A personalized approach to selecting antiplatelet therapy for patients with ACS may reduce ischemic and bleeding events. (Pharmacogenetics of Clopidogrel in Patients With Acute Coronary Syndromes [PHARMCLO]; NCT03347435).
SUMMARY Hemodynamic monitoring after a single dose (10 mg) of nifedipine in 27 primary hypertensive subjects (diastolic pressure > 110 mm Hg) documented that this calcium antagonistic agent exerts a potent arteriolar vasodilating action, which results in prompt (-21% of control at 30 minutes) and persistent (-16% of control at 120 minutes) fall in mean arterial pressure associated with a rise in cardiac output and pulse rate.The same patients received oral treatment for 3 weeks. Hourly pressure readings showed that 1) the antihypertensive response to each dose lasts 8-12 hours; and 2) nifedipine every 6 hours significantly reduced blood pressure throughout the 24 hours, without postural hypotension.Side effects were short-lasting (headache in five patients, palpitation without arrhythmias in eight patients, burning sensation in the face and legs in five patients and sporadic extrasystoles in five patients) and tended to disappear with continued treatment.Development of drug resistance, sodium retention, plasma volume expansion, renin release or angina pectoris were not observed during the study. Although these findings seem to differentiate nifedipine from other vasodilators currently used in the treatment of hypertension, broader experience and more prolonged trials with nifedipine as an antihypertensive agent will be needed before conclusions can be drawn on these particular aspects.HIGH VASCULAR RESISTANCE is the proximate cause of elevated arterial pressure in most patients with chronic hypertension. Blood pressure can be normalized either by decreasing cardiac output or by lowering vascular resistance. The former, however, makes circulation doubly abnormal, since vascular resistance remains excessive and cardiac output becomes abnormally low. This situation may be associated-with tissue hypoperfusion, involving kidneys, heart and brain. The desired hemodynamic effect in antihypertensive therapy is dilatation of constricted arterioles by a compound that acts directly on the smooth muscle, relaxes arterioles independently of the vasoconstrictor mechanism, and does not affect the heart or decrease the venous return.Hydralazine, diazoxide, minoxidil and guancydine act directly on vascular smooth muscle to produce vasodilatation, and were introduced with variable degrees of success in the chronic treatment of hypertension. These agents share several common side effects, including an exaggeration of cardiac action that may precipitate angina pectoris in patients with coronary disease and the promotion of renin release, sodium retention and plasma volume expansion. In most circumstances ,B-blockers and diuretics should be added to counteract these effects.' 3
Oral (17 cases) or sublingual (9 cases) administration of nifedipine (10 mg), a new coronary dilator, induced a prompt and large pressure reduction in patients with severe primary hypertension. Pressure started to fall within 20 and 5 min after oral and sublingual administration, respectively, and reached the lowest levels in the next 10 min. Maximal mean arterial pressure reduction averaged 36 mm Hg; 120 min after the drug, mean arterial pressure was diminished by 19.5% of control. The hypotension was mediated through diminished peripheral resistance associated with rise of cardiac output and pulse rate. Nifedipine was also administered sublingually in 3 cases with hypertensive encephalopathy and acute left ventricular failure with average systemic and pulmonary arterial pressures from 307/164 and 9 I/55 mm Hg, respectively, which fell to 2371115 and 68135 mm Hg 15 min after 10 mg of the drug, and were further reduced to 176189 and to 47/19 mm Hg by an additional 10 mg.
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