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Cross-sectional and longitudinal studies are reviewed that address the effects of training on several measures of central circulatory function, including gas exchange, cardiac output, left ventricular structure, and left ventricular function. Responses to training in healthy individuals, athletes, and patients with ischemic cardiovascular disease are compared.
The use of early coronary angiography to assess the benefits of coronary patency on left ventricular size and function fails to account for subsequent reocclusion or spontaneous reperfusion. To investigate the relationship between late vessel patency and changes in left ventricular structure and function after thrombolysis, echocardiography was performed within 48 hours and at 6 to 12 weeks in 30 patients treated with intravenous thrombolysis. Left ventricular endocardial surface area index (ESAj; cm2/m2) and extent of abnormal wall motion were quantitated in those with a patent (n = 20) and those with an occluded (n = 10) infarct-related artery on coronary angiography performed 8 +/- 6 days after thrombolysis. Mean ESAi increased from (53 +/- 7 to 61 +/- 10 cm2/m2; p less than 0.02) in the occluded group during the follow-up period but remained unchanged (60 +/- 11 to 62 +/- 11 cm2/m2; p = NS) in the patient group. Mean percentage of abnormal wall motion decreased in the patent group (27 +/- 16% to 18 +/- 16%; p less than 0.01), whereas no significant change was noted in the occluded group (20 +/- 13% to 23 +/- 17%; p = NS). Thus coronary patency at days after thrombolysis is associated with both improvement in regional left ventricular function and attenuated left ventricular dilatation.
Use of echocardiography to quantify left ventricular structure and function requires standardization of recording conditions and techniques, accurate machine calibration, and definition of requirements for measurable images. Measurement of left ventricular muscle mass should use M-mode, two-dimensional, or three-dimensional echocardiographic methods that have been anatomically validated to maximize accuracy and comparability of results among studies. Body size and sex influence ventricular muscle mass sufficiently to be taken into account for clinical and research purposes, while age and physical activity are of less certain importance. Echocardiographic studies have clarified the prevalence of left ventricular hypertrophy in hypertensive patients and the effect of blood pressure during normal activity on left ventricular muscle mass, and they have provided data suggesting that left ventricular hypertrophy is a major cardiac risk factor in hypertensive and general populations. Further research is needed to obtain definitive results in these areas, to track the hitherto elusive transition from functionally compensated cardiac hypertrophy to congestive heart failure, and to determine the degree and selectivity of beneficial cardiac effects of antihypertensive treatment. Three-dimensional echocardiographic reconstruction and Doppler measurement of intracardiac blood flow and systemic hemodynamics are likely to extend the usefulness of echocardiography for hypertension and general population research.
OBJECTIVE: To evaluate the left ventricular function of hypertensive patients with abnormal diurnal change in blood pressure. DESIGN: We compared left ventricular structural and functional characteristics between hypertensive patients with a normal diurnal change in blood pressure (H2 group) and those with a nocturnal blood pressure increment (H1 group) using echocardiography. METHODS: The study group consisted of 36 hypertensives and 16 normotensives whose 24-h ambulatory blood pressure monitorings were measured non-invasively. The hypertensive group was subdivided into the H1 group, consisting of 11 patients (76 +/- 7 years), and the H2 group with 25 patients (73 +/- 7 years). The normotensive control group had a mean age of 73 +/- 6 years. Echocardiographic examinations were performed before and at the end of isometric exercise (handgrip for 3 min) and isoproterenol infusion (0.02 micrograms/kg per min for 5 min). RESULTS: The left ventricular mass index in the H1 group was significantly greater than in the H2 or control group. Left ventricular fractional shortening (LVFS) at rest in the H1 group was also significantly greater than in the other two groups. However, the peak late: early diastolic filling ratio, which indicated diastolic function, significantly deteriorated in the H1 group compared with the H2 and control groups. Furthermore, changes in LVFS after isometric exercise in the H1 group were more suppressed than in the H2 or control group. In addition, a significantly lower increment in LVFS after isoproterenol was observed in the H1 group compared with the H2 or control group. CONCLUSION: The H1 group had greater left ventricular mass and impaired left ventricular functional reserve than the H2 group.
