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Biomedical subjects

D Himbert

Publications and source records attributed to D Himbert.

At least 73 records · Page 4Linked to original sources
PubMed1992

A patency-oriented strategy for early management of acute myocardial infarction using emergency coronary angiography and selective coronary angioplasty.

From June 1988 to March 1991, an unselected cohort of 150 consecutive patients with acute myocardial infarction (AMI) (less than 6 hours) was managed according to a strategy designed to ensure early patency of the infarct-related artery in the maximum number of patients. The following procedures were used: (1) intravenous thrombolysis, which was the usual treatment (n = 103), followed in 98 cases by emergency coronary angiography 90 minutes after the beginning of thrombolysis. This identified 31 thrombolysis failures (32%) and led to 19 rescue angioplasties (18 successes). All patients were then scheduled for predischarge angiography. (2) Direct angioplasty, which was performed in 40 patients because of contraindications to thrombolysis (n = 23), cardiogenic shock (n = 3), diagnostic doubt (n = 7) or "ideal" conditions for direct angioplasty (n = 7). Success (defined as Thrombolysis in Myocardial Infarction [TIMI] flow greater than 1, with a residual stenosis less than 50% in the infarct-related artery) was achieved in 36 of 40 patients (90%). (3) The 7 remaining patients were given conventional medical treatment because of advanced age, contraindications to thrombolysis and angioplasty, or spontaneous reperfusion (confirmed by emergency angiography). In all, emergency angioplasty was performed in the acute phase in 39% of the 150 patients in this nonselected cohort.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

[Feasibility, indications and immediate results of direct angioplasty without thrombolysis during the acute period of myocardial infarction].

Between June 1988 and November 1991, 64 out of 200 consecutive admissions (32%) before the 6th hour of myocardial infarction underwent angioplasty of first intention. Fifty men and 14 women (average age 62 +/- 11 years) benefitted from this 24 hour emergency interventional cardiology service. The indication was formal in 22% of patients because of a contra-indication to thrombolysis (N = 40) or cardiogenic shock (N = 4); in 6%, the choice was logical because of diagnostic uncertainty (N = 12); it was a deliberate choice in 4% of cases (N = 8). Successful angioplasty was defined as reperfusion of the occluded artery without circulatory delay or > 50% residual stenosis. Arterial recanalisation was attempted in all patients (associated with intraaortic balloon pumping in 3 cases) and was successful in 59 patients (92%) within 231 +/- 100 minutes of the onset of chest pain and within 49 +/- 29 minutes of hospital admission. The outcome was uncomplicated without any other intervention in 81% of patients (48/59). Three reocclusions were observed, two of which were symptomatic and treated successfully by repeat emergency angioplasty. Six surgical revascularisations were necessary (2 emergency, 4 secondary). One major complication related to the angioplasty was observed (haemopericardium). Global hospital mortality was 9% (6/64): three of the 4 patients admitted in cardiogenic shock, 3 of the 40 high risk patients with contra-indications to thrombolytic therapy, none of the 20 patients considered to be at low risk (uncertain diagnosis and deliberate choice).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1992

[Acute hemodynamic effects of SIN-1 and isosorbide dinitrate in stable left ventricular failure: a comparative double-blind, cross-over study].

The acute hemodynamic effects of intravenous SIN-1 (1 mg) and sublingual isosorbide dinitrate (5 mg) were investigated in 12 patients (8 men and 4 women) between 38 and 80 years of age and suffering from stable chronic left ventricular failure (NYHA Classes III-IV) secondary to ischemic myocardiopathy (n = 5), hypertensive disease (n = 2) or idiopathic disorder (n = 5) corresponding to the following hemodynamic inclusion criteria: stable condition, cardiac index > or = 2 l/min/m2, mean capillary pressure > or = 18 mmHg and < or = 28 mmHg. Previous treatments were continued with the exception of vasodilators and diuretics which were stopped 24 hours earlier. The hemodynamic data from this cross-over, double-blind double-dummy trial were collected for two 60-hour periods separated by a washout period of 120 minutes. Simultaneously, venous samples were taken for the assay of plasma levels of SIN-1. The heart rate, cardiac output, pulmonary artery resistance and blood pressure were not affected by either SIN-1 or isosorbide dinitrate. An obvious reduction (> 15% of the basal value) in the mean capillary pressure, pulmonary artery pressure and mean right atrial pressure was observed in 10 subjects after SIN-1 and in 7 patients isosorbide dinitrate. A statistically non-significant trend towards a more marked effect (number of patients responding and maximum amplitude of pressure reduction) which occurred more rapidly and lasted longer was observed after SIN-1. Analysis of the relationship between the pharmacodynamics and pharmacokinetics of SIN-1 suggests that an active metabolites is involved. No adverse effects were reported.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

[How to evaluate the hemodynamic risk after myocardial infarction?].

