Ruvin Gabriel

Rationale and design of the Sodium Lowering In Dialysate (SoLID) trial: a randomised controlled trial of low versus standard dialysate sodium concentration during hemodialysis for regression of left ventricular mass.

BackgroundThe current literature recognises that left ventricular hypertrophy makes a key contribution to the high rate of premature cardiovascular mortality in dialysis patients. Determining how we might intervene to ameliorate left ventricular hypertrophy in dialysis populations has become a research priority. Reducing sodium exposure through lower dialysate sodium may be a promising intervention in this regard. However there is clinical equipoise around this intervention because the benefit has not yet been demonstrated in a robust prospective clinical trial, and several observational studies have suggested sodium lowering interventions may be deleterious in some dialysis patients.Methods/designThe Sodium Lowering in Dialysate (SoLID) study is funded by the Health Research Council of New Zealand. It is a multi-centre, prospective, randomised, single-blind (outcomes assessor), controlled parallel assignment 3-year clinical trial. The SoLID study is designed to study what impact low dialysate sodium has upon cardiovascular risk in dialysis patients. The study intends to enrol 118 home hemodialysis patients from 6 sites in New Zealand over 24 months and follow up each participant over 12 months. Key exclusion criteria are: patients who dialyse more frequently than 3.5 times per week, pre-dialysis serum sodium of <135 mM, and maintenance hemodiafiltration. In addition, some medical conditions, treatments or participation in other dialysis trials, which contraindicate the SoLID study intervention or confound its effects, will be exclusion criteria. The intervention and control groups will be dialysed using dialysate sodium 135 mM and 140 mM respectively, for 12 months. The primary outcome measure is left ventricular mass index, as measured by cardiac magnetic resonance imaging, after 12 months of intervention. Eleven or more secondary outcomes will be studied in an attempt to better understand the physiologic and clinical mechanisms by which lower dialysate sodium alters the primary end point.DiscussionThe SoLID study is designed to clarify the effect of low dialysate sodium upon the cardiovascular outcomes of dialysis patients. The study results will provide much needed information about the efficacy of a cost effective, economically sustainable solution to a condition which is curtailing the lives of so many dialysis patients.Trial registrationAustralian and New Zealand Clinical Trials Registry number: ACTRN12611000975998

Clinical Characteristics and Outcomes of Patients with Amphetamine-Associated Cardiomyopathy in South Auckland, New Zealand

BACKGROUND Amphetamine-associated cardiomyopathy (AAC) is becoming an increasingly recognised entity. The characteristics and outcomes of these patients are poorly understood. METHODS Thirty patients admitted with heart failure and echocardiographic evidence of cardiomyopathy between 2005 and 2014 and who had a documented history of amphetamine abuse that was considered an important factor in the causation of their cardiomyopathy were retrospectively identified. RESULTS Mean age at presentation was 40±10 years with a male predominance (n=25, 83%). The majority were of indigenous Maori ethnicity. At presentation, four patients were in cardiogenic shock. Five patients required intensive care unit (ICU) admission for inotropic support and mechanical ventilation. Fifteen had severe left ventricular (LV) dilation (mean LV end-diastolic dimension 6.8±1.0cm) and all patients had severe LV dysfunction (mean LV ejection fraction 22±8%). Despite optimal heart failure therapy, LV size remained significantly dilated with minimal improvement in LV function. During median follow-up of 18 months, five patients died from end-stage heart failure and 17 had at least one readmission with decompensated heart failure. CONCLUSION Amphetamine-associated cardiomyopathy was seen predominantly in young indigenous Maori men. They presented with severe cardiomyopathy, often requiring ICU admission. Severe LV dilation and significant LV dysfunction persisted despite treatment and mortality was high.

Left ventricular morphology and response to beta-adrenergic stimulation in apical ballooning syndrome

AIMS The patho-physiology of apical ballooning syndrome (ABS) has not been clearly defined. The aim of this study was to determine whether patients with a history of ABS are more likely to develop left ventricular (LV) mid-cavity or outflow tract obstruction, or have a greater regional LV contractile response to an adrenergic stimulus compared with normal controls. METHODS AND RESULTS Twenty patients who had recovered from ABS and 15 age-and sex-matched controls had dobutamine stress echocardiography with incremental doses up to 20 µg/kg/min. On average ABS subjects had slightly greater basal LV interventricular septal (1.1 ± 0.24 cm vs. 0.93 ± 0.12, P = 0.03) and posterior wall (1.04 ± 0.16 vs. 0.91 ± 0.11 cm, P = 0.02) diameters compared with controls but LV end-diastolic and end-systolic volumes and LV ejection fraction were similar both at rest and after dobutamine. Regional and global LV contractility, measured with the strain rate and tissue velocity imaging were also similar during the dobutamine infusion up to 10 µg/kg/min in ABS and controls. Mid-LV or LV outflow tract obstruction was not present at rest in any subjects, but was common during peak dobutamine infusion both in the ABS (45%) and controls (53%, P = 0.62). CONCLUSIONS Dynamic LV obstruction with dobutamine is common in those with and without prior ABS. However, this study did not identify a