[Problem of differential therapy of arrythmias in acute myocardial infarct].
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Biomedical subjects
Publications and source records attributed to W Meesmann.
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Epicardial electrocardiographic maps were used to assess the effect of heart rate, myocardial contractility, and oxygen need on the severity of myocardial ischaemic injury after acute coronary artery occlusion in dogs. The experimental data indicate statistically significant dependence of the severity of ischaemia on heart rate, contractility, and oxygen need of the heart. These dependences are highly influenced by the spontaneous collateral vessels of the heart.
Fibrillation threshold (FS) were determined in 27 mongrel dogs by direct electrical stimulation of the myocardium by 50 Hz AC impulses of 0.20-0.28 sec during the vulnerable period. The FS is the current which just suffices to produce ventricular fibrillation. Sinus rhythm was restored 10 sec after onset of ventricular fibrillation by defibrillation. Determinations of FS were carried out for each animal repeatedly before and 3 min after acute ligation of the circumflex ramus respectively the descendens ramus of the left coronary artery. Post mortem selective coronary angiography was performed in all cases and the extent of spontaneous collateral vessels was estimated by the rate of retrograde contrast radiography of the ligated coronary artery. The FS fell appreciably following acute ligation of both the circumflex ramus and the sescendens ramus. Beside the size of the ligated area (the circumflex ramus supplies a larger area of the myocardium in the dog than the ramus descendens) the extent of collateral supply was the determining factor for the reductions of the FS: Following coronary ligation of the circumflex ramus the FS fell on the average from 24.0 mA to 4.1 mA if no collateral vessels were detectable; in the animals with well developed collaterals the FS was reduced from 24.8 to only 14.1 mA. After acute occlusion of the descendens ramus the FS fell from 27.9 mA to 11.5 mA in the group with not sufficient collateral supply and from 31.2 mA to only 21.5 mA in the group with well developed collaterals. The comparison of the different decreases of the FS after coronary occlusion clearly shows that the influence of the in size differing ischemic areas on the decrease of the FS is particularly evident if no collateral vessels are existent. If collateral vessels are well developed this difference is not significant. These results demonstrate that the influence of well developed collaterals on the decrease of the FS after coronary occlusion exceeds the dependence on the size of the ischemic area.
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In animals without myocardial infarction the new beta-sympathicolytic agent atenolol (4-[2'-hydroxy-3'-iso-propylaminopropoxy]-phenyl acetamide, ICI 66 082) dose-dependently decreased heart rate, systolic aortic pressure and cardiac output. Coronary mean flow, coronary resistance, stroke volume, left ventricular enddiastolic pressure and total peripheral vascular resistance did not change significantly. Atenolol significantly reduced myocardial contractility, expressed by (dp/dtmax), Vpm, t-(dp/dtmax) and pre-ejection period. Furthermore, the comparative studies in animals with myocardial infarction and concomitant reduced cardial efficiency revealed, that atenolol has neither a positive intrinsic activity as has practolol nor a negative intrinsic activity as has propranolol. The dose-contractility relation of atenolol resembles that of practolol: in low dosages a strong decrease is achieved, in higher dosages no further reduction of the contractility parameters is observed. Because of the strong negative inotropic and blood pressure lowering effect it is suggested to use atenolol only with great caution in patients with reduced cardiac efficiency.
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