The hemodynamic prognosis of myocardial infarction is determined, at medium and long term, by the function of the left ventricle. This is related to the infarct size, the dilatation and geometry of the ventricle secondary to left ventricular remodeling which often follows infarction. In addition to clinical criteria, the hemodynamic parameters which are essential for patient evaluation are the ejection fraction (by radionuclide or conventional ventriculography), rapidly progressive ventricular dilatation (by repeated echocardiography) and circulatory reserve from the exercise stress test data.

Angiocardiography↗
PubMed1991

Ventilatory threshold during exercise in patients with mild to moderate chronic heart failure: determination, relation with lactate threshold and reproducibility.

Detection of the ventilatory threshold during exercise has been proposed in order to assess exercise tolerance in patients with chronic heart failure. The relation between the different methods of detecting the ventilatory threshold and the lactate threshold, however, and their reproducibility, have not really been assessed. Forty-three patients with chronic heart failure underwent an exercise test with respiratory gas analysis. A lactate threshold could be determined in 36 patients and a ventilatory threshold in 27 to 38 patients, depending on the method of determination of the ventilatory threshold. The greatest number of determinations (38) and the best correlation coefficient with the lactate threshold (r = 0.87 and 0.88, respectively) were obtained with the method of the ventilatory equivalent for oxygen and by averaging the different methods of determination. Reproducibility of the ventilatory threshold was only moderately good (r = 0.83) and less satisfactory than that of the peak oxygen uptake (r = 0.97). We conclude that unless the way of detecting the ventilatory threshold is improved in patients with chronic heart failure, the peak oxygen uptake will remain more reproducible.

Adult↗
PubMed1991

[Do antihypertensive agents change the incidence of cardiovascular complications of hypertension?].

The main aim of the treatment of hypertension is to reduce the incidence and severity of its complications. Despite some bias affecting the major clinical trials of diuretics and/or beta blockers, the results of the meta-analysis taking them into account demonstrate the effectiveness of the prevention of cerebrovascular complications and the less effective prevention of coronary complications. Progress can be hoped for as a result of new therapeutic categories (converting enzyme inhibitors, calcium channel inhibitors ...) and to a greater extent from new treatment strategies, involving better identification of "genuinely high risk" subjects.

Adrenergic beta-Antagonists↗
PubMed1991

[Left ventricular remodeling and ischemic heart diseases. Therapeutic possibilities].

Left ventricular modeling after myocardial infarction may be modified in three ways: firstly, by limiting the infarct size; secondly, by administering ACE inhibitors: these drugs limit infarct expansion and ventricular dilatation. They reduce the prevalence of secondary left ventricular failure and, in the animal, improve the prognosis. Glyceryl trinitrate also appears to be effective. The third therapeutic option is maintaining the patency of the artery responsible for the infarction, which has a beneficial effect on ventricular remodeling. The respective therapeutic indications of these three options are still a matter of discussion.

Adrenergic beta-Antagonists↗
PubMed1991

[Ventricular "remodeling" after myocardial infarction].

Cardiac failure is the principal medium-term complication of myocardial infarction. Changes in left ventricular geometry are observed after infarction, called ventricular remodeling, which, though compensatory initially, cause ventricular failure in the long-term. Experimental and clinical studies suggest that early treatment by coronary recanalisation, trinitrin and angiotensin converting enzyme inhibitors may prevent or limit the expansion and left ventricular dilatation after infarction, so improving ventricular function, and, at least in the animal, reduce mortality. Large scale trials with converting enzyme inhibitors are currently under way to determine the effects of this new therapeutic option. It would seem possible at present, independently of any reduction in the size of the infarction, to reduce or delay left ventricular dysfunction by interfering with the natural process of dilatation and ventricular modeling after infarction.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1991

[Properties of arteries, cardiac function and structure in chronic hypertension].

Hypertension is a condition which demonstrates the relationship between the properties of the left ventricle and arterial system. The spectrum of aortic impedence expresses the principal factors which oppose LV ejection into the initial aorta: 1) capacitive forces related to the viscoelastic properties of the arterial wall, directly proportional to its rigidity, 2) forces of inertia which increase with the acceleration of the blood and which are inversely proportional to the aortic cross sectional area, 3) reflection. With respect to a stroke volume which is usually normal, hypertension is characterised by: 1) an increase in mean aortic pressure (MAP), 2) with respect to the increase in MAP, an increase in systolic, late systolic and differential pressures. These changes in the level and morphology of aortic pressure are due to: a) the increase in systemic arterial resistances, a continuous expression of the spectrum of the module, b) an increase in the elastic forces (increased rigidity of the aorta related to increased pressure and structural wall changes) usually insufficiently compensated by a decrease in the inertial forces (aortic dilatation), c) an earlier return of the reflected pulse wave, well before the end of the anterograde wave. Overall, there is a relationship between the mass, the geometry (concentric hypertrophy) and pump function of the left ventricle and the properties of the arterial system expressed in terms of pulse wave velocity, characteristic impedence or the late systolic pressure/stroke volume ratio. The relationship is much closer than that of the properties of the LV and aortic pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1991

[Hemopericardium caused by coronary perforation during angioplasty. A surgical diagnosis].

