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 case of a girl who presented with gastrointestinal upsets with nausea, vomiting and occasional hypoglycaemic attacks during childhood is reported. At about 5 years of age generalised muscular weakness with severe amyotrophy, cardiomegaly with a cardiothoracic ratio of 0,63, left ventricular hypertrophy on electrocardiography and left ventricular dilatation with hypokinesis on echocardiography were observed. A few weeks later she developed severe cardiac failure. Muscle biopsy showed muscular dystrophy with lipid infiltration due to carnitine deficiency )serum carnitine 9 nmoles/ml, normal values: 46 +/- 6,9 nmoles/ml; muscle carnitine 0,27 nmoles/mg, normal values: 3,0 +/- 0,79 nmoles/mg fresh frozen weight). She improved rapidly with carnitine chlorhydrate and a diet low in lipids and high in medium chain triglycerides. Regression of muscular symptoms and cardiac failure was observed. After 13 months follow-up with no tonicardiac therapy she is much improved; the signs of heart failure have disappeared, the cardiothoracic ratio is now 0,55 and the electrocardiogramme and echocardiogramme are normal.
Arch Mal Coeur Vaiss 1979 May
PMID:[Lipidic myopathy with severe cardiomyopathy caused by a generalized carnitine deficiency. Favourable course during carnitine hydrochloride treatment]. 11 7

A series of 20 patients with pure and severe major aortic incompetence was studied, and three different groups were distinguished: group I, with no previous defect in function; group II, with cardiac failure as a result of aortic incompetence of more than 5 years' standing; group III, with cardiac failure secondary to acute aortic incompetence. The internal diameter of the left ventricle and the mode of closure of the mitral valve were studied by echocardiography, and compared with the clinical and haemodynamic findings. Left ventricular dilatation appeared early, and occurred to the same degree in the three groups. The diastolic diameter of the left ventricle showed a fairly close correlation (r equals 0.61) with the degree of regurgitation as measured from clour dilution curves; by contrast, the length of time the aortic incompetence had been present had little influence on the degree of dilatation of the left ventricle. Premature closure of the mitral valve was significantly associated with a raised LVEDP and a low systolic index; it represents a defect in the compliance of the left ventricle, and is a poor prognostic factor because of the clinical progression into very rapid and severe heart failure. Moreover, there is a distinct aetiological factor (Infective endocaditis) in the most marked forms of premature closure. The other ecocardiographic findings (appearances of the aorta, mitral echo, slope EF of the mitral valve) give no information on the degree of tolerance to the cardiac defect.
Arch Mal Coeur Vaiss 1977 Jul
PMID:[Echocardiographic study of the left ventricle in aortic insufficiency. Comparison with the data of clinical development and hemodynamic results]. 41 49

The aim of this study was to determine whether the percentage of akinesia on echocardiography during the acute phase of transmural anterior myocardial infarction could predict secondary left ventricular dilatation. The study group comprised 24 patients (18 men and 6 women) with an average age of 59 years. The patients underwent two echocardiographic examinations, the first during the acute (< 72 hours) phase and the second, 6 months later. Ventricular volumes were calculated by the ellipse monoplane method in the apical 4 chamber view. The percentage of akinesia was defined as the ratio between the length of the akinetic segment and the left ventricular end diastolic perimeter in the apical 4 chamber view. An increase in end diastolic volume (83 +/- 25 vs 62 +/- 18 ml/m2; p < 0.01) and in end systolic volume (51 +/- 27 vs 34 +/- 11 ml/m2; p < 0.01) was observed 6 months after infarction without a significant change in ejection fractions (42 +/- 17% vs 44 +/- 10%). The percentage of akinesia in the acute phase was > 30% in 15 patients (Group I) and < 30% in 9 patients (Group II). The increase in ventricular volumes at 6 months after infarction was significant in Group I (p < 0.02) but not in Group II. At 6 months after infarction, the end systolic volumes were greater (60 +/- 27 vs 37 +/- 22 ml/m2, p < 0.5) and the ejection fractions were lower (35 +/- 13% vs 53 +/- 18%, p < 0.01) in Group I than in Group II.(ABSTRACT TRUNCATED AT 250 WORDS)
Arch Mal Coeur Vaiss 1992 Oct
PMID:[Left ventricular dilatation after primary transmural anterior myocardial infarction. Influence of the percentage of akinesia on echocardiography]. 129 91

