The purpose of this report is to examine the incidence and etiological classification of the valvular heart diseases in the aged. Among 1, 000 consecutive autopsy, a total of 122 cases (42 men and 80 women) was clinically diagnosed as having valvular disease, who were the subjects of this study. Their ages ranged from 60 to 100 with an average of 78.7 years.
Incidence of valvular disease was 12.2% (122 among 1, 000 cases). Ten cases (8.2%) of mitral stenosis (MS) consisted of 8 cases of rheumatic MS and 2 mitral ring calcification. Thirty-nine cases (32%) of mitral regurgitation (MR) included 28 cases of papillary muscle dysfunction, 4 ruptured chordae tendineae, 4 mitral valve prolapse, 2 mitral ring calcification, and 1 rheumatic etiology. Aortic stenosis (AS) was found in 10 cases (8.2%), consisting of 7 calcified, 2 rheumatic, and 1 congenital (discrete subaortic) stenosis. Aortic regurgitation (AR) was found in 59 cases (48.3%), including 48 degenerative, 8 syphilitic, 1 rheumatic origin, and 2 of unknown aortitis. There were 4 cases (3.3%) of tricuspid regurgitation (TR). Subjective symptoms were present in 64.8%. Incidence of congestive heart failure was 54%, cardiac death 37%, atrial fibrillation 37%, and hypertension was found in 59%.
Combining the previously reported 120 cases and present 122 cases of valvular disease among 2, 000 consecutive autopsy, following conclusions were obtained. (1) Incidence of valvular disease was 12.1%. (2) Valvular heart disease included 18 cases of MS (7.4%), 76 MR (31.4%), 22 AS (9.1%), 122 AR (50.4%), and 4 TR (1.7%). (3) High incidence of MR and AR was noted in the aged, which were mainly related to papillary muscle dysfunction (58% of MR) and degenerative AR (68% of AR), respectively.

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Clinicopathologic correlation studies were performed to clarify the characteristic features of myocardial infarction (MI) in the elderly. A total of 203 cases of MI were found in 1, 000 consecutive autopsy of the aged. There were 113 men and 90 women with an average age of 78.5 years.
There were 117 cases of large MI and 82 fresh MI. With aging, there was a tendency of decrease in ratio of large MI, and increase in middle-sized MI. When coronary stenosis of more than 75% was considered to be significant, there were 97 cases of 3 vessel disease, 51 of 2 vessel dis-ease, and 30 of 1 vessel disease; that is 178 cases (87.7%) showed significant stenosis in at least 1 vessel. Remaining 25 cases of MI had no sig-nificant coronary stenosis. In general, large MI had marked coronary stenosis. Some of the MI without significant coronary stenosis were explained by uncommon pathogenesis such as disseminated intravascular coagulation or atrial fibrillation. Incidence of coronary thrombi was the highest (76.7%) in large and fresh MI.
Electrocardiographic diagnosis was correct in 65% of large fresh MI. Incidence of chest pain was 48% in large acute MI and 27.8% in middle MI, whereas various complications such as shock (60%), congestive heart failure (53.3%), and arrhythmia (65%) were frequently found. Causes of death in large acute MI were arrhythmia in 16 cases, cardiac rupture in 13, and sudden death in 8.
There were 15 cases of cardiac rupture, which occurred within 5 days from the onset of acute MI in all. Site of MI and rupture was anterior in 8, inferior in 5, and lateral in 2, including 1 case of septal perforation in anterior MI. There were 21 cases of papillary muscle dysfunction. From analysis of clinical sequence of MI and mitral regurgitation, 3 types of the syndrome were classified; 15 cases due to old MI, 2 cases due to acute MI, and 4 cases of mitral regurgitation followed by MI. There were 24 cases of conduction disturbances in 82 cases of acute MI (29%). In atrioventricular (A-V) block, site of lesions in conduction system was examined by the serial sections, which was located at the A-V node in 2, A-V bundle in 4, and bilateral bundle branches in 4.

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Left ventricular dimension and function were studied by echocardio-graphy in 28 "non-cardiac" patients with chronic alcoholism. Concentric left ventricular hypertrophy was the prevalent abnormality. Gross hypertrophy with wall thickness exceeding 14mm was seen in 8 patients, and was associated with higher incidence of mild exertional dyspnea and paroxysmal tachyarrhythmia during drinking bouts than in 16 patients with almost normal left ventricle. Left ventricular ejection fraction was decreased in 2 and diastolic descent rate of the anterior mitral valve was decreased in 1 of the hypertrophied left ventricle. The concentric hypertrophy may represent a preclinical stage of alcoholic cardiomyopathy. In addition to the 24 patients with normal sized left ventricular cavity, there were 4 patients with dilated left ventricle and increased wall mass. Left ventricular ejection fraction and mitral valve motion were normal in all the 4, and cardiac output was suggested to be increased. The relations of this type of abnormality to the concentric hypertrophy and to clinical alcoholic cardiomyopathy were obscure.

