The E/e filling index and right ventricular pressure in relation to applied international Doppler recommendations of left ventricular filling assessment.

AIM: A ratio>15 between the early diastolic pulsed Doppler velocities of the mitral inflow (E) and the basal left ventricular (LV) tissue (e) has been demonstrated to predict an elevated LV filling pressure (FP). An elevated LVFP implies an elevated right ventricular pressure (RVp). In order to investigate the sensitivity of the E/e filling index, we compared E/e and RVp, in their ability to identify a Doppler-assumed elevation of LVFP. METHODS AND RESULTS: Application of pulsed Doppler international recommendations grouped 134 patients with acute coronary syndromes (ACS) and 50 age- and sex-matched controls, according to LV filling: normal; delayed relaxation; an isolated pathological mitral-pulmonary venous-A-wave-duration difference; pseudo normal; or a restrictive filling pattern. An E/e>15 and an RVp>30 mmHg showed the following (%) sensitivity (32/94), specificity (95/76), positive (68/59), and negative (80/97) predictive values of a Doppler-assumed elevation of LVFP, in terms of either a pseudo normal or a restrictive filling pattern. CONCLUSION: The low sensitivity of E/e to detect a Doppler-assumed elevation of LVFP could limit its clinical usefulness as a single variable, in ACS. The high sensitivity and negative predictive value of RVp support its use as an additional LV filling variable in these patients.     

Can the left ventricular early diastolic tissue-to-blood time interval be used to identify a normal pulmonary capillary wedge pressure?

The pulsed Doppler early diastolic left ventricular (LV) tissue (e)-blood (E) onset temporal relationship (e-E) is suggested to predict pulmonary capillary wedge pressure (PCWP), through the formulas: tau = 32 + 0.7(e-E) and PCWP = LV end-systolic pressure x e(-IVRT/tau). Small changes/errors in E could influence the quotient IVRT/tau by oppositely affecting IVRT and e-E. At rest in 50 healthy individuals we noted: e-E: 2 +/- 14 ms; IVRT: 89 +/- 17 ms; calculated tau: 33 +/- 10 ms; and PCWP: 9 +/- 9 mmHg (> 12 mmHg in 28%). Non-pharmacological preload alterations in 14 individuals rendered an intraindividual 'PCWP'-fluctuation of up to 40 mmHg. This application may therefore not be clinically robust.     

Acute renal failure after a holiday in the tropics

A 20-year-old, previously healthy woman, presented with high fever, headache and myalgia 3 days after her return from a holiday in Southeast Asia. Laboratory data on admission demonstrated a pronounced increase in plasma creatinine, marked thrombocytopenia and moderately elevated liver aminotransferases. After having ruled out malaria, dengue fever was primarily suspected and supportive intravenous fluid therapy was initiated. Still, 1 day after admission, platelet counts dropped even further and she became anuric although she did not appear hypovolemic. On day 2 after admission, urine production commenced spontaneously and the patient slowly recovered. All laboratory test results had returned to normal approximately 2 months later. Serological analysis for dengue fever was negative. It turned out that the patient had been trekking in the jungle while in Thailand and we, therefore, analyzed serology for Leptospira spirochetes which was clearly positive. The patient was diagnosed with leptospirosis which is a serious condition associated with a high mortality when complicated by acute renal failure. Differential diagnoses in patients with acute renal failure and tropical infections are reviewed. The importance of early recognition of leptospirosis, and prompt treatment with antibiotics in suspected cases, is emphasized.     

Herbicide poisoning: A diagnostic challenge

Despite widespread availability, reports of herbicide poisoning from India are not common. Diagnosis is often difficult in the absence of proper history, non-specific clinical features and lack of diagnostic tests. A case of Paraquat poisoning is reported where diagnosis could be established only after the recovery of the patient. The literature is reviewed.     

