Multidisciplinary network in heart failure management in a community-based population: results and benefits at 2 years.

OBJECTIVE: To study the effects of a network using simple routine tools, in a community-based population. METHODS: This is a non-randomized controlled study. Cardiosaintonge network set up on January 1st 2004, offered coordinating care involving general practitioners, cardiologists, nurses, physical therapists and dieticians to patients with heart failure. RESULTS: After 2 years, 362 patients were included, 129 in the network and 233 in the usual care control group. The 2 groups were different for age but not for gender. The readmission rate was of 2.5 days per patient included in the network versus 4.8 in the control group. Twenty four patients (19%) died in the network and 82 (35%) in the control group (p=0.001). Survival analysis estimated a median survival time of >4 months (median survival not achieved within the follow-up) for the network group and 20 months for the non-network group (p=0.0004). The Cox model, adjusting on gender, age and NYHA stage determined the independent role of the network on longer survival since, the adjusted hazard ratio was of 0.37 for the network group (p=0.02). The Duke quality of life score marked a global improvement since admission, at months 6, 12, 18 and 24. CONCLUSIONS: Cardiosaintonge network permits less readmissions and longer survival with better quality of life for patients with chronic heart failure.

Short- and long-term risk factors for sudden death in patients with stable angina.

Sudden death is most common and often the first manifestation of coronary heart disease although its risk is difficult to predict. It has been studied mainly in patients with severe ventricular arrhythmia or recent myocardial infarction, but little is known about the different risk factors for short- and long-term risk of sudden death in patients with stable angina. To assess risk factors for sudden death in patients with stable angina and angiographically proven coronary artery disease, 319 consecutive patients were recruited prospectively and followed-up. Patients with clinical heart failure or recent myocardial infarction were excluded. Clinical, angiographic and biological variables were recorded. The association between each variable and the risk of sudden death was assessed in univariate and logistic multivariate analysis. There were 25 sudden deaths during the follow-up period (97+/-29 months). The univariate predictors in the short-term (2 years) were: peripheral arterial disease, left ventricular hypertrophy, low density lipoprotein cholesterol and ejection fraction. The independent predictors were: peripheral arterial disease (relative risk: 6.3), ejection fraction (relative risk 1.05) and low density lipoprotein (relative risk: 1.8). In the long-term (8-10 years), body mass index, coronary score, ejection fraction and fibrinogen were univariate predictors. Only body mass index (relative risk: 1. 2), ejection fraction (relative risk: 1.06) and fibrinogen (relative risk: 2) remained independent predictors. The risk factors for sudden death in stable angina were time-dependent, peripheral arterial disease appeared as the best predictor with LDL for short time, and body mass index (obesity: index >27) and fibrinogen for long time. Ejection fraction was the only time-independent predictor.

Detection of coronary stenoses by stress echocardiography using a previously implanted pacemaker for ventricular pacing: preliminary report of a new method.

BACKGROUND: The number of patients with pacemakers has been increasing and a large number of them will present with chest pain or symptoms suggesting angina pectoris. Myocardial ischemia and presence of coronary artery disease are difficult to detect and assess by noninvasive methods in patients with a pacemaker; the electrocardiogram (ECG) at rest and during exercise is usually very difficult to analyze in terms of ischemia or even presence of an acute myocardial infarction. HYPOTHESIS: To detect significant coronary stenosis in patients with previously implanted pacemakers, we tested a new stress echocardiography method using incremental ventricular pacing by already implanted pacemakers. METHODS: We studied prospectively 25 consecutive patients who underwent stress echocardiography with increasing ventricular pacing up to either 85% of the age-predicted maximal heart rate or chest pain. Positive tests were defined by new hypokinesia or worsening of a preexisting alteration in wall motion in at least two adjacent territories. All patients underwent coronary angiograms to define the presence and severity of coronary stenoses. RESULTS: Among the 25 tests, 11 (44%) were stopped for chest pain. 1 (4%) for moderate discomfort, 1 (4%) for a drop in blood pressure, and the target pacing rate was achieved in the tests of the remaining 12 patients (48%). There were no complications. Thirteen patients had significant stenoses. In 10 cases, stress echocardiography was a true positive test with respect to coronary angiography. There were 11 true negative, 1 false positive, and 3 false negative tests. The sensitivity was 77%, specificity was 90%, the positive predictive value was 91%, and the negative predictive value 79%. The accuracy was 84%. CONCLUSIONS: This new stress echocardiography method appears feasible, easy, safe, and effective for detection of significant coronary stenoses in patients with pacemakers.

