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Biomedical subjects

M Degeorges

Publications and source records attributed to M Degeorges.

At least 37 records · Page 2Linked to original sources
PubMed1986

Nifedipine and thallium-201 myocardial perfusion in progressive systemic sclerosis.

Heart disease in patients with progressive systemic sclerosis may be due in part to myocardial ischemia caused by a disturbance of the coronary microcirculation. To determine whether abnormalities of myocardial perfusion in this disorder are potentially reversible, we evaluated the effect of the coronary vasodilator nifedipine on myocardial perfusion assessed by thallium-201 scanning in 20 patients. Thallium-201 single-photon-emission computerized tomography was performed under control conditions and 90 minutes after 20 mg of oral nifedipine. The mean (+/- SD) number of left ventricular segments with perfusion defects decreased from 5.3 +/- 2.0 to 3.3 +/- 2.2 after nifedipine (P = 0.0003). Perfusion abnormalities were quantified by a perfusion score (0 to 2.0) assigned to each left ventricular segment and by a global perfusion score (0 to 18) for the entire left ventricle. The mean perfusion score in segments with resting defects increased from 0.97 +/- 0.24 to 1.26 +/- 0.44 after nifedipine (P less than 0.00001). The mean global perfusion score increased from 11.2 +/- 1.7 to 12.8 +/- 2.4 after nifedipine (P = 0.003). The global perfusion score increased by at least 2.0 in 10 patients and decreased by at least 2.0 in only 1. These observations reveal short-term improvement in thallium-201 myocardial perfusion with nifedipine in patients with progressive systemic sclerosis. The results are consistent with a potentially reversible abnormality of coronary vasomotion in this disorder, but the long-term therapeutic effects of nifedipine remain to be determined.

Adult↗
PubMed1986

Pharmacodynamic effect of dipyridamole on thallium-201 myocardial perfusion in progressive systemic sclerosis with diffuse scleroderma.

We evaluated the effect of dipyridamole on thallium-201 myocardial perfusion in 23 patients with progressive systemic sclerosis (PSS) with diffuse scleroderma. Thallium-201 single photon emission computed tomography (SPECT) was performed at rest and after coronary artery vasodilatation with intravenous dipyridamole (0.14 mg/kg/min for four minutes). The left myocardium was divided into nine segments; each segment was graded as 2.0, 1.5, 1.0, 0.5, 0 (zero represents no activity). Dipyridamole significantly improved resting thallium-201 myocardial perfusion: the mean (SD) number of segments with thallium defects decreased from 6.0 (2.1) at rest to 4.1 (2.5) after dipyridamole (p less than 0.0001); the mean (SD) score in segments with resting defects increased from 0.92 (0.24) at rest to 1.13 (0.38) after dipyridamole (p less than 0.0001); the mean (SD) global score per patient increased from 10.2 (1.8) at rest to 11.4 (2.1) after dipyridamole (p less than 0.02); the global score increased by at least 2.0 in 12 patients and worsened by at least 2.0 in three patients only (p = 0.05). The results of this acute study suggest that some drugs with potent vasodilator activity on small coronary arteries may be beneficial in the treatment of PSS patients with thallium-201 myocardial perfusion abnormalities.

Adult↗
PubMed1986

[Double mitral orifice. An anatomical case].

A double mitral orifice was discovered at autopsy in a 74 year old woman. Death resulted after several episodes of cardiac failure complicating mixed mitral and aortic valve disease. A vertical limbus bridged the mitral annulus separating it into two distinct right and left orifices, with oblique long axes aligned towards the lower part of the limbus perpendicular to each other from the left atrial view. After opening the left ventricle, both orifices were observed to have their own sets of chordae tendinae attached to normal papillary muscles: the right orifice to the posterior and the left to the anterior papillary muscle. The inferior end of the limbus was attached to a supplementary papillary muscle. Echocardiography and CT scanning were performed before dissection. This malformation results from symphysis of the mid parts of the two mitral leaflets during embryonic stages 15 and 16 (8-10 mm vertex-coccyx, 31st-33rd days).