Association between Level of Tumor Markers and Development of VTE in Patients with Pancreatic,Colorectal and Ovarian Ca: Retrospective Case- Control Study in Two Community Hospitals

The risk of venous thromboembolism (VTE) is increased in patients with cancer. However, the role of tumor markers as potential indicators of increased risk of VTE is still undetermined. In this retrospective observational case control study, levels of the tumor markers CEA, CA 19–9 and CA 125 in patients with colorectal, pancreatic, and ovarian cancer respectively, who were admitted to two community hospitals between January 2001 and December 2011, were compared between patients who were VTE positive and those who were VTE negative. The primary goal of this study was to determine whether VTE positive cancer patients had higher tumor marker levels compared to VTE negative cancer patients. In our study, 66.7% (48/72) of patients who were positive for VTE had elevated tumor markers while 65.3% (66/101) of patients who were negative for VTE had low (normal) tumor markers, indicating an association of high tumor marker levels with the diagnosis of VTE. This was statistically significant with an odds ratio of 3.77 and p-value of <0.0001 (95% CI of 1.99–7.14). When the VTE group was further divided into DVT and PE groups, 70.2% (40/57) of patients in the DVT positive group had high tumor markers with a p value of <0.0001 and an odds ratio of 3.99 (95% CI of 2.02 to 7.89) while 57.9% (11/19) of patients in pulmonary embolism positive group had high tumor markers; this was, however, not statistically significant (p-value of 0.35 and a CI of 0.59 to 4.10). In this retrospective study of 173 individuals with a diagnosis of either colorectal, pancreatic, or ovarian Cancer, higher tumor marker levels (CEA, CA 19–9, and CA 125 respectively) were associated with an increased risk of VTE, either DVT or PE. However, when further divided into either DVT or PE groups, the association remained statistically significant only for DVT but not for PE.     

Perturbed medullary tubulogenesis in neonatal rat exposed to renin-angiotensin system inhibition.

BACKGROUND: Pharmacological interruption of the angiotensin II type-1 receptor (AT(1)) signalling during nephrogenesis in rats induces irreversible abnormalities in kidney morphology, comprising papillary atrophy and tubulointerstitial damage, which are characterized by tubular dilatation/atrophy and interstitial inflammation/fibrosis. This study determined the time course for development of tubular structural and inflammatory changes and possible cytokine production in the renal medulla of newborn rats exposed to angiotensin-converting enzyme (ACE) inhibition. Additionally, medullary expression of E-cadherin, a marker for tubular formation, was investigated in ACE-inhibited rats. METHODS: Newborn rats were exposed (postnatal days 0-12) to ACE inhibitor enalapril and killed at days 1, 2, 4, 9 and 13. One kidney was used for morphological evaluation and the other for immunohistochemistry, using antibodies directed against monocytes/macrophages, T cells and E-cadherin on frozen sections. In a separate experiment, rats were treated for 9 days and had their kidneys processed for western immunoblot and immunohistochemistry, where antibodies directed against monocyte chemoattractant protein-1 (MCP-1) and tumour necrosis factor-alpha (TNF-alpha) were used on paraffin sections. RESULTS: In renal medulla from enalapril-treated rats, volume fractions of tubular lumens and interstitium were increased from postnatal days 2 and 4, respectively, while that of tubular cells was decreased from 4 days of age. Concomitant loss and/or reduction in E-cadherin expression (from day 2) was observed in dilated medullary tubules of enalapril-treated rats. Furthermore, in the medulla of enalapril-treated rats, the increased number of ED2+ (resident macrophages) cells, followed by the increase in ED1+ (monocytes/macrophages) and CD4+ T cells, was observed at days 9 and 13, respectively. This was accompanied by increased medullary expression of TNF-alpha at day 9. CONCLUSIONS: Neonatal ACE inhibition perturbs medullary tubulogenesis, as indicated by tubular dilatation and a lack of E-cadherin expression in these tubules. Macrophage/monocyte-mediated immune response is a secondary event, coincidentally associated with the up-regulation of TNF-alpha.