[Patients with the highest cardiovascular risk are the least compliant with their antihypertensive therapy (DESIR study)]. / Les hypertendus les plus à risque sont les moins observants (étude DESIR).

AIM OF THE STUDY: To identify the sociodemographic and clinical profile of hypertensive patients who are not compliant with their antihypertensive treatment. METHODS: each cardiologist described his or her next 4 hypertensive patients from a clinical standpoint and gave them a self-administered compliance questionnaire developed by the French Committee to Fight Hypertension, which they returned directly to the analysis center using a postage-paid reply envelope. RESULTS: 1965 patients 63.9 +/- 12.1 years old, 55.3% of whom were male, were included in the study. According to the specific questionnaire, compliance is definitely satisfactory in 35.9% of patients, is probably satisfactory in 28.3%, is probably poor in 19.4% and is definitely poor in 16.4%. Poor compliance is more frequent among men (38.1 vs. 33.4%; p < 0.05), overweight or obese patients (35.8 and 43.0% vs. 30.0%; p < 0.001), diabetics (46.7 vs. 32.3%; p < 0.0001), dyslipidemic patients (39.3 vs. 31.8%; p < 0.001), smokers (50.2 vs. 33.8%; p < 0.0001), those whose father died of cardiovascular causes before 55 years of age (51.6 vs. 34.1%; p < 0.0001) or those with a previous history of CV events (40.6 vs. 32.8%; p < 0.001). The rate of poor compliance increases with the number of risk factors: 27.3% with no risk factor other than high BP, 32.2% with one, 37.2 with 2 and 51.5% with 3 or more (p < 0.0001). Multifactorial analyses confirm the independent effect of obesity, diabetes, smoking, and father's CV death before age 55 on patient compliance. CONCLUSION: patients with the highest CV risk are those who are the least compliant with their antihypertensive treatment. These results raise the question of the appropriateness of the prevention information given to the most at-risk patients.

Human cardiac myosin ATPase and light subunits. A comparative study.

Myosin was extracted from normal human hearts (autopsy material) and compared to that of pig heart and rabbit white skeletal muscle. Myosin light subunits were isolated by a preparative urea gel electrophoresis. These subunits were shown by urea and sodium dodecylsulfate gel electrophoresis to be only slightly affected by the time lapse between death and the beginning of myosin extraction. This was also true for myosin ATPases. The Ca-2+-activated ATPases of pig and human heart myosins have the same apparent Km and V, whereas white skeletal muscle myosin ATPase has the same Km with a higher V. Human myosin light subunits, when compared to those of pig heart possess: (i) different molecular weights: 27 999 and 18 000 datlons for pig heart, and 25 000 and 19 000 daltons for human heart. (ii) for both the light chains, different ultraviolet spectra and a higher helical content for the subunit molecular weight 25 000. (iii) a different composition for several amino acids (Tyr, Pro, Lys). A third light subunit (molecular weight 15 000) was occasionally seen in human as well as pig heart myosin. It concentration varied inversely with that of the subunit molecular weight 27 000-25 000, and so was probably a degradation product of the heaviest subunit.

Post-extrasystolic left ventricular peak pressure with and without left ventricular failure.

18 patients without valvular pathology, coronary artery disease, or idiopathic hypertrophic subaortic stenosis were haemodynamically and angiographically investigated in order to analyse the effects of a ventricular extrasystolic beat upon the post-extrasystolic left ventricular peak pressure. In eight normal patients (group I), the post-extrasystolic peak pressure (P.ES.P.P.) was lower than that of the pre-extrasystolic beat; in 10 patients with symptoms of left ventricular failure (group II) the P.ES.P.P. significantly increased. The reasons are: 1) cardiac origin: stroke volume increased more in group II; 2) arterial origin. a) aortic compliance was lower in group II (this is probably related to the older age of patients in group II), and by decrease in end-diastolic aortic pressure was smaller in group II. Part of this arterial effect (2b) may probably be explained from the fact that post-extrasystolic compensatory pauses are equal in both groups, but the decay time of arterial pressure during diastole (assuming an exponential decay) is larger in group II. At the same age and with the identical aortic compliance only the two factors 1 and 2b play a part in the changes in P.ES.P.P.

Protein and 28S ribosomal RNA fractional turnover rates in the rat heart after abdominal aortic stenosis.

