M. McGee

Heart Failure Hospitalisations in the Hunter New England Area Over 10 years. A Changing Trend

BACKGROUND Heart failure carries a major burden on our health system, mainly related to the high rate of hospital admission. An understanding of the recent trends in heart failure hospitalisation is essential to the future allocation of health resources. Our aim is to analyse the temporal trends in heart failure hospitalisation. METHODS We extracted all separations in the Hunter New England Local Health District between 2005-2014 (n=40,119) with an ICD 10 code for heart failure (I-50) in the first four diagnoses on discharge. The numbers of hospitalisations were age-standardised to the 2001 Australian population and compared based on gender and remoteness. RESULTS There was a decline in the age-standardised hospitalisation. However, there was a clear inflection point between 2009-2010, after which the decline levelled off. The absolute number of hospitalisations increased between 2010 and 2014. Heart failure hospitalisation was higher in males compared to females and rural compared to metropolitan inhabitants. CONCLUSION The gains in heart failure treatment noted in recent years seem to have come to an end. Patients aged 75 years and older are contributing the majority of age-standardised hospitalisations.

Specificity of Myocardial Perfusion Imaging: Issues With Proposed MBS Item Review

Myocardial perfusion scanning (MPS) is commonly used to assess patients with an intermediate to high risk of coronary artery disease. Concerns have been raised about the accuracy of this test. There is little recent data regarding the specificity of the MPS in the context of current medical therapy. The primary objective of this study is to determine the specificity of MPS in diagnosing obstructive coronary artery disease. A total of 184 patients fulfilled study criteria. The overall specificity of MPS for obstructive coronary artery disease was 54%.The only demographic variable that influenced specificity was gender: males with a specificity of 66% and females with a specificity of 29% (p-value=0.001). These results suggest that the real world specificity of MPS is lower than previously indicated, particularly in the female population. The limitations proposed by the Cardiac Services Committee Report are therefore unlikely to improve patient outcomes.

Groin Haemostasis with a Purse String Suture for Patients Following Catheter Ablation Procedures (GITAR Study)

BACKGROUND The most frequent complications from percutaneous electrophysiology procedures relate to vascular access. We sought to perform the first randomised controlled trial for femoral venous haemostasis utilising a simple and novel purse string suture (PSS) technique. METHODS We randomised 200 consecutive patients who were referred for electrophysiology procedures at two different hospitals to either 10minutes of manual pressure or a PSS over the femoral vein and determined the incidence of vascular access site complications. RESULTS The mean age was 61.8±12.1years and 138 (69%) were male. Bleeding requiring addition pressure or a FemStop (Abbott Laboratories, Abbott Park, IL, USA) for complete haemostasis occurred in 17/99 (17%) patients in the PSS arm and 19/101 (19%) patients in the manual pressure arm (p=0.72). There were no cases of haematoma prolonging hospital stay, arterio-venous fistula, pseudoaneurysm or retroperitoneal bleeding. The mean duration to achieve haemostasis was 45seconds in the PSS arm and 10minutes 44seconds in the manual pressure arm (p<0.001). Pain/discomfort associated with haemostasis occurred in 15/99 (15%) patients in the PSS arm and in 29/101 (29%) patients receiving manual pressure (p=0.03). CONCLUSIONS In this randomised trial we demonstrate that an easy to perform PSS is as effective at achieving haemostasis as 10minutes of manual pressure for catheter ablation procedures. The PSS is considerably faster to perform and is more comfortable for patients than manual pressure.

Drug-associated pulmonary arterial hypertension

Abstract Introduction: While pulmonary arterial hypertension remains an uncommon diagnosis, various therapeutic agents are recognized as important associations. These agents are typically categorized into “definite”, “likely”, “possible”, or “unlikely” to cause pulmonary arterial hypertension, based on the strength of evidence. Objective: This review will focus on those therapeutic agents where there is sufficient literature to adequately comment on the role of the agent in the pathogenesis of pulmonary arterial hypertension. Methods: A systematic search was conducted using PubMed covering the period September 1970– 2017. The search term utilized was “drug induced pulmonary hypertension”. This resulted in the identification of 853 peer-reviewed articles including case reports. Each paper was then reviewed by the authors for its relevance. The majority of these papers (599) were excluded as they related to systemic hypertension, chronic obstructive pulmonary disease, human immunodeficiency virus, pulmonary fibrosis, alternate differential diagnosis, treatment, basic science, adverse effects of treatment, and pulmonary hypertension secondary to pulmonary embolism. Agents affecting serotonin metabolism (and related anorexigens): Anorexigens, such as aminorex, fenfluramine, benfluorex, phenylpropanolamine, and dexfenfluramine were the first class of medications recognized to cause pulmonary arterial hypertension. Although most of these medications have now been withdrawn worldwide, they remain important not only from a historical perspective, but because their impact on serotonin metabolism remains relevant. Selective serotonin reuptake inhibitors, tryptophan, and lithium, which affect serotonin metabolism, have also been implicated in the development of pulmonary arterial hypertension. Interferon and related medications: Interferon alfa and sofosbuvir have been linked to the development of pulmonary arterial hypertension in patients with other risk factors, such as human immunodeficiency virus co-infection. Antiviral therapies: Sofosbuvir has been associated with two cases of pulmonary artery hypertension in patients with multiple risk factors for its development. Its role in pathogenesis remains unclear. Small molecule tyrosine kinase inhibitors: Small molecule tyrosine kinase inhibitors represent a relatively new class of medications. Of these dasatinib has the strongest evidence in drug-induced pulmonary arterial hypertension, considered a recognized cause. Nilotinib, ponatinib, carfilzomib, and ruxolitinib are newer agents, which paradoxically have been linked to both cause and treatment for pulmonary arterial hypertension. Monoclonal antibodies and immune regulating medications: Several case reports have linked some monoclonal antibodies and immune modulating therapies to pulmonary arterial hypertension. There are no large series documenting an increased prevalence of pulmonary arterial hypertension complicating these agents; nonetheless, trastuzumab emtansine, rituximab, bevacizumab, cyclosporine, and leflunomide have all been implicated in case reports. Opioids and substances of abuse: Buprenorphine and cocaine have been identified as potential causes of pulmonary arterial hypertension. The mechanism by which this occurs is unclear. Tramadol has been demonstrated to cause severe, transient, and reversible pulmonary hypertension. Chemotherapeutic agents: Alkylating and alkylating-like agents, such as bleomycin, cyclophosphamide, and mitomycin have increased the risk of pulmonary veno-occlusive disease, which may be clinically indistinct from pulmonary arterial hypertension. Thalidomide and paclitaxel have also been implicated as potential causes. Miscellaneous medications: Protamine appears to be able to cause acute, reversible pulmonary hypertension when bound to heparin. Amiodarone is also capable of causing pulmonary hypertension by way of recognized side effects. Conclusions: Pulmonary arterial hypertension remains a rare diagnosis, with drug-induced causes even more uncommon, accounting for only 10.5% of cases in large registry series. Despite several agents being implicated in the development of PAH, the supportive evidence is typically limited, based on case series and observational data. Furthermore, even in the drugs with relatively strong associations, factors that predispose an individual to PAH have yet to be elucidated.

