European Society of Cardiology quality indicators for the prevention and management of cancer therapy-related cardiovascular toxicity in cancer treatment.

AIMS: To develop quality indicators (QIs) for the evaluation of the prevention and management of cancer therapy-related cardiovascular toxicity. METHODS AND RESULTS: We followed the European Society of Cardiology (ESC) methodology for QI development which comprises (i) identifying the key domains of care for the prevention and management of cancer therapy-related cardiovascular toxicity in patients on cancer treatment, (ii) performing a systematic review of the literature to develop candidate QIs, and (iii) selecting of the final set of QIs using a modified Delphi process. Work was undertaken in parallel with the writing of the 2022 ESC Guidelines on Cardio-Oncology and in collaboration with the European Haematology Association, the European Society for Therapeutic Radiology and Oncology and the International Cardio-Oncology Society. In total, 5 main and 9 secondary QIs were selected across five domains of care: (i) Structural framework, (ii) Baseline cardiovascular risk assessment, (iii) Cancer therapy related cardiovascular toxicity, (iv) Predictors of outcomes, and (v) Monitoring of cardiovascular complications during cancer therapy. CONCLUSION: We present the ESC Cardio-Oncology QIs with their development process and provide an overview of the scientific rationale for their selection. These indicators are aimed at quantifying and improving the adherence to guideline-recommended clinical practice and improving patient outcomes.

Inflammation versus mechanical stretch biomarkers over time in acutely decompensated heart failure with reduced ejection fraction.

Heart failure can be associated with inflammation but it is unclear if inflammation is directly related to hemodynamic worsening or is an independent pathway. Our aim was to investigate inflammation and mechanical stress using serial measurements of biomarkers in acute and chronic heart failure with reduced ejection fraction (AHF and CHF). METHOD: The following biomarkers were measured on admission, at discharge and one month after discharge: B-type natriuretic peptide (BNP), high-sensitivity C-Reactive protein (hsCRP), Tumour Necrosis Factor alpha (TNFα), interleukin 6 (IL6), myeloperoxidase (MPO), suppression of tumorigenicity 2 (ST2), mid-regional pro-adrenomedullin (MR-proADM), galectin 3 (Gal3), Growth differentiating factor 15 (GDF15) and procalcitonin (PCT). RESULTS: In control CHF group (n=20, 69±11y, NYHA 1-2), most biomarker levels were low and stable over time. In AHF (n=55, 71±14y), BNP, ST2 and GDF15 levels were highly increased on admission and then decreased rapidly with clinical improvement; BNP, ST2 and GDF15 levels were statistically correlated (r=0.64, 0.46 and 0.39; p<0.001 for both). Both hsCRP, MPO, TNFα and Gal3 levels were increased in most AHF patients (70, 56, 83 and 98% respectively) with poor change over time. HsCRP, MPO and TNFα levels were correlated. IL6, MR-proADM and PCT levels were slightly increased, without change over time. Highest quartiles of BNP and ST2 were associated with death or readmission at one year (HR 2.33 [95CI 1.13-4.80] and 2.42 [1.27-4.60]). CONCLUSION: AHF is associated with systemic inflammation. This inflammatory response continued up to one month after discharge despite normalisation of mechanical stress-related markers.

Trends in death attributed to myocardial infarction, heart failure and pulmonary embolism in Europe and Canada over the last decade.

BACKGROUND: Worldwide, cardiovascular diseases and cancer account for ∼40% of deaths. Certain reports have shown a progressive decrease in mortality. Our main objective was to assess mortality trends related to myocardial infarction (MI), heart failure (HF) and pulmonary embolism (PE). METHODS: MI, HF and PE were studied as cause of death based on the analysis of death certificates in Canada (C), England and Wales (E), France (F) and Sweden (S). We also used a multiple cause approach. Age-standardized death rates (SDR) were calculated. RESULTS: The SDR for MI, HF or PE as the underlying cause of death, all decreased during the last decade. The decrease in SDR secondary to MI exceeded that for HF or PE. Concerning multiple cause of death, a greater decrease was also found for MI, compared with HF or PE. CONCLUSIONS: We confirm the beneficial trends in SDR with MI, HF or PE both as underlying or multiple causes in the studied countries. For HF and PE, multiple cause approach seems more accurate to describe the burden of these two pathologies. Our study also suggests that more efforts should be dedicated to HF and PE in order to achieve similar trends than in MI.

