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Biomedical subjects

G Montalescot

Publications and source records attributed to G Montalescot.

At least 109 records · Page 6Linked to original sources
PubMed1992

[Vascular action of prostaglandins: atheroma, vasoconstriction and ischemia].

Prostaglandins seem to be involved in all stages of the atheromatous process, especially coronary artery disease. This condition is associated with decreased prostacyclin synthesis. Prostacyclin, by the intermediary of cAMP, regulates cholesterol metabolism in the smooth muscle cell by mobilising intracellular cholesterol. Thromboxane is liberated in great quantities in acute coronary syndromes such as myocardial infarction (especially when fibrinolysis is performed) and unstable angina. It is also found in high concentrations in coronary sinus blood during stress tests inducing transient ischaemia in patients with stable angina. There is a relationship between the degree of ischaemia and plasma concentrations of thromboxane whereas prostacyclin levels remain unchanged, causing an imbalance between these two substances during ischaemia. Thromboxane is also responsible for the acute pulmonary vasoconstriction induced by the neutralisation of heparin by protamine. The introduction of molecules modifying the synthesis of these prostaglandins or inhibiting their effects by specifically blocking their receptors should open up new therapeutic possibilities.

Arteriosclerosis↗
PubMed1992

[Peripheral calcific embolism after percutaneous mitral valvuloplasty].

The authors report a case of calcific embolization after percutaneous mitral valvuloplasty. The nature of the embolism was confirmed by anatomopathological examination after popliteal embolectomy. This complication would appear to be extremely rare but represents an additional risk in patients with calcific mitral stenosis.

Adult↗
PubMed1992

[Value of antimyosin monoclonal antibody scintigraphy in the diagnosis of acute myocardial infarction].

A 53 year old woman developed chest pain with transient anterior subepicardial ischaemic ECG changes and a mild increase in serum myocardial enzyme concentrations. She was admitted to hospital some time later but there were no electrocardiographic signs of infarction. Echocardiography was considered to be normal. Coronary angiography showed no significant stenosis and there were no segmental wall motion abnormalities on left ventriculography. The diagnosis of a non-Q wave infarct was confirmed by myocardial scintigraphy using antimyosin monoclonal antibodies labelled with Indium 111. The site and size of the necrosis were also determined by this non-invasive investigation.

Antibodies, Monoclonal↗
PubMed1991

Haemodynamic effects of intravenous quinacainol with and without autonomic nervous system blockade.

Normal subjects are able to compensate negative inotropic drug effects by adrenergic stimulation. This may limit the relevance of hemodynamic investigations with new drugs. Therefore, the haemodynamic effects of a new class 1 antiarrhythmic drug, quinacainol, were evaluated in 16 patients with normal left ventricular function 5 and 25 minutes after intravenous administration in 2 settings: 12 patients were untreated, and 4 patients were pretreated with beta-blockers and atropine to block a reflex adrenergic discharge and vagolytic reaction. Cardiac contractility decreased in all patients: in the untreated group, the heart rate increased from 74 +/- 10 beats per minute to 80 +/- 9 and Vmax decreased from 1.56 +/- 0.56 circ/sec to 1.36 +/- 0.45 at 5 minutes and 1.36 +/- 0.61 at 25 minutes; in the pretreated group, the heart rate did not change. Vmax decreased from 1.61 +/- 0.19 circ/sec to 1.33 +/- 0.08 at 5 minutes and to 1.09 +/- 0.13 at 25 minutes. Autonomic nervous system blockade unmasked a significant persistent negative inotropic effect of the drug in this series of patients with normal left ventricular function. This method may be useful for evaluating the haemodynamic effects of antiarrhythmic drugs in preliminary studies before administration to patients with impaired left ventricular function.

Adrenergic beta-Antagonists↗
PubMed1991

Intra-myocardial haemorrhage following recanalisation of a venous coronary arterial bypass by balloon angioplasty.

