Echocardiographic studies were performed on 3 patients with torn chordae tendineae of the mitral valve proven by open heart surgery or during autopsy. Mitral regurgitation was noted after episodes of bacterial endocarditis in 3 patients ; one had had rheumatic valvular disease before the episode. Conventional M-mode echocardiograms showed coarse diastolic fluttering of the mitral valve, multiple mitral valve echoes in systole, and diastolic mid-echoes between both anterior and posterior leaflets. The last pattern was found in all 3 patients. There was only one patient with an unusual systolic echo in the left atrium. Two-dimensional echocardiograms from 2 patients revealed an abnormal echo in the left ventricle in diastole which moved into the left atrium in systole, slightly beyond the closure line of the mitral valve. This moving abnormal echo observed in two-dimensional echograms presumably originated from torn chordae tendineae and was consistent with the diastolic mid-echo noted in M-mode echograms. Thus, the diastolic mid-echo of the mitral valve by M-mode echocardiography is an important finding in the diagnosis of torn chordae tendineae of the mitral valve, and two-dimensional echocardiography can identify the movement of torn chorda itself.

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This study was done to evaluate the quantification of thallium-201 myocardial perfusion imaging (MPI) for the detection of coronary artery disease (CAD). Segmental analysis of stress and delayed MPI was performed in 33 patients with angiographically proved CAD. They were divided into two groups : 22 patients without previous infarction (Group 1) and 11 patients with prior myocardial infarction (Group 2). Using computer analysis of MPI, 9 region-of-interests (ROIs) were set on the left ventricular image. We defined 3 indices as follows : initial uptake (%) = a ratio of ROI counts to the highest ROI counts on the exercise image ; washout rate (WR) = a ratio of [(ROI counts of the exercise image) - (those on the delayed image)] to those on the exercise image : redistribution index (ROI)= a ratio of the maximal WR to WR. Coronary arteriograms were evaluated according to Pujadas' method. In group 1, the region supplied by the coronary artery with significant stenosis showed a lower initial uptake (p < 0.005) and a higher ROI (p < 0.001) than the region supplied by the coronary artery without significant stenosis. If an initial uptake less than 83% and/or a RDI greater than 1.15 are defined as abnormal, the sensitivity for detecting CAD, including the detection of a stenosis site, was 76% and the specificity was 84%. In group 2, the sensitivity was 76% and the specificity was 80%. The mean WR could also indicate the severity of CAD. In all patients studied., the average of mean WR was 0.451 in one-vessel disease (n=18), 0.446 in two-vessel disease (n=6) and 0.305 in three-vessel disease (n=8). In conclusion, the quantitative evaluation of stress MPI using initial uptake, RDI and WR appear to be useful for noninvasive and objective diagnosis of CAD, particularly in detecting the severity and location of stenotic coronary arteries.

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Platelet aggregation was studied in patients with angina pectoris in whom coronary sclerosis was found by arteriography. The subjects consisted of 20 patients with stable angina pectoris, 12 with unstable angina pectoris and 4 with variant form of angina pectoris. Fifteen healthy subjects served as controls. ADP- and collagen-induced platelet aggregations were estimated during resting conditions before and immediately after an exercise test. In patients with unstable angina pectoris, ADP-induced as well as collagen-induced platelet aggregations during resting conditions were significantly less than those in normal subjects. After exercise, however, they significantly increased. In stable angina pectoris, they did not differ from those in the control group and their responses to exercise were also not significant. In general, platelet aggregation during resting conditions was accelerated in relation to an increase in the number of coronary arteries involved. The results demonstrate that examination of platelet aggregation during resting conditions and following exercise aids in a more accurate evaluation of the types and the stages of patients with angina pectoris.

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A case of cardiac sarcoma was reported. The tumor, which arose from the posterior wall of the left atrium, was demonstrated by echocardiography, contrast-enhanced computed tomography and direct observation during surgery. The tumor was successfully excised under emergency operation and was diagnosed as malignant fibrous histiocytoma after histologic examination. The patient had been free of symptoms for several months, but died of rapidly progressive congestive heart failure 6 months after surgery.

