Contemporary review on spontaneous coronary artery dissection: insights into the angiographic finding and differential diagnosis.

Spontaneous coronary artery dissection (SCAD), although in the majority of cases presents as an acute coronary syndrome (ACS), has different pathophysiology from atherosclerosis that influences specific angiography findings and enables most patients to be solved by optimal medical therapy rather than percutaneous coronary intervention (PCI). Therefore, accurate diagnosis is essential for adequate treatment of each patient as management of SCAD differs from that of ACS of atherosclerotic aetiology. So far, invasive coronary angiography remains the most important diagnostic tool in suspected SCAD. However, there are ambiguous cases that can mimic SCAD. In this review, the authors summarize current knowledge about the diagnostic algorithms, particularly angiographic features of SCAD, pitfalls of angiography, and the role of intracoronary imaging in the context of SCAD diagnosis. Finally, apart from the pathognomonic angiographic features of SCAD that are thoroughly discussed in this review, the authors focus on obscure angiography findings and findings that can mimic SCAD as well. Differential diagnosis and the timely recognition of SCAD are crucial as there are differences in the acute and long-term management of SCAD and other causes of ACS.

Control of the terminal step of intracellular membrane fusion by protein phosphatase 1.

Intracellular membrane fusion is crucial for the biogenesis and maintenance of cellular compartments, for vesicular traffic between them, and for exo- and endocytosis. Parts of the molecular machinery underlying this process have been identified, but most of these components operate in mutual recognition of the membranes. Here it is shown that protein phosphatase 1 (PP1) is essential for bilayer mixing, the last step of membrane fusion. PP1 was also identified in a complex that contained calmodulin, the second known factor implicated in the regulation of bilayer mixing. The PP1-calmodulin complex was required at multiple sites of intracellular trafficking; hence, PP1 may be a general factor controlling membrane bilayer mixing.

Influence of non-dipping pattern of blood pressure in gestational hypertension on maternal cardiac function, hemodynamics and intrauterine growth restriction.

BACKGROUND: An association between gestational hypertension (GH) and changes of maternal cardiac function was previously reported. AIM: The study assessed the effect of non-dipping pattern of blood pressure (BP) in GH on haemodynamic function and intrauterine growth restriction (IUGR). METHODS: This study included 126 women (91 with GH and 35 normotensive controls). Based on the BP values measured by ambulatory blood pressure monitoring (ABPM), all hypertensive women were classified in dipper (46 women) or in non-dipper group (45 women). All participants underwent echocardiography and ABPM during the third trimester. RESULTS: Participants with GH and non-dipping pattern had significantly lower velocity of longitudinal systolic function (s') (p<0.0005), and cardiac output index (COi) compared to dippers (p<0.0005) and controls (p=0.002). Diastolic velocities at the mitral valve annulus were also lower in non-dippers e's (non-dippers vs dippers p=0.023; non-dippers vs controls p<0.0005) and e'l (non-dippers vs dippers p=0.048; non-dippers vs controls p<0.0005). There were significant differences in the index of the left ventricle filling pressure E/e' and myocardial mass index between women with GH and controls, but with no significant difference among dippers and non-dippers. Total vascular resistance was increased in non-dipping group compared to normotensives and dippers (p<0.0005). Multivariate regression analysis revealed that the peak night-time diastolic BP, left ventricular mass index and CO index were identified as independent predictors of IUGR. CONCLUSION: Changes in maternal hemodynamics, as well as IUGR, are strongly related to the non-dipping pattern of BP.

Breast cancer survivorship symptom management: current perspective and future development.

Increasing numbers and longevity of cancer survivors has furthered our insight into the factors affecting their health outcomes, suggesting that multiple factors play a role (e.g., effects of cancer treatments and health behaviors). Emotional and physical symptoms may not always receive sufficient attention. In this short narrative review highlighting recent literature, we describe the most common physical and emotional symptoms of breast cancer survivors aged 50 years and older and outline a multidisciplinary symptom management approach, regardless of symptom etiology.

[Comparative analysis in the use of natural and artificial vascular grafts on hematologic characteristics in patients]. / Uporedna analiza efekata primene prirodnih i vestackih vaskularnih graftova na hematoloske karakteristike krvi i bolesnika.