We report the case of a patient presenting an intra-myocardial hematoma after recanalisation of a saphenous aorto-right coronary arterial bypass graft implanted 10 years previously after posterior myocardial infarction. The intra-myocardial hematoma occurred immediately after recanalisation of the graft and was complicated by transient complete atrio-ventricular block. An acute increase of coronary capillary perfusion pressure may cause intramyocardial bleeding when capillary permeability is altered by prolonged ischemia or necrosis. In this case the resulting hematoma was limited to the segment of left ventricular wall affected by the previous necrosis and there was no further myocardial damage.

Angioplasty, Balloon, Coronary↗
PubMed1991

Anomalous coronary arteries coursing between the aorta and pulmonary trunk: clinical indications for coronary artery bypass.

Coronary arteries of anomalous origin with subsequent coursing between the aorta and pulmonary trunk can cause ischaemia, infarction or sudden death. However, reports of surgical correction are sparse due to the rarity of ante-mortem diagnosis. We report two cases in which symptoms were related to anomalous origin of a non-atherosclerotic coronary artery. Surgical repair was performed to prevent sudden death or recurrent ischaemia.

Adult↗
PubMed1991

Coronary blood flow reserve measured by contrast media injection depends on myocardial viability.

Coronary blood flow reserve may be affected by several physiological variables besides hydraulic impediment to flow. A hyperaemic response induced by hyperosmolar radiopaque contrast medium was recorded in the left anterior descending and left circumflex arteries with a steerable pulsed Doppler system in four patients with Q wave anterior myocardial infarction chronic scar and non-stenotic coronary arteries. Resting flow velocities were similar in both arteries. The magnitude of the hyperaemic response induced by contrast media in the circumflex artery (mean flow velocity increase from 5.9 +/- 2.5 baseline to 12.2 +/- 0.6 cm s-1 at peak flow, P less than 0.05) was almost twice that induced in the left anterior descending artery (mean flow velocity increase from 6.1 +/- 2.2 baseline to 7.4 +/- 2.6 cm s-1 at peak flow, P = N.S.). The peak flow to baseline flow velocities ratios were 1.22 +/- 0.15 in the left anterior descending artery vs 2.23 +/- 0.75 in the circumflex artery. Thus when a post-myocardial infarction chronic scar is supplied by a non-stenotic coronary artery, the coronary blood flow hyperaemic response to contrast media-induced transient ischaemia is decreased, suggesting that coronary blood flow reserve depends on a myocardial metabolic stimulus which is impaired by ischaemic cell death.

Adult↗
PubMed1991

Evaluation of thromboxane production and complement activation during myocardial ischemia in patients with angina pectoris.

