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PubMed1990

Long-term cardiorespiratory effects of amelioration of renal anaemia by erythropoietin.

The long-term cardiorespiratory effects of recombinant human erythropoietin treatment were investigated in ten haemodialysis patients by means of maximum exercise testing, lung function tests, echocardiography, chest X-ray, and rheological assessment over 12 months. There were significant rises in exercise time (mean [SD] 13.2 [5.5] to 20.0 [6.2] min), maximum oxygen consumption (19.1 [7.0] to 25.0 [6.7] ml.min-1.kg-1), and anaerobic threshold (11.7 [3.6] to 15.4 [4.8] ml.min-1.kg-1) after 2 months of erythropoietin treatment. The improvements were maintained but not augmented on repeat testing after 4, 8, and 12 months of therapy. Carbon monoxide transfer [corrected] rose from 15.5 (2.9) to 18.6 (3.7) ml.min-1.mm Hg-1. There was a substantial reduction in exercise-induced cardiac ischaemia (eight patients had significant ST segment depression before erythropoietin, only one after 2 months' treatment, and none after 12 months' treatment), despite a significant rise in whole blood viscosity. Left ventricular mass, as estimated by echocardiography, progressively decreased from 354 (169) g to 251 (95) g after 12 months' treatment, and four patients showed a reduction in cardiothoracic ratio on chest X-ray.

Adult↗

PubMed1990

[Left auricular hypertrophy in aortic stenosis in adults].

Left atrial hypertrophy (LAH) was noted from the electrocardiograms of 72 of 98 adult patients (81%) who underwent hemodynamic evaluation of calcified aortostenosis (CAS). The relations between LAH and clinical, echographic and hemodynamic findings are specified. The frequency of LAH was not higher in cases of a history of hypertension, angina pectoris, lipothymia or exercise-induced syncope. In contrast, dyspnea was more frequently associated with LAH (84%) than not (17%). An approximately linear relation was seen between LAH and the mean pulmonary capillary pressure, the mean rate of circumferential decrease (RCF), the coefficient of muscle rigidity (ks of Mirsky), the left ventricular mass (LVM) and the left ventricle-aorta gradient. LAH is, therefore, a frequent sign in patients presenting CAS. Its origin is multifactorial, with a predominance of increased mean capillary pressure in cases of clinical signs of poor safety.

Aortic Valve Stenosis↗

PubMed1988

Antimitochondrial autoantibodies in myocardial hypertrophy: comparison between hypertrophic cardiomyopathy, hypertensive heart disease, and athlete's heart.

Antimitochondrial autoantibodies (AMA) were tested by indirect immunofluorescence in three groups of subjects with different types of myocardial hypertrophy: 35 patients affected with hypertrophic cardiomyopathy (HC), 20 patients with cardiac hypertrophy secondary to essential hypertension, and 35 active endurance athletes with exercise-induced left ventricular hypertrophy. Forty-two healthy subjects served as a control group. Left ventricular hypertrophy was considered a left ventricular mass (LVM) echocardiographically calculated (Devereux formula), exceeding 244 gm or a LVM index exceeding 122 gm/m2 (greater than 2 SD from a previously studied normal population). AMA were found in 15 of 35 (43%) patients with HC and in 6 of 20 (30%) patients with hypertensive heart disease (p less than 0.01); in contrast, AMA were not present in the sera of athletes or in the sera of controls. Although the significance of AMA in subjects with pathologic myocardial hypertrophy has not yet been established, their absence in the sera of athletes strengthens the opinion that cellular changes, as a compensatory response of the myocardium to a work overload, have a physiologic fashion in these cases. Moreover, identification of AMA in the sera of athletes with disproportionate severe left ventricular hypertrophy of uncertain origin may be helpful to ensure a single diagnosis.

Adolescent↗

PubMed1988

Impaired myocardial perfusion in patients with hypertrophic cardiomyopathy: assessment with digital subtraction coronary arteriography.

