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Biomedical subjects

J M Juliard

Publications and source records attributed to J M Juliard.

At least 91 records · Page 5Linked to original sources
PubMed1987

[Total pericardectomy. Exceptional treatment for recurrent idiopathic cortico-dependent pericarditis].

The authors report a case of definitive treatment of idiopathic relapsing pericarditis by total pericardectomy in the absence of signs of constrictive pericarditis after a 15 month period marked by multiple invalidating recurrences and the development of dependence on corticosteroid therapy. The indications of total pericardectomy must be discussed in these exceptional cases of failure of medical therapy in idiopathic relapsing pericarditis.

Humans↗
PubMed1987

[Reduction of auricular fibrillation and tachycardia using intravenous flecainide].

Fifty-one consecutive patients with atrial tachycardia [atrial fibrillation (FA) 37, atrial flutter (Fl) 10, tachycardia (TSA) 4] received a single 2 mg/kg dose of flecainide injected intravenously over 5 to 10 minutes. Patients over 75 years of age or presenting with heart failure or disorders of conduction were excluded from the study. Sinus rhythm was restored during the injection or within the following 5 minutes in 15 patients (FA 12, Fl 1, TSA 2). The most frequent side-effects were visual disorders (5 cases) and moderate prolongation of QRS (all cases). Five patients had more pronounced disorders of conduction, but none developed heart failure. Reduction was obtained in 12 of the 18 patients whose arrhythmia had lasted for less than 8 days, against only 3 of the patients whose arrhythmia was more than 8 days old. Drug-induced reduction always failed in patients with left atrial dilatation (greater than 45 mm at echocardiography). An increase in the ventricular rate of unreduced flutter was observed in only one patient. Plasma flecainide levels were high (1.5 and 5.5 mg/l) at the end of the injection, but they fell to the therapeutic range within less than 10 minutes. Flecainide therefore appears to be effective in reducing recent atrial fibrillation on a non-dilated atrium. In cases with disorders of conduction, altered ventricular function or flutter, the therapeutic risk is such that another method of conversion should be used.

Adult↗
PubMed1987

[Drug treatment of left ventricular insufficiency. Current aspects].

The medical treatment of left ventricular failure classically relies upon the use of diuretics with or without digitalis. The recent arrival of vasodilators allows for both an improvement in the quality of life as well as a prolongation of survival for people in heart failure. The "new" positive inotropic agents which can be used orally in the longterm have not yet given the results which were anticipated. The prognosis of left ventricular failure remains poor, underlining the importance of preventive treatment and in the last resort the possibility of cardiac transplantation.

Cardiotonic Agents↗
PubMed1987

[Esophageal motility in cases of chest pain with normal coronarography].

The aim of this study was to assess the incidence of oesophageal abnormalities and to determine their nature in patients with retrosternal chest pain and normal coronary angiography with a negative coronary spasm provocation test. Oesophageal manometry was carried out in all cases with or without a spasm provocation (usually alkalosis) test. Forty consecutive patients were studied: 19 men (47.7 +/- 10.0 years) and 21 women (54.7 +/- 7.5 years). A history of gastro-intestinal disorder was obtained in 57 p. 100 of cases (hiatal hernia and/or gastro-oesophageal reflux, biliary lithiasis and/or cholecystectomy, gastritis). Seventeen patients had broad based powerful oesophageal contractions which are an established cause of pain; they were recorded under basal conditions in 5 cases and after a provocation test in 12 cases. Two patients had a megaoesophagus without giant waves. Thirteen patients had manometric signs of reflux (malposition and hypotonia of the lower oesophageal sphincter) of whom 7 had giant waves on provocation. In addition, three patients experienced pain during gastro-oesophageal reflux (1 case) or hypotonia of the lower oesophageal sphincter (2 cases). In all, a very probable oesophageal origin of the chest pain was demonstrated in 22 patients (55 p. 100 of cases).

Angina Pectoris↗
PubMed1987

[Non-obstructive hypertrophic cardiomyopathy and systolic compression of 3 coronary arteries. Long-term improvement with verapamil].

Systolic compression of the three main coronary vessels was observed during the investigation of a 23 year old African with hypertrophic cardiomyopathy. The patient was admitted in 1982 for evaluation of retrosternal chest pain and one syncopal attack during exercise. The ECG showed left ventricular hypertrophy with important ST-T wave changes which became more severe on exercise. Diffuse myocardial hypertrophy without obstruction was confirmed by echocardiography and cardiac catheterisation. Coronary angiography showed systolic compression of the three main coronary arteries. There was no coronary vasodilatory response to rapid atrial pacing; increased left ventricular end diastolic pressure confirmed the poor tolerance of exercise. The therapeutic failure of betablockers suggested a possible coronary spasm. Long-term (4 years) clinical improvement was obtained with calcium antagonists (Verapamil 360 mg/day) without significant regression of the hypertrophy. Coronary vasodilation under Verapamil led to improved tolerance of rapid atrial pacing. Control angiography showed only mild systolic compression of the three main coronary vessels. The improvement of this functional coronary insufficiency with Verapamil was attributed to its negative inotropic effects associated with improved myocardial relaxation and ventricular filling.

