Time-course of diastolic dysfunction in different stages of chronic HCV related liver diseases.

AIM: A hyperdynamic circulatory pattern in advanced liver disease is known since a long time. The first studies evaluating cardiac function in cirrhosis were performed in patients with alcoholic liver disease and thus this condition was attributed to the toxic effects of ethanol. A reduced performance of the left ventricle after physical and pharmacological strains along with an altered diastolic function has been demonstrated also in postviral cirrhosis. Many factors are involved in advanced cirrhosis whereas little is known in the earlier stages of disease. METHODS: To this aim we have investigated patients with different stages of hepatitis C virus (HCV)-related liver disease to detect the time-course of diastolic dysfunction. An impaired relaxation and increased thickness of left ventricular walls along with an altered pattern of transmitral flow can be easily detected by means of echocardiography. RESULTS: In chronic hepatitis diastolic function is preserved but increased thickness of left ventricle parietal walls can be detected in patients with fibrosis on liver biopsy. The typical pattern of diastolic dysfunction is observed in Child A cirrhotic patients and in Child C ascitic patients but thickness of parietal walls is more relevant in the former group. Chronic aldosterone blockade could exert favourable effects in heart remodeling suggesting a potential role of these drugs in cirrhotic cardiomyopathy. CONCLUSIONS: The presence of increased thickness of left ventricle parietal walls in chronic hepatitis C in the precirrhotic stage point to a putative role of HCV in this heart structural abnormality that can become a co-factor in the more advanced stages of cirrhosis when portal hypertension and its deleterious effects on systemic hemodynamics, cardiac function and structure become manifest.

Radial artery flow-mediated dilatation in heart failure patients: effects of pharmacological and nonpharmacological treatment.

Congestive heart failure (CHF) is associated with an impaired flow-mediated vasodilation that reflects an impaired endothelial function. Limited information is available, however, on whether and to what extent this impairment is improved by pharmacological or nonpharmacological treatment. We measured radial artery diameter and blood flow by an echo-tracking Doppler device both at baseline and after 4 minutes of hand ischemia, which increases diameter through NO secretion mediated by an increase in flow and shear stress. Data were collected from 44 CHF patients (New York Heart Association class I to III) under standard treatment (diuretic, digitalis, and enalapril, 20 mg/d), in whom CHF severity was assessed by a cardiopulmonary stress test, and from 16 age- and sex-matched controls. CHF patients were then randomized to maintain for (A) 2 months of standard treatment (n=11), (B) treatment with double the ACE inhibitor dose (n=11), (C) standard treatment with an angiotensin II antagonist (losartan, 50 mg/d; n=11), or (D) standard treatment with bicycle training for 30 minutes, 3 times a week (n=11). At baseline, radial artery diameter and flow were similar in CHF patients and controls; CHF patients had a modest although significant impairment in flow increase (-36%) and a striking impairment (-78%) in diameter increase following the 4 minutes of ischemia. After 2 months, baseline diameter and flow remained unaltered in the 4 groups. After the 4 minutes of ischemia, radial artery flow and diameter increased as before in the group under standard treatment (A), whereas in the other 3 groups, the increase was significantly (P<0.05) and, for diameter, markedly (B, 83%; C, 92%; and D, 95%) greater. The vasodilatation induced by trinitroglycerin was similar in CHF and control subjects and not affected by treatments. In CHF, radial artery shows a marked reduction in flow-mediated vasodilation, reflecting impairment of endothelial function. This impairment can be markedly improved by treatments that effectively block the renin-angiotensin system either at ACE or at ACE plus angiotensin receptor level. This is the case also with nonpharmacological treatment of CHF.

Progression of functional and structural cardiac alterations in young normotensive uncomplicated patients with type 1 diabetes mellitus.

OBJECTIVE: We have recently observed that in young, normotensive patients with a type I diabetes mellitus and no macro or microvascular complications, large artery structure and function are already altered. This study has been done to assess whether this condition is also characterized by early alterations in cardiac structure and function, and whether these alterations progress with time. DESIGN AND METHODS: In 56 insulin-treated, normotensive uncomplicated type I diabetic patients (age 35.0 +/- 2 years, means +/- SE) in good metabolic control, left ventricular wall thickness and diameter were measured by echocardiography together with left ventricular ejection fraction and diastolic function E/A (ratio between early and late ventricular filling), before and after 23 +/- 1 months. The same measurements were made in 20 age and sex-matched subjects who served as controls (C). RESULTS: Compared to C, diabetic patients had a significant increase in left ventricular wall (septal plus posterior wall) thickness (+ 8.4%), left ventricular mass index (+ 11%) and h/r ratio (left ventricular wall thickness/ventricular end diastolic diameter, + 16.0%) whereas they showed a reduction of E/A (-6%). In C, all echocardiographic values were unchanged after 2 years. This was the case also for diabetic patients, except for left ventricular ejection fraction and diastolic diameter which showed a significant reduction (-7.2%) and increase (+ 3.8%), respectively, with a reduction of ratio between LV wall thickness and diameter, h/r (-6.8%). CONCLUSIONS: Uncomplicated type I diabetes mellitus is characterized by early structural and functional cardiac alterations. Some of these alterations show a measurable progression within a relatively short time span.

