Kinetics of oxygen consumption during and after exercise in patients with dilated cardiomyopathy. New markers of exercise intolerance with clinical implications.

OBJECTIVES: This study analyzed the kinetics of oxygen consumption during and after a maximal cardiopulmonary exercise test in patients with dilated cardiomyopathy. The prognostic information derived from indexes of recovery was also studied. BACKGROUND: Previous studies have examined the kinetics of oxygen consumption during a short recovery period in a limited number of patients. To our knowledge, no study has examined the prognostic information derived from indexes of recovery. METHODS: We studied 153 patients and 55 control subjects. We calculated the ratio between total oxygen consumption during exercise and recovery, the half-recovery time of peak oxygen consumption, the time constant of recovery, the recovery time and the ratio between duration of exercise and recovery time. RESULTS: Recovery of oxygen consumption was significantly delayed in patients, and this delay was related to the degree of exercise intolerance. After a median follow-up period of 439 days, for the total study group, percent of predicted peak oxygen consumption (p = 0.003) and ejection fraction (p = 0.03) were independent predictors of survival. In a subgroup of patients with moderate exercise intolerance (percent peak oxygen consumption > 40%), the ratio between total oxygen consumption during exercise and recovery (p = 0.013) and the ejection fraction (p = 0.013) were independent predictors of survival. CONCLUSIONS: The kinetics of oxygen consumption during recovery was delayed in patients with dilated cardiomyopathy. Although indexes of recovery were not prognostic markers in the total study group, the ratio between total oxygen consumption during exercise and recovery was an independent prognostic marker in patients with moderate exercise intolerance.

Right ventricular ejection fraction is an independent predictor of survival in patients with moderate heart failure.

OBJECTIVES: We sought to study the relationship between survival and right ventricular ejection fraction (RVEF) in a subgroup of patients with moderate congestive heart failure (CHF). BACKGROUND: It has been demonstrated that RVEF is an independent predictor of survival in patients with advanced CHF. METHODS: Cardiopulmonary exercise testing and radionuclide angiography (to determine right and left ventricular ejection fraction) were prospectively performed in 205 consecutive patients with moderate CHF (140 patients in New York Heart Association [NYHA] class II, 65 in class III). RESULTS: Left ventricular ejection fraction was 29.3%+/-10.1%, RVEF was 37.5%+/-14.6% and peak oxygen consumption (VO2) was 16.2+/-5.4 ml/min/kg (60.2%+/-19% of maximal predicted VO2). After a median follow-up period of 755 days, there were 44 cardiac-related deaths, 3 deaths from noncardiac causes and 15 transplantations of whom 2 were urgent; 1 patient was lost to follow-up. Multivariate analysis showed that three variables-NYHA classification, percent of maximal predicted VO2 and RVEF-were independent predictors of both survival and event-free cardiac survival. Left ventricular ejection fraction and peak VO2 normalized to body weight had no predictive value. The event-free survival rates from cardiovascular mortality and urgent transplantation at 1 year were 80%, 90% and 95% in patients with an RVEF <25%, with a RVEF > or =25% and <35% and with a RVEF > or =35%, respectively. At 2 years, survival rates were 59%, 77% and 93% in the same subgroups, respectively. CONCLUSIONS: In addition to the NYHA classification and to the percent of maximal predicted VO2, RVEF is an independent predictor of survival in patients with moderate CHF.

Lack of association between polymorphisms of eight candidate genes and idiopathic dilated cardiomyopathy: the CARDIGENE study.

OBJECTIVES: The study investigated the potential role of eight candidate genes in the susceptibility to idiopathic dilated cardiomyopathy (IDC). BACKGROUND: Idiopathic dilated cardiomyopathy has a familial origin in 20% to 25% of cases, and several genetic loci have been identified in rare monogenic forms of the disease. These findings led to the hypothesis that genetic factors might also be involved in sporadic forms of the disease. In complex diseases that do not exhibit a clear pattern of familial aggregation, the candidate gene approach is a strategy widely used to identify susceptibility genes. All genes coding for proteins involved in biochemical or physiological abnormalities of cardiac function are potential candidates for IDC. METHODS: We studied 433 patients with IDC and 401 gender- and age-matched controls. Polymorphisms investigated were the I/D polymorphism of the angiotensin I-converting enzyme (ACE) gene, the T174M and M235T polymorphisms of the angiotensinogen (AGT) gene, the A-153G and A+39C polymorphisms of the angiotensin-II type 1 receptor (AGTR1) gene, the T-344C polymorphism of the aldosterone synthase (CYP11B2) gene, the G-308A polymorphism of the tumor necrosis factor-alpha (TNF) gene, the R25P polymorphism of the transforming growth factor beta1 (TGFB1) gene, the G+11/in23T polymorphism of the endothelial nitric oxide synthase (NOS3) gene and the C-1563T polymorphism of the brain natriuretic peptide (BNP) gene. RESULTS: None of the polymorphisms were significantly associated with the risk or the severity of the disease. CONCLUSIONS: We did not find evidence for an involvement of any of the 10 investigated polymorphisms in the susceptibility to IDC.

