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)

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.
 ...
PMID:The electrocardiogram in acute pulmonary embolism. 12 74

Postoperative echocardiogram often demonstrate persistent right ventricular dilatation and paradoxic ventricular septal motion after repair of an atrial septal defect. To determine the prevalence, causes and significance of these echocardiographic abnormalities, 31 patients were studied with catheterization and echocardiography before and after repair of an atrial septal defect. Before operation, every patient manifested right ventricular dilatation, and all but one had abnormal septal motion. After operation, right ventricular dilatation was noted in 24 (77%) and abnormal septal motion in 21 (68%) patients despite the absence of residual left to right shunting in 30 (97%). These echocardiographic abnormalities could be correlated with age at operation and length of postoperative follow-up study but did not correlate with the degree of preoperative right ventricular enlargement or with shunt size or right ventricular pressure before or after operation. There was no associated functional deficit as demonstrated by the normal maximal oxygen consumption in all 13 patients who underwent treadmill exercise testing 5 to 38 months after operation; these patients included 9 with persistent right ventricular enlargement and abnormal septal motion.
 ...
PMID:Abnormal right ventricular size and ventricular septal motion after atrial septal defect closure: etiology and functional significance. 14 24

Persistence of the fetal circulation is a recently recognized cause of severe cyanosis in newborn full term infants. Abnormally elevated pulmonary vascular resistance apparently stimulated by hypoxia, acidosis, and/or hyperviscosity results in cyanosis due to large right-to-left shunts through persistent fetal channels (patent foramen ovale and patent ductus arteriosus). Initial chest radiographs demonstrate clear lungs, decreased, normal, or mildly prominent pulmonary vascularity, and normal to moderately enlarged cardiac silhouettes. Angiocardiography, when required to rule out cyanotic congenital heart disease, demonstrates normal intracardiac anatomy, normal great vessel relationships, and right-to-left shunting across the patent foramen ovale and patent ductus arteriosus. Significant tricuspid regurgitation occurs in some of these infants, associated with variable right ventricular dilatation; the left ventricle is normal. The majority of babies with this condition ultimately survive. Treatment consists of intensive care including oxygen therapy and correction of acidosis. Vasodilators such as tolazoline may be helpful.
 ...
PMID:Persistence of the fetal circulation: radiologic considerations. 40 2

In the first few hours after the onset of coronary occlusion the infarct zone stretches due to myocyte slippage. Subsequently the noninfarct zone develops volume overload hypertrophy with series addition of new sarcomeres and fibre elongation. Dilatation is detrimental as it increases ventricular wall stress and oxygen demand, and re-entry of electrical impulses may be influenced by stretching of the ischaemic scar resulting in ventricular fibrillation. Left ventricular remodelling and dilatation is a progressive process which begins early and continues in the months after infarction. The major determinants of the extent of remodelling are infarct size and patency of the infarct-related artery. Late reperfusion may reverse initial infarct dilatation and decrease left ventricular volumes by inducing calcium-activated contracture of the actomyosin complex. Expansion may also be inhibited by acceleration of healing, splinting of the infarct zone by salvage of subepicardial cells, and blood in the coronary arteries and veins supporting the infarct zone. End-systolic volume is the strongest predictor of long-term prognosis after infarction. A number of therapies including thrombolysis, angiotensin-converting enzyme (ACE) inhibition and nitrates have been shown to decrease left ventricular dilatation. The optimal time for commencement, dose, duration and the effects of combinations of therapy are yet to be determined.
 ...
PMID:Remodelling of the heart after myocardial infarction. 144 47

In heart failure, many alterations occur in the ventricle as a whole, as well as in the myocardial cell. In the first part of this review we report on the macroscopic structure of the left ventricle by analysing the relation between left ventricular dilatation and left ventricular hypertrophy in terms of ventricular wall stress. Peak systolic stress in dilated ventricles of patients with compensated heart failure does not differ from values obtained in normal ventricles, whereas the systolic stress-time integral is increased by more than 40%. The stress-time integral is a major determinant of myocardial oxygen consumption, and its reduction by peripheral vasodilation leads to a proportional decrease in left ventricular oxygen consumption. In contrast, the phosphodiesterase inhibitor, enoximone, decreases the stress-time integral without a proportional decrease in myocardial oxygen consumption, due to the competition between positive inotropic effect with increased oxygen consumption and a vasodilating effect with decreased oxygen consumption. Beta-1 adrenoceptor agonists increase myocardial oxygen consumption. In the second part of this review we report on the functional alterations of the following subcellular and molecular structures in the failing myocardium: (1) adrenoceptors and G-proteins; (2) sarcoplasmic reticulum with an altered force-frequency relationship; (3) the acto-myosin system with decreased velocity of shortening and increased economy of force generation. On the basis of these alterations, a disadvantageous chain of events develops in the failing myocardial cell.
 ...
PMID:The heart in heart failure. Ventricular and myocardial alterations. 183 95