Aged↗
PubMed1985

Nifedipine and alpha 1-adrenergic blockade in Raynaud's phenomenon.

The efficacy of nifedipine and prazosin in the treatment of Raynaud's phenomenon was assessed in a prospective double-blind randomized cross-over trial in 15 patients. Each patient received one week of nifedipine 20 mg TID, one week of prazosin 1 mg TID, and 2 weeks of placebo. Nifedipine was shown to be effective in reducing both the frequency and the severity of Raynaud's phenomenon, whereas prazosin was ineffective. Before initiation of therapy in the 15 patients, pressor responses to the intravenous alpha 1-agonist phenylephrine were assessed in the basal state, 30 min after 20 mg oral nifedipine, and 30 min after 1 mg oral prazosin; the shift to the right of the log dose-vasopressor response curves to phenylephrine was similar with nifedipine and prazosin.

Adult↗
PubMed1985

Prevention with molsidomine of coronary artery spasm caused by alkalosis.

A provocative test of coronary artery spasm caused by alkalosis was used to evaluate a possible anti-coronary artery spasm effect of molsidomine. The rapid infusion of an alkaline buffer followed by maximal voluntary hyperventilation in 10 patients with angina at rest led to the appearance of anginal pain and significant, transient ischemic changes of the ST segment resulting from alkalosis-induced coronary spasm. A second provocative test was performed under the same conditions, 24 hours later, after the administration of 4 mg of molsidomine. Molsidomine prevented the development of coronary artery spasm in 8 of the 10 patients in the study group. These preliminary results justify further clinical evaluation of molsidomine in the treatment of vasospastic angina.

Alkalosis↗
PubMed1985

[Classification and principles of the use of vasodilators in the treatment of left ventricular insufficiency].

Vasodilators have been widely used in recent years for the treatment of severe left ventricular failure (LVF). However, amongst these drugs, not all have the same therapeutic effects, but they differ from one another in molecular structures, cellular mechanisms, haemodynamic actions and modes of administration. A three tier classification is proposed with the single objective of facilitating the therapeutic choice: mechanism of action: this property distinguishes the alpha-blockers from the beta-2 sympathomimetics, calcium antagonists, angiotensin converting enzyme inhibitors and prostacyclin biosynthesis inducers. Some molecules such as hydralazine, whose mechanism of action remains unclear, cannot be classified in this way; haemodynamic effects: these effects can be used to distinguish vasodilators which act mainly on the venous sector from arterial and mixed vasodilators. The knowledge of the preferential site ol action of these molecules helps to adapt the choice of treatment to the initial haemodynamic profile of each patient; pharmacokinetics: these properties distinguish molecules active only by intravenous administration, better adapted for the treatment of acute LVF in the intensive care unit, from those active orally which can be used for long-term ambulatory therapy of chronic cardiac failure. Trinitrin and its derivatives occupy an intermediate position because of their relatively low bioavailability after oral administration: long-term administration is not always easy and may require special modes of administration (i.e. percutaneous). Vasodilators have been widely used in cardiac failure for about 5 years; the results of some medium term controlled therapeutic trials are now available and confirm the efficacy of these drugs but also define their limitations: variable therapeutic efficacy: the number of responders ranges from 30 to 60 p. 100 according to the molecule used.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcium Channel Blockers↗
PubMed1984

[Use of beta-blockers in the acute phase of myocardial infarction].

Several experimental studies have demonstrated that the early administration of beta blockers in the setting of an acute myocardial infarction (in the first six hours) tended to diminish the area of myocardial necrosis. Numerous attempts to limit infarct size with beta blockers have occurred over the past ten years. Without a reliable and reproducible method to measure necrosed tissue, it has been difficult to evaluate the effectiveness of this therapy. Presently available studies have demonstrated, however, that beta blockers are well tolerated in the setting of an acute infarction as long as none of the usual contraindications are present. The majority (but not all) of these studies indicated improvement in parameters used to determine the amount of tissue necrosis and a tendency (not always significant due to the small numbers studied) to decrease morbidity and mortality during hospitalization. One study using metoprolol administered during the acute phase and continued during the first three months demonstrated a significant decrease in mortality. The results of this study are very demonstrative, nevertheless, once the acute necrotic phase is over, it is difficult to ascertain whether diminished tissue necrosis or the preventive effect of beta blockers is responsible for these findings until a recurrence or sudden death occurs.