Adult↗
PubMed1986

[Left ventricular hypertrophy. Advantages and drawbacks].

The increase of the muscular mass of the left ventricle represents, for the ventricular pump, a mechanism of adaptation to a normal process (growth, sport, etc.) or a pathological process (mechanical overload or cardiomyopathy). The geometrical variations which are associated, tend to normalize the performances and/or the systolic constraints, determining elements of the metabolic needs of the myocardium. If left ventricular hypertrophy is not quantitatively, geometrically and functionally adequate and if the contractility and precharge reserves become exhausted, the systolic performance of the ventricular pump is altered and becomes extremely dependent upon the systolic constraints which are then increased. It may be difficult to take into consideration an insufficiency of the contractility of the ventricular muscle in front of clinical signs of cardiac insufficiency which is conditioned by abnormalities in the filling of the ventricular pump. In addition, some "pathological" hyperthophies may secondarily induce an alteration of the intrinsic properties of the muscle (during its contraction, relaxation an/or extension), susceptible to induce or aggravate a ventricular insufficiency. The causes remain uncertain, since a metabolic imbalance of the myocardium by increase of the needs as well as a decrease of the coronary reserve and the exchange capabilities are commonly accepted. What are the mediators of these mechanisms of quantitative, geometric adaptation and also--at least in some animals--structural adaptation (isoenzymes of myosin)? Why do they seem, at times, strangely absent or quickly out-of-date, or sometimes excessive, with all the drawbacks specific to hypertrophy? The answer to these questions would perhaps represent a new therapeutic approach to left ventricular insufficiency.

Adaptation, Physiological↗
PubMed1986

[Long-term course of septal rupture operated on during the acute phase of a myocardial infarct].

Between 1970 and 1979, 28 patients (18 men and 10 women, aged 46 to 76 years, average 62 years) with acute myocardial infarction complicated by septal rupture survived surgery performed during the acute phase. In the same period 62 patients were admitted to the Cardiology Department and were operated early for septal rupture complicating myocardial infarction. The site of infarction was the anterior wall in 22 cases and the posterior wall in 6 cases; septal rupture occurred on average after 4.2 days (range 1 to 10 days); 15 patients including 13 with cardiogenic shock underwent intraaortic balloon pumping for an average of 3:7 (range 1 to 11 days) before surgery; the operation performed after an average interval of 11 days consisted in direct suture of the defect in 3 cases and a patch repair in the other 25 cases, associated in all cases with infarctectomy and LAD coronary bypass grafting in 1 case. The immediate postoperative course was simple; three patients with residual shunts were not reoperated. Five to 14 years later, in 1984, 4 patients had been lost to follow-up; 4 patients had died, 2 of cardiac causes (LVF after 1 year and an arrhythmia after 4 years). Of the 20 survivors, 2 were successfully reoperated (1 coronary bypass after 10 years and 1 false aneurysm after 5 years). Only one patient had recurrent myocardial infarction. The quality and longevity of long-term survival encourage early surgery. The factors affecting long-term survival are discussed: correction of associated valvular defects, resifual shunts, conservation of left ventricular function and evaluation of the coronary circulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1985

[Coronary and renal circulation in patients with cardiac failure after converting enzyme inhibitors].

The cardiac output and its peripheral distribution must fulfill the metabolic and/or functional requirements of the different organs. The various techniques used to measure blood flow rates in the coronary and renal arteries provide much information on this point, but they do not tell us all we would like to know about the distribution and "utilization" of these flows in tissues. In normal subjects the myocardial oxygen consumption is not markedly different from the renal oxygen consumption, but the mechanisms that regulate the coronary and renal circulations are not the same. The flow rate in the coronary vessels is about 10% of the cardiac output, the arteriovenous oxygen gradient is superior to 10 vol % and regulation is metabolic. In the renal vessels, which are primarily "functional", the flow rate is about 25% of the cardiac output and the arteriovenous oxygen gradient is inferior to 2 vol %. In heart failure patients, despite reduced cardiac output the blood pressure is kept normal for a long time by vasoconstriction of the arterioles, a process which involves, at least partly, the renin-angiotensin system. The vasoconstriction predominates in some circuits (the renal flow rate is less than 15% of the cardiac output) and spares the "privileged" circuits (the coronary flow rate is more than 15% of the cardiac output). Under the influence of angiotensin converting enzyme inhibitors, the cardiac output increases and its distribution is modified. The coronary flow rate remains stable or is reduced in proportion to the decrease in myocardial oxygen consumption, the metabolic regulation is preserved and there is no "coronary steal". The percent increase in renal flow rate is usually superior to that of the cardiac output. This peripheral redistribution of coronary and renal blood flow rates in heart failure patients after treatment with converting enzyme inhibitors seems to correspond to the physiological purposes of the two regional blood flows.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1985

Hemodynamic and coronary effects of molsidomine at basal state, during atrial pacing, and during cold pressor test in patients with stable angina pectoris.

