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

The cardiovascular, coagulation and haematological effects of prothrombin activator from Tiger Snake (Notechis scutatus) venom were investigated in anaesthetized mechanically ventilated dogs. Infusion caused dose-related systemic hypotension, marked decreases in cardiac output and stroke volume, marked increases in pulmonary artery pressure, pulmonary artery occlusion pressure and pulmonary vascular resistance. Effects occurred within several minutes but abated over 30 to 40 minutes. Evidence of procoagulation included prolongation of prothrombin and partial thromboplastin times and depletion of serum fibrinogen. Thrombocytopenia and leucopenia occurred. All effects were prevented by prior administration of heparin but none by inhaled nitric oxide. Oesophageal echocardiography during infusion identified thrombi within the heart, right ventricular dilatation and dyskinesia. Electrocardiography suggested myocardial ischaemia. Pulmonary thromboemboli were identified histologically post mortem. Cardiovascular effects of the activator were not due to a variety of endogenous substances as indicated by use of antagonists to platelet activating factor and thromboxane A2 indomethacin, dexamethasone, serotonin, ketanserin, histamine, promethazine and ondansetron. Tiger Snake prothrombin activator causes bilateral ventricular failure by thrombotic obstruction of the pulmonary vasculature and possibly by coronary ischaemia.
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PMID:The cardiovascular, coagulation and haematological effects of tiger snake (Notechis scutatus) prothrombin activator and investigation of release of vasoactive substances. 980 10

Although it is generally accepted that ventricular geometric configuration plays an important role for manifestation of cardiac pumping failure, the relative significance of structural dilatation vs impaired myocardial performance- and the interaction of these factors-have not been thoroughly addressed. Besides its unfavorable effects on coronary circulation, cardiac energetics, and arrhythmogenesis, structural ventricular dilatation has direct consequences for stroke volume for geometrical reasons. As demonstrated by model calculations, the slope of the curve describing the relation between stroke volume and anatomical ventricular size is flattened and the maximum of the curve is shifted toward smaller end-diastolic volumes in the presence of reduced "contractility" or distensibility or after loss of contractile tissue. Further determinants of this curve are wall thickness and end-diastolic and systemic pressure. Based on the examples of human dilative cardiomyopathy and spontaneously hypertensive rats it can be shown that symptoms of pumping failure occur when the ventricular operating point has reached the maximum of the stroke volume-ventricular size relation or has even passed over the maximum, so that compensation via increase in ventricular size has been exhausted. However, neither ventricular dilatation nor severe myocardial impairment are a precondition for the occurrence of congestive symptoms if diastolic dysfunction is predominant or if hemodynamics and neuroendocrine reactions are substantially influenced by peripheral factors.
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PMID:The functional significance of ventricular geometry for the transition from hypertrophy to cardiac failure. Does a critical degree of structural dilatation exist? 987 47

To clarify the relationship between long-term prognosis of patients with stroke and their MRI findings, 103 patients with initial cerebral thrombosis, who survived more than three months after the ictus, were studied for five years. The mean age of 98 patients (T group), who were followed up completely, was 73.1 years-old and 65 were men. The age-matched controls consisted of two groups: 65 subjects, who had hypertension and/or diabetes without a history of stroke (R group), and 85 subjects, who had any hypertension, diabetes and stroke (N group). MRI findings were divided into six categories: 1) types of causative lesion, 2) grades of periventricular hyperintensity (none, rims/caps, patchy, diffuse PVH), 3) number of spotty lesions, 4) presence of silent infarction. 5) ventricular dilatation, and 6) extents of brain atrophy. Types of causative lesion were subdivided into 3 subtypes; infarction of the perforating artery territory (P type), infarction of the cortical artery territory (C type), and brainstem infarction (B type). The presence of vascular risks and dementia, and the extent of activity of daily living (ADL) were assessed. The P, C, and B types were identified by MRI in 46, 36, and 16 of the T group, respectively. Motor impairment, dementia, and an ADL status of complete dependence at discharge were also seen in 84, 44, and 22, respectively. In the T group, 33 patients died during five years, which resulted in a cumulative mortality rate of 33.7% and an annual mortality rate of 8.2%. Based on log-rank analysis, the survival rate of the T group revealed was significantly lower than those of the R and N groups. The recurrent rate in the T group (annual stroke recurrence rate was 4.0%) was higher than in the R and N groups, but stroke recurrence was not the cause of death and two thirds of deaths were due to aspiration pneumonia and/or asphyxia. Cox hazard regression analysis for death due to respiratory diseases showed that the hazard ratios of infarction, patchy PVH, and more than 4 spotty lesions were 8.87 (p < .001), 0.31 (p = .058), and 0.44 (p = .098), respectively. Compared to the survival group, rates of complete dependence in ADL, dementia, and brain atrophy were significantly higher in the death group with low incidences of the P type and patchy PVH, which indicated small vessel disease. These findings suggested that in patients with cerebral thrombosis, even in the chronic phase, care should be taken to prevent pneumonia and/or asphyxia due to bulbar palsy. Furthermore, no MRI findings were distinct predictors of long-term prognosis, although infarction based on the small vessel disease had rather good outcome in terms of respiratory disease.
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PMID:[Long-term prognosis of patients with initial cerebral thrombosis and the MRI findings]. 1036 31

