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PubMed1998

[Differential expression of cardiac immediate early and late response gene in exercise-induced and hypertensive cardiac hypertrophic remodeling].

Our previous studies have shown that the myocardial phenotypes between exercise-induced and hypertensive cardiac hypertrophy are different. However, alteration of cardiac gene expression in the two kinds of hypertrophy is not clear. We therefore studied the expression of immediate early and late responsive gene in Wistar rats subject to a 12-weeks swimming program and spontaneously hypertensive rats (SHR) by Northern blot. The autoradiographs were analyzed by scanning densitometry. When compared with matched sedentary control, swimming rats and SHR increased their heart/body weight by 29% and 61% respectively (P < 0.01). After a series of swimming program, levels of c-fos and atrial natriuretic factor (ANF) mRNA were instantly increased 203% and 214% respectively in the swimming rats. However in 24 h after swimming, ANF mRNA was decreased to the level of control but c-fos mRNA was still higher than than in control. The levels of c-fos and ANF mRNA were increased by 80% and 298% in SHR respectively. The expression of beta-myosin heavy chain (MHC) mRNA was increased by 117% in SHR but decreased by 12% in swimming rats. The expression of alpha-MHC mRNA was decreased by 42% in SHR but unchanged in swimming rats. The abundance alpha/beta-MHC mRNA in swimming rats is 336% higher than in SHR. These results showed differential expression of the immediate early and late responsive gene in exercise-induced and SHR hypertrophied heart remodeling. It is suggested that (1) the differential expression of c-fos gene may differently regulate remodeling of these two cardiac hypertrophies; (2) the differential expression of ANF gene may be a molecular marker for distinguishing the two kinds of cardiac hypertrophy; and (3) the differential expression of alpha/beta-MHC gene ratio may regulate exercise-induced and hypertensive hypertrophied myocardial cell changing to contractile phenotype and synthetic phenotype respectively, at the gene transcription level.

Animals↗

PubMed1981

Comparison of ambulatory electrocardiography and exercise testing.

Ambulatory electrocardiography and exercise testing are two noninvasive diagnostic procedures widely employed to evaluate patients for cardiac arrhythmias and S-T segment changes. This review addresses the differences and similarities of the two techniques, and examines the relative diagnostic and prognostic merit of the arrhythmia and S-T segment changes detected with each method. Ambulatory electrocardiography is more sensitive than exercise testing in detecting cardiac arrhythmias. The recording of ventricular arrhythmia is of value in predicting sudden death in survivors of myocardial infarction, whereas exercise-induced ventricular arrhythmia has limited predictive value. Nevertheless, exercise-induced S-T depression is of great prognostic value in predicting mortality and sudden death in patients with acute and chronic coronary heart disease.

Ambulatory Care↗

PubMedDate not supplied

[ECG mapping in heart muscle hypertrophy].

67 test persons (15 healthy persons, 52 patients with coronary heart disease, of them 28 patients with and 24 patients without myocardial hypertrophy) were examined by means of a mapping ECG (69 leads) and the echocardiography. For every individual lead of the mapping ECG the mean values and simple scattering of the R and S potentials of 15 normal persons have been established. Of this we led the limit values for left heart and right heart hypertrophy for every individual lead. We are able to make evident that for the determination of a myocardial hypertrophy the principle of Sokolow's index can be transferred to R (max) and S (min) of the mapping ECG. A quantification of the myocardial hypertrophy by means of the R-potential summation method presupposes a correction of the normal potential decrease in the cardio-electric field. A regionally differently characterized myocardial hypertrophy can be recognized with the help of the mapping ECG. By means of an exercise-induced mapping ECG hypertrophy-caused repolarisation disturbances can highly significantly be demarcated (p less than 0.001) from ischaemia-caused ones. The difference mapping is suitable as mapping ECG documentation for a myocardial hypertrophy.

Cardiomegaly↗

PubMed1987

Adaptation of the left ventricle to exercise-induced hypertrophy.

