[Pathology and dental care in the context of cardiovascular conditions: myths, beliefs and realities]. / Pathologies et soins dentaires dans le cadre des affections cardiovasculaires: mythes, croyances et réalités.

The knowledge regarding the links between dental and cardiac affections are generally based on empirical concepts and lead to unjustified clinical practices. Infectious endocarditis (IE) is the principal cardiac diseases concerned with dental procedures. Although in France, the incidence of IE is stable, the incidence of oral bacteria at the origin of IE is diminishing. The risk of IE and thus the indication of antibioprophylaxis depend upon the subjacent cardiopathy and dental treatment. Antibioprophylaxis has to be very strict in patients with high or moderate risks of IE but is not necessary in low risk patients. In all cases, a good oral and dental hygiene and a regular dentist follow up are the most effective methods of preventing IE. Coronary artery disease and dental affections are associated because they present similar risk factors (i.e. smoking, excessive sugar consumption) and also because inflammation increases the risk of acute coronary syndrome. Today, dental cares are not contraindicated in patients with recent coronary syndrome if precise protocols are followed. Concerning the hemorrhagic risk during dental care in patients treated by anticoagulants and/or antithrombotics, dental cares and extractions are possible if INR or heparinemy are within the therapeutic limits and local haemostasis is meticulous. In addition, aspirin does not require to be stopped before minor dental treatments. Finally a better collaboration between dentists and cardiologists would allow an optimum management of patients with cardiac disease requiring dental cares.

[Future molecules in heart failure]. / Molécules du futur dans l'insuffisance cardiaque.

TODAY: The management of heart failure (HF) has considerably progressed over the last two decades. Treatment today relies on prevention and treatment of congestion (limited salt intake, diuretics, converting enzyme inhibitors) and limiting neurohormone stimulation (converting enzyme inhibitors +/- aldactone, beta-blockers). IN THE YEARS TO COME: Based on new concepts, several therapeutic strategies are interesting: blocking over vasoconstrictor systems which have not been taking into account; stimulation of vasodilator and natriuretic systems; modulation of cardiac remodelling; modulation of the immune and inflammatory systems; modification in intrinsic contractility; prevention of rhythm disorders. Among these differing strategies and molecules, it is not easy to predict those that will change the HF prognosis. In any event, their efficacy and safety remain to be demonstrated with large cohort randomised studies. THE PRINCIPLES: To reduce the number of drugs administered, two options appear particularly interesting: measurement of hormone levels (BNP) in order to adjust treatment and administration of molecules with greatest efficacy and safety profiles; limit cardiac remodelling by using new imaging techniques to detect it more precisely and select the molecule(s) exerting the required effect. To target the new molecules better, patients should be classified according to their etiology, stage and progressive profile of their disease, cardiac remodelling, expression of principle endocrine systems and pro-inflammatory cytokines, expression of inflammatory and immune systems and inherent genetic characteristics and response to treatment. This would permit the adaptation of treatment to each individual patient with heart failure.

Aortic stenosis with severe left ventricular dysfunction and low transvalvular pressure gradients: risk stratification by low-dose dobutamine echocardiography.

OBJECTIVES: We sought to assess risk stratification by using dobutamine stress echocardiography (DSE) in patients with aortic stenosis (AS) and severe left ventricular (LV) dysfunction. BACKGROUND: Few data are available on risk stratification for valve replacement in patients with AS, LV dysfunction and low transvalvular gradients. METHODS: Low-dose DSE was performed in 45 patients (16 women and 29 men; median [quartile range] age in years: 75 [69 to 79]; left ventricular ejection fraction: 0.29 [0.23 to 0.32]; aortic valve area [cm2]: 0.7 [0.5 to 0.8]; mean transaortic gradient [mm Hg]: 26 [21 to 33]). Patients were classified into two groups: group I (n = 32, LV contractile reserve on DSE) and group II (n = 13, no contractile reserve). Valve replacement was performed in 24 and 6 patients in groups I and II, respectively. RESULTS: Perioperative mortality was 8% in group I and 50% in group II (p = 0.014). Survival at five years after the operation was 88% in group I. Compared with medical therapy, valve surgery was associated with better long-term survival in group I (hazard ratio for death [HR-D] 0.13, 95% confidence interval [CI] 0.002 to 0.49) and reduced survival in group II (HR-D 19.6, 95% CI 2.7 to 142). The effect of valve surgery on survival remained significant in both groups after adjustment for age, diabetes, respiratory disease and hypertension. Medical therapy had the same effect in both groups. CONCLUSIONS: In patients with AS, LV dysfunction and low transvalvular gradients, contractile reserve on DSE is associated with a low operative risk and good long-term prognosis after valve surgery. In contrast, operative mortality remains high in the absence of contractile reserve.