BACKGROUND: The complement system and arachidonic acid metabolites are involved in severe myocardial ischemia such as myocardial infarction. Furthermore, there is experimental evidence for C5a participation in thromboxane production. METHODS AND RESULTS: We examined whether C5a and thromboxane are produced during brief and reversible episodes of myocardial ischemia induced in patients with stable angina. Twenty-five patients underwent either atrial pacing or percutaneous transluminal coronary angioplasty associated with arterial and coronary sinus blood sampling. Rapid atrial stimulation of patients with effort angina caused significant ST segment depression (delta ST = -1.7 +/- 0.2 mm), decreased fractional lactate extraction (from +12.8 +/- 2.5% baseline to -13.7 +/- 4.6% at peak ischemia, n = 13, p less than 0.001), and increased coronary sinus plasma thromboxane B2 levels (from 345 +/- 85 pg/ml baseline to 1,684 +/- 64 pg/ml at peak ischemia, p less than 0.01). Changes of fractional lactate extraction correlated significantly with changes of coronary sinus plasma levels of thromboxane B2. There was no change of coronary sinus 6-keto-PGF1 alpha levels. Similar pacing of control subjects (n = 6) did not cause release of lactate or thromboxane. Seventeen other patients underwent exercise testing with noninvasive measurements of thromboxane and prostacyclin metabolites in urinary samples collected before and after the test. No detectable increase of urinary 11-dehydrothromboxane B2 was measured in patients with stable angina after exercise-induced myocardial ischemia. However, basal 11-dehydrothromboxane B2 levels were significantly higher in patients with angina (105 +/- 25 pg/mmol creatinine, n = 9) than in control patients (45 +/- 8 pg/mmol creatinine, n = 8, p less than 0.05 between groups). Coronary sinus plasma levels of the anaphylatoxin C5a always remained below 4 ng/ml in patients undergoing pacing. More severe myocardial ischemia after coronary angioplasty (percent lactate extraction decreased from +24.8 +/- 2.7% baseline to -41.6 +/- 22.4% at peak ischemia, p less than 0.05) was not associated with C3a or C5b-9 generation. In all patients, there was neither platelet sequestration nor platelet alpha-granule release (no changes of beta-thromboglobulin/platelet factor 4 levels) into the coronary sinus plasma. CONCLUSIONS: Patients with stable angina have chronically increased thromboxane synthesis as assessed by excretion of urinary metabolites. Thromboxane is acutely released into the coronary sinus during pacing-induced ischemia without significant intracoronary platelet aggregation. Complement does not appear to be activated in stable angina during brief and reversible episodes of myocardial ischemia and does not contribute to thromboxane production.

Angina Pectoris↗
PubMed1991

[Focus on anticoagulants].

More and more heparins are available to the prescriber and low molecular weight heparins have brought about a modification of prescribing habits. Some complications linked to the use of heparins remain insufficiently known: thrombocytopenia and acute pulmonary hypertension during neutralization for example. Treatment monitoring must be clearly codified to increase effectiveness and reduce the number of accidents thus achieving a better risk/benefit ratio for such treatment. Some of the Vitamin K antagonists have specific properties which should be known, particularly relating to their half-life. Monitoring is important, it is provided by INR and adapted to the indications. The world of anticoagulants is in flux; the movement must be followed as it may well accelerate with the arrival of new antithrombotic drugs.

Anticoagulants↗
PubMed1991

[Mitral valvuloplasty during the 4th month of pregnancy. Fetal protection with a lead mantle].

A 27 year old woman who had undergone closed heart surgical commissurotomy 10 years previously, underwent percutaneous mitral valvuloplasty during the fourth month of her pregnancy. Despite significant valvular thickening with calcification, the balloon dilatation led to an increase in valve surface area from 1.1 to 2 cm2 with no complications and with relief of the pulmonary hypertension. Foetal protection against ionising radiation was assured by a lead mantle completely surrounding the patient's abdomen. This protection reduced irradiation of the pelvic region to 0.5 milliSievert which corresponds to 1/100 of the permitted irradiation of pregnant women professionally exposed to ionising radiation.

Adult↗
PubMed1990

Nitroglycerin-resistant coronary spasm treated with intracoronary linsidomine chlorhydrate (SIN-1).

Spontaneous left anterior descending coronary artery spasm occurred in two patients during coronary angiography. After intravenous injection of 0.75 mg of nitroglycerin, the narrowing was unchanged in one patient and only partially relieved in the other. The coronary narrowing completely disappeared after intracoronary injection of 1 mg of the active metabolite of molsidomine, linsidomine chlorhydrate (SIN-1). In the first patient, this injection was performed just prior to the initiation of coronary balloon dilatation, which was then cancelled. Although rare, these two observations demonstrate the limitations of the intravenous use of nitroglycerin during diagnostic coronary angiography and point out the efficacy of intracoronary administration of SIN-1.

Angiography↗
PubMed1990

Neutralization of low molecular weight heparin by polybrene prevents thromboxane release and severe pulmonary hypertension in awake sheep.

