Pulmonary hypertension is a frequent complication of left heart disease arising from a wide range of cardiac disorders and is associated with poor prognosis. Its pathophysiology is complex with both passive mechanisms of elevated filling pressures in left cavities and occasionally reactive mechanisms of arterial vasoconstriction and remodelling to interplay. This stage, called <> pulmonary hypertension, further worsens the heart failure patients' prognosis but is still a matter of debate concerning the criteria to apply for its diagnosis and concerning the best way to manage it. This article gives an overview of the importance and pathophysiology of pulmonary hypertension associated with left heart disease, and discusses the challenges associated with its diagnosis and treatment.
Pulmonary hypertension (PH) is a complex disease leading, in its advance form, to a decreased quality of life and early mortality. In the early stage, non specific signs and symptoms are the rule. The diagnosis is often missed, leaving the patient alone to face the disease and its repercussion on his daily life. This article reviews the main PH causes and predisposing conditions. Signs and symptoms suggesting the diagnosis are reviewed as well as conditions recognised at high risk for the disease. The key role of echocardiography in establishing the diagnosis, assessing PH severity, cardiac repercussions and/or potential aetiologies, is addressed. Finally the importance of a multidisciplinary approach is recommended.
L'hypertension pulmonaire (HP) est une maladie invalidante, responsable a un stade avance d'une baisse importante de la qualite de vie et d'une mortalite precoce. Un debut insidieux, aux symptomes non specifiques, retarde trop souvent le diagnostic, laissant le patient demuni face a sa maladie. Cet article revoit les causes principales de l'HP ainsi que les conditions jugees a risque pour son developpement. Les signes et les symptomes evocateurs d'une HP ainsi que les situations necessitant un depistage periodique sont revus. L'interet majeur de l'echocardiographie Doppler dans le depistage, le bilan et le suivi d'une HP est discute. Il est aussi rappele que la prise en charge d'un patient avec HP necessite une collaboration multidisciplinaire pour une prise en charge diagnostique et therapeutique optimalisee.
Hypertrophic cardiomyopathy (HCM) is a complex disease of multiple genetic origins. It is usually a familial cardiac disorder, recognised to be of heterogeneous expression with diverse clinical manifestations and outcome. This structural and functional abnormality of the myocardium is the phenotype of many genetic disorders of encoding proteins of the sarcomere. The diagnostic disorder is a thickened and non-dilated left ventricle in the absence of an associated condition that could explain the hypertrophy.
BACKGROUND The therapeutic options for hypertrophic obstructive cardiomyopathy (HOCM) classically include medical treatment with beta-blockers and calcium antagonists or myectomy-myotomy as a surgical possibility for refractory cases. The observation that pacemaker activation of the heart in HOCM reduces the subaortic gradient is well known but less well investigated. METHODS Eighty-three patients (33 female and 50 male) mean age 53 (18-82) years, with symptoms refractory to drug treatment and a resting gradient above 30 mmHg, who responded favourably to temporary pacing, were included in this prospective study and had a pacemaker (DDD) implanted. After an initial double-blind crossover phase of 6 months, patients were reinvestigated at 12 months and followed for a mean of 36 months. RESULTS As observed during a screening investigation, the obstruction was significantly reduced from 72 +/- 35 mmHg to 29 +/- 24 mmHg (P < 0.01) when the pacemaker was on, while no major effect was seen during the sham phase. The effect was persistent at 1 year with a remaining resting gradient of 28 +/- 24 mmHg. In parallel, we documented an improvement in functional capacity, according to the NYHA classification and by quality of life analysis, and a significant improvement in dyspnoea and angina. Exercise on treadmill improved only in patients with reduced initial tolerance (< 8 min). During the mean follow-up of 36 months, 65 patients remained on pacing alone, with eight patients having additional AV-node ablation and five patients finally having surgery. CONCLUSION This controlled multicentre study shows that pacemaker treatment is an option for HOCM patients; it is inoffensive and does not exclude alternative methods, but satisfies 79% of patients beyond 3 years.
A 76-year-old woman had a permanent transvenous DDDR pacemaker implanted for complete atrioventricular block. She was hospitalized 4 years later for recurrent transient ischaemic attacks related to dislodgment of the atrial lead into the left atrium through a patent foramen ovale. The patient was successfuly treated by transvenous extraction of the atrial lead. The follow-up has been uneventful 12 months after the procedure. Left atrially dislodged pacemaker leads have to be retracted under full anticoagulation.