Effect of mitral valve surgery on exercise capacity, ventricular ejection fraction and neurohormonal activation in patients with severe mitral regurgitation.

OBJECTIVES: The purpose of this study was to prospectively investigate the effects of surgical correction of mitral regurgitation (MR) on exercise performance, cardiac function and neurohormonal activation. BACKGROUND: Little is known about the effect of surgical correction of MR on functional status or on neurohormonal activation. METHODS: Cardiopulmonary exercise test, radionuclide angiography and blood samples for assessment of neurohormonal status were obtained in 40 patients with nonischemic MR before and within one year (216+/-80 days) after surgery. Twenty-four patients underwent mitral valve repair (MVr), and 16 underwent valve replacement (VR) with anterior chordal transection. RESULTS: Despite an improvement in New York Heart Association functional class, exercise performance did not change (peak oxygen consumption: 19.3+/-6.1 to 18.5+/-5.6 ml/kg/min, percentage of maximal predicted oxygen consumption: 79.5+/-18.2% to 76.8+/-16.9%). After surgery, left ventricular (LV) ejection fraction (EF) decreased (64.2+/-10.3% to 59.9+/-11.4%, p = 0.003) while right ventricular (RV) EF increased (41.4+/-9.6% to 44.7+/-9.5%, p = 0.03). Left ventricular EF did not change after MVr (64.3+/-11.5% to 61.5+/-12.2%), but RVEF improved (40.4+/-9.2% to 46.0+/-10.0%, p = 0.02). In contrast, VR was associated with an impairment of LV function in the apicolateral area and a decrease in LVEF (64.1+/-8.5% to 57.4+/-10.0%, p = 0.01), whereas RVEF did not change (42.9+/-10.3% to 42.8+/-8.6%). Moreover, there was only a slight decrease in neurohormonal activation after surgery. CONCLUSIONS: Despite an improvement in symptomatic status, exercise performance was not improved seven months after either MVr or VR for MR, and neurohormonal activation persisted. Compared with MVr, VR resulted in a significant impairment of cardiac function in this study.

Expanding the phenotype of LMNA mutations in dilated cardiomyopathy and functional consequences of these mutations.

AIMS: Mutations in the lamin A/C gene (LMNA) have been reported to be involved in dilated cardiomyopathy (DCM) associated with conduction system disease and/or skeletal myopathy. The aim of this study was to perform a mutational analysis of LMNA in a large white population of patients affected by dilated cardiomyopathy with or without associated symptoms. METHODS: We performed screening of the coding sequence of LMNA on DNA samples from 66 index cases, and carried out cell transfection experiments to examine the functional consequences of the mutations identified. RESULTS: A new missense (E161K) mutation was identified in a family with early atrial fibrillation and a previously described (R377H) mutation in another family with a quadriceps myopathy associated with DCM. A new mutation (28insA) leading to a premature stop codon was identified in a family affected by DCM with conduction defects. No mutation in LMNA was found in cases with isolated dilated cardiomyopathy. Functional analyses have identified potential physiopathological mechanisms involving identified mutations, such as haploinsufficiency (28insA) or intermediate filament disorganisation (E161K, R377H). CONCLUSION: For the first time, a specific phenotype characterised by early atrial fibrillation is associated with LMNA mutation. Conversely, mutations in LMNA appear as a rare cause of isolated dilated cardiomyopathy. The variable phenotypes observed in LMNA-DCM might be explained by the variability of functional consequences of LMNA mutations.

Patients with familial partial lipodystrophy of the Dunnigan type due to a LMNA R482W mutation show muscular and cardiac abnormalities.

