To assess the effects of oral verapamil therapy on global and regional left ventricular (LV) diastolic filling of hypertrophic cardiomyopathy (HCM), we studied 9 patients with HCM by radionuclide ventriculography and M-mode echocardiography before and after 2 weeks of oral verapamil therapy (240 mg/day). LV regional function was assessed by subdividing the LV region of interest into 4 regions from which global, septal, apical and lateral time-activity curves and their first-derivative curves were derived. Diastolic asynchrony during early diastole was measured as the sum of the absolute values (total Δt) of the time differences ( Δt) from peak filling rate in the global left ventricle to that in each of the 3 regions. Verapamil did not alter LV systolic function globally and regionally. Global LV peak filling rate improved after verapamil therapy from 1.92±0.59 to 2.35±0.63 end-diastolic counts/s (p<0.02) without altering regional peak filling rates significantly. Global and regional times to peak filling rate showed a shortening or no change despite a tendency to increase in the diastolic time after verapamil therapy. The total Δt decreased from 93±61 to 41±23 ms after verapamil (p<0.05), indicating more synchronous LV diastolic filling after verapamil. There was a negative correlation between the global peak filling rate and the total Δt (r= -0.54, p<0.05, n=18), suggesting that the global peak filling rate may improve after verapamil therapy in association with the decrease in the asynchronous LV diastolic filling. Thus, verapamil was effective in improving impaired LV filling in HCM, which might be related to reduction in regional LV diastolic asynchronous filling.

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To examine the effects of dialysis on left ventricular (LV) filling, gated radionuclide ventriculography was conducted in 15 patients with renal failure before and after dialysis. The LV regional function was assessed by subdividing the LV region of interest into 4 regions from which global and regional time-activity curves and their first-derivative curves were obtained. Early diastolic asynchrony was measured as the sum of the absolute values (total Δt) of the time differences (Δt) between the global peak LV filling rate (PFR) and that for each of the other 3 regions. Dialysis produced an increase in the peak LV ejection rate (PER), heart rate, total Δt and total Δt/diastolic time. It caused a delay or tendency to delay in the time to PFR without significant changes in the PFR either globally or regionally, and the PFR/PER ratio decreased both globally and regionally. These alterations indicated a failure of improvement of the global and regional LV filling, with more asynchronous filling occurring after dialysis despite the increases in PER and, heart rate, both of which are expected to increase PFR and shorten the time to PFR. There was a negative correlation between the change in total Δ t/diastolic time and the change in the PFR/PER ratio (r= -0.62, p<0.01), with a greater increase in asynchrony occurring with the relative greater reduction in the relative global PFR compared with the global PER after dialysis. Dialysis can produce early diastolic asynchronous filling, which will be associated with a failure of improvement of LV filling despite the increases in LV peak ejection rate and the heart rate. Thus, LV filling requires careful attention in patients undergoing dialysis, since the pattern and timing of the filling is altered, and the excessive water removal by dialysis may affect the LV diastolic filling.

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In 1977, 92 male patients with mild hypertension (persistent diastolic blood pressure between 90 and 104 mmHg) were found from among 1608 men aged between 18 and 40 years old who were employees of an industrial company. Of these, 81 patients were followed-up for 10 years. After that time, blood pressures (BP) of 44.4% of the mild hypertensive patients became normotensive (group N); BP of 22.2% remained mild hypertensive (group M); and BP of 33.4% increased to higher levels than the starting BP (group H). Higher levels of systolic and diastolic BP, a higher incidence of family history of hypertension, a higher voltage of SV₁+RV₅ on ECG and a lower concentration of serum triglycerides at the starting point were risk factors for the progression to higher levels of hypertension. Body weights of patients in group H increased significantly during the follow-up period. These results indicate that male mild hypertensive patients with the above-mentioned risk factors should be followed carefully, especially with regard to increased body weights.