Restenosis or rapid progression in non-dilated sites are not predictors of late spontaneous coronary events.

The present study was designed to assess the prognostic value of clinical and angiographic factors, and especially restenosis or rapid progression in non-dilated sites, on major spontaneous coronary events at long-term follow-up after a first successful coronary angioplasty performed for angina pectoris. A second aim was to assess the prognostic factors and especially restenosis in asymptomatic patients after angioplasty. The first 352 consecutive patients undergoing a successful coronary angioplasty were selected and followed-up. The following variables: age, sex, unstable angina, previous myocardial infarction, diabetes, hypercholesterolemia, tobacco consumption, hypertension, fibrinogen, coronary extent, single or multiple dilatation, restenosis, new progression, clinical deterioration of anginal status just before angiographic restudy or asymptomatic status were subjected to a stepwise regression analysis. Restenosis (a loss of 30% in diameter and/or a return to a >50% stenosis) and progression in non-dilated segments (a 20% reduction in diameter) were assessed by a computer-assisted method. Cardiac death, new myocardial infarction or new unstable angina, at long-term follow-up after angiographic restudy, were regarded as spontaneous coronary events and pooled in a single dependent variable. Thus 41 patients had a coronary event. In the overall population, clinical deterioration of anginal status (p<0.001, relative risk: 3.65) and fibrinogen (p<0.05, relative risk: 1.03) were independent predictors of spontaneous coronary events. Restenosis or new progression were not predictors. In asymptomatic patients (n=187), fibrinogen (p<0.01, relative risk=1.06) was the only predictor and restenosis was not an independent predictor of spontaneous coronary events. The best predictor of spontaneous coronary events at long-term follow-up after a first successful coronary angioplasty is clinical deterioration in anginal status in the months following the procedure. Restenosis does not appear as an independent predictor. Rapid progression observed in non-dilated sites is not an important prognostic factor.

Progression of coronary artery disease in non-dilated sites in the months following balloon angioplasty: time-dependent relation with restenosis.

There is scant information on the progression of coronary artery disease in non-dilated sites in the months following percutaneous transluminal coronary angioplasty (PTCA) or on its relationship with restenosis. To assess the incidence of this progression and its relationship with restenosis at various times after PTCA, the authors selected 371 consecutive patients who had undergone a first successful PTCA for angina on native coronaries followed by a repeat angiographic study. The angiograms were analysed by a computer-assisted method; progression was defined as a 20% decrease in diameter and restenosis as a 30% decrease in diameter or a return to > 50% stenosis. The relationship between progression and restenosis was analysed in the whole population and then, using the Mantel-Haenszel chi-square test, in two subgroups: patients with a stable clinical state, who were restudied routinely and those whose worsened state had prompted repeat angiography. The relationship was assessed at different times between angioplasty and the repeat angiography. Progression was observed in 80 patients (22%) and restenosis in 155 patients (42%). There was a highly significant relationship between progression and restenosis in the total population (chi 2 = 26.4, odds ratio = 3.9 and P < 0.0003) and in the group of patients that were routinely restudied (chi 2 = 31.6, odds ratio = 5.3 and P < 0.0001), but not in the group of patients in whom restudy was performed because of clinical worsening (chi 2 = 0.13, odds ratio = 1.5 and P = NS). With respect to the length of follow-up, in the total population the relationship was significant only at 6 and 7 months (P < 0.0001), and in the group receiving a routine restudy only at 4-5 and 6-7 months (P < 0.001). Progression in non-dilated sites appeared to be strongly and transiently linked with restenosis, suggesting that PTCA may enhance both restenosis and progression over a short period.

Predictive value of hemostatic factors for sudden death in patients with stable angina pectoris.