To study the clinical significance of abnormal myocardial perfusion in patients with hypertrophic cardiomyopathy (HCM), we performed a computerized washout analysis of digital subtraction coronary arteriograms in 28 patients with HCM and 16 control subjects. The contrast disappearance half-life (T1/2) was calculated from a time-density curve generated in the four sectors of the myocardium perfused by the left anterior descending coronary artery and the mean T1/2 was calculated by averaging T1/2 values for these four sectors. Patients with HCM demonstrated longer T1/2 in the ventricular septal region than control subjects. Thirteen (46%) of the patients with HCM presented abnormally longer mean T1/2 values, suggesting impaired myocardial perfusion. Family histories of HCM were more frequent in patients with abnormal mean T1/2 values (92% vs 47%; p less than 0.05). On the exercise stress test, patients with abnormal T1/2 values presented significantly lower exercise tolerance with more frequent exercise-induced ST segment depression (62% vs 13%; p less than 0.05). However, there were no significant differences between the two groups with regard to ventricular wall thickness, left ventricular end-diastolic pressure, or the severity of systolic narrowing of the coronary arteries. These findings suggest that 13 (46%) of the patients with HCM have impaired myocardial perfusion, which may be a manifestation of intramural coronary artery disease in addition to left ventricular hypertrophy, elevated left ventricular end-diastolic pressure, or systolic narrowing of the coronary arteries. Additionally, significant association of the prolonged T1/2 with a familial occurrence of HCM and depressed exercise tolerance with ST segment depression imply that impaired myocardial perfusion could be an important inherent pathophysiological state leading to myocardial ischemia during exercise.

Adolescent↗

PubMed1988

Electrocardiographic diagnosis of exercise-induced left ventricular hypertrophy.

To assess the prevalence of physiologic left ventricular hypertrophy and the usefulness of ECG criteria for its diagnosis, we compared ECGs and M-mode echocardiograms from 44 ultraendurance athletes and 20 similarly aged sedentary control subjects. Left ventricular mass was elevated in 25 of 44 (57%) athletes including 17 of 29 (59%) men greater than 134 gm/m2 and 8 of 15 (53%) women greater than 110 gm/m2. The sensitivity and specificity of the three ECG criteria used to diagnose left ventricular hypertrophy were: Sokolow-Lyon voltage (S-V1 + R-V5 greater than or equal to 3.5 mV), 65% and 61%; Romhilt-Estes score (greater than or equal to 4), 16% and 84%; and Cornell voltage (R-aVL + S-V3 greater than 2.8 mV in men and greater than 2.0 mV in women), 8% and 95%, respectively. Left ventricular mass, mass index, posterior wall thickness, chamber diameter, and relative wall thickness were not related to any measurement of QRS voltage. Nonvoltage ECG criteria for left ventricular hypertrophy were rare in athletes. Thus hypertrophy is a common but not universal adaptation to exercise. It is only moderately well detected by standard voltage criteria for left ventricular hypertrophy and is not reflected in nonvoltage criteria.

Adult↗

PubMed1979

Idiopathic hypertrophic subaortic stenosis: evaluation of anginal symptoms with thallium-201 myocardial imaging.

The evaluation of angina pectoris in patients with idiopathic hypertrophic subaortic stenosis is difficult in those in the age group prone to coronary artery disease. Ten patients with angina pectoris, normal coronary angiograms and idiopathic hypertrophic subaortic stenosis were studied with thallium-201 myocardial imaging performed in conjunction with submaximal treadmill exercise testing. The resting electrocardiogram demonstrated left ventricular hypertrophy with S-T segment abnormalities in seven patients, thereby vitiating the further increase in S-T segment abnormalities that developed in these patients during exercise or in the postexercise period. Of the three patients with a normal resting electrocardiogram, one had significant exercise-induced S-T segment depression. Thallium-201 myocardial imaging revealed no significant perfusion defects in 9 of the 10 patients (90 percent). In one patient with severe left ventricular hypertrophy significant perfusion defects developed after exercise that were not present at rest. Stress thallium-201 myocardial perfusion imaging is a useful noninvasive technique that assists in ruling out the presence of significant coronary artery disease in patients with idiopathic hypertrophic subaortic stenosis.

Adolescent↗

PubMed1982

Exercise electrocardiogram, blood pressure, and working capacity in young patients with valvular or discrete subvalvular aortic stenosis.

