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Current costs in AF patients are driven by the consequences of AF, while costs for specific treatments for AF are low. The addition of new, effective and safe treatment options could potentially reduce overall healthcare costs in AF.

Residual blood flow in pigs (n = 8) and dogs (n = 11) was measured by tracer microspheres (85Sr) 1 hour after occlusion of the left anterior descending coronary artery (LAD). Collateral blood flow was distinguished from overlap flow, defined as the blood flow of non-ischemic myocardium interdigitating into the ischemic area, by direct LAD injection of isotope-labelled microspheres (125I) prior to ligation. In the center of the acutely ischemic pig myocardium the residual blood flow, i.e., the myocardial perfusion remaining after LAD occlusion, was 0.01 +/- 0.01 ml/min/g subendocardially and 0.02 +/- 0.01 ml/min/g subepicardially , as estimated with 85Sr-labelled microspheres. These values were significantly lower than the corresponding values for the dog, 0.13 +/- 0.05 ml/min/kg (p less than 0.05) subendocardially and 0.28 +/- 0.08 ml/min/g (p less than 0.01) subepicardially . In the lateral aspects of the ischemic area, calculations of overlap flow were made with the aid of the distribution of the microspheres injected into the LAD. Values of the residual blood flow were normalized and non-ischemic myocardial perfusion was set to 100 units. In subepicardial layers of the myocardium with calculated overlap flows corresponding to 20, 50 or 80 units, respectively, the residual blood flow (overlap flow + collateral flow) actually measured in the pig was 31 +/- 4, 55 +/- 4 and 75 +/- 7 units and in the dog 65 +/- 6, 79 +/- 5 and 91 +/- 2 units. The values for the dog were significantly different from the respective value for the pig (p less than 0.01). In the subendocardial layers the difference between the two species regarding residual blood flow was similar, although the difference was statistically significant only for myocardium with a calculated overlap flow of 80 units. When the calculated overlap flow was subtracted from the measured residual blood flow, the collateral blood flow was found to be extensive in the dog and virtually absent in the pig. When, in the dog, the collateral blood flow across the lateral border of the ischemic area was related to the amount of myocardium it supplies, it was found to be homogeneously distributed. Thus neither subendocardially nor subepicardially could a gradient of collateral blood flow be detected. It is concluded that in the pig the collateral blood flow is almost nil throughout the acutely ischemic myocardium, both in subendocardial and subepicardial layers. In contrast, the dog has an extensive collateral flow. No lateral gradient of this collateral blood flow could, however, be detected.

Left coronary artery ligation was performed in pentobarbitone anaesthetised rats. Following 1/2 and 2 1/2 h of coronary artery occlusion or sham-operation the right and left ventricular myocardium and the interventricular septum were analysed for tissue content of catecholamines. In control rats and in rats with coronary artery ligation for various time periods (1/2, 2 1/2 and 5 h), the Hillarp-Falck fluorescence histochemical technique was used to visualise the catecholamines of the ventricular myocardium. The tissue noradrenaline content of the left ventricle was markedly reduced after 2 1/2 h of ischaemia while noradrenaline levels in the other parts of the ventricles were unaffected. The adrenergic innervation of the normal rat ventricles is described for the purpose of comparing the normal innervation picture with the appearance after ischaemia. A reduced catecholamine fluorescence was found mainly in the centre of the left ventricular free wall 30 min after coronary artery occlusion. After 2 1/2 and 5 h large areas of the ischaemic myocardium were found to be completely devoid of fluorescent terminals. The border zone between the areas of fluorescence disappearance and normally innervated myocardial tissue was generally quite sharp and occasionally terminals with a diffuse appearance were found in this zone. It is concluded that coronary artery ligation caused a time-dependent loss of noradrenaline from the adrenergic nerve terminals in the ischaemic myocardium. Catecholamine thus released may activate myocardial adrenoceptors and hence be related to increased ischaemic damage and ventricular arrhythmias.

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