Atrial filling fraction obtained by left ventricular echocardiogram (AFF by LV echo) is considered to be a reliable measure of AFF of LV. However, in patients with LV asynergy, AFF by LV echo cannot be evaluated correctly by this method. To obtain AFF, we devised a new echocardiographic index of AFF, obtained from the aortic-left atrial echogram (AFF by Ao echo), and examined the significance of this index in 9 normal subjects (Normals) and 49 patients with various heart diseases. The correlation between AFF by Ao echo and left ventricular end-diastolic pressure (LVEDP) also was examined. In an additional 20 patients with acute myocardial infarction (acute MI), the relationship between AFF by Ao echo and pulmonary arterial end-diastolic pressure (PAEDP) was studied for several days following the onset of MI. Results were as follows: 1) In Normal patients and patients without asynergy, a significant correlation was seen between AFF by LV echo and AFF by Ao echo (r=0.710, p < 0.001). The value of AFF by Ao echo was always greater than that by LV echo. 2) AFF by Ao echo in patients with hypertensive heart disease (HHD), angina pectoris (AP) and old myocardial infarction (old MI) was significantly higher than that in Normal patients. 3) A significant curvilinear correlation was seen between AFF by Ao echo and LVEDP (r=0.673, p < 0.005). 4) In patients with acute MI, AFF by Ao echo correlated well with PAEDP. Therefore, AFF by Ao echo, a newly devised parameter, may be a useful, convenient and non-invasive index for estimating actual AFF and for evaluating the day to day changes of LV end-diastolic performance in acute MI.

View full abstract

By definition, the pulmonary "venous" system consists of the pulmonary veins and the left atrium. The stiffness of the pulmonary "venous" (P'V') system and the left ventricle (LV) at the end of the slow filling period (at the point of pre-a) were estimated sequentially in a total of 26 patients, divided into a control group and mitral stenosis (MS), angina pectoris (AP), hypertrophic cardiomyopathy (HCM) groups. The stiffness (ΔP/ΔV) of the P'V' system was estimated from the pulmonary artery wedge (PAW) pressure tracings and the stroke volume. The stiffness (dP/dV) of LV was obtained from the pressure-volume (P-V) relationship of LV with a model of P = be^aV. The present study is aimed primarily at obtaining factual information. The stiffness of the P'V'system was 0.063 ± 0.022 mmHg/ml (mean ± SD) in the control group and 0.052 ± 0.006 mmHg/ml in the HCM group (p > 0.1). The stiffness of LV in diastole was 0.091 ± 0.016 mmHg/ml in the control group and 0.199 ± 0.056 mmHg/ml in the HCM group (p < 0.01). The ratio of the stiffness of LV in diastole to that of the P'V' system was 1.6 ± 0.6 in the control group and 3.8 ± 0.7 in the HCM group. The volume elastic constant (a) of the P'V' system was 0.008 ± 0.005 ml^-1 in the control group and the values of (a) occupied a range of 0.007 to 0.008 ml^-1 in the remaining 3 groups of patients. The values of (a) of LV were 0.011 ± 0.004 ml^-1 in the control group and 0.022 ± 0.007 ml^-1 in the HCM group (p < 0.01). The present study suggests that the P'V' system is usually 2 to 3 times more compliant than LV in diastole. On the other hand, the P'V' system remained compliant in spite of the decreased compliance of LV in diastole in the HCM group, maintaining the reservoir function with which pulmonary edema is prevented.

View full abstract

An attempt was made to analyze bifid T waves which appeared in different clinical conditions. Bifid T waves occured in 16% of 600 normal children, 92% of 37 cases of childhood ventricular septal defect (VSD), 6 of 10 cases of tetralogy of Fallot (children) and 33% of 193 patients with cerebrovascular accidents (including 3 children). Sixteen cases of bifid T waves which appeared after amiodarone treatment were also analyzed. It was thought that in normal children, bifid T waves might be due to right ventricular preponderance. In VSD, the bifid T waves assumed a peculiar "dome and dart" appearance. In cerebrovascular accidents, autonomic imbalance might be at fault. In cases of treatment with adriamycin, myocardial toxicity is the most probable cause. The conclusion was made that bifid T waves can appear in different clinical settings, which must be considered individually.

View full abstract

The inhibitory effects ofβ-blocking agents against the action of phospholipase (PLase) were investigated. Using micelles of dimyristoyl (-)-α-phosphatidylcholine (DMPC) as a substrate, myristic acid (MA) released from DMPC by PLase A₂ was determined by gas chromatography. β-Blocking agents were divided into 4 groups depending on their inhibitory effects on PLase. Their inhibitory effects on PLase could be due to their displacing ability with Ca⁺⁺ on membrane phospholipids, since Ca⁺⁺ is an essential factor for the activation of PLase.

