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Prinzmetal’s angina

Verapamil. Verapamil hydrochloride is a pbenyl alkyl amine and is considered the prototype of the Class I calcium channel blockers. Verapamil is also a potent inhibitor of coronary artery spasm and is useful in Prinzmetal s angina and in unstable angina at rest. Verapamil produces negative chronotropic and inotropic effects. These two actions reduce myocardial oxygen consumption and probably account for the effectiveness of verapamil in chronic stable effort angina (98,99). Moreover, verapamil is an effective antihypertensive agent. [Pg.126]

The answer is a. (Hardman, pp 762-764.) Experimentally, nitrates dilate coronary vessels. This occurs in normal subjects, resulting in an overall increase in coronary blood flow. In arteriosclerotic coronaries, the ability to dilate is lost, and the ischemic area may actually have less blood flow under the influence of nitrates. Improvement in the ischemic conditions is the result of decreased myocardial oxygen demand because of a reduction of preload and afterload. Nitrates dilate both arteries and veins and thereby reduce the work of the heart. Should systemic blood pressure fall, a reflex tachycardia will occur. In pure coronary spasm, such as Prinzmetal s angina, the effect of increased coronary blood flow is relevant, while in severe left ventricular hypertrophy with minimal obstruction, the effect on preload and afterload becomes important. [Pg.132]

Patients with variant (Prinzmetal s) angina or cocaine-induced ACS may benefit from calcium channel blockers as initial therapy because they can reverse coronary vasospasm. /J-Blockers generally should be avoided in these situations because they may worsen vasospasm through an unopposed /T-blocking effect on smooth muscle. [Pg.67]

Verapamil (Isoptin, Covera), in addition to its use as an antiarrhythmic agent, has been employed extensively in the management of variant (Prinzmetal s) angina and effort-induced angina pectoris (see Chapters 17 and 19). It selectively inhibits the voltage-gated calcium channel that is vital for action potential genesis in slow-response myocytes, such as those found in the sinoatrial and A-V nodes. [Pg.191]

All agents are also effective in the control of variant (Prinzmetal s) angina, in which spasm of the coronary arteries is the main factor. Their usefulness in the more complex unstable (preinfarction) angina is less definite, depending on the hemodynamic status and the susceptibility of the patient to infarction. [Pg.221]

Contraindications Basilar or hemiplegic migraine, coronary artery disease, ischemic heart disease (including angina pectoris, history of Ml, silent ischemia, and Prinzmetal s angina), uncontrolled hypertension, use within 24 hours of ergotamine-contain-ing preparations or another serotonin receptor agonist, use within 14 days of MAOls... [Pg.1100]

Keller KB, Lemberg L. Prinzmetal s angina. AmJ Crit Care. 2004 13 350-354. [Pg.318]

Schroeder JS, Feldman RL, Giles TD, Friedman MJ, DeMaria AN, Kinney EL, Mahon SM, Pit B, Meyer R, Basta LL, Curry RC Jr, Groves BM, MacAlpin RN. Multichnic controUed trial of dhtiazem for Prinzmetal s angina. Am J Med 1982 72(2) 227-32. [Pg.1129]

Kleiman NS, Lehane DE, Geyer CE Jr, Pratt CM, Young JB. Prinzmetal s angina during 5-fluorouracil chemotherapy. Am J Med 1987 82(3) 566-8. [Pg.1416]

IV use ischemic heart disease silent ischemia, Prinzmetal s angina, uncontrolled hypertension, concurrent ergotamine-containing preparations, hemiplegic or basilar migraine Caution with liver and kidney problems... [Pg.198]

Good candidates for calcium channel blockers in angina include patients with contraindications to or intolerance of /3-blockers, those with coexisting conduction system disease (except for verapamil and diltiazem), those with Prinzmetal s angina (vasospastic or variable-threshold angina), those with peripheral vascular disease, those with severe ventricular dysfunction (amlopidine is probably the calcium channel blocker of choice, and others need to be used with caution if the ejection fraction is less than 40%), and those with concurrent hypertension. [Pg.284]

Two groups of patients may benefit from calcium chaimel blockers as opposed to /8-blockers as initial therapy. Cocaine-induced ACS and variant (or Prinzmetal s) angina are two conditions in which coronary vasospasm plays an important role. Calcium channel blockers and/or NTG generally are considered the agents of choice in these... [Pg.306]

Unlike skeletal muscles, which contain endogenons stores of calcium ions, both cardiac muscle and vascnlar smooth muscle require extracellular calcium for contractile function. Therefore, cardiac muscle and vascnlar smooth muscle are subject to regulation by calcium antagonists or calcium entry blockers (Figure 103 and Table 21), which are used in the treatment of hypertension, Raynand s disease, Prinzmetal s angina, and migraine syndromes. [Pg.120]

Although anecdotal evidence suggested that prazosin might be useful in the treatment of patients with variant angina (Prinzmetal s angina) due to coronary vasospasm, several small controlled trials have failed to demonstrate a clear benefit. Some studies have indicated that prazosin can decrease the incidence of digital vasospasm in patients with Raynaud s disease however, its relative efficacy as compared with other vasodilators (e.g., Ca -channel blockers) is not known. Prazosin may have some benefit in patients with other vasospastic disorders. Prazosin decreases ventricular arrhythmias induced by coronary artery ligation or reperfusion in laboratory animals the therapeutic potential for this use in humans is not known. Prazosin also may be useful for the treatment of patients with mitral or aortic valvular insufficiency, presumably because of reduction of afterload. [Pg.670]

Amlodipine is a potent peripheral vasodilator, which decreases cardiac afterload and thus decreases cardiac work and myocardial oxygen consumption. Coronary arteries are also dilated, increasing oxygen delivery to the myocardium. Amlodipine is useful in both chronic stable angina and Prinzmetal s angina. [Pg.130]

Prinzmetal s angina) constipation, peripheral edema, angina, bradycardia, AV block, flushing, rash, nasal congestion, cough ... [Pg.383]

Variant (Prinzmetal s) Angina Hypoxia and ischemia to myocardium is caused by vasospasm (rather than progressive narrowing of coronary arteries). Episodes may occur at rest, often at the same time each day. S-T elevation on ECG. [Pg.70]

Some pathophysiological states are characterized by perturbations in receptor dynamics. Prinzmetal s angina is thought to be characterized by an imbalance between vasodilatory P2-adrenoceptor function and vasoconstrictor -adrenoceptor function. In this disease state, the excessive alpha vasoconstriction of... [Pg.160]

Rozanski, J.J. and M. Kleinfeld, Altemans of the ST segment of T wave. A sign of electrical instability in Prinzmetal s angina. Pacing Clin Electrophysiol, 1982. 5(3) p. 359-65. [Pg.537]


See other pages where Prinzmetal’s angina is mentioned: [Pg.811]    [Pg.383]    [Pg.383]    [Pg.65]    [Pg.35]    [Pg.543]    [Pg.848]    [Pg.1325]    [Pg.811]    [Pg.263]    [Pg.261]    [Pg.266]    [Pg.1115]    [Pg.283]    [Pg.273]    [Pg.112]    [Pg.128]    [Pg.128]    [Pg.528]    [Pg.539]    [Pg.383]    [Pg.110]    [Pg.417]   
See also in sourсe #XX -- [ Pg.484 ]

See also in sourсe #XX -- [ Pg.16 ]

See also in sourсe #XX -- [ Pg.3 , Pg.9 ]




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Angina Prinzmetal

Prinzmetals angina

Prinzmetal’s variant angina

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