Use of tamoxifen in a German shepherd dog with sclerosing encapsulating peritonitis.

A German shepherd dog was diagnosed with sclerosing encapsulating peritonitis after an episode of peritonitis caused by a free intra-abdominal foreign body (stick). The foreign body had initially been treated by surgical removal and abdominal lavage. Postoperatively, peritoneal effusion persisted despite the use of methylprednisolone for 1 month and a second surgical exploration and abdominal lavage. After a third surgery at our institution (to breakdown abdominal adhesions) followed by open abdominal drainage, treatment with tamoxifen orally was initiated and within 2 weeks the dog's condition improved dramatically. Two months later, no fluid was present in the abdomen. The only apparent adverse reaction to tamoxifen therapy was swelling of the vulva. In humans, sclerosing encapsulating peritonitis is a known life-threatening complication following peritoneal dialysis. In veterinary medicine, most animals with sclerosing encapsulating peritonitis die because of chronic weight loss, peritoneal effusion and progression of concurrent disease. This dog's condition was unresponsive to methylprednisolone alone but was successfully treated with aggressive surgery including enterolysis and open abdominal lavage and the addition of tamoxifen.

[Diabetes and heart failure, a fatal association]. / Diabète et insuffisance cardiaque, une association morbide.

The prevalence of heart failure and diabetes are both increasing: 25 to 30% of patients with heart failure suffer from diabetes, and the latter aggravates heart failure. The presence of macro- or micro-angiopathy, cardiac neuropathy or renal failure worsens the clinical pattern and disturbs treatment strategies. Doppler-echocardiography and the dosage of BNP can probably help to detect and consequently to treat prematurely heart failure in the diabetic patient. The usual treatments in heart failure have similar or lower efficacy in the diabetic patient, and treatment intolerance is frequent. Treatments used for diabetes can be handled with difficulty in case of heart failure (metformin, glitazones). In the future, it is therefore extremely important: 1--to prevent the occurrence of diabetes in patients with glucose intolerance; 2--in diabetic patients, to prematurely detect cardiac dysfunction and optimally control diabetes, in order to avoid its occurrence; 3--and finally, in diabetic patients with heart failure, to optimize the medical treatment, in order that these patients have similar benefits compared to non-diabetic patients with heart failure. The ACE-inhibitors and angiotensin-2 antagonists seem to have an important role. Treatments breaking the glycation bridges, as well as statins, appear as interesting therapeutic options. Finally, the exact role of myocardial revascularization, either by angioplasty or surgery, might probably be important.

[Exercise training in cardiac patients: usefulness of the cardiopulmonary exercise test]. / Réadaptation des patients porteurs d'une cardiopathie: intérêt de la mesure des echanges gazeux a l'effort (VO2).

Exercise training is currently including in the treatment of coronary arterial disease patients, in patients with left ventricular dysfunction as well as in patients who underwent cardiac transplantation or cardiac surgery. However methods of prescribing exercise-training programs are difficult to determine and must be adapted for each patient Exercise test with gas analysis through the determination of anaerobic threshold may help to understand the physiopathological mechanism related to exercise limitation in these patients. Exercise test may help to precise exercise intensity during cardiac rehabilitation and may assess the benefits on exercise tolerance.

[Massive pulmonary embolism and stroke due to thrombus across the foramen ovale]. / Thrombus enclavé dans le foramen ovale responsable d'embolie pulmonaire et d'accident vasculaire cérébral.

We report the case of a man admitted for massive pulmonary embolism. Transthoracic echocardiography showed a serpentine thrombus in the right atrium across the foramen oval. Because of an acute worsening of the circulatory insufficiency, an intravenous thrombolysis was prescribed and the patient recovered progressively. An early control echocardiography showed the disappearing of the intracardiac thrombus and no evidence of abnormality of interatrial septum. While there was no evidence of venous thrombosis in legs, a renal cancer was diagnosed by echography. Silent stroke were highlighted at the scanner. This clinical case leads to discuss the origin of thrombus (in situ formation or thrombus migration) as well as the treatment (heparinotherapy, thrombolysis, surgical embolectomy, definitive closure of the foramen oval).

[Heart failure and cachexia]. / Insuffisance cardiaque et cachexie.