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Definition of and criteria for borderline hypertension were reviewed. Prevalence of borderline hypertension and hypertension combined was estimated to be 12.4 million in Japan. Because of this magnitude, further studies on etiology, mechanism and natural history are warranted to prevent or treat borderline hypertension efficiently.

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The natural history of borderline hypertension was studied in a general population sample of 1, 621 Hisayama residents aged 40 or over, followed for 18 years. The causes of death during the study were verified by postmortem examination in most of the cases. The prevalence of borderline hypertension determined by a single casual blood pressure was almost equivalent at the 3 different cross-sectional surveys (1961, 1973-74, 1978) accounting for approximately 20% of the population. Prospectively, "borderline hypertension" was associated with an intermediate risk of cardiovascular mortality between normotensives and hypertensives. Borderline hypertensives with hypertensive organ damage manifested by left ventricular hypertrophy on electrocardiogram, retinal arterial changes and/or proteinuria, were much more related to cardiovascular deaths than those without. Blood pressure (BP) in persons not prescribed antihypertensive medications was examined at 3- or 6-year intervals during the follow up period, and the relationship of long-term changes in BP to subsequent cardiovascular mortality was determined. After adjusting for age, an elevation of BP to the hypertensive range from borderline was significantly associated with subsequent cardiovascular catastrophe, and a perspective labile BP was less related to that. The later evidence of hypertensive BP values in borderline was strongly correlated with initial BP levels in both systolic and diastolic, and also with old-age at the time of entry. It should also be emphasized that borderline hypertension was much more common than severely hypertensive disease in this community. If control of BP in this category is successful, a large number of cardiovascular deaths can hopefully be prevented, because the population-attributable risk of borderline hypertension is high.

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Among 157 patients with borderline hypertension 33.8% developed established hypertension (H), 28.6% became normotensive (N), and 37.6% still had borderline hypertension (BH) during a 3 to 10 year follow-up period (an average of 6.4 years). Significant differences in the clinical data among these 3 groups at the first examination were observed in systolic blood pressure (SBP), diastolic blood pressure (DBP), age, obesity, known duration of hypertension and SV₁ + RV₅ on an electrocardiogram. Analysis of variance showed that SBP increased with age in both sexes, while DBP of men less than 49 years of age was higher in the H group than in the other groups. Obesity and duration of hypertension appeared to contribute to the later development of hypertension because of a higher blood pressure. Obese men in the H group generally had higher DBP than nonobese patients in the other groups. Men with a longer history of hypertension in the H group also had a higher initial blood pressure. SV₁ + RV₅ in many of the subgroups of the H group was often higher in similar subgroups of the other groups. These inter-subgroup differences may affect the statistical differences in the above-mentioned parameters among the 3 groups. The mean value and standard deviation of SBP and DBP of diurnal blood pressure measurements were in the order of established hypertensives, borderline hypertensives and normotensive subjects when power-normal distribution was applied. There was no evidence that lability of blood pressure was a characteristic feature of borderline hypertension.

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The hemodynamics and the baroreflex function were studied and compared between patients with borderline and established hypertension. 1) As compared to patients with established hypertension, the heart rate, the cardiac output and the left ventricular ejection fraction were higher in patients with borderline hypertension in the young group, but these characteristics were not found in the patients of the middle-aged group. 2) In regard to the cardiac output and the total peripheral resistance, patients with borderline hypertension predominantly shoed a high cardiac output, especially in the young group, while patients with established hypertension predominantly showed a high total peripheral resistance, especially in the middle-aged group. 3) At higher and lower blood pressure levels during one day, no difference of hemodynamic pattern was observed in the same subjects. 4) The hemodynamic response to exercise, isoproterenol and noradrenaline was greatest in the borderline hypertensives of the young group. 5) The baroreceptor slope decreased in the order of normal subjects, borderline hypertensives and established hypertensives. It decreased with age in each group. The hemodynamics and the baroreflex function in borderline hypertensives differed slightly between the young and the middle-aged groups. Although the borderline hypertension in the middle-aged group is considered to be a pre-stage of established hypertension, detailed analysis of case histories may be required to assess how borderline hypertension develops into established hypertension in the young group.