OBJECTIVE: The aim was to determine left and right ventricular functional reserves and collagen concentration during the development of cardiac hypertrophy and after its regression. METHODS: Two experimental models of cardiac hypertrophy (chronic thyroxine or isoprenaline treatment of adult rats) were compared 24 h and five weeks after the agent was last given. Pressure changes in the left (right) ventricle before and after acute aortic (pulmonary artery) ligation were recorded in open chest anaesthetised animals. The difference in dP/dtmax after and before ligation was regarded as the functional reserve. The total collagen concentration was determined in both ventricles separately by means of hydroxyproline. RESULTS: Left and right ventricular weight increased by 20% and 30% respectively in the two models employed. In the thyroxine treated group, the functional reserve of the left ventricle rose very noticeably, whereas in the isoprenaline treated group it decreased. The right ventricular functional reserve did not differ from that in the controls in either of the two groups. The collagen concentration rose in the left ventricle in the isoprenaline group only. Five weeks after the last administration of the agent, cardiac mass and ventricular function did not differ from the control values in either of the models studied; the only exception was the incomplete regression of left ventricular hypertrophy and persistent structural and functional impairment of the left ventricle in the isoprenaline treated group. CONCLUSIONS: Our results indicate that hearts undergoing a comparable degree of experimental hypertrophy may have different functional and structural properties; significant differences were found between the right and left ventricular response. Regression of hypertrophy together with a reversal of ventricular function usually occurs unless the myocardium has received severe structural damage.
The pathogenesis of reduced systolic left ventricular function in dilated cardiomyopathy is yet unclear. To analyze a possible involvement of contractile protein, function and structure of left ventricular myofibrils were examined in hearts of patients with advanced cardiomyopathy undergoing heart transplantation and in normal control hearts (from renal transplant donors). Myosin and actin content of the left ventricular myocardium was slightly reduced in cardiomyopathic hearts. Myofibrillar polypeptide composition was determined using two-dimensional electrophoresis and immunoblotting. No differences in constituting polypeptides were apparent, including Z-line proteins and proteins of the endosarcomeric lattice. M-line-bound creatine kinase was identical in both groups. Further, basal and maximal myofibrillar adenosine triphosphatase (ATPase) activities were unaltered in dilated cardiomyopathy. The structure of purified myosin was identical in both groups by the following criteria: electrophoretic mobility of native myosin, identical pattern of light chains after isoelectric focusing, identical cleavage peptides of myosin's heavy chain, and identical patterns after immunoblotting of heavy chain cleavage peptides using polyclonal antibodies generated against myosin from normal and cardiomyopathic ventricles. Ca2+-activated, K+-EDTA-activated and actin-activated myosin ATPase activities were identical in control and cardiomyopathic hearts. A structural alteration or functional defect of myofibrils does not seem to be primarily involved in the pathogenesis of reduced myocardial contractility in dilated cardiomyopathy.
As the effects of anabolic steroids on left ventricular structure and function are unknown, we carried out clinical examination, 12 lead electrocardiography and echocardiography on a 23 year old male bodybuilder using these drugs. In this subject we found values of ECG voltage criteria, left ventricular-mass, posterior wall and interventricular septal thickness which exceeded those found in normal subjects and also in other competitive, power athletes. Despite these values, however, ejection fraction remained normal. This would suggest that anabolic steroids perhaps have a direct effect on the myocardium, in addition to the effects of training, but whether this is of pathological significance is unclear.
In 14 essential hypertensive patients, aged 26-59 years, blood pressure, left ventricular mass index (LVMI), systolic function (M-mode echo, two-dimensionally guided), post-ischaemic 'maximal' forearm blood flow (strain gauge venous occlusion plethysmography), plasma renin activity, plasma catecholamines and aldosterone were measured before and after 6 and 12 months of treatment (eight patients were given captopril, 100 mg/day, + hydrochlorothiazide 25 mg/day in five patients, and six patients were given nitrendipine, 20 mg/day, + atenolol 50 mg/day in four patients). Minimal vascular resistance (mean blood pressure/peak forearm blood flow) was taken as an index of arterial structural changes. After 6 months of treatment significant reductions in blood pressure (P less than 0.001), LVMI (P less than 0.001) and minimal vascular resistance were observed. After 12 months of treatment blood pressure, LVMI and minimal vascular resistance were further reduced. The LVMI was normalized in nine cases and the minimal vascular resistance in two cases only. Aldosterone and plasma catecholamines did not change, whereas plasma renin activity was increased during captopril only. Before and during treatment the left-ventricular shortening fraction in relation to end-systolic stress in each patient at rest, and at peak of handgrip and cold pressor tests, fell within the 95% confidence limits of correlation obtained in normals. Thus, in essential hypertensives long-term treatment can induce normalization of LVMI before complete regression of arterial structural changes in the forearm. Left ventricular systolic function is preserved after normalization of LVMI, both at rest and during stress.