Investigation of two groups of patients was performed. Both male and female patients, 34 to 69 years old, in which extracorporeal circulation was established in the course of open heart and ascendental aorta surgeries were included in the investigation. The first group consisted of 20 patients with surgically revascularized miokard by triple venous grafts, and the second included 20 patients with partial replacement of ascendental aorta using synthetic dacron graft. It was concluded that extracorporeal circulation leads to a significant decrease of platelet count and agreability after surgery, as well as decrease of red blood cell count and hemoglobin and hematocrit value. However, contact of circulating blood with the synthetic dacron graft surface, in surgical procedures on ascendental aorta, leads consequently to a significantly higher decrease of platelet count and agreability, with the significant decrease of red blood cell count and decrease of hemoglobin and hematocrit value. Based on the obtained results it is possible to plan requirements for allogenous blood/red blood cells which are significantly higher in patients undergoing partial replacement of ascendental aorta using artificial dacron graft compared with patients after surgical revascularization of miocard with triple venous graft.

Extent of oncological resection in laparoscopic vs. open colorectal surgery: meta-analysis.

BACKGROUND: Laparoscopy is not yet wide accepted in cancer colorectal surgery. This study investigated whether the extent of anatomical resection in laparoscopic colorectal surgery is equivalent to that in the open colorectal surgery. MATERIALS AND METHODS: We examined reports on the results of laparoscopic or open colorectal procedures published between 1990 and 1999 and selected 35 with data on lymph node count and distal margin clearance (total of 3935 patients). There were 16 comparative studies, 6 open series, and 13 laparoscopic series of patients. Several meta-analytic models were used to evaluate the difference between open and laparoscopic surgery, including multiple-outcome random-effects models that account for correlation between multiple-outcomes. RESULTS: More lymph nodes were extracted laparoscopically (0.3-2.14 lymph nodes more); however, only for the fixed-effects single-outcome model this difference was statistically significant. The average distal margin clearance was 4.6 cm with the laparoscopic approach and 5.3 with the open approach Accounting for random variation among the studies, the estimate of this difference obtained from meta-analysis was 0.64-1.19 cm, favoring the open approach; this difference was statistically significant. The estimated within-study correlation between lymph node count and distal margin clearance was 0.26 with the open and 0.19 with the laparoscopic procedure. The estimated within-study correlation between outcomes of laparoscopic and open procedures was 0.86 for the lymph node count and 0.96 for the distal margin clearance. CONCLUSIONS: This meta-analysis shows that laparoscopic approach is as adequate as the conventional approach. Estimates of difference between the two therapeutic options obtained from random-effects models were more precise than those from fixed-effects models.

[Interleukin-8 serum levels in patients with various types of open heart surgical procedures performed under extracorporeal circulation]. / Ispitivanje serumskih koncentracija interleukina-8 u bolesnika sa razlicitim vrstama hirurskih procedura na otvorenom srcu uz uspostavljen vantelesni krovotok.

Serum concentrations of proinflammatory cytokine interleukin-8 (IL-8) in 15 patients with surgically revascularized myocardium by triple venous cardiopulmonary bypass (CPB x 3) and in 10 patients with implanted artificial aortic valves (AV) were measured. Average IL-8 concentrations in (CPB x 3) patients and in those with artificial aortic valve were 7.3 +/- 11.6 pg/mL 24 hours before surgery, i.e. 3.3 +/- 3.4 pg/mL; six hours after surgical procedure 32.7 +/- 71.4 pg/mL, i.e. 8.9 +/- 9.9 pg/mL; and 24 hours after surgery 10.9 +/- 9.7 pg/mL, i.e. 8.3 +/- 4.6 pg/mL. Extracorporeal circulation (ECC) caused significant increase of IL-8 serum concentration in both investigated groups six hours after surgery. Comparing preoperative values of the both groups, as well as those of 6 and 24 hours after surgery, no significant values of IL-8 were found. Various types of open heart surgical procedures had no influence on the extent of the production and secretion of proinflammatory IL-8 cytokine measured in patients during 24 hours after surgery.

Hypogonadism precedes liver feminization in chronic alcohol-fed male rats.

