ISRN cardiology最新文献

Background. We evaluated the incidence of mortality and myocardial infarction (MI) in endovascular repair (EVAR) as compared to open aneurysm repair (OAR) in both elective and ruptured abdominal aortic aneurysm (AAA ) setting. Methods. We analyzed the rates of 30-day mortality, 30-day MI, and hospital length of stay (LOS) based on comparative observation and randomized control trials involving EVAR and OAR. Results. 41 trials compared EVAR to OAR with a total pooled population of 37,781 patients. Analysis of elective and ruptured AAA repair favored EVAR with respect to 30-day mortality with a pooled odds ratio of 0.19 (95% CI 0.17-0.20; I (2) = 88.9%; P < 0.001). There were a total of 1,835 30-day MI events reported in the EVAR group as compared to 2,483 events in the OAR group. The pooled odds ratio for elective AAA was 0.74 (95% CI 0.58-0.96; P = 0.02) in favor of EVAR. The average LOS was reduced by 296.75 hrs (95% CI 156.68-436.82 hrs; P < 0.001) in the EVAR population. Conclusions. EVAR has lower rates of 30-day mortality, 30-day MI, and LOS in both elective and ruptured AAA repair.

Background. Radiotherapy is commonly used to treat breast and thoracic cancers but it also causes delayed microvascular damage and increases the risk of cardiac mortality. Endothelial cell proliferation and revascularization are crucial to restore microvasculature damage and maintain function of the irradiated heart. We have therefore examined the potential of bone marrow-derived endothelial progenitor cells (BM-derived EPCs) for restoration of radiation-induced microvascular damage. Material & Methods. 16 Gy was delivered to the heart of adult C57BL/6 mice. Mice were injected with BM-derived EPCs, obtained from Eng(+/+) or Eng(+/-) mice, 16 weeks and 28 weeks after irradiation. Morphological damage was evaluated at 40 weeks in transplanted mice, relative to radiation only and age-matched controls. Results. Cardiac irradiation decreased microvascular density and increased endothelial damage in surviving capillaries (decrease alkaline phosphatase expression and increased von Willebrand factor). Microvascular damage was not diminished by treatment with BM-derived EPCs. However, BM-derived EPCs from both Eng(+/+) and Eng(+/-) mice diminished radiation-induced collagen deposition. Conclusion. Treatment with BM-derived EPCs did not restore radiation-induced microvascular damage but it did inhibit fibrosis. Endoglin deficiency did not impair this process.

Background. Transesophageal echocardiography (TEE) is used for the evaluation of the presence of left atrial appendage (LAA) thrombus prior to pulmonary vein isolation (PVI), while coronary computed tomography angiography (CCTA) is used for anatomic mapping during PVI. Methods. We compared the diagnostic performance of single phase CCTA to TEE in excluding the presence of LAA thrombus in patients undergoing PVI in 172 subjects performed during index hospitalization. Results. The mean age was 51 ± 13 years, a median CHADS2 score of 1 [IQR25,75 0,1, range 0-3] and a mean periprocedural INR of 2.1 ± 0.6. The prevalence of an LAA filling defect on single phase CCTA was 9.3% (6/183) and on TEE was 1.2% (2/183). Sensitivity, specificity, positive predictive value, and negative predictive value were 100% (95% CI, 19.8-100%), 91.8% (95% CI, 94-99%), 12.5% (95% CI, 60-76%), and 91.8% (95% CI, 97-100%) for the detection of LAA filling defect, respectively. Conclusion. Given the utility of a preprocedural single phase CCTA for the performance of PVI, the absence of a filling defect negates the need for a subsequent TEE as an adjunct for exclusion of LAA thrombus.

We aimed to evaluate the frequency, clinical profiles and outcomes of abdominal aortic aneurysms (AAA), and their association with coronary artery disease (CAD) in a small country with high cardiovascular burden. Methods. Data were collected for all adult patients who underwent abdominal computed tomography scans at Hamad General Hospital in Qatar between 2004 and 2008. Results. Out of 13,115 screened patients for various reasons, 61 patients (0.5%) had abdominal aneurysms. The majority of AAA patients were male (82%) with a mean age of 67 ± 12 years. The incidence of AAA substantially increased with age reaching up to 5% in patients >80 yrs. Hypertension was the most prevalent risk factor for AAA followed by smoking, dyslipidemia, renal impairment, and diabetes mellitus. CAD and peripheral arterial disease (PAD) were observed in 36% and 13% of AAA patients, respectively. There were no significant correlations between CAD or PAD and site and size of AAA. Conclusion. This is the largest study in our region that describes the epidemiology of AAA with concomitant CAD. As the mortality rate is quite high in this high risk population, routine screening for AAA in CAD patients and vice versa needs further studies for proper risk stratification.

