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Медицинская библиотека · Cardiologia (Rome, Italy) · 1992

[An analysis of the variability in the heart rate in relation to the presence of transient ischemia and to its physiopathological mechanism].

Meloni C, Carandente O, Bonetti F, Ferrario F, Carandente F, Chierchia S L

Сравнительное исследованиеАннотация на английскомСтатьяПеревод в очереди

Аннотация

To assess the differences in the pathogenesis of cardiac ischemic events and the role of the autonomic nervous system, we studied the electrocardiographic measures of tonic vagal activity during 24-hour Holter monitoring. We tested the circadian rhythm of the power in the high frequency energy (HF: 0.15-0.40 Hz) of the normal R-R interval power spectrum, the daily percent of successive normal R-R greater than 50 ms (pNN50) and the roots mean square of successive difference of normal R-R intervals (MMSD) in patients with coronary artery disease of comparable angiographic severity. Group A consisted of 5 patients (mean age 62 +/- 8) with chronic stable angina and Group B of 5 patients (mean age 61 +/- 8) with variant angina. Characteristic anginal pattern, typical ST changes during ischemic events on Holter monitoring and angiographic evidence of vasoconstriction induced by hyperventilation distinguished the 2 groups. Mean Cosinor analysis showed the presence of a significant circadian rhythm of HF only in Group A with a peak in the early morning hours (phi at 03.45, % rhythm 50.0, p less than 0.03); a significant reduction of parasympathetic activation was also found in Group B (MSSD: 27.8 vs 15.4, p less than 0.05; pNN50: 2.9 vs 0.6, p less than 0.05). These results suggest a different pattern in circadian variation of HF and lower degree of time and frequency domain of heart rate variability, as a marker of vagal tone in patients with high susceptibility to coronary vasospasm.

Для цитирования: Meloni C, Carandente O, Bonetti F, Ferrario F, Carandente F, Chierchia S L. [An analysis of the variability in the heart rate in relation to the presence of transient ischemia and to its physiopathological mechanism].. Cardiologia (Rome, Italy). 1992.

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