Hemodynamic Effects of Isradipine and Nifedipine in Chronic Sustained Hypertension

As isradipine is known to be less cardiodepressant than nifedipine, myocardial wall stress–an important determinant of cardiac oxygen demand–may also be more favorably influenced by isradipine. Therefore, the acute effects of an intravenous (i.v.) infusion of isradipine (0.4 mg) vs. nifedipine (2.0...

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Veröffentlicht in:Journal of cardiovascular pharmacology 1992, Vol.19 (3 Suppl), p.84-86
Hauptverfasser: Gross, P, Koppenhagen, K, Wudel, E, Burger, K J, Welzel, W, Distler, G.-A
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container_end_page 86
container_issue 3 Suppl
container_start_page 84
container_title Journal of cardiovascular pharmacology
container_volume 19
creator Gross, P
Koppenhagen, K
Wudel, E
Burger, K J
Welzel, W
Distler, G.-A
description As isradipine is known to be less cardiodepressant than nifedipine, myocardial wall stress–an important determinant of cardiac oxygen demand–may also be more favorably influenced by isradipine. Therefore, the acute effects of an intravenous (i.v.) infusion of isradipine (0.4 mg) vs. nifedipine (2.0 mg) on cardiac hemodynamics and systolic wall stress were investigated in a crossover study of 12 hypertensive patients. Vasodilation-induced reflex activation was limited by pretreatment with i.v. propranolol at 0.1 mg/kg of body weight. The hemodynamic parameters measured were statistically comparable at baseline and after propranolol with both calcium antagonists, as was blood pressure reduction. However, the end-systolic volume decreased with isradipine, but not with nifedipine [before69 ± 7.0 ml (mean ± SEM); after61 ± 6.1 ml; 2p < 0.01 vs. before62 ± 6.1 ml; after64 ± 7.0 ml; NS, (difference between changes in response to treatments2p < 0.05)]. The ejection fraction increased only with isradipine vs. nifedipine [before48 ± 2.3%; after54 ± 2.3%; 2p < 0.001 vs. before52 ± 2.0%; after52 ± 2.3%; NS (difference between changes in response to treatments2p < 0.05)]. Systolic wall stress decreased significantly more with isradipine than with nifedipine [before2,767 ± 231; after2,153 ± 162 relative units; 2p < 0.001 vs. before2,636 ± 212; after2,310 ± 199 relative units; 2p < 0.05 (difference between changes in response to treatments2p < 0.05)]. These results suggest that isradipine, given acutely, unloads the heart more than does nifedipine.
doi_str_mv 10.1097/00005344-199200193-00020
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Therefore, the acute effects of an intravenous (i.v.) infusion of isradipine (0.4 mg) vs. nifedipine (2.0 mg) on cardiac hemodynamics and systolic wall stress were investigated in a crossover study of 12 hypertensive patients. Vasodilation-induced reflex activation was limited by pretreatment with i.v. propranolol at 0.1 mg/kg of body weight. The hemodynamic parameters measured were statistically comparable at baseline and after propranolol with both calcium antagonists, as was blood pressure reduction. However, the end-systolic volume decreased with isradipine, but not with nifedipine [before69 ± 7.0 ml (mean ± SEM); after61 ± 6.1 ml; 2p < 0.01 vs. before62 ± 6.1 ml; after64 ± 7.0 ml; NS, (difference between changes in response to treatments2p < 0.05)]. The ejection fraction increased only with isradipine vs. nifedipine [before48 ± 2.3%; after54 ± 2.3%; 2p < 0.001 vs. before52 ± 2.0%; after52 ± 2.3%; NS (difference between changes in response to treatments2p < 0.05)]. Systolic wall stress decreased significantly more with isradipine than with nifedipine [before2,767 ± 231; after2,153 ± 162 relative units; 2p < 0.001 vs. before2,636 ± 212; after2,310 ± 199 relative units; 2p < 0.05 (difference between changes in response to treatments2p < 0.05)]. 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Therefore, the acute effects of an intravenous (i.v.) infusion of isradipine (0.4 mg) vs. nifedipine (2.0 mg) on cardiac hemodynamics and systolic wall stress were investigated in a crossover study of 12 hypertensive patients. Vasodilation-induced reflex activation was limited by pretreatment with i.v. propranolol at 0.1 mg/kg of body weight. The hemodynamic parameters measured were statistically comparable at baseline and after propranolol with both calcium antagonists, as was blood pressure reduction. However, the end-systolic volume decreased with isradipine, but not with nifedipine [before69 ± 7.0 ml (mean ± SEM); after61 ± 6.1 ml; 2p < 0.01 vs. before62 ± 6.1 ml; after64 ± 7.0 ml; NS, (difference between changes in response to treatments2p < 0.05)]. The ejection fraction increased only with isradipine vs. nifedipine [before48 ± 2.3%; after54 ± 2.3%; 2p < 0.001 vs. before52 ± 2.0%; after52 ± 2.3%; NS (difference between changes in response to treatments2p < 0.05)]. Systolic wall stress decreased significantly more with isradipine than with nifedipine [before2,767 ± 231; after2,153 ± 162 relative units; 2p < 0.001 vs. before2,636 ± 212; after2,310 ± 199 relative units; 2p < 0.05 (difference between changes in response to treatments2p < 0.05)]. 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Therefore, the acute effects of an intravenous (i.v.) infusion of isradipine (0.4 mg) vs. nifedipine (2.0 mg) on cardiac hemodynamics and systolic wall stress were investigated in a crossover study of 12 hypertensive patients. Vasodilation-induced reflex activation was limited by pretreatment with i.v. propranolol at 0.1 mg/kg of body weight. The hemodynamic parameters measured were statistically comparable at baseline and after propranolol with both calcium antagonists, as was blood pressure reduction. However, the end-systolic volume decreased with isradipine, but not with nifedipine [before69 ± 7.0 ml (mean ± SEM); after61 ± 6.1 ml; 2p < 0.01 vs. before62 ± 6.1 ml; after64 ± 7.0 ml; NS, (difference between changes in response to treatments2p < 0.05)]. The ejection fraction increased only with isradipine vs. nifedipine [before48 ± 2.3%; after54 ± 2.3%; 2p < 0.001 vs. before52 ± 2.0%; after52 ± 2.3%; NS (difference between changes in response to treatments2p < 0.05)]. Systolic wall stress decreased significantly more with isradipine than with nifedipine [before2,767 ± 231; after2,153 ± 162 relative units; 2p < 0.001 vs. before2,636 ± 212; after2,310 ± 199 relative units; 2p < 0.05 (difference between changes in response to treatments2p < 0.05)]. These results suggest that isradipine, given acutely, unloads the heart more than does nifedipine.]]></abstract><pub>Lippincott-Raven Publishers</pub><doi>10.1097/00005344-199200193-00020</doi><tpages>3</tpages><oa>free_for_read</oa></addata></record>
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title Hemodynamic Effects of Isradipine and Nifedipine in Chronic Sustained Hypertension
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