There is some controversy regarding the indications for transesophageal echocardiography in patients with suspected systemic embolism. The present case report refers to a 65 year old male admitted to the hospital for ischemic acute cerebrovascular accident, which was confirmed by cerebral computerized tomography. A transthoracic echocardiogram was performed showing right atrial and ventricular dilatation. A transesophageal echocardiogram was also performed to exclude thromboembolism and clarify dilatation of the right cavities. Mild spontaneous echocontrast was present in the left atrium without images of thrombus; an interatrial septal aneurysm with patent foramen ovale was found with right to left flow; an image compatible with a very mobile, large, proximal thrombus in the main pulmonary artery was observed. A venous duplex scan was performed, demonstrating venous thrombosis in the right popliteal and femoral veins. Pulmonary arteriography showed a large thrombus in the right pulmonary branch extending to the median lobe and a smaller thrombus in the left pulmonary branch. Apparently, the patient had no predisposing factors for thromboembolism. Full-dose heparin was started followed by oral anticoagulation. An inferior vena cava filter was implanted. At hospital discharge the pulmonary thrombus had disappeared and the right cardiac cavities had returned to normal size. The interatrial aneurysm had disappeared and foramen ovale was no longer patent. After 36 months of clinical follow up on oral anticoagulation, the patient remains asymptomatic without neurological sequelae nor respiratory distress.
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PMID:[Diagnosis of paradoxal and concomitant pulmonary thromboembolism with transesophageal echocardiography: a clinical case]. 1101 85

The electron microscopic structure of heart muscle and the ultrastructural basis of cardiac contraction have been reviewed. The relation between muscle length and developed tension has been explained in terms of the structure of the sarcomere, which is the basic unit of contraction. Using the derived length-tension curve of the sarcomere, developed tension has been attributed to the overlap of thick and thin filaments within the sarcomere, lending support to the "sliding" mechanism in heart muscle. It has been shown that initial sarcomere length is a function of ventricular filling pressure and that this relation explains the normal limits of the heart as a pump, including: (1) the Starling mechanism whereby increased diastolic volume (EDV) engenders an increased stroke volume (SV), (2) the upper limits to ventricular filling pressure and volume, and (3) the normal range to the ventricular ejection fraction (SV/EDV). Further, ultrastructure helps to define the processes which occur with acute and chronic ventricular dilatation. In this regard, the importance of sarcomere dispersion and "fiber slippage," which may lead to disordered ventricular function, have been discussed.
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PMID:Correlation of myocardial ultrastructure and function. 1171 90

Pulmonary hypertension is characterised by the chronic elevation of pulmonary artery pressure (PAP) and pulmonary vascular resistance (PVR) leading to right ventricular enlargement and hypertrophy. Pulmonary hypertension may result from respiratory and cardiac diseases, the most severe forms occurring in thromboembolic and primary pulmonary hypertension. Pulmonary hypertension is most often defined as a mean PAP >25 mmHg at rest or >30 mmHg during exercise, the pressure being measured invasively with a pulmonary artery catheter. Doppler echocardiography allows serial, noninvasive follow-up of PAPs and right heart function. When the adaptive mechanisms of right ventricular dilatation and hypertrophy cannot compensate for the haemodynamic burden, right heart failure occurs and is associated with poor prognosis. The haemodynamic profile is the major determinant of prognosis. In both primary and secondary pulmonary hypertension, special attention must be paid to the assessment of pulmonary vascular resistance index (PVRI), right heart function and pulmonary vasodilatory reserve. Recent studies have stressed the prognostic values of exercise capacity (6-min walk test), right atrial pressure, stroke index and vasodilator challenge responses, as well as an interest in new imaging techniques and natriuretic peptide determinations. Overall, careful haemodynamic evaluation may optimise new diagnostic and therapeutic strategies in pulmonary hypertension.
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PMID:Haemodynamic evaluation of pulmonary hypertension. 1244 89

