Articles

Permanent pacemaker implantation is conventionally done via upper limb veins. But in 1% - 6% cases, usual sub clavicular approach is either not possible or contraindicated due to complete occlusion of superior vena cava (SVC) or bilateral subclavian vein and/or bilateral implant site infection or thin skin [1]. Alternative approaches are warranted, including leadless pacemaker or complex lead extraction techniques, before considering surgical epicardial lead placement as a last resort because it has own hazards. We report a patient with complete heart block, total SVC obstruction, and a previously implanted malfunctioning epicardial lead presenting with pacemaker end of life. In view of exhaustion of the surgical option and in a resource constrained situation for lead extraction or leadless pacemaker, transiliac endocardial pacemaker implantation was done and a repeat surgery was averted. Learning objective: Complete venous occlusion is not very often encountered after pacemaker/ICD implantation. Apart from the risk of general anesthesia and invasive surgery, epicardial leads increase battery drain, and have a shorter operating life compared to an endocardial lead. The sparingly utilized iliac venous approach for permanent pacemaker implantation is a valuable, safe and minimally invasive alternative, when the conventional percutaneous access is unavailable, and surgery is undesirable or not possible. 

A 60-year-old female patient presented with typical anginal pain on exertion and relieved by rest for about one month. Percutaneous coronary angiography was done and showed an abnormal left circumflex coronary artery connecting to intercostal artery. Embolization of that abnormal connection was done successfully and the patient discharged from hospital after 24 hours. This case shows a new form of coronary steal syndrome. This cause could be missed if not put under the differential diagnosis of typical anginal pain with normal coronary arteries.

Background: Inflammation is associated with enhanced cardiovascular risk profile and increased cardiovascular mortality in end-stage kidney disease patients undergoing hemodialysis. Mechanisms of activated acute phase reaction in patients on chronic hemodialysis remain to be identified. As successful treatment of the inflammatory condition in these patients may improve long-term survival, we studied potential changes in different inflammatory biomarkers of cardiovascular risk in end-stage kidney disease patients after a mid-week hemodialysis session. Methods: Inflammatory biomarkers of cardiovascular risk (cystatin-C, homocysteine, C-reactive protein, procalcitonin, pentraxin-3, serum amyloid-A) and atherogenic plasma lipoproteins (Lipoprotein(a), cholesterol low and high density lipoproteins) were studied in 21 end-stage kidney disease patients previously and after a mid-week hemodialysis session. Results: We found a significant reduction in serum levels of low molecular weight molecules: cystatin-C (5.56 to 1.85 mg/L, 66.73%, p < 0.001), homocysteine (22.85 to 13.25 µmol/L, 42.01%, p < 0.001) and procalcitonin (0.788 to 0.457 ng/mL, 42.01%, p < 0.001). Large molecules as C-reactive protein (9.70 to 9.90 mg/L, 2.06%, p = 0.022) and pentraxin-3 (1.67 to 4.28 ng/mL, 156%, p < 0.001) increased, but serum amyloid-A decreased (15.90 to 12.70 mg/L, 20.13%, p < 0.05). There was no change in Lipoprotein (a) levels. Conclusion: Pentraxin-3 was a more specific inflammatory vascular marker than C-reactive protein, and the best inflammatory marker associated with hemodialysis. Homocysteine, procalcitonin and the other small proteins could be released and removed during hemodialysis session. Further studies are needed to understand the behavior and significance of these markers after successive hemodialysis.

We hypothesize that, with elevated cerebral spinal fluid (CSF) pressure, cerebral micro-vascular obstruction and congestion may occur despite (subdural) large-vein pressures being normal. Smaller veins emptying into these larger, dura-enveloped veins are not immune to the compressive effects of elevated CSF pressure and a “Starling Resistor” mechanism might explain why elevated CSF pressures collapse these smaller veins. This small cerebral venous starling resistor compression mechanism may be the final common pathway for many patients suffering from increased CSF pressures and might also be an important contributor to impaired focal venous drainage presenting as a headache with normal venous sinus pressures.

