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Biomedical subjects

G Drobinski

Publications and source records attributed to G Drobinski.

At least 55 records · Page 3Linked to original sources
PubMed1992

[Coronary pathology after heart transplantation].

Graft coronary disease is a frequent and devastating complication with rapid development after heart transplantation. Until now, non-invasive and invasive methods have proved to be insensitive in the prediction and detection of the early stages of this disease. Conventional arteriography is considered as the only reliable means of diagnosis, but it remains insensitive in the accurate evaluation of the severity of graft coronary lesions (obliterative, diffuse and distal lesions). Precise quantitation of coronary lumen changes may be a sensitive method for the accurate evaluation of graft coronary disease and help in the understanding of the natural course of development of this disease. The pathogenesis of the disease is still unclear. It is possible that graft coronary disease is a consequence of non-treated low-grade cellular rejections. In most cases, retransplantation must be considered as the unique solution.

Coronary Angiography↗
PubMed1992

Systemic embolism as a complication of percutaneous mitral valvuloplasty.

Systemic embolism is a potential and severe complication of percutaneous mitral valve dilatation. In our series of 80 cases, the incidence of systemic embolism was 3.75% (3 cases). Two cases occurred during the procedure itself. The cause of embolism was different in each case: cruoric thrombus formation occurred in 2 cases during or after dilatation, and was attributable to inappropriate heparinization, and catheter and guidewire thrombogenicity. In both cases heparin administration was delayed or given at a lower dosage. In the third case, calcific embolism occurred several days after valve dilatation. We think that the embolic calcified fragment was detached from the mitral leaflet at the time of or after balloon inflation. In these 3 cases, intraatrial thrombus mobilization was not the mechanism of systemic embolism. In 2 cases, transesophageal echocardiography had been performed before dilatation and excluded the presence of an atrial thrombus the day before the procedure. It is concluded that, together with mobilisation of left atrial thrombi, which can be adequately detected by transesophageal echocardiography, catheter-induced thrombi represent a significant cause of embolic complications and must be prevented by giving full-dose heparin during the total duration of the procedure. Calcific embolism may also occur, and may become more frequent if mitral valve balloon dilatation is proposed to a larger number of patients with valvular and subvalvular calcifications.

Aged↗
PubMed1992

Model-based determination of cut-off values for left ventricular hypertrophy from echocardiographic myocardial mass data.

1. The left ventricular myocardial mass is a measurement that is easy to obtain by echocardiography. It is currently used for the definition of left ventricular hypertrophy, but cut-off values are often critical, since they depend on covariates of left ventricular myocardial mass such as sex, age, body surface area, physical training, blood pressure, etc. As it is very difficult in any laboratory to obtain a sufficient number of normal subjects for the establishment of left ventricular myocardial mass experimental distributions, we propose a non-linear model for the calculation of echocardiographic left ventricular myocardial mass distribution in normal subjects, from personal and literature data. left ventricular myocardial mass probability density function was computed from the following two assumptions: the joint distribution of the internal and external left ventricular diameters is assumed to be bivariate normal, and the relation between left ventricular myocardial mass and ventricular diameters is given by the formula of Devereux & Reicheck (Devereux, R. B. & Reicheck, N. Circulation 1977; 55, 613-8). 2. The Gaussian assumption was tested by using skewness tests. The model was further developed for the myocardial mass index distribution. The calculated probability density functions were compared with experimental data and showed very good agreement. Furthermore, they were used to define cut-off values of left ventricular hypertrophy at selected false-positive ratios. Finally, since left ventricular myocardial mass may vary under normal conditions with co-variates, the model may provide co-variate-matched cut-off values for any, even small, series of non-diseased control subjects.

Adult↗
PubMed1992

Lack of platelet-activating factor release during reversible myocardial ischaemia.

Platelet-activating factor (PAF) is involved in experimental models of myocardial ischaemia, and PAF infusion can cause thromboxane release. Thromboxane is produced during brief episodes of reversible myocardial ischaemia in patients with coronary heart disease. To learn whether PAF synthesis is associated with thromboxane production in mild myocardial ischaemia, we performed rapid atrial pacing in four patients with angina pectoris which caused chest pain, ST segment depression (delta ST = -1.8 +/- 0.2 mm) and lactate excretion in the coronary sinus (percent lactate extraction decreased from 20 +/- 6% to -15 +/- 9%). Thromboxane B2 was produced causing a positive transmyocardial gradient (from 88 +/- 154 pg.ml-1 baseline to 1770 +/- 1407 pg.ml-1 at the peak) but there was no PAF release into coronary sinus blood. In four other patients we determined whether more pronounced ischaemia could be associated with PAF synthesis. Coronary sinus blood was sampled before and during balloon occlusion of a major coronary artery: PAF was not detected in coronary sinus, whereas percent lactate extraction decreased from 24 +/- 6% to -63 +/- 22% (n = 4). We conclude that PAF plays a minor role in short episodes of reversible ischaemia and does not participate in thromboxane production.

Angina Pectoris↗
PubMed1992

Diagnosis of pulmonary embolism by transoesophageal echocardiography.

A 68-year-old woman was admitted for major dyspnoea. A transoesophageal echocardiogram was performed after the occurrence of acute circulatory shock. During the examination, the patient was under mechanical ventilation. We found a thrombus that had almost occluded the right pulmonary artery and which was later confirmed by selective angiography. Despite treatment, the patient died 2 days later; autopsy confirmed the thrombus in the right pulmonary artery.