To clarify the hemodynamic effects of verapamil, we investigated in normal volunteers the effects of 4-day treatment with verapamil (240 mg/day) on left ventricular function and on systemic and brachial artery haemodynamics, in comparison with the effects of placebo and atenolol (100 mg/day). Left ventricular structure and function was evaluated by echocardiography, systemic hemodynamics were assessed by pulsed Doppler velocimetry of the ascending aorta, and brachial artery hemodynamics were assessed pulsed Doppler velocimetry of the brachial artery. Verapamil decreased systemic and brachial artery vascular resistance (p less than 0.05), increased cardiac output (CO, p less than 0.01) and brachial flow (p = 0.054), and did not affect blood pressure (BP) and heart rate (HR). In contrast, atenolol decreased BP, HR, and CO (p less than 0.001) but did not significantly affect brachial flow and systemic and brachial artery vascular resistance. We conclude that short-term administration of verapamil in normal humans produces systemic and brachial artery vasodilatation, with a reflex increase of stroke volume but not of HR.
To study the time course of left ventricular structural and functional responses to chronic aortic regurgitation, aortic regurgitation was surgically induced in rabbits, and Doppler echocardiography was performed preoperatively and serially postoperatively for up to 2.5 yr. Twenty-five New Zealand White rabbits underwent surgical induction of aortic regurgitation and 13 control animals underwent sham operation. Left ventricular endocardial and epicardial surfaces were digitized from M-mode echocardiograms to measure the rates of change of cavity dimensions and wall thicknesses during diastolic relaxation and systolic contraction. Aortic regurgitant animals developed left ventricular dilatation and eccentric hypertrophy that remained relatively stable throughout the follow-up period. Compared with baseline values, left ventricular mass increased 120% and left ventricular internal dimension at end diastole increased 40%, whereas posterior wall thickness at end diastole and fractional shortening remained relatively stable. Left ventricular diastolic performance was enhanced at 6 mo after operation, a finding associated with increased volume load and heart rate following induction of aortic regurgitation. Diastolic performance was then reduced at 12 mo after operation and demonstrated no further decline throughout the remainder of the follow-up period. In contrast, left ventricular systolic performance was not altered following operation and remained preserved until the final assessment at up to 2.5 yr. Thus alterations in diastolic performance occurred without impairment of systolic performance during long-term follow-up of chronic experimental aortic regurgitation.
This study evaluated by noninvasive methods the cardiac structure and functional characteristics of world class athletes participating in different types of training programs. Fourteen subjects, including 4 strength-trained (discus and shot put), 4 endurance-trained (long distance runners), 4 decathlon-trained (strength and endurance), 2 wheelchair athletes and 31 college-age control subjects were evaluated using electrocardiography, M-mode echocardiography and maximal oxygen consumption. M-mode echocardiography measurements of left ventricular structure and function were compared before and after normalization for lean body weight. As expected, endurance athletes had greater maximal O2 consumption than the other groups (p less than 0.05). Before normalization for lean body weight, there were no significant differences in end-diastolic dimensions. After normalization, the endurance, wheelchair and control subjects had end-diastolic dimensions larger than those of strength athletes. Strength athletes appeared to have a much larger posterior wall and septal thickness than all groups except the decathlon athletes. However, when normalized, there was no difference among any of the groups. Previous investigators have attempted to determine "normalcy" of cardiac hypertrophy by looking at the ratio of left ventricular wall thickness to left ventricular radius. In the present study, the thickness to radius ratio in strength athletes was 33% greater than that in endurance athletes. It appears that the left ventricular wall thickness in the strength athletes occurred without a concomitant increase in left ventricular radius and that the left ventricular hypertrophy of world class athletes is related to the total increase in lean body weight. However, ventricular dimensions may be related more to the type of overload experienced.
