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

Electrocardiograms of 90 patients with arteriographically documented acute submassive or massive pulmonary embolism and no associated cardiac or pulmonary disease were studied. Patients were derived from the Urokinase-Pulmonary Embolism Trial National Cooperative Study. In massive embolism, the electrocardiogram was normal in 6 per cent (3 of 50) of patients. With submassive embolism, 23 per cent of patients (9 of 40) had a normal electrocardiogram. Since one or more of the traditional manifestations of acute cor pulmonale (S1Q3T3, right bundle branch block, P pulmonale, or right axis deviation) occurred in only 26 per cent of patients, one could not rely exclusively upon these electrocardiographic abnormalities for the diagnosis of pulmonary embolism. The most common electrocardiographic abnormalities were nonspecific T wave changes which occurred in 42 per cent of patients and nonspecific abnormalities (elevation or depression) of the RST segment which occurred in 41 per cent of patients. Left axis deviation occurring in 7 per cent of the patients was as frequent as right axis deviation. Low voltage QRS complexes, previously undescribed in pulmonary embolism, occurred in 6 per cent of patients. None of the patients had atrial flutter or atrial fibrillation, which appears to occur more typically in patients with pulmonary embolism who have preexistent cardiac disease. All of the varieties of electrocardiographic abnormalities disappeared in some of the patients by 2 wk. Inversion of the T wave was the most persistent abnormality. Larger defects on the lung scan or pulmonary arteriogram occurred in patients with various abnormalities on the electrocardiogram than in patients with normal electrocardiograms. The pulmonary arterial mean pressure and/or right ventricular end-diastolic pressure was significantly higher in patients with several varieties of abnormal electrocardiograms, although the partial pressure of oxygen in arterial blood, in general, did not differ from that in patients with normal electrocardiograms. These hemodynamic correlations, made for the first time in patients, suggest that acute ventricular dilatation, possibly in combination with hypoxemia, is a causative factor of the electrocardiographic changes in acute massive or submassive pulmonary embolism.
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PMID:The electrocardiogram in acute pulmonary embolism. 12 74

A study was made of 34 patients with valve defects or arterial hypertension and a haemodynamic picture of left ventricle pressure or volume load. Echocardiography and haemodynamic investigated-established the size and mass of the left ventricle and also enabled its indices of contractility, relaxation and distensibility to be determined. The series was divided in accordance with the dynamic geometry of the left ventricle. In concentric hypertrophy, telediastolic rigidity increased in proportion to ventricular thickness and mass. In eccentric forms and ventricular dilatation, diastolic distensibility was reduced in cases with a high filling pressure. The relaxation values bore no relationship to distensibility and telediastolic compliance. The relaxation rate in protodiastole diminishes in proportion to functional depression of the left ventricle.
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PMID:[Dynamic geometry of the left ventricle. Relaxation and elasticity indices]. 15 May 54

Eighty-five studies of regional cerebral blood flow (rCBF) were performed on 49 patients with ruptured intracranial aneurysms. The changes in rCBF were analyzed under various pathophysiological conditions, The degree of flow abnormalities correlated well with the clinical severity of neurological deficits. All of the patients with diffuse vasospasm of severe grade, to less than half of their control value, showed focal areas of decreased flow below 30 ml/100 gm/min, in addition to a reduction in mean CBF. The relief or disappearance of vasospasm in angiograms was followed by the increase of rCBF in the ischemic focus and mean CBF. Marked reduction in rCBF was found in patients with intracerebral hematoma and ventricular dilatation. Impaired CO2 response and autoregulation were found in patients with severe neurological deficits, a severe degree of vasospasm and marked depression of CBF. In this series direct operation was delayed in patients with impaired vascular reactivity as well as marked decrease of mean CBF below 30 ml/100 gm/min; good clinical results were obtained in thses patients.
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PMID:Regional cerebral blood flow in patients with ruptured intracranial aneurysms. 43 Jan 52

Four to 5 months after exposure of the right occipital lobe of the monkey to 3500 rads of X-irradiation there is a proliferative and degenerative lesion accompanied by a massive break in the blood-brain barrier. The resulting vasogenic edema causes gross swelling in the ipsilateral hemisphere, compression of the contralateral hemisphere with ventricular dilatation, and distortion of midline structures, which may result in herniation through the incisura and foramen magnum. The regional cerebral blood flow, determined by [14C]antipyrine method, at successive stages in the development and resolution of the delayed brain swelling shows a reduction of blood flow in white and gray matter, first regionally, then throughout the ipsilateral hemisphere and finally throughout the brain. This is accompanied by an increase in CSF pressure, CSF lactic dehydrogenase and total protein, and clinical signs of increased intracranial pressure. With resolution of CSF pressure, there is a return to baseline of CSF chemistry and partial resolution of the other parameters. The cerebral blood flow shows a greater recovery in gray than white matter, but there remains a diffuse depression suggesting a long-term impairment in cellular metabolism and/or blood flow regulatory mechanisms.
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PMID:Regional cerebral blood flow in delayed brain swelling following x-irradiation of the right occipital lobe in the monkey. 80 11