Cardiac functional and structural adaptations to exercise-induced hypertrophy were studied in 68 pigs. Pigs were exercise trained on a treadmill for 10 wk. Sequential measurements were made of cardiac dimensions, [left ventricular end-diastolic diameter (EDD), changes in diameter (delta D%), wall thickness (WTh), wall thickening (WTh%), left ventricular pressure (LVP), time derivative of pressure (dP/dt), stroke volume, total body O2 consumption (VO2), blood gases, and systemic hemodynamics] at rest and during moderate and severe exercise. Postmortem studies included morphometric measurements of capillary density, arteriolar density, mitochondria, and myofibrils. All of the exercise-trained pigs showed significant increases in aerobic capacity. Maximum O2 consumption (VO2 max) increased by 37.5% in group 1 (moderate exercise training) and 34% in group 3 (heavy exercise training). Cardiac hypertrophy ranged from less than 15% in a group (n = 8) subjected to moderate exercise training to greater than 30% in a group (n = 11) subjected to heavy exercise training. Before training, exercise was characterized by a decreasing EDD during progressive exercise; this was reversed after exercise training. Stroke volume and end-diastolic volumes during exercise showed a highly significant increase after exercise training and hypertrophy. Morphometric measurements showed that mitochondria and cell membranes increased with increasing myocyte growth in all exercise groups, but there was only a partially compensated adaptation of capillary proliferation. Arteriolar number and length increased in all exercise groups. Intrinsic contractility as measured by delta D%, WTh%, or left ventricular dP/dt did not increase with exercise training and in some instances decreased. Therefore, left ventricular adaptation to strenuous exercise in the pig heart is primarily one of changes in left ventricular dimensions and a compensated hypertrophy. Exercise-induced increases in EDD and stroke volume can be accounted for by decreases in peripheral resistance and increased cardiac dimensions.

Acclimatization↗

PubMed1992

Prognostic significance of exercise blood pressure and heart rate in middle-aged men.

Systolic blood pressure and heart rate measured at rest and during a standardized exercise test were analyzed in the cohort of middle-aged male employees followed-up an average of 17 years in the Paris Prospective Study I. The population sample selected for the analysis included 4,907 men who completed at least 5 minutes of bicycle ergometry, who had no heart disease at entry, and whose resting blood pressure was less than or equal to 180/105 mm Hg. Exercise-induced increase in systolic blood pressure was positively correlated with resting systolic blood pressure (r = 0.104, p less than 0.0001), whereas the correlation of exercise-induced heart rate increase with resting heart rate was negative (r = -0.169, p less than 0.001). Using Cox regression analysis with the inclusion of resting systolic blood pressure and heart rate; exercise-induced elevations of systolic blood pressure and heart rate; and controlling for age, smoking, total cholesterol, body mass index, electrical left ventricular hypertrophy, and sports activities, cardiovascular mortality was found to be associated with the systolic blood pressure increase (p less than 0.05), whereas no association with resting systolic blood pressure was found. Total mortality was predicted by resting systolic blood pressure and its elevation (p less than 0.01 for both) and by resting heart rate (p less than 0.0001). The heart rate increase did not contribute to death prediction. In conclusion, the magnitude of the exercise-induced increase of systolic blood pressure, but not of heart rate, may represent a risk factor for death from cardiovascular as well as noncardiovascular causes, independently of resting blood pressure and heart rate.

Aging↗

PubMed1981

Natural history of myocardial infarction--relevance for secondary prevention.

Numerous variables have been identified as having prognostic value after infarction. The significance of each of these depends both on the time after the event when the observation is made and the length of follow-up. Although much prognostic information has been published, its validity is difficult to establish because the criteria for infarction have seldom been stated, the effect of treatment has been ignored and the case material has been either ill-defined or atypical. Most of the most powerful predictors of medium and long-term prognosis are not susceptible to correction, e.g. age, previous myocardial infarction, cardiomegaly, enzyme levels, intraventricular conduction defects and indices of left ventricular dysfunction. Others, e.g. "warning arrhythmias" may be treatable but there is, as yet, no evidence that suppressing them improves prognosis. The most clinically relevant prognostic factors are those which are of relatively high predictive value but are potentially correctable. These include smoking, hypertension, diabetes, life-threatening arrhythmias, and exercise-induced ischaemia, as manifested by angina and ST changes. Secondary prevention is most likely to be successful if appropriate approaches are aimed at specific subsets. Thus, beta-blockade, anti-arrhythmic therapy, platelet active agents, and surgery may each be beneficial in different although possibly overlapping sub-sets. Even if it is shown that any one of these forms of therapy produces a statistical benefit when given to the whole post-infarct population, it does not follow that it should be given to all members of such a population.

Humans↗

PubMed2000

D-Ribose as a supplement for cardiac energy metabolism.