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A quantitative pathologic study was performed on papillary muscles in 15 cases of chronic rheumatic mitral stenosis. The papillary muscles were grossly hypertrophied as compared with papillary muscles in 10 normal specimens. Hypertrophy of papillary muscles was associated with pronounced fibrosis. Angiographically, these hearts were remarkable in small left ventricular cavity with almost complete cavity elimination at end systole. Left ventricular wall dyskinesia was also present. It is probable that derangement of the mitral valve structure due to rheumatic process leads to more stress on the supporting elements, thus resulting in papillary muscle hypertrophy.

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To determine the usefulness of the time intervals obtained from the first derivative of apexcardiogram (dA/dt) in assessing contraction and relaxation in cardiomyopathy, 11 patients with hypertrophic obstructive cardiomyopathy (HOCM) and 9 patients with congestive cardiomyopathy (COCM) with hemodynamically and angiographically documented diagnosis were studied. As a control group 50 normal subjects were used. Since contraction and relaxation is dependent on preload and afterload, the time interval from R wave of electrocardiogram to the positive peak of dA/dt (R to dA/dt) and 2 relaxation parameters derived from negative peak dA/dt, early relaxation index (ERI) and total relaxation index (TRI) were investigated. In HOCM the R to dA/dt were shortened (55±13msec versus 76±14msec in controls, P<0.01) and both ERI and TRI were augmented (ERI: 12.5±9 versus 4.3±5 in controls, p<0.001; TRI: 147±29 versus 70±18 in controls, p<0.02). In COCM the R to dA/dt were elongated (124±14msec versus 76±14msec in controls, P<0.001) and both ERI and TRI were decreased (ERI: 2.1±4 versus 4.3±5 in controls, p<0.005; TRI: 41±17 versus 70±18 in controls, p<0.002). Significant correlation between these indices and some internal parameters of myocardial performance were observed.
These findings indicate that systolic and diastolic time intervals measured from the first derivative of apexcardiogram may by used as a reliable indices for evaluation of contraction and relaxation independently of preload and afterload.

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To study clinical significance and possible mechanism of negative U-wave observed in hypertensive patients, we applied handgrip test (HG) to 35 patients with hypertension and 20 age-matched normal subjects. HG was sustained for 3min at 50% of maximum voluntary contraction. ECG recording and measurement of blood pressure were made before, during, and after HG.
During HG, systolic blood pressure was 188.7±3.4mmHg (mean±SE) and diastolic blood pressure was 114.8±2.1mmHg in hypertensives, while 145.3±2.6mmHg and 93.8±1.1mmHg in normals; the difference between hypertensives and normals was statistically significant (p<0.001). Incidence of HG-induced negative U-wave was 0% in normals, while 68.6% in hypertensives. In hypertensive subjects, HG-induced negative U-wave appeared in 24 of the 28 patients (85.7%) with minimum to moderate left ventricular hypertrophy, while it was not seen in all 7 patients (0%) with marked left ventricular hypertrophy shown by ECG and/or UCG findings (QRS-T angle>130° with left high voltage: left ventricular wall thickness>12mm). Further we recorded UCG during HG in 14 subjects. In 4 patients, negative U waves appeared simultaneously with increase in left ventricular dimension during diastole. In the remaining 10 cases that included both normals and hypertensives, however, neither increase in left ventricular end diastolic dimension nor negative U waves were observed.
Thus we conclude that HG-induced negative U waves may be caused by stretch of the ventricular wall resulting from acute left ventricular volume overload.

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The 4 year prospective trial on the effectiveness of the antihypertensive treatment was performed in 100 mild hypertensive patients of the aged, the average age being 76.1 years. Dropouts during the drug-off control period were 9 cases. The matched pair group was selected by the age, sex, and blood pressure. Forty-four drug treated cases and 47 placebo treated cases were comparable in blood pressure as well as in laboratory data.
Cerebrovascular and cardiac complications were observed in 4 cases or 10.5% in the drug group, and in 9 cases or 22.0% in the placebo group. When 8 cases of blood pressure elevation over 200/110mmHg in the placebo group were added to the cardiovascular complications, dropouts in placebo group reached 41.5%, and this showed the significant difference. Other complications were observed in 12 cases or 31.6% in the drug group and in 17 cases or 41.5% in the placebo group. Major complications were cancers, infections, and bone or joint diseases.
Blood pressure was decreased from 171/87 to 151/80 in the drug group, and the average decrease was 20/7mmHg in 4 year period. No significant changes in hematocrit, serum protein, urea nitrogen, uric acid, sodium, and potassium were observed during the trial period. The present study suggested that antihypertensive treatment was effective in the aged with mild hypertension, and that careful follow up was needed not only for cardiovascular complications but also for general health condition.