To assess hemostatic risk factors for sudden death in patients with stable angina, 323 consecutive patients were recruited prospectively. Patients with clinical heart failure or recent myocardial infarction were excluded. The following clinical variables were recorded: age, gender, smoking habits, hypertension, previous myocardial infarction, left ventricular hypertrophy, and severe ventricular arrhythmia. Angiographic variables included coronary extent, assessed from Jenkins' and mean atherosclerotic scores, and left ventricular ejection fraction. Lipid variables included total cholesterol, triglycerides, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and apolipoproteins A-I and B. Hemostatic factors included fibrinogen, fibrinopeptide A, antithrombin III, factor VIII antigen, factor VIII coagulant, protein C, plasminogen, alpha 2 antiplasmin, euglobulin clot lysis time, tissue plasminogen activator before and after venous occlusion, and plasminogen activator inhibitor. There were 34 deaths, 19 of which were sudden during the follow-up period (60 +/- 17 months). The association between each variable and the risk of sudden death was assessed by calculating the relative risk with the Cox univariate model. All significant predictors from the univariate analysis were then incorporated in a Cox multivariate model to select the independent predictors of sudden death. The independent predictors of sudden death were left ventricular hypertrophy (p < 0.04), lower left ventricular ejection fraction (p < 0.04), and shorter euglobulin clot lysis time after venous occlusion (p < 0.02), whereas fibrinogen (p < 0.07) and Jenkins' score (p < 0.08) were borderline. Determination of hemostatic variables, especially those pertaining to dynamic fibrinolysis, may thus be of value in assessing risk of sudden death.

Biological risk factors for restenosis after percutaneous transluminal coronary angioplasty.

In an attempt to discern biological (such as thrombotic or fibrinolytic) risk factors in patients developing restenosis after percutaneous transluminal coronary angioplasty, the following factors were measured prior to angiography in a population of 23 patients (20 men, 3 women, mean age 57 +/- 5 yr) treated by a successful angioplasty (gain > 20% and residual stenosis < 50%) for stable angina pectoris and who had a routine angiographic restudy. The following factors were thus assessed: lipid factors: cholesterol, triglycerides, high density lipoprotein cholesterol, low density lipoprotein cholesterol, apolipoprotein AI, apolipoprotein B; coagulation factors: fibrinogen, antithrombin III, fibrinopeptide A, factor VIII coagulant, factor VIII antigen, protein C; factors of physiological fibrinolysis: plasminogen, alpha 2-antiplasmin, tissue plasminogen activator and euglobulin clot lysis time before and after venous occlusion, plasminogen activator inhibitor before venous occlusion; and factors of platelet release: beta-thromboglobulin, platelet factor 4. Also studied were clinical characteristics: age, gender, diabetes, hypertension, smoking habits, previous myocardial infarction; angiographic data: global extent of coronary artery disease, location of the stenosis in a bend or branch point, complexity of the lesion, initial and residual stenosis and treatment during follow-up. The coronary angiograms were analyzed by a computer-assisted method with automatic edge detection. On angiographic criteria, 6 patients (restenosis group) were judged to have developed a restenosis (30% decrease in diameter and/or return to a 50% stenosis). The other 17 patients (those without restenosis) were considered to have a persistent success. Apart from age (group without restenosis: 55 +/- 6; restenosis group 61 +/- 5, p < 0.04), there were no differences in clinical, angiographic or treatment variables. There were no differences in lipid factors, but significant differences were observed in hemostatic variables: fibrinogen (without restenosis: 3.18 +/- 0.83; restenosis: 3.83 +/- 0.51 milligrams, p = 0.05), tissue plasminogen activator before venous occlusion (without restenosis: 10.9 +/- 26.8; restenosis: 232.5 +/- 371.2 IU, p < 0.04), euglobulin clot lysis time after venous occlusion (without restenosis: 176.5 +/- 100.5; restenosis: 78.6 +/- 40.2 min, p < 0.05) and for marker of the platelet release: platelet factor 4 (without restenosis: 10.8 +/- 7.9; restenosis: 20.5 +/- 7.5 ng/l, p < 0.04). These findings indicate that patients developing restenosis after coronary angioplasty tend to have an imbalance in the prothrombotic-antithrombotic equilibrium prior to the procedure.

Biological risk factors for sudden death in patients with coronary artery disease and without heart failure.