We investigated the effects of a dual thromboxane (TX)A2 synthase inhibitor and TXA2 receptor antagonist (BM-573) on right ventricular-arterial coupling in a porcine model of endotoxic shock. Thirty minutes before the onset of 0.5 mg/kg endotoxin infusion, six pigs (Endo group) received an infusion with a placebo solution, and six other pigs (Anta group) with BM-573. Right ventricular pressure-volume loops were obtained by the conductance catheter technique. The slope (Ees) of the end-systolic pressure-volume relationship and its volume intercept at 25 mmHg were calculated as measures of right ventricular systolic function. RV afterload was quantified by pulmonary arterial elastance (Ea), and Ees/Ea ratio represented right ventricular-arterial coupling. Mechanical efficiency was defined as the ratio of stroke work and pressure-volume area. In this model of endotoxic shock, BM-573 blunted the early phase of pulmonary hypertension, improved arterial oxygenation, and prevented a decrease in right ventricular myocardial efficiency and right ventricular dilatation. However, the drug could not prevent the loss of homeometric regulation and alterations in right ventricular-arterial coupling. In conclusion, dual TXA2 synthase inhibitor and receptor antagonists such as BM-573 have potential therapeutic applications, improving right ventricular efficiency and arterial oxygenation in endotoxic shock.
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PMID:Effect of a novel thromboxane A2 inhibitor on right ventricular-arterial coupling in endotoxic shock. 1467 83

Beta-blockade efficiency and safety in anthracycline induced cardiomyopathy (AIC) are poorly documented. Cardiac Heart Failure (CHF) due to an AIC has haemodynamic and histologic particularities: only mild ventricular dilatation, restriction pattern and myocardial and endocardial fibrous thickening. Therefore, beta blockade therapy initiation may cause heart failure decompensation by absence of the usual left ventricular adaptation (improvement of left ventricular compliance allowing maintenance of stroke volume). We describe an AIC patient in whom a first beta-blockade initial administration caused a global cardiac failure; after stabilisation, one month later, a second attempt caused a new cardiac failure. We raise the question of beta-blockade safety in restrictive cardiomyopathies.
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PMID:Beta-blockade intolerance in anthracycline-induced cardiomyopathy. 1599 49

The feasibility and safety of total arterial coronary revascularization with 2 arterial conduits in patients with impaired left ventricular function was evaluated. Data were prospectively collected on all patients with multiple vessel discase and moderately or severely impaired left ventricular function, who underwent coronary surgery with the intention of total arterial revascularization with 2 conduits between March 1995 and August 2002. One hundred and seventy-nine patients were included in the study. Acute coronary insufficiency was present in 3 patients and 43 had unstable angina. Severe left ventricular impairment was present in 29 patients. There were 17 redo operations including 3 redo-redo procedures. Eighty-two percent of patients had a Y graft configuration from the left internal mammary artery (right internal mammary artery 40.8%, radial artery 33.5%, other 7.8%). The perioperative mortality was 2.2%, myocardial infarction 1.7% and stroke 0.6%. Total arterial revascularization in patients with ischaemic left ventricular dysfunction can be safely performed with 2 arterial conduits. The radial artery provides conduit length greater than the right internal mammary artery and allows full revascularization despite left ventricular dilatation.
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PMID:Total arterial revascularisation in left ventricular dysfunction. 1671 Oct 14

Intraventricular extension of hemorrhage after intraparenchymal hemorrhage is associated with significant morbidity and mortality. Clinical improvement is reported in a patient with thalamic hemorrhage with intraventricular extension after third and fourth ventricular blood clot resolution with instillation of urokinase intraventricularly. A 49-year-old man with hypertension collapsed while at work. A computed tomography (CT) scan of the head revealed a left thalamic hemorrhage with extension into the lateral, third, and fourth ventricles and associated hydrocephalus. A left frontal intraventricular catheter (IVC) was placed and intraventricular urokinase was administered at a dose of 25,000 U every 12 hours. The CT scan revealed resolution of the lateral ventricular dilatation and blood clot but no decrease in third or fourth ventricular hemorrhage. No clinical improvement was noted. The IVC was reinserted on the right side with the catheter tip placed through the foramen of Monroe into the third ventricle. Twelve hours after receiving the first dose of urokinase through the new catheter, the patient's condition improved. The CT scan showed a reduction in the volume of blood of the third and fourth ventricles. This case report shows that treatment of hydrocephalus with an IVC was not sufficient to provide a therapeutic effect. Substantial clinical improvement occurred only after the blood clot was cleared from the third and fourth ventricles.
J Stroke Cerebrovasc Dis
PMID:Clinical improvement related to thrombolysis of third ventricular blood clot in a patient with thalamic hemorrhage. 1790 95


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