[Hospital mortality in cardiology. Analysis of deaths occurring in the Federation of Cardiology of a university hospital center]. / Mortalité hospitalière en cardiologie. Analyse des décès survenus au sein de la fédération de cardiologie d'un centre hospitalo-universitaire.

The aim of this study was to examine the nature of cardiovascular deaths occurring in a University Hospital. All the hospital files of 1999 of the Federation of Cardiology of Henri Mondor Hospital, Creteil, of patients who died in the department or after transfer to the intensive care unit or cardiac surgery department, were analysed. Myocardial ischaemia was the leading cause of death, occurring either in the acute phase of transmural infarction or in patients with chronic cardiac failure. Deaths occurring during acute myocardial infarction were associated with late treatment and/or non-reperfusion of the culprit artery. The delay of diagnosis seemed to be secondary to late consultation or difficulty in diagnosis. This resulted in severe left ventricular dysfunction and, in a quarter of cases, mechanical complications. They led to the early death of the patients (2.9 +/- 3.5 days after admission). Campaigns of patient information and education of doctors who see these patients would seem to be the most appropriate approach to reduce the delay before hospital admission in order to reduce mortality related to myocardial infarction. Cardiac failure is a common cause of death in cardiology departments. The deaths of patients occurred after a long follow-up and several days after hospital admission (11 +/- 10 days). Optimisation of the treatment of cardiac failure, the investigation of ischaemic heart disease, the search for new therapeutic strategies of acute cardiac failure and information of patients about their disease, seem to be the principal measures to take to improve the poor prognosis of this disease.

Prediction of functional recovery of viable myocardium after delayed revascularization in postinfarction patients: accuracy of dobutamine stress echocardiography and influence of long-term vessel patency.

OBJECTIVES: We sought to evaluate dobutamine stress echocardiography (DSE) for predicting recovery of viable myocardium after revascularization with cineangiography as a gold standard for left ventricular (LV) function. We studied the influence of late vessel reocclusion on regional LV function. BACKGROUND: Dobutamine stress echocardiography is a well established evaluation method for myocardial viability assessment. In previous studies the reference method for assessing LV recovery was echocardiography, long-term vessel patency has not been systematically addressed. METHODS: Sixty-eight patients with a first acute myocardial infarction (AMI) and residual stenosis of the infarct related artery (IRA) underwent DSE (mean +/- standard deviation) 21 +/- 12 days after AMI to evaluate myocardial viability. Revascularization of the IRA was performed in 54 patients by angioplasty (n = 43) or bypass grafting (n = 11). Coronary angiography and LV cineangiography were repeated at four months to assess LV function and IRA patency. RESULTS: Sensitivity and specificity of DSE for predicting myocardial recovery after revascularization were 83% and 82%. In the case of late IRA patency, specificity increased to 95%, whereas sensitivity remained unchanged. In the 16 patients with myocardial viability and late IRA patency, echocardiographic wall motion score index decreased after revascularization from 1.83 +/- 0.15 to 1.36 +/- 0.17 (p = 0.0001), and left ventricular ejection fraction (LVEF) increased from 0.52 +/- 0.06 to 0.57 +/- 0.06 (p = 0.0004), whereas in five patients, reocclusion of the IRA prevented improvement of segmental or global LV function despite initially viable myocardium. CONCLUSIONS: Dobutamine stress echocardiography is reliable to predict recovery of viable myocardium after revascularization in postinfarction patients. Late reocclusion of the IRA may prevent LV recovery and influence the accuracy of DSE.

Quantitative systolic and diastolic transmyocardial velocity gradients assessed by M-mode colour Doppler tissue imaging as reliable indicators of regional left ventricular function after acute myocardial infarction.