In a study of biological risk factors for sudden death in patients with coronary artery disease, 320 patients were, prospectively, recruited and followed-up over two years. None of the patients had heart failure or recent myocardial infarction. The following variables were recorded: previous acute myocardial infarction, hypertension, smoking habits, ventricular arrhythmia; the angiographic variables included: left ventricular ejection fraction, Jenkins' and mean atherosclerotic scores; lipid profile: cholesterol, triglycerides, high density lipoprotein cholesterol, low density lipoprotein cholesterol, apolipoproteins Al and B; hemostatic profile: fibrinogen, fibrinopeptide A, antithrombin III, factor VIII antigen, factor VIII coagulant, protein C, plasminogen, alpha 2-antiplasmin, euglobulin clot lysis time and tissue plasminogen activator before and after venous occlusion, tissue plasminogen activator inhibitor, platelet factor 4, beta-thromboglobulin. During the follow-up period, 12 of the patients died suddenly. In these patients, ejection fraction was lower: 49 +/- 16% versus 61 +/- 14% for the other patients (P less than 0.02), fibrinogen higher: 3.9 +/- 0.8 g/l versus 3.5 +/- 0.8 for the living patients (P less than 0.05) and protein C lower: 89 +/- 39% versus 111 +/- 39% (P = 0.06) for the other patients. In multivariate analysis: lower ejection fraction (P less than 0.008), older age (P less than 0.03) and lower protein C (P less than 0.01) were correlated with sudden death. Among the patients with coronary artery disease, the raised fibrinogen and the decreased protein C appeared to be risk factors for sudden cardiac death. These alterations reflected a prothrombotic state which might increase the ischemic risk, due to an acute thrombosis, leading to the fatal ventricular arrhythmia. Determination of these hemostatic variables might be a useful adjunct for assessment of the vital prognosis of patients with coronary artery disease, especially the risk of sudden death in addition to other known clinical, electrocardiographic, hemodynamic risk factors. This would also guide both the instigation of complementary investigations and appropriate therapy in such high risk group of patients.

[Cardiac lesions in Takayasu's disease. A case with initial pericarditis and tamponade]. / Atteintes cardiaques de la maladie de Takayasu. Un cas de pancardite inaugurale avec tamponnade.

The authors report the case of 21-year old female patient with a particular form of Takayasu's disease remarkable for its initial presentation and its cardiac and coronary lesions. The disease began with miscarriage at the 5th months of pregnancy, followed by acute pericarditis with tamponade. Subsequently, lesions of the aortic and mitral valves developed, while the myocardium became involved with left ventricular dilatation and hypokinesia confirmed by echocardiography and cineangiography. Coronary arteriography revealed large coronary aneurysms which are exceptional in this disease. This case prompted the authors to discuss the various cardiac lesions and the relationship of Takayasu's disease with pregnancy.

Risk factors for progression of atherosclerosis six months after balloon angioplasty of coronary stenosis.

To assess the possible progression of coronary artery disease after percutaneous transluminal coronary angioplasty (PTCA) and its relation to risk factors and restenosis, 124 patients who underwent a first successful PTCA were studied. All had routine follow-up angiography 5 to 8 months after PTCA. Restenosis was defined as a 30% decrease in diameter stenosis or a return to greater than 50% stenosis, and progression (in any nondilated site) as a 20% decrease in diameter stenosis, assessed by a video-densitometric computer-assisted technique. Univariate and multivariate analysis with respect to progression was carried out for age, sex, initial unstable angina, previous myocardial infarction, diabetes mellitus, hypertension, hypercholesterolemia (greater than or equal to 6.2 mmol), smoking habits, Jenkins' score, dilated artery and restenosis. Forty-one patients (33%) had restenosis, and 23 (19%) had evidence of progression; 20 (87%) of these latter patients had restenosis and 3 (13%) did not. Univariate correlates of progression were: previous myocardial infarction (p less than 0.05), higher Jenkins' score (p less than 0.0003) and restenosis (p less than 0.0001). Restenosis was the only multivariate correlate (p less than 0.00003). Progression at routine angiography after PTCA is not rare, and appears to be related to both the initial extent of coronary artery disease and restenosis.