Cachexia is related to a malnutrition state related to hypercatabolism. Initially described in cancer, it is also related to several chronic diseases including heart failure. Defined by an unintentional weight loss exceeding 7.5% of body mass during more than 6 months, it is presented by the association of nutritional deficiencies, digestive and/or urinary losses as well as metabolic abnormalities causing fat and lean mass loss and is associated to a poor prognosis. The pathophysiology of cachexia and heart failure presented some similarities associating especially neuro-hormonal activation, a cortisol/DHEA ratio imbalance, as well as pro-inflammatory cytokines activation. Currently the treatment of cachexia is mainly preventive, based on ACE-inhibitors and beta-blockers therapy and physical reconditioning. The benefits of hormonal and nutritional substitutes remains to be evidenced.

[Heart insufficiency in the elderly]. / Insuffisance cardiaque du sujet âgé.

Congestive heart failure in the elderly differs from the one in the younger. The ageing of the cardiovascular system makes the organism weaker. When a myocardial infarction or an other cardiovascular disease happens, the occurrence of congestive heart failure is precipitated. The symptoms which are often misleading and the polypathologies make the assumption of relationship difficult between a symptom like dyspnea and congestive heart failure. Further examinations are limited because of the reduced physical performances in the elderly (stress test) or because of an increased risk of side-effects (coronary angiogram). The echocardiography has a central role in the exploration of congestive heart failure. The medical treatment has the same principles than in the younger but with cautions especially regarding the renal insufficiency and the multiple treatments that an elderly patient has.

[Brain natriuretic peptide (BNP) in coronary insufficiency: relationship with left ventricular filling and exercise tolerance]. / Brain natriuretic peptide (BNP) dans l'insuffisance cardiaque: relations avec le remplissage ventriculaire gauche et la tolérance à l'effort.

Brain natriuretic peptide (BNP) is a recently discovered peptide, secreted by the atria and ventricles in response to parietal distension. It was recently proposed as a screening test for left ventricular failure. The authors assayed this peptide at rest in 37 patients with chronic heart failure due to left ventricular systolic dysfunction and another 20 patients with various diseases (respiratory failure, cirrhosis, heart transplantation, "diastolic" heart failure) but normal left ventricular systolic function. A significant increase compared to normal values was observed not only in the group of heart failure patients, but also in patients with all other diseases. BNP was significantly higher in NYHA class IV patients. The relationship between plasma BNP levels and ejection fraction was not significant. On the other hand, a good correlation was observed between BNP and left ventricular filling parameters evaluated by cardiac Doppler: E wave deceleration time (r = -0.53, p = 0.001), E/A ratio: r = 0.57 p = 0.005) or VO2 max (r = -0.55, p < 0.005).

Study of muscular and ventricular function in dynamic cardiomyoplasty: a ten-year follow-up.

BACKGROUND: The basic physiologic principle underlying cardiomyoplasty is long-term electrostimulation of a latissimus dorsi muscle (LDM) wrapped around the heart to obtain a phasic activity that could be integrated with ventricular kinetics. The aim of cardiomyoplasty is to prolong survival and to improve the quality of life of patients with severe chronic and irreversible myocardial failure by improving systolic contraction and correcting diastolic dysfunction. METHODS: To evaluate the long-term outcome of cardiomyoplasty, we investigated 82 patients electively undergoing this procedure in-our hospital. All patients had severe chronic heart failure that did not respond to optimal medical treatment. Patients had a mean age of 50 +/- 12 years (84% males). The cause of heart failure was ischemic (55%), idiopathic cardiomyopathy (34%), ventricular tumor (6%), and other (5%). The mean follow-up was 4.3 years. RESULTS: The mean New York Heart Association functional class improved after operation from 3.2 to 1.8. Average radioisotopic left ventricular ejection fraction increased from 17% +/- 6% to 28% +/- 3% (p < 0.05). Stroke volume index increased from 35 +/- 9 to 46 +/- 8 ml/beat/m2 (p < 0.05). The heart size remained stable at long term (evaluated by echo and computed tomography scanning). After cardiomyoplasty the number of successive hospitalizations resulting from congestive heart failure was reduced to 0.4 hospitalizations/patient/year (before operation 2.5, p < 0.05). Computed tomography scans showed at long-term a preserved LDM structure in 82% of patients who underwent operation. Survival probability at 7 years was 54% for the totality of patients, and 66% for patients who underwent operation in New York Heart Association functional class 3. Five patients underwent heart transplantation after cardiomyoplasty (mean delay 29 months), principally as a result of the natural evolution of their underlying heart disease, without major technical difficulties. CONCLUSIONS: Our 10-year clinical experience demonstrates that cardiomyoplasty increases ejection fraction, improves functional class, and ameliorates quality of life. Ventricular volumes and diameters remain stable long term. LDM structure is maintained long term if electrostimulation is performed avoiding excessive myostimulation. Patient selection is the most important determinant for early and late outcome. Late death in patients undergoing cardiomyoplasty is principally due to sudden death. Our future aim is to incorporate a cardioverter-defibrillator in the cardiomyostimulator, thus improving long-term results. Cardiomyoplasty may delay or prevent end-stage heart failure and the need for heart transplantation.