The rate of synthesis of myocardial proteins and ribosomal ribonucleic acid (rRNA) was measured during the development of cardiac hypertrophy in rats using a continuous intracardiac infusion of 14C-tyrosine and 3H-uridine in unanaesthetised animals. Cardiac overload was induced by abdominal aortic stenosis. Left ventricular weight and total myocardial RNA concentration were significantly increased on day 4 after aortic stenosis (+19% and +18% respectively). On day 8 left ventricular weight reached +52% whereas RNA concentration had not increased further (+13%). The fractional turnover rates were calculated using the specific activities of intracellular free tyrosine and free uracil nucleotides (precursors) and those of protein bound tyrosine and 28S rRNA bound uridine monophosphate (products) respectively. The fractional rate of synthesis of proteins and rRNA (expressed as percentage per day) increased from 24% to 45% for proteins and from 25% to 34% for rRNA and peaked by day 2. The RNA activity, expressed as gram of protein synthesised per day and per gram of total RNA, was unchanged on day 1 and reached a maximal value on day 2 (+107%). These results suggest that the pre-existing ribosomal RNA could be underutilized under control conditions and that the boosting of RNA transcription, associated with that of protein translation, is a complementary process rather than a prerequisite for the transition period leading to hypertrophy.

A new T-287C polymorphism in the 5' regulatory region of the tissue factor pathway inhibitor gene. Association study of the T-287C and C-399T polymorphisms with coronary artery disease and plasma TFPI levels.

Tissue factor pathway inhibitor (TFPI) is an important regulator of the extrinsic blood coagulation pathway. We screened the untranslated 5' region of the TFPI gene for polymorphisms and investigated their possible involvement in arterial thrombosis. The allele frequencies of a new polymorphism, located 287 base pairs upstream of the transcription start site (T-287C), and that of the previously described C-399T polymorphism, were similar in cases and controls. In controls, the -287C allele was associated with significantly higher levels of total TFPI antigen, arguing for an effect of this polymorphism on TFPI gene expression. In controls, the C-399T polymorphism did not alter TFPI levels. In the cases, however, decreased total and post-heparin free TFPI levels and increased F1+2 levels were significantly associated with the -399T allele. These findings suggest that the T-287C and C-399T polymorphisms are not associated with an increased risk of coronary heart disease, a result which should be confirmed by a larger study. However, their influence on outcome, or a link with subtypes of acute coronary syndromes, cannot be excluded.

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)

Primary coronary angioplasty for acute myocardial infarction with contraindication to thrombolysis.

Patients with acute myocardial infarction (AMI) and contraindication to thrombolysis have a high mortality and morbidity with conventional medical treatment. Among 226 consecutive patients hospitalized within 6 hours of the onset of Q-wave AMI, 45 (20%) had contraindications to thrombolysis. All were treated by emergent primary angioplasty. Mean age of the 45 patients was 60 +/- 11 years and 8 (18%) were > or = 70 years old; 17 (38%) had multivessel disease and 5 (11%) presented with cardiogenic shock. Successful angioplasty was achieved in 42 of the 45 patients (93%) 52 +/- 27 minutes after admission and 238 +/- 100 minutes after the onset of pain. Overall in-hospital mortality was 9% (4 of 45). Neither major bleeding nor stroke occurred. There was 1 case of early symptomatic reocclusion, treated with emergent repeat angioplasty without reinfarction. Predischarge angiography in 33 patients showed only 1 silent reocclusion (3%). Ejection fraction at discharge was 46 +/- 13%. Repeat catheterization at 6 months in 19 patients showed 4 restenoses (21%) and 4 reocclusions (21%) of the infarct-related artery. There were 3 late deaths (2 noncardiac), which gave survival rates of 87 and 85% at 1 and 3 years, respectively, and event-free survival rates of 71 and 69% including in-hospital deaths. There were no cases of late reinfarction. Consequently, in this series, primary coronary angioplasty proved safe and highly effective in rapidly restoring sustained infarct-vessel patency during AMI, and led to a greater improvement in early and late outcomes than that reported in the literature for medically treated subjects in this high-risk subset for which thrombolytic therapy is contraindicated.

Acute assessment of microvascular perfusion patterns by myocardial contrast echocardiography during myocardial infarction: relation to timing and extent of functional recovery.