Protamine reversal of heparin anticoagulation in patients is occasionally associated with life-threatening acute pulmonary hypertension. In a sheep model, we evaluated the effect on this adverse cardiopulmonary reaction of modifying the type of heparin (low molecular weight heparin compared with unfractionated heparin) and the type of heparin antagonist (polybrene compared with protamine). Protamine reversal of low molecular weight heparin (LMWH) and polybrene reversal of unfractionated heparin induced more than a 10-fold increase of plasma thromboxane B2 levels, a threefold increase of pulmonary vascular resistance and pulmonary artery pressure, and a 25% decrease of PaO2. A similar adverse reaction followed protamine reversal of conventional unfractionated heparin. However, with polybrene (1 mg/kg) reversal of LMWH (1 mg/kg), we measured neither pulmonary hypertension (pulmonary artery pressure was 22.6 +/- 3.6 mm Hg at 1 minute after polybrene reversal of LMWH compared with 47.9 +/- 4.2 mm Hg after protamine reversal of unfractionated heparin, p less than 0.005 groups differ), hypoxemia (PaO2 was unchanged 2 minutes after polybrene compared with a decrease of 26 mm Hg 2 minutes after protamine, p less than 0.05), nor acute release of thromboxane into arterial plasma (thromboxane B2 was 0.2 +/- 0.1 at 1 minute after polybrene compared with 3.7 +/- 1.7 ng/ml at 1 minute after protamine, p less than 0.005). The hemodynamic effects and mediator release were also benign after neutralization of larger doses of LMWH (3 mg/kg) by polybrene (3 mg/kg). The increases of activated clotting time and activated partial thromboplastin time due to both types of heparin were completely reversed with polybrene. Anti-Xa activity increased to more than 3 IU/ml 4 minutes after LMWH anticoagulation (p less than 0.01) but was only partially neutralized by polybrene. Various polyanion-polycation complexes that are formed when heparin anticoagulation is reversed induce thromboxane release and acute pulmonary vasoconstriction in awake sheep. Reversal of LMWH anticoagulation with polybrene does not elicit this adverse reaction.

Animals↗
PubMed1990

Thromboxane receptor blockade prevents pulmonary hypertension induced by heparin-protamine reactions in awake sheep.

We used competitive thromboxane A2-prostaglandin endoperoxide receptor blockade (SQ 30,741) as a probe to evaluate the role of thromboxane in ovine pulmonary vasoconstriction associated with protamine reversal of heparin anticoagulation. Control heparin-protamine reactions induced rapid release of thromboxane into arterial plasma (more than 1 ng/ml plasma), a 2.5-fold increase of pulmonary artery pressure, a 20% decrease of PaO2, and a 30% reduction in arterial white blood cell concentration. After giving SQ 30,741 despite similar thromboxane release into arterial plasma after heparin-protamine challenge, acute pulmonary hypertension was significantly reduced when 94% of pulmonary vascular smooth muscle thromboxane receptors were occupied with SQ 30,741 (p less than 0.01 at 1 minute after protamine versus control heparin-protamine reaction) and was completely abolished by a 10 mg/kg i.v. bolus (p less than 0.0001 at 1 minute after protamine versus control). Peripheral leukopenia was not affected by SQ 30,741 prophylaxis, but hypoxemia was prevented. We conclude that thromboxane causes pulmonary vasoconstriction in ovine heparin-protamine-induced pulmonary hypertension. Pulmonary vasoconstriction and hypoxemia can be completely prevented by thromboxane receptor blockade.

Animals↗
PubMed1990

[Cellular mechanisms of pulmonary vasoconstriction in an experimental model of protamine reversal of heparin].

