Articles

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.

Objective: To investigate in an animal model of Pulmonary Hypertension (PH) by monocrotaline whether a lower exercise intensity, which has lower potential to provoke dyspnea symptoms, could prevent the increase the right ventricle pressure and the decrease in respiratory compliance. Setting: A research laboratory. ANIMALS: twenty-one Wistar rats were randomized to the groups: Control (CO; saline solution); PH-sedentary; PH-low and PH-moderate intensity of exercise training (ET). Interventions: They received a single saline or monocrotaline subcutaneous injection (50 mg/kg). The exercise program was performed during 3-weeks. Main Outcome Measures: Rats were evaluated by their morphometric and hemodynamic changes and by the respiratory mechanic responses induced by the exercise protocols. Results: Both protocols of ET significantly (p < 0.05) attenuated the increase in the right ventricular systolic pressure. However, the lower intensity was more effective to prevent the impairment in the respiratory and quasi-static compliance. Conclusion: Collectively, our results showed for the first time the benefits of ET to the respiratory system mechanics. We also demonstrated that intensity is crucial in PH, probably due to the difficulty to match VO2 capacity and O2 demand during exercise. The improvement in quasi-static compliance not only might improve the ability to breathe, and capture oxygen, but also welfare.

A key platform underpinning the traditional understanding of the cardiovascular system, with respect to the behavior of large arterial vessels, is Otto Frank’s Windkessel Hypothesis [1]. This hypothesis posits simply that the smooth muscle walls of large arteries do not undergo rhythmic contractions in synchrony with the heartbeat but, rather, behave as passive elastic tubes undergoing distension from pulsatile pressure waves. The Windkessel Hypothesis is elegant, well described for over a century, ingrained in the understanding of cardiovascular medicine and physiology, and simply wrong. Several groups have now shown that the arterial smooth muscle wall undergoes rhythmic activation in synchrony with the heartbeat in a variety of tissues, including human brachial artery; canine coronary, femoral, and carotid arteries; rabbit aorta; feline pulmonary artery and rodent aorta [2-8]. The phasing of these events is such that the upstroke of the contraction slightly precedes the upstroke of the pulse wave, suggesting nomenclature for the events as pulse synchronized contractions, or PSCs [3,6-8]. PSCs have been found to be of neurogenic origin, sensitive to the neural blocker tetrodotoxin [3,8]. Although the specific neural pathways regulating PSCs have not been elucidated, the alpha-adrenergic system is at least partially involved, as evidenced by reduction or blockade of PSCs by the alpha-adrenergic blocker phentolamine [8]. Further, PSCs have not been observed following vessel excision in in vitro studies, as an intact nervous system is not present. The pacemaker for the PSC resides in the right atrium, as suggested by two lines of evidence. First, pacing of the right atrial region to faster than spontaneous frequencies leads to a one-to-one correspondence of PSC frequency with the stimulation rate [3]. Additionally, excision of the right, but not the left, atrial appendage results in elimination of PSCs [3]. As the pacemaker region for PSCs and the heartbeat both lie in the right atrium, this may potentially allow for coordination between the heartbeat and pulse wave with PSCs [3,5,8]. Extensive evaluations also have been performed showing the PSC was not an artifact produced either by cardiac contractility or from the vessel distension from the pulse wave [3,5,6].