We studied 16 patients with chronic mitral regurgitation by echocardiography before, and at 3 weeks, at 6-8 months and at 1-9 years after mitral valve replacement (MVR) to investigate serial changes in left ventricular (LV) function and reversal of ventricular dilatation. All patients at an average of 2.6 years after, and 8 patients before MVR were also studied by echocardiography and, except for 3 patients by measuring plasma catecholamines from the right atrium during bicycle exercise. Before operation, all patients were divided into group A (n = 12) with end-systolic dimension (ESD) < 4 cm and systolic blood pressure (SBP)/ESD > 3, and group B (n = 4) with ESD > 4 cm and SBP/ESD < 3. Maximum reduction in end-diastolic dimension (EDD) occurred at 3 weeks in all patients after MVR (from 60.5 +/- 3.7 to 49.0 +/- 4.5 mm, p < 0.05). ESD was reduced significantly (p < 0.5) only in group A. LV function was normal in group A, but it was depressed in group B at early and late periods after MVR. The slopes of the relationship between the mean velocity of circumferential fiber shortening (Vcf) and plasma norepinephrine (NE) during exercise in all patients in group B decreased along with the depression in LV function. After operation, all patients in group A reached New York Heart Association (NYHA) functional class I, while patients in group B were in NYHA class II. It is concluded that the surgical outcome after MVR for chronic MR will be better if preoperative ESD < 4 cm and SBP/ESD > 3. The relationship between mean Vcf and plasma NE during exercise seemed to be a useful index to evaluate the inotropic reserve of the LV.
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PMID:Determinants of subsequent late postoperative left ventricular function and reversal of ventricular dilatation after mitral valve replacement for chronic mitral regurgitation. 128 93

Serial electrocardiograms as well as echocardiographic studies of 51 pilgrims suffering from acute heat stroke (mean rectal temperature 41.6 degrees C) were performed. All patients were examined immediately after cooling and 24 h later whenever possible. Regional wall motion abnormalities were detected in 9 cases (17.6%) while pericardial effusion was observed in 13 cases (25%) and asymmetrical septal hypertrophy was detected in 8 cases (15.6%). Other cardiac abnormalities included right ventricular dilatation and increased in left ventricular internal dimensions in 4 cases (7.8%), respectively. Thirteen cases (25.5%) had normal echocardiographic findings. Forty (78%) patients had sinus tachycardia while 8 cases (15.7%) showed atrial fibrillation with uncontrolled ventricular rate, and 3 (5.8%) had sinus bradycardia. Heat stroke electrocardiograms showed tracings demonstrating ST segment depression, compatible with ischaemia in 9 cases, while in 6 cases there were nonspecific T wave changes, whereas in another 4 cases the tracings demonstrated different conduction abnormalities. The collected data were analysed and compared to those of 43 control patients. The adverse effects of heat stroke on the heart are multifactorial requiring the utmost attention and understanding, as they reflect the patient's cardiovascular status.
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PMID:Non-invasive evaluation of cardiac abnormalities in heat stroke pilgrims. 145 70

One hundred thirty-four patients with redistribution on a thallium-201 exercise test who did not experience angina (group 1) were compared with 134 patients also having redistribution who had angina during the test (group 2). The groups were matched by age, sex, and peak exercise heart rate. Although patients in both groups achieved an equivalent exercise level, patients in group 1 had less frequent (53 vs 71%, p less than 0.005) and less severe (0.15 +/- 0.13 vs 0.20 +/- 0.13 mV, p less than 0.005) ischemic ST-segment depression. Group 1 also had less ischemic thallium-201 images in terms of the number of redistributing defects, the severity of the worst redistributing defect, and an ischemic index composite of both extent and severity. Patients in group 1 were less likely to undergo early revascularization (12 vs 29%, p less than 0.005), but in the remaining patients the occurrence of adverse cardiac events was similar (21% vs 29%, p = not significant). By multivariate analysis, only the ischemic index correlated with early revascularization in group 1 (p = 0.0017), whereas the percent maximal predicted heart rate correlated best in group 2 (p = 0.0003). In group 1 the ratio of lung/heart thallium-201 uptake correlated best with an outcome of nonfatal myocardial infarction or cardiac death (p = 0.0024); in group 2 the presence of fixed left ventricular dilatation did (p = 0.0022). Thus, patients with exercise-induced thallium-201 redistribution without angina have less ischemia than patients experiencing angina.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Silent versus symptomatic ischemia during a thallium-201 exercise test. 174 60

