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Biomedical subjects

P Cosnay

Publications and source records attributed to P Cosnay.

107 records · Page 6Linked to original sources

[Paroxysmal mitral insufficiency caused by ischemic dysfunction of the papillary muscles. Apropos of 39 cases].

Episodic mitral regurgitation due to ischaemia of one or both papillary muscles was studied in a review of 39 cases with complementary investigations and compared with previously reported data. The condition occurred after myocardial infarction in 69 p. 100 of cases (usually after inferior infarction: 54 p. 100) associated with ischaemia of the controlateral territory; there was no history of myocardial infarction in 31 p. 100 of cases. The patients were usually elderly (73 years), often hypertensive (77 p. 100) and diabetic (62 p. 100). The clinical syndrome was that of severe anginal pain, mitral regurgitation and left ventricular failure which was critical in some cases. The ECG showed typical ST depression (4.1 +/- 1.6 mm) especially in the antero-lateral leads; left bundle branch block (28 p. 100) with left axis deviation (18 p. 100), sometimes associated with changes of chronic infarction (64 p. 100) was also recorded. Mitral regurgitation and left ventricular failure regressed almost completely in typical cases between attacks, whilst the ECG showed slight residual sub-endocardial ischaemia (ST depression of 1.5 +/- 0.4 mm) in 30 cases and/or subepicardial ischaemia observed in the anterolateral leads in 13 cases. Phonomechanographic recordings (n = 32) showed moderate mitral regurgitation (1-2/6), usually parasystolic (47 p. 100) or early and mid systolic (36 p. 100) in 87.5 p. 100 of cases between attacks, aggravated by handgrip exercise and improved by trinitrin administration. Echocardiography (n = 27) only showed mitral valve changes in 2 patients (increased density of the papillary muscle in 1 case and prolapse of the anterior leaflet in 1 case); however, segmental wall hypokinetic (51 p. 100) or dyskinetic (15 p. 100) motion, was common with increased left ventricular end diastolic dimensions (mean 56.3 +/- 8.0 mm) and decreased fractional shortening (mean 0.30 +/- 0.07) (67 p. 100). Left atrial dimensions were increased (mean 39.7 +/- 6.4 mm) in 52 p. 100 of patients. Thallium 201 myocardial scintigraphy (n = 32) showed hypofixation in 57 (36 p. 100) and a lacuna in 23 (14 p. 100) of the 160 segments analysed. Left ventricular angioscintigraphy (n = 27; 135 segments) showed hypokinesia in 72 segments (53 p. 100); 2.7 segments per patient), akinesia in 19 segments (15 p. 100; 0.7 segment per patient) and dyskinesia in 2 segments (1.5 p. 100); 0.1 segment per patient). The global ejection fraction was 46 +/- 13 p. 100. Coronary angiography (n = 8) showed significant diffuse atherosclerosis.(ABSTRACT TRUNCATED AT 400 WORDS)

Aged↗

[Paroxysmal mitral insufficiency caused by ischemic dysfunction of the papillary muscles. Hemodynamic and angiographic study of 18 cases. Pathogenic hypotheses].

18 of 39 cases of ischaemic papillary muscle dysfunction reported elsewhere underwent cardiac catheterisation and angiography. Fifteen patients had previous myocardial infarction. The average age of the patients was less than in the overall series (69 vs 73 years) but the incidence of infarction and the degree of cardiac disease were greater. The absence of catheter data in the other patients is explained by their older age (76.4 years) and the longer period of recruitment. Their results and outcome of medical or surgical treatment are reported. The pathogenesis of the syndrome is reconsidered in the perspective of paroxysmal forms. A protocol for investigation is suggested to guide the therapeutic options. Right heart catheterisation at rest (n = 16), on exercise (n = 12), under vasodilator therapy (n = 6) and during angiography (n = 2) does not show a specific profile. These investigations only provide haemodynamic data related to therapy but they are essential for the interpretation of ventriculography. Ventriculography (n = 8) demonstrated 4 cases of mitral regurgitation (2 major and 2 minor), a reduced EF (0.47 +/- 0.17), asynergy of 36.1 p. 100 of segments analysed, predominantly in the inferior and lateral zones. Coronary angiography showed triple vessel disease in 6 cases, double vessel disease in 1 case and 1 stenosis of the left main coronary artery. Stenosis was commonest on the left circumflex (87.5 p. 100) and right coronary arteries (87.5 p. 100) but also frequently involved the left anterior descending artery (75 p. 100). Of the 12 patients treated medically, 8 died (66.6 p. 100) and the survivors remain symptomatic (33.3 p. 100), half with and half without attacks. After surgery (n = 8) comprising coronary bypass surgery (n = 6) or mitral valve replacement (n = 2), patients were asymptomatic. 1 patient died of cancer. These paroxysmal forms of mitral regurgitation may be explained by the association of aggravating, reversible ischaemic or haemodynamic factors to organic mitral lesions. Mitral valve replacement is justified when dysfunction becomes permanent and coronary bypass surgery is advocated whenever possible. The indications for surgery can only be taken into account after complete haemodynamic and angiographic investigation. A protocol for the interpretation of these investigations is suggested.

