3.1 Genetics of Cardiovascular Risk in the Elderly: the ROVIGO study (Risk of Vascular Complication: Impact of Genetics in Old People)

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Endocrine arterial hypertension: therapeutic approach in clinical practice

This review describes the therapeutic approach of endocrine arterial hypertension in clinical practice. In mineralocorticoid-related hypertension, adrenalectomy is the treatment of choice for aldosterone-producing adenomas and monolateral primary aldosteronism, whereas pharmacologic blood pressure (BP) control is indicated for the other forms of primary aldosteronism such as bilateral adrenal hyperplasia. Spironolactone is the drug of choice, but intolerable side effects limit its use; amiloride or eplerenone are a valid alternative. If BP remains uncontrolled, angiotensin converting enzyme inhibitors (ACE-I), angiotensin II receptor antagonists (AII-RA) and calcium channel blockers (CCB) may be added. Hypertension accompanying Cushing's syndrome can be approached with surgery, but antihypertensive treatment both pre- and postoperative is required as well. Eplerenone, AII-RA and ACE-I are indicated, while peroxisome proliferator activated receptor upsilon agonists may help for the insulin resistance syndrome. Drugs that suppress steroidogenesis should be used with care because of their serious side effects. Subjects with catecholamine-dependent hypertension due to a neuroendocrine neoplasm need to undergo preoperative alpha-adrenergic blockade with phenoxybenzamine or doxazozine. When adequate alpha-adrenergic blockade is achieved, beta-adrenergic blockade with low dose propranolol may be added. If target BP is not achieved, CCB and/or metyrosine are indicated. Laparoscopic adrenalectomy is the procedure of choice for solitary intra-adrenal neoplasms <8 cm. Acute hypertensive crises that may occur before or during surgery should be treated intravenously with sodium nitroprusside, phentolamine, nicardipine or labetalol. For malignant neoplasms, chemo- and radiopharmaceutical therapy may be considered

EFFETTI EMODINAMICI ED ELETTROFISIOLOGICI DELL\u2019IPNOSI CON E SENZA RILASSAMENTO. STUDIO SPERIMENTALE IN 12 VOLONTARI

Effetti elettrofisiologici /EEG e LORETA) ed emdinamici di due diversi metodi di induzione inotica, con e senza rilassamento

EFFETTI EMODINAMICI ED ELETTROFISIOLOGICI DELL\u2019IPNOSI CON E SENZA RILASSAMENTO. STUDIO SPERIMENTALE IN 12 VOLONTARI

Effetti elettrofisiologici (mediante EEG e LORETA) ed emodinamici di due diverse modalit\ue0 di induzione ipnotica, con e senza rilassamento

Hypnosis prevents the cardiovascular response to cold pressor test.

To highlight the effects of hypnotic focused analgesia (HFA), 20 healthy participants underwent a cold pressor test (CPT) in waking basal conditions (WBC) by keeping the right hand in icy water until tolerable (pain tolerance); subjective pain was quantified by visual scale immediately before extracting the hand from water. The test was then repeated while the participants were under hypnosis and underwent HFA suggestions. Cardiovascular parameters were continuously monitored. Pain tolerance was 121.5+/-96.1 sec in WBC and 411.0+/-186.7 sec during HFA (p < 0.0001), and visual rating score 7.75+/-2.29 and 2.45+/-2.98 (p < 0.0001), respectively. CPT-induced increase of total peripheral resistance was non significant during HFA and +21% (p < 0.01) in WBC. HFA therefore reduced both perception and the reflex cardiovascular consequences of pain as well. This indicates that hypnotic analgesia implies a decrease of sensitivity and/or a block of transmission of painful stimuli, with depression of the nervous reflex arc