The diagnostic value of maximum corrected sinus node recovery time (CSNRT) and sinoatrial conduction time (SACT) was assessed in I 5 patients with clinical evidence of sinus node (SN) dysfunction and I 6 control subjects. The SACT was calculated by a modified method using only those sinus cycles with A 1-A 1 intervals falling within one standard deviation of the mean. We also obtained a maximum SACT and a ratio of maximum/mean SACT. We found that the maximum/mean SACT ratio being useful for identifying patients with sinus arrest or sinoatrial block. Abnormal value of the ratio (⩾ 1 .85) was also more frequently observed in patients with syncope or dizzy spells than those without (55.6% vs. 33.3%). By applying mean SACT and maximum/mean SACT ratio, calculated by the modified method, together with maximum CSNRT, all patients with SN dysfunction could be completely isolated from the normal subjects.

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In 20 patients with acute myocardial infarction (AMI), serial Tl-201 myocardial scintigraphy was performed and scintigraphic infarct size (SIS) was determined 1 (or less), 2 and 8 weeks after AMI. Hemodynamic indices were determined with a Swan-Ganz catheter at a mean of 27.7 hours after AMI. Left ventricular ejection fraction (EF) was determined with Tc-99m HSA cardiac blood pool scintigram at 8 weeks after AMI. Mapping ECG was also observed serially. Of 20 patients, SIS decreased in 12, was unchanged in 2 and increased in 5 . No image defect was observed on the initial scintigram in one case. When the patients were classified into two groups, i.e. those with initial SIS more than 25% and those with initial SIS less than 25%, hemodynamic indices were demonstrated to be more markedly impaired in the former than in the latter. However, when all patients were pooled, correlations between the initial SIS and hemodynamic indies (CI, SI, SWI, PADP) were poor. There was a good correlation between SIS and EF both determined 8 weeks after AMI. When the patients were clasified into the improved and unimproved groups according to the per cent change of SIS (CIS), both hemodynamic indies on admission and EF at 8 weeks were better in the improved than in the unimproved group, and especially significant correlation was found between CIS and each of SI and PADP. There was a good correlation between maximum ΣST in mapping ECG and SIS at 1 week after AMI. From these results, it is suggested that a decrease in SIS in serial Tl-201 myocardial scintigrams represents the presence of transiently ischemic area and that serial Tl-201 myocardial scintigraphy performed from the initial stage after AMI may provide a useful information for evaluating the effect of therapeutic intervention and predicting the prognosis.

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A simplified screening test for differentiating primary aldosteronism (PA) from low renin essential hypertension (LREH) is presented. Nine patients with LREH and 5 patients with PA due to adrenal adenoma were studied. In the patients with LREH, the levels of plasma renin activity (PRA) before and after treatment with furosemide (0.7 mg/kg, i.v.) and a 2hour ambulation under treatment with dexamethasone (1.0 mg) (dexamethasone + furosemide test) increased briskly, compared to the levels of PRA before and after treatment with furosemide (0.7 mg/kg, i.v.) and a 2hour ambulation (furosemide test). In patients with PA, there was no significant difference between the mean levels before the furosemide test and before the dexamethasone + furosemide test, or between the mean levels after the furosemide test and after the dexamethasone + furosemide test. These results suggest that the suppression of PRA in patients with LREH may be related to a factor controlled by dexamethasone. It is concluded that the dexamethasone + furosemide test is useful for differentiating PA due to adenoma from LREH.

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According to Schnitker, Mandel, Hirst and their associates, approximately half of the dissecting aneurysms in women under 40 years of age are associated with pregnancy. This significant relationship between dissecting aneurysm and pregnancy has been discussed by considering hemodynamic stress and also the hormonal changes of pregnancy. In this report, we describe five patients with dissecting aneurysm during pregnancy or the puerperium, review the literature and discuss the influence of pregnancy on the pathogenesis of this disease.