AIMS: The aim of this study was to determine whether myocardial velocity gradients assessed by M-mode colour Doppler tissue imaging could be of clinical relevance and represent reliable indicators of regional left ventricular function after acute myocardial infarction. METHODS AND RESULTS: Among 64 consecutive patients with a first acute myocardial infarction, in 50 who had a marked asynergy in the parasternal short-axis view at the mid-papillary muscle level, myocardial velocities and velocity gradients were assessed in the anteroseptum and posterior wall by M-mode Doppler tissue imaging. Similar measurements were obtained in 11 matched healthy volunteers who served as a control group. In patients with anterior myocardial infarction, the peak myocardial velocity gradient in the anteroseptum was significantly lower when compared with controls (mean +/- [SD] 0.0 +/- 0.5 vs 1.1 +/- 0.7 s-1 during systole, P < 0.01; and 0.3 +/- 0.6 vs 2.0 +/- 0.5 s-1 during diastole, P < 0.01). Conversely, the peak systolic myocardial velocity gradient in the posterior wall was significantly higher than in controls (2.6 +/- 1.2 vs 1.8 +/- 1.2 s-1, P < 0.05). In patients with inferior myocardial infarction, the peak velocity gradient in the posterior wall was significantly lower when compared with healthy subjects (0.9 +/- 0.6 vs 1.8 +/- 1.2 s-1 during systole and 1.4 +/- 1.4 vs 4.9 +/- 1.2 s-1 during diastole, both P < 0.01). The peak systolic tissue velocity gradient in the anteroseptum was significantly higher than in controls (2.1 +/- 1.0 vs 1.1 +/- 0.7 s-1, P < 0.01). CONCLUSION: The present study indicates that myocardial velocity gradients assessed by M-mode Doppler tissue imaging are of clinical relevance for the characterization of ischaemic myocardial dysfunction after infarction and may provide quantitative assessment of segmental left ventricular function in this clinical setting.

[Physiopathological basis of the treatment of heart failure]. / Bases physiopathologiques du traitement de l'insuffisance cardiaque.

Therapeutic advances have changed the mode of presentation of cardiac failure over the last decades: the main cause, nowadays, is myocardial ischaemia. The modern treatment of cardiac failure is based on relatively simple physiopathological mechanisms which take into account the different aspects of cardiac physiology: a pump, a muscle, a coronary circulation supplying oxygen to the myocardium, an automatic contraction. The concept of vasodilatation and the blocking of vasoconstrictive systems introduced during the 70s is the basis of modern treatment of cardiac failure which involves angiotensin converting enzyme inhibitors and, increasingly, betablockers. In the near future, with earlier treatment of cardiac failure, the stimulation of vasodilator systems could become a new therapeutic strategy. Early detection of ischaemia and its complications with the aim of limiting the loss of cardiac myocytes is a priority for slowing the progression of cardiac failure. The prevention of cardiac failure also depends on educating cardiologists to treat rapidly the factors predisposing to or prolonging episodes of even mild cardiac failure.

Comparison of regional myocardial velocities assessed by quantitative 2-dimensional and M-mode color Doppler tissue imaging: influence of the signal-to-noise ratio of color Doppler myocardial images on velocity estimators of the Doppler tissue imaging system.

M-mode color Doppler imaging of the myocardium affords a greater sampling rate and signal-to-noise (S/N) ratio than 2-dimensional (2D) imaging. In this study, we compared myocardial velocities assessed by 2D and M-mode Doppler tissue imaging (DTI) at the same site and evaluated the influence of the S/N ratio on velocity estimates of the currently used DTI systems. In patients with and without impaired regional left ventricular function, myocardial velocities assessed by 2D DTI were lower than those obtained with M-mode DTI. The difference between regional velocities derived from both imaging techniques was positively correlated with the extent of the "black zone," which could be considered as indirectly reflecting the S/N ratio for each frame. Thus in the clinical setting and on currently used echocardiographs, 2D DTI may provide underestimated regional myocardial velocities when compared with M-mode, mainly because of the influence of the lower sampling rate and S/N ratio on velocity estimators of the imaging system.

Alteration of left ventricular diastolic function during coronary angioplasty-induced ischemia: a color M-mode Doppler study.