Effects of physical training of the dominant arm on ipsilateral radial artery distensibility and structure.

BACKGROUND: Exercise training induces cardiovascular changes that are both generalized and restricted to the microcirculation of the tissues more actively involved in the exercise itself. Whether the local effect of exercise extends to larger arteries is unknown, however. METHODS: In the right and left upper limb of 17 right-handed subjects performing an asymmetric training of the upper limbs (hammer throwers and baseball players) and 16 age-matched sedentary controls, we continuously measured radial artery diameter, distensibility and wall thickness by an echotracking and a beat-to-beat finger blood pressure device. Arterial distensibility was calculated by the arctangent model of Langewouters and expressed as continuous values from diastolic to systolic blood pressure. Measurements were made: (1) in baseline conditions; (2) after release from prolonged proximal ischaemia; and (3) after an increase in radial artery blood flow caused by a short (4 min) distal ischaemia to determine the endothelial involvement in the training-induced change in arterial distensibility. RESULTS: In athletes the radial artery distensibility was markedly greater in the right than in the left arm, the latter showing values slightly greater than those seen in the two arms of sedentary subjects. In both arms and groups radial artery distensibility increased markedly after prolonged ischaemia, the between arm and group differences being preserved, however. The radial artery response to distal short ischaemia was, on the other hand, similar in the two arms of the athletes, although greater in these subjects than in the sedentary ones. Radial artery wall thickness was greater in the trained than in the untrained arm of athletes, both values being greater than in sedentary subjects. CONCLUSIONS: Asymmetrical training of the upper limbs is accompanied by a greater distensibility of the middle-sized arteries of the more trained side. This is not associated with asymmetrical changes in endothelial structure or function. It is associated with a greater wall thickness in the trained side, suggesting that, at least in part, a training-induced asymmetrical change in wall structure (possibly with a predominance of more distensible tissues such as elastine and smooth muscle) is responsible.

Pharmacological improvement of large arteries properties.

Arterial distensibility reflects mechanical properties of the arterial wall and have, thus a clearcut clinical relevance. This because an arterial distensibility reduction is associated with an increased pulse pressure, an increased cardiac work and a reduced diastolic vital organ perfusion. In recent years it has been demonstrated that arterial distensibility is reduced in marked and mild hypercholesterolemia, in a manner independent from arterial blood pressure values. Arterial mechanical properties are also impaired in heart failure, this leading to a further cardiac damage. This important vascular properties however, can be improved by appropriate treatment, while the time needed for that can be extremely long.

Effects of cigarette smoking on carotid and radial artery distensibility.

OBJECTIVE: Cigarette smoking acutely induces a marked increase of blood pressure and heart rate. This is accompanied by a marked reduction of radial artery distensibility. Whether this reflects an alteration of arterial mechanics of large elastic arteries as well is not established, however. DESIGN AND METHODS: In this study we addressed the acute effects of smoking on the stiffness of a peripheral medium-sized muscular artery and a large elastic vessel. We studied seven healthy normotensive smokers (age 28+/-7 years, mean+/-SEM), in the absence of smoking for at least 24 h. Radial artery (NIUS 02) and carotid artery diameter (WTS) were concomitantly acquired beat-to-beat in the 5 min before, during and after smoking of a cigarette containing 1.2 mg of nicotine. Blood pressure and heart rate were concomitantly recorded by a Finapres device. Radial and carotid artery distensibility were calculated according to the Langewouters and Reneman formulae, respectively. Data were collected for consecutive 30 s periods. Statistical comparisons were performed between the three different phases and, within each phase, between 30 s periods. In five subjects the protocol was repeated after 1 week using a stran rather than a cigarette to obtain data under sham smoking. RESULTS: Smoking increased systolic blood pressure by 14%, diastolic blood pressure by 10% and heart rate by 27%. Radial artery diameter was reduced during smoking (-3.7%) and more so after smoking (-14.8%), while carotid artery diameter did not change significantly either during or after smoking. Radial artery distensibility was also significantly reduced only after smoking (-41.3%, P < 0.01), while carotid artery distensibility was significantly reduced both during (-33.3%) and after smoking (-27.2%) (P < 0.01 versus before). No changes in blood pressure, heart rate and arterial wall mechanics were induced by sham smoking. CONCLUSIONS: Acute cigarette smoking reduces distensibility not only in medium-sized but also in large elastic arteries, therefore causing a systemic artery stiffening. The mechanisms of these effects remain to be determined. However, it is likely that adrenergic mechanisms are responsible for the arterial distensibility alterations.