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PubMed1978

Left ventricular function in exercise-induced hypertrophy in dogs.

Indexes of left ventricular function and diastolic compliance were studied in 10 awake exercise-trained greyhounds with left ventricular hypertrophy. Mean left ventricular to body weight ratio and mean myocardial cell diameter were significantly greater than in normal dogs (8.73 +/- 2.7 [standard error of the mean] versus 4.63 +/- 0.24 g/kg, P less than 0.01; and 18.3 +/- 0.67 versus 12.5 +/- 0.71 mu, P less than 0.01, respectively). In awake resting animals, 7 to 50 days after implantation of a high fidelity micromanometer and sonomicrometer crystals, left ventricular contractility indexes were similar to those measured previously in normal dogs (maximal derivative of left ventricular pressure [dP/dt] 3,800 +/- 250 versus 3,810 +/- 330 mm Hg/sec, difference not significant; and mean rate of circumferential fiber shortening 1.54 +/- 0.12 versus 1.43 +/- 0.12 sec-1, difference not significant). During volume loading sufficient to produce a left ventricular end-diastolic pressure of 20 mm Hg, changes in contractility indexes were similar to those in normal dogs; however, heart rate increased significantly (74 percent, P less than 0.005) in the trained greyhounds but not in normal dogs. Left ventricular diastolic stiffness did not differ from normal (51.6 +/- 3.0 versus 45.9 +/- 5.9 mm Hg/cm, P less than 0.01). These findings suggest that left ventricular function in exercise-induced left ventricular hypertrophy is substantially normal.

Animals↗

PubMed1992

Blunted cardiac responses to exercise-induced sympathetic stimulation in non-failing aortic regurgitation: insight into role of cardiac dilation in hyporesponse of failing hearts.

Although blunted cardiac response to sympathetic stimulation in patients with heart failure is usually attributed to myocardial beta 1-adrenoceptor downregulation secondary to elevated circulating catecholamines, cardiomegaly per se may also play a role through presynaptic mechanisms such as reduction in cardiac norepinephrine (NE) concentration. To evaluate effects of cardiac dilatation on cardiac response to sympathetic stimulation, we studied left ventricular contractile and heart rate responses to plasma NE levels increased by exercise in 10 asymptomatic patients with a dilated left ventricle due to aortic regurgitation (AR), but with normal resting plasma NE levels, using 10 normal subjects and 10 patients with heart failure due to dilated cardiomyopathy (DCM) as controls. Plasma NE levels, systemic blood pressure, echocardiographic left ventricular dimensions, and heart rate were measured at rest, and at 3 submaximal levels of supine bicycle exercise. The ratio of peak systolic blood pressure to end-systolic dimension (P/D ratio), heart rate, and plasma NE increased with the intensity of exercise. In each subject, both P/D ratio and heart rate increased in a logarithmic manner against plasma NE levels. The slope of the regression line for log (plasma NE)--P/D ratio relation, and that for log (plasma NE)--heart rate relation, were significantly less in patients with AR than in normal subjects (p less than 0.001 and p less than 0.05, respectively), and were less in patients with DCM than in patients with AR (p less than 0.005 and p = 0.051, respectively). Thus, the left ventricular contractile and heart rate responses to sympathetic stimulation are blunted in patients with dilated hearts due to AR, even in the absence of overt heart failure and elevated plasma NE levels. These responses were further decreased in patients with heart failure due to DCM. Cardiac responses to sympathetic stimulation appear to be blunted by cardiac dilatation per se, independently of myocardial beta 1-receptor downregulation secondary to high circulating catecholamines. The decrease in mechanical response to sympathetic stimulation in failing hearts is likely to be combined result of cardiac dilatation and beta 1-receptor downregulation.

Adult↗

PubMed1990

Iodine-123 phenylpentadecanoic acid myocardial scintigraphy in patients with left ventricular hypertrophy: alterations in left ventricular distribution and utilization.

Regional alterations in myocardial substrate uptake and/or utilization have been demonstrated in rats with hypertension. To determine whether alterations in left ventricular fatty acid uptake and/or utilization are present in patients with left ventricular hypertrophy (LVH), we compared the results of rest and exercise iodine-123 phenylpentadecanoic acid (IPPA) myocardial scintigraphy in 10 patients with hypertension who had concentric LVH without evidence of coronary artery disease and in 15 normal subjects. Patients with LVH had more heterogeneous left ventricular activity of IPPA compared to normal subjects after exercise but not at rest (23 +/- 8% versus 13 +/- 5% difference in maximum segmental activity at 4 minutes after exercise; p = 0.005). Although IPPA clearance was similar in both patients with LVH and normal subjects, postexercise washout in segments showing decreased initial IPPA uptake was reduced compared to washout at rest in patients with LVH (11.7 +/- 7.5% versus 21.5 +/- 8.4% at 20 minutes after injection, n = 15; p = 0.005). Exercise thallium-201 (TI-201) scintigraphy was normal in all seven patients with LVH tested. Patients with LVH showed significantly greater heterogeneity in IPPA uptake compared to TI-201 uptake immediately after exercise (25 +/- 5% versus 16 +/- 6%; p = 0.013). We conclude that (1) compared to normal subjects, patients with LVH show heterogeneous myocardial IPPA activity after exercise but not at rest; (2) postexercise washout of IPPA was decreased in segments with reduced uptake after exercise in patients with LVH; and (3) the distribution of IPPA is more heterogeneous than that of TI-201 immediately after exercise in patients with concentric LVH. The postexercise heterogeneity in IPPA uptake and delayed washout in segments with reduced initial uptake is consistent with exercise-induced myocardial ischemia in patients with LVH.