Epidemiological studies suggest that VVI pacing is associated with a higher risk of embolic complications than atrial or dual chamber pacing. However, no studies have been performed on pacemaker patients admitted to a neurological department with a cerebral embolism. The authors report the cases of 8 patients (6 men and 2 women) with an average age of 74 years and having the following characteristics: 1) a cerebral embolism, 2) a permanent cardiac pacemaker (7 VVI and 1 DDD mode). The average delay between implantation of the pacemaker and the neurological complication was 31 months. Cardiological investigations at the time of admission showed: a clinically evident cause of cardiac embolism in 3 cases (2 with VVI and 1 with DDD pacing); paroxysmal or permanent atrial fibrillation in 4 cases with VVI pacing at the time of the embolic event (in only one case at the time of implantation); various echocardiographic abnormalities in 6 of the 7 patients who underwent this examination, mainly left atrial dilatation (6/7), septal wall motion abnormalities in all related to ventricular pacing and unexplained left ventricular dilatation in 2 patients with VVI pacemakers. These results suggest that although the etiology of cerebral embolism was probably multifactorial in some patients, VVI packing probably a predisposing role, though not the only cause, and could be considered to be an embolic risk factor as suggested by previous epidemiological studies. These preliminary retrospective data should be interpreted cautiously taking into account the small population size. Prospective studies on pacemaker patients with cerebral embolism are required.
Arch Mal Coeur Vaiss 1992 Nov
PMID:[VVI mode cardiac pacing: cause or risk factor of cerebral embolism?]. 130 Sep 52

The hemodynamic prognosis of myocardial infarction is determined, at medium and long term, by the function of the left ventricle. This is related to the infarct size, the dilatation and geometry of the ventricle secondary to left ventricular remodeling which often follows infarction. In addition to clinical criteria, the hemodynamic parameters which are essential for patient evaluation are the ejection fraction (by radionuclide or conventional ventriculography), rapidly progressive ventricular dilatation (by repeated echocardiography) and circulatory reserve from the exercise stress test data.
Arch Mal Coeur Vaiss 1992 Nov
PMID:[How to evaluate the hemodynamic risk after myocardial infarction?]. 130 39

Ventricular tachycardia by bundle branch reentry is a special type of ventricular tachycardia. A rare arrhythmia, it occurs in very particular conditions of ventricular dilatation and conduction defects. The diagnosis is based on electrophysiological findings associating a His potential preceding the ventriculogramme with a HV interval comparable to that observed in sinus rhythm, and spontaneous variations of the cycle length between two ventriculogrammes preceded by those of the His potentials. Contrary to what is observed in other forms of ventricular tachycardia, pacing is possible from the atrium without changes of the QRS complexes and the presence of fusion complexes excludes the diagnosis. Treatment consists of radiofrequency ablation of the right bundle branch.
Arch Mal Coeur Vaiss 1992 Dec
PMID:[Ventricular tachycardia caused by bundle branch reentry]. 130 97

Incessant, rapid, supraventricular tachycardia may be complicated by cardiac failure with ventricular dilatation and hypokinetic wall motion on echocardiography: so-called tachycardia-induced cardiomyopathy. The diagnosis is simple when the cardiac rhythm is not sinus rhythm. The authors report the cases of 4 children aged 7 months to 12 years, referred for diagnosis and treatment of apparently primary cardiomyopathy. The findings of spontaneous or vagally-induced atrioventricular conduction defects, a permanently rapid atrial rhythm though influenced by 24 hour variations, or periodic abnormal rate increases, suggested myocardial dysfunction due to an ectopic atrial tachycardia. This was an essential step in management as the control of the tachycardia by amiodarone or betablocker therapy resulted in regression of symptoms and normalisation of left ventricular function. However, some atrial tachycardias are very resistant to medical treatment and, in such cases, there should be no hesitation in using more radical approaches, surgery or ablation, even and especially in patients with severe cardiac failure. In conclusion, apparently primary dilated cardiomyopathy in children may be due to chronic atrial arrhythmia and it is essential to perform at least Holter monitoring in order not to miss this diagnosis.
Arch Mal Coeur Vaiss 1992 May
PMID:[Rhythmogenic cardiomyopathies of atrial origin in children. Myth or reality?]. 135 26

