Luigi Aronne

Visceral adiposity and arterial stiffness: echocardiographic epicardial fat thickness reflects, better than waist circumference, carotid arterial stiffness in a large population of hypertensives

AIMS Relationship between obesity and cardiovascular (CV) disease depends not only on the amount of body fat, but also on its distribution. For example, individuals with increased fat accumulation in the abdominal region have atherogenic lipid profiles and are at increased CV risk. The loss of elasticity in medium and large arteries is an early manifestation of atherosclerosis. The aim of this study was to evaluate whether echocardiographic epicardial adipose tissue, an index of cardiac adiposity, is related to carotid stiffness and carotid intima-media thickness (IMT), indexes of subclinical atherosclerosis, better than waist circumference in hypertensive patients. METHODS AND RESULTS We studied 459 patients with Grade I and II essential hypertension who were referred to our outpatient clinic over a period from May 2007 to March 2008. The population was first sorted by waist circumference and then by epicardial fat < or = 7 or >7 mm. We measured epicardial fat thickness, waist circumference, carotid artery stiffness, and carotid IMT in all patients. Patients divided according to waist circumference showed no statistical differences in carotid artery stiffness between the two groups. Subjects with epicardial fat >7 mm were older, had higher systolic, diastolic, and pulse pressure, increased left ventricular mass index, carotid IMT, diastolic parameters, and stiffness parameters compared with those with epicardial fat < or = 7 mm (P < 0.001). A positive correlation was found between epicardial fat and age, pulse pressure, stiffness parameters, carotid IMT, systolic blood pressure, and duration of hypertension, and a negative correlation was found with diastolic parameters. Age, carotid IMT, and stiffness parameters were independently related to epicardial fat. CONCLUSION Our findings indicate that epicardial fat reflects carotid artery stiffness in hypertension-induced organ damage.

Worsening of rosacea in patients treated with dihydropyridine calcium channel blockers: a clinical observation.

Worsening of rosacea in patients treated with dihydropyridine calcium channel blockers: a clinical observation

Ambulatory arterial stiffness index: a marker of subclinical organ damage in treated and untreated dipper hypertensive patients.

Ambulatory arterial stiffness index: a marker of subclinical organ damage in treated and untreated dipper hypertensive patients

When chewing gum is more than just a bad habit.

In November, 2008 a 13-year-old boy (weight 45 kg, height 160 cm) was taken by his parents to the emergency department. His parents reported that after school the boy had been agitated and aggressive, in contrast with his normal mood. He denied feeling stressed or having used drugs or stimulants. He complained of abdominal discomfort, increased diuresis, dysuria, and prickling sensations in his legs. On examination, he was restless, with sinus tachycardia (147 beats per min [bpm] on electrocardiogram [ECG]), tachypnoea (25 breaths per min), and raised blood pressure (145/90 mm Hg). Chest radiography and laboratory blood test results were normal. Toxicological screen was negative for cocaine, heroin, and amphetamine. Psychiatric consultation was unremarkable. Our patient’s condition improved overnight without any treatment and he was discharged the following morning. At discharge he was noted to have sinus bradycardia (40 bpm).Later that day, his mother returned to the emergency unit with two empty packets of stimulant (“energy”) chewing gum that she had found in her son’s bag; he had admitted consuming the confectionery at school. The chewing gum contained 160 mg caff eine per packet (0·57% caff eine per gum pellet) and non-specifi ed amounts of guarana,

Which is the correct management of patients with asymptomatic severe calcific aortic stenosis after symptomatic spontaneous calcium cerebral embolism

Elective surgery cannot be recommended in every patient with asymptomatic severe aortic stenosis, and predictors identifying high-risk patients need to be identified. In guidelines we read that elective surgery, at the asymptomatic stage, can only be recommended in selected patients, at low operative risk (see guidelines of European Society of Cardiology and American Heart Association), but we have not read any reference to patients with severe calcific aortic stenosis after symptomatic spontaneous calcium cerebral embolism. Because cardioembolic stroke is associated with poor prognosis compared to other stroke subtypes, in patients with asymptomatic severe aortic stenosis and spontaneous calcific embolic stroke valve replacement appears to offer the best hope of avoiding a recidivation of stroke and should be considered in most cases. On the contrary, is it still correct to consider as asymptomatic patients with severe aortic stenosis and cerebral thromboembolism from a calcified aortic valve?