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To evaluate left ventricular (LV) and left atrial (LA) function in patients with borderline and established hypertension, 7 indexes of LV systolic function (cardiac index, end-diastolic volume index, ejection fraction, LV network, mean VCF, Vmax and peak dp/dt), 7 indexes of LV diastolic properties (specific compliance, LV mass index, LV wall thickness, stiffness constant, time constant T, end-diastolic pressure and peak negative dp/dt) and 3 indexes of LA function (volume index, chamber stiffness constant and muscle stiffness constant), all obtained form the data of cardiac catheterization and cineangiogram, were analyzed in patients with normotension (N, n=12), borderline hypertension (BH, n=13) and established hypertension (EH, n=17). LV systolic function was not impaired in the BH and EH groups. In the BH group, LV diastolic function was not affected, but LV wall thickness and stiffness constant were significantly greater in the EH group than in the N group. There was no significant difference in LA volume index among the 3 groups, but a significant increase of LA chamber stiffness constant was found only in the EH group as compared to the values of the N group. On the other hand, LA muscle stiffness constant was significantly greater in the BH group than in the N group, and significantly greater in the EH group than in the BH group. From these results it seemed that LV systolic and diastolic functions were not impaired in patients with borderline hypertension, and that LV systolic function was not affected, but LV diastolic function was possibly impaired in patients with established hypertension. Moreover, it was suggested that LA compliance was impaired already not only in patients with established hypertension, but also in patients with borderline hypertension.

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There has been yet no report, to our knowledge, which clarified the affinity ("sensitivity") of catecholamines to cardiac chronotropic beta-adrenergic receptor or to vasoconstrictive alpha-adrenergic receptor of skeletal muscle resistance vessels in human borderline hypertension (BHT), using an analysis of the kinetics of the drug-receptor interaction. In the first half of this study, isoproterenol (ISO) infusion test was performed on "normal" subjects (n=12) and subjects with BHT (n=10). Dose-response relation was obtained in terms of various doses of ISO and the increments of heart rate (ΔHR) produced by ISO. In the latter half of this study, phenylephrine (PHE) infusion test was carried out in the series of "normal" subjects (n=5) and subjects with BHT (n=6), a partly different series from the first series of subjects. Dose-response relation, again, was obtained in terms of various doses of PHE and the increments of total peripheral resistance (ΔTPR) produced by PHE. These relations were displayed on Lineweaver-Burk's plot and the "affinity" of ISO to cardiac chronotropic beta-receptor or that of PHE to vasoconstrictive alpha-receptor of skeletal muscle resistance vessels was estimated, graphically, assuming that 1)drugs were diluted by a volume of body fluid equal to the blood volume which was actually measured in each individual and 2) this concentration of drugs existed around the receptor site, i.e., there was no significant individual variations in terms of the metabolism and the distribution of the drugs. Estimated "affinity" of ISO to cardiac chronotropic beta-receptor was 0.168 ± 0.014 × 10⁴ ml·ug^-1 (mean ± SE, n=10) in patients with BHT, while it was 0.170 ± 0.015 ×10⁴ (n=12) in "normal" subjects. Estimated "affinity" of PHE to vasoconstrictive alpha-receptor of skeletal muscle resistance vessels was 0.171 ± 0.011 × 10² ml·ug^-1 (n=6) in patients with BHT, while it was 0.183 ± 0.012 × 10² (n=5) in "normal" subjects. It is concluded from these data, almost fairly, that there is no difference in terms of the estimated "affinity" of ISO to cardiac chronotropic beta-receptor or that of PHE to vasoconstrictive alpha-receptor between "normal" subjects and patients with BHT. It was also found, in PHE infusion tests, that the plasma adrenaline concentration was significantly higher in patients with BHT than in "normal" subjects, at least at two points of time in the test : a) immediately before PHE infusion, when every individual appeared to be considerably restful and b) at the end of 1-2 min after the completion of the infusion of the largest dose of PHE used.

