Ability of calcium-entry blockade by felodipine to disclose different pathogenetic mechanisms behind hyperventilation-induced myocardial ischemia in men

Diego Ardissino, Stefano Savonitto, Paola Zanini, Paolo Barberis, Stefano De Servi, Alberto Rolla, Giuseppe Specchia

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

To verify that myocardial ischemia occurring during ither the overbreathing or recovery phase of the hyperventilation test is based on different pathogenetic mechanisms, 2 consecutive series of patients, selected on the basis of their response to a run-in hyperventilation test, were studied. Group I comprised 15 patients who developed ST-segment depression early during overbreathing, whereas group II consisted of 12 patients showing ST-segment depression late during the recovery phase. A single oral dose of felodipine 10 mg or of placebo was administered on 2 consecutive days according to a randomized, double-blind, crossover design, and the hyperventilation test was repeated, on both days of the study, 3 to 5 hours after drug intake. In group I, ST-segment depression occurred after placebo in all patients during overbreathing, with an increase in rate pressure product (from 112 ± 31 at baseline to 168 ± 55 mm Hg × beats/min/100 at the onset of ST-segment depression; p <0.01). After felodipine, 13 patients continued to show ST-segment depression during overbreathing, together with an increase in rate pressure product (from 107 ± 24 at baseline to 158 ± 46 mm Hg × beats/ min/100 at the onset of electrocardiographic changes; p <0.01). In group II, all 12 patients showed ST-segment depression during recovery after placebo, with a rate pressure product comparable to baseline conditions (112 ± 35 at baseline vs 102 ± 27 mm Hg × beats/min/100 at the onset of ST-segment depression; difference not significant). After felodipine, no patient developed ST-segment depression or chest pain. These findings confirm that early hyperventilation-induced ST-segment depression is related to increased oxygen consumption, which cannot be prevented by felodipine. On the other hand, felodipine is highly effective in preventing delayed ischemia, which is due to a primary reduction in coronary blood flow.

Original languageEnglish
Pages (from-to)1304-1308
Number of pages5
JournalThe American Journal of Cardiology
Volume66
Issue number19
DOIs
Publication statusPublished - Dec 1 1990

Fingerprint

Felodipine
Hyperventilation
Myocardial Ischemia
Calcium
Placebos
Pressure
Chest Pain
Oxygen Consumption
Cross-Over Studies
Ischemia

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Ability of calcium-entry blockade by felodipine to disclose different pathogenetic mechanisms behind hyperventilation-induced myocardial ischemia in men. / Ardissino, Diego; Savonitto, Stefano; Zanini, Paola; Barberis, Paolo; De Servi, Stefano; Rolla, Alberto; Specchia, Giuseppe.

In: The American Journal of Cardiology, Vol. 66, No. 19, 01.12.1990, p. 1304-1308.

Research output: Contribution to journalArticle

Ardissino, Diego ; Savonitto, Stefano ; Zanini, Paola ; Barberis, Paolo ; De Servi, Stefano ; Rolla, Alberto ; Specchia, Giuseppe. / Ability of calcium-entry blockade by felodipine to disclose different pathogenetic mechanisms behind hyperventilation-induced myocardial ischemia in men. In: The American Journal of Cardiology. 1990 ; Vol. 66, No. 19. pp. 1304-1308.
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abstract = "To verify that myocardial ischemia occurring during ither the overbreathing or recovery phase of the hyperventilation test is based on different pathogenetic mechanisms, 2 consecutive series of patients, selected on the basis of their response to a run-in hyperventilation test, were studied. Group I comprised 15 patients who developed ST-segment depression early during overbreathing, whereas group II consisted of 12 patients showing ST-segment depression late during the recovery phase. A single oral dose of felodipine 10 mg or of placebo was administered on 2 consecutive days according to a randomized, double-blind, crossover design, and the hyperventilation test was repeated, on both days of the study, 3 to 5 hours after drug intake. In group I, ST-segment depression occurred after placebo in all patients during overbreathing, with an increase in rate pressure product (from 112 ± 31 at baseline to 168 ± 55 mm Hg × beats/min/100 at the onset of ST-segment depression; p <0.01). After felodipine, 13 patients continued to show ST-segment depression during overbreathing, together with an increase in rate pressure product (from 107 ± 24 at baseline to 158 ± 46 mm Hg × beats/ min/100 at the onset of electrocardiographic changes; p <0.01). In group II, all 12 patients showed ST-segment depression during recovery after placebo, with a rate pressure product comparable to baseline conditions (112 ± 35 at baseline vs 102 ± 27 mm Hg × beats/min/100 at the onset of ST-segment depression; difference not significant). After felodipine, no patient developed ST-segment depression or chest pain. These findings confirm that early hyperventilation-induced ST-segment depression is related to increased oxygen consumption, which cannot be prevented by felodipine. On the other hand, felodipine is highly effective in preventing delayed ischemia, which is due to a primary reduction in coronary blood flow.",
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