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This study aimed to evaluate the change in external work and its control mechanism in the concentric hypertrophied heart induced by systemic hypertension. The calculated stroke work, myocardial contractility, afterload, and preload were examined in the baseline period (Control Stage, CS) and in the eighth week after the induction of perinephritic hypertension (Hypertensive Stage, HS) in unanesthetized dogs. These variables were examined with echocardiograms and high-fidelity left ventricular (LV) and ascending aortic pressures. Mean aortic pressure was significantly (p<0.05) elevated from 95±10 to 134±27 mmHg in HS. The ratio of end-diastolic wall thickness to radius significantly (p<0.05) increased in the HS. The calculated stroke work of the LV chamber was significantly (p<0.05) increased from 7022±1203 to 8860±1548×10³ erg in HS while the stroke work normalized for wall thickness by calculating the wall stress was not altered (3069±1086 v.s. 2989±866 erg; CS v.s. HS) with no significant change in heart rate in HS. In the HS, the end-systolic wall stress (afterload) and the slope of end-systolic wall stress-dimension relationship (myocardial contractility) were unchanged while the end-diastolic wall stress (preload) slightly reduced. These results suggest that, in the concentric hypertrophied left ventricle induced by systemic hypertension, the LV myocardial external work is normal, whereas the LV chamber external work increases. Furthermore, the major role for allowing the LV myocardial external work to remain normal seems to be not the compensatory changes in preload, myocardial contractility, or heart rate, but rather myocardial hypertrophy; an adaptation to preserve normal ejecting wall stress to chronic pressure overload.

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Vein graft atherosclerosis characterized by smooth muscle cell proliferation has become the most serious cause of late graft failure. This study was designed to elucidate why marked histological differences occur in atherosclerotic changes between the vein graft and the artery. Fourteen rabbits underwent autonomous transplantation of femoral vein sections (10 - 12 mm in length) into femoral arteries on the same side. They were then kept on either commercial or 1% cholesterol diet. At 4. 8. 15 and 30 weeks after the operation. they were sacrificed and histochemical & immunocytochemical studies on atherosclerotic changes found in graft and arteries were carried out. using monoclonal antibodies for macrophages (RAM 11) and smooth muscle cells (HHF 35). Atherosclerotic lesions found in arteries of rabbits fed by cholesterol for more than 8 weeks were characterized with the accumulation of macrophage-derived foamy cells with fibrous caps. In contrast, the lesions found in the grafts of the same rabbits were occupied with proliferating smooth muscle cells and very few macrophages. Furthermore, in lesions of the vein grafts of rabbits fed cholesterol for 4 weeks. macrophages were rather frequently encountered in the bottom of the lesions and/or its medial layer. scattering and sometimes forming mass-lesions. These results may suggest structural differences in the vein with its thin and sparse internial elastic lamina and with its thin medial layer, allowing macrophages to pass easily through the elastic lamina and scatter into the media. This may be the reason why autonomous vein graft atherosclerosis is mainly composed of proliferated smooth muscle cells.

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To clarify the central effects of physical training on patients with coronary heart disease, 81 subjects were selected for the present study. Evaluations of the oxygen transport system function were performed according to the definition proposed by Bruce and others in terms of FAI (functional aerobic impairment), LVI (left ventricular impairment) or MRI (myocardial reserve impairment). CRI (chronotropic reserve impairment) and PCI (peripheral circulatory impairment). Remarkable improvement in left ventricular impairment was found in those patients with single vessel disease or those who experienced disappearance of chest pain after the completion of the program. In another series of study on myocardial perfusion performed on 11 patients with coronary heart disease, improvement in ischemia was also demonstrated in 7 of 8 patients who revealed redistribution pattern in ²⁰¹TL exercise stress images specifying myocardial ischemia. In conclusion, exercise training could induce improvements not only the left ventricular functions characterized by increased maximal pressure rate product and maximal heart rate, but also in myocardial ischemia. Further studies are needed to specify its effects, since natural progression or regression of the disease process itself may influence the results.