Adrenergic beta-Antagonists↗
PubMed1983

Nosocomial infections by chlorhexidine solution contaminated with Pseudomonas pickettii (Biovar VA-I).

Over a period of 10 days, six patients in a cardiac intensive care unit developed Pseudomonas pickettii (biovar VA-I) septicaemia after installation of a venous catheter. The organism was also recovered from all the vials of the aqueous solution of 0.05 per cent chlorhexidine ('Hibitane') prepared with contaminated bidistilled water. There were no further cases of infection when the use of this water was prohibited.

Adult↗
PubMed1983

Calcium entry blocking agents in digital vasospasm (Raynaud's phenomenon).

We have evaluated the therapeutic effect of the calcium entry blocking agent nifedipine in Raynaud's phenomenon associated with connective tissue diseases and in idiopathic digital vasospasm. In a preliminary study 16 patients with a digital vasospasm that could be induced by hand-immersion in cold water (4 degrees C) were challenged a second time with cold water 1 and 6h after 20 mg oral nifedipine. Nifedipine provided an effective protection against this cold-induced vasospasm in 14 of the 16 patients. Thirty patients were included in a short-term ambulatory study: Raynaud's phenomenon was associated with progressive systemic sclerosis (PSS) in 10 patients, systemic lupus erythematosus (SLE) in five and rheumatoid arthritis (RA) in three; it was idiopathic (I) in 12 patients. Each patient received, in a double-blind manner and random order, on two consecutive weeks, nifedipine (20 mg three times daily) and placebo. Nifedipine proved to be effective: the mean number of digital vasospastic attacks per week decreased from 27.3 to 5.8 (P less than 0.01). The results in the SLE and RA groups were similar and were pooled. The improvement (in % decrease) was better in the idiopathic group (90.9) than in the SLE and RA group (78.6, P less than 0.02) and the PSS group (64.0, P less than 0.01).

Adult↗
PubMed1983

Mitral reconstructive operations. A series of 130 consecutive cases.

Between January, 1975, and January, 1982, 130 patients underwent mitral valvuloplasty for pure or predominant mitral insufficiency. Mean age at operation was 30 +/- 17 years. Twenty-five patients were under 15 years of age. Mitral insufficiency was mainly (112/130) due to rheumatic disease. Fifty-nine patients (45.4%) had another diseased valve which necessitated a surgical correction (tricuspid in 36 and aortic in 23). Surgical technique for mitral valvuloplasty varied according to the lesions. Three patients died in the first month after operation (2.3%). Five patients are lost to follow-up. The mean follow-up period for the 122 remaining patients is 38 +/- 27 months. Seven patients required reoperation and three of them died. An additional patient died without reoperation. Therefore, the late mortality was 3.1% (4/122). Almost all (116/118) of the remaining patients are in Class I (105) or II (11) of the New York Heart Association. Mean cardiothoracic ratio decreased from 60.6% +/- 7.7% preoperatively to 53.7% +/- 6.2% postoperatively (p less than 0.001). Thromboembolic episodes were noted in four patients, all of them in atrial fibrillation. Actuarial curves including hospital mortality showed a 92.0% survival rate at 7 years for the overall series (1.0% +/- 0.5%/patient-year), 93.7% +/- 4.9% at 7 years for isolated mitral reconstruction and 89.9% +/- 5.6% for mitral-tricuspid valvuloplasty at 5 years. The embolism-free rate at 7 years was 91.2%, with a rate of thromboembolic episodes of 1.0 +/- 0.5%/patient-year. Eighty-eight percent were free of reoperation at 7 years, with a rate of reoperation of 1.7 +/- 0.7%/patient-year. This system of mitral repair can provide stable functional results, low surgical and late mortality, and an acceptable rate of reoperation.

Adolescent↗
PubMed1983

[Course of pulmonary embolism].

