Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0264733 (ventricular dilatation)
 2,163 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In forty-one patients with various heart diseases including 29 with LVH, the vectorcardiograms of Frank system and angiocardiographic findings correlated minutely. Based on the left ventricular wall thickness in end-diastole, left ventricular end-diastolic volume, and the length of the long axis of the left ventricle obtained in angiocardiograms, typical left ventricular hypertrophy was classified into types 1a, 1b, 2a, 2b anatomically. The vectorcardiograms in these 4 types represented different patterns with regard to the QRS and T loops respectively. The QRS voltage in the left ventricular hypertrophy closely correlated to the left ventricular wall thickness in end-diastole, the left ventricular end-diastolic volume, and the left ventricular mass. Marked ST and T changes in the left ventricular concentric hypertrophy characterized by increase in wall thickness without definite chamber enlargement may be closely related to the abnormal muscle state with the increased left ventricular wall thickness, the probably due to relative hypoxia in origin. The Q loop of patients with severe left ventricular concentric hypertrophy was definitely differentiated from that of most patients with the pure left ventricular eccentric hypertrophy which was characterized by chamber enlargement with usually slight thickening of the wall. A possible mechanism regarding inconspicuous or prominent Q loops in both concentric and eccentric LVH was presented. An important factor of the delay of the time of occurrence of the spatial R vector in the left ventricular eccentric hypertrophy is the greater distance of the intraventricular conducting pathways caused by the left ventricular dilatation. By means of assessing the vectorcardiogram of the left ventricular hypertrophy, relatively exact anatomy of the left ventricular hypertrophy can be determined.
 ...
PMID:Vectorcardiographic findings in concentric and eccentric left ventricular hypertrophy as determined by angiocardiograms. 1. Preliminary report. 12 81

Echocardiograms (ECHO) and Frank vectorcardiograms (VCGs) were obtained in three groups of patients: Group I (n = 16), concentric left ventricular hypertrophy (LVH) with increased interventricular septal (IVS) and left ventricular posterior wall (LVPW) thickness in the presence of a normal left ventricular internal dimension (LVID); Group II (n = 17), left ventricular dilatation (LVD) with an enlarged LVID, normal IVS and LVPW thickness, and Group III (n = 22), no catheterization evidence of heart disease with normal IVS, LVPW and LVID. VCGs were analyzed with respect to magnitude of the QRS maximal deflection vector (MDV) and +/- 10 msec QRS vectors, horizontal plane (HP) maximal posterior force, time of HP MDV inscription, distal and proximal HP loop areas and HP loop configuration utlizing criteria of Varriale et al. The results indicate that: 1) HP QRS vector magnitude cannot reliably differentiate concentric LVH from isolated LVD and 2) proximal-distal loop area relationships and pattern of the HP QRS loop, when reviewed together, are superior to other criteria for distinguishing whether ECHO determined LVH or LVD is the primary correlate of an enlarged left ventricle.
 ...
PMID:Hypertrophy or dilatation? A vectorial analysis of echocardiographically determined left ventricular enlargement. 14 78

Two grams of methylprednisolone was administratered to ten patients with acute myocardial infarction at an average of 13 hours from the onset of symptoms; pain in the chest was not relieved in six of the ten patients. In one hour, no significant improvement was noted in the function of the ischemic segments (examined using a multiaxis echocardiographic method) or in the S-T segments of the 12-lead electrocardiogram. Left ventricular filling pressure soon increased by an average of 4 mm Hg (P less than 0.005), without ventricular dilatation or a Frank-Starling response, suggesting a decrease (ischemic?) in myocardial compliance. Cardiac output by Swan-Ganz thermodilution later increased by 21 percent (P less than 0.01) when a decrease in peripheral vasoconstriction was evident. In contrast, small-dose beta-adrenergic blockade using 0.2 mg of pindolol intravenously after administration of methylprednisolone immediately relieved pain in the chest in all six patients. Elevation of the S-T segments was reduced by 34 percent (P less than 0.05) within 15 minutes, and the contractile function of the ischemic segments improved markedly, by 3 mm or to 34 percent of normal, from the 4 percent of normal before administration of pindolol (P less than 0.005). Hemodynamic function did not deteriorate in the eight patients with uncomplicated infarction or moderate left ventricular failure. Therapy with pindolol thus reduced clinical, electrocardiographic, and myocardial mechanical signs of acute ischemia safely, while administration of methylprednisolone had no short-term protective effect.
 ...
PMID:Failure of methylprednisolone to protect acutely ischemic myocardium: a contrast with subsequent beta-adrenergic blockade in man. 34 14

