Summary
The influence of atrial fibrillation on coronary circulation was studied in 21 anesthetized open-chest dogs. Atrial fibrillation was induced either by local application of acetylcholine (10% in normal saline) on the left atrial appendage or by electric stimulation (2–7 volts, 2 ms, 50 Hz). When atrial fibrillation was induced (n=10), mean aortic pressure fell and heart rate rose significantly; coronary blood flow (CBF) remained unchanged (78±6 vs. 75±5 ml/min×10 g) while coronary vascular resistance (CVR) (1.16±0.05 vs. 0.87±0.07 [mHg×min×100 gl/ml [RU], p<0.0001) and sinus oxygen saturation (26±2 vs. 22±1%, p<0.05) decreased. Following the application of carbochromen (5 mg/kg in 3 min i.v.) resulting in maximal coronary dilatation, atrial fibrillation resulted in a reduction in CBF (311±48 vs. 205±30 ml/min×100 g, p<0.01) and coronary sinus oxygen saturation (65±6 vs. 42±6%, p<0.01), while CVR (0.27±0.03 vs. 0.37±0.04 RU, p<0.0001) was 38±8% (p<0.0005) higher during atrial fibrillation than at sinus rhythm.
When hearts were paced to a rate which was identical to the average heart rate at atrial fibrillation (n=11), CBF (92±9 vs. 125±14 ml/min×100 g, p<0.001) and sinus oxygen saturation (24±2 vs. 30±2%, p<0.0025) were higher and CVR (1.16±0.11 vs. 0.97±0.10 RU, p<0.0005) lower than during atrial fibrillation; during maximal coronary dilatation by carbochromen, pacing also resulted in a higher CBF (233±24 vs. 168±16 ml/min×100 g, p<0.0005) and sinus oxygen saturation (70±3 vs. 57±2%, p<0.0005), while CVR (0.35±0.02 vs. 0.46±0.02 RU, p<0.0005) was lower than during atrial fibrillation.
Thus atrial fibrillation results in a decrease in coronary vascular resistance but an increase in coronary oxygen extraction. When heart rate is controlled, the vasoconstrictor effect of atrial fibrillation becomes unmasked. Coronary vasoconstriction during atrial fibrillation appears to be greater during maximal coronary dilatation than during control.
Zusammenfassung
An 21 narkotisierten thorakotomierten Hunden wurde der Einfluß von Vorhofflimmern auf die Koronardurchblutung untersucht. Vorhofflimmern wurde entweder durch lokale Applikation einer 10%-Acetylcholinlösung auf das linke Herzohr oder durch elektrische Stimulation (2–7 Volt, 2 ms, 50 Hz) induziert. Unter Vorhofflimmern (n=10) kam es zu einem signifikanten Abfall des mittleren Aortendruckes und Anstieg der Herzfrequenz; die Koronardurchblutung änderte sich nicht (78±6 gegenüber 75±5 ml/min×100 g), dagegen nahmen der Koronargefäßwiderstand von 1,16±0.05 auf 0,87±0.07 (mmHg×min×100 g)/ml (RU), p<0,0001 und die koronarvenöse Sauerstoffsättigung von 26±2% auf 22±1%, p<0,05, ab. Nach maximaler Koronardilatation durch Carbochromen (5mg/kg in 3 min i.v.) waren Koronardurchblutung (311±48 gegenüber 205±30 ml/min×100 g, p<0,01) und koronarvenöse Sauerstoffsättigung (65±6 gegenüber 42±6%, p<0,01) bei Vorhofflimmern deutlich niedriger, der Koronargefäßwiderstand (0,27±0,03 gegenüber 0,37±0,04 RU, p<0,0001) hingegen um 38±8% (p<0,0005) größer als bei Sinusrhythmus. Während der ebenfalls durch elektrische Vorhofstimulation ausgelösten supraventrikulären Tachykardie mit identischer Herzfrequenz wie bei Vorhofflimmern (n=11) waren Koronardurchblutung (92±9 gegenüber 125±14 ml/min×100 g, p<0,001) und koronarvenöse Sauerstoffsättigung (24±2 gegenüber 30±2%, p<0,0025) größer, der Koronargefäßwiderstand (1,16±0,11 gegenüber 0,97±0,10 RU, p<0,0005) niedriger als bei Vorhofflimmern; auch bei maximaler Koronardilatation waren Koronardurchblutung (168±16 gegenüber 233±24 ml/min×100 g, p<0,0005) und koronarvenöse Sauerstoffsättigung (57±2 gegenüber 70±3%, p<0,0005) größer, der Koronargefäßwiderstand (0,46±0,02 gegenüber 0,35±0,02 RU, p±0,0005) niedriger als bei Vorhofflimmern.