Metabolic support for the heart has been an attractive concept since the pioneering work of Sodi-Pallares et al. four decades ago.* Recently, interest has increased in the use of over-the-counter supplements and naturally occurring nutriceuticals for enhancement of cardiac and skeletal muscle performance. These include amino acids such as creatine, L-carnitine, and L-arginine, as well as vitamins and cofactors such as alpha-tocopherol and coenzyme Q. Like these other molecules, D-ribose is a naturally occurring compound. It is the sugar moiety of ATP and has also received interest as a metabolic supplement for the heart. The general hypothesis is that under certain pathologic cardiac conditions, nucleotides (particularly ATP, ADP, and AMP) are degraded and lost from the heart. The heart's ability to resynthesize ATP is then limited by the supply of D-ribose, which is a necessary component of the adenine nucleotide structure. In support of this hypothesis, recent reports have used D-ribose to increase tolerance to myocardial ischemia. Its use in patients with stable coronary artery disease improves time to exercise-induced angina and electrocardiographic changes. In conjunction with thallium imaging or dobutamine stress echocardiography, D-ribose supplementation has been used to enhance detection of hibernating myocardium. In this article, we review the biochemical basis for using supplemental D-ribose as metabolic support for the heart and discuss the experimental evidence for its benefit.

Adenosine Triphosphate↗

PubMed2003

Exercise-induced cardiac hypertrophy: a substrate for sudden death in athletes?

Cardiac hypertrophy is a general term signifying an increase in cardiac mass in response to applied stress. In mild, early hypertrophy, cardiac myocyte contractile performance may be normal or enhanced, whereas in severe hypertrophy associated with cardiac failure, myocyte contraction is reduced in amplitude and increased in duration. In contrast to the varied contractile response, the duration of electrical excitation shows similar changes in both mild and severe hypertrophy. Action potential duration in mid-myocardial and sub-epicardial layers is increased, which is associated with ventricular arrhythmias (in a similar manner to the long QT syndromes from other causes), based on afterdepolarizations and enhanced automaticity. Single-cell studies following exercise training in animal models show that exercise-induced cardiac hypertrophy displays features similar to mild, compensated hypertrophy from other causes. Developed shortening of unloaded single cells is increased or unchanged, and developed force in single myocytes is enhanced. Action potential duration is increased, apart from in the sub-endocardial layer. As with mild hypertrophy from other causes, this will be pro-arrhythmic because of altered dispersion of repolarization and enhanced automaticity. Major abnormalities of the ECG in man include frequent and complex ventricular ectopy, ST segment changes and prolongation of repolarization. In this review a case is presented for regarding exercise-induced cardiac hypertrophy as being no different from mild cardiac hypertrophy resulting from other, pathological causes. The cellular electrophysiological changes are sufficient to account for many of the abnormalities of the ECG, including high-grade ventricular ectopy. Sudden death in trained athletes who have no evidence of specific heart disease may be a direct consequence of cardiac hypertrophy and altered repolarization.

Adaptation, Physiological↗

PubMedDate not supplied

The electrocardiogram and the athlete.

Physiological adaptations of the heart to prolonged, intense physical training produce electrocardiographic changes considered abnormal in untrained persons. Increased vagal tone, anatomical changes in the heart, and other less understood mechanisms are thought to cause a spectrum of surface ECG changes characteristic of trained athletes. Arrhythmias frequently seen include sinus bradycardia, sinus pauses, and supraventricular ectopic beats. Conduction abnormalities such as prolonged P-R interval, first degree AV heart block, Wenckebach type I AV heart block, non-sinus escape rhythms, and intraventricular conduction delays of right bundle branch type are also found. Other commonly seen abnormalities include right axis deviation, increased right and left ventricular voltage, ST segment elevation, diphasic and inverted T waves, and prominent U waves. Changes in ECG parameters with exercise include a shortening of the P-R interval with a concomitant increase in the P wave/P-R interval ratio, improved AV conduction with cessation of Wenckebach phenomenon, and normalisation of ST segment and other T wave changes. Thallium scintigraphy and radionuclide angiography have been very useful in ruling out ischaemic heart disease in athletes with rest- and exercise-induced repolarisation abnormalities. Racial differences in QRS voltage and repolarisation changes have been documented. In summary, it is important to consider the type of physical activity, intensity of training, race of athlete, body habitus, and the time the ECG was obtained in relation to training in order to better understand the "normal' spectrum of ECG changes in athletes.