Based on animal experiments in rats (spontaneous and renal hypertension, experimental aortic stenosis, thyroxine and training-induced hypertrophy, and aorto-caval fistula with and without additional unilateral renal artery coarctation) as well as clinical data and literature, the functional consequences of cardiac hypertrophy and structural ventricular dilatation are analyzed and discussed. A methodological approach, developed on the basis of Frank's diagram and model calculations, permits quantitatively estimating the significance of ventricular geometry (wall thickness and inner dimensions) compared to myocardial alterations (decrease in contractility and distensibility) and hemodynamic load (preload and systolic pressure). As a rule, hypertrophy causes an increase in ventricular working capacity, which allows the heart to cope with an increased hemodynamic load without a decrease in stroke volume and without enhanced systolic stress requirement. Adverse consequences mainly concern ventricular compliance, cardiac energetics, and electrophysiological parameters. Particularly from the example of the aorto-caval fistula, it can be seen that enhanced systolic wall stress does not necessarily lead to heart failure within a few months. However, the length of time for which the additional wall stress, with correspondingly increased energy demand, can be tolerated remains to be determined. In later stages, a multitude of alterations on the cellular, tissue, and organ level occurs, affecting myocardial and ventricular mechanics and energetics, depending on the type, velocity of development, and duration of overload. A distinction should be made between the adverse alterations, which can be related to myocardial growth, and those that are not necessarily related to a certain cell size (receptors, transformation of the contractile proteins) as well as those changes that do not primarily influence the myocardial cell (arteriosclerosis, microangiopathy). Structural dilatation alone could lead to insufficiency only in the case of substantial increase in inner ventricular radius. Reduced contractility, myocardial distensibility, and increased pressure load aggravate the negative effects of dilatation in a predictable manner, as demonstrated on the basis of a representative case of dilative cardiomyopathy. Using the example of spontaneously hypertensive rats, it is shown that ventricular mass and shape are differently influenced by various blood-pressure lowering agents, e.g., atenolol, nifedipine, and dietary interventions. It is concluded from the analysis of chronic cardiac reactions that adaptive processes are, in principle, ambiguous in character, revealing negative components even in the case of regular adaptation. However, it seems unjustified to aim at a regression of hypertrophy without reducing the underlying hemodynamic overload.
 ...
PMID:Functional consequences of cardiac hypertrophy and dilatation. 182 78

Loss of contractile myocardial tissue by myocardial infarction would result in depressed cardiac output if compensatory mechanisms would not be operative. Frank-Straub-Starling-mechanism and increased heart rate and contractility due to sympathetic stimulation are unlikely to chronically compensate for cardiac dysfunction. Structural left ventricular dilatation may be compensatory, but results in increased wall stress and, ultimately, in progressive dilatation and heart failure. In patients with myocardial infarction, we have shown left-ventricular dilatation in dependence of infarct size and time after infarction. Dilatation is compensatory first and normalizes stroke volume. However, left ventricular dilatation progresses without further hemodynamic profit and, thus, may participate in development of heart failure.
 ...
PMID:Compensatory mechanisms for cardiac dysfunction in myocardial infarction. 183 46

Both peripheral vascular abnormalities and changes in myocardial function are hallmarks of septic shock. Their complex interactions result in inadequate and maldistributed microcirculatory flow and progressive organ dysfunction. Inappropriate vasodilation, microembolization and endothelial cell injury are proposed mechanisms that may induce maldistribution of flow in the microcirculation and inefficient, defective peripheral oxygen extraction. Abnormal myocardial function is manifested by diminished right and left ventricular ejection fractions, ventricular dilatation, altered Frank-Starling curves and diastolic pressure-volume relationships. These changes are already observed in an early stage of septic shock and are entirely reversible in survivors.
 ...
PMID:The haemodynamics of septic shock. 228 87

The Frank-Starling mechanism was investigated in 88 athletes exposed to physical stress and was shown to operate under physical stress in athletes with ventricular cavities of normal or moderately increased size. In athletes with physiological ventricular dilatation as a result of endurance training (over 160 ml in ultimate diastolic volume), the Frank-Starling mechanism is not normally triggered under stress: increased cardiac output is provided by greater basal blood volume reserve. With ultimate diastolic volumes of 115-159 ml, the Frank-Starling mechanism provides an optimum increase in peak stroke volume. The effectiveness of the heterometric mechanism activated by physical stress in subjects with small ultimate diastolic volumes is not sufficient as additive reserve volume cannot be increased essentially.
 ...
PMID:[Efficacy of the Frank-Starling mechanism during physical stress]. 688 71