Electrocardiographic changes, blood pressure, and working capacity (total work) were recorded during an upright cycle exercise test in 65 children and young adults (mean age 12 years) with valvular or discrete subvalvular aortic stenosis. All patients had cardiac catheterization, but none had surgical treatment. Controls consisted of 164 normal subjects (mean age 15 years). In the patients, the intervals between the exercise test and cardiac catheterization were 1 month or less in 66%, 2 to 12 months in 28%, and 12 to 24 months in 6%. The patients were classified by resting left ventricular to aortic peak systolic pressure gradient into Groups I (gradient less than 30 mm Hg), II (30 to 49 mm Hg), III (50 to 69 mm Hg), and IV (70 mm Hg or greater). The mean frequency and magnitude of exercise-induced S-T depression were greater in the patients than in the control subjects (p less than 0.005) and increased with increasing obstruction in the patients. Mean total work and peak exercise systolic pressure were significantly decreased in the patients with a left ventricular to aortic systolic gradient of 30 mm Hg or greater as compared with the control subjects (p less than 0.03). An exercise profile consisting of S-T depression of 2 mm or more, and markedly decreased total work and systolic blood pressure were characteristic of the 19 patients (Group IV) with a resting left ventricular to aortic systolic gradient of 70 mm Hg or greater. At least 2 or more components of this exercise profile occurred in 11 (24%) of the 46 patients with a resting left ventricular to aortic systolic gradient less than 70 mm Hg. This study demonstrates that exercise testing reveals serious abnormalities in patients otherwise classified as having trivial or moderate obstruction, and that a properly performed exercise study can be done at minimal risk to the patient.

Adolescent↗

PubMed1985

Exercise-induced myocardial capillary growth in the spontaneously hypertensive rat.

Spontaneously hypertensive rats (SHR) were studied to test the hypothesis that endurance exercise training can stimulate capillary growth and offset the decrement associated with the development of myocardial hypertrophy. The exercise group (SHR-T) was trained on a treadmill for 10 weeks at 70-90% maximum VO2 and compared to nontrained SHR and normotensive Wistar-Kyoto (WKY) at 16 weeks of age. Thus, the training program coincided with the development of hypertension and hypertrophy in SHR. Image analysis was used to study capillaries in one micron thick left ventricular tissue samples from perfuse-fixed hearts. Training did not affect left ventricular mass or blood pressure, but reversed the characteristic decrements in capillary surface area (CSA), volume (CV), and numerical density (CD). CSA and CV were most markedly affected by exercise, as mean values for these parameters increased by 31 and 40%, respectively, compared to SHR. The magnitude of these changes approximated the magnitude of hypertrophy as evidenced by left ventricular weight/body weight ratios (42% in SHR and 37% in SHR-T). Anatomical intercapillary distance was also normalized by training (means +/- SEM): SHR-T, 11.65 +/- 0.31; SHR, 13.97 +/- 0.37; WKY, 11.19 +/- 0.37. These data indicate that exercise stimulates capillary growth in the face of developing hypertension and its related left ventricular hypertrophy.

Animals↗

PubMed1983

Changes in lysosomal enzyme activities in exercise-induced cardiac hypertrophy of mice.

The activities of several lysosomal enzymes were assayed in control and in exercise-hypertrophied cardiac muscle of mice (Mus musculus). The repeated running program increased the activity of beta-glucuronidase (16.1%) in mouse cardiac muscle. Decreased activities of beta-N-acetylglucosaminidase (10.8%), acid ribonuclease (10.7%), and arylsulphatase (14.2%) were observed in the hypertrophied myocardium. The activities of acid deoxyribonuclease, cathepsin C, cathepsin D, and p-nitrophenylphosphatase as well as the activities of citrate synthase and cytochrome c oxidase, mitochondrial enzymes, were unaffected in cardiac muscle. We suggest that lysosomal enzyme responses are selective and highly different in physiologically and pathologically induced cardiac hypertrophies.

Acetylglucosaminidase↗

PubMed1989

Pathophysiologic assessment of left ventricular hypertrophy and strain in asymptomatic patients with essential hypertension.

