Effects of intravenous nifedipine in patients with chronic stable angina pectoris

two-dimensional excercise echocardiographic study

F. Fedele, C. D. Vizza, F. Fabietti, S. Sciomer, A. Dagianti

Research output: Contribution to journalArticle

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Abstract

To study the effects of nifedipine on exercise tolerance in patients with stable angina and to clarify the mechanisms underlying the drug's action, the authors studied ten patients with stable effort angina (nine men, 1 woman; mean age, 58 ± 16 years). All patients performed two ergometric tests (limited by symptoms and/or electrocardiographic echo signs of myocardial ischemia) preceded by randomized intravenous administration of placebo or nifedipine (1 mg). In addition to the normal parameters, the behavior of left ventricular function was also evaluated during the tests, using two-dimensional echocardiography. In the post-nifedipine test at intermediate loads, there were no statistically significant differences with respect to placebo for all the measured parameters; at the point of highest stress a net improvement was observed in stress tolerance (baseline, 1,862 ± 962 kgm; placebo, 1,914 ± 948 kgm; nifedipine, 2,836 ± 1,188 kgm; nifedipine vs baseline, P <0.05; nifedipine vs placebo, P <0.05) and higher double product (DP) values were achieved (baseline, 19,500 ± 4,512 mmHg x beat/min x 10-2; placeboo, 19,753 ± 4,611 mmHg x beat/min x 10-2; nifedipine, 21,869 ± 4,989 mmHg x beat/min x 10-2; nifedipine vs baseline, P <0.05; nifedipine vs placebo, P <0.05) with lower incidence of angor (baseline, 9/10; placebo, 8/10; nifedipine, 4/10), electrocardiogram ST slope (baseline, 1.3 ± 0.05 mm; placebo, 1.3 ± 0.5 mm; nifedipine, 0.8 ± 0.5 mm; nifedipine vs baseline, P <0.05; nifedipine vs placebo, P <0.05), two-dimensional echo reversible asynergies (WMS: baseline, 1.9 ± 0.5; placebo, 1.9 ± 0.5; nifedipine, 1.1 ± 0.3; nifedipine vs baseline, P <0.05; nifedipine vs placebo, P <0.05), and improved left ventricular function (EF: baseline, 48.5 ± 3.8; placebo, 48.8 ± 3.8, nifedipine 51.5 ± 3.8, P <0.05). In conclusion, the antianginal effect of IV nifedipine appears to be attributable to an improvement in coronary flow rather than to a decrease in myocardial oxygen consumption (higher DP values and no significant variation in ventricular volumes).

Original languageEnglish
Pages (from-to)379-389
Number of pages11
JournalCurrent Therapeutic Research
Volume47
Issue number2
Publication statusPublished - 1990

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Stable Angina
Nifedipine
Placebos
Left Ventricular Function
Exercise Tolerance

ASJC Scopus subject areas

  • Medicine(all)

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Effects of intravenous nifedipine in patients with chronic stable angina pectoris : two-dimensional excercise echocardiographic study. / Fedele, F.; Vizza, C. D.; Fabietti, F.; Sciomer, S.; Dagianti, A.

In: Current Therapeutic Research, Vol. 47, No. 2, 1990, p. 379-389.

Research output: Contribution to journalArticle

Fedele, F. ; Vizza, C. D. ; Fabietti, F. ; Sciomer, S. ; Dagianti, A. / Effects of intravenous nifedipine in patients with chronic stable angina pectoris : two-dimensional excercise echocardiographic study. In: Current Therapeutic Research. 1990 ; Vol. 47, No. 2. pp. 379-389.
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abstract = "To study the effects of nifedipine on exercise tolerance in patients with stable angina and to clarify the mechanisms underlying the drug's action, the authors studied ten patients with stable effort angina (nine men, 1 woman; mean age, 58 ± 16 years). All patients performed two ergometric tests (limited by symptoms and/or electrocardiographic echo signs of myocardial ischemia) preceded by randomized intravenous administration of placebo or nifedipine (1 mg). In addition to the normal parameters, the behavior of left ventricular function was also evaluated during the tests, using two-dimensional echocardiography. In the post-nifedipine test at intermediate loads, there were no statistically significant differences with respect to placebo for all the measured parameters; at the point of highest stress a net improvement was observed in stress tolerance (baseline, 1,862 ± 962 kgm; placebo, 1,914 ± 948 kgm; nifedipine, 2,836 ± 1,188 kgm; nifedipine vs baseline, P <0.05; nifedipine vs placebo, P <0.05) and higher double product (DP) values were achieved (baseline, 19,500 ± 4,512 mmHg x beat/min x 10-2; placeboo, 19,753 ± 4,611 mmHg x beat/min x 10-2; nifedipine, 21,869 ± 4,989 mmHg x beat/min x 10-2; nifedipine vs baseline, P <0.05; nifedipine vs placebo, P <0.05) with lower incidence of angor (baseline, 9/10; placebo, 8/10; nifedipine, 4/10), electrocardiogram ST slope (baseline, 1.3 ± 0.05 mm; placebo, 1.3 ± 0.5 mm; nifedipine, 0.8 ± 0.5 mm; nifedipine vs baseline, P <0.05; nifedipine vs placebo, P <0.05), two-dimensional echo reversible asynergies (WMS: baseline, 1.9 ± 0.5; placebo, 1.9 ± 0.5; nifedipine, 1.1 ± 0.3; nifedipine vs baseline, P <0.05; nifedipine vs placebo, P <0.05), and improved left ventricular function (EF: baseline, 48.5 ± 3.8; placebo, 48.8 ± 3.8, nifedipine 51.5 ± 3.8, P <0.05). In conclusion, the antianginal effect of IV nifedipine appears to be attributable to an improvement in coronary flow rather than to a decrease in myocardial oxygen consumption (higher DP values and no significant variation in ventricular volumes).",
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AU - Fedele, F.