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Vectorcardiogram (VCG) was studied in four patients with hypertrophic cardiomyopathy (HCM) with RSR' pattern in right chest leads. In these patients there was an anterior QRS loop with a slow inscription in the initial part of the QRS loop, the pathognomonic initial pig-tail curl pattern was also observed in two patients. Though mid-terminal conduction delay was also observed in two patients, the slowly inscribed terminal QRS vector oriented anteriorly and to the right, thus characteristic of right bundle branch block (RBBB), was not observed. The initial conduction delay was attributed to the conduction disturbance as the result of hypertrophy and disarray of the muscle fiber, particularly in the septal area. The recognition of this VCG pattern provides a pertinent clue in the clinical detection of HCM.

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The aim of this study was to investigate whether insulin-glucose (IG) is able to prevent detrimental systemic and myocardial changes induced in healthy dog by adrenaline (AD) infused at a rate which mimics spontaneous secretion after coronary occlusion. Insulin (0.3 u/kg) and glucose ( 10%, 10 ml/kg) mixture was infused intravenously concurrently with AD (1 .2 μg/kg/min) for 4 h and blood values of FFA, triiodothyronine (T₃ ) immunoreactive insulin (IRI) and glucose measured initially, after 2 and 4 h of infusion were compared with the values found in dogs infused with AD alone and with saline. IG suppressed a rise in FFA, attenuated a fall in T₃, reversed AD-induced histoenzymatic changes in SDH and ATPase activity and completely prevented the development of mitochondrial alterations shown by electron microscopic study. These data provide evidence for usefulness of IG in preventing the consequences of catecholamine excess in acute stage of MI.

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It is known that oxygen inhalation induces coronary vessel constriction as well as brings about a reduction in myocardial oxygen consumption. The present study was performed to clarify whether or not this constriction of the coronary vessels resulting from oxygen is secondary to the reduction in myocardial oxygen consumption. The regional myocardium in 12 mongrel dogs was perfused with femoral arterial blood at a constant rate of flow. While maintaining myocardial oxygen consumption equal by adjusting heart rate, coronary vascular resistance was compared under the two following conditions: 1 ) perfusion of the coronary artery with the dog's own femoral arterial blood (pO₂ : 95±14 mmHg) and 2) perfusion with blood with a high level of oxygen tension (pO₂ : 497±56 mmHg). Coronary vascular resistance was increased (p<0.001) from 3.00±1.25 to 3.36±1.28 mmHg/ml/min by increasing the pO₂ in the perfusing blood, even though myocardial oxygen consumption was kept at the same level. This increase in coronary vascular resistance resulting from the increase in oxygen tension was independent of the coronary perfusion rate as well as independent of the presence or absence of myocardial ischemia. This suggests that coronary vasoconstriction due to oxygen is not secondary to decreases in myocardial oxygen demand.

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The effects of prostacyclin (PGI₂ ) were compared with those of prostaglandin E₁ (PGE₁) on the cardiac hemodynamics (coronary blood flow, systemic blood pressure, cardiac output and max dp/dt of the left ventricle) in closed-chest dogs. Moreover, the effects of PGI₂ were compared with those of PGE₁ on the concentrations of the coronary arterial and myocardial cyclic adenosine 3': 5'-monophosphate (cyclic AMP) and cyclic guanosin 3': 5'-monophosphate (cyclic GMP) in open-chest dogs. The intraventricular and intravenous injection of 0.1 to 4.0 μg/kg of PGI₂ increased the coronary blood flow and decreased the mean systemic blood pressure. Comparison of dose response curves for PGI₂ and PGE₁ in relation to the coronary blood flow indicated that PGI₂ was 4 times as potent as PGE₁ . On the other hand, the effect of PGI₂ on the systemic blood pressure was twice as potent as PGE₁ . The concentration of the coronary arterial cyclic AMP was significantly increased by the administration of PGI₂ and PGE₁ (control group: PGI₂ group was 0.201±0.022 vs. 0.264±0.017 pmoles/mg tissue, p<0.05; control: PGE₁ was 0.201±0.022 vs. 0.286±0.027 pmoles/mg tissue, p<0.05). The concentrations of the coronary arterial cyclic GMP were not significantly changed by the administration of PGI₂ and PGE₁, nor were those of myocardial cyclic AMP and cyclic GMP. The changes in cyclic nucleotide levels and cardiac hemodynamics induced by PGI₂ were qualitatively similar to those induced by PGE₁, but the change caused by PGI₂ was greater than PGE₁ in the coronary and systemic hemodynamics.

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