To investigate the significance of the electrocardiographic (ECG) pattern of left ventricular hypertrophy and strain, two groups of asymptomatic patients with essential hypertension were compared. The patients were similar in terms of age, smoking habit, serum cholesterol and blood pressure levels, but differed in the presence (Group I, n = 23) or absence (Group II, n = 23) of the ECG pattern of left ventricular hypertrophy and strain. Group I patients had significantly more episodes of exercise-induced ST segment depression (14 versus 4, p less than 0.05) and reversible thallium perfusion abnormalities (11 of 23 versus 3 of 23, p less than 0.05) despite similar exercise capacity and absence of chest pain. Nonsustained ventricular tachycardia was detected on 24 h ambulatory ECG monitoring in two patients in Group I, but no patient in Group II. Coronary arteriography performed in 20 Group I patients demonstrated significant coronary artery disease in 8 patients. This study has shown that there is a subgroup of hypertensive patients with ECG left ventricular hypertrophy and strain who have covert coronary artery disease. This can be detected by thallium perfusion scintigraphy, and may contribute to the increased risk known to be associated with this ECG abnormality.

Angiography↗

PubMed1983

Exercise-induced cardiac dysfunction in sickle cell anemia. A radionuclide study.

Cardiac performance was studied by radionuclide angiography at rest and during exercise in 22 adolescents with sickle cell (SC) anemia and the results were compared with those in 12 control subjects. At rest, cardiac contractility was normal; cardiac output and end-diastolic volume were increased. At maximal exercise, heart rate, cardiac output response, and work capacity were reduced; the reduction was related to the degree of anemia. Left ventricular end-diastolic volume decreased with exercise most markedly in patients with ischemic exercise electrocardiograms. An abnormal ejection fraction response to exercise occurred in 4 patients; electrocardiographic signs of ischemia developed in all 4, and wall motion abnormalities in 2. Those patients who had electrocardiographic signs of ischemia had a significantly lower heart rate, ejection fraction, and cardiac output response to exercise, and a lower hematocrit level than subjects with normal results on exercise electrocardiography. The increase in cardiac output was not sufficient to maintain a normal level of exercise. The decrease in end-diastolic volume suggests that diastolic function was abnormal during exercise. Cardiac dysfunction was manifested by an abnormal ejection fraction response, wall motion abnormalities, and incomplete left ventricular filling during exercise.

Adolescent↗

PubMed1987

Dissociation between regional myocardial dysfunction and subendocardial ST segment elevation during and after exercise-induced ischemia in dogs.

The onset and resolution of electrical and functional measures of regional myocardial ischemia were examined in nine conscious dogs during control exercise and exercise after beta-receptor blockade. The dogs had been instrumented with an ameroid constrictor and were studied when no regional dysfunction was evident at rest, although severe coronary stenosis or coronary occlusion with collateral circulation development was present. ST segment elevation was measured on subendocardial electrograms, and regional wall motion was studied by sonomicrometry. During control exercise, subendocardial myocardial blood flow in the ischemic zone, normalized to blood flow in the nonischemic zone, decreased. Subendocardial ST elevation increased slowly, was significantly different from control standing values by 2.5 minutes of exercise and returned quickly to control values within 5 minutes after exercise. Percent systolic wall thickening decreased rapidly, was significantly depressed by 1 minute of exercise and did not return to control values until 30 minutes after exercise. A second, identical exercise stress was performed on the same day after a single oral dose (1 mg/kg body weight) of atenolol. In the ischemic zone during exercise after atenolol compared with control exercise, normalized subendocardial myocardial blood flow was improved and significantly less ST elevation occurred, but the onset and resolution of ST elevation were not altered. Systolic wall dysfunction during exercise was significantly less after atenolol, and function returned toward preexercise values by 1 minute after exercise, even more rapidly than ST segment resolution.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1979

Development and regression of exercise-induced cardiac hypertrophy in rats.

Adult female rats were exercised by daily swimming. All the increase in heart weight induced by the exercise occurred within 14 days and averaged 30%. The half times of the increases in heart weight and total protein content were about 4.5 days, whereas that of cytochrome c, which was used as a mitochondrial marker, was 6.5 days. The total amounts of DNA and of hydroxyproline in the heart, which were used to evaluate the degree of connective tissue hyperplasia, increased only slightly (8% and 10%, respectively). Other animals were subjected to the same swimming program for 21 days. Groups of rats were killed at various time intervals after stopping exercise. Heart weight, total protein content, and total cytochrome c content decreased rapidly initially, with 60% of the total regression of hypertrophy occurring during the first week. Thereafter, heart weight fell more gradually toward the sedentary control value. The hydroxyproline content of the heart, which was increased 10%, did not decrease during the regression of the hypertrophy.