OBJECTIVES: The aim of this study was to assess the effects of ischemia on diastolic function by analyzing flow propagation velocity with color M-mode Doppler echocardigraphy. BACKGROUND: Color M-mode Doppler echocardiography has been proposed as a method of assessing left ventricular filling. METHODS: Color M-mode Doppler echocardiography and measurement of hemodynamic data were performed simultaneously at baseline and during angioplasty-induced ischemia. Tau was compared with flow propagation velocity. Late diastolic indexes, left ventricular pressure and flow cessation time were also investigated. RESULTS: During ischemia, left ventricular relaxation rate (tau) increased, whereas flow propagation velocity decreased, from (mean +/- SD) 46.8 +/- 10 ms to 72.6 +/- 18.3 ms and from 59.8 +/- 15.8 cm/s to 30 +/- 8 cm/s, respectively (all p < 0.0001). The maximal slowing of flow propagation velocity was observed 20 to 30 s after the beginning of the inflation, coexisting with a notch on the ascending limb of the negative rate of rise of the left ventricular pressure (dP/dt) curve. Flow propagation velocity was correlated with tau both at baseline (r = 0.53, p < 0.05) and during inflation (r = 0.53, p < 0.03). Left ventricular end-diastolic pressure increased during ischemia from 13.5 +/- 8 mm Hg at baseline to 27.5 +/- 7 mm Hg, while a premature cessation of the entering flow occurred -13.8 +/- 23 ms before the next Q wave onset, compared with 4.5 +/- 19.6 ms after the Q wave onset at baseline (all p < 0.0001). CONCLUSIONS: The analysis of flow propagation velocity showed that early filling is highly dependent on left ventricular relaxation rate, particularly through the phenomenon of asynchrony. During ischemia, the premature cessation of late filling is associated with increased diastolic pressures.

[Adaptation to effort in patients with chronic cardiac insufficiency; study by post-exercise Doppler echocardiography, comparative results with a control population]. / Adaptation à l'effort chez l'insuffisant cardiaque chronique; étude par échocardiographie doppler post-effort, résultats comparatifs avec une population témoin.

Adaptation to exercise was studied by post-exercise Doppler echocardiography in patients with chronic cardiac failure and an apparently healthy control population matched for age. This post-exercise Doppler echocardiographic method initially introduced for the detection of myocardial ischaemia has already been validated in normal subjects for the analysis of haemodynamic changes caused by exercise providing the data is recorded in the first 5 minutes following recovery in the recumbent position. Eleven patients with chronic cardiac failure in NYHA classes II or III with a mean age of 54 +/- 11 years and 6 controls (mean age: 46 +/- 9 years) were investigated. The patients had been stabilised for at least 3 months with a vasodilator and diuretic therapy: the control subjects had no medication. After bicycle ergometry performed to 70% of maximum capacity, the subjects were positioned in the left lateral recumbent position. Doppler echocardiography was then performed in the immediate recovery phase. When compared to the control population, the patients with cardiac failure had a reduced chronotropic reserve, a smaller increase in the parameters of myocardial contractility (maximal aortic velocity, maximal aortic acceleration and left ventricular fractional shortening) without an increase in left ventricular end diastolic dimensions in subjects with severe dilatation under basal conditions (left ventricular end diastolic dimension 69 +/- 3 mm). This result suggests the absence of a Frank-Starling effect. The lack of adaptation of the peripheral vascular system was demonstrated by the lack of reduction of left ventricular end systolic stress, already greatly increased at rest (176 vs 77 +/- 10 g/cm2 for patients, compared with controls; p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Improvement of subendocardial myocardial perfusion after percutaneous transluminal coronary angioplasty. A myocardial contrast echocardiography study with correlation between myocardial contrast reserve and Doppler coronary reserve.