View full abstract

Prostacyclin (PGI₂) generation has been known to be regulated by several endogenous vasoactive substances, and in this study the relationship between angiotensin I-converting enzyme (ACE) related substances and PGI₂ generation was investigated using cultured human vascular endothelial cells. Addition of angiotensin I(AI) or bradykinin(BK) enhanced PGI₂ generation and increased the level of ACE activity in the culture medium, while the addition of ACE inhibitor (captopril) caused a dose dependent suppression of PGI₂ generation and ACE activity. The enhancement of PGI₂ generation induced by AI or BK was not affected by pretreatment with captopril, and angiotensin II(AII) did not show any effect on either PGI₂ generation or ACE activity. Through these experimental results, the conversion of AI to AII by ACE was considered not to cause the enhancement of PGI₂ generation. Captopril solely inhibited PGI₂ generation and the reported hypothesis that captopril enhances PGI₂ generation by the accumulation of AI or BK via inhibition of ACE was not confirmed in this experimental system. Rather, it is proposed that AI or BK induced PGI₂ generation may be regulated by the increased breakdown of AI or BK, as an autoregulation mechanism, that is derived from increased ACE activity by AI or BK.

View full abstract

By measuring ECG ST segment deviation and regional mechanical dysfunction, we assessed the effects of an alteration in afterload pressure on regional myocardial ischemia due to a partial coronary occlusion of the left circumflex coronary artery (CFX). Eight isolated, perfused and paced dog hearts were loaded with an artificial arterial system which simulated the aortic input impedance of the dog arterial tree. Afterload pressure was altered by stepwise changes in peripheral resistance (Rp), while left ventricular end-diastolic pressure (LVEDP) and heart rate were kept constant. Coronary perfusion pressure (CPP) was kept equal to mean aortic pressure (AoP). ECG and myocardial systolic segment shortening (SS) were measured in both areas perfused by the CFX and the left anterior descending coronary artery (LAD). In the presence of CFX stenosis, mean AoP decreased from 96 ± 7 to 46 ± 7 mmHg following a decrease in Rp and cardiac output increased progressively from 465 ± 30 to 1055 ± 100 ml/min. In this situation, CFX coronary blood flow decreased from 75 ± 2 to 28 ± 6 ml/100g/min. Epicardial CFX stenosis: ST segment elevation and ST segment degression. Moreover, following afterload reduction, these individual ECG ST segment changes showed further deviations. The levels of mean AoP, below which further ST segment deviations significantly occurred, were as follows: 71 ± 6 mmHg in ST segment elevation cases and 52 ± 7 mmHg in ST segment depression cases. Myocardial systolic segment shortening in the ischemic region also significantly decreased following CFX stenosis (91 ± 8% of pre-ischemic control, p < 0.05). Then, during afterload reduction, SS in the CFX area appeared to be bimodal and it definitely decreased when mean AoP was 46 ± 7 mmHg. To enhance the sensitivity of detection of further mechanical dysfunction throughout afterload reduction following regional myocardial ischemia, we calculated percentage values of the SS in the CFX area to the SS in the LAD area at each Rp. By this normalization, mechanical dysfunction was found when mean AoP was below 67 ± 5 mmHg. These results suggest that reduction in afterload pressure below a certain level aggravated the regional ischemia, despite an increase in cardiac output, and to detect this change in the ischemic region during afterload reduction, ECG ST segment deviation seems to be a useful indicator. On the other hand, unless the normalization for systolic segment shortening is performed, regional myocardial mechanical dysfunction in the ischemic area would not necessarily be a sensitive indicator for detecting the worsening of myocardial ischemia.

View full abstract

The Wistar rat, with a blood pressure range of 120-160 mmHg, and two strains of spontaneously hypertensive rats (SHR), stroke-prone (SHRSP, range 210-270 mmHg) and stroke-resistant (SHRSR, range 160-240 mmHg), were used to determine the degree of damage after ischemic insult induced by bilateral carotid artery ligation (BLCL). The survival rate and McGraw Stroke Index correlated well with the degree of hypertension. After BLCL, impairment of cerebral blood flow is abrupt and residual flow is near zero in rats with initial blood pressures greater than 200 mmHg. A markedly deteriorated aerobic metabolism, as measured by the concentrations of ATP, c-AMP and lactate, is seen to precipitate in rats with initial blood pressures greater than 180 mmHg and severe edema occurs if the pressure is more than 160 mmHg. The degree of hypertension that produces high vulnerability to stroke and severe damage to the brain after ischemic insult is indicated as beginning at about 180 mmHg.