Animals↗

PubMed1986

Exercise-induced cardiac hypertrophy: a correlation of blood flow and microvasculature.

The effects of exercise conditioning on the myocardium were studied in seven instrumented pigs strenuously exercised for 12 wk by treadmill running. Data were compared with eight instrumented untrained pigs. O2 consumption measured during maximum exercise effort was significantly elevated in the trained pigs (71.7 +/- 4.0 vs. 56.3 +/- 3.0 ml X ml-1 X kg-1). Absolute right and left ventricular mass increased by 20 and 13%, respectively, in response to exercise. Myocyte cross-sectional area increased by 21% in the trained hearts compared with the untrained hearts. Transmural left ventricular myocardial blood flow (ml X min-1 X g-1) was not significantly different at rest, during maximum exercise, or during exercise with adenosine infusion. However, training caused an elevation of the regional epicardial blood flow noted during exercise and exercise with adenosine. In the trained pigs mean aortic pressure during maximum exercise with adenosine infusion was not significantly different compared with untrained pigs. Coronary resistance during exercise with adenosine infusion was the same in both animal groups. In the trained group capillary numerical (no./mm2) and length (mm/mm3) densities were reduced, whereas arteriolar numerical and length densities were significantly increased compared with the untrained group. Measurements of capillary luminal surface density (mm2/mm3) in the trained group were unchanged compared with the untrained group. These results suggest that strenuous exercise does not stimulate the production of new capillaries, but this is modified by the ability of existing capillaries to increase their luminal surface area to parallel increases in myocyte growth. The arteriolar data suggest that exercise promotes the formation of new arterioles.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1986

Exercise training-induced alterations of cardiac morphology.

The data to date are ambivalent regarding exercise-induced cardiac enlargement in previously sedentary individuals. The training regimens used in previous longitudinal studies probably did not provide an optimum training stimulus. Accordingly we studied echocardiograms of the left ventricle of 11 relatively inactive individuals pre and post an intense endurance training program, when intensity was increased relative to improvement, thereby providing an optimum training stimulus. Subjects trained 6 days/wk for 7 wk, alternating days of continuous cycling (40 min) and interval running (5 5-min bouts). Exercise intensity was maintained at 85-90% of peak cycle ergometer O2 uptake (VO2) for cycle training by increasing power output approximately 11 W/wk and at approximately 100% of VO2max for run training by increased (P less than 0.01) approximately 950 ml/min (approximately 32%) and was correlated with training duration (r = 0.91; P less than 0.01). Training-induced increases (P less than 0.05) in interventricular septal thickness (IVS, mm) during both systole (13.4 +/- 0.9 to 14.9 +/- 0.8) and diastole (10.4 +/- 0.6 to 11.5 +/- 0.7) and in left ventricular end-diastolic dimension (4.96 +/- 0.16 to 5.13 +/- 0.19 cm). The absolute values of left ventricular end diastolic volume (LVEDV), stroke volume, ejection fraction, and left ventricular mass (LVM) increased (P less than 0.05) after training. Increases (P less than 0.05) in LVEDV index (64.3 +/- 3.3 to 69.0 +/- 3.4 ml/m2) and LVM index (114.1 +/- 6.5 to 124.5 +/- 7.3 g/m2) were also evident.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗

PubMed1976

The effect of complete and partial deconditioning on exercise-induced cardiovascular changes in the rat.

