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Cardiovascular (CV) risk factors, primarily arterial hypertension, modify the structural and functional features of the myocardium and the blood vessels, a process known as CV remodeling. Cardiac remodeling refers to changes in left ventricular (LV) geometry, such as concentric LV geometry and LV hypertrophy (LVH), an independent hallmark of CV risk. Vascular remodeling consists of structural changes of the arterial walls, such as increased intima-media thickness, arterial stiffening, and deteriorating endothelial function. CV remodeling is to a large extent a result of compensatory mechanisms, and its pathophysiology is partially mediated by the activation of the renin-angiotensin-aldosterone system and its primary effector peptide angiotensin II, which together play a key role in the progression of CV disease. Angiotensin-converting enzyme (ACE) inhibitors, a class of drugs used in the treatment of arterial hypertension, appear to be effective in controlling or even reversing CV remodeling, independently of simple blood pressure reduction. Evidence shows that ACE inhibitors counteract CV remodeling by reducing LV mass and regressing LVH, attenuating vascular atherosclerosis and improving vascular compliance. ACE inhibitors possessing a sulfhydryl moiety appear to have additional benefits in increasing nitric-oxide release and improving vascular endothelial function.

Objective: The aim of this study was to evaluate the incremental diagnostic role of tissue Doppler in primary cardiac amyloidosis (CA)., Methods: Eleven patients with CA at diagnosis and 11 healthy controls, matched for sex and age, underwent standard Doppler echocardiography and pulsed tissue Doppler of the left ventricular (LV) lateral annulus, in the apical four-chamber view. The ratio of early transmitral flow velocity to early diastolic mitral annular velocity (E/E(m) ratio) was derived as an index of LV filling pressure., Results: The two groups were comparable for body mass index, blood pressure, heart rate and standard Doppler diastolic measurements. Patients with CA had a significantly higher sum of wall thickness (SWT) and LV mass, a lower E(m) peak velocity (P < 0.002) and a higher E/E(m) ratio (P < 0.001) than controls. By dividing CA patients according to the transmitral E/A ratio, patients with an E/A ratio < 1 (abnormal relaxation) (n = 5) and patients with an E/A ratio > 1 (likely pseudonormal/restrictive pattern) (n = 6) did not show any difference in the E/E(m) ratio (14.5 + or - 7.1 vs. 15.1 + or - 6.4, P = NS). In the overall population, the E/E(m) ratio was related to SWT (r = 0.84, P < 0.0001) and LV mass index (r = 0.72, P < 0.0001). After adjusting for age and heart rate by separate multivariate models, SWT (beta = 0.78, P < 0.0001; cumulative r(2) = 0.63, SE = 3.38, P < 0.0001) and LV mass index (beta = 0.71, P < 0.0001; cumulative r(2) = 0.53, SE = 3.80, P < 0.002) were both independently associated with the E/E(m) ratio., Conclusions: Pulsed tissue Doppler is able to detect early myocardial diastolic impairment in CA. The E/E(m) ratio is very useful in diagnosing increased LV filling pressure, regardless of the transmitral pattern, and may, therefore, be helpful in the clinical management of these patients.

Purpose: Our goal was (a) to test the ability of functional MRI (fMRI) to localize the hand primary motor cortex in patients with brain neoplasms using a conventional scanner and (b) to compare within the same subject the location and morphology of the activated motor areas in the affected hemisphere with the contralateral ones., Method: Seventeen right-handed patients with frontoparietal intra- and extraaxial tumors were studied. Hand motor performance ranged from normal to slight impairment of finger dexterity. The fMRI study was based on a series of FLASH images. Two or three contiguous slices parallel to the bicommissural plane were acquired through the level of frontoparietal cortex. Each patient was requested to perform with each hand a finger-tapping task or a simpler repetitive flexion-extension of the last four fingers. Pseudo-color activation maps were then calculated by a Z-score method and superimposed on high resolution images., Results: Five patients were excluded because of gross motion artifacts. In all other patients, areas of significant signal increase were detected on the precentral gyrus. They had a spot-like appearance, and no substantial side-to-side differences in shape or extension could be observed. In the presence of severe compression of the gyri, a displacement of the activated areas in the affected hemisphere with respect to the contralateral ones was noticeable., Conclusion: fMRI localization of the primary motor area using a conventional scanner can be obtained also in patients with brain tumors, although with a lower success rate than in normal volunteer studies, mainly because of subject compliance problems. Areas of significantly increased signal are detectable even in cortex where normal anatomical patterns are lost.