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Long-term clinical effects of beta-blockers (propranolol in most cases) and calcium inhibitors (nifedipine in most cases) were studied in 16 patients with hypertrophic cardiomyopathy.
On overall subjective symptoms, beta-blockers were effective in 50% of symptomatic patients, while calcium inhibitors were effective in only 33%. On angina pectoris, however, calcium inhibitors were superior to beta-blockers in our patients. Blood pressure decreased with each drug, and the decrease was significant with nifedipine. Otherwise there was no change in physical findings with either drug.
Long-term (more than 6 months) use of beta-blockers resulted in an increase in cardiothoracic ratio on chest X-ray, a decrease in left ventricular ejection fraction on echocardiogram and more pronounced ST-T change on electrocardiogram. Prolonged use of nifedipine resulted in a slight decrease in cardiothoracic ratio, but no systematic change on echocardiogram and on electrocardiogram.

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Atrioventricular conduction characteristics were examined by atrial extrastimulus technique in 45 children aged 50 days to 14 years following diagnostic cardiac catheterization. None of the patients had a history of supraventricular tachycardia and none had evidence of pre-excitation on routine electrocardiogram. By plotting the A2H2 and H1H2 intervals against corresponding S1S2 intervals 2 types of conduction curve were obtained. Eight of the 45 children (17.7%) showed discontinuous conduction curves, characteristic of dual atrioventricular nodal pathways, whereas 37 patients had continuous curves. Of the 8 patients with discontinuous curves 3 showed unsustained echo beats following extrastimuli, after the effective refractory period of the fast pathway was reached. This study showed that, as in adults, the atrioventricular node was frequently functionally dissociated in children.

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We have developed a new X-ray visible suture. It is a polyester suture containing platinum wires.
The radiopaque suture was used clinically in 43 cases, and was useful in the following situations:
(1) as a marker for post-operative angiography (post-operative graft angiography of aorto-coronary bypass or Brockenbrough's method), (2) as a marker for evaluation of valve reconstructive surgery or surgery of intracardiac anomalies, and (3) as a guideline for second radical repair after primary operation.

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Previous experiments showed the cases in which end ejection of the ventricle did not always coincide with end systole as identified by the time for Emax corresponding to the maximally contracted pressure-volume relationship line of the ventricle. The purpose of the present study is to obtain a better insight into the ventricular afterloading conditions that enable end ejection to coincide with end systole of the ventricle by a simulation method. The left ventricle was simulated by a time-varying elastance, E(t), and the afterload by a constant pressure connected to the ventricle via a valve with resistance R and inertance L in series. A sinusoidal wave starting from 0 at onset of systole, reaching Emax at end systole, and returning to 0 at end diastole in each cycle was assigned for E(t). Parameters of the system elements were changed individually. Ventricular pressure, volume and flow were computed by solving the system of ordinary differential equations with a time-varying parameter, E(t). Results indicate that end ejection coincides with end systole only when R and L values fall on a specific curve in an R-L domain for a given set of the other system parameters, and otherwise the 2 ends variably dissociate from each other. Consequently, end ejection should not blindly be used as a substitute for end systole when Emax and end-systolic pressure-volume relations are to be assesse

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Arterial dilatation distal to a stenosis has been known as poststenotic dilatation (PSD). This paper describes arterial constriction enough to produce PSD, time course of PSD, structural changes of the dilated segments and influence of hypertension on the development of PSD. These problems were studied in 2 experimental protocols. In protocol I, 87 carotid arteries of 45 rabbits were constricted by silver clip of 0.65 to 2.0mm in diameter. The arterial diameter was measured at the sites both proximal and distal to the constriction after 3 days to 8 weeks. In protocol II, 22 carotid arteries of 12 rabbits with experimental one-or two-kidney Goldblatt hypertension were constricted and the development of PSD was compared with age matched controls. Remarkable PSD developed in arteries with moderate stenosis of 45 to 60% constriction. The degree of dilatation expressed as ratio of distal to proximal diameter reached about 1.5 at the end of the second week and remained unchanged thereafter. Destrucion of the elastic fibers with intimal hyperplasia was observed in the dilated segments even at the early stages of the PSD. Both mild and severe stenosis failed to produce prominent PSD. In protocol II, the PSD averaged 1.18±0.05 (mean±SE) in hypertensive, and 1.32±0.03 in normotensive animals (p<0.05). The result suggests that chronic hypertension decreases the distensibility of the arteries

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Reciprocating tachycardia in a patient with concealed septal accessory pathway is described. His arrhythmia is characterized by incessant form of tachycardia which is not initiated by a triggering extrasystole but by critical shortening of P-P interval. Electrophysiological studies showed that the occurrence of the reciprocating tachycardia was dependent on atrial pacing rate. By comparing effective refractory period of the atrium, retrograde effective refractory period of the accessory pathway, the conduction time over the reentrant circuit and the difference of conduction time via normal conduction system and via the accessory pathway to the ventricular end of the accessory pathway, it was found that an atrial echo was elicited only at atrial pacing rates at which the difference of conduction times to the ventricular end of the accessory pathway was greater than the effective refractory period of retrograde accessory pathway.
These observations suggest that the initiation of the tachycardia in this patient is related to a critical antegrade conduction delay necessary for complete recovery of the ventricular end of the accessory pathway from the preceding antegrade depolarization.

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