Exercise conditioning of young male rats by swimming for 1 h, 5 times per week for 10 weeks results in a reduced gain in body weight, cardiac hypertrophy and hyperplasia, an increase in myocardial capillary density, and an increase in cross-sectional laminal areas of extracoronary collateral arteries. The effects of partial or complete deconditioning on these changes were studied by randomizing young male rats exercise-conditioned for 10 weeks to groups either kept sedentary or subjected to varying amounts of exercise for a second 10-week period. Their hearts were compared with those of unexercised controls using quantitative histologic measurements. During the second 10 weeks, exercise conditioning was found not to continue to suppress weight gain. However, frequent relative short-duration exercise sessions (as little as 15 min per session) frequently prevented an accelerated increase in body weight associated with deconditioning. A complete regression of exercise-induced cardiovascular adaptive changes occurred when wxercise was discontinued completely for 10 weeks or the duration of sessions was cut to 15 min. In order to maintain cardiac hypertrophy, exercise had to be continued for 1 h, 5 times per week while hyperplasia could be maintained with shorter duration, less frequent sessions (30 min, twice a week). The maintenance of increased myocardial capillary density required a similar amount of exercise, and at least 1 h of exercise once a week was necessary to maintain the enlargement of ECA.20

Adaptation, Physiological↗

PubMed1990

Exercise-induced subendocardial dysfunction in dogs with left ventricular hypertrophy.

The effects of treadmill exercise on regional myocardial blood flow and function were examined in 10 adult, conscious dogs with left ventricular hypertrophy (LVH) induced by aortic banding in puppies, which resulted in a left ventricular (LV) weight/body weight ratio of 8.5 +/- 0.3. Data were compared with results from eight control dogs with an LV weight/body weight ratio of 4.9 +/- 0.2. At rest, LV systolic and end-diastolic pressures were significantly greater (p less than 0.01), and mean arterial pressure was significantly less (p less than 0.05) in LVH dogs. Mean myocardial blood flow (control dogs, 0.98 +/- 0.11 ml/min/g; LVH dogs, 1.16 +/- 0.06 ml/min/g) and the transmural blood flow distribution at baseline, as assessed by endocardial/epicardial blood flow ratio (control, 1.35 +/- 0.12; LVH, 1.21 +/- 0.09), were similar in the two groups. During exercise to a target heart rate (240 beats/min), LVH dogs demonstrated greater (p less than 0.01) increases in LV systolic and end-diastolic pressures. In control dogs, as expected, exercise augmented velocity of circumferential fiber shortening (16 +/- 9%) and shortening fraction (15 +/- 5%), but in LVH dogs, exercise reduced the velocity of circumferential fiber shortening (-14 +/- 6%) and shortening fraction (-17 +/- 5%). Exercise also increased full wall thickening (35 +/- 5%), subendocardial wall thickening (66 +/- 10%), and subepicardial wall thickening (44 +/- 9%) in control dogs. In LVH dogs, exercise increased subepicardial wall thickening (31 +/- 9%) and reduced subendocardial wall thickening (-40 +/- 7%); full wall thickening did not change (-11 +/- 9%). This was associated with a fall in endocardial/epicardial flow ratio to 0.72 +/- 0.05 (p less than 0.01) in LVH dogs. The subendocardial dysfunction persisted late into recovery, at a time when the transmural blood flow distribution had returned to baseline; this occurrence suggested myocardial stunning. Thus, in dogs with LVH, selective subendocardial hypoperfusion and profound selective depression in subendocardial wall thickening are observed during exercise. The subendocardial dysfunction persisted into recovery despite resolution of the perfusion abnormality.

Animals↗

PubMed1992

[Cardiac and humoral mechanisms of the preventive effect of physical activity on cardiovascular diseases].

Many recent studies on the effects of regular exercise on the heart, coronary arteries and the balance between haemostasis and fibrinolysis suggest several mechanisms that are able to explain the epidemiologically well-documented association of habitual physical activity with a reduced risk of cardiovascular disease. Based on a review of current evidence, it is proposed that i) the haemodynamic adaptation of an aerobically-trained heart is an important cardioprotective mechanism, ii) the importance of exercise-induced effects on the coronary vessels may currently be somewhat underestimated, and iii) the importance of training-related changes in the haemostatic-fibrinolytic balance is equivocal at present, since the relative intensity of exercise seems to be a modifying factor that has not been taken into account appropriately so far. Further biomedical research into the cardiac and humoral effect of physical training is, thus, needed to corroborate the recent epidemiological observation that moderate-intensity exercise is just as--or even more--cardioprotective than high-intensity sports activity.

Cardiomegaly↗