View full abstract

The effect of plasma potassium concentration on the vascular response to the pressor agent angiotensin II (ANG II) and to the depressor agent prostaglandin E₂ (PGE₂) was investigated in dog kidney. Renal vascular reactivity to the vasoactive agents was assessed from the change in renal blood flow (RBF) after infusion of the agent into the renal artery. Plasma potassium concentration was increased by intravenous infusion of potassium L-asparate solution. The vascular response to ANG II was attenuated when plasma potassium was increased, i.e. percent decrease in RBF produced by ANG II (26.1 ± 8.4%) during potassium infusion (plasma K⁺, 5.68 ± 0.31 mEq/L) was significantly lower than those (35.8 ± 9.8, 30.4 ± 7.8%) obtained in the control period (plasma K⁺, 3.60 ± 0.40 mEq/L) and in the postinfusion period (plasma K⁺, 4.70 ± 0.42 mEq/L). On the other hand, the vascular response to PGE₂ showed a tendency to be potentiated by elevation of plasma potassium concentration, i.e. percent increases in RBF produced by PGE₂ were 44.9 ± 10.5% in the control period (plasma K⁺, 3.47 ± 0.25 mEq/L), 50.5 ± 6.8% during potassium infusion (plasma K⁺, 5.45 ± 0.25 mEq/L) and 44.9 ± 7.2% in the recovery period (plasma K⁺, 4.55 ± 0.21 mEq/L). These changes in the vascular response obtained by elevation of plasma potassium appear to act towards lowering blood pressure.

View full abstract

Effects of the intracerebroventricular (IVT) infusion of a subpressor dose (3 ng/kg/min) of angiotensin II (ang II) on the pressor responses to intravenous (IV) infusions of ang II and to IV bolus injections of norepinephrine (NE) were studied in conscious rats. This study was undertaken to determine whether activations of the brain renin-angiotensin system alter pressor responsiveness to IV infusions of ang II and IV injections of NE in the conscious state. Pressor responses to IV infusions of ang II and IV injections of NE were potentiated by the concurrent IVT infusion of the subpressor dose of ang II. Plasma renin activity (PRA), plasma corticosterone (B), and plasma prolactin concentration (PRL) were also measured before and during the IVT infusion of the subpressor (3 ng/kg/min) or the pressor (50 ng/kg/min) dose of ang II in order to determine the mechanisms for this pressor hyperresponsiveness to vasoconstrictor substances. The IVT subpressor dose of ang II increased PRA, but did not significantly change B and PRL. The IVT pressor dose of ang II decreased PRA and increased B, but did not significantly change PRL. These results suggest that the brain renin-angiotensin system plays an important role in pressor responsiveness to IV ang II and NE. Although the mechanisms are not fully understood, pressor hyperresponsiveness to IV ang II and NE by an intracerebroventricularly administered subpressor dose of ang II may be related to increased sympathetic outflow, because of the increment in PRA.

View full abstract

In a 64-year-old male, recurrent syncope, hypotension and bradycardia developed repeatedly. The systolic blood pressure fell and could not be measured by auscultation method and the heart rate decreased to under 20 bpm. He recovered from unconsciousness in several minutes. No precipitating cause was apparent for such episodes. Physical examination revealed swollen lymph nodes in the upper cervical regions .Carotid sinus massage caused a fall of systolic blood pressure by 40 mmHg and the P-P interval lengthened to 1.96 sec. The otolaryngeal examination showed neoplasma in the pharynx. He received irradiation therapy on the primary lesion and the bilateral metastatic lesions. After irradiation (4, 000 rad), the paroxysmal hypotension and bradycardia disappeared concomitantly with the reduction in size of the metastatic tumor. Hypersensitiveness to carotid sinus massage, however, remained unchanged. In this case, the metastatic tumor around the carotid sinus seemed to be related to the syncope and the hemodynamic collapse.

View full abstract

A female patient had recurrent sustained ventricular tachycardia (VT) as a late sequela after complete repair of tetralogy of Fallot, and the clinically documented VT could be induced and terminated in a reproducible manner by programmed stimulation. VT was accompanied by fragmented electrical activities when the electrode was positioned at the outflow tract of the right ventricle where myotomy was added on the previous scar. The electrophysiological study revealed that the mechanism of VT was re-entry and that the focus of VT was located at the right ventricular outflow tract.

View full abstract