Adult↗

PubMed1989

Exercise body surface mapping in patients with left ventricular hypertrophy: comparison with stress thallium scans (SPECT).

To evaluate exercise-induced myocardial ischemia in patients with electrocardiographic evidence of left ventricular hypertrophy (LVH), including ST.T changes, body surface maps (QRST area maps) were recorded using 87 lead points before and after exercise. The patterns of the subtraction QRST area maps (S-maps) were compared with the findings of stress thallium (T1) scans in 31 patients with hypertrophic cardiomyopathy and in five with essential hypertension. All 18 patients whose S-maps revealed changes less than -40 muVS or only an increase over the anterior chest region showed no positive findings on the stress T1 scans. However, there were clearly positive findings on stress T1 scans in eight (89%) of nine patients whose S-maps revealed changes greater than -40 muVS over a wide precordial region or in six (67%) of nine patients whose S-maps revealed increases over the anterior chest region and had accompanying changes greater than -40 muVS somewhere over the precordial region. These results suggested that exercise QRST area maps could differentiate exercise-induced myocardial ischemia from LVH with ST.T changes.

Aged↗

PubMed1990

The effect of baseline electrocardiographic abnormalities on the diagnostic accuracy of exercise-induced ST segment changes.

Although exercise-induced ST segment depression is thought to be unreliable marker of myocardial ischemia in the presence of resting electrocardiographic changes, this conclusion is based on limited and disparate data from studies often lacking acceptable measures of ischemia. To determine the diagnostic accuracy of the ST segment response in a blinded prospective protocol, we compared ST deviation to thallium201 SPECT scintigraphy in 95 patients during exercise. Diagnostic accuracy was poor in the 95 patients with resting abnormalities: left bundle branch block (LBBB) = 70%, complete right bundle branch block (cRBBB) = 75%, incomplete right bundle branch block (incRBBB) = 79%, intraventricular conduction delay (IVCD) = 44%, left ventricular hypertrophy (LVH) = 59%, digitalis = 53%, compared with a diagnostic accuracy of 90% in 29 patients without resting changes. There were 20 false negative and 17 false positive ST segment responses. The extent and direction of resting ST deviation varied substantially and had no influence on diagnostic accuracy. The extent of change in ST deviation with exercise required for a positive response did not alter diagnostic accuracy: -1.0 mm = 61%, -1.5 mm = 63%, and -2.0 = 61%. While the location of regional ischemia did not influence the accuracy of ST segment analysis, a QRS duration less than 120 msec did improve diagnostic accuracy. Our data confirm that ST segment analysis with exercise testing is not reliable in patients with resting electrocardiographic abnormalities and demonstrates that accuracy is not improved by adjusting for either resting or exercise-induced ST segment changes or for location of the ischemic region.

Aged↗

PubMed1979

Exercise-induced ST elevation in patients without myocardial infarction.

A review of 6040 consecutive exercise tests yielded 106 patients without previous myocardial infarction (MI) who had exercise-induced ST elevation (greater than or equal to 0.5 mm in a 15-lead ECG system). In 46, ST elevation was correlated with left ventriculography and coronary angiography. Coronary artery disease (CAD) (greater than or equal to 70% narrowing) was detected in 40 of 46 patients: 12 patients had one-vessel disease, 13 had two-vessel disease, and 15 had three-vessel disease. Resting ventriculograms were normal in 36 of 40 patients. Of 21 patients with anterior (V1-V3) ST elevation, 86% had a left anterior descending (LAD) obstruction and 78% had obstruction proximal to the first diagonal branch. LAD disease occurred significantly more frequently than right and circumflex CAD. There was no anatomic correlation of three persons with lateral (leads V4--6, I or aVL) or 27 patients with inferior-posterior (leads II, III, aVF, Y or Z) exercise-induced ST elevation. Therefore, exercise-induced ST elevation is strongly correlated with CAD but not resting wall motion abnormalities. Further, anterior exercise-induced ST elevation in patients without a previous MI often predicts a significant proximal LAD obstruction.

Adult↗

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↗

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↗

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↗

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↗

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↗

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↗

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↗