Objectives. The aim of this study was to investigate the occurrence of myocardial injury in critically ill children through assessment of cardiac troponin T levels and whether levels are associated with disease severity and myocardial dysfunction measured by echocardiography. Methods. Over a 6-month period, this case control study included 50 patients admitted to Pediatric Intensive Care Unit of Zagazig University Children's Hospital. Twenty-five healthy children were included as a control group. Demographic and clinical data including the pediatric index of mortality II score were recorded. Echocardiographic examination was done and level of cardiac troponin T was measured using Elecsys Troponin T STAT Immunoassay. Results. Cardiac troponin T levels were significantly higher in critically ill in comparison to healthy children (median 22 (18-28) pg/mL versus 10 (10-10) pg/mL, P < 0.05). Cardiac troponin T levels correlated positively with duration of ventilation as well as with disease severity and correlated negatively with left ventricular fractional shortening. Moreover, cardiac troponin T levels were significantly higher in nonsurvivors when compared to survivors (median 34.5 (27.5-41.5) pg/mL versus 20 (18-24) pg/mL, P < 0.05). Conclusion. In critically ill children, cardiac troponin T levels were elevated and were associated with duration of ventilation and disease severity.

In an experimental model of atherogenesis induced by hyperfibrinogenemia (HF), the pharmacological response of vitamin E was studied in order to assess its antioxidant effect on the mitochondrial morphofunctional alterations in aortic smooth muscle cells. Three groups of male rats were used: (Ctr) control, (AI) atherogenesis induced for 120 days, and (AIE) atherogenesis induced for 120 days and treated with vitamin E. HF was induced by adrenalin injection (0.1 mg/day/rat) for 120 days. AIE group was treated with the administration of 3.42 mg/day/rat of vitamin E for 105 days after the first induction. Mitochondria morphology was analyzed by electronic microscopy (EM) and mitochondrial complexes (MC) by spectrophotometry. In group AI the total and mean number of mitochondria reduced significantly, the intermembranous matrix increased, and swelling was observed with respect to Ctr and AIE (P < 0.01). These damages were related to a significant decrease in the activity of citrate synthase and complexes I, II, III, and IV in group AI in comparison to Ctr (P < 0.001). Similar behavior was presented by group AI compared to AIE (P < 0.001). These results show that vitamin E produces a significative regression of inflammatory and oxidative stress process and it resolved the morphofunctional mitochondrial alterations in this experimental model of atherogenic disease.

Objectives. Assess the impact of associating thrombolytics, anticoagulants, antiplatelets, and primary angioplasty (PA) on death, reinfarction (AMI), and major bleeding (MB) in STEMI therapy. Methods. Medline search was performed to identify randomized trials comparing these classes in STEMI treatment, at least 500 patients, providing death, AMI, and MB rates. Similar arms were grouped. Correlation between number of drugs and PA and the outcomes was evaluated, as well as correlation between the year of the study and the outcomes. Results. Fifty-nine papers remained after exclusions. 404.556 patients were divided into 35 groups of arms. There was correlation between the number of drugs and rates of death (r = -0.466, P = 0.005) and MB (r = 0.403, P = 0.016), confirmed by multivariate regression. This model also showed that PA is associated with lower mortality and increased MB. Year and period of publication correlated with the outcomes: death (r = -0.380, P < 0.001), MB (r = 0.212, P = 0.014), and AMI (r = -0.231, P = 0.009). Conclusion. The increasing complexity of STEMI treatment has resulted in significant reduction in mortality along with increased rates of MB. Overall, however, the benefits of treatment outweigh the associated risks of MB.

International guidelines recommend ICD implantation in patients with severe left ventricular dysfunction of any origin only after careful optimization of medical therapy. Indeed, major randomized clinical trials suggest that suboptimal use of fundamental drugs, such as ACE inhibitors (ACE-i) and beta-blockers, may affect ICD shock-free survival, sudden cardiac death (SCD), and overall mortality. While solid evidence in favour of pharmacological therapy based on ACE-i with or without beta-blockers is available, data on SCD in HF patients treated with angiotensin receptor blockers (ARBs) are limited. The present paper systematically analyses the impact of ARBs on SCD in HF and reviews the contributory role of the renin-angiotensin system (RAS) to the establishment of arrhythmic substrates. The following hypothesis is supported: (1) the RAS is a critical component of the electrical remodelling of the failing myocardium, (2) RAS blockade reduces the risk of SCD, and (3) ARBs represent a powerful tool to improve overall survival and possibly reduce the risk of SCD provided that high doses are employed to achieve optimal AT1-receptor blockade.

The pericardium plays an important role in optimizing cardiac motion and chamber pressures and serves as a barrier to pathology. In addition to pericardial anatomy and function, this review article covers a variety of pericardial conditions, with mention of potential pitfalls encountered during interpretation of diagnostic imaging. Normal and abnormal appearance of pericardium on CT and MR imaging is emphasized, including dynamic imaging correlates of pericardial pathophysiology.

Objectives. Doxapram hydrochloride is a respiratory stimulant that has an inhibitory effect on myocardial IK1 potassium channels and is thought to increase membrane instability and excitability in myocardial cells. We examined the arrhythmogenic effects of doxapram hydrochloride in a rat model of halothane adrenaline-induced arrhythmia. Methods. Thirteen female Wistar rats (12-14 weeks old) were used in the study. Animals were anesthetized with inhalation of halothane to permit observation of the effects of doxapram hydrochloride on halothane adrenaline-induced arrhythmia. Time-dependent changes in ECG repolarization characteristics (QT, QTc, JTp, JT, and Tp-e intervals) were studied. Results. Doxapram hydrochloride itself did not induce arrhythmia but did induce bidirectional ventricular tachycardia after addition of adrenaline. Conclusion. Drug-induced impairment of intracellular Ca(2+) regulation caused BVT in the absence of genetic abnormalities in proteins in the sarcoplasmic reticulum.