Hemodynamic evaluation of a vasodilator drug is a difficult exercise in which Doppler echocardiography can be a useful tool. We studied the hemodynamic effect of isosorbide dinitrate (ISDN) by Doppler echocardiography in 7 patients with severe cardiac failure despite prolonged therapy with usually effective doses of captopril. The patients were evaluated before (H0) and 24 hours after treatment by ISDN (120 mg/24 hr) (H24) and 10 minutes after sublingual 0.75 mg of trinitrin (H24 + T). M mode echocardiography did not show any significant changes in chamber dimension as reported after vasodilator therapy in patients without cardiac dilation: in patients with severe left ventricular dilatation a reduction in LV filling pressures causes little if any changes in fractional shortening and ventricular dimensions. Two-dimensional echocardiography showed a reduction in end systolic volume and an increase in ejection fraction, emphasizing the superiority of this technique in cases of abnormal left ventricular function and the sensitivity of indices of systolic function to changes in afterload in these patients. Cardiac output measured by Doppler increased during the study. The maximal acceleration did not change significantly and pulmonary artery pressures were stable after administration of nitrates. ISDN caused a marked change in diastolic mitral flow patterns for which there are several explanations: an effect of ISDN on relaxation or LV compliance or on the conditions of LV filling or on both factors together. The presence of mitral regurgitation and/or atrial arrhythmia prevents the use of Doppler indices for analysis of diastolic LV function.(ABSTRACT TRUNCATED AT 250 WORDS)
Arch Mal Coeur Vaiss 1992 Apr
PMID:[Doppler echocardiographic evaluation of vasodilator treatments in patients with cardiac insufficiency. Contribution to the combination of isosorbide dinitrate and captopril]. 153 Apr 26

ST segment elevation in the anterior precordial chest leads may be observed in some cases of right ventricular infarction alone or associated with left ventricular inferior wall infarction. Six out of 700 patients admitted to our Coronary Care Unit over a 2 year period had right ventricular infarction with these electrocardiographic changes. In three cases, isolated right ventricular infarction was due to occlusion of a right marginal artery (N = 2) or of a small right coronary artery (N = 1) which only vascularised the right ventricle. In 2 cases, right ventricular infarction was associated with a recent or chronic left ventricular inferior wall infarct. This type of ST segment elevation may suggest a left ventricular anterior wall infarct especially when there are no changes in the inferior leads, as was the case in our first patient. However, the dome-like appearance of the ST segment, the reduction in amplitude of ST elevation from V2 to V5, the progressive regression of the ST changes without the appearance of Q waves, are more suggestive of the diagnosis of right ventricular infarction. In addition, normal left ventricular dilatation on echocardiographic examination rapidly confirms the diagnosis.
Arch Mal Coeur Vaiss 1992 Jan
PMID:[ST segment elevation in anterior precordial leads and right ventricular infarction. Apropos of 6 cases]. 155 Apr 36

Left ventricular modeling after myocardial infarction may be modified in three ways: firstly, by limiting the infarct size; secondly, by administering ACE inhibitors: these drugs limit infarct expansion and ventricular dilatation. They reduce the prevalence of secondary left ventricular failure and, in the animal, improve the prognosis. Glyceryl trinitrate also appears to be effective. The third therapeutic option is maintaining the patency of the artery responsible for the infarction, which has a beneficial effect on ventricular remodeling. The respective therapeutic indications of these three options are still a matter of discussion.
Arch Mal Coeur Vaiss 1991 Dec
PMID:[Left ventricular remodeling and ischemic heart diseases. Therapeutic possibilities]. 168 44


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