Men who chronically abuse alcohol may display a spectrum of endocrine abnormalities including hypogonadism and feminization, with elevated serum estradiol and low serum testosterone. We examined factors that may result in disruption of hepatic sex hormone homeostasis in alcohol-fed male rats and possible consequences of such changes. Rats were fed alcohol-containing or isocaloric diets for 30, 60, and 90 days. In alcohol-fed rats, serum testosterone levels and hepatic activity of 2 androgen-dependent estrogen metabolizing enzymes were reduced (P <.05) at all times, as was activity of androgen receptor. There was also a significant early and progressive decrease in testes/body ratio in alcohol-fed rats. Compared with this early decrease in testosterone-related parameters, there was a significant increase in serum estrogen levels (at 30 and 90 days, 132% and 168% of control values, respectively). An increase in serum ceruloplasmin, an estrogen-responsive liver protein, was apparent at 60 and 90 days, but not at 30 days of alcohol exposure, suggesting that hypogonadism precedes liver feminization. Hepatic estrogen receptor activity was decreased in alcohol-fed rats at 60 and 90 days, the latter despite elevated serum estrogen levels. Hepatic aromatase was slightly increased in alcohol-fed rats, an elevation probably not sufficient to account for observed increases in serum estrogen. Taken together, these data suggest that (1) alcohol induces profound reduction of serum testosterone, resulting in loss of androgen-regulated hepatic functions such as estrogen-metabolizing enzyme activity and activity of androgen receptors; and (2) such alcohol-induced hypogonadism precedes changes in hepatic sex hormone homeostasis and subsequent feminization.

Downregulation of nuclear sex steroid receptor activity correlates with severity of alcoholic liver injury.

Chronic ethanol ingestion in rats and humans results in significant alterations in sex steroid levels and expression of sex hormone-dependent phenotype. In this study, we used the intragastric feeding model in male rats to determine hepatic sex hormone receptor activity under circumstances of chronic ethanol exposure and differing degrees of liver injury induced by type of dietary fat. Pathological analysis and quantitation of hepatic androgen receptor (AR) and estrogen receptor (ER) activity, serum sex hormones, and sex hormone-responsive protein and mRNA expression were performed. The activity of the physiologically relevant nuclear form of both AR and ER was significantly decreased with ethanol and correlated inversely with the severity of liver injury. Serum testosterone levels, as well as expression of an androgen-dependent hepatic mRNA, were decreased by ethanol and progressive liver injury. Serum estradiol increased with liver injury. We postulate that these changes in receptor activity may be due to the oxidative stress, reduced cellular energy, and/or altered cytokine milieu known to occur in this model.

Hepatic hyperplasia and cancer in rats: alterations in copper metabolism.

We previously demonstrated that rats exposed to the peroxisome proliferator (PP) diethylhexylphthalate (DEHP) had reduced serum ceruloplasmin (CP) oxidase activity, which suggests tissue copper deposition. Copper is highly toxic in excess, and results in cellular damage and hepatocellular carcinomas (HCC). This study addresses changes in expression of copper-related genes and metal accumulation in hyperplastic liver and tumors induced by PP. Male rats were fed diets containing DEHP or clofibrate (CLF) for 3-60 days (hyperplasia) and 4-chloro-6-(2,3 xylidino)-2-pyrimidinyl-thio(N-beta-hydroxyethyl) acetamide for 10 months (HCC). During hyperplasia, an immediate and progressive decrease in serum CP activity was observed (P < 0.05), as were reductions in mRNA levels for both CP and Wilson's disease gene (WD gene, a P-type ATPase) (P < 0.05). Tumor-bearing rats had lower serum CP activity (P < 0.05), and CP and WD gene mRNA levels were reduced in tumors (P < 0.05), and in liver surrounding tumors (SL) (P < 0.05). Metallothionein mRNA showed no consistent changes during hyperplasia. Tumors showed a 2.5-fold induction of metallothionein mRNA (P < 0.05), and a 1.2-fold increase in SL. Temporal increases in liver copper content occurred during hyperplasia, with increases of 2-fold (DEHP) and 3.3-fold (CLF) at 60 days (P < 0.05). Copper content was 2.2-fold higher in tumors (P < 0.05) and 1.7-fold higher in SL; iron did not increase and zinc decreased temporally. Thus, copper accumulation and changes in copper-related gene expression may be contributing factors in liver neoplasia in PP-treated rats. Loss of CP results in decreased free radical scavenger capacity and thus may enhance oxidative damage induced by PPs.