Few models of heart failure (HF) are available for physiological and pharmacological studies. We report here a model of pressure plus volume overload induced in rabbits in which left ventricular (LV) function was studied in the conscious state after instrumentation of the animals with LV pressure catheter and ultrasonic crystals measuring LV diameter. Beta-Adrenoceptors were studied on crude membranes obtained from control (C) and HF rabbits using [3H]CGP 12177. LV weights and end-diastolic diameters were significantly increased in the HF group compared with the C group (by 79 and 38%, respectively). The percentage of diameter systolic shortening was decreased, in the control state, in rabbits with HF (15.3 +/- 1.6%) as compared with C rabbits (29.6 +/- 2.5%) and remained lower in the HF group when end-systolic pressures were matched. Chronotropic response to isoproterenol injection was significantly decreased in rabbits with HF compared with that of C rabbits. Beta-Adrenergic receptor density was decreased in rabbits with HF (39.3 +/- 3.7 fmol/mg) compared with C rabbits (56.7 +/- 4.2 fmol/mg) without affinity changes. This model of chronic HF thus produces a marked hypertrophy with ventricular dilatation and a depression of LV function within 2 mo, factors that are associated with a reduced cardiac responsiveness to catecholamines and a decreased ventricular beta-adrenergic receptor density.
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PMID:Left ventricular function and beta-adrenoceptors in rabbit failing heart. 215 52

Septic shock is the commonest cause of death in intensive care units. Although sepsis usually produces a low systemic vascular resistance and elevated cardiac output, strong evidence (decreased ejection fraction and reduced response to fluid administration) suggests that the ventricular myocardium is depressed and the ventricle dilated. In survivors, these abnormalities are reversible. Failure to develop ventricular dilatation in nonsurvivors suggests that dilatation is a compensatory mechanism needed to maintain adequate cardiac output. With a canine model of septic shock that is very similar to human sepsis, myocardial depression was confirmed using load-independent measures of ventricular performance. Endotoxin administration to humans simulates the qualitative, cardiovascular abnormalities of sepsis. The pathogenesis of septic shock is extraordinarily complex. Diverse microorganisms can generate toxins, stimulating release of potent mediators that act on vasculature and myocardium. A circulating myocardial depressant substance has been closely associated with the myocardial depression of human septic shock. Therapy has emphasized early use of antibiotics, critical care monitoring, aggressive volume resuscitation, and, if shock continues, use of inotropic agents and vasopressors. Pharmacologic or immunologic antagonism of endotoxin or other mediators may prove to enhance survival in this highly lethal syndrome.
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PMID:Septic shock in humans. Advances in the understanding of pathogenesis, cardiovascular dysfunction, and therapy. 224 Sep 23

Septic shock in humans is usually characterized by a high cardiac output, a low systemic vascular resistance, reversible depression of left ventricular ejection fraction, and transient left ventricular dilatation. The relationship of left ventricular to right ventricular function in septic shock is poorly understood. To evaluate right ventricular vs left ventricular performance and to evaluate the relation of biventricular performance to survival, we performed serial hemodynamic and radionuclide angiographic studies in 39 patients with septic shock. Right ventricular ejection fraction was calculated using the two regions of interest method. There were 22 survivors and 17 nonsurvivors. Comparing initial with final (after recovery for survivors; within 24 hours of death for nonsurvivors) studies, each survivor's cardiovascular performance returned toward normal, with significant increases in mean arterial pressure, left and right ventricular ejection fraction, and right ventricular stroke work index. Their profiles also demonstrated significant decreases in central venous pressure, pulmonary artery wedge pressure, pulmonary artery mean pressure, and left and right ventricular end-diastolic volume indices. From initial to final study in the nonsurvivors, there was a statistically significant increase in heart rate but no change in any other cardiovascular parameter, indicating a persistence of the initial cardiovascular dysfunction until death. Comparing serial studies, the pattern of change in right vs left ventricular function was very similar (same direction in 82 percent of patients). Thus, myocardial depression in human septic shock affects both ventricles simultaneously with a similar pattern of dysfunction.
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PMID:Right ventricular dysfunction and dilatation, similar to left ventricular changes, characterize the cardiac depression of septic shock in humans. 229 31


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