Aged↗

[Treatment of supraventricular and paroxysmal ventricular tachycardia with bepridil].

Bepridil is a molecule which, apart from its anti-anginal properties, also has antiarrhythmic effects due to its calcium antagonist action which depresses antero and retrograde AV conduction in the physiological pathways. Conduction in accessory AV pathways is also depressed to a lesser and more variable extent. It also has an anti-ventricular arrhythmic action probably due to an associated membrane-stabilising effect. This drug was used intravenously to treat attacks of reciprocating supra-ventricular tachycardia (SVT) (60 p. 100 conversion to sinus rhythm: 6 out of 10 cases of intra-nodal reentry, 6 out of 10 cases of reentry via an accessory pathway) and also in ventricular tachycardia (VT) (7 conversions in 15 patients within 2 to 9 minutes). It was impossible to induce attacks of SVT after administering the drug in about a third of patients; better results were obtained in intra-nodal SVT (5 cases of effective prevention out of 10) than in SVT involving an accessory pathway (1 case out of 10). It was not possible to reinitiate VT after treatment in 3 out of 6 cases (very aggressive pacing methods, a long QT interval and accelerated idio-ventricular rhythm were responsible for the failures). Oral therapy (400 to 800 mg, usually 600 mg daily in 3 doses) prevented any recurrence of SVT in over half the patients (prevention of intranodal SVT: 80 p. 100; prevention of SVT involving an accessory pathway: 13 p. 100) and in 4 out of 6 patients with VT. Provocative pacing studies after intravenous or oral bepridil provide a good indication of long-term efficacy. The drug is generally well tolerated.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗

[Effects of oral and injectable flecainide in patients with an accessory atrioventricular pathway].

Flecainide, a new Vaughan-Williams Class Ic anti-arrhythmic agent, was used in 21 patients with an accessory AV conduction pathway which was apparent in 16 cases (WPW syndrome), latent in 1 case and concealed in 4 cases (block in the anterograde direction). Seventeen patients had spontaneous and inducible arrhythmias; 13 supraventricular tachycardias (SVT) due to orthodromic reentry including the accessory AV pathway and 4 atrial arrhythmias. Intravenous flecainide (2 mg/kg over 5 minute period) terminated the 13 cases of SVT in an average of 3 minutes by depressing then blocking retrograde conduction in the accessory pathway and 3 out of 4 cases of atrial arrhythmias. Conduction in the accessory pathway was blocked in the anterograde direction in 75% of cases and depressed in the rest; it was blocked in the retrograde direction in about half the cases and depressed in the rest. Intravenous flecainide completely prevented the induction or arrhythmias in 13 out of 17 patients (76%). Oral flecainide blocked the accessory pathway in the anterograde direction in 68.7%, and in the retrograde direction in 62% of patients, and prevented arrhythmias during provocative testing in 82% of patients (14 out of 17). With an average follow-up of 20.7 +/- 2.6 months with oral doses adapted to body weight and to the response to IV flecainide only one recurrence of atrial fibrillation was observed, a 100% prevention of spontaneous SVT and 94% prevention of all arrhythmias (16 out of 17 cases). The predictive value for the response to oral therapy of the tests of regularisation of SVT by IV flecainide and of the tests of non-provocation of SVT with oral or IV flecainide was excellent (100%). The cardiac tolerance was very good in these 21 patients (17 of whom had no valvular or myocardial lesion). There were 6 minor cases of general intolerance to oral therapy which were not dose related, only 1 of which required interruption of therapy. Flecainide appears one of the best choices for the treatment of preexcitation syndromes and their related arrhythmias at the present time.

Administration, Oral↗

Phase quadrature shift between left and right ventricles during a ventricular tachycardia attack.

Equilibrium gated nuclear angiography was performed on a patient during an attack of ventricular tachycardia and then after conversion to sinus rhythm. Global and regional wall motion was assessed by means of isocontours, Fourier phase analysis and factor analysis. Ventricular phase histograms showed a 100 degrees difference between ventricles: left ventricular filling time occurred during right ventricular contraction. The earliest phase was located in the septum and the sequence of activation showed a large delay of left ventricular activation. After conversion to sinus rhythm, a right bundle branch block was observed, being almost the inverse of the latter situation.

