Should we try to determine the specific cause of cardiac tamponade?

INTRODUCTION: The causes of cardiac tamponade vary and it has been suggested that underlying causes should be sought in all cases. The purpose of this study was to determine the causes of cardiac tamponade in our environment, distinguishing between specific and idiopathic causes, and analyzing the proportion and causes in the subgroup of patients with relapsing tamponade. PATIENTS AND METHOD: We retrospectively studied all patients who underwent therapeutic pericardiocentesis between 1985 and 2001. The clinical and radiographic features and macroscopic characteristics of the pericardial fluid were analyzed. The final diagnosis in each patient was based on the clinical history, follow-up, pericardial fluid cytology, and pericardial biopsy, if available. RESULTS: Ninety-six patients were included (52 men/44 women), mean age 56.1 16.1 years. The cause of pericardial effusion was neoplasm in 50 patients (52.1%), 14 idiopathic pericarditis (14.6%), 12 renal failure (12.5%), 7 iatrogenic cases (7.3%), 4 mechanical tamponades (4.2%), 2 tuberculosis (2.1%), and 7 other causes (7.3%). Thirty-five patients had relapsing tamponade; only 2 of them had idiopathic pericarditis (5.7%). We found no significant differences in age, development time, extracted volume or fluid features between tamponade of specific or idiopathic origin. CONCLUSIONS: Most of the cardiac tamponades in our series had a specific cause. This made it necessary to identify a specific underlying cause in each case, especially in relapsing effusions. However, we did not find any variable suggestive of the cause of the disease.     

Thrombogenic and endothelial damage markers in patients with ischemic systolic impairment

INTRODUCTION: Anticoagulation is rarely indicated in patients with left ventricular dysfunction who show an increased risk for thromboembolism. In theory, the three arms of the Virchow' triad may be present: abnormal blood flow, endothelial damage and prothrombotic markers. The aim of this study was to identify the last two arms. PATIENTS AND METHOD: We studied 82 consecutive patients with demonstrated ischaemic heart disease and sinus rhythm, and compared them with a control group comprised of 32 healthy subjects matched for age and sex. None or the patients had had an acute coronary event or hemodynamic decompensation within the 3 months prior to inclusion in the study. The plasma concentration or von Willebrand factor and fibrin d-dimer and fibrinogen were determined as endothelial damage and prothrombotic markers, respectively. A fractional shortening less than 29% by echography was defined as ventricular systolic dysfunction. RESULTS: The patients showed significantly higher levels of von Willebrand factor with respect to the control group (109.2 31.9 vs 85.5 32.6%, p < 0.01), with no differences in fibrinogen and fibrin d-dimer values. Twenty-six patients fulfilled criteria of left ventricular systolic dysfunction. Patients with left ventricular dysfunction showed higher fibrinogen (386 118 vs 322 102 mg/dl, p = 0.03) and fibrin d-dimer (0.36 0.22 vs 0.26 0.10 g/ml; p = 0.04) levels, with no differences in von Willebrand factor levels. CONCLUSIONS: After acute coronary events, patients with ischaemic heart disease show markers of endothelial damage. However, patients with left ventricular dysfunction show a hypercoagulable state.     

Biventricular impairment of diastolic function in acromegaly

AIM: Left ventricle impairment is very common in acromegaly. Concentric hypertrophy and diastolic dysfunction are observed at an early stage. Late left ventricle dilatation with systolic dysfunction may appear. Few reports have studied right ventricle diastolic function. METHODS: Twenty-seven acromegalic patients were included. Biventricular diastolic function was assessed using Doppler-echocardiography. Possible associations with hormonal activity, evolution time of illness, hypertension, left ventricular hypertrophy and systolic impairment on echocardiography were studied. RESULTS: Fifteen patients showed left ventricular diastolic dysfunction, whereas thirteen patients showed right ventricular diastolic dysfunction. A good correlation was observed between E/A relation of both ventricles (r = 0.70; p < 0.01) and isovolumetric relaxation time (r = -0.60; p < 0.01). The right ventricular E/A relation correlated with left ventricular mass index and significance was almost achieved with the presence of hypertension. There was no statistical correlations between the right ventricular E/A relation and hormone values or evolution time of illness. The left ventricular E/A relation showed a significant association with left ventricular mass index, isovolumetric time index and evolution time of illness. There were no statistical association with hormone values. CONCLUSIONS: The high prevalence of right ventricular diastolic dysfunction observed in acromegaly suggests the presence of acromegalic myocardiopathy.     