Heart rate (HR), cardiac output (CO), coronary sinus blood flow (CSF), left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), mean arterial (MAP), and coronary arteriovenous difference for oxygen (AVDcO2) were measured in patients with stable angina pectoris without cardiac failure before and 40 to 60 minutes after administration of 2 or 3 mg of molsidomine. In 20 patients these measurements were made in basal state during spontaneous rhythm. In eight of these patients (including three receiving beta blockers) the measurements were made during atrial pacing. In eight other patients, all receiving long-term beta-blocker therapy, the measurements were made during cold pressor test. At the basal state in spontaneous rhythm, a gradual reduction in the LVSP to 70% or less of its initial value was observed in four patients receiving 3 mg of molsidomine (two of whom received beta-blocker treatment). The LVSP was immediately restored by vascular filling. In the 16 other patients molsidomine decreased LVSP, LVEDP, MAP, CO, and double product (DP = LVSP X HR). The AVDcO2 was unchanged. CSF and myocardial oxygen uptake index (MVO2 = CSF X AVDcO2) were decreased. During atrial pacing, hemodynamic and coronary effects were similar to those seen in the basal state. During the cold pressor test, the increases in LVSP, MAP, and LVEDP were significantly reduced by molsidomine. The variations in CSF and coronary resistance (MAP/CSF) were also significantly different after administration of molsidomine, with better metabolic regulation of the coronary circulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Changes in left ventricular performance during chronic pressure or volume overload: importance of physical properties of the arterial system.

The present study was aimed at evaluation of changes in systolic and diastolic left ventricular function during chronic pressure of volume overload, in comparison with normal subjects. Sixty-two patients were included: group 1 was composed of 25 normal subjects, group 2 was composed of 20 subjects with essential hypertension, and group 3 was composed of 17 subjects with aortic regurgitation without congestive heart failure. Cardiac output, aortic and left ventricular pressures (micromanometers), ventricular volume and ascending aortic radius (cineangiography), ejection fraction (EF), mean velocity of fiber shortening (VCF), ventricular mass (m), and the ratio m/EDV (EDV, end diastolic volume) were determined. Also measured were maxima for end systolic pressure (ESP), end systolic stress (ESS), and end systolic volume (ESV) and radius (ESR), as well as the modulus of left ventricular chamber and muscle stiffness (method of Gaash et al.) (1) and characteristic impedance of the ascending aorta (Zc). In hypertensive patients, m and m/EDV were increased, as was the ESP/ESV ratio, whereas EF and VCF were not modified and the ESS/ESR was normal or sometimes decreased. The systolic "pump" function thus appeared to be increased, whereas the muscle function appeared normal or decreased. The moduli of left ventricular chamber stiffness and muscle stiffness were increased. Zc was increased because of a greater pulse wave velocity, although aortic radius was larger. A close relationship was found between Zc and the ratio m/EDV. In patients with aortic regurgitation, the increased left ventricular mass was closely related to the regurgitant fraction (RF). The m/EDV ratio was normal. EF was unmodified and VCF and the ESP/ESV ratio were decreased.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

[Effects of molsidomine during the cold test in stable coronary insufficiency under beta-blocker treatment].

The heart rate, cardiac output, coronary sinus blood flow, systolic and end diastolic left ventricular pressures, femoral arterial pressure and coronary oxygen arterio-venous difference were measured in 12 patients with stable coronary artery disease without cardiac failure on long-term betablocker therapy, before and 45 minutes after 2 or 3 mg sublingual molsidomine. The measurements were repeated in 8 patients during a cold pressor test. Under basal conditions, molsidomine decreased the systolic and end diastolic left ventricular pressures, mean femoral arterial pressure, cardiac output and double product. The coronary oxygen arterio-venous difference was unchanged. Coronary sinus flow and myocardial oxygen consumption decreased. In the 2 patients who were given 3 mg molsidomine, a progressive reduction in systolic left ventricular pressure to 70% or less than its initial value, necessitated immediate treatment with volume expanders. During the cold pressor test before molsidomine the systolic and end diastolic left ventricular pressures, mean femoral arterial pressure and the double product increased. Coronary sinus flow was unchanged overall: it decreased in 6 patients, increased in 2 patients and remained the same in 1 patient. Coronary resistance increased in 6 patients and decreased in only one patient. During the cold pressor test after molsidomine there was a significant reduction in the increase of systolic left ventricular pressure, mean femoral artery pressure and double product. Coronary sinus blood flow increased in 5 patients and decreased in only one case. Coronary resistance decreased in half the cases.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1984

[Transformation of cerebral infarction into hemorrhage during x-ray computed tomography in a patient under anticoagulant treatment].

Repeated CT scans provide the only means of confirming the initial ischemic nature of a cerebrovascular accident and its eventual course towards a hemorrhage. Precise data can be obtained as to the frequency of this complication as a function of factors such as the embolic origin of the infarct or associated anticoagulant therapy. The present case shows that contrast medium, at least in patients receiving anticoagulant treatment, may constitute a risk factor by increasing the possibility of transformation of a pale infarct into a hemorrhagic one. Possible relevant properties of iodized contrast media with respect to this type of complication are considered.

Aged↗