Adult↗

[Traumatic myocardial infarction. Apropos of 2 cases].

Two cases of anterior transmural myocardial infarction occurring after closed chest injuries in young adults (26 and 29 years) are reported. In one case, the infarct was detected after 42 days when the patient gradually developed left ventricular failure after thoracic injury (fracture of the left 9th rib). In the other case, the diagnosis was made during the initial evaluation of a patient with multiple injuries by routine electrocardiography. Radio-isotopic investigations showed an antero-septo-apical and lateral defect with akinetic wall motion in the first case, and apical hypofixation with limited akinesis in the second one. Coronary angiography with left ventriculography was performed after 2 and 3 months respectively, and showed a prolonged non-atheromatous stenosis of the proximal left anterior descending artery with anterior wall hypokinesia, apical akinesia and mitral incompetence (Case n 1) and slight changes of the distal part of the left anterior descending artery with apical hypokinesia (Case n 2). These two cases bring the number of documented reported cases to 37 and illustrate the two possible mechanisms of myocardial infarction after closed chest trauma: direct trauma to the coronary arteries with vascular lesions and secondary myocardial infarction associated with a poor prognosis, and myocardial contusion resulting in random myocardial lesions which usually carry a better prognosis.

Adult↗

[The heart and hyperkalemia].

Hyperkalaemia is a common and serious clinical condition in medical and surgical intensive care units. It is mainly encountered in patients with overt or latent cardiac and/or renal failure, and often aggravated by dietetic and therapeutic mismanagement. Hyperkalaemia depresses cardiac contractility, automaticity, conductivity and excitability, leading to ECG changes which must be recognized before clinical cardiovascular deterioration occurs if treatment is to be given to reverse an irremediably fatal evolution: ST-T changes and widening of the QRS with axial deviation shortly precede sinoatrial, intraatrial and atrioventricular block, the characteristic appearances of atrial standstill and ventricular and junctional hyperexcitability. The ECG changes faithfully follow the rise in serum potassium with few exceptions, such as associated electrolytic and acid-base disturbances (usually acidosis). Treatment must be administered as soon as a rise in potassium is observed. It may be administered intravenously (hypertonic glucose and insulin, calcium gluconate, furosemide, buffer solution and, above all, sodium bicarbonate or hypertonic saline) or orally (cation exchange resin). Renal dialysis may be required secondarily.

Arrhythmias, Cardiac↗

[Radioisotopic quantification of isolated mitral insufficiency].

A group of 23 consecutive patients with isolated mitral regurgitation confirmed by angiography, 8 of whom had normal and 15 abnormal coronary arteriographies, were compared with a control group of 27 subjects without valvular heart disease (normal coronary arteriography in 7 cases, abnormal coronary arteriography in 20 cases). After injection of technetium 99m labelled albumin, gamma-angiocardiography was performed in the left anterior oblique plane at equilibrium with electrocardiographic synchronisation. Fourier's analysis of the images excluded hepatic pulsation and dephasing of the two ventricles: amplitude images were used to trace the right and left ventricular zones of interest. The ratio of right to left ventricular ejection fraction was calculated in these zones from the radioactive count at end diastole and end systole. The ratio of the ejection fractions was 1.15 +/- 0.18 in subjects without valvular disease compared to 2.66 +/- 0.47 in patients with mitral regurgitation and normal coronary arteries, and 2.50 +/- 1.28 in mitral regurgitation with coronary artery disease (no significant difference between these two sub-groups). When compared with angiographic quantification of the mitral regurgitation, the ratio of ejection fractions increased progressively with the severity of the leak: 1.81 +/- 0.44 for grade I (9 cases), 2.37 +/- 0.80 for grade 2 (5 cases), 3.02 +/- 1.07 for grade 3 (4 cases) and 3.73 +/- 1.50 for grade 4 (5 cases). The differences between each sub-group are not statistically significant because of the small number of patients in each sub-group but all the values are significantly higher than the reference values.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

[Auriculo-ventricular block in the Kearns-Sayre syndrome. Apropos of a case].

