We attempted to fit heart rate (HR) changes induced by constant exercise loads of different intensities to an exponential hyperbolic sine curve by the least-squares method, and we compared the results with the fitting of the changes to exponential curves. Seven healthy male volunteers performed three different intensities of constant-load exercise on a bicycle ergometer. The exponential hyperbolic sine function adequately fitted the HR responses induced by all three different intensities of loads: low (30 W: correlation coefficient, r = 0.68 +/- 0.13, mean +/- SD), moderate (75 W: r = 0.93 +/- 0.07) and high (125 W: r = 0.97 +/- 0.02). The first-order exponential curve fitted only the moderate load response. Although the second-order exponential equation fitted the HR response for both the moderate and high loads, the equation did not fit the low-load response (r = 0.43 +/- 0.26). In low-load exercise, the sum of the power of the residuals for the exponential hyperbolic sine curve fitting was significantly smaller than that for the first- or second-order exponential curve fitting. In conclusion, the exponential hyperbolic sine function is useful for quantitative analyses of the HR response to exercise loads of various intensities.
Abstract A total of 51 patients with hypertrophic cardiomyopathy (HCM) were followed for at least 3 years (mean follow‐up period 6.5 years) by serial M‐mode and two‐dimensional echocardiography. An increase of the left ventricular diastolic dimension (LVDd) to ≥ 55 mm with a decrease in the left ventricular ejection fraction (LVEF) to < 55% was observed in eight (15.7%) patients (progressive disease group). In five of these eight patients, the LVDd was ≥ 60 mm and the LVEF was < 40%. Ventricular enlargement was closely related to mortality and death due to congestive heart failure occurred in three of these patients. No deaths occurred among the 37 patients without significant progression of ventricular enlargement (nonprogressive group). The annual changes of LVEF and LVDd in the progressive disease group were larger than in the nonprogressive group (LVEF – 0.18 ± 1.45 vs. – 2.46 ± 1.47 %/year; LVDd 0.22 ± 0.81 vs. 1.43 ± 0.77 mm/year). An increment in LVDs occurred earlier than the enlargement of the LVDd. Therefore, close attention to the LVDs seems to be important to detect early left ventricular morphological changes in HCM. In summary, this study indicates that HCM patients include a subgroup with symptoms resembling dilated cardiomyopathy, in whom the left ventricle enlarges with hypofunction and in whom there is high mortality due to congestive heart failure.
The association between the extent of left ventricular (LV) hypertrophy and severity of ventricular or atrial arrhythmias are examined. Two-dimensional echocardiography and 24-h Holter electrocardiography monitoring were performed in 60 patients with hypertrophic cardiomyopathy (HCM). According to the distribution of the LV hypertrophy, the patients were divided into three groups: 1. Apical hypertrophy (APH), 2. Septal hypertrophy, and 3. Extensive hypertrophy. Ventricular arrhythmias were found in 82% of the patients and supraventricular arrhythmias were detected in 70% of the patients. Lown grade III and IV arrhythmias occurred significantly more frequently in patients with extensive than with septal hypertrophy. Lown grade III to IV arrhythmias did not occur in patients with APH. Present results show a significant association between the extent of LV hypertrophy and the severity of ventricular arrhythmias in HCM.
Aim Ventricular remodeling following acute myocardial infarction is an important factor in prognosis. The healing process, involving changes in type I and III collagens, is one of the major factors in remodelling. We therefore examined sequential changes in type I and III collagens after experimental myocardial infarction. Materials and methods Hearts were excised from 1 day to 10 weeks after permanent left coronary ligation in rats. Immunohistochemical staining with a polyclonal antibody to each collagen was performed by the avidin-biotin-peroxidase method. Results Type I collagen initially appeared in the peripheral zone of the infarct from 3 days after ligation, the extent of staining gradually increasing until it reached a maximal level on days 21–28, after which the distribution remained unchanged. Type III collagen appeared in the peripheral zone of the infarct from 3 days after ligation; the extent of staining reached the maximal level after 11–28 days, after which a slight decrease in the distribution was observed, although the staining did not entirely disappear. Conclusions Type I collagen was a major factor in collagen matrix formation, especially in the relatively late phase. Type III collagen, however, contributed particularly to collagen matrix formation in the relatively early phase. This study improves current understanding of the time-dependent alterations in type I and III collagens involved in the healing process after coronary artery occlusion.