A case of haemopericardium occurring during angioplasty of the left anterior descending artery complicated by an occlusive dissection is reported. The haemopericardium was diagnosed and evacuated during surgical myocardial revascularisation indicated by the failure of angioplasty. This complication, though rare, underlines the necessity of a real surgical stand-by for this procedure.

Angioplasty, Balloon, Coronary↗
PubMed1990

[Cardiac insufficiency. Definition, mechanisms, principles of treatment].

Cardiac failure is defined as the inability of the heart to provide the necessary blood flow for the metabolic and functional needs of the vital organs under normal conditions. The underlying physiopathological mechanisms are multiple: cardiac failure without ventricular failure, ventricular failure with or without abnormal ventricular systolic function, prolonged tachycardias or tachyarrhythmias in normal hearts. The association of several mechanisms aggravates the prognosis. Peripheral and central compensatory mechanisms in such situations are not always beneficial. The principles of treatment depend on the type of cardiac failure encountered. The medium and long-term therapeutic objectives are not only to correct the haemodynamic abnormalities but to improve the quality of life and, if possible, the duration of survival.

Arrhythmias, Cardiac↗
PubMed1989

[Immediate postoperative results following conservative surgery of rheumatic mitral valve insufficiency in children].

The immediate post-operative results of conservative surgery were evaluated objectively in 31 children aged under 13 years referred to us for surgical correction of severe rheumatic mitral valve regurgitation. 16 patients had pure mitral regurgitation. In the others, lesions which required additional surgery were aortic regurgitation in 7 cases, tricuspid of the mitral valve and left ventricle was studied by two-dimensional TM-mode echocardiography. This examination was combined with a pulsed doppler study in search of a possible residual mitral regurgitation signal, with special attention to the depth at which it was recorded in the left atrium -- a semi-quantitative indication of the severity of residual leakage. Two mitral valve replacements were performed, and two early reoperations were needed for residual regurgitation developed between the 5th and 8th post-operative days. Three deaths occurred due to supra-systemic pulmonary arterial hypertension. The post-operative evaluation of mitral valvuloplasty results therefore involved 25 patients. In the absence of significant residual mitral regurgitation, two-dimensional echocardiography was inconclusive since the images obtained varied considerably according to the surgical procedures performed. There was a distinct reduction of end-diastolic diameters (43.5 +/- 5.9 versus 62.1 +/- 8.7 mm pre-operatively), reflecting the disappearance or marked decrease of the pre-operative ventricular volume overload consecutive to mitral regurgitation. The reduction of end-systolic diameters was also significant (31.2 +/- 6.7 mm versus 39.2 +/- 7.1 mm pre-operatively), though less pronounced than that of end-diastolic diameters, which explains the diminution observed in the percentage of fibre shortening, although the figures remained within normal limits (28.7 +/- 9.7 p. 100 versus 37.0 +/- 6.8 p. 100).(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Surgical Procedures↗
PubMed1989

Phenylephrine, vasopressin and angiotensin II as determinants of proto-oncogene and heat-shock protein gene expression in adult rat heart and aorta.

The expression of two oncogenes (conc) c-myc and c-fos, coding for nuclear proteins which play a regulatory role in growth and differentiation, and of two genes coding for two heat shock proteins (HSP) 68 (molecular weight 68,000) and 70 (molecular weight 70,000), which have a protective function during stress, have been investigated by Northern blot analysis of the total RNA, extracted from adult rat ventricle and aorta. (1) The two onc transcripts are absent from these tissues but their expression can be enhanced by a pretreatment with cycloheximide. (2) The HSP70 is, in part, constitutive, while HSP68 is not; both are thermo-inducible in an isolated coronary perfused rat heart. (3) The four messenger RNA (mRNA) are expressed in both ventricles and aorta, 1 or 2 hours after i.p. injection of 6 mg/kg phenylephrine or 12 IU/kg of vasopressin. (4) They are also induced by a continuous or discontinuous injection of angiotensin II (7.5 micrograms/kg per min) for 1-2 h, but only in the aorta. The lack of ventricular response to angiotensin II in rat ventricles has been attributed to the lack of angiotensin II receptors in this tissue. This indicates that, in addition to mechanical factors, circulating hormones which have in common the use of the phosphoinositol pathway, may activate the expression of genes coding for regulatory proteins. This may play a role in the genesis of both ventricular and aortic hypertrophy.

Angiotensin II↗
PubMed1987

[Left ventricular insufficiency: definitions and mechanisms].

Left ventricular failure is defined as an inability to maintain, under resting conditions, a cardiac output sufficient for the oxygen requirement. It is accompanied by a rise in trans-mural ventricular filling pressure and/or a reduction in systolic volume. It may be linked to an alteration in the systolic performance and/or an alteration in the characteristics of the left ventricle. The compensatory mechanisms are represented by the noradrenergic stimulation; a rise in the muscular mass of the left ventricle and the associated changes in its geometry the heterometric regulation of Frank Starling. Some peripheral adaptive mechanisms such as salt and water retention, arteriolar vaso-constriction and a rise in the peripheral extraction of oxygen contribute to compensating for the lower systemic cardiac output.

Cardiomegaly↗