Arrhythmia, Sinus↗

PubMedDate not supplied

Effects of the cessation of training on left ventricular function in the racing greyhound. Serial studies in a model of cardiac hypertrophy.

Exercise-induced cardiac hypertrophy has been associated with normal resting left ventricular function and, after cessation of training, variable degrees of regression. The racing greyhound is an animal with cardiac hypertrophy said to be part congenital and part exercise-induced. Racing greyhounds underwent serial cardiac catheterization three times during an 8-month period after cessation of racing/training to determine the functional consequences of the cessation of training. At the end of 8 months of inactivity the animals' hearts were excised and weighed in order to compare heart weight/body weight (HW/BW) ratios with those obtained in a group of racing greyhounds killed within one month, 19 +/- 16 days (mean +/- SD), of the cessation of training. Comparison of HW/BW ratios failed to reveal a significant difference between the serially studied group, 12.1 +/- 1.9 g/kg (mean +/- SD), and the more recently exercising group, 12.7 +/- 1.4 g/kg (mean +/- SD) of dogs. After 2 months of inactivity, 9 of 12 greyhounds in the serially studied group showed increases in max dP/dt and dP/dt normalized to a pressure of 50 mmHg. Modified pre-ejection period and peak negative dP/dt also increased significantly (p less than .004) during this same period. No further changes in these variables were found at the final 8-month study. Our failure to demonstrate a difference in HW/BW ratios between these two groups of dogs suggests that the exercise-induced component of cardiac hypertrophy in the trained racing greyhound is probably very small and, if it exists, regresses very early (less than 1 month). Changes in contractility indices that were observed occurred after this time period (between 1 and 2 months) and are therefore probably not due to regression of cardiac hypertrophy.

Animals↗

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↗

PubMed2002

[Stress and stress tolerance in chronic heart failure].

BACKGROUND: Exercise intolerance in patients with chronic heart failure (CHF) shows no correlation to the degree of left ventricular dysfunction. This surprising finding has directed attention to peripheral changes in CHF. During the last years several different peripheral factors as determinants of exercise intolerance have been defined, i.e. abnormalities in ventilation, reduced endothelium-dependent vasodilatation of peripheral conduit and resistance vessels, and altered skeletal muscle metabolism. Skeletal muscle alterations are characterized by a reduced oxidative capacity, a catabolic state with reduced local IGF-I expression and muscle atrophy, chronic inflammation with local expression of the inducible isoform of nitric oxide synthase (iNOS) and an accelerated rate of programmed cell death (apoptosis). EFFECTS OF PHYSICAL EXERCISE: Physical exercise training has evolved as an important therapeutic approach to influence these non-cardiac causes of exercise intolerance. After the first studies documenting the effect of aerobic training on the peripheral causes of exercise intolerance in CHF the question was asked: Should we treat the heart or the periphery to improve exercise intolerance in CHF? Today, we have come closer to the answer: It is now clear that these two systems are not mutually exclusive. Exercise training in CHF has been shown to improve skeletal muscle metabolism and function, to avert muscle catabolism, to reduce neurohumoral overactivation, to reverse endothelial dysfunction and to contribute to the prevention of pathologic left ventricular remodeling. After 6 months of regular exercise training oxidative capacity of the working skeletal muscle increases by approximately 40%. Regular exercise training leads to a significant improvement of endothelium-dependent vasodilatory capacity of peripheral resistance vessels, thereby reducting peripheral resistance in particular during exercise. These beneficial training effects result in a small, but significant improvement of stroke volume and reduction in cardiomegaly. CONCLUSION: Although several questions regarding patient selection, optimal training protocol and training intensity remain unanswered, exercise training can been seen as an established adjunct to pharmacotherapy in CHF. We may soon reach the conclusion that by treating the periphery with exercise programs we are in fact treating the heart, as well. All exercise-induced adaptations converge to increase peak oxygen uptake by up to 2 ml/kg.min. For patients in stable CHF on optimal cardiac medication a combination of in-hospital and home-based aerobic endurance training in combination with local muscle strength training seems most promising. Although exercise training offers no causal treatment of CHF, it has great potentials as an adjunct therapy directed at improving exercise tolerance and expanding the physical limits of CHF patients.

Chronic Disease↗

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↗