Diseases due to mutations in the lamin A/C gene (LMNA) are highly heterogeneous, including neuromuscular and cardiac dystrophies, lipodystrophies, and premature ageing syndromes. In this study we characterized the neuromuscular and cardiac phenotypes of patients bearing the heterozygous LMNA R482W mutation, which is the most frequent genotype associated with the familial partial lipodystrophy of the Dunnigan type (FPLD). Fourteen patients from two unrelated families, including 10 affected subjects, were studied. The two probands had been referred for lipoatrophy and/or diabetes. Lipodystrophy, exclusively observed in LMNA-mutated patients, was of variable severity and limited to postpubertal subjects. Lipodystrophy and metabolic disturbances were more severe in women, even if an enlarged neck was a constant finding. The severity of hypertriglyceridemia and hirsutism in females was related to that of insulin resistance. Clinical muscular alterations were only present in LMNA-mutated patients. Clinical and histological examination showed an invalidating, progressive limb-girdle muscular dystrophy in a 42-yr-old woman that had been present since childhood, associated with a typical postpubertal FPLD phenotype. Six of eight adults presented the association of calf hypertrophy, perihumeral muscular atrophy, and a rolling gait due to proximal lower limb weakness. Muscular histology was compatible with muscular dystrophy in one of them and/or showed a nonspecific excess of lipid droplets (in three cases). Immunostaining of lamin A/C was normal in the six muscular biopsies. Surprisingly, calpain 3 expression was undetectable in the patient with the severe limb-girdle muscular dystrophy, although the gene did not reveal any molecular alterations. At the cardiac level, cardiac septal hypertrophy and atherosclerosis were frequent in FPLD patients. In addition, a 24-yr-old FPLD patient had a symptomatic second degree atrioventricular block. In conclusion, we showed that most lipodystrophic patients affected by the FPLD-linked LMNA R482W mutation show muscular and cardiac abnormalities. The occurrence and severity of the myopathic and lipoatrophic phenotypes varied and were not related. The muscular phenotype was evocative of limb girdle muscular dystrophy. Cardiac hypertrophy and advanced atherosclerosis were frequent. FPLD patients should receive careful neuromuscular and cardiac examination whatever the underlying LMNA mutation.

Association between anticardiolipin antibodies and mortality in patients with peripheral arterial disease.

PURPOSE: Anticardiolipin antibodies may be associated with recurrent thromboembolic events in patients with myocardial infarction or stroke. We sought to determine the prevalence of anticardiolipin antibodies in patients with peripheral arterial disease and their association with subsequent thromboembolic events and mortality. METHODS: We ascertained anticardiolipin antibodies using a standardized enzyme-linked immunosorbent assay (immunoglobulin G [IgG] anticardiolipin > or =15 GPL units or IgM anticardiolipin > or =15 MPL units) in 232 patients with peripheral arterial disease and 100 control subjects. Patients were observed to determine overall and cardiovascular mortality, and incident thromboembolic events. RESULTS: IgG anticardiolipin antibodies were significantly more common in the patients with peripheral arterial disease (36 of 232 [16%]) than in the controls (7 of 100 [7%], P = 0.03). During a median follow-up of 3.5 years, 3 of the 232 patients were lost to follow-up and 56 (24%) died. Overall mortality was significantly greater in the IgG anticardiolipin-positive patients (16 of 35 [46%]) compared with those who were IgG anticardiolipin-negative (40 of 194 [21%], P = 0.0003), largely due to an increase in cardiovascular mortality among the IgG anticardiolipin-positive patients. In a multivariate proportional hazards analysis, IgG anticardiolipin antibodies were an independent risk factor for overall mortality (hazard ratio [HR] = 2.1, 95% confidence interval [CI]: 1.2 to 4.0) and cardiovascular mortality (HR = 4.4, 95% CI: 1.6 to 12). CONCLUSIONS: IgG anticardiolipin antibodies are common in patients with peripheral arterial disease and are associated with an increased risk of overall and cardiovascular mortality.

Compound heterozygosity in a family with protein C deficiency illustrating the complexity of the underlying molecular mechanism.

The association of two missense mutations, a Leu 223 to Phe and an Ile 403 to Met, is described in a family presenting with various protein C deficiency phenotypes. In this family, two subjects were compound heterozygotes with protein C levels of about 25%, the other members being heterozygous for only one of the mutations. The Leu 223 to Phe mutation was also found in 9 members of 3 other families and, in all cases but one, resulted in protein C levels below 60% associated with a high incidence of thrombotic complications. The other mutation, an Ile 403 to Met, was identified in those of the family' members who presented with borderline protein C concentrations. In such a family, the genomic DNA analysis represents the only way to differentiate between the genetic status of each family member. The results highlight the importance of the genotype determination and the poor discriminative power of the plasma assays currently used.