Left ventricular functional and structural adaptations to mild essential hypertension were assessed by 2D-guided M-mode echocardiography in a population of premenopausal and postmenopausal women (n = 29) who were matched with the same number of men with regard to mean arterial pressure, age and race. Premenopausal women had a thinner posterial wall (P less than 0.05), a smaller left ventricular systolic and diastolic diameter, and a smaller left ventricular mass than men with the same level of arterial pressure. Left ventricular performance indices, ejection fraction, velocity of circumferential fibre shortening, and the ratio of the end-systolic wall stress to the end-systolic volume index (a load-insensitive contractility index) were higher in women than in men. These sex differences were most pronounced before the menopause and tended to disappear thereafter. We conclude that in the presence of the same level of arterial pressure, women have smaller left ventricular dimensions and enhanced ventricular performance compared with men. These differences in cardiac adaptations between the genders may account for the lower risk of cardiovascular morbidity and mortality in premenopausal women with essential hypertension.
Fifteen children and adolescents who had repair of coarctation of the aorta before age 15, who were not hypertensive at rest, and who had resting arm-leg blood pressure gradients of less than 20 mm Hg underwent noninvasive evaluation of left ventricular structure and function, aortic stiffness, and residual coarctation as well as bicycle exercise testing. These results were compared with those in 15 age- and sex-matched control subjects. The mean resting age-related systolic blood pressure percentiles (63% versus 46%), transverse aortic stiffness measured by the elastic modulus (Ep) (42.1 versus 23.2 kPa), stiffness index beta (beta) (3.66 versus 2.17), echocardiographic left ventricular fractional shortening (0.42 versus 0.36), left ventricular mass index (99.3 versus 81.0 gm/m2), maximum exercise right arm systolic blood pressure (173 versus 156 mm Hg), and exercise arm-leg blood pressure gradient (35 versus 6 mm Hg) were significantly increased in the coarctectomy patients compared with controls. Univariate correlations in the coarctectomy group showed significant relationships of residual aortic narrowing with left ventricular mass index (r = 0.68, p less than 0.01) and resting systolic blood pressure percentile for age (r = 0.55, p less than 0.05). Residual aortic narrowing did not significantly correlate with aortic stiffness, resting blood pressure gradient, or exercise blood pressure gradient. Neither left ventricular mass index nor resting systolic blood pressure percentile significantly correlated with age of repair or years after repair. These results demonstrate persistent abnormalities in aortic stiffness and left ventricular mass and function after successful repair of coarctation of the aorta in childhood and adolescence.(ABSTRACT TRUNCATED AT 250 WORDS)
In order to investigate the potential role of atrial natriuretic peptide (ANP) in mild to moderate essential hypertension, a study was conducted in groups of normotensive and hypertensive middle-aged men born in 1926 and 1927. Venous plasma concentrations of immunoreactive ANP (irANP) were studied in relation to measurements of cardiac structure and function, urinary electrolytes as well as some cardiovascular hormones. Plasma irANP did not differ between normotensive controls (31 +/- 14 pmol l-1) and borderline or untreated hypertensive patients. However, irANP concentrations were slightly but significantly (P less than 0.05) lower in the borderline (26 +/- 8 pmol l-1) compared to the untreated established hypertensives (35 +/- 14 pmol l-1). No relationships were found between irANP and blood pressure, indices of left ventricular structure and function or hormone parameters in subgroups or the whole study group. Our data do not support the view that plasma irANP is increased in uncomplicated essential hypertension, since our groups of borderline or established hypertensive middle-aged men without major cardiac involvement did not differ in irANP concentrations compared to normotensive controls. Thus, during the development or in the early stages of essential hypertension, ANP secretion does not seem to be abnormal.