The Influence of the growth hormone in the profile of blood pressure. Results in adult patients with deficiency in this hormone

INTRODUCTION AND OBJECTIVES: There is an increasing interest in the relationship between the growth hormone (GH) and the heart since the GH has an important inotropic effect and its use has been tested in patients with severe systolic dysfunction. However, cardiovascular diseases are the main cause of increased morbimortality observed in patients with acromegaly. Growth hormone deficiency has been related to different clinical findings depending on the age of onset. Recent studies have demonstrated that GH deficiency in adults is associated with alterations in blood pressure. The aim of our study was to assess the influence of GH in blood pressure. PATIENTS AND METHODS: We studied 14 adult patients with GH deficiency and 15 healthy subjects, matched for sex and age. The diagnosis of GH deficiency was based on GH response to intravenous insulin tolerance test < 5 ng/ml and IGF-1 levels lower than the normal limit for each age group. In all the patients 24-hour Holter blood pressure monitorization was performed in addition to a treadmill test and echographic evaluation. RESULTS: All patients showed normal systolic and diastolic function in the echocardiographic study. Only one patient had an increased left ventricular mass. Blood pressure was lower in the patients than in the control subjects (p < 0.05). Moreover, the difference remained significant when analysis was based on the time of day. However, the patients showed normal blood pressure response to the effort test with a mean increase of 60%. The length of the exercise on the treadmill test was shorter in the subgroup of GH deficient patients. CONCLUSIONS: Lower systolic blood pressure was observed in GH deficiency patients. The patients studied did not show structural heart alterations. Blood pressure and chronotrophic response to the effort test were similar in both groups.     

The osseous genioplasty

Despite its existence for nearly half a century and its versatility in solving a complex range of chin deformities, osseous genioplasty through an intraoral approach remains a rusty tool in many surgeons' armamentarium. The osseous genioplasty is not solely within the domain of the maxillofacial or craniofacial surgeon; it is well within the reach of any surgeon whose practice involves facial aesthetics. The surgeon who masters this relatively simple procedure can solve a broad range of chin deformities that an implant cannot solve: a chin that is too long, too short, or asymmetric.     

Caco-2 intestinal epithelial cells absorb soybean ferritin by mu2 (AP2)-dependent endocytosis

Iron deficiency, a condition currently affecting approximately 3 billion people, persists in the 21st century despite half a millennium of medical treatment. Soybean ferritin (SBFn), a large, stable protein nanocage around a mineral with hundreds of iron and oxygen atoms, is a source of nutritional iron with an unknown mechanism for intestinal absorption. Iron absorption from SBFn is insensitive to phytate, suggesting an absorption mechanism different from for the ferrous transport. Here, we investigated the mechanism of iron absorption from mineralized SBFn using Caco-2 cells (polarized in bicameral inserts) as an intestinal cell mode and analyzed binding, internalization and degradation with labeled SBFn ((131)I or fluorescent labels), confocal microscopy, and immunoanalyses to show: 1) saturable binding to the apical cell surface; dissociation constant of 7.75 +/- 0.88 nmol/L; 2) internalization of SBFn that was dependent on temperature, concentration, and time; 3) entrance of SBFn iron into the labile iron pool (calcein quenching); 4) degradation of the SBFn protein cage; and 5) assembly peptide 2 (AP2)-/clathrin-dependent endocytosis (sensitivity of SBFn uptake to hyperosmolarity, acidity, and RNA interference to the mu(2) subunit of AP2), and resistance to filipin, a caveolar endocytosis inhibitor. The results support a model of SBFn endocytosis through the apical cell membrane, followed by protein cage degradation, mineral reduction/dissolution, and iron entry to the cytosolic iron pool. The large number of iron atoms in SBFn makes iron transport across the cell membrane a much more efficient event for SBFn than for single iron atoms as heme or ferrous ions.