Articles

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].

Background: Contrast-induced acute kidney injury (CI-AKI) is an important cause of increasing the hospital stay and in-hospital mortality. By increasing intra-renal vasoconstriction, left ventricular ejection fraction (LVEF) can increase the risk of CI-AKI. We sought to investigate whether LVEF can impact the incidence of CI-AKI after cardiac catheterization and whether it can be used to predict CI-AKI. Methods: Patients underwent cardiac catheterization from December 2017 to February 2018 at Jersey Shore University Medical Center were enrolled in the study. Contrast-induced acute kidney injury (CI-AKI) was defined as an increase in serum creatinine of ≥ 0.5 mg/dL or an increase of ≥ 25% from the pre-procedure value within 72 hours post-procedure. The maximum allowable contrast dose was calculated using the following formula: (5* (weight (kg)/creatinine level (mg/dL)). A multivariable logistic regression analyses, controlling for potential confounders, were used to test associations between LVEF and CI-AKI. Results: 9.6% had post catheterization CI-AKI. A total of 18 out of 44 (44%) of patients who had CI-AKI also had ongoing congestive heart failure. No statistically significant association found neither with maximum allowable contrast (p = 0.009) nor ejection fraction (p = 0.099) with the development of CI-AKI. Conclusion: In spite of the fact that no statistically significant relationship found between the percentage maximum contrast dose and the ejection fraction with the post-procedure CI-AKI, we heighten the essential of employing Maximum Allowable Contrast Dose (MACD) and ejection fraction in patients undergoing PCI to be used as a clinical guide to predict CI-AKI.

Background: Subclavian venous access for pacemaker lead insertion is a common procedure and is normally considered safe in the hands of an expert. However, subclavian venepuncture is not without complications, starting from mild subcutaneous hematoma to pneumothorax. We here present a case of hemoptysis occurring after difficult subclavian vein puncture, which subsequently improved on conservative management only. Case Summary: A 65-year-old gentleman, post aortic valve replacement had persistent high-grade AV block and was taken up for a dual chamber pacemaker implantation. Immediately following venous access, he had a bout of hemoptysis, which recovered on its own. Post procedure chest x-ray was suggestive of alveolar hemorrhage which cleared gradually in next three-four days. Discussion: Post subclavian venepuncture hemoptysis is known; but it is a rare complication, arising either because of lung parenchyma injury or arterial injury. This is mostly benign and improves on conservative management only; however rarely it may be massive and life threatening where transcatheter arterial embolization may be required.

Background: Hypertrophic cardiomyopathy (HCM) patients have a predisposition for malignant VT/VF and consequently, sudden cardiac death (SCD). In single center studies, late gadolinium enhancement (LGE) defined fibrosis has been linked to VT/VF. However, despite innumerable investigations, SCD has not been definitely attributable to LGE. Explanations for these are believed to be related to insufficient statistical power. Methods: We performed an electronic search of MEDLINE, PubMed: and CMR abstracts for original data published or presented between Jan 2001 to Mar 2011. Key search terms: HCM, LV fibrosis, SCD and LGE. Studies were screened for eligibility based on inclusion criteria: referral for CMR exam with LGE for HCM; and follow-up for incidence of VT/VF and SCD. Categorical variables were evaluated between patient groups via Chi-square test. Results: A total of 64 studies were initially identified. Of these, 4 (6.3%) were identified and included (n = 1063 patients). Three prospective and one retrospective study were included. LGE was detected in 59.6% of patients. As expected, the presence of myocardial fibrosis was associated with VT/VF (x2 = 6.5, p < 0.05; OR 9.0, (95% CI 1.2 to 68.7). Moreover, myocardial fibrosis strongly predicted SCD (x2 = 6.6, p < 0.05; OR 3.3 (95% CI 1.2 to 9.7). Conclusion: Despite single center CMR studies, LGE has consistently predicted VT/VF while prediction of SCD has remained paradoxically unlinked. Although the lack of studies meeting our criteria limited our ability to perform a comprehensive meta-analysis, we have been able to demonstrate for the first time that LGE-defined fibrosis is a predictor of SCD in patients with HCM0.

Chronic heart failure has been extensively characterized as a disorder arising from a complex interaction between impaired ventricular performance and neurohormonal activation. Since beta adrenoceptor blocking agents are currently considered an integral component of therapy for the management of patients with severe chronic heart failure; several well designed clinical trials have been conducted to determine the morbidity and mortality benefits of these agents these studies, however did not yield the same results in terms of morbidity and mortality benefits. Currently only Bisoprolol, Carvedilol and sustained release metoprolol succinate have clinically proven and convincing morbidity and mortality benefits the current list of approved medicines of the National Health Insurance Scheme (NHIS) of the republic of Ghana does not provide coverage for these lifesaving therapeutic agents. The objective of this review was to collate the relevant scientific evidence that will convince the authorities at the National Health Insurance Authority (NHIA) of the Republic of Ghana to include at least one of the evidence based beta adrenoceptor blocking agents in the list of approved medicines. A thorough search on the internet was conducted using Google scholar to obtain only the clinically relevant studies associated with the benefits of beta adrenoceptor blocking agents in patients with chronic heart failure published in the English language. The phrases beta adrenoceptor blocking agents and chronic heart failure were used as search engines. The search engine yielded several studies that met the predefined inclusion criteria. However, only the Cardiac Insufficiency BIsoprolol Studies (CIBIS-I and CIBIS-II), Carvedilol Prospective Randomized Cumulative Survival Study (COPERNICUS) and Metoprolol CR/XL Randomized Intervention Trial (MERIF-HF) because of the clinical relevance of their findings Beta adrenoceptor blocking agents such as atenolol and propranolol have been used in the management of patients with chronic heart failure. However, their efficacy and optimal dose in reducing mortality have not been scientifically established not all beta adrenoceptor blocking agents scientifically studied provide the same degree of clinically meaningful and convincing morbidity and mortality benefits in patients with chronic heart failure.

Critical congenital heart defects (CCHDs) are preferably diagnosed prenatally or soon after birth. Late diagnosis has been related to poorer prognosis. The aim of this study is to assess when CCHDs are diagnosed in Iceland and whether late diagnosis is a problem. All live born children in Iceland and foetuses diagnosed with CCHDs during the years 2000-2014 were included. CCHD was defined as a defect requiring intervention or causing death in the first year of life, or leading to abortion. The total number of pre- and postnatal diagnosis of CCHDs was 188. Prenatal diagnosis was made in 69 of 188 (36.7%). Of 69 diagnosed prenatally 33 were terminated due to CCHD. Of the 155 live born children with CCHD, 36 (23.2%) had a prenatal diagnosis and 100 (64.5%) were diagnosed shortly after birth, before discharge from birth facility. 19 children (12.3%) were diagnosed late, that is after discharge from birth facility. Coarctation of the aorta was the most common CCHD diagnosed late (6/19). Prenatal screening and newborn examination give good results in diagnosis of CCHDs in Iceland. Late diagnosis are relatively few, but both the number of prenatally diagnosed CCHDs and CCHDs diagnosed shortly after birth can be further improved.