To compare the efficacy of new calcium blocker nitrendipine and ACE-inhibitor captopril on the regression of hypertensive left ventricular hypertrophy (LVH), 134 hypertensive subjects with LVH were divided randomly into two groups. 2DE, M-mode and pulsed Doppler echocardiography was used to measure the left ventricular structure and function. In the nitrendipine group (n = 67, mean age 48 +/- 11 years), nitrendipine (20-40 mg/day) was administered for 24 months, and in the captopril group (n = 67, mean age 47 +/- 12 years), captopril (75-150 mg/day) was also given for 24 months. Blood pressure decreased significantly in all the patients. In the nitrendipine group, the thickness of the interventricular septum (IVST) and the posterior wall of the left ventricle (PWT) as well as the left ventricular mass index (LVMI) decreased by 20.3%, 15.5% and 25.7% (P less than 0.01) respectively. The cardiac index (CI), left ventricular ejection fraction (EF) and fractional shortening (FS) remained unchanged. The early peak filling velocity (E, 0.64 +/- 0.15 to 0.86 +/- 0.22, P less than 0.01) of the mitral valve and E to late peak filling velocity ratio (E/A, 0.88 +/- 0.20 to 1.31 +/- 0.31, P less than 0.01) increased significantly. In the captopril group, IVST, PWT, and LVMI were 20%, 17.1% and 23.6% respectively (P less than 0.01). CI (2.6 +/- 0.5 to 3.7 +/- 0.6L/min/m, P less than 0.01) and EF (60 +/- 4 to 78 +/- 6%, P less than 0.01) increased. Both E and E/A were elevated in a similar degree as in the nitrendipine group.(ABSTRACT TRUNCATED AT 250 WORDS)
UNLABELLED: Between June 1978 and 1986, 93 consecutive patients underwent electrophysiologically guided operations for life-threatening recurrent sustained ventricular tachycardia mostly associated with other surgical procedures, such as left ventricular resection (aneurysmectomy) and coronary artery bypass grafting. DATA: Eighty-seven percent of the surviving patients were free of spontaneous ventricular tachycardia return or sudden death 1 year after the operation and 77% at 5 years. The instantaneous risk of ventricular tachycardia return was highest immediately after operation, declined rapidly, and by 2 weeks postoperatively had merged with the constant hazard phase, which persisted as long as the patients were observed. Endocardial resection, rather than encircling endocardial myotomy, increased the risk of spontaneous ventricular tachycardia return/sudden death. Survival rates, including hospital deaths, were 95% at 30 days, 89% at 1 year, and 70% at 5 years after operation. The most prevalent mode of death was heart failure. The absence of anterolateral left ventricular aneurysms and the use of more extended encircling incisional techniques for ventricular tachycardia ablation increased the risk of early and late death. Survival was particularly poor in that subset of patients in whom recurrent sustained ventricular tachycardia returned after operation; the most prevalent mode of death in this group was also progressive left ventricular failure. Inferences: (1) Complete and partial encircling endocardial myotomy incisions are the most effective surgical techniques for malignant ventricular tachycardia ablation. (2) Because of their adverse effects on left ventricular structure and function, the arrhythmogenic tissues have to be localized as precisely as possible, and the encompassing incisions should be kept as limited as possible. (3) The late return of ventricular tachycardia may be more related to a progressive ischemic left ventricular cardiomyopathy than to an inadequate operation.
To assess left ventricular structure and function at rest and during exercise in endurance athletes, 10 elite marathon runners, aged 28 to 37 years, and 10 matched nonathletes were studied by echocardiography and supine bicycle ergometry. Each athlete's best marathon time was less than 2 h 16 min. Echocardiography was performed at rest, at a 60 W work load and at an individually adjusted work load, at which heart rate was 110 beats/min (physical working capacity 110 [PWC110]). Oxygen uptake at PWC110 averaged (+/- SD) 1.14 +/- 0.2 liters/min in the nonathletes and 2.0 +/- 0.2 liters/min in the runners (p less than 0.001). The left ventricular internal diameter at end-diastole was similar at the three activity levels in the control subjects but increased significantly from rest to exercise in the runners (p less than 0.001). Left ventricular systolic meridional wall stress remained unchanged during exercise in the nonathletes but was significantly higher at PWC110 in the athletes (p less than 0.05). Both the systolic peak velocity of posterior wall endocardial displacement and fractional shortening of the left ventricular internal diameter increased with exercise; at PWC110 the endocardial peak velocity was higher in the runners than in the control subjects (p less than 0.01). The endocardial peak velocity during relaxation was comparable in athletes and control subjects at rest, increased similarly at a 60 W work load, but was higher in the runners at PWC110 (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
To study the earliest changes in left ventricular structure and function appearing in response to hypertensive heart disease the study was started with an initial group of subjects detected for the first time in their lives with elevated levels of systemic blood pressures. A careful follow up of these subjects during the next year allowed the division of these subjects into a group of healthy not hypertensive subjects and a group of subjects with mild essential systemic hypertension detected in an early phase. The next six years of repeated controls (arterial blood pressure measurement, clinical examination, routine chest X-ray pictures, standard 12 leads ECG and M-mode echocardiography) allowed a further division of the hypertensive subjects into two groups of patients: one correctly treated and the other treated incorrectly or not at all. It was found that left ventricular diastolic functions expressed by left ventricular relaxation time index (LVRTI) and left atrial emptying index (LAEI) are the earliest indicators of hypertensive heart disease due to mild essential systemic hypertension.