Anoxia has been compared with ischaemia. The abrupt restoration of either oxygen or flow may accelerate cardiac damage. Anoxic stimulation of glycolysis (Pasteur effect) is inhibited during ischaemia by lactate and proton accumulation at the levels of phosphofructokinase and glyceraldehyde-3-phosphate dehydrogenase. Anaerobic glycolysis provides lactate and ATP; breakdown of the latter provides protons. During partial respiration thought to occur in partial ischaemia, continued production of CO₂ is a factor contributing to intracellular acidosis; mitochondrial ATP when formed by continued respiration also yields protons when ultimately broken down. The endproducts of aerobic glycolysis (pyruvate and NADH) are transported into the mitochondria by the malate-aspartate cycle and by pyruvate dehydrogenase activity. Adenine nucleotide transferase activity normally transfers the mitochondrially-made ATP to the cytoplasm, but acyl CoA accumulates in ischaemia (or during perfusions with high circulating free fatty acids) to inhibit the transferase. The mitochondrial creatine kinase is thought to transform ATP transported outwards into creatine phosphate which can permeate the outer mitochondrial membrane. Further compartmentation of ATP may be by other creatine kinase isoenzymes or in relation to the cell membrane. The glycogenolytic-sarcoplasmic reticulum complex links a glycogen pool to the sarcoplasmic reticulum. Cyclic AMP may regulate admission of calcium to the cell during the plateau of the action potential and promote calcium uptake by the sarcoplasmic reticulum by phosphorylation of phospholamban. The latter promotes the activity of the calcium-transport ATPase. Calcium and cyclic AMP may also interact at the level of the contractile proteins where cyclic AMP phosphrylates troponin. Cyclic GMP generally has opposite effects to cyclic AMP and undergoes opposite changes in the frog cardiac cycle to those of cyclic AMP. At present it is reasonable to suppose that physiological effects of adrenaline or of cholinergic agents on the myocardium are mediated by cyclic AMP or cyclic GMP, respectively, but this hypothesis still lacks firm support. There is an association between tissue cyclic AMP and ventricular fibrillation after coronary ligation, and direct evidence for a role of cyclic AMP in promoting arrhythmias has been obtained by studies on the ventricular fibrillation threshold in the rat heart. However, there are other mechanisms, involving first the effects of substrates on the action potential duration, and secondly, the fast channel, which can also give rise to the development of malignant arrhythmias.

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Attempts have been made to demonstrate that the presence of coronary collateral development can preserve and improve the regional contractile force in the ischemic myocardium. Studies were carried out in dogs with developed collaterals and in control dogs. Contractile force was measured with strain-gauge sutured onto the ischemic and the border areas of the myocardium. After ligation of the anterior descending coronary artery, an augmentation of coronary collateral flow via the left circumflex artery was carried out by means of infusion pump up to two and a half fold level. In dogs with developed collaterals, contractile force decreased by 57.6±11.1% (p<0.01) in the ischemic area and 27.2±5.4% (p<0.01) in the border area after coronary ligation. The marked recovery of contractile force up to 63.5±20.4% (p<0.05) of control level in the ischemic are and 70.4±20.4% (p<0.01) in the border are was observed by the augmentation. In control dogs, however, contractile force decreased by 93.2±17.2% (p<0.01) in the ischemic area and 24.6±5.5% (p<0.01) in the border area after the ligation. The augmentation of coronary flow did not recover the depressed contractile force in both areas. These results indicated that the beneficial effect was observed only when the ischemic area was supplied by developed collaterals and closely correlated with the extent of coronary collateral development.