Die Ergebnisse zeigen, daß bei Vorhofflimmern zwar der Koronargefäßwiderstand abnimmt, dennoch die Sauerstoffausschöpfung ansteigt. Dieser vasokonstriktorische Effekt des Vorhofflimmerns wird dann sichtbar, wenn die Herzfrequenz kontrolliert wird. Das vasokonstriktorische Effekt ist unter maximaler Koronardilatation größer als unter Ausgangsbedingungen.
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References
Abildskov, J. A., F. K. Millar, M. J. Burgess: Atrial fibrillation. Amer. J. Cardiol.28, 263 (1971).
Adams, Z. S., A. Alella, P. Di Lavore, D. Gatullo, G. Losano, G. Vacca: The coronary flow during atrial flutter-fibrillation. G. Ital. Cardiol.9, 676 (1979).
Benchimol, A., H. M. Lowe, P. R. Akve: Cardiovascular response to exercise during atrial fibrillation and after conversion to sinus rhythm. Amer. J. Cardiol.16, 31 (1965).
Blinks, J. R., J. Koch-Weser: Analysis of the effects of changes in rate and rhythm upon myocardial contractility. J. Pharmacol. Exp. Ther.134, 373 (1961).
Bretschneider, H. J.: Aktuelle Probleme der Koronardurchblutung und des Myokardstoffwechsels: Regensburg, Jb. ärztl. Fortbild.15, 1 (1967).
Broch, O. J., O. Müller: Hemodynamic studies during auricular fibrillation and after restoration of sinus rhythm. Brit. Heart J.19, 222 (1957).
Corday, E., H. Gold, L. B. De Vera, J. H. Williams, J. Fields: Effect of the cardiac arrhythmias on the coronary circulation. Annals of Internal Medicine50, 535 (1959).
Duff, F., E. Berglund, H. Borst: The effect of heart rate on ventricular function and coronary circulation in dogs. Amer. J. Physiol.183, 611 (1955).
Edmands, R. E., K. Greenspan, C. Fisch: The role of inotropic variation in ventricular function during atrial fibrillation. J. Clin. Invest.49, 73 (1970).
Feigl, E. O.: Control of myocardial oxygen tension by sympathetic coronary vasoconstriction in the dog. Circulat. Res.37, 88 (1975).
Formann, R., E. S. Kirk, J. M. Downey, E. H. Sonnenblick: Nitroglycerin and heterogeneity of myocardial blood flow. Reduced subendocardial blood flow and ventricular contractile force. J. Clin. Invest.52, 905 (1973).
Gilbert, R., R. H. Eich, H. Smulyan, J. Keighley, J. H. Auchincloss, Jr.: Effect on circulation of conversion of atrial fibrillation to sinus rhythm. Circulation27, 1079 (1963).
Goble, A. J., G. Sloman, J. S. Robinson: Mortality reduction in a coronary care unit. Brit. Med.J. 1966/I, 1005.
Graettinger, J. S., R. A. Carleton, J. J. Muenster: Circulatory consequences of changes in cardiac rhythm produced in patients by transthoracic direct current shock. J. Clin. Invest.43, 2290 (1964).
Hecht, H. H., W. J. Osher, A. J. Samuels: Cardiovascular adjustments in subjects with organic heart disease before and after conversion of atrial fibrillation to normal sinus rhythm. J. Clin. Invest.30, 647 (1961).
Hiss, R. G., L. E. Lamb: Electrocardiographic findings in 122,043 individuals. Circulation25, 947 (1962).
Hunt, D., G. Sloman, C. Penington: Effects of atrial fibrillation on prognosis of acute myocardia infarction. Brit. Heart J.40, 303 (1978).
Jevith, D. E., R. Balcon, E. B. Raltery, S. Cram: Incidence and management of supraventricular arrhythmias after acute myocardial infarction. Lancet1967/II, 734.
Johannsen, U. J., L. M. Allyn, L. M. Melvin: Responsiveness to cardiac sympathetic nerve stimulation during maximal coronary dilatation produced by adenosine. Circulat. Res.50, 510 (1982).
Julian, D. G., P. A. Valentine, G. G. Miller: Disturbances of rate, rhythm and conduction in acute myocardial infarction. Amer. J. Med.37, 915 (1964).
Killip, T., R. A. Baer: Hemodynamic effects after reversion from atrial fibrillation to sinus rhythm by precardial shock. J. Clin. Invest.45, 658 (1966).
Killip, T., J. H. Grault: Mode of onset of atrial fibrillation. Amer. Heart. J.70, 172 (1965).
Kory, R. C., G. R. Meneely: Cardiac output in auricular fibrillation with observations on the effects of conversation to normal sinus rhythm. J. Clin. Invest.30, 653 (1961).
Lendrum, B., H. Feinberg, E. Boyd, et al.: Rhythm effects on contractility of the beating isovolumic left ventricle. Amer. J. Physiol.199, 1115 (1960).
Lewis, T.: Fibrillation of the auricles: its effects upon the circulation. J. Exp. Med.16, 395 (1912).