BACKGROUND: After angioplasty coronary reserve improves but does not normalize in most patients. The purpose of this study was to examine before and after angioplasty coronary reserve and transmural myocardial blood flow distribution using myocardial contrast echocardiography. METHODS AND RESULTS: Twelve patients with left anterior descending coronary artery stenosis were investigated before and immediately after angioplasty. A Doppler catheter was placed in the proximal segment. Myocardial contrast echocardiography was performed by imaging the septum in M mode in a parasternal view using a 3.0-mL bolus of sonicated amidotrizoate sodium meglumine through the guiding catheter. The gray level before injection was subtracted from the gray level after injection to maximize contrast time-intensity curves. The area under the curve was used as an indicator of myocardial blood flow, and subendocardial/subepicardial ratios were measured. After baseline measurements were obtained, Doppler and echographic data were recorded after a bolus infusion of papaverine into the left main coronary artery. The same protocol was performed in patients after angioplasty and in five control subjects with normal coronary arteries. Before angioplasty, echocardiographic and Doppler coronary reserve were 2.57 +/- 0.48 and 2.54 +/- 0.57, respectively. Both increased after angioplasty to 3.65 +/- 0.57 and 3.36 +/- 0.70, respectively (P < .05). Coronary reserve values obtained in patients with these two methods under the different conditions and in control subjects were correlated (r = .81; P = .0001). Before angioplasty, subendocardial/subepicardial septal ratios decreased from 0.80 +/- 0.48 to 0.60 +/- 0.27 after papaverine (P < .05). However, after angioplasty, these ratios tended to increase, from 0.72 +/- 0.27 to 0.92 +/- 0.45 after papaverine, but they did not change in control subjects (1.11 +/- 0.23 to 0.92 +/- 0.11). CONCLUSIONS: These results show that myocardial contrast echocardiography yields flow reserve values that correlate with values obtained using intracoronary Doppler. This technique may be considered as an accurate tool to assess coronary reserve in humans.

Post-exercise Doppler-echocardiographic haemodynamics in idiopathic dilated cardiomyopathy after metoprolol infusion.

1. The physiological effects of the acute administration of a beta-adrenoceptor antagonist in patients with idiopathic dilated cardiomyopathy were assessed by performing post-exercise Doppler-echocardiography study. Eleven patients and six control subjects were studied. According to a double-blind randomized protocol, 5 mg of metoprolol or placebo was administered before cycloergometer exercise. 2. In patients, after metoprolol, a significant decrease in heart rate and systolic blood pressure, as well as in peak aortic acceleration and cardiac output, was observed 2 min after exercise. Left ventricular end-diastolic diameter did not change from baseline values either after placebo or metoprolol. In normal subjects, as compared with placebo, a decrease in heart rate and peak aortic acceleration was observed after metoprolol, whereas systolic blood pressure did not change. A similar increase in cardiac output occurred after metoprolol, as compared with placebo, associated with an increase in left ventricular end-diastolic diameter and stroke volume. 3. Post-exercise Doppler echocardiography is a means of assessing haemodynamic changes occurring during exercise in patients with congestive heart failure. Although acute metoprolol administration does not provide beneficial haemodynamic effects, a decrease in the energy requirements of the heart and a faster recovery after exercise may participate in the long-term beneficial action of beta-adrenoceptor antagonists.

Coronary vasodilating action of dobutamine in patients with idiopathic dilated cardiomyopathy.

To assess the coronary hemodynamic effects of dobutamine in patients with idiopathic dilated cardiomyopathy, dobutamine was infused at the incremental infusion rates of 25, 50, 100, and 200 micrograms/min into the left main coronary artery of nine patients undergoing cardiac catheterization. In response to dobutamine infusion, systemic hemodynamic effects were dose related. At the highest infusion rate cardiac index and left ventricular peak positive rate of rise in ventricular pressure increased from 2.33 +/- 0.54 to 2.97 +/- 0.65 L/min/m (p = 0.001) and from 690 +/- 177 to 1157 +/- 275 mm Hg/sec (p = 0.001), respectively. Left ventricular end-diastolic pressure decreased from 17 +/- 8 to 8 +/- 7 mm Hg (p = 0.001) and a trend toward decrease in left ventricular wall stress was observed (from 166 +/- 75 to 148 +/- 66 gm/cm2, not significant). Heart rate and mean arterial pressure remained unchanged. The coronary hemodynamic response to dobutamine infusion was also dose related. At the highest infusion rate coronary sinus blood flow increased from 133 +/- 35 to 179 +/- 47 ml/min (p < 0.01) and was associated with an increase in coronary oxygen blood content from 4.5 +/- 0.6 to 7.8 +/- 1.7 ml per 100 ml (p < 0.01) whereas myocardial oxygen consumption remained unchanged. During dobutamine infusion norepinephrine decreased in the femoral artery and in the coronary sinus from 1.03 +/- 0.34 to 0.641 +/- 0.179 ng/ml (p < 0.05) and from 1.76 +/- 0.98 to 1.38 +/- 0.65 ng/ml (p < 0.05), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Physiologic assessment of milrinone therapy in severe heart failure patients.

