cholesterol, smoking habit, or sex, were independent correlates of IMT (multiple R=0.54, P<0.0001), whereas carotid stiffness was independently associated with age, body surface area, and sex (R=0. 38, P<0.0001). In conclusion, hypertension is a potent stimulus of vascular hypertrophy. The superimposition of hypercholesterolemia does not substantially augment these changes or further increase arterial stiffness in uncomplicated hypertensive subjects.

Cardiovascular health in migrants: current status and issues for prevention. A collaborative multidisciplinary task force report.

Objectives To review information on cardiovascular health and migration, to stress the attention of researchers that much needs to be done in the collection of sound data in Italy and to allow policy makers identifying this issue as an important public health concern. Background In Italy, the rate of immigrants in the total number of residents increased from 2.5% in 1990 to 7.4% in 2010, and currently exceeds 10% in regions such as Lombardia, Emilia Romagna and Toscana. Methods A consensus statement was developed by approaching relevant Italian national scientific societies involved in cardiovascular prevention. Task force members were identified by the president and/or the boards of each relevant scientific society or working group, as appropriate. To obtain a widespread consensus, drafts were merged and distributed to the scientific societies for local evaluation and revision by as many experts as possible. The ensuing final draft was finally approved by scientific societies. Results In several western European countries, the prevalence of hypertension, diabetes, chronic kidney disease, obesity and metabolic syndrome was found to be higher among immigrants than in the native population. Although migrants are often initially healthier than non-migrant populations in their host countries, genetic factors, and changing environments with lifestyle changes, social exclusion and insufficient medical control may expose them to health challenges. Cultural reasons may also hamper both the dissemination of prevention strategies and migrant communication with healthcare providers. However, great diversity exists across and within different groups of migrants, making generalizations very difficult and many countries do not collect registry or survey data for migrants health. Conclusions In the present economic context, the European Union is placing great attention to improve data collection for migrant health and to support the implementation of specific prevention policies aimed at limiting the future burden of cardiovascular and renal disease, and the consequent load for health systems. Wider initiatives on the topic are awaited in Italy.

An Update on hypertensive emergencies and urgencies

Severe acute arterial hypertension is usually defined as ‘hypertensive crisis’, although ‘hypertensive emergencies’ or ‘hypertensive urgencies’, as suggested by the Joint National Committee and the European Society of Hypertension, have completely different diagnostic and therapeutic approaches. The prevalence and demographics of hypertensive emergencies and urgencies have changed over the last four decades, but hypertensive emergencies and urgencies are still associated with significant morbidity and mortality. Different scientific societies have repeatedly produced up-to-date guidelines; however, the treatment of hypertensive emergencies and urgencies is still inappropriate, with potential clinical implications. This review focuses on hypertensive emergencies and urgencies management and treatment, as suggested by recent data.

Left ventricular diastolic function in hypertension: methodological considerations and clinical implications.

The assessment of left ventricular (LV) diastolic function should be an integral part of a routine examination of hypertensive patient; indeed when LV diastolic function is impaired, it is possible to have heart failure even with preserved LV ejection fraction. Left ventricular diastolic dysfunction (LVDD) occurs frequently and is associated to heart disease. Doppler echocardiography is the best tool for early LVDD diagnosis. Hypertension affects LV relaxation and when left ventricular hypertrophy (LVH) occurs, it decreases compliance too, so it is important to calculate Doppler echocardiography parameters, for diastolic function evaluation, in all hypertensive patients. The purpose of our review was to discuss about the strong relationship between LVDD and hypertension, and their relationship with LV systolic function. Furthermore, we aimed to assess the relationship between the arterial stiffness and LV structure and function in hypertensive patients.