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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 18 adult mongrel dogs (24.6 kg) a statistically significant left ventricular hypertrophy (LVH) was induced by chronic aortic coarctation (180 days). In 12 anesthetized dogs (LVH 1) the effect of increasing doses of catecholamines on maximum contractility, expressed by (dp/dt)max, Vpm, t-(dp/dt)max was determined in comparison to a control group (KO 1; N = 6). There was no depression of the acute maximum contractility of hypertrophied hearts compared with the controls, also in respect to other haemodynamic parameters (SV/10 kg, HR, LVEP). In 6 other LVH-dogs (LVH 2) the maximum reached left ventricular pressure - obtained by complete clamping of the ascending aorta - was significantly higher. Either pressure per 100 g left ventricle did not differ significantly.
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PMID:[Contractility, pressure and volume reserve of pressure-hypertrophied hearts in situ]. 13 Jul 49

This study examined the recuperative potential of cat hearts subjected to experimental right ventricular pressure overload (for a 10- to 14-day period) which provoked hypertrophy with and without congestive heart failure. Five groups of cats were studied: normal controls; one group with 70% pulmonary artery constriction which produced right ventricular hypertrophy (RVH); one group with an 87% constriction which also produced right ventricular hypertrophy but with congestive heart failure (CHF); and two groups which had been similarly subjected to pressure overload but which had been allowed a recovery period of 30 days after relief of the pressure overload. Both the 70% and 87% pulmonic constrictions were associated with extensive right ventricular hypertrophy, depression of myocardial contractile function, and severe redlction of cardiac norepinephrine stores (normal, 1.42 mug/g: RVH, 0.11 mug/g; CHF, 0.01 mug/g). After a 30-day period of relief from the pulmonic constriction normal hemodynamic function returned. In cats in which RVH had been relieved, right ventricular weight and contractile function were normal but catecholamine depletion persisted. Cats with relieved CHF showed depressed contractile function and depleted myocardial norepinephrine, and the right ventricular weight did not return to normal. Cardiac muscle of all pressure-overloaded nonrelieved hearts showed depressed velocity of shortening and depressed ability to sustain load. Cats with RVH alone regained normal muscle shortening velocity and load-bearing ability after relief. However, cardiac muscle from the CHF-relieved group recovered only unloaded shortening velocity while the ability to sustain load remained depressed. We conclude that the recuperative potential of myocardium damaged by pressure overload is adequate provided congestive heart failure has not occurred. Heart failure produces a persistent reduction in force-generating ability of the myocardium. Hypertrophy due to pressure overload, with or without CHF, leads to cardiac catecholamine depletion which is not readily reversed by relief of the overload.
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PMID:Recuperative potential of cardiac muscle following relief of pressure overload hypertrophy and right ventricular failure in the cat. 13 86

To assess the adaptation of the left ventricle to a chronic pressure overload we used echocardiography to study 18 patients with left ventricular hypertrophy caused by systemic arterial hypertension. Increased values for either posterior wall or interventricular septal thickness or both confirmed the presence of left ventricular hypertrophy in all patients and an increase in the average wall thickness to radius ratio was consistent with the development of concentric hypertrophy. No patient had clinical evidence of ischaemic heart disease. Ejection phase indices of left ventricular performance (mean Vcf, fractional per cent of shortening, normalised posterior wall velocity, and ejection fraction) were within the normal range in the basal state in 16 of the 18 patients. The hypothesis is advanced that patients with concentric left ventricular hypertrophy resulting from systemic arterial hypertension usually have normal left ventricular performance in the basal state because values for wall stress remain within the normal range. We conclude that the hypertrophic response to a chronic increase in systemic arterial pressure does not per se result in depression of the basal inotropic state of the left ventricle.
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PMID:Left ventricular performance in patients with left ventricular hypertrophy caused by systemic arterial hypertension. 14 28

Sixty-two autopsied hearts, with left ventricular hypertrophy (LVH) caused by mitral regurgitation (MR), aortic failure (AR), combined valvular disease (CVD), hypertension (HHD), or ischemia (IHD), and 23 control hearts with normal left ventricles were studied morphologically for analysis of modes of hypertrophy and for ECG-pathology correlation. Basic disorders modify the mode of hypertrophy; that is, elongated AR-type LV makes muscle fiber orientation in the outer layer more vertical, and globular MR-type LV makes it more horizontal than normal. High-voltage QRS correlates with hypertrophy of the outer layer which is often associated with that of the inner layer. ST depression and T changes correspond to relative deterioration of the inner and median layers, respectively.
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PMID:Histopathological study of hypertrophied myocardium of known etiologies with special reference to correlation of ECG changes. 14 36