OBJECTIVE: To examine the relation between the initial microvascular perfusion pattern, as assessed by intracoronary myocardial contrast echocardiography (MCE), immediately after restoration of TIMI (thrombolysis in myocardial infarction) (TIMI) grade 3 flow during acute myocardial infarction, and the extent and timing of functional recovery in the area at risk. SETTING: Referral centre for interventional cardiology. METHODS: Intracoronary MCE was performed 15 minutes after TIMI grade 3 recanalisation of the infarct artery in 25 patients. Segmental myocardial contrast patterns were graded semiquantitatively (0, none; 0.5, heterogeneous; 1, homogeneous). Functional recovery was assessed by echocardiography on days 9 and 42. RESULTS: Among 174 myocardial segments in the area at risk, wall motion recovery on day 9 was observed in 40% of MCE grade 1 segments but there was no significant recovery in grade 0 or 0.5 segments. On day 42, recovery had occurred in 56% of MCE grade 1 segments (p < 0. 0001 v MCE grade 0 and 0.5; p = 0.0001 v MCE grade 1 on day 9), and 22% of MCE grade 0.5 segments (p = 0.02 v MCE grade 0; p = 0.0005 v MCE grade 0.5 on day 9); MCE grade 0 segments did not recover. Negative predictive value in predicting recovery by contrast enhancement was 95% and 89% by days 9 and 42, respectively. CONCLUSIONS: Contractile recovery occurs earliest in well reperfused segments. Up to one quarter of segments with heterogeneous contrast enhancement show wall motion recovery within the first six weeks. Myocardial perfusion after recanalisation in acute myocardial infarction, even if heterogeneous, is a prerequisite for postischaemic functional recovery. Thus preservation of acute myocardial perfusion is associated with more complete and early functional recovery.

Kinetics of in vivo binding of antagonist to muscarinic cholinergic receptor in the human heart studied by positron emission tomography.

Positron Emission Tomography (PET) was used to analyse in vivo antagonist binding to human myocardial muscarinic cholinergic receptor. The methiodide salt of the muscarinic antagonist, quinuclidinyl benzilate (MQNB), was labeled with the positron emitter, Carbon-11, and injected intravenously to 8 normal subjects. 11C-MQNB concentration was determined in vivo in the ventricular septum from 40 cross-sectional images acquired at the same transverse level over a period of 70 minutes. In 4 subjects, various amounts of unlabeled atropine were rapidly injected at 20 minutes to study whether atropine competitively inhibited MQNB. The kinetics of binding of 11C-MQNB were not the same in vivo and in vitro. The apparent dissociation rate of 11C-MQNB in vivo was much slower (by 1 to 2 orders of magnitude) than that observed in vitro with 3H-QNB. After atropine injection, 11C-MQNB dissociated from its binding sites at a rate that apparently depended on the amount of atropine present. 11C-MQNB kinetics were analysed with a mathematical model which assumes the existence of a boundary layer containing free ligand in the vicinity of the binding sites. The dissociation rate of the radioligand depends on the probability of its rebinding to a free receptor site.

Studies of isolated adult rat heart cells: the surface morphology and the influence of extracellular calcium ion concentration on cellular viability.

Rat cardiac muscle was dissociated into single cells by a coronary perfusion technique with collagenase and hyaluronidase in a Ca-free medium. Retention of the cylindrical shape of isolated muscle cells could be achieved by regulation of [Ca2+]0 and temperature. Cells kept at 4 degrees C, and 0-01 mM CaCl2 remained cylindrical for more than a week and contracted spontaneously upon warming at 37 degrees C. At [Ca2+]0 between 0-1-2 mM and 37 degrees C, cells underwent contracture and rounded up. Scanning (SEM) and transmission electron microscopy were used to analyze the structure of cylindrical and rounded muscle cells. The extracellular aspect of the sarcolemma at lateral cell surfaces and intercalated disc regions were clearly revealed for SEM analysis. Both the distribution and number of T-tubule openings on the surfaces can be estimated and a three-dimensional description of the intercalated disc obtained. This study reveals that isolated adult heart cells are extremely sensitive to [Ca2+]0, but with careful control of this cation, this preparation should be helpful in the analysis of both sarcolemmal structure and the pathological changes which accompany myocardial injury.