Background The therapeutic options for hypertrophic obstructive cardiomyopathy (HOCM) classically include medical treatment with beta-blockers and calcium antagonists or myectomy-myotomy as a surgical possibility for refractory cases. The observation that pacemaker activation of the heart in HOCM reduces the subaortic gradient is well known but less well investigated. Methods Eighty-three patients (33 female and 50 male) mean age 53 (18-82) years, with symptoms refractory to drug treatment and a resting gradient above 30 mmHg, who responded favourably to temporary pacing, were included in this prospective study and had a pacemaker (DDD) implanted. After an initial double-blind crossover phase of 6 months, patients were reinvestigated at 12 months and followed for a mean of 36 months. Results As observed during a screening investigation, the obstruction was significantly reduced from 72 +/- 35 mmHg to 29 +/- 24 mmHg (P<0.01) when the pacemaker was on, while no major effect was seen during the sham phase. The effect was persistent at 1 year with a remaining resting gradient of 28 +/- 24 mmHg. In parallel, we documented an improvement in functional capacity, according to the NYHA classification and by quality of Life analysis, and a significant improvement in dyspnoea and angina. Exercise on treadmill improved only in patients with reduced initial tolerance (<8 min). During the mean follow-up of 36 months. 65 patients remained on pacing alone, with eight patients having additional AV-node ablation and five patients finally having surgery. Conclusion This controlled multicentre study shows that pacemaker treatment is an option for HOCM patients; it is inoffensive and does not exclude alternative methods, but satisfies 79% of patients beyond 3 years.
In this study, which included 56 patients with aortic stenosis, the predictive value of the fractional shortening velocity ratio was evaluated. This Doppler index allowed detection of significant aortic stenosis (0.53 cm2/m2), with a positive predictive value of 93% and a negative predictive value of 92% for a cutoff value of 0.8.
Clinical improvement with dual chamber pacing bas largely been reported in patients suffering from hypertrophic obstructive cardiomyopathy and mainly attributed to the reduction of the subaortic pressure gradient. To be effective, pacing must induce a permanent and complete capture of the LV. In two patients of our collective, symptoms (angina and dyspnea NYHA Class III and/or syncopes) persisted or relapsed despite pacing. This was related to the inability to obtain full LV capture due to a too‐short native PR interval. RF ablation of the AV junction was therefore performed in botb patients, resulting in permanent AV block in one and prolonged PR interval up to 310 ms in the second. Pacing was thereafter associated with an immediate and significant clinical improvement related to permanent LV capture, whatever the patient's activity. After RF ablation, the AV delay was set up to induce the best LV filling, as assessed by Doppler analysis of mitral flow. Our observations suggest that RF ablation or modification of the AV junction can be a successful procedure in some patients with residual or recurrent symptoms, when the latter result from a loss of capture or from the inability to program an AV delay tbat does not compromise the active component to LV filling. Doppler echocardiography is a simple and effective mean to assess the hemodynamic effect of AV interval modulation in this setting.
P = .017). There were statistically significant differences between the patients with the CDAD and the carriers in terms of the presence of more than three active medical problems (i.e., requiring treatment in the ICU; 65% vs. 27%; P = .05), the presence of more than three underlying diseases (65% vs. 27%; P = .05), and longer duration of antibiotic therapy (88% vs. 45%; P = .02) (table 1). A total of 68 stool specimens were positive for C. difficile, and 62 of the isolates were preserved for further research. Fifty-nine (95%) of the 62 isolates, evenly distributed in CDAD group and carrier group, were positive for toxins. PCR ribotyping yielded five ribotypes, and the RAPD method yielded seven types. The combination of these two methods generated eight distinctive fingerprints. The most frequently isolated type was type I (isolated from 29 [47%] of 62 patients), which could be isolated from nine (53%) of 17 patients with CDAD and from two (18%) of 11 asymptomatic carriers (P = .08). In addition, types II, III, IV, and V were variably associated with diseases. Types VI, VII, and VIII were recovered only from asymptomatic carriers, but the numbers of isolates of these types were small. Our data show that there was no correlation between genotypes, toxin production, and clinical manifestations of infection. There was no strain-specific difference for asymptomatic carriers vs. patients with CDAD. The predominant type (type I) was variably associated with diseases, and five of eight types were associated with diarrhea. Toxigenic C. difficile strains could be isolated both from patients with CDAD and from asymptomatic carriers. Actually, most strains from both groups were toxigenic in vitro. The results of our study also failed to support the belief that the pathogenicity of an isolate depended on strain variation and toxin production. Host factors, especially debilitat d status, appear to be important determ nants fo the clinical expr ssion of CDAD.