A review of electrocardiograms from 33 patients with nonobstructive hypertrophic cardiomyopathy was made. In 22 patients there was noted a high QRS voltage, depression of the ST segment, and inversion of the T wave, satisfying the diagnostic criteria of left ventricular hypertrophy with the abnormal changes not only extending to the midprecordial leads but showing the most striking abnormal changes in Lead V4 in 20 patients. The frontal plane electrical axis was normal (around 60 degrees), with the most remarkable changes in Lead II. In the VCG, the magnitude of the QRS loop was increased and directed anteriorly and to the left, and the T loop was deviated posteriorly and to the right opposite the QRS loop. The asymmetric septal and apical hypertrophy was noted on echocardiography and/or angiocardiography. The coronary arteries were normal without significant obstruction in selective coronary angiography. It was postulated that the asymmetric septal and apical hypertrophy was reflected in this ECG pattern. The recognition of this ECG pattern provides pertinent information in the clinical detection of nonobstructive HCM.
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PMID:ECG pattern of left ventricular hypertrophy in nonobstructive hypertrophic cardiomyopathy: the significance of the mid-precordial changes. 15 93

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.
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PMID:Idiopathic hypertrophic subaortic stenosis: evaluation of anginal symptoms with thallium-201 myocardial imaging. 15 76

One third of 160 operatives working in a permanently noisy industrial environment, within the range of 63-8000 Hz and intensity of sound of about 100 db, were found to suffer from a syndrome of neurocirculatory asthenia and 8.1% from arterial hypertension. Study of the ECG according to the criteria of the Minnesota code showed an increased frequency of upward deflection of ST segment (index 9-2) in 20.6% of the cases, depression of the ST segment with an ascending orientation in 50.62% of the cases and left ventricular hypertrophy (index 3-1 and 3-3) in 20% of the cases. Audiometry revealed loss of hearing at frequencies of 4000 CS in 16.1% of the cases. The results obtained suggest that the detrimental effects are not restricted only to hearing, but also that the alterations detected might evolve towards organic cardiac disorders.
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PMID:Study of cardiovascular and auditory pathophysiological implications in a group of operatives working in noisy industrial surroundings. 40 53

Hypertrophic cardiomyopathy is a common cause of prominent non-infarctional Q waves. A retrospective analysis of previously published cases confirmed a characteristic Q wave T wave vector discordance in hypertrophic cardiomyopathy. In 41 of 44 cases with predominant Q waves (as part of QS or Qr complexes where Q wave amplitude exceeded R wave height), the T wave was positive, and in all cases with QS type complexes the T wave was positive. This characteristic electrocardiographic sign probably represents a pattern of septal hypertrophy and strain (Q waves with positive T waves and ST segment elevation) which is the inverse of the classical pattern of left ventricular hypertrophy and strain (tall R waves with inverted T waves and ST segment depression).
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PMID:Q wave T wave vector discordance in hypertrophic cardiomyopathy: septal hypertrophy and strain pattern. 57 21

A group of 215 men and 272 women aged 62 to 90 forming a randomly-selected sample of the older population was studied by cardiovascular survey methods and followed for 5 years. The 5-year mortality of 28 per cent was related to age and was higher in men. Ischaemic heart disease was the certified cause of 28 per cent of the deaths. Mortality was greater in those with systolic hypertension. Among electrocardiographic features ST depression, T inversion, and atrial fibrillation increased overall and ischaemic heart disease mortality independently of their association with age. A positive response to an angina and infarct questionnaire was poorly related to subsequent mortality. Re-examination of 72 per cent of 5-year survivors was possible. Systolic and diastolic blood pressures were significantly lower and the frequency of electrocardiographic abnormalities, particularly left axis deviation, left ventricular hypertrophy, and ST and T wave changes, was increased.
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PMID:Longitudinal survey of ischaemic heart disease in randomly selected sample of older population. 90 84

The incidence of positive submaximal treadmill exercise tests was evaluated in patients with mitral stenosis and aortic stenosis, no electrocardiographic evidence of left ventricular hypertrophy, and normal coronary arteries on angiography. Seven of 19 patients (37 percent) with aortic stenosis (53 to 80 mm Hg gradient across the aortic valve) had greater than or equal to 1.0 mm of ischemic S-T segment depression during or after a submaximal treadmill test. Three of 15 patients (20 percent) with mitral stenosis (11 to 22 mm Hg mean gradient across the mitral valve) had greater than or equal to 1.0 mm of ischemic S-T segment depression during or after a submaximal treadmill exercise test. Patients with significant valvular disease, no electrocardiographic evidence of left ventricular hypertrophy, and normal coronary arteries may have a positive submaximal treadmill exercise test due to an unfavorable balance between myocardial oxygen supply and myocardial oxygen demand.
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PMID:Treadmill exercise test in aortic stenosis and mitral stenosis. 117 8


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