Syndecan-1 and fibroglycan, heparan sulphate proteoglycans, play important roles in extracellular matrix formation via their biological functions.To examine experimentally the sequential changes in syndecan-1 and fibroglycan messenger RNA (mRNA) expression after acute myocardial infarction.The left coronary arteries of male Sprague-Dawley rats were ligated and the hearts were excised on days 1-14, 28 and 42. Syndecan-1 and fibroglycan mRNA expression in the infarct and non-infarct zones and in sham-operated hearts was determined by reverse transcriptase-polymerase chain reaction. Amplified products were quantified by densitometry of the electrophoresed bands stained with ethidium bromide and standardized relative to the glyceraldehyde 3-phosphate dehydrogenase or beta-actin mRNA expression. Northern hybridization was also performed in the infarct and non-infarct zones on day 3.Expression both of syndecan-1 and of fibroglycan mRNA began to increase on day 2. The expression attained maximum levels on day 3. The maximum levels of syndecan-1 and fibroglycan expression were, respectively, sevenfold and fivefold the preligation level and the level in the sham-operated hearts. The levels remained elevated until day 14, whereupon they declined gradually, returning to the control levels by around day 42. Northern blotting also demonstrated that there was an increased expression both of syndecan-1 and of fibroglycan mRNA in the infarct compared with that in the non-infarct zone on day 3.Our results demonstrated that there are sequential increases in the expression both of syndecan-1 and of fibroglycan mRNA in the infarct zone after experimentally induced myocardial infarction in rats, suggesting that these proteoglycans play some role in the pathological course of infarction.
We studied the factors which may induce acute high grade restenosis in emergency percutaneous transluminal coronary angioplasty (PTCA). PTCA was attempted in 50 patients with acute myocardial infarction, and the balloon catheter passed successfully across the occlusion site in 47 (94%) of the patients. These 47 patients were analyzed. "Acute restenosis" was defined as a lesion which was revascularized to less than 50% luminal reduction narrowed again to more than 75% luminal reduction 5 min after the balloon inflation. Univariate and multivariate analyses were used for determining factors which significantly influenced acute restenosis. The incidence of at least one restenosis episode was 45%. Multiple regression analysis selected 5 factors associated significantly with an increased rate of acute restenosis: 1) angiographic evidence of dissection, 2) lesion in the right coronary artery (RCA), 3) lack of or insufficient administration of thrombolytic agent preceding PTCA, 4) curved lesion and 5) relatively small balloon/artery diameter ratio. Acute restenosis correlated significantly with late reocclusion. This study indicates that it is important to administer a thrombolytic agent prior to emergency PTCA, and to use an adequately sized balloon to the artery when the acute restenosis occurs by using relatively smaller sized balloon. The present data also demonstrated that patients with RCA and a curved lesion have a relatively high risk of acute restenosis. This study indicates how patients with relatively high risk of acute restenosis may be identified.
We successfully implanted coronary stents into refractory reoccluded lesions after failed coronary angioplasty in three patients with acute myocardial infarction (AMI). Lesion location was the proximal left anterior descending coronary artery in two patients and the dominant right coronary artery in one patient. The reference diameters of the lesions were 3.64, 3.33, and 3.50 mm, respectively. A stent with a luminal diameter of 3.0 mm was implanted in all patients. Poststenting dilation of the stent was performed at high pressure (18 atm), and urokinase was administered immediately thereafter. Heparin was administered for 24 h with maintenance of activated coagulation time within 180-200 s. Warfarin was then administered to keep the international normalized ratio within 2.5-3.5. Luminal diameters immediately after stenting were 3.14, 2.89, and 3.26 mm, and those at 1 month after stenting were 3.09, 2.81, and 3.12 mm, respectively, indicating good patency. Our experience in these cases suggests that coronary stenting can be applied after unsuccessful coronary angioplasty in selected patients with AMI. The present report includes informative reference data on diameter, postdilation, adjunctive thrombolytic agent administration, and adequate anticoagulation therapy in coronary stenting in this acute application.