A 21 year old patient was operated for bilateral ptosis and external ophthalmoplegia at 13 years of age. At this time there were no signs of retinitis pigmentosa or atrioventricular block, features of the Kearns and Sayre Syndrome (1958) which were detected five years later. His bundle recording showed an intrahisian block (1 degree proximal and a complete distal block) with a trifascicular block, the latter persisting alone during a brief return to sinus rhythm. This is one of the rare cases of the Kearns and Sayre Syndrome with documented His bundle recordings and the only reported case with intrahisian block. The patient also suffered from bilateral neural deafness. The patient's condition remains stable after implantation of an isotopic cardiac pacemaker and he now leads a normal life. A review of 52 previously published cases shows that this rare condition appears to be caused by a mitochondrial abnormality, which, for an unknown reason, affects only the neuromuscular and cardiac conduction systems. The prognosis is poor when swallowing and respiration are affected, but this does not occur in all cases. As cardiac conduction abnormalities are the other life-threatening complication, cardiac pacing has greatly improved the prognosis of these patients.

Adult↗

Fourier phase analysis of SPECT equilibrium radionuclide angiography in symptomatic patients with mitral valve prolapse without significant mitral regurgitation: assessment of biventricular functional abnormalities suggesting a cardiomyopathy.

BACKGROUND: Ventricular premature beats are common in patients with mitral valve prolapse (MVP). The purpose of this study was to determine whether symptomatic patients with MVP had certain functional characteristics and if ventricular arrhythmia (VA) could be explained by functional extravalvular abnormalities. Single photon emission computed tomography equilibrium radionuclide angiography with Fourier phase analysis was preferred to the planar radionuclide method. Only patients without significant mitral regurgitation were studied. METHODS AND RESULTS: A total of 23 symptomatic patients with MVP (13 men, 10 women, mean age, 47+/-14 years) without mitral regurgitation underwent single photon emission computed tomography equilibrium radionuclide angiography. Symptoms were present in 20 patients, and VA was present in 14 patients. Ejection fraction, regional wall motion, and Fourier phase analysis were examined in both ventricles and compared with results for normal subjects. Ventricular abnormalities were observed in 20 (87%) patients: decreased left ventricular and right ventricular ejection fractions, increased standard deviations of the mean phase and focal wall motion, and/or delayed phase abnormalities. Abnormalities were less frequent but more marked in the right ventricular free wall, the infundibulum, or the septum compared with left ventricular delayed abnormalities, which were more frequent but limited. In 12 of 14 patients with VA, phase-delayed areas were observed in the ventricle where the origin of ventricular premature beats was suspected on the basis of their electrocardiographic morphologic features. A relation was found between late potentials and delayed-phase areas (right ventricle or septum) and left bundle branch block morphologic features of VA. CONCLUSIONS: Symptomatic patients with MVP frequently have ventricular dysfunction in 1 or both ventricles, sometimes limited but more marked in the presence of severe VA even without significant mitral regurgitation, suggesting structural modification. The use of a sensitive, accurate, and 3-dimensional method such as single photon emission computed tomography equilibrium radionuclide angiography may be of interest for a noninvasive investigation, especially in young symptomatic patients with MVP and VA.

Arrhythmias, Cardiac↗

[Treatment of chronic refractory cardiac insufficiency with an inhibitor of converting enzyme. Long-term results].

44 patients with refractory heart failure (RHF) were treated with a conversion enzyme inhibitor, captopril. Prior to treatment, 26 patients had stage IV RHF and 18 patients had stage III RHF (NYHA). The course of the trial was marked by early deaths (6 months) in 9 cases (20.4%), early treatment failure in 8 cases (18.2%), intolerance in 3 cases (6.8%) and 3 patients (6.8%) were lost to follow-up. 21 patients (48%) were improved by the treatment and were followed for a mean of 16 months +/- 8.6. The mean dosage of captopril was 157 mg per day in 3 oral doses (range: 75 to 300 mg per day). The pulmonary capillary pressure dropped, on average, from 30 +/- 10 mm Hg to 21 +/- 7 mm Hg (p less than 0.01) by the 8th day and remained stable thereafter. The cardiac index increased by 40%. The heart rate decreased by a mean of 10.4%, by the time of the first examination. The mean blood pressure was not significantly modified. Side effects which resolved after changing the dosage were seen in one third of cases: renal failure (4 cases), hypotension (2 cases), hyperkalaemia (1 case). In the long term, 6 patients (2.6%) died after a mean delay of 15.6 +/- 5.3 months.

Adult↗

[Tumor of the adrenal gland associating pheochromocytoma and ganglioneuroma (author's transl)].

An adrenal gland tumor associating of both a pheochromocytoma and a ganglioneuroma was discovered upon its fissuration in a 58-year-old male having a family history of neurofibromatosis. The patient's clinical course was fatal due to complications of necrotizing enteritis which was discovered at laparotomy. The association of pheochromocytoma, ganglioneuroma, and "café au lait" spots in the same patient illustrates the polymorphism of neural crest dysgenetic pathology.

Adrenal Gland Neoplasms↗