Serial assessment of cardiopulmonary exercise capacity after cardiomyoplasty for either ischemic or idiopathic dilated cardiomyopathy.

Cardiomyoplasty is a surgical procedure aimed at assisting the left ventricle during ejection. We describe the long-term effects of cardiomyoplasty on peak exercise capacity, with serial assessments for up to 3 years after operation. Sixteen patients (12 in New York Heart Association class III and 4 in class IV) were enrolled. The mean left ventricular ejection fraction was 18 +/- 8%. Bicycle exercise tests with respiratory gas analysis were performed preoperatively and 6, 12, 18, 24, and 36 months after operation. Mean follow-up was 12 +/- 5 months (range 6 to 24). At 6 months, peak oxygen consumption and the ventilatory threshold were unchanged (from 17.8 +/- 5.8 to 15.8 +/- 5.3 ml/min/kg, and from 12.1 +/- 2.7 to 11.4 +/- 3.4 ml/min/kg, respectively). Ventilation at 50 W, viewed as an index of polypnea at submaximal exercise, was also unchanged. Serial assessment of exercise capacity thereafter showed no changes. However, ejection fraction tended to increase from 18 +/- 8% to 21 +/- 9% (p=0.08) and 14 patients reported an improvement in their functional status, resulting in a significant change in New York Heart Association functional class (3.3 +/- 0.5 to 2.2 +/- 0.4 at 6 months and 2.4 +/- 0.4 at the last visit, p <0.005) and improvement in quality-of-life scores. Thus, cardiomyoplasty does not appear to increase peak exercise capacity in the long term, despite an improvement in the left ventricular ejection fraction. Symptoms and quality of life, however, appear to improve. This may be related in part to an insufficient number of assisted systoles during exercise, persistent deconditioning, or changes in pulmonary mechanics.

Close association of the alpha subunits of Gq and G11 G proteins with actin filaments in WRK1 cells: relation to G protein-mediated phospholipase C activation.

A selective polyclonal antibody directed toward the C-terminal decapeptide common to the alpha subunits of Gq and G11 G proteins (G alpha q/G alpha 11) was prepared and used to investigate the subcellular distribution fo these proteins in WRK1 cells, a rat mammary tumor cell line. In immunoblots, the antibody recognized purified G alpha q and G alpha 11 proteins and labeled only two bands corresponding to these alpha subunits. Functional studies indicated that this antibody inhibited vasopressin- and guanosine 5'-[alpha-thio]triphosphate-sensitive phospholipase C activities. Immunofluorescence experiments done with this antibody revealed a filamentous labeling corresponding to intracytoplasmic and perimembranous actin-like filament structures. Colocalization of G alpha q/G alpha 11 and F-actin filaments (F-actin) was demonstrated by double-labeling experiments with anti-G alpha q/G alpha 11 and anti-actin antibodies. Immunoblot analysis of membrane, cytoskeletal, and F-actin-rich fractions confirmed the close association of G alpha q/G alpha 11 with actin. Large amounts of G alpha q/G alpha 11 were recovered in the desmin- and tubulin-free F-actin-rich fraction obtained by a double depolymerization-repolymerization cycle. Disorganization of F-actin filaments with cytochalasin D preserved G alpha q/G alpha 11 and F-actin colocalization but partially inhibited vasopressin- and fluoroaluminate-sensitive phospholipase C activity, suggesting that actin-associated G alpha q/G alpha 11 proteins play a role in signal transduction.

Prolonged kinetics of recovery of oxygen consumption after maximal graded exercise in patients with chronic heart failure. Analysis with gas exchange measurements and NMR spectroscopy.