Plasma levels of atrial natriuretic peptide at peak exercise: a prognostic marker of cardiovascular-related death and heart transplantation in patients with moderate congestive heart failure.

BACKGROUND: Conflicting data have been published concerning exercise performance and hormonal activation. Previous studies have demonstrated the prognostic information of plasma levels of neurohormones at rest in patients with congestive heart failure. No study has examined the prognostic information of plasma levels of hormones at peak exercise. METHODS: Fifty-five consecutive ambulatory patients with stable moderate congestive heart failure (New York Heart Association class II to III) performed a maximal symptom limited cardiopulmonary exercise test with the determination of peak oxygen consumption. Blood samples were drawn at rest and at peak exercise for the determination of plasma levels of atrial natriuretic peptide, aldosterone, and plasma renin activity. RESULTS: Hormonal activation was present at rest, and exercise significantly increased hormonal values. There was no correlation between exercise parameters and hormonal values either at rest or at peak exercise. After a median follow-up period of 724 days, in univariate and multivariate Cox analysis, the most significant independent prognostic marker was the plasma level of atrial natriuretic peptide at peak exercise. Patients with a plasma level of atrial natriuretic peptide > 38 pmol/L had an event rate of 48% compared with an event rate of 14.8% in the other subgroup (p < 0.01). CONCLUSIONS: In patients with stable moderate congestive heart failure, exercise increased hormonal values, but there was no relationship between hormonal activation and exercise performance. Plasma level of atrial natriuretic peptide at peak exercise was the most significant independent marker of cardiovascular-related death and of cardiovascular-related death and heart transplantation.

A miniature cesium iodide-photodiode detector for ambulatory monitoring of left ventricular function.

The physical characteristics of a portable nonimaging scintillation probe system for continuous ambulatory monitoring of the left ventricular function are described. The detector of the equilibrium radionuclide labeled blood pool is a single cesium iodide (CsI) crystal coupled to a silicium photodiode and interfaced to a microcomputer. The spatial properties of this small CsI crystal (1 x 1 x 1 cm3) were evaluated with various single-hole collimators. Linearity was studied in nonattenuating medium. Saturation began at 3000 cps, count loss was 10% at 4000 cps, maximal count rate was 24,000 cps. In attenuating medium, isocount curve of 5% of the maximal count rate was 100 mm deep and 160 mm wide. The most appropriate tested lead collimator to record the global ejection fraction of the left ventricle was a disc-shaped (thickness 5 mm, diameter 41 mm) single-hole (proximal aperture 8 mm, distal aperture 18 mm) collimator. Sensitivity was similar to the sensitivity of a sodium iodide nuclear probe. The detection performance appeared comparable to other available detector systems. Our results indicate that such a CsI-photodiode probe is a promising candidate for left ventricular function monitoring. The application to an ambulatory multicrystal detector system is presented and discussed.

Plasma levels of endothelin-1 at rest and after exercise in patients with moderate congestive heart failure.

Plasma levels of endothelin-1 are increased in patients with severe congestive heart failure related to various etiologies. However, conflicting data have been published in patients with moderate congestive heart failure. Moreover, the effect of exercise on plasma levels of endothelin-1 is not precisely known. We determined the plasma levels of endothelin-1 in a homogenous group of patients with idiopathic dilated cardiomyopathy in stage II of the New York Heart Association functional classification at rest and at peak exercise. In this group of patients, plasma levels of endothelin-1 were increased compared to a control group (2.9 +/- 0.27 vs. 1.96 +/- 0.24 pmol/l, P < 0.01, mean +/- S.E.M.), as were plasma levels of atrial natriuretic peptide (26.3 +/- 6.3 vs. 2.95 +/- 0.7 pmol/l, P < 0.001), plasma renin activity (12.6 +/- 2.98 vs. 1.75 +/- 0.23 ng/ml per h, P < 0.001) and plasma levels of aldosterone (217 +/- 29.3 vs. 154 +/- 18.8 pg/ml, P < 0.05). In contrast to the other hormones, exercise did not increase plasma levels of endothelin-1. There was no correlation between plasma levels of endothelin-1 and plasma levels of atrial natriuretic peptide, and no correlation between left ventricular ejection fraction, peak oxygen consumption and hormonal values. In conclusion, plasma levels of endothelin-1 are increased in a homogeneous group of patients with idiopathic dilated cardiomyopathy and moderate congestive heart failure. Endothelin-1 could participate in the progression of heart failure. Exercise did not increase the plasma levels of endothelin-1 in contrast to the other hormones.