Staphylococcus aureus Myocarditis with Associated Left Ventricular Apical Thrombus

Staphylococcus aureus myocarditis is a rare diagnosis with a high mortality rate, usually seen in people who are immunocompromised. Here, we report a case of a 44-year-old man on methotrexate for rheumatoid arthritis who presented in septic shock and was diagnosed with staphylococcus aureus myocarditis. The myocarditis was associated with a left ventricular apical thrombus, with normal systolic function. The myocarditis and associated thrombus were characterised on transthoracic echocardiogram and subsequently on cardiac magnetic resonance imaging. Cardiac magnetic resonance (CMR) imaging showed oedema in the endomyocardium, consistent with acute myocarditis, associated with an apical mural thrombus. Repeat CMR 3 weeks following discharge from hospital showed marked improvement in endomyocardial oedema and complete resolution of the apical mural thrombus. He was treated with a 12-week course of antibiotics and anticoagulated with apixaban. The patient was successfully managed with intravenous antibiotics and anticoagulation with complete recovery.

Polypharmacy is Associated with Co-morbidity and Predicts outcome in Patients undergoing Index Pulmonary Hypertension Assessment

Aims: We sought to evaluate the incidence of polypharmacy in patients referred for pulmonary hypertension assessment, assess the relationship of polypharmacy to the presence of co-morbidity and document the influence of polypharmacy and co-morbidity on unplanned readmissions and mortality in this cohort.Methods: We performed an audit of outpatient clinical medical records for 215 consecutive patients referred to a tertiary referral centre for pulmonary hypertension assessment between March 2009 and April 2016. Data on number and class of medications were recorded, as well as past medical history and investigations relevant to assessment of pulmonary hypertension.Results: At the time of pulmonary hypertension evaluation, patients were prescribed a mean of 8 ± 4 medications with 83.2% of patients being on 5 or more regularly prescribed medications. Taking 8 or more medications was associated with co-morbidity, as assessed by the Charlson Co-morbidity Index, and reduced exercise capacity. The presence of co-morbidity resulted in a significantly higher risk of unplanned admission. The presence of polypharmacy is a marker of important co-morbidity, identifying a group at high risk.Conclusion: Patients referred for assessment of pulmonary hypertension had high rates of polypharmacy reflecting extensive comorbidity, which in turn predicts adverse outcome in this patient population. The presence of polypharmacy should be considered a simple clinical marker of co-morbidity, increased risk and adverse outcome.

Adenoid Cystic Carcinoma of the Trachea Resulting in Fatal Asphyxia

Primary malignant tumors of the trachea are uncommon. The authors report a case of a 72‐year‐old female who died from asphyxia due to an undiagnosed obstructing adenoid cystic carcinoma of the trachea. The decedent became unresponsive while eating cereal and was pronounced upon arrival at the local hospital. The autopsy revealed a near occlusive tumor mass just superior to the bifurcation of the distal trachea. There was no evidence of aspiration. The death was the result of asphyxia due to obstruction of the trachea by an adenoid cystic carcinoma. This case demonstrates that an obstructive tumor mass may remain undiagnosed until an obstructive episode results in a sudden death.

ST elevation myocardial infarction in patients with anomalous left main coronary artery: Case series and review of the literature☆

Anomalous left main coronary artery is rare. We present four cases where anomalous left main coronary artery was diagnosed during emergent cardiac catheterization for ST elevation myocardial infarction. Procedural characteristics, technical challenges, and relevant literature are discussed.

Ebstein's Anomaly, Left Ventricular Noncompaction, and Sudden Cardiac Death

Ebsteins anomaly is a congenital disorder characterized by apical displacement of the septal leaflet of the tricuspid valve. Ebsteins anomaly may be seen in association with other cardiac conditions, including patent foramen ovale, atrial septal defect, and left ventricular noncompaction (LVNC). LVNC is characterized by increased trabeculation within the left ventricular apex. Echocardiography is often used to diagnose LVNC; however, magnetic resonance (MR) imaging offers superior characterization of the myocardium. We report a case of sudden cardiac death in a patient with Ebsteins anomaly with unrecognized LVNC noted on post mortem examination with screening documenting the presence of LVNC in one of the patients twin sons.