Lewis, F. B., J. D. Coffmann, D. E. Gregg: Effect of heart rate and intracoronary flow and resistance. Circulat. Res.9, 89 (1961).
Linden, R. J., J. H. Mitchell: Relation between left ventricular diastolic pressure and myocardial segment length and observations on the contribution of atrial systole. Circulat. Res.8, 1092 (1960).
Martin, R. H., L. A. Cobb: Observation on the effect of atrial systole in man. J. Lab. Clin. Med.68, 224 (1966).
Martin, R. H., S. T. Lim, R. L. van Citters: Atrial fibrillation in the intact unanesthetized dog: hemodynamic effects during rest, exercise, and beta-adrenergic blockade. J. Clin. Invest.46, 205 (1967).
Millar, K., R. R. Eich, M. J. Burgess, et al.: Entrancement of cardiac output by irregular rhythms (Abstr.). Circulation 40, Suppl. 3, 146 (1969).
Mitchell, J. H., W. Shapiro: Atrial function and the hemodynamic consequences of atrial fibrillation in man. Amer. J. Cardiol.23, 556 (1964).
Mohrmann, D. E., E. O. Feigl: Competition between sympathetic vasoconstriction and metabolic vasodilation in the canine coronary circulation. Circulat. Res.46, 79 (1978).
Morris, Jr. J. J., M. Entman, W. C. North, Y. Kong, H. MacIntosh: The changes in cardiac output with reversion of atrial fibrillation to sinus rhythm. Circulation31, 670 (1965).
Mudge, Jr. G. H., S. Goldberg, S. Gunther, T. Mann, W. Grossman: Comparison of metabolic and vasoconstrictor stimuli on coronary vascular resistance in man. Circulation59, 544 (1979).
Murray, P. A., S. F. Vatner: Alpha-adrenoreceptor attenuation of the coronary vascular response to severe exercise in the conscious dog. Circulat. Res.45, 654 (1979).
Nakano, J.: Effects of atrial and ventricular tachycardias on the cardiovascular dynamics. Amer. J. Physiol.206, 547 (1964).
Olsson, R. A.: Myocardial reactive hyperemia. Circulat. Res.37, 263 (1975).
Raff, W. K., F. Kosche, W. Lochner: Extravascular coronary resistance and its relation to micro-circulation. Amer. J. Cardiol.29, 598 (1972).
Reid, J. V., C. J. Baghat: Effect on coronary flow atrial contraction. S. Afr. J. med. Sci.40 (4), 117 (1975).
Sabiston, D. C., D. E. Gregg: Effect of cardiac contraction on coronary blood flow. Circulation15, 14 (1957).
Saito, D., S. Haraoka, M. Ueda, T. Fujimoto, H. Yoshida, Y. Ogino: Effect of atrial fibrillation on coronary circulation and blood flow distribution across the left ventricular wall in anesthetized open-chest dogs. Jap. Circulat. J.42, 417 (1978).
Schütz, E.: Über den Einfluß des intraventrikulären systolischen Druckes auf die Koronardurchblutung. Z. Kreislaufforsch.45, 708 (1956).
Skinner, N., J. J. Mitchell, A. G. Wallace, S. J. Sarnoff: Hemodynamic consequences of atrial fibrillation at constant ventricular rates. Amer. J. Med.36, 342 (1964).
Stock, E., A. Goble, G. Slomen: Assessment of arrhythmias in myocardial infarction. Brit. Med. J.1967/II, 719.
Tauchert, M., B. E. Strauer, H. W. Heiss, K. Kochsiek: On the influence of atrial fibrillation on coronary hemodynamics in patients with mitral stenosis. Europ. J. Clin. Invest.1, 393 (1971).
Wegria, R., C. W. Frank, G. A. Misrahy, R. S. Sioussat, L. S. Sommer, G. H. McCormack: Effect of auricular fibrillation on cardiac output, coronary blood flow and mean arterial blood pressure. J. Clin. Invest.29, 851 (1956).
Wegria, R., R. P. Keating, H. P. Ward, F. Dreyfuss, C. W. Frank, M. R. Blumenthal: Effect of auricular fibrillation on coronaly blood flow. Amer. J. Physiol.160, 177 (1950).
Wiggers, C. J.: The interplay of vascular resistance and myocardial compression in regulating coronary flow. Circulat. Res.2, 271 (1954).
White, C. W., R. E. Kerber, H. R. Weiss, M. L. Marcus: The effects of atrial fibrillation on atrial pressure-volume and flow relationships. Circulat. Res.51, 205 (1982).
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The paper was supported by the Deutsche Forschungsgemeinschaft (Wi 596/2)
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Wichmann, J., Ertl, G., Rudolph, G. et al. Effect of experimentally induced atrial fibrillation on coronary circulation in dogs. Basic Res Cardiol 78, 473–491 (1983). https://doi.org/10.1007/BF01906459
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DOI: https://doi.org/10.1007/BF01906459