Purpose: This was a prospective study conducted at Benha University hospital and National Heart Institute on one hundred patients undwent coronary artery bypass grafting (CABG) to evaluate the effect of CABG on the right ventricular (RV) function using speckle tracking echocardiography (STE). Methods: All cases were subjected to detailed medical history, full physical examination, 12 leads electrocardiogram (ECG), routine laboratory tests including (complete blood picture, liver functions, renal functions and lipid profile) and echocardiography either conventional echocardiography or STE, all parameters obtained before and within 2 weeks after surgery. Results: By conventional echocardiography there was statistically significant decrease in peak right ventricle systolic velociy (RVS) from (12.76 ± 1.72) to (7.33 ± 1.71) and tricuspid annular plane systolic excursion (TAPSE) from (22.8 ± 3.99) to (13.77 ± 4.63) among the studied patients after CABG. While there was significant increase in right ventricle fractional area change (RVFAC) from (44.69 ± 3.25) to (49.01 ± 3.36). On the other hand, there was non-significant change in right ventricle end diastolic diameter (RVEDD) at mid-cavity from (26.37 ± 2.72) to (26.53 ± 2.72) and basal segment from (36.05 ± 2.98) to (36.29 ± 3.04), right ventricle stroke volume (RVSV) from (65.44 ± 7.02) to (65.85 ± 6.86) and right myocardial performance index (RMPI) from (0.491 ± 0.088) to (0.498 ± 0.086). By STE There was statistically significant decrease in right ventricle global longitudinal strain (RVGLS) from (-20.63 to -14.1) after CABG. There was statistically significant decrease in right ventricle free wall longitudinal strain [apical decreased from (-23.73 to -13.7), mid-cavity decreased from (-25.76 to -11.53), basal decreased from (-20.39 to -10.13) and lateral wall declined from (-23.01 to -9.13)]. There was statistically significant decrease in interventricular septum longitudinal strain [apical decreased from (-19.77 to -10.06), mid-cavity decreased from (-17.81 to -10.87) and basal decreased from (-15.89 to -11.13)]. There was statistically significant increase in RV circumferential strain of lateral free wall from (-12.04 to -16.21), while there was non-significant change in RV circumferential strain of septum from (-19.77 ± 4.86) to (-20.37 ± 5.14). Conclusion: Distorted RV geometry after CABG can lead to altered deformation parameters, in other words longitudinal functional parameters may underestimate RV function and the decrease in RVGLS was compensated by increase in circumferential strain of lateral free wall of RV without change in RVSV or RMPI. Therefor changes in deformation parameters should always be interpreted in relation to change in geometry.

A 56-year-old man was admitted to our hospital because of sudden onset of right-sided thoracic pain. The ECG showed inferior ST segment elevations. He has been treated with aspirin, clopidogrel, unfractionated heparin and tenecteplase, and his symptoms resolved after 30 minutes. About half an hour later, the patient developed again left-sided thoracic pain and the signs of an anterior myocardial ST-segment elevation infarction. 90 minutes after receiving the initial medications, the performed coronary angiography revealed a long dissection of a large ramus circumflexus. Furthermore, the left anterior descending coronary artery was occluded at about the mid-level. The left ventriculography showed a reduced ventricular function and a Stanford type A aortic dissection. Immediate patient transfer for emergency surgical intervention was arranged. However, ventricular fibrillation occurred during transport and he required endotracheal intubation and prolonged cardiopulmonary resuscitation. Unfortunately, he died during further transport. In a patient with massive thoracic pain of initially uncommon localization in combination with fluctuation of ST-segment elevations, aortic dissection should be seriously taken into the differential diagnosis as well as into therapeutic management decisions (in particular antiplatelet and thrombolytic therapy).

Background: Adoption of the Lung Allocation Score (LAS) has led to increased listing of older patients and those with idiopathic pulmonary fibrosis (IPF) for lung transplantation (LTX). Older patients and those with IPF have higher prevalence of coronary artery disease (CAD), a relative contraindication for LTX. The impact of the LAS on CAD prevalence and cardiovascular morbidity in LTX recipients is unknown. Methods: Retrospective review of single institution database from January 2000 to December 2010. Patients with and without CAD were compared by age, gender, LAS, single vs double LTX, and transplant indication. Survival was calculated by Kaplan-Meier method, and statistical significance determined by log-rank method. Survival analysis was performed on all patients and by 3:1 propensity matching. Differences in CAD, gender, and indication were determined by Chi-squared test. Differences in LAS and age were calculated with a two-tailed t - test. Results: In the pre-LAS era, 6.2% (9/145) recipients had CAD vs. 9.2% (17/184) in the post-LAS era (p = 0.411). Among all patients, recipients with CAD had a worse long term survival as estimated by Kaplan-Meier method (p = 0.001), although there was no statistically significant difference after propensity matching ((p = 0.14). Although more recipients in the post-LAS era had a diagnosis of IPF [15/145 vs. 71/184 patients, (p < 0.001)], there was no difference in the prevalence of CAD in the IPF cohort compared to others. There were no differences in cardiovascular deaths among recipients with CAD, with IPF, or in the post-LAS era. Patients with a pre-transplant diagnosis of CAD had an descreased risk of new onset postoperative atrial fibrillation (AF) (p = 0.007; HR:0.133; CI:0.030-0.583). Conclusion: Adoption of the LAS was not associated with a significant change in proportion of recipients with CAD who underwent LTX at our institution, despite an increase in recipients with IPF. Recipients with CAD had a higher risk of developing new postoperative AF and worse survival than patients without CAD. Differences in survival, however, could not be attributed directly to CAD based on propensity matched analysis