Response of atrial natriuretic factor to surgical pericardial drainage in patients with chronic pericardial effusion.

Previous studies have demonstrated the importance of atrial transmural pressure in the secretion of atrial natriuretic peptide. These studies have been performed in patients with pericardial effusion and hemodynamic compromise. The response of atrial natriuretic peptide to the drainage of chronic pericardial effusion without clinical evidence of tamponade is unknown. We studied 13 patients with chronic abundant pericardial effusion but without hemodynamic compromise. Blood samples for hormonal determinations were drawn before and after surgical pericardiocentesis. Right atrial pressure was measured during the procedure. Drainage induced a significant increase of atrial natriuretic peptide (from 12 +/- 3.9 to 105 +/- 22.8 pmol/l, P < 0.001, mean +/- S.E.M.), correlated with the fall in right atrial pressure (from 7.65 +/- 1.18 to 4.31 +/- 1.46 mmHg, P < 0.05, r = 0.68, P = 0.01). This increase was inversely correlated with the rise of mean blood pressure after surgery (from 84 +/- 2.37 to 100 +/- 5.3 mmHg, P < 0.05, r = 0.65, P < 0.02). Plasma renin activity decreased after drainage (from 8.12 +/- 2.57 to 3.27 +/- 0.65 ng/ml/h, P < 0.05). Surgery induced an increase of plasma levels of aldosterone (from 811 +/- 241 to 1199 +/- 249 pmol/l, P < 0.05), which were reduced after pericardiocentesis (371 +/- 102 pmol/l, P < 0.02). In patients with chronic abundant pericardial effusion, surgical pericardiocentesis induced a significant increase of atrial natriuretic peptide, correlated with a fall in right atrial pressure. The increase of atrial natriuretic peptide was similar than in patients with tamponade, despite a moderate fall in right atrial pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Pericardoscopy for primary management of pericardial effusion in cancer patients.

OBJECTIVE: To assess the usefulness of pericardoscopy via the subxyphoid route for the diagnosis and treatment of pericardial effusion in patients with a history of cancer. METHODS: All patients with a recent or remote history of cancer and a pericardial effusion of unknown origin requiring drainage for diagnostic and therapeutic purposes were included in the study. They underwent complete exploration and cleansing of the pericardial cavity. Abnormal structures or deposits were biopsied under direct visual control, with a 24 cm long rigid pericardoscope. RESULTS: Between 1985 and 1998, pericardoscopy was completed in 112 of the 114 patients included (feasibility 98%), resulting in the immediate relief of symptoms in all the cases. Peri-operative mortality was 3.5%, and post-operative morbidity, 6.1%. After pericardioscopy pericardial effusions were considered malignant in 43 cases. One more case (2.3%) due to a false negative result of pericardioscopy was diagnosed during follow-up. Overall, 44 of the 114 patients (38.6%) had a malignant effusion, and 70 (61.4%), a non-malignant effusion according the follow up. In 10 of the 44 patients with a malignant pericardial effusion (22.7%), pericardoscopy corrected the results of cytological pericardial fluid studies and pericardial window biopsy, both false negatives. The sensitivities of cytological studies of the pericardial fluid, pathological examinations of pericardial window biopsy and pericardioscopy were 75, 65 and 97%, respectively. One patient with a malignant effusion had a non-symptomatic recurrence 1 month after pericardioscopy (2.3%). CONCLUSION: We recommend pericardioscopy to ascertain the malignant nature of the effusion and to diminish the recurrence rate, this avoiding repeat procedures in patients with a short life expectancy.

Congenital high flow coronary cameral fistula in an 81-year-old woman: management problems.