Aged↗
PubMed1992

Myocardial viability in patients with Q wave myocardial infarction and no residual ischemia.

BACKGROUND: Coronary revascularization in patients with persistent angina after myocardial infarction reduces the incidence of recurrent angina pectoris and myocardial infarction and improves left ventricular function. The results of revascularization after a Q wave myocardial infarction when there is no residual ischemia may depend on myocardial viability. METHODS AND RESULTS: To determine whether there was viable myocardium in the infarct area in the absence of clinical and scintigraphic evidence of myocardial ischemia, 15 asymptomatic patients with a Q wave myocardial infarction, no redistribution on stress 201Tl test, and single-vessel disease (greater than 70% stenosis) with persistent anterograde blood flow were randomized to percutaneous transluminal coronary artery angioplasty (PTCA) or conservative medical treatment. After 2 months of follow-up, mean coronary blood flow measured by Doppler catheter in the infarct-related artery was higher in the PTCA treatment group (33 +/- 6 ml/min, n = 8) than in the conservative treatment group (16 +/- 4 ml/min, n = 7; p less than 0.05 between groups). The 201Tl pathological-to-normal ratios measured on postexercise images did not change in patients treated conservatively during the follow-up period (delta = +1.1 +/- 2.2%; NS from baseline) but increased significantly in patients treated by PTCA (delta = +8.5 +/- 2.3%; p less than 0.01 from baseline; p less than 0.05 between groups). Segmental wall motion improved on left ventricular angiography 2 months after PTCA (delta = +11.5 +/- 2.2%; p less than 0.001 from baseline) significantly more than in the conservative treatment group (delta = +4.1 +/- 1.4%; p less than 0.05 between both groups). Improvements of 201Tl ratios and segmental wall motion indexes correlated significantly (r = 0.73, p = 0.002). The mild improvement of global left ventricular ejection fraction measured in the PTCA treatment group did not differ significantly from changes in the conservative treatment group. CONCLUSIONS: Successful angioplasty of the stenotic infarct artery in patients with a Q wave myocardial infarction and no residual ischemia improved coronary flow, 201Tl uptake in the infarct area, and regional wall motion. Therefore, myocardial viability may last several weeks, as long as residual blood flow persists in the infarct-related artery. Optimal assessment of viability by imaging techniques should identify patients who are most likely to benefit from revascularization.

Angioplasty, Balloon, Coronary↗
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

Renal tolerance for ioxaglate in patients with chronic renal failure.

The authors sought to evaluate renal tolerance for ioxaglate sodium meglumine used as a contrast agent in patients with chronic renal failure. Eight male patients (mean age, 55 years +/- 5) with chronic renal insufficiency (glomerular filtration rate less than 60 mL/min) who underwent diagnostic cardiac catheterization were enrolled. Renal clearance of inulin and rho-aminohippuric acid and urinary enzyme excretion were studied 1 day before and 1 day after administration of 167 mL +/- 43 of ioxaglate. None of the patients experienced any adverse reactions. All the patients had markedly depressed renal clearance values before angiography. Mean serum creatinine level, glomerular filtration rate, effective renal plasma flow, and urinary beta 2-microglobulin excretion were unaltered by angiography. After the procedure, only one patient had an increase in serum creatinine level of more than 10% (from 115 to 159 mumol/L [1.3 to 1.8 mg/dL]), with a decrease in glomerular filtration rate from 34 to 27 mL/min. In this patient, serum creatinine level and glomerular filtration rate normalized within 72 hours. Using accurate and sensitive renal function tests, the authors have shown that ioxaglate may be used safely in patients with chronic renal failure.

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

[Search for emboligenic heart disease in case of ischemic cerebral accidents].

The demonstration of a cardiac source of systemic embolism in patients who have suffered a cerebral ischemic event may have important therapeutic implications. This explains the large demand for echocardiography and Holter monitoring in these patients. The frequency of cerebral embolism of cardiac origin, the simplification of the diagnostic approach by non-invasive investigations and the precision of ultrasound techniques explains the tendency towards the indiscriminate generalisation of this attitude. However, the large number of potential patients for investigation, the limited facilities of investigation and the incertitude over the responsibility of certain cardiac abnormalities with respect to the context and age, are arguments in favour of a more selective investigative approach. The keystone of diagnosis is careful history taking and clinical examination with interpretation of the ECG and chest X-ray. Three clinical situations may then be identified: 1) A cardiac abnormality known to be highly embolic is diagnosed from the outset (e.g. mitral stenosis, valve prosthesis, endocarditis, myocardial infarction). The diagnostic work-up is no longer etiological: echocardiography may show intracardiac thrombi or a valvular vegetation, reinforcing the causal relationship, but the complementary investigations are mainly useful for evaluation the cardiac disease and for deciding on curative or preventive therapy. 2) A cardiac abnormality is diagnosed but its responsibility is doubtful due to its high prevalence and low embolic potential. This is the case of patients with mitral valve prolapse, mitral annular calcification, calcific aortic stenosis and VVI pacing. Complementary investigations are not discriminative for the etiological diagnosis of the cerebral embolism.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗
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↗