Objectives: Cardioembolic etiology is a frequent source of ischemic stroke. Echocardiogram is the mainstay of cardioembolic source detection with regard to plan secondary stroke management, however it remains unclear how often clinically actionable findings are provided hereby. In addition, it is uncertain whether echocardiography should be performed transthoracic or transesophageal (TEE). In a monocenter study, we evaluated the frequency of pathological findings from TEE evaluation in patients with ischemic stroke with suspected cardioembolic and cryptogenic source and determined whether there was an associated adjustment in the prescribed administration of antithrombotic therapy. Materials and Methods: Over a 21-month period (2012-2013), we enrolled 143 patients in a prospective monocenter study (mean age ± standard deviation, 70 ± 12 years; females, 44.1%) who were admitted to the Department of Neurology at the University of Lübeck due to ischemic stroke and who underwent TEE due to supposed cardiac embolism. We assessed the presence of atrial fibrillation; days from admission to TEE; and TEE findings, including atrial septal aneurysm, thrombogenic aortic arch, valve failure, presence of left atrial thrombus, and patent foramen ovale. Demografic information and medical history were drawn from patient records and the hospital information system. Results: On average, TEE was performed 4 days after admission to the hospital. Left atrial thrombus was detected in 3 patients (2.1%), patent foramen ovale (PFO) in 27 (18.9%), atrial septum aneurysm in 17 (11.9%), and thrombogenic aortic arch in 29 (20.3%). Findings from TEE were commonly associated with therapeutic adjustment; antiplatelet therapy increased from 30.1% to 80.4%, oral anticoagulation therapy increased from 2.8% to 27.3%. Conclusion: Findings from TEE for the evaluation of ischemic stroke lead to frequent adjustment of prior antithrombotic therapy, antiplatelet as well as anticoagulation.

Wegener’s granulomatosis is a systemic granulomatous focus on small to medium sized vessels. It typically affects sinuses, lungs and kidneys due to necrotizing granulomatous vasculitis. Less commonly, cardiac involvement is reported up to 8%-44% of cases [1-3]. It often rises to supraventricular arrhythmia, left ventricular systolic dysfunction, pericarditis, myocarditis, and valvulitis [4,5]. Cardiac conducting tissue involvement is rare and associated with increased mortality. It was only reported in fourteen previous cases, some of them were reversible to medical treatment [6]. 

Idiopathic Pulmonary Fibrosis (IPF) is a chronic and progressive disease without treatment that leads to death. Therefore, to control its progression to pulmonary hypertension is still a challenge. Moreover, there is no study that has investigated the Renin-Angiotensin System in patients with IPF. Objective: Verify the plasma concentrations of Angiotensin I, Angiotensin II (AngII), Angiotensin-(1-7) [Ang- (1-7)] and Alamandine in patients with IPF. Methods: Ten IPF patients, with or without PH, were included, and ten controls matched by sex and age. Quantitative plasma peptide concentrations (PPC) were expressed as mean and standard deviation or median and interquartile range. The Student Newman-Keuls t test was used for parametric data, Mann-Whitney for nonparametric data and, to compare proportions, the Fisher exact test was performed. The associations between clinical variables and the PPC were evaluated by Pearson or Spearman correlation coefficients. A p ≤ 0.05 was considered statistically significant. Results: The Alamandine plasma concentration was significantly (365%) lower in the IPF group and positively associated (r = 0.876) with pulmonary artery pressure (PAP). In addition, only in control group, the forced expiratory volume (FEV1%) was positively associated (p = 0.758) with Ang-(1-7). Conclusion: This study showed, for the first time, that there is a decrease in Alamandine participation in patients with IPF. The ACE-AngII-AT1 axis may be more active in this disease. In addition, our results suggest that Alamandine might be compensating the increase in PAP, as well as the Ang-(1-7) is improving the forced expiratory volume.