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Maximal vasodilator capacity of arteries as well as venous distensibility in the forearm were decreased in young patients with borderline hypertension as compared to those in age-matched normotensive men. These results are consistent with the consideration that there is structural vascular abnormality in arteries and veins in young patients with borderline hypertension.

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Role of neurohumoral factors in borderline hypertension was evaluated in comparison to those in established hypertension. although there was no significant difference in urinary noradrenaline between the 2 groups, urinary adrenaline was significantly higher in borderline hypertension than in established hypertension. During head-up tilt and Schellong's test a significant increase of diastolic blood pressure was demonstrated n borderline hypertension, whereas a significant decrease of systolic blood pressure was observed without any significant change of diastolic pressure in established hypertension. There was no significant difference in blood pressure response to cold pressor test, plasma volume, total body potassium and plasma renin activity (PRA) between the 2 groups. Blood pressure did not change after administration of captopril in normal subjects but it decreased significantly after captopril in patients with borderline hypertension even when blood pressure became normotensive during hospitalization. Blood pressure decreased significantly after captopril in patients with established hypertension. However, no significant relationship between the pretreatment PRA and the reduction of mean blood pressure was observed in both groups. It can be concluded from the present study that borderline hypertension is intermediate between normal subjects and established hypertension and that both the renin-angiotensin system and the kinin-prostaglandin system play some role in the maintenance of blood pressure in borderline hypertension.

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Seventeen patients with borderline hypertension and 11 patients with sustained hypertension were instructed to reduce their salt intake to 5-8 g/day. We checked whether or not the patients were following instructions by estimating their 24-hour urinary sodium excretion (U_NaV). In borderline hypertension, the U_NaV was 5.6 ± 0.4 g/24-hour on a normal salt diet and 3.7 ± 0.3 (p < 0.01) on a salt-restricted diet, while in sustained hypertension it was 4.9 ± 0.3 g and 3.6 ± 0.4 g/24-hour (p < 0.01), respectively. After moderate salt restriction there was a significant fall in blood pressure in the supine, sitting and standing positions in both the borderline and the sustained hypertensives. There was a significant relationship between the fall of mean blood pressure in the supine position and the decrease in the 24-hour urinary soidum excretion, which was corrected for 24-hour creatinine excretion, in overall hypertensive patients (r=0.39, p < 0.05). In the borderline hypertensive group, both the systolic and diastolic blood pressure in the sitting position were 8.7 mmHg or 6.3% (p < 0.01) and 6.2 mmHg or 6.6% lower (p < 0.01) on salt-restricted diets than those on normal salt diets, respectively. In 9 of 14 patients with borderline hypertension, the diastolic blood pressure moved into the normal range during the salt restriction. We suggest that moderate salt restriction is an effective management of borderline hypertension.

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To clarify the possible risk factors for the development of hypertension, we examined the influences of heredity and environment on blood pressure regulation and whether or not the physiological condition differed in high school students with different levels of blood pressure. A borderline hypertensive (BH) group, consisting of 75 male students with systolic blood pressure (SBP) consistently (N) group of 84 male students with SBP below 130 mmHg. In the BH group, 43% of students had a family history of hypertension within two generations of relatives, while 18% had one in the N group (p<0.05). The BH group was characterized by a gain in weight, a slight increase in 24-hour urinary sodium excretion, a higher heart rate, elavated values of plasma renin and urinary aldosterone, and an elevated sodium concentration in erythrocytes. Nevertheless, urinary excretion of potassium and kallikrein did not differ between the two groups. In each group, students with familial hypertension had a significantly (p < 0.05) lower 24-hour urinary kallikrein excretion than those without it. Although kallikrein excretion correlated fairly well with aldosterone excretion (r=0.47, p < 0.01) or creatinine clearance (r=0.59, p < 0.01) in the BH students without familial hypertension, no such correlations were found in those with familial hypertension. These results indicate that the abnormal relationships of aldosterone to kallikrein metabolism and of kallikrein to renal function control may be involved as hereditary factors in the development of hypertension.

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