Late thrombotic obstruction of an aortic bioprosthetic valve: successful treatment by oral anticoagulation.

Thrombotic obstruction of aortic bioprostheses is rare. Few cases have been reported involving the use of the Carpentier-Edwards (CE) prosthesis, the Hancock bioprosthesis, or the Medtronic Intact porcine valve. Thrombolytic therapy for mechanical valve thrombosis has been used frequently even though it is known to carry a high risk of embolism and recurrence. However, the use of this therapy was reported for the first time only recently, in a case of acute aortic thrombosis which occurred 3 1/2 months after bioprosthesis insertion. We report a case of late progressive thrombotic obstruction of a CE aortic valve 3 years after insertion. The case was successfully treated with coumadin therapy, as confirmed by serial Doppler echocardiographic examinations and a 3-year follow-up.

[Resistance to ACE inhibitors. Myth or reality?]. / Echappement aux inhibiteurs de l'enzyme de conversion. Mythe ou réalité?

Angiotensin Converting Enzyme (ACE) inhibitors represent a major advance in the treatment of: hypertension, and generally speaking, in cardiovascular prevention; myocardial infarction; cardiac failure. They have a cardio and vascular protective action by tending to correct hypertension, left ventricular hypertrophy and remodelling, endothelial dysfunction, arterial smooth muscle proliferation and thrombotic phenomena. However, besides the cough that this therapeutic class engenders, a major question remains unanswered: is there resistance to this family of drugs? In other words, does left ventricular remodelling and arterial smooth muscle proliferation continue with regular treatment at the prescribed dosages? The synthesis of angiotensin II does not only depend on the angiotensin converting enzyme but also on the quality of angiotensin I and the presence of other enzymes such as chymase. A secondary increase of angiotensin II with ACE inhibitor therapy may reflect insufficient blockade of the renin-angiotensin system or a synthesis of angiotensin II by an alternative pathway to the converting enzyme. In vivo measurement of ACE inhibition shows that blockade of the renin-angiotensin system is automatically limited due to the very accurate regulation of angiotensin II concentrations.

[Secondary prevention after myocardial infarction; rôle of platelet antiaggregants and hypolipemic agents]. / Prévention secondaire de l'infarctus du myocarde; place des antiagrégants plaquettaires et des hypolipémiants.

The goals of secondary prevention after myocardial infarction are to avoid the complications of infarction itself, to prevent reinfarction, to detect and treat ischaemic episodes and to slow the progression of atherosclerosis. Antiplatelet therapy, especially with aspirin, has a clearcut beneficial effect decreasing cardiovascular mortality and of non-fatal reinfarction. A metaanalysis of ten trials has shown a 25% decrease in vascular events in the long-term, irrespective of age, gender, blood pressure blood glucose level, and dosage whether low (75 to 160 mg) or moderate (160 to 325 mg/day). Apart from the irreversible inhibition of cyclooxygenase, a beneficial effect on remodelling may be observed. Lipid lowering therapy has made significant advances since the introduction of the statimes. Compared with fibrates, statines have the advantage of reducing total mortality in addition to coronary mortality, whereas the fibrates, though reducing the latter, have been reported to increase total mortality and non-coronary mortality, but in a non-significant manner. Fibrates remain the drugs of choice for the treatment of pure hypertriglyceridaemia. The mechanisms of action of the statine are diverse: effects on endothelium-dependent relaxation, haemostasis, stabilisation of the atheromatous plaque and prevention of its rupture. The cost/effectiveness ratio of aspirin and statines is very high, the latter being much more cost-effective than, for example, the treatment of mild hypertension.

[Baroreflexes and congestive heart failure]. / Baroréflexes et insuffisance cardiaque.