AU - Vizza, C. D.

AU - Fabietti, F.

AU - Sciomer, S.

AU - Dagianti, A.

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N2 - To study the effects of nifedipine on exercise tolerance in patients with stable angina and to clarify the mechanisms underlying the drug's action, the authors studied ten patients with stable effort angina (nine men, 1 woman; mean age, 58 ± 16 years). All patients performed two ergometric tests (limited by symptoms and/or electrocardiographic echo signs of myocardial ischemia) preceded by randomized intravenous administration of placebo or nifedipine (1 mg). In addition to the normal parameters, the behavior of left ventricular function was also evaluated during the tests, using two-dimensional echocardiography. In the post-nifedipine test at intermediate loads, there were no statistically significant differences with respect to placebo for all the measured parameters; at the point of highest stress a net improvement was observed in stress tolerance (baseline, 1,862 ± 962 kgm; placebo, 1,914 ± 948 kgm; nifedipine, 2,836 ± 1,188 kgm; nifedipine vs baseline, P <0.05; nifedipine vs placebo, P <0.05) and higher double product (DP) values were achieved (baseline, 19,500 ± 4,512 mmHg x beat/min x 10-2; placeboo, 19,753 ± 4,611 mmHg x beat/min x 10-2; nifedipine, 21,869 ± 4,989 mmHg x beat/min x 10-2; nifedipine vs baseline, P <0.05; nifedipine vs placebo, P <0.05) with lower incidence of angor (baseline, 9/10; placebo, 8/10; nifedipine, 4/10), electrocardiogram ST slope (baseline, 1.3 ± 0.05 mm; placebo, 1.3 ± 0.5 mm; nifedipine, 0.8 ± 0.5 mm; nifedipine vs baseline, P <0.05; nifedipine vs placebo, P <0.05), two-dimensional echo reversible asynergies (WMS: baseline, 1.9 ± 0.5; placebo, 1.9 ± 0.5; nifedipine, 1.1 ± 0.3; nifedipine vs baseline, P <0.05; nifedipine vs placebo, P <0.05), and improved left ventricular function (EF: baseline, 48.5 ± 3.8; placebo, 48.8 ± 3.8, nifedipine 51.5 ± 3.8, P <0.05). In conclusion, the antianginal effect of IV nifedipine appears to be attributable to an improvement in coronary flow rather than to a decrease in myocardial oxygen consumption (higher DP values and no significant variation in ventricular volumes).

AB - To study the effects of nifedipine on exercise tolerance in patients with stable angina and to clarify the mechanisms underlying the drug's action, the authors studied ten patients with stable effort angina (nine men, 1 woman; mean age, 58 ± 16 years). All patients performed two ergometric tests (limited by symptoms and/or electrocardiographic echo signs of myocardial ischemia) preceded by randomized intravenous administration of placebo or nifedipine (1 mg). In addition to the normal parameters, the behavior of left ventricular function was also evaluated during the tests, using two-dimensional echocardiography. In the post-nifedipine test at intermediate loads, there were no statistically significant differences with respect to placebo for all the measured parameters; at the point of highest stress a net improvement was observed in stress tolerance (baseline, 1,862 ± 962 kgm; placebo, 1,914 ± 948 kgm; nifedipine, 2,836 ± 1,188 kgm; nifedipine vs baseline, P <0.05; nifedipine vs placebo, P <0.05) and higher double product (DP) values were achieved (baseline, 19,500 ± 4,512 mmHg x beat/min x 10-2; placeboo, 19,753 ± 4,611 mmHg x beat/min x 10-2; nifedipine, 21,869 ± 4,989 mmHg x beat/min x 10-2; nifedipine vs baseline, P <0.05; nifedipine vs placebo, P <0.05) with lower incidence of angor (baseline, 9/10; placebo, 8/10; nifedipine, 4/10), electrocardiogram ST slope (baseline, 1.3 ± 0.05 mm; placebo, 1.3 ± 0.5 mm; nifedipine, 0.8 ± 0.5 mm; nifedipine vs baseline, P <0.05; nifedipine vs placebo, P <0.05), two-dimensional echo reversible asynergies (WMS: baseline, 1.9 ± 0.5; placebo, 1.9 ± 0.5; nifedipine, 1.1 ± 0.3; nifedipine vs baseline, P <0.05; nifedipine vs placebo, P <0.05), and improved left ventricular function (EF: baseline, 48.5 ± 3.8; placebo, 48.8 ± 3.8, nifedipine 51.5 ± 3.8, P <0.05). In conclusion, the antianginal effect of IV nifedipine appears to be attributable to an improvement in coronary flow rather than to a decrease in myocardial oxygen consumption (higher DP values and no significant variation in ventricular volumes).

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