The effect of nifedipine on ventriculoarterial coupling in old myocardial infarction
Autor: | Takashi Fujii, Kohzaburo Seki, Kazuhiro Katayama, Takafumi Hiro, Toshiro Miura, Michihiro Kohno, Masunori Matsuzaki, Masafumi Yano |
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Rok vydání: | 1996 |
Předmět: |
Male
medicine.medical_specialty Nifedipine Physiology Heart Ventricles Vasodilator Agents Myocardial Infarction Hemodynamics Blood Pressure Sublingual administration Afterload Heart Rate Internal medicine Heart rate Medicine Humans Ventricular Function Myocardial infarction Aged Heart Failure Ejection fraction business.industry Stroke Volume Arteries Middle Aged medicine.disease medicine.anatomical_structure Cardiology Female Cardiology and Cardiovascular Medicine business Artery medicine.drug |
Zdroj: | Japanese circulation journal. 60(1) |
ISSN: | 0047-1828 |
Popis: | The effect of nifedipine on ventriculoarterial coupling was examined in 8 patients with old myocardial infarction who showed a depressed ejection fraction (37 +/- 7%). Left ventricular (LV) pressure and LV volume were determined simultaneously by micromanometer and conductance catheter, respectively. We measured the slope (Ees) of the end-systolic pressure-volume relation during transient inferior vena caval occlusion, the slope (Ea) of the end-systolic pressure-stroke volume relation, the ratio of Ea to Ees (Ea/Ees), and the work efficiency (the ratio of external work to the systolic pressure-volume area) at baseline and after the sublingual administration of nifedipine (10 mg). Nifedipine slightly increased the heart rate from 71 +/- 14 to 78 +/- 17 beats/min. Although nifedipine had little effect on Ees (2.54 +/- 0.68 vs 2.47 +/- 0.62 mmHg/ml/m2, ns), it significantly decreased Ea from 3.47 +/- 1.16 to 2.37 +/- 0.54 mmHg/ml/m2. Consequently, Ea/Ees decreased from 1.42 +/- 0.47 to 0.97 +/- 0.31 and work efficiency increased from 48 +/- 12 to 59 +/- 13% after nifedipine administration. These data suggest that nifedipine reduces afterload (Ea) and improves left ventriculoarterial coupling without depressing left ventricular contractility in patients with failing hearts due to old myocardial infarction. |
Databáze: | OpenAIRE |
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