1979
DOI: 10.1016/0002-9149(79)90055-9
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Biochemical aspects of arrhythmogenesis and ventricular fibrillation

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1981
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Cited by 181 publications
(31 citation statements)
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“…Raised cAMP concentrations result in an increase in intracellular calcium which may exacerbate ischemia. 21 Levosimendan, with its negligible effect on myocardial oxygen demand, is better tolerated by patients with ischemic cardiomyopathy, as demonstrated by an open-label dosecontrolled study in patients with AMI. 22 Moreover, a recent study demonstrated that levosimendan is safe in patients with acute coronary syndromes who underwent a percutaneous coronary intervention (PCI) and improves the function of stunned myocardium.…”
Section: Discussionmentioning
confidence: 97%
“…Raised cAMP concentrations result in an increase in intracellular calcium which may exacerbate ischemia. 21 Levosimendan, with its negligible effect on myocardial oxygen demand, is better tolerated by patients with ischemic cardiomyopathy, as demonstrated by an open-label dosecontrolled study in patients with AMI. 22 Moreover, a recent study demonstrated that levosimendan is safe in patients with acute coronary syndromes who underwent a percutaneous coronary intervention (PCI) and improves the function of stunned myocardium.…”
Section: Discussionmentioning
confidence: 97%
“…Nevertheless, the decrease in the amplitude of MAP is probably caused by the decrease in the resting potential, because the amplitude of MAP markedly decreased at T4 after verapamil. It has been reported that acidosis and several metabolic factors besides K+ accumulation in the extracellular space also contribute to electrical abnormalities during ischaemia (Dower et aL, 1977a;Vogel & Sperelakis, 1977;Carmeliet, 1978;Opie, Nathan & Lubbe, 1979;Hill & Gettes, 1980;Morena, Janse, Folet, Krieger, Crijns & Durrer, 1980). Therefore, it is probable that verapamil attenuated these metabolic changes resulting in the inhibition of ST-T alternans and conduction abnormalities.…”
Section: Discussionmentioning
confidence: 99%
“…The development of ventricular fibrillation is strengthened by the difference between the duration of the refractory period and irregular electrical activity in the various parts of the heart. The probability of the development of such irregular activity is increased by an increased resting excitability, a decreased conduction velocity, and an increase in automaticity (Fisch, 1973;Opie et al, 1979;Carmeliet, 1988). The resistance of the heart to these disorders is dependent on its electrical stability, which can be measured by several parameters such as the duration of the vulnerable period (Wegria et al, 1941;Axelrod et al, 1975), ventricular flutter threshold (Szekeres & Papp, 1967), excitability threshold (Jones & Klein, 1982), or ventricular fibrillation threshold (Wegria et al, 1941;Gerst et al, 1966).…”
Section: Introductionmentioning
confidence: 99%
“…The vulnerable duration period was prolonged during hypoventilation. These disorders can be explained by a sudden increase in extracellular K + concentration, which plays a crucial role in the changes in resting membrane potential, and can produce ectopic activity as well as inhibition of the rapid reaction (Opie et al, 1979). The rapid increase in extracellular K + concentration is the result of K ATP channel activation.…”
mentioning
confidence: 99%