The neutralisation of heparin by protamine can cause life-threatening pulmonary hypertension. We studied this reaction in animal experimental models (sheep and rat) to determine the cellular mechanisms of the pulmonary vasoconstriction. The heparin-protamine reaction (H-P) with pulmonary hypertension (peak of mean pulmonary artery pressure = 57.3 +/- 2.2 mmHg), decreased cardiac output (-20%), leukopenia (-30%) and plasma release of high concentrations of thromboxane B2 (6.03 +/- 0.03 ng/ml) was constantly observed in sheep. The reaction was identical in sheep with induced thrombocytopenia by administration of antiplatelet antibodies. On the other hand, the neutralisation of heparin by protamine in rats did not cause thromboxane release or pulmonary vasoconstriction although the leukopenia was identical to that observed in sheep. Therefore, the platelets and white blood cells did not seem to cause the pulmonary vasoconstriction induced by the H-P complexes. The inter-species difference observed suggests that pulmonary intravascular macrophages may be responsible for the liberation of eicosanoids and acute pulmonary vasoconstriction occurring during the neutralisation of heparin by protamine.

Animals↗
PubMed1989

Clinical and ultrasound results after aortic valve replacement: intermediate-term follow-up with the St. Jude Medical prosthesis.

Mortality, morbidity, quality of life, and left ventricular (LV) function were evaluated in 49 patients after aortic valve replacement with the St. Jude prosthesis. Total follow-up was 2577 patient-months; survivors were followed-up for 4 to 7 years by clinical examination and echocardiography. The actuarial survival rate at 6 years was 79.6%, and there were no valve-related deaths. The linearized rates for thromboembolism and hemorrhage were 0.93% and 3.26% per patient-year, respectively. In 34% of the survivors the quality of life was poor. In the first three postoperative months, patients with aortic stenosis (n = 12) had a significant decrease in the muscle cross-sectional area (p less than 0.01) and patients with aortic regurgitation (n = 11) had decreases in both LV end-diastolic diameter (p less than 0.05) and cross-sectional area (p less than 0.001). All of these results were maintained at 5 years without modification of LV systolic function. Despite the good overall results, six patients deteriorated and had major LV dilatation. Multivariate logistic regression analysis identified two independent preoperative variables associated with a poor outcome defined as death of LV dysfunction (p less than 0.05): age and end-diastolic diameter. Thus meticulous follow-up showed a high incidence of hemorrhage and a poor quality of life in many of the survivors. It was concluded that in high-risk patients (age and end-diastolic diameter) surgery should probably be considered earlier.

Aortic Valve↗
PubMed1989

Arteriolar vasoconstriction and tachyphylaxis with intraarterial angiotensin II.

Several aspects of the differences between the responses of the second- to fifth-order arterioles (A2 to A5) to intraarterial administration of angiotensin II (AII) were studied by intravital microscopy on an original preparation of rat cremaster muscle. Dose-response curves displayed a leftward shift when the arteriolar order increased. Doses inducing 50% vasoconstriction were 15.1, 0.51, and 0.08 micrograms for A3, A4, and A5, respectively. For A2, very small vasoconstriction was found even at the highest dose of angiotensin II. The dynamics of the response were also dependent on the arteriolar order. The duration of the peak of vasoconstriction increased from A3 to A5, and the interval between the contact of vascular wall with drug and the response was smaller in A4 and A5 than in A3. To understand the effect of diameter as a determinant of heterogeneity in the degree of arteriolar vasoconstriction, norepinephrine was administered under the same conditions as angiotensin II, and responses were measured on arterioles with the same morphological characteristics as those examined after angiotensin II. When comparing the regression curves for the percentage of vasoconstriction vs diameter, we found that this relationship was drug dependent. The significantly steeper slope for angiotensin II than for norepinephrine excluded the possibility that heterogeneity of the degree of vasoconstriction is solely due to differences between the morphological characteristics of the arterioles. Since tachyphylaxis to AII is considered to be a reflection of the drug-receptor interaction, we also studied the magnitude of this phenomenon from proximal to distal parts of the arteriolar network. We showed that the degree of partial tachyphylaxis after 1 microgram AII was dependent on the arteriolar order and a decreasing tachyphylaxis gradient was evidenced from A3 to A5 arterioles.

Angiotensin II↗