A new character on the scene of cardiorenal syndrome

Arterial stiffness has a strong influence onthe kidney because of the distinctive structureof the renal microcirculation. Certain tissues,such as the brain, heart, skin and skeletalmuscle tissues, contain precapillary arteriolesand metarterioles that disperse the majorityof the mean and pulsatile energy content ofthe advancing pressure and flow waveformbefore it reaches the capillary. In contrast,glomerular capillaries are located betweenafferent and efferent arterioles. Because effer-ent arteriolar resistance is physiologicallygreater than afferent resistance, the meanand pulsatile pressures in the glomerulusare relatively elevated. This high hydrostaticpressure ensures the maintenance of anelevated glomerular filtration fraction, whichis normally B20% of renal plasma flow,but exposes the glomerular capillary topotentially harmful pulsatile pressures ifarterial stiffness and pulse pressure are high.Moreover, the myogenic tone of the afferentarteriole is influenced by pressure pulsatility.

CAROTID ARTERIAL STIFFNESS AND LEFT VENTRICULAR DIASTOLIC FUNCTION IN DIABETICS AND HYPERTENSIVE PATIENTS WITH CORNARY MICROCIRCULATION DISEASE: PP.2.67

In diabetic and hypertensive patients increased arterial stiffness and diastolic dysfunction are early expression of organ damage and are related with a higher cardiovascular risk. Subjects with increased arterial stiffness PWV is high, and the backward waves from the periphery return earlier to the ascending aorta. Since this backward waves coming from the periphery arrive during the LV ejection, they raise the central systolic blood pressure and the LV afterload and decrease the central diastolic pressure and the coronary perfusion pressure. These changes may cause ischaemia particularly in the subendocardium, which if chronic is associated with left ventricular interstitial fibrosis. We assessed the arterial stiffness by a non-invasive new tool known as “e-tracking, Aloka, Japan” and the diastolic function with Doppler tissue imaging in patients with coronary microcirculation disease proved by typical anginous synthomatology, negative coronary angiography, positive myocardial scintigraphy stress test. Methods: We have observed 40 consecutive patients with angina, proved by typical clinical history, positive myocardial scintigraphy stress test and negative coronary angiography. We compared the data of arterial stiffness with the measurements of 50 healthy volunteers. We performed e-tracking on the left carotid with ALOKA a 10 ultrasound system. Arterial compliance (AC), pulse wave velocity (PWV), elastic pressure (Ep) stiffness parameter (ß) and augmentation index (AI) were measured. Results: Pwv(m/s)7 +/− 2,AC(mm2/Kpa)1 +/− 0.4,Ep(Kpa)102 +/− 31, ß 7.53 +/− 2, AI (%) (17 +/− 8), normalized for age, were increased when compared with healthy subjects. Stiffness parameters correlate significantly with Tissue Doppler imaging diastolic parameters pwv (r = 0.56,p < 0.05),Ep(r = 0.55,p < 0.05)andAi (r = 0.75,p < 0.01). Conclusion: These results suggest that increased arterial stiffness could be involved in the pathogenesis o fthe left ventricle microcirculation disease. The positive correlation between Em and arterial stiffness parameters show that diastolic disfunction may be also linked to health status of artery.

ASSOCIATION BETWEEN CAROTID ARTERY STIFFNESS ESTIMATED WITH E-TRACKING AND DIASTOLIC DYSFUNCTION ASSESSED WITH TDI IN 105 PATIENTS WITH MASKED HYPERTENSION: PP.31.237

A normal blood pressure in the clinic or office but an elevated blood pressure out of the clinic is defined as masked hypertension. It may occurs in as many 10% of the general population. Increased arterial stiffness directly increase end-diastolic left ventricular pressure and compromise myocardial relaxation properties. Thanks to our study we can evaluate the role of carotid artery stiffness parameters on diastolic function in patients with masked hypertension. Methods: Observing 105 consecutive patients with masked hypertension (proved by 24 H- ambulatory blood pressure monitoring), we have noticed that diastolic early (E’) and late (A’) velocities were recorded by pulse wave tissue. Doppler imaging of the lateral mitral anulus in the apical 4- chamber view and carotid artery stiffness parameters were valued by e-tracking on the left carotid with ALOKA a 10 ultrasound system. Pulse wawe velocity (PWV), elastic pressure (Ep) and stiffness parameter (ß) were measured. Results: Pwv (m/s) 8+/-2, Ep (Kpa) 134+/-23, ß 12+/-2, normalized for age, were increased when compared with healthy subjects. Stiffness parameters correlate significantly with Tissue Doppler imaging diastolic parameters in particularly with E’ pwv (r = 0.68, p < 0.05), Ep (r = 0.60, p < 0.05) and ß (r = 0.68, p < 0.01). Conclusion: patients with masked hypertension increased arterial stiffness and abnormal left ventricular diastolic function (particularly with E’), was associated with arterial stiffness, expression of a greater contribution of atrial contraction to left ventricular filling for increased left ventricular end-diastolic pressure due to an high afterload.