To assess the inotropic, vasodilator, and after-load-reducing effects of intravenous milrinone in patients with severe congestive heart failure, a simple noninvasive echocardiographic study coupled with a right catheterization was performed in 12 patients. Milrinone was administered intravenously as a 50 micrograms.kg-1 bolus followed by a 24-h milrinone infusion at a rate of 0.5 mg.kg-1.min-1 [corrected]. Echocardiographic left ventricular end-diastolic diameter (Ded), end-systolic diameter (Des), and wall thickness were measured at baseline and at 24 h of milrinone infusion, before and after a sublingual nitrate administration (0.8 mg of nitroglycerin) that induced load variations. Hemodynamic measurements were performed simultaneously. Left ventricular end-systolic meridional wall stress (Ses) was then calculated. The slopes of percent fractional shortening (percent FS)/Ses and Ses/Des, obtained during sublingual nitrate administration, were traced. Both end-systolic relations are an index of the contractile state. Milrinone therapy improved hemodynamics in all patients, resulting in stabilized hemodynamic conditions between 12 and 24 h of continuous milrinone infusion. At these times, the cardiac index increased to 30% while the capillary pulmonary wedge pressure and systemic vascular resistance decreased to 26 and 24%, respectively (all p less than 0.01). The average slope of Ses/Des shifted upward from 47.5 +/- 30 to 69.25 +/- 34 (p less than 0.05) and the average slope of (percent FS)/Ses shifted from -0.032 +/- 0.025 to -0.082 +/- 0.061 (p less than 0.01), both variations attesting the inotropic effect of milrinone.(ABSTRACT TRUNCATED AT 250 WORDS)

[Treatment of chronic left ventricular insufficiency]. / Traitement de l'insuffisance ventriculaire gauche chronique.

Left ventricular failure results from many myocardial diseases: the symptoms of left ventricular failure are the consequence of adaptations which the left ventricle and circulatory system activate to counteract the initial myocardial disease. The aims of treatment of cardiac failure are diverse depending on whether treatment is directed to correct the initial myocardial disease, its myocardial consequences, its circulatory consequences or, more simply, the patient's symptoms. The ideal treatment of cardiac failure would include a drug acting on the cause, a drug restoring left ventricular contraction and relaxation adapted to the conditions of cardiac load, a drug correcting regional blood flow disturbances and a drug relieving symptoms related to salt retention. An ideal drug for chronic left ventricular failure does not exist, and so treatment is a composite effort. Should it be in first intention? This is the current trend.

[The role of Doppler echography in the evaluation of systolic and/or diastolic dysfunction of the left ventricle]. / Rôle de l'écho-doppler dans l'évaluation des dysfonctions systoliques et/ou diastoliques du ventricule gauche.

The doppler-echocardiographic assessment of left ventricular systolic and diastolic dysfunction involves numerous indices. Preload is evaluated by measurement of the end-diastolic left ventricular diameter and sometimes by the rapid filling E wave on doppler recordings. The best index of of afterload is the end-systolic stress. Most indices of contractility are load-dependent, including percentage of fibre shortening, FCV, FCVc, EF. This leads to the construction of end-systolic regression slopes by varying the load to determine the myocardial contractile value. In the future, automated analysis of doppler curves will be used to determine the aortic flow maximal acceleration. The diastolic function is easily evaluated through the transmitral flow, but its interpretation must take into account the patient's age, heart rate and filling state. Two aspects are regarded as pathological: the filling disorder aspect with E/A under 1, and the hypernormal assay described by Appleton. In doppler-echocardiographic studies as well as in haemodynamic studies all these indices are interrelated, which shows the complexity of cardiac physiology and the interdependence of its factors.

[The treatment of chronic left ventricular insufficiency]. / Traitement de l'insuffisance ventriculaire gauche chronique.

