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MIDAS = Multicenter isradipine diuretic atherosclerotic study; VHAS = verapamil in hypertension and atherosclerosis study; ELSA = European lacidipine study on atherosclerosis; INSIGHT IMT = international nifedipine GITS study: intervention as a goal in hypertension treatment. * Statistically significant difference vs. control drug.

MIDAS = Multicenter isradipine diuretic atherosclerotic study; VHAS = verapamil in hypertension and atherosclerosis study; ELSA = European lacidipine study on atherosclerosis; INSIGHT IMT = international nifedipine GITS study: intervention as a goal in hypertension treatment. * Statistically significant difference vs. control drug.

Effect of Drug Treatment

Therapeutic double-blind trials have assessed the long-term effect mainly of antihypertensive (table 2), and of lipid-lowering drugs on carotid IMT progression.

In hypertensive patients the results indicate a greater effect of calcium antagonists over diuretics and ^-blockers on IMT progression [12,21-23]. In the ELSA [22] a greater effect of lacidipine in plaque progression and regression was shown; the study did not have statistical power to detect differences in clinical events between the two treatment groups. In a small study the effect of a calcium antagonist and of an ACE inhibitor was similar [24].

The effect of angiotensin II antagonists needs to be evaluated in larger studies; available data from small studies indicate that this class of drugs is more effective than P-blockers and similar to ACE inhibitors. As ultrasound methodology is continuously improving, the measurement of plaque volume by three-dimensional reconstruction will be possible, in addition to IMT, for a more precise evaluation of atherosclerotic changes; IMT and plaque volume changes are the endpoint of an ongoing European study comparing an angiotensin II antagonist to a P-blocker [25].

Plaque tissue composition and its changes may be indirectly evaluated by radiofrequency signal or videodensitometric analyses, differentiating the relative amount of lipid-rich macrophages or fibrous tissue. A recent analysis of the plaque composition in the ELSA study has pointed out that in about 70% of patients included in the study plaques are fibrolipidic. After 4 years of treatment with either lacidipine or atenolol, no significant changes in plaque composition were observed, suggesting that treatment with a calcium antagonist may slow IMT progression, without influencing the characteristics of plaque tissue [26].

ACE inhibitors reduce the progression of IMT as compared with placebo or diuretic, in hypertensive hypercholesterolemic patients [27].

In high-risk patients, treatment with an ACE inhibitor, or with a calcium antagonist or a ^-blocker, is more effective than administration of placebo (over a conventional treatment) in delaying the progression of IMT [28-30].

A recent meta-regression analysis, including 22 randomized controlled trials, has evaluated the effects of an antihypertensive drug versus placebo or another antihypertensive agent of a different class on carotid IMT. The results have shown that, compared with no treatment, diuretics/^-blockers or ACE inhibitors, CCBs attenuate the rate of progression of carotid intima-media thickening. In the prevention of carotid intima-media thickening, calcium antagonists are more effective than ACE inhibitors, which in turn are more effective than placebo or no treatment, but not more active than diuretics/^-blockers. Among all studies, 9 trials inadequately powered for hard outcomes, reported morbidity and mortality results and the odds ratio for all fatal and non-fatal cardiovascular events in trials comparing active treatment with placebo reached statistical significance (p = 0.007). Therefore, it remains to be demonstrated whether IMT changes may have implications for the long-term prevention of cardiovascular complications such as stroke [31].

In patients with hypercholesterolemia, long-term treatment with a statin may reduce the progression of carotid IMT and favor plaque regression. The changes induced on IMT by statin treatment have about twice the effect observed with antihypertensive drugs. A recent analysis of nine studies, aimed to assess the efficacy of statin treatment on common carotid wall thickness, has demonstrated that carotid IMT reduction was strongly related with LDL decrease. It has been calculated that a 10% reduction in LDL cholesterol concentration is associated with a 0.73% per year decrease in IMT. In the LIPID study and in smaller studies, the occurrence of stroke was significantly lower in the group of patients treated with the active drug in respect to the control group. No correlation between changes in IMT and incidence of stroke is reported [32].

In a recent, randomized, controlled study, the effects of pioglitazone (45 mg/day) and glimepiride (2.7 8 1.6 mg/day) were compared on carotid

IMT in a large group of 173 patients with type 2 diabetes; despite similar gly-cemic control, an improvement in insulin resistance and a decrease in carotid IMT were observed only in patients treated with pioglitazone [33].

In perimenopausal women [34] the use of hormone replacement therapy was associated with a delayed progression of IMT in the common carotid artery.

Arterial Stiffness


Basically, three main methods are used in clinical practice to assess non-invasive measures of arterial stiffness [35].

Aortic stiffness may be obtained by measurement of pulse wave velocity (PWV) along the thoracic and abdominal aorta. Wave forms of the right common carotid artery and the right femoral artery can be detected by applanation tonometry or pressure-sensitive transducers, and the time delay between the feet of the two waveforms is measured. The distance traveled by the pulse wave is measured over the body surface, and the PWV is calculated as the ratio of distance over time (m/s).

In addition, carotid stiffness can be measured directly from the ratio of local pulse pressure (measured by applanation tonometry) to relative stroke change in diameter (measured by ultrasound scan).

Aortic stiffness can be estimated from the augmentation index, i.e. the additional increase in pressure caused by the pressure wave reflected back from the periphery.

Other parameters and indices of arterial mechanics can also be calculated: (1) the cross-sectional compliance, i.e. the relationship between decline in pressure and decline in volume in the arterial tree during the diastolic pressure decay, which takes into account the volume of the artery, and mainly the age-induced enlargement; (2) the cross-sectional distensibility, i.e. the relative change in vessel diameter (or area) for a given change in pressure, which is related to the mechanical behaviour of the artery as a whole; (3) the Peterson elastic modulus, which is the pressure change required for 100% (theoretical) stretch from resting diameter, and is inversely related to cross-sectional dis-tensibility; (4) the Young's incremental elastic modulus (Einc), which corresponds to the elastic modulus per unit area, requires measurement of wall thickness and may give insights on the mechanical behaviour of the wall material, and (5) the P stiffness index, which corresponds to the ratio of natural logarithm of systolic/diastolic blood pressure to the relative change in diameter, and is supposed to be independent of distending pressure.

Relative risk 1.0

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