An 81-year-old woman presenting with severe congestive heart failure was found to have a congenital right coronary fistula draining into the superior vena cava. The diagnosis was suspected on transthoracic two-dimensional echo-Doppler study and confirmed with coronary angiography. Transesophageal echocardiography and magnetic resonance imaging were nondiagnostic. An attempt to close the fistula with transcatheter embolization using a detachable latex balloon was unsuccessful because of the very large size of the fistula. Follow-up showed a favorable outcome with medical therapy. Despite the advent of more recent diagnostic and therapeutic techniques, management of such large fistulae remains unresolved.

The ergometrine test: effects on esophageal motility in patients with chest pain and normal coronary arteries.

Ergometrine can evoke coronary spasm in patients with variant angina. The cause of ergometrine-induced chest pain in the absence of coronary spasm is not clear. To determine whether ergometrine produced esophageal dysfunction and chest pain, we evaluated 28 patients by esophageal manometry. Six had chest pain in response to ergometrine during cardiac catheterization (group I) and 22 did not (group II). Results of cardiac catheterization were normal in all patients. Seven volunteers with no history of chest pain formed a control group (group III). Esophageal manometry was performed before and after ergometrine administration (0.4 mg I.V.). Ergometrine provocation during esophageal manometry caused significant deterioration in esophageal motility associated with familiar pain in 5/6 group 1 patients. The motility disorders were characterized by repetitive contracts of high amplitude and long duration in the distal esophagus. No patient from group II or III experienced chest pain after ergometrine and only 2 from group II developed long duration contractions. Thus, we conclude that in patients with normal coronary angiograms, ergometrine-induced chest pain without associated coronary spasm suggests that esophageal motility disorders originate chest pain.

Multifocal peripheral and coronary angioplasties.

Multifocal atherosclerotic lesions are frequent. It could thus be expected that multifocal angioplasties (performed in one particular patient on several [iliofemoral, renal, subclavian, mesenteric, coronary] sites) are frequent. To study multifocal angioplasty, we considered the 5344 angioplasties (PTA) (4151 coronary and 1193 peripheral PTA) which had been performed over 10 years in our institution. Eighty PTA (1.5%) were considered as multifocal angioplasty. They were performed in 30 patients who were followed up during 7 to 132 months (mean = 55). In case of primary PTA (72 PTA), the most frequent involved site was the iliofemoral site (47%) followed by renal (35%), coronary (8%), subclavian (7%) and mesenteric sites (3%). Eight PTA were performed after primary failure (3 cases) or after restenosis (5 cases). The 30 patients were divided into 2 groups according to the chronology of multifocal PTA. In group I, 20 patients had multifocal lesions on the first workup and multifocal angiopathy over a short operative period (< 3 months). The 10 patients of group II initially had a single procedure. They subsequently had multifocal angioplasty over a longer period (> 2 years) on different sites of the first PTA. Compared to group I, mean age was lower in group II (46 vs 52 year; ns), primary success rate higher (100 vs 90%; p < 0.05), complications less frequent (3 vs 20%, p < 0.05) and restenosis rate lower (7 vs 21%; p < 0.01). In conclusion, multifocal angioplasty is infrequent. A specific group of patients who had multifocal angioplasty spread over several months or years could be individualized.(ABSTRACT TRUNCATED AT 250 WORDS)

Comparative diagnostic value of ankle-to-brachial index and transcutaneous oxygen tension at rest and after exercise in patients with intermittent claudication.

BACKGROUND: Few studies have compared sensitivities of ankle-to-brachial index (ABI) and transcutaneous oxygen tension (TcPO2) in a large group of patients with Leriche stage II intermittent claudication. METHOD AND RESULTS: 111 patients (138 limbs) with a stable chronic (> three months) intermittent claudication and significant peripheral vascular disease (PVD) proved by angiography were studied. They performed a treadmill test (10%, 3 km/hr) limited by limb pain. ABI and TcPO2 were measured before, just after exercise, and after three and ten minutes of recovery in supine position. Sensitivities per patient for ABI and TcPO2 were respectively at rest: 82.9% and 28.8%, and after exercise: 88.3% and 62.2%. Sensitivities per leg (n = 138) for ABI and TcPO2 were respectively at rest: 73.9% and 26.8%, and after exercise: 82.6% and 34%. The sensitivity of TcPO2 increased to 56.5% after three minutes of recovery but was always less than that of ABI, which was maximal just after exercise (82.6%). The sensitivity of the regional perfusion index was similar to that of TcPO2. The sensitivity of TcPO2 increased with respect to the Leriche stage and the number of lesions but was always lower than that of ABI. There was a weak correlation between TcPO2 and ABI after exercise, but no correlation was noted between maximal walking distance, ABI, and TcPO2. CONCLUSION: TcPO2 is not required in patients with Leriche stage II intermittent claudication but might be useful either in severely affected patients (Leriche stage III or IV) or in selected patients.