Left ventricular failure is caused by a variety of myocardial diseases and its symptoms results from adjustments attempted by the left ventricle and the circulatory system to cope with the initial myocardial pathology. Treatment of heart failure has various objectives, depending on whether one tries to correct the initial myocardial disease, or its consequences on the myocardium, or its repercussions on blood circulation, or, more simply, to alleviate the symptoms experienced by the patient. The ideal treatment of heart failure would include a drug acting on its cause, another drug to restore a degree of contraction and relaxation adjusted to the amount of load, a third drug bringing back to normal a perturbed peripheral circulation and a fourth drug to relieve the symptoms due to sodium retention. Such a treatment does not exist, and the management of chronic left ventricular failure can only be composite. Should it be prescribed from the start? This, increasingly, is the current trend.

[Medical strategy in patients awaiting emergency heart transplantation]. / Stratégie médicale chez les patients en attente de greffe cardiaque en urgence.

Cardiac transplantation is theoretically the optimal final treatment of terminal cardiac failure but the indications, especially in the emergency situation, should be carefully considered. Sympathomimetic agents are of limited use in patients with severe cardiac failure partly because of the down regulation of the myocardial beta-receptors. The phosphodiesterase inhibitors, represented by enoximone, are valuable because of their action on the cardiac muscle (inotropic and lusitropic) and their direct systemic vasodilator effect. Enoximone can be administered by intravenous bolus resulting in a rapid onset of action (peak at 30 minutes) with a prolonged effect due to its hepatic metabolites. The authors' experience in this indication dates over 5 years and over 50 patients were included. A preliminary study in 34 patients with cardiac failure resistant to betamimetic drugs, referred to the intensive care unit for urgent cardiac transplantation, or, in the absence of a donor, circulatory assistance is reported. A Swan Ganz catheter and radial artery canula were inserted for haemodynamic monitoring and enoximone was administered in an intravenous bolus over 15 minutes every 8 hours in addition to sympathomimetic agents. A haemodynamic improvement was observed after the 30th minute in 30 patients. The cardiac index increased from 1.82 to 2.67 l/mn/m2 and the pulmonary capillary pressures decreased from 30.8 to 18.9 mmHg. Systemic arterial resistances fell from 2,170 to 1,520 dynes.s.cm-5. No haemodynamic improvement was observed in 4 patients who were treated by mechanical ventricular assistance. After investigations to detect contra-indications to cardiac transplantation, 12 of the 30 patients remained candidates for cardiac transplantation.(ABSTRACT TRUNCATED AT 250 WORDS)

Pre-hospital thrombolysis, is it useful?

Thrombolytic treatment efficacy is greater when the delay between onset of pain and treatment is short. One way to shorten this delay is to give treatment at home, but one cannot recommend this technique if it has not been demonstrated first, that pre-hospital thrombolysis is feasible and safe, and second, that it is useful. We have been able to demonstrate that pre-hospital thrombolysis with APSAC is feasible and safe. Our findings are similar to those of other teams using other drugs. Whether pre-hospital thrombolysis is useful has not been adequately assessed; and we consider that first, the benefit of pre-hospital vs in-hospital thrombolysis must be determined, and second, the results of a study involving many centres, with various levels of training, practicing pre-hospital thrombolysis must be examined. Two large scale studies are currently being performed. One in Seattle, uses left ventricular ejection fraction as the major end-point, whereas the other, the European Myocardial Infarction Project, (EMIP) is using total mortality. Data currently available indicate that pre-hospital thrombolysis with APSAC is feasible, easy and safe. We hope that we will very soon be able to answer the last question: is it useful?

[Pre-hospital thrombolysis]. / Thrombolyse préhospitalière.

Too few myocardial infarctions are thrombolysed, and the thrombolytic agent is usually administered too late. This situation can conceivably be improved by educating both physicians and patients, by promoting thrombolysis in all hospitals and by performing thrombolysis before admission. We report here our experience of pre-hospital thrombolysis with Eminase in the Val-de-Marne department. This preliminary study is just a small stone added to the big heap of small series of thrombolysis at home published throughout the world. But while the feasibility of pre-admission thrombolysis has been well demonstrated, its effectiveness remains to be accurately determined. Two studies involving large groups of patients are currently in progress: one in Seattle with the left ventricular function as principal criterion of judgment, the other in Europe (The European Myocardial Infarction Project) with mortality as main criterion of judgment. We must wait for the results of these studies to know whether pre-hospital thrombolysis will become the standard treatment of myocardial infarction and if so, to implement the relevant changes required in health structures.