Right ventricular function was measured in ten patients with severe COPD (mean FEV1 = 0.48 +/- 0.2 L/s) as part of an evaluation for single lung transplant (SLT). Right ventricular ejection fraction (RVEF) was determined by two methods: first-pass radionuclide scan by multigated acquisition (MUGA) and by using a fast thermistor tipped RVEF/volumetric pulmonary artery catheter. None of the patients had clinical evidence of active right heart failure, although mild resting pulmonary hypertension (mean pulmonary artery pressure [PAP] = 24 +/- 4 mm Hg) that worsened with minimal exercise (mean PAP = 39 +/- 11 mm Hg) was present. There was a significant difference in RVEF measured by the two methods (mean MUGA RVEF = 57 +/- 10%, mean catheter RVEF = 27 +/- 8%; p < 0.00005). RVEF determined by both methods was correlated with hemodynamic and gas exchange variables obtained during rest and at maximal exercise. There were significant, yet inverse, correlations between RVEF measured by catheter and cardiac index measured during exercise (CIex), as well as with exercise pulmonary vascular resistance index (PVRI). There were no significant correlations found between MUGA RVEF and any gas exchange or hemodynamic variables. Significant correlations were found with the catheter-measured right ventricular end-diastolic volume (RVEDV) and CIex (r = 0.9 p < 0.005), with maximal oxygen consumption during exercise (VO2max) (r = 0.86 p < 0.0025), with exercise stroke volume index (SVI) (r = 0.76 p < 0.01), and exercise central venous pressure (CVP) (r = 0.62 p < 0.05). Echocardiographic studies revealed right ventricular dilatation and mild tricuspid regurgitation (TR) in all patients. The strong correlation between RVEDV, CIex, and VO2max supports the concept that in these patients, as long as there is no clinical evidence of right heart failure (resting CVP still within normal limits), those with the largest RVEDVs use the Frank Starling principle to their best advantage to remain more functional.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Right ventricular function in patients with severe COPD evaluated for lung transplantation. Lung Transplant Group. 778 38

The goal of this study was to elucidate the ability of the left ventricle to accommodate an increase in preload (Frank-Starling mechanism) in the presence of congestive heart failure (CHF) but in the absence of the complicating effects of hypertrophy and fibrosis. To accomplish this, the effects of volume loading were examined in eight conscious dogs during the control state and after 3 wk of right ventricular pacing (240 beats/min). CHF increased heart rate (by 16 +/- 5 from 92 +/- 5 beats/min), left ventricular (LV) end-diastolic pressure (by 17 +/- 2 from 10 +/- 1 mmHg), and LV end-diastolic volume (EDV; by 23 +/- 4 from 57 +/- 3 ml). Despite reduced LV ejection fraction (from 54 +/- 3 to 31 +/- 3%), there was no significant change in cardiac output (2.5 +/- 0.3 l/min) compared with control (2.7 +/- 0.2 l/min). Stroke volume was preserved (control 19 +/- 2 ml; CHF 18 +/- 2 ml) at a constant heart rate by a shift to the right in the relationship between LV stroke volume and EDV, indicating the importance of chronic ventricular dilatation in maintaining pump performance. In the control state, acute volume load increased LV EDV (by 17 +/- 2 ml) and stroke volume (by 11 +/- 2 ml), whereas in CHF it did not increase LV EDV or stroke volume. Scanning electron microscopy revealed areas of reduced collagen weave pattern surrounding myofibers. Myocyte cross-sectional area by transmission electron microscopy was significantly reduced, and there were multiple electron-dense expansions of the Z lines with disruption of the normal lateral sarcomere alignment. These morphological findings suggest that chronic ventricular dilatation utilized in CHF results from myocyte stretch and morphological intracellular rearrangement. Furthermore, the failing heart cannot further augment stroke volume by acutely increasing EDV in CHF, suggesting that the Frank-Starling reserve is essentially exhausted.
 ...
PMID:Exhaustion of Frank-Starling mechanism in conscious dogs with heart failure. 823 98

Coronary heart disease and beta-blocker treatment can increase the use of the Frank-Starling mechanism during exercise. The aim of the study was to assess whether this could be influenced by physical training. Male patients on beta-blocker treatment after myocardial infarction were randomised to four weeks of training (ET, n = 19) or to a control group (Ctr, n = 18). Cardiac output (CO) at rest and at identical submaximal exercise levels in each patient were determined by radionuclide ventriculography at baseline and after the intervention period. CO was calculated as end diastolic volume (EDV) x ejection fraction x heart rate, and deltaCO and deltaEDV as change in parameter from rest to exercise. The mean (SD) deltaCO decreased from 6.5 (2.1) L/min(-1) to 5.1 (2.4) in ET patients and increased from 5.0 (1.7) to 5.8 (2.7) in Ctr, p = 0.004. deltaEDV decreased from 30 (30) mL to 12 (35) in ET and increased from 11 (20) to 36 (33) in Ctr, p = 0.005. When adjusting for baseline dissimilarities between the groups in a multivariate linear regression analysis, these differences were still statistically significant, p = 0.018 and p = 0.044, respectively. Physical training reduces the CO increase needed to perform identical submaximal exercise, and this is accompanied by less left ventricular dilatation, with a potential for reducing exercise-induced ischaemia.
 ...
PMID:Short-term physical training reduces left ventricular dilatation during exercise soon after myocardial infarction. 1093 71


1 2 Next >>