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Angina heart rate

We examined the effects of selective activation of histamine Hj receptors on coronary hemodynamics in two groups patients with atypical chest pain and normal coronary arteries, and patients with vasospastic angina [48]. Selective Hj receptor stimulation was achieved by infusing histamine intravenously (0.5 pg/kg/min) for 5 min after pretreatment with cimetidine to antagonize the H2 receptors. Heart rate was kept constant (100 beats/min) by coronary sinus pacing. [Pg.104]

Ivabradine is used in the treatment of angina in patients in normal sinus rhythm. It acts on the sinus node resulting in a reduction of the heart rate. It is contraindicated in severe bradycardia (heart rate lower than 60 beats/ minute), cardiogenic shock, acute myocardial infarction, moderate-to-severe heart failure, immediately after a cerebrovascular accident, second and third-degree heart block and patients with unstable angina or a pacemaker. Side-effects include bradycardia, first-degree heart block, ventricular extrasystoles, headache, dizziness and visual disturbances, including blurred vision. [Pg.119]

Indications. Verapamil is used as an antiarrhythmic drug in supraventricular tachyarrhythmias. In atrial flutter or fibrillation, it is effective in reducing ventricular rate by virtue of inhibiting AV-conduction. Verapamil is also employed in the prophylaxis of angina pectoris attacks (p. 308) and the treatment of hypertension (p. 312). Adverse effects Because of verapamil s effects on the sinus node, a drop in blood pressure fails to evoke a reflex tachycardia Heart rate hardly changes bradycardia may even develop. AV-block and myocardial insufficiency can occur. Patients frequently complain of constipation. [Pg.122]

Tachycardia/Angina Minoxidil increases heart rate this can be prevented by coadministration of a -adrenergic blocking drug or other sympathetic nervous system suppressants. In addition, angina may worsen or appear for the first time... [Pg.569]

All of the aforementioned beneficial effects of the /3-blockers are caused by the blockade of /3i-adrenoceptors. The beneficial effect of /3-blockers in the treatment of angina is largely caused by the reduction of heart rate and the concomitant decrease in myocardial oxygen consumption, thus improving the imbalance between oxygen supply and consumption which underlies myocardial ischaemia. [Pg.325]

Angina pectoris requires a /3-blocker which clearly lowers heart rate. For this reason ISA-/3-blockers should not be used in this condition. As in the treatment of hypertension a /3i-selective blocker seems preferable. [Pg.326]

Verapamil and a few newer dmgs of this category are vasodilator agents, which in addition impair AV conduction, reduce heart rate and cardiac contractile force. Verapamil was initially developed for the treatment of supraventricular tachycardia and it continues to be an important drug for the management of this condition, also postoperatively. Verapamil is the CA of choice in the management of hypertrophic cardiomyopathy. Verapamil is also used in the treatment of stable angina and, less frequently, essential hypertension. [Pg.331]

Fig. 4. Schematic presentation of the mechanism of calcium antagonists with respect to their beneficial effect in angina pectoris. The final result is an improvement of the imbalance between myocardial oxygen demand and supply. TPR = total peripheral resistance HR = heart rate. Fig. 4. Schematic presentation of the mechanism of calcium antagonists with respect to their beneficial effect in angina pectoris. The final result is an improvement of the imbalance between myocardial oxygen demand and supply. TPR = total peripheral resistance HR = heart rate.
Arterial blood pressure (afterload) is also reduced by propranolol. Although the mechanisms responsible for this antihypertensive effect are not completely understood, they are thought to involve (1) a reduction in cardiac output, (2) a decrease in plasma renin activity, (3) an action in the central nervous system, and (4) a resetting of the baroreceptors. Thus, propranolol may exert a part of its benehcial effects in secondary angina by decreasing three of the major determinants of myocardial oxygen demand, that is, heart rate, contractihty, and systolic wall tension. [Pg.201]

L A patient comes to your office with effort-induced angina and resting tachycardia. You choose the following drug to treat the patient because it slows heart rate by blocking L-type calcium channels in the SA node ... [Pg.204]

Monitor patients with a cardiovascular disease for an increase in the frequency duration, or severity of angina or changes in blood pressure or heart rate... [Pg.240]

Angina-. Reduction in nitroglycerin usage frequency, severity, onset, and duration of angina pain heart rate... [Pg.456]

Tachycardia and angina pectoris may occur because of increased oxygen demands associated with increased heart rate and cardiac output. [Pg.811]


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See also in sourсe #XX -- [ Pg.299 ]




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