Background and Purpose: Low-density lipoprotein apheresis is currently used for the treatment of familial hypercholesterolemia, an inherited disorder of metabolism associated with premature development of cardiovascular disease. We wanted to evaluate cerebral blood flow velocity, cardiac output, and systemic vascular resistance in patients with familial hypercholesterolemia before and after low-density lipoprotein apheresis., Methods: Ten patients (age range, 14 to 46 years; 4 males, 6 females) with familial hypercholesterolemia (8 homozygotes, 2 heterozygotes) and 10 healthy control subjects of comparable age and sex distribution participated in the study. Low-density lipoprotein apheresis by dextran sulfate was performed in 8 patients (7 homozygotes, 1 heterozygote). Six patients (4 homozygotes, 2 heterozygotes) underwent a procedure of extracorporeal erythrocyte filtration with the same extracorporeal volume as for low-density lipoprotein apheresis, but with the exclusion of the passage of plasma through the dextran sulfate column. Cerebral blood flow velocity (transcranial Doppler), cardiac output, and systemic vascular resistance (electric bioimpedance cardiography) were determined by noninvasive techniques before and 1 day and 7 days after low-density lipoprotein apheresis or extracorporeal erythrocyte filtration. Plasma and blood viscosities were measured at the same time., Results: Before apheresis, mean and diastolic cerebral flow velocities were abnormally low in hypercholesterolemic patients (P < .01 and P < .02 vs healthy control subjects, respectively). After apheresis, low-density lipoprotein cholesterol was lowered by 40% to 60% from baseline, and cerebral blood flow velocities (mean, systolic, and diastolic velocities) were increased (P < .01). Cardiac output, systemic vascular resistance, and viscosity values were not significantly modified. Extracorporeal erythrocyte filtration (without passage of plasma through the dextran sulfate column) did not modify serum lipids, hemodynamic parameters, or viscosity values., Conclusions: Low-density lipoprotein apheresis produces potentially useful hemodynamic effects. They are not adequately explained by changes in blood viscosity alone and might reflect a restoration of endothelium-mediated vasodilation, which is inhibited by high concentrations of low-density lipoprotein.

Our aim was to assess echocardiographic parameters and the effort blood pressure of 50 children of hypertensives with respect to 50 children of normotensives. Systolic and diastolic blood pressures at rest were comparable between the two groups. Left ventricular mass index (LVMI), interventricular septum and posterior wall thicknesses were higher in children of hypertensives (P less than 0.01). Systolic blood pressure was higher in children of hypertensives at maximal effort until 5 min of recovery (P less than 0.01). Similarly, diastolic blood pressure was higher at 1 and 2 min of recovery (P less than 0.01). Direct correlations of mean diastolic wall thickness (r = 0.39, P less than 0.01) and LVMI (r = 0.33, P less than 0.05) with percentage effort systolic blood pressure increases were found in children of hypertensives but not in children of normotensives. In conclusion, we confirmed early cardiac alterations and a tendency for effort hypertension in children of hypertensives. The relationship between these data could be explained either by effort systolic overload or by a common response to an increased adrenergic stimulus.

In order to clarify the role of age and hypertension in determining arrhythmias, we evaluated the average heart rate, and the number of supraventricular and ventricular premature beats and their severity (Lown grade) by 24-h Holter electrocardiography of 336 patients. We excluded 54 patients with prolonged runs of atrial fibrillation or supraventricular tachycardia because these arrhythmias reduce the possibility of determining the number of premature beats. Analysis of variance, carried out after dividing the patients into four different groups according to age and blood pressure (excluding patients aged 60-65 years with diastolic blood pressure of 91-94 mmHg) showed that the hypertensives had a higher average heart rate (P less than 0.01) and more supraventricular (P less than 0.05) and premature ventricular (P less than 0.01) beats than the normotensives; no difference was found among groups of different ages. The severity of premature ventricular beats was higher in hypertensives than in normotensives, and also higher in elderly than in 'young' patients (P less than 0.01). In the evaluation of all 336 patients we found correlations between age and severity of premature ventricular beats in both normotensives (P less than 0.05) and hypertensives (P less than 0.001). Multilinear regression showed that mean blood pressure was independently related to the average heart rate, and supraventricular and premature ventricular beats and their severity, while age was correlated independently only with the severity of premature ventricular beats (P less than 0.001). We conclude that hypertension induces arrhythmias, and that age increases their severity.

We studied 10 obese volunteers, mean age 36.5 +/- 10.3 years, who weighed 123.56 +/- 28.7 g and were 69.96 +/- 22.5 kg overweight. The subjects did not have diabetes, arterial hypertension or signs of cardiac and respiratory failure or disease and all underwent right- and left-heart catheterization. cardiac output and stroke volume were high, according to increased oxygen consumption and to the degree of obesity. Ventricular end-diastolic and atrial pressures ranged from normal to high and correlated with body weight, signs of volume overloading and reduced left ventricular (LV) compliance. The mean pulmonary artery pressure was elevated and correlated well with weight, pulmonary resistance being normal; mean aortic pressure did not correlate with weight, and systemic arterial resistance tended to have a negative correlation. The LV function curve showed impaired ventricular function, particularly for the heaviest subjects, in whom Vmax and the ratio of the stroke work index to LV end-diastolic pressure were reduced. These indexes correlated well with each other and both correlated negatively with the degree of obesity. In contrast, maximal dP/dt was normal and did not correlate with excess weight. These observations show that depressed LV function is already present in relatively young obese people, even if they are free from signs of cardiopathy and other associate diseases. The degree of impairment of heart function seems to parallel the degree of obesity.