BACKGROUND: Patients with chronic heart failure (CHF) often complain of prolonged dyspnea after exercise. The determinants of oxygen consumption after exercise in these patients are unknown. We hypothesized that the kinetics of oxygen consumption recovery after graded exercise was prolonged in parallel with the recovery of muscle energy stores, was not affected by the exercise level, and could be used to assess the circulatory response to exercise. METHODS AND RESULTS: Seventy-two patients with CHF in Weber's class A (n = 28), B (n = 21), and C/D (n = 23) and 13 healthy subjects performed maximal upright bicycle exercise with breath-by-breath respiratory gas analysis. Kinetics of recovery of ventilation (VE), oxygen consumption (VO2), and CO2 production (VCO2) after exercise were characterized by T1/2, the time to reach 50% of the peak value. T1/2 VO2 (seconds) increased with the severity of CHF (97 +/- 17 for CHF A [P < .05 versus CHF B, P < .05 versus CHF C/D], 119 +/- 22 for CHF B [P < .05 versus control subjects, P < .05 versus CHF A, and P < .05 versus CHF C/D], 155 +/- 55 for CHF C/D [P < .05 versus control subjects, P < .05 versus CHF A, and P < .05 versus CHF B] compared with 77 +/- 17 for control subjects). T1/2 VCO2 and T1/2 VE also increased similarly with the worsening of CHF. T1/2 VO2 was correlated negatively with peak VO2 (r = .65) and was reproducible (r = .96). To study the relation between T1/2 VO2 and the duration of exercise, 10 healthy subjects and 22 patients underwent a second graded test at 75% and/or 50% of peak workload. T1/2 VO2 was minimally shortened, at only 50% of peak workload (P = .02). Finally, 19 patients underwent 31P nuclear magnetic resonance spectroscopy of the anterior compartment of the leg during exercise; the half-time of recovery of the ratio of inorganic phosphate to creatine phosphate (T1/2 Pi/PCr), reflecting the level of involvement of oxidative metabolism in the restoration of energetic metabolites after exercise, was linearly correlated with the half-time of VO2 recovery (r = .70, P < .01). CONCLUSIONS: Postexercise T1/2 VO2 increases when CHF worsens, perhaps in part a result of slower kinetics of recovery of muscle energy stores. The time course of oxygen consumption recovery may represent a simple new criterion for measuring the impairment of the circulatory response to exercise in CHF, even submaximal exercise.

Immunological detection of prohormone convertases in two different proglucagon processing cell lines.

The distribution of the prohormone convertases, PC1/3, PC2 and PC5/6, was determined by immunoblotting in two cell lines. In alpha TC1-6 cells, the proglucagon processing occurred according to the pancreatic A-cell type. In STC-1 cells, proglucagon was processed in a manner reminiscent of the intestinal L-cell type. PC1/3 was undetectable in both proglucagon processing cell lines whereas PC2 displayed a strong immunostaining in the alpha TC1-6 cells and was barely detectable in the STC-1 cells. PC5/6 was detected as a 70 kDa protein in both cell lines. These results suggest a possible role of PC2 in the processing of proglucagon into glucagon in the A-cells, whereas in L-cells it would require still undetermined endoproteases.

Endopeptidase from rat liver membranes, which generates miniglucagon from glucagon.

An endopeptidase activity that cleaves glucagon, producing miniglucagon or glucagon (19-29), a Ca2+ pump inhibitory peptide, was isolated from rat liver membranes. The purified enzyme has a molecular mass of approximately 100 kDa and a pH optimum of approximately 8. It is inhibited by both sulfhydryl-blocking reagents and metal-chelating reagents and activated by thiol compounds. The partial N-terminal amino acid sequence of the 100-kDa protein does not correspond to any known protein. An antiserum was raised against a synthetic octapeptide corresponding to the N-terminal sequence. Immunoblot analysis of crude liver membranes revealed a single band at 100 kDa. Immunoreactivity was found in liver, pancreas, and heart, which are glucagon and miniglucagon target tissues, and in gastric mucosa and kidney. Low levels were detected in spleen, whereas immunoreactivity was undetectable in skeletal muscle and intestinal mucosa. The endopeptidase activity was inhibited by insulin, glucagon-like peptide-1, and glucagon-like peptide-1 (7-36) amide, whereas other peptides that contain dibasic sites had no effect on its activity, indicating that the endopeptidase does not display strict selectivity toward basic doublets.