Abnormal responses are found in the early stages of heart failure with increased sympathetic and decreased parasympathetic activity, causing peripheral arteriolar vasconstriction and tachycardia respectively. The cardiopulmonary baroreflex may be studied by decreasing venous return ("low body negative pressure") and by measuring vascular resistance forearm. The arterial baroreflex may be studied by changing aortic pressures (by intravenous phenylephrine or nitroglycerin). Orthostatism and the tilt test deactivate the cardiopulmonary and arterial baroreflexes simultaneously. These baroreflexes are impaired in patients with heart failure. Their activation does not cause the usual sympatho-inhibition so contributing to increased sympathetic tone. This dysfunction may result from a change at any point on the reflex pathway: the baroreceptors themselves, the afferent, central and efferent pathways. It is selective as during the cold pressor test, the vasoconstrictor response remains intact. One of the possible mechanisms of baroreflex dysfunction in heart failure is loss of sensitivities of the baroreceptors. This may be multifactorial: structural abnormalities, changes in compliance or functional abnormality. Even if the loss of sensitivity is partially related to a change in compliance, other factors play a role. It is more functional than structural abnormalities because, after cardiac transplantation, the baroreceptors regain their sensitivity within 2 to 3 weeks. Excessive Na-K dependent ATPase activation of the smooth muscle cells of the carotid sinus could lead to hyperpolarization of the cell membrane, so reducing the excitability of the receptor. Aldosterone is one of the factors which could activate the Na-K ATPase, as this hormone directly increases pump activity and favorizes the synthesis of new pumps in the vascular smooth muscle cells.(ABSTRACT TRUNCATED AT 250 WORDS)

["Diastolic" heart failure and pulsed pressure]. / Insuffisance cardiaque "diastolique" et pression pulsée.

Cardiac failure is the leading cause of hospital admission after 65 years of age. Several studies have confirmed the frequency of cardiac failure with normal systolic function ("diastolic" cardiac failure) in the elderly (nearly half the cases). The cause is commonly isolated systolic hypertension. The pulsed pressure depends on ventricular ejection, arterial rigidity and the precocity of reflected pulse waves. In the elderly, the pulse pressure is a powerful predictive factor for mortality and adverse cardiovascular events (acute coronary syndromes, cardiac failure and cerebrovascular accidents). Patients with isolated systolic hypertension or an increased pulsed pressure usually have left ventricular hypertrophy or concentric remodelling, abnormal relaxation, alteration of hypertrophied myocytes with increased myocardial oxygen consumption and subendocardial ischaemia, especially when the coronary reserve is reduced. The decrease of the diastolic blood pressure reduces the presence of coronary perfusion. Moreover, an increase in the pulsed pressure predisposes to coronary atherosclerosis. These patients are very symptomatic on exercise because they do not have a reserve of preload and easily develop acute pulmonary oedema after a volume overload (increased salt intake, postoperative rehydratation). A recent study showed that the left ventricular ejection fraction was preserved during acute pulmonary oedema of hypertensive patients. The diagnosis of "diastolic" cardiac failure is often suspected by elimination (clinical signs of cardiac failure with a normal left ventricular ejection fraction), and echographers have proposed many criteria to detect abnormal relaxation, filling or distensibility of the left ventricle. Mortality would seem to be half that of systolic cardiac failure. Treatment should normalise the hypertension, ischaemia, tachycardia, and maintain or reestablish sinus rhythm, but it remains empirical.

[Thrombocytopenia after cardiac surgery due to anti-platelet allo-immunization. Apropos of a case]. / Thrombopénie après chirurgie cardiaque par allo-immunisation antiplaquettaire. A propos d'un cas.

Thrombocytopaenia is rare after cardiac surgery but carries a very high risk of bleeding and thrombotic complications. It is generally due to heparinisation but may be secondary to the surgical procedure itself (cardiopulmonary bypass, sepsis, platelet consumption by the prosthesis), or associated factors (massive blood transfusion, drug reaction, rare antiplatelet allo-immunisation). One case of post-transfusion thrombocytopenia with antiplatelet anti-HPA-la allo-antibodies with a favourable outcome with high dose polyvalent gammaglobulins is reported. The authors describe the diagnostic and therapeutic approaches to this problem.

[Classic treatment of chronic heart insufficiency. What if new?]. / Le traitement classique de l'insuffisance cardiaque chronique. Quoi de neuf?