One hundred and fifty-five patients with a mean age of 59 years and suffering a recent pulmonary embolism (P.E.) underwent angiopneumography and phlebocavography before and after treatment. The P.E. was minimal in 42 cases (Muller less than 11) and severe in 113 cases (Muller greater than 11). There was an associated venous thrombosis (V.T.) in 134 cases (86%) affecting the iliac veins or vena cava in 44 cases (28%). Several types of treatment were used: heparin 66, SK 24, high dose UK 16, low dose UK + heparin 37, surgery 16. Fifty-two patients underwent a procedure to interrupt the I.V.C. Four patients received two types of treatment in succession. SK resulted in more rapid disappearance of the pulmonary clot than UK at the dose used but the results were comparable on the 15th day (SK = UK = H). With regard to V.T., the Marder index failed to reveal any significant difference between the types of treatment. However, SK resulted in the lowest therapeutic failure rate (19%) and it was the only agent which produced disobliteration of iliac or vena cava thromboses (6 cases out of 13), other types of treatment being ineffective (0 cases out of 28). The mortality rate was high (14%) but 86% of the patients who died had a massive P.E. (greater than 60%). The recurrence rate was less (6%) but recurrences were fatal in 6 cases out of 10. Sixty-four patients were seen again after a mean period of 20.7 months. Pulmonary sequelae were minor (CPC 4.6%, dyspnoea 18%). By contrast, one patient in two suffered from post-phlebitis syndrome. The latter was all the more common when obstruction of the proximal veins persisted after treatment. On the basis of these data, the authors emphasise the gravity of pulmonary thrombo-embolic disease: fatal in the early phase essentially as a result of recurrences, incapacitating in the late phase as a result of post-phlebitis syndrome. They note that proximal V.T. associated with P.E. is responsible for such complications. Such iliocaval disease must therefore be sought routinely by phlebocavography. Their presence justifies aggressive treatment designed to destroy them (SK) or protect against their consequences (I.V.C.I.).

Drug Therapy, Combination↗
PubMed1983

[Molsidomine prevention of coronary artery spasm caused by alkalosis].

A test provocation of coronary artery spasm by alkalosis was used to evaluate a possible anti-coronary artery spasm effect of molsidomine. The rapid infusion of an alkaline buffer followed by maximal voluntary hyperventilation in 10 patients with angina at rest led to the appearance of angina pain and significant, transient ischaemic changes of the ST segment, due to alkalosis induced coronary spasm. A second provocation test was performed under the same conditions, 24 hours later, after the prior administration of 4 mg of molsidomine. Molsidomine prevented the development of coronary artery spasm in 8 of the 10 patients in the study group. These preliminary results justify further clinical evaluation of molsidomine in the treatment of vasospastic angina.

Alkalosis↗
PubMed1983

[Comparative effects of dopamine and dobutaine in subendocardial perfusion in the acute phase of myocardial infarct].

Dobutamine, a selective agonist of beta I adrenergic receptors was proposed as an inotropic support of the failing left ventricle in the acute phase of myocardial infarction. We studied the action of Dobutamine (10 micrograms/kg/min) on subendocardial perfusion, compared to the effects of an equipotent dose of Dopamine, in 10 patients with acute transmural infarction. Subendocardial perfusion was assessed by subendocardial viability ratio (EVR), ratio of the diastolic pressure-time index to the systolic pressure-time index. A mean 35 p. cent increase in cardiac index was observed with 10 micrograms/kg/min Dopamine, and with 6,75 micrograms/kg/min Dobutamine; heart rate increased by 13 p. cent with both drugs; with Dobutamine, systolic arterial pressure increased by 9,6 p. cent while pulmonary wedge pressure decreased by 34 p. cent; Dopamine increased systolic arterial pressure by 19 p. cent while pulmonary wedge pressure remained unchanged. Subendocardial viability ratio decreased by 25 p. cent with Dopamine (p less than 0,01) but only by 14 p. cent with Dobutamine (p less than 0,01). Thus, there was significantly less impairment of subendocardial perfusion with Dobutamine and its use is preferable when inotropic support of the failing left ventricle is necessary in the acute stage of myocardial infarction.

Aged↗