[Multiparameter correlative study of respiratory gas exchange during exercise]. / Etude corrélative multiparamétrique des échanges gazeux respiratoires à l'effort.

Patients with chronic heart failure were evaluated simultaneously by conventional methods and by heart-lung exploration during exercise with the purpose of validating the latter method. Only 50 patients were evaluated on two occasions and therefore included in the correlative statistical study. In this study such data as NYHA classification, cardiothoracic ratio, ejection fraction, echocardiographic fibre shortening fraction and biochemical values (venous lactate, plasma noradrenaline levels) were compared with data obtained from evaluation during exercise, i.e. VO2 max, VO2 peak, anaerobic threshold, oxygen pulse, VCO2, O2 equivalent and respiratory quotient, alveolar ventilation per minute, duration and load of exercise. Very good correlation was found with the indices obtained from VO2 and in particular with the O2 pulse and the VO2 max percentage. Good correlation was also found with VCO2 and the O2 equivalent as well as with alveolar ventilation per minute. In contrast, the anaerobic threshold and respiratory quotient correlated poorly with the first set of data and therefore were disappointing. It appears from this study that the indices obtained from VO2 are highly representative of the heart-lung unit in patients with heart failure. It seems, however, that the muscular status of the patients plays a considerable role in their exercise capacity. We suggest that these indices should be used in clinical pharmacology studies.

[Neuroendocrine changes in chronic cardiac insufficiency]. / Modifications neuro-endocrines au cours de l'insuffisance cardiaque chronique.

Throughout the course of chronic congestive heart failure cardiac and peripheral compensatory mechanisms are at play, most of them under the influence of the neuroendocrine system. The reserves of heart rate and contractility are regulated essentially by the noradrenergic system (NAS), but this mechanism is partial and transient owing to the gradual decrease in the density and sensitivity of myocardial beta-adrenergic receptors induced by overstimulation. Adaptation of the heart to exercise may be reduced. This escape phenomenon is also observed with almost all cardiotonic drugs which interfere with cyclic adenosine monophosphate (cAMP), in contrast with the paradoxically favourable effects of beta-blockers in small doses or of drugs that are both agonists and antagonists of beta-adrenergic receptors. The mechanisms which contribute to the induction of left ventricular hypertrophy are imperfectly known. The noradrenergic system and the renin-angiotensin-aldosterone system (RAAS) are probably not the only ones involved. The setting in action of Frank-Sterling heterometric regulation, at first during exercise then permanently, requires an increase in filling pressure obtained by venous constriction (predominantly controlled by the NAS) and, mostly, by an increase in circulating blood volume. NAS and RAAS intervene in the kidneys to produce water-and-salt retention.(ABSTRACT TRUNCATED AT 250 WORDS)

[Evaluation of bidimensional echography in the etiological orientation of pericardial disease. Apropos of 39 anatomo-echographic comparisons]. / Evaluation de l'échographie bidimensionnelle dans l'orientation étiologique des maladies du péricarde. A propos de 39 confrontations anatomo-échographiques.

Echocardiography provides a firm diagnosis of pericardial effusion and evaluates its repercussions on the cardiac cavities. The images obtained with two-dimensional echocardiography are of such quality that the anatomical lesions can be analyzed, but the predictive value of this examination for the aetiological diagnosis has not yet been established. To investigate this point we have compared the images recorded in 39 episodes of pericardial disease with the corresponding anatomical data provided by surgery (n = 38)) or necropsy (n = 1) less than 48 hours after the ultrasonic examination. In one case, the purely solid nature of the pericardial content, suspected on the presence of an echo-filled cavity with adherent membranes, was confirmed at surgery. Conversely, the totally or partly liquid nature of the effusion was ascertained whenever the two pericardial membranes were separated by an echo-free cavity in at least one portion of the region examined, and there was no false-positive result (n = 38). The images obtained could be compared with the anatomical lesions in 28 out of 38 cases of partly or totally liquid pericarditis. The pericardial cavity was entirely echo-free in 12 of these cases, and this was confirmed by the anatomical examination, except in one case where epicardial nodules were found at surgery. Abnormal intrapericardial images were detected in the other 16 echocardiographic examinations, viz.: round masses in 2 cases, linear echoes in 2 cases and mattress-like deposits in 12 cases. In 9 of these 16 cases corresponding intrapericardial formations were discovered at surgery.(ABSTRACT TRUNCATED AT 250 WORDS)