The aims of treatment of chronic heart failure are to improve the symptoms and the quality of life, reduce mortality and prevent left ventricular dysfunction. Before the first symptom occurs, neurohormonal activation takes place (increased catecholamines and atrial natriuretic peptide levels). Diuretics improve symptoms and are irreplaceable for the elimination of salt and water overload. Loop diuretics are used more often than the thiazides. Their deleterious effects on electrolyte balance are well known. The fact that they activate the renin angiotensin system is a more recent acquisition; the increase in plasma renin activity is a poor prognostic factor. Diuretics potentialize the vasodilator effect of angiotensin converting enzyme inhibitors which inhibit the neurohumoral activation induced by the diuretics. This therapeutic association is very logical, effective and allows reduction in the dosage of the diuretic. To date, there are no large scale controlled studies of the effects of diuretics on mortality. Spironolactone corrects hypokalaemia and hypomagnesaemia induced by loop diuretics. Moreover, it has been shown experimentally in renovascular hypertension and in hyperaldosteronism, that this molecule can prevent myocardial fibrosis, a factor which leads to ventricular dysfunction. The RALES study will analyse the effect of associating spironolactone to diuretic and ACE inhibitor therapy on the mortality of patients in NYHA classes III-IV. The value of digitalis in heart failure patients with sinus rhythm is a classical controversy. Digitalis has a positive inotropic effect (inhibition of NaK-dependent ATPase). More recently, a favourable neurohormonal effect has been reported; digitalis decreases the activation of the sympathetic and renin-angiotensin systems.(ABSTRACT TRUNCATED AT 250 WORDS)

[Treatment of chronic cardiac insufficiency with normal left ventricular systolic function]. / Traitement de l'insuffisance cardiaque chronique à fonction ventriculaire gauche systolique d'éjection normale.

Chronic cardiac failure with normal left ventricular systolic function is observed in conditions without ventricular failure (pericardial adiastole, obstruction to intracardiac blood flow) or with ventricular failure due to isolated abnormalities of left ventricular filling. These forms of cardiac failure are often subject to diagnostic error. However, it is essential that they be recognised because traditional therapy must be used with caution and because of the efficacy of treatment of the underlying pathology whenever this is possible.

[Determination of the ventilatory threshold during the exercise test in patients with cardiac insufficiency. Relation of the lactate threshold]. / Détermination du seuil ventilatoire au cours d'une épreuve d'effort chez l'insuffisant cardiaque. Relation avec le seuil du lactate.

The non-invasive assessment of the lactate threshold during exercise test is possible in normal subjects by the study of respiratory gas exchange: a ventilatory threshold may be determined using Wasserman's criteria. This determination is more unreliable in cardiac failure. Forty-four patients with cardiac failure underwent exercise tests with measurement of lactate concentrations and respiratory gas exchanges during the exercise. Despite a regular increase in the lactate concentration from the onset of exercise, it was possible to determine a lactate threshold in the majority of patients. A ventilatory threshold could be determined in 27 to 38 patients depending on the method used. The correlation between these two thresholds was excellent (r = 0.87). The determination of the ventilatory threshold during exercise is therefore possible in cardiac failure. The main limitation of the method is that no result can be obtained in a large number of patients (15 to 20%) which restricts its value as a principal method of therapeutic evaluation.

[The clinician's view of restenosis: methodological and therapeutic aspects]. / La resténose vue par le clinicien. Aspects méthodologiques et thérapeutiques.

The study of restenosis after angioplasty poses serious methodological problems. The first is the definition of angiographic criteria of restenosis. These should be based on quantitative angiographic measurements in absolute values of coronary diameter rather than on the use of percentage stenosis which is an inaccurate indication of the true severity of the coronary disease. Moreover, the use of an arbitrary threshold > or = 50% stenosis at angiographic control tends to "pre-select" poor initial results of angioplasty as restenosis. Criteria based on absolute values of coronary artery diameter have enabled the demonstration of a close correlation between an excellent result of angioplasty and the degree of the restenosis 6 months later which suggests that a too good result of angioplasty may be related to increased intimal hyperplasia. This is a real dilemma for those performing angioplasty knowing that a mediocre initial result does not guarantee a good long-term result. In addition, it seems that the diameters of coronary arteries 6 months after angioplasty have a Gaussian distribution. This would imply that intimal hyperplasia is a constant phenomenon after angioplasty and that it is its degree which varies between patients with and without restenosis. Restenosis would therefore be more of a quantitative than a qualitative phenomenon. This justifies the use of continuous variables in the study of restenosis and a categorical approach would therefore be less valuable, not as powerful statistically and based on thresholds of an arbitrary nature. This could also explain the contradictory results concerning predictive factors of restenosis in the literature.(ABSTRACT TRUNCATED AT 250 WORDS)