Long-term follow-up after peripheral and coronary angioplasty in patients undergoing both types of procedure.

Restenosis rates after peripheral and coronary angioplasties have been assessed only in patients who had either peripheral angioplasty or coronary angioplasty but never in patients who had both types. Among the 6364 angioplasties performed in the authors' institution since 1980, they studied 38 patients (36 men, 2 women, mean age fifty-five years, range thirty-four to seventy-seven) who had both peripheral and coronary angioplasty. The peripheral angioplasties were most often performed on iliac artery stenoses. They were performed before coronary angioplasty in 22 patients (58%) and after coronary angioplasty in 16 patients (42%). The follow-up after peripheral angioplasty was based on clinical data; ultrasound investigation was performed when the result of the clinical follow-up was poor (maximal walking distance lower than 500 meters). Follow-up after coronary angioplasty was assessed by a systematic coronary angiography at six months and with long-term clinical follow-up. The mean durations of the follow-up after peripheral or coronary angioplasty were not significantly different (respectively fifty-six +/- eleven and forty-two +/- nine months [mean +/- 2 SEM]). No patient was lost to clinical follow-up; 17 (45%) ultrasound investigations, 12 (32%) peripheral angiographies, and 34 (89%) coronary angiographies were performed. The restenosis rate after peripheral angioplasty was 18% and that after coronary angioplasty was 34%. These rates are similar to the classic rates observed in the literature. In conclusion, as reported for either procedure alone, the restenosis rates after peripheral angioplasty and after coronary angioplasty are different when assessed in patients who undergo both types of angioplasty.

RF-transmitted CsI radio-isotopic ambulatory recorder for left ventricular ejection fraction monitoring.

We have developed a CsI multidetector probe in order to produce a nuclear ambulatory recorder to study simultaneously cardiac electric activity and the left ventricular ejection fraction. To make the device lighter, the electronics were designed with surface-mounted technology, and a serial data RF transmission system was used. The data are processed on a real-time basis using a portable microcomputer. Unlike other commercially available devices, this monitor avoids the problems of volume, weight, recording time capacity and slow off-line data processing. Our device permits global and regional analysis of the ejection fraction for a moderate manufacturing cost. It is intended primarily for ambulatory use and can easily be adapted to perform a monitoring function. The first tests on patients conducted using the prototype demonstrate the technical reliability and satisfactory operation of the device.

[Surgical treatment of hypertrophic cardiomyopathy; techniques, indications and results]. / Le traitement chirurgical des cardiomyopathies hypertrophiques; techniques, indications et résultats.

Many techniques have been proposed for the treatment of hypertrophic cardiomyopathy over the last 35 years: myotomy, septal myotomy-myectomy, isolated mitral valve replacement with a low profile prosthesis, cardiac transplantation. Usually, the patients referred for surgery are those who do not respond or are resistant to medical therapy (patients in NYHA classes III or IV). The usual indication for myomectomy is a significant subaortic gradient and major septal hypertrophy (> 18 mm). When mitral regurgitation is severe or organic, mitral valve replacement is associated. When septal hypertrophy is moderate (< 18 mm) or not evenly distributed, or after ineffective myomectomy, mitral valve replacement may be proposed. Cardiac transplantation is only considered when all medical and surgical possibilities have been exhausted. Analysis of the results of surgery (over 1,000 published cases) is hindered by the variability of the techniques employed, the indications and experience of the different groups. The operative mortality has significantly decreased (25% in the 1960s to 2 to 11% at present). The complications of myomectomy are mainly postoperative ventricular septal defects and atrioventricular block, some of which require implantation of a pacemaker. Peroperative transoesophageal echocardiography could help to reduce the operative risk even further. Surgery improves symptoms and increases exercise capacity. The benefits seem greater, more frequent and longer lasting than with medical therapy. Surgery should not, however, be considered to be curative as some patients remain at risk of developing symptoms related to physiopathological phenomena other than intraventricular obstruction (poor left ventricular filling, myocardial ischaemia, arrhythmias). Although some workers suggest improved survival, there have been no controlled trials on this subject.(ABSTRACT TRUNCATED AT 250 WORDS)