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The effects of diltiazem hydrochloride, a new Ca⁺⁺ antagonistic antianginal drug, on the cardiac conductivity were evaluated in 10 patients with atherosclerotic heart disease. His bundle electrograms were obtained by catheter technique. R-R, A-H and H-V intervals were measured before and after intravenous administration of diltiazem. Diltiazem acted towards significant prolongation in A-H interval. R-R and H-V intervals were insensitive to diltiazem. Diltiazem did not interrupt the cardiac effects of atropine when A-H prolongation was still observed in the subject pretreated with atropine. In short, diltiazem depresses the conductivity of the atrioventricular node selectively and this is not mediated through vagus tone change. This Ca⁺⁺ antagonist induced A-H prolongation strongly suggests the contribution of Ca⁺⁺ current on the generation of atrioventricular nodal action potential in humans.

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The conduction system of 14 autopsied hearts with complete AV block, was examined with the serial sectioning method and the following results and conclusions were obtained. (1) The lesion at the upper AV conduction system covering from the AV node and its approaches to the proximal branching portion of the bundle of His mainly corresponded to the complete AV block with narrow QRS complex (5/6). On the contrary, the lesion at the lower AV conduction system in or distal to the branching portion of the bundle of His fully corresponded to the complete AV block with wide QRS complex (8/8). (2) An exceptional case had the lesion at the distal penetrating portion of the bundle of His which corresponded to the complete AV block with wide QRS complex and the complete right bundle branch block with left axis deviation during sinus rhythm. This case could be explained by the anatomical longitudinal dissociation in the bundle of His. (3) Correlation of the HBE and histological findings was studied in 4 cases. There were 2 cases with AH block and narrow QRS configuration; one case had the lesion in the AV node and its approaches and the other had the lesion at the proximal branching portion of the bundle of His. There were 2 cases with HV block and wide QRS complex; one case had the lesion at the branching portion of the bundle of His and the bundle branches and the other had the lesion only at the bundle branches. (4) In EKC, the so-called "trifascicular blocks" pattern was observed in 6 cases. Three among the 6 cases had main lesions of the bundle branches. An one case among the 6, had coexisting lesions at both the portions of the bundle of His and the bundle branches and the remaining one had the lesion at the distal penetrating portion of the bundle of His. (5) Moderate to severe reduction of the conducting cells lesion was observed in some level in the AV conduction system in all case studied. Especially severe reduction of conducting cells was observed in all case having permanent complete AV block with long duration. (6) Etiologies of the complete AV blocks were assumed as follows; 6 senile degeneration type, 3 acute myocardial infarction, 2 chronic ischemia, 1 congenital malformation, 1 metastatic neoplasm and 1 of uncertain cause.

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A 16-years-old girl with myocarditis and hepatitis in the course of mycoplasma pneumoniae infection was reported. She had fever and coughed for ten days prior to admission. At the time of admission infiltrations of the left lower lung field were revealed on the chest X-ray films. The ESR was elevated and CRP⁺⁶. There were no leukocytosis and anemia, but S-GOT, S-GPT and LDH were moderately increased. On the 11th day of admission VPC in bigeminy appeared and the third sound was heard. Subsequently biphasic and inverted T waves in leads V2 and V3 and flattening of T waves in leads III and aVF appeared. At the same time, the cardiac shadow was enlarged. Antibody titer to mycoplasma pneumoniae increased to more than 1 : 640 two weeks after admission and then it decreased gradually. The cold agglutinin test was 1 : 64 on the 8th day of the disease and then it became normal. ASO, antibodies to DNA and immunoglobulins were normal; ANA, Coombs test and LE test were negative. The abnormal ECG-findings were normalized three months later.

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A necropsy of a 21-year-old male with isolated stenosis of the pulmonary artery was presented. The pulmonary artery branches showed various fibrous thickening including atheromata and mural thrombi. Those findings appeared mostly in elastic and large muscular pulmonary arteries as well as in medium sized arteries, while the small arteries and arterioles remained in slight changes. Systemic large elastic arteries seemed to be small and showed atheromatous lesions similar to those of the main pulmonary arteries. Moreover, eight autopsy cases with pulmonary artery stenosis form the literature were shortly reviewed and some pathological findings as an aid for angiographic cardiovascular studies were discussed.

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