It is clearly settled that the management of overt heart failure offers poor prognostic impact due to the advanced setting of the disease. Relief of symptoms, objective benefits, as testified by short-term hemodynamic improvements, are as a matter of fact not reliable prognostic markers. Myocardial dysfunction starts early in the natural history of many cardiac diseases, and runs through the steps of progressive wall remodeling, witnessed by quantitative and qualitative changes in cells, interstitium and connective tissue. Experimental studies offered keys to interventions modulated to oppose the pathophysiological changes present in early myocardial dysfunction. At present, medical therapy has made great strides in testing early myocardial dysfunction. Angiotensin-converting enzyme inhibitors, which retard ventricular dilatation and thus may lower myocardial oxygen consumption requirements seem to offer a unique prognostic profile. Preliminary pilot studies on them and some of many large-scale multicentre trials still in progress reached evidence that this class of drugs is by this time a cornerstone of medical therapy, useful to lower cardiac events-rate in patients with heart failure.
 ...
PMID:[The effects of pharmacological treatment in asymptomatic left ventricular dysfunction]. 184 2

Chronic cor pulmonale is defined as right heart hypertrophy or right ventricular dilatation and/or chronic right heart failure. There are many etiologies which largely determine mortality and drug therapy, but the common cause is increased right ventricular work from primary or secondary pulmonary hypertension assuming two prototypes, the asphyxial and the vascular obliterative type. The main focus of this review concentrates on the various drugs to reduce pulmonary vascular pressure and resistance. The value to correct hypoxaemia is mentioned with regard to its demonstrated important effect of asthmatic patients with cor pulmonale. Continuous oxygen therapy and a potential therapy by almitrine, a respiratory stimulant, have been suggested. Phosphodiesterase inhibitors and dopaminergic drugs have been used successfully to improve right cardiac function in a small number of patients. The use of prostacyclin has a large potential to effectively correct pulmonary vascular haemodynamics but its use is fairly limited by the need of continuous intravenous application. New oral drugs under investigation which stimulate endogenous prostacyclin as well as thromboxane synthetase inhibitors still need further evaluation but might be of potential benefit. The comparison of the side-effects due to vasodilators and calcium antagonists argues for the use of calcium channel blockade for patients with pulmonary hypertension. To define the role of angiotensin converting enzyme inhibitors or the more recently introduced potassium channel openers for treatment of chronic cor pulmonale still await detailed, controlled studies.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[The drug therapy of chronic cor pulmonale]. 186 13

Challenge to a new therapeutic principle to treat heart failure is to ameliorate or eliminate symptoms, decelerate progression of the disease and reduce mortality. However, to begin, one would request improvement of objective hemodynamic parameters. Angiotensin converting enzyme (ACE) inhibitors may have acute and chronic, global and regional effects. ACE inhibitors acutely and chronically reduce pre- and afterload without reflex tachycardia. They lower myocardial oxygen consumption and improve the relation of coronary blood flow to myocardial oxygen consumption. Cerebral and renal blood flow generally are beneficially influenced if the blood pressure is not lowered too much. Left ventricular dilatation following extensive myocardial infarction which is prognostically unfavourable, may be retarded or prevented by ACE-inhibitors. It is not yet clear whether mortality may thus be reduced as in patients with severe heart failure. Large multicenter studies currently address this question. It is unclear as well whether the effects of ACE-inhibitors are exclusively due to a reduction of circulating angiotensin II. Most likely, interference is of major importance with local renin-angiotensin systems, other hormone systems and the central and peripheral nervous system.
 ...
PMID:[Modification of hemodynamics by angiotensin converting enzyme inhibitors in heart failure]. 219 16

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

Beta-adrenoceptor antagonists do not directly depress myocardial contractile function. The primary pharmacological target of these drugs is to attenuate the increase in myocardial oxygen consumption resulting from sympathoadrenal stimulation of the heart. Pure beta blockade achieves this by modulating the increases in heart rate and myocardial contractility. This brings in its train the unwanted secondary and tertiary consequences of ventricular dilatation, impaired cardiac output response to exercise, and reflex increases in systemic vascular resistance and left ventricular afterload. Together these physiological effects offset much of the primary therapeutic benefit of these drugs. The ancillary pharmacological properties possessed by newer generations of beta-adrenoceptor antagonists have reduced some of the undesirable hemodynamic consequences of pure beta blockade. In this respect, positive inotropic activity and vasodilator effects, however achieved, are desirable properties in a drug with beta-blocking activity. Such additional pharmacodynamic activities afford direct support of cardiac contractile activity and reduce the undesirable increase in peripheral vasoconstriction that results from beta blockade alone. Celiprolol is a new dimension in beta-blocking therapy in that it achieves these additional hemodynamic benefits by widespread modulation of sympathoadrenal activity.
 ...
PMID:Beta-blocking drugs and myocardial function. 242 56


1 2 3 4 5 6 7 Next >>