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The aim of this study was to assess the effectivenss of an early predischarge exercise therapy, started 2 weeks following acute myocardial infarction (AMI), to working functional capacity. Seventeen AMI patients (10 males, 7 females, mean age 62±11 years) were examined in this study. Six, serious clinical symptoms and complications, were excluded, while the remaining 11 patients completed, the ewhole exercise therapy protocol (2 weeks). Patients performed exercise performed for 20-30 min twice daily at a target heart rate (90% level of heart rate at AT) on the basis of anaerobic threshold (AT) determined using treadmill ramp exercise with our protocol. Heart rates (HR) at rest, warming-up and AT point decreased sigificantly (p<0.05) after exercise therapy, although peak HR remained unchanged. O₂ pulse at the AT point and endpoint, after exercise therapy, improved significantly (p<0.05), when compared to that before therapy. Moreover, AT and peak Vo₂ improved remarkably (p<0.05), as did exercise time to the AT point and endpoint after exercise therapy (p<0.05), when compared to that before therapy. These results indicate that the predischarge early exercise therapy begun 2 weeks after AMI will be effective and beneficial in improving working capacity with improvement of physical deconditioning. Additionally, it is necessary that patients with severe clinical symptoms and complications be excluded.

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An optimal target of exercise therapy for the chronic stage of myocardial infarction (OMI) was proposed by investigating a daily total energy consumption (DTEC) in 172 outpatients (142 males and 30 females) with OMI. DTEC was significantly lower in OMI than in the preinfarction state : 2005.8±487.8 vs. 2451.6±631.7 Kcal (p<0.01) in the male, 1389.9±367.4 vs. 1626.2±426.0 Kcal (p<0.01) in the female. Limiting factors of a daily physical activity (DPA) in OMI were selected from various non-cardiac and cardiac factors by using multi-factorial analysis (Hayashi III). Non-cardiac limiting factors included; age of >60, house-wife, joblessness and female, sex, and cardiac limiting factors included; NYHA class II, III, low anaerobic threshold (AT), treadmill exercise tolerance of <6 min. Forrester subset III, IV, heart failure in OMI and the recurrence of MI. Eighty percent of patients without cardiac limiting factors restricted DPA by 25% of DTEC of the preinfarction state. Our optimal target of exercise therapy for OMI was set to resume DTEC up to the level before MI. For patients without exercise habits, activities requiring 100 to 150 Kcal a day were requested. Also, this regimen had an educational purpose to obtain self-confidence both mentally and physically and was expected to raise the level of DPA to that of preinfarction state.

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Out of 636 patients with acute myocardial infarction (AMI) admitted to our institution, 183 patients enrolled in our non-supervised home exercise program immediately after their discharge from the hospital. The first 40 patients were randomized to control and training group, while the remaining 143 patients were included in the training group. Before and after the trial, all patients underwent cardiopulmonary exercise testing; submaximal graded treadmill exercise test with the application of expiratory gas analysis. In the training group, patients performed 2km walk-jog exercise everyday for 1 month, keeping their heart rate (HR) at 90 - 100% of that in the anaerobic threshold. HR during exercise was monitored by patients themselves, using HR-meter. The anaerobic threshold significantly increased in the training group ; while control group had no significant changes. V^^·O₂ and HR significantly increased at the same Borg's indices. Psychological improvement was also obtained in the training group compared to control group. It is concluded that non-supervised home exercise program is effective and easily applicapable in the convalescent phase of AMI.

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This paper summarizes data gathered from an 8 years sports cardiac rehabilitation program at Kyoto University and satellite hospital (Takeda Hospital). In total, 185 patients were rehabilitated under our original program with no serious cardiac accidents. Compliance was 58.2% after 6 months of this rehabilitation. In patients selected to evaluate the value of rehabilitation, exercise study with treadmill and ²⁰¹Tl scintigraphic study showed improvement in exercise tolerance (in 58% of patients) and in perfusion on exercise (in 40%). Coronary angiographic study showed regression of arterial narrowing in 16% of the patients studied. We conclude that in addition to emotional and psychological support, our sports cardiac rehabilitation is safe and effective in improving exercise tolerance and cardiac perfusion.

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The necessity, the methodology and clinical benefit of physical training were evaluated in 85 patients with valvular heart surgery. In 21 patients who had undergone the exercise stress test before surgery, corrective valvular surgery increased maximal oxygen uptake (max·V^^·O₂) from 15.4 before to 18.9 ml/min/kg. while 11 (52%) of them failed to increase exercise capacity over 5 METs. Of the total 85 patients. 41 (58%) again showed reduced exercise capacity in the initial postoperative stress test, suggesting that a return to work might be difficult without rehabilitation in these patients. We then compared two training programs: program A of short duration and frequent exercise and program B of longer duration and less frequent exercise, both using a bicycle exercise set at an intensity of 70% of the max.V^^·O₂, Both programs similarly increased max.V^^·O₂, while patients preferred program A. suggesting that exercise of longer duration could not be tolerated because of deconditioning. Program A was then prescribed to 62 patients, and it increased max.V^^·O₂ from 18.2 to 20.7 ml/min/kg after 4 weeks training without any complication. In 9 patients who served as controls undergoing no physical training. no spontaneous improvement in exercise capacity was observed. Of the 76 patients who recieved either program A or B, 28 patients failed to increase the max.V^^·O₂ by 10% or more. These patients presented atrial fibrillation, a cardiothoracic ratio >__=60% or execise-induced ST depression more frequently, suggesting that residual cardiac dysfunction might inhibit the training effects. These observations indicated that physical training is beneficial to patients after valvular heart surgery, by increasing exercise capacity, promoting an earlier return to daily activities and to work and improving generally, the quality of life.

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The effects of exercise (10000 walk steps/day) and diet (1500 kcal/day) for 4 months on coronary risk factors (obesity, hypertension, serum lipid and lipoprotein abnormalites) were studied in 332 obese, middle-aged subjects. Body weight, skinfold thickenss, systolic and diastolic blood pressures, serum lipid and lipoproteins (total cholesterol, triglyceride, and β-lipoprotein) improved significantly (p<0.05) during the program. The degree of improvement in blood pressures, serum lipids and lipoproteins was greater in abnormal blood pressure (greater than 140/90 mmHg) or abnormal serum lipid group than in normal group. A significant correlation was observed between daily number of walk steps and the improvement of body weight, diastolic blood pressure and HDL-cholesterol. Increase of daily steps during the program showed a significant (p<0.05) correlation to the change in HDL-cholesterol. It was suggested that mild exercise characterized by brisk walking was effective in the treatment of obesity, hypertension and low HDL-cholesterolemia in obese, middle-aged subjects.

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Physical training is considered as fundamental in the functional activation of aged people. The authors studied the effects of training especially on cardiovascular function and serum lipids. The subjects consisted of 2 large groups subdivided into males (M) and females (F). Group A lived with their families and were relatively active, Group B lived in a home for retired aged people and were physically inactive. AM: N=25, 65.0±19.1YO AF: N=8. 63.1±6.7YO BM: N= 13, 69.1±20.8YO BF: N= 17, 67.5±18.0YO. 63 persons in all. Training heart rates (THR) were calculated using Karvonen's formula from the symptom limited maximal heart rate (HR max, S.L.) on a low grade treadmill test. Subjects received tasked physical training under the surveillance of a physician every hour twice a week for 4 months. Endopint treadmill speeds were AM46.8±25.4. AF42.5±20.5. BM31.7±19.0. BF24.7±18.1 m/min, reflecting capacity for physical work. As expected. HR response to the same load decreased in all groups after 4 months of training. Systolic blood pressure response decreased significantly in the active group but, surprisingly, increased in Group B. Diastolic blood pressure response showed a similar decreasing tendency in both groups. Triglyceride decreased in both groups but the decrease was marked in Group A. HDL-cholesterol increased significantly in all groups. The ratio of pre-ejection period over ejection time decreased in all groups reflecting increased cardiac muscle contractility. Cardiothoracic ratio decreased in Group B but increased in Group A. Basal metabolic rate increased in Group B . Thus the effects of training varied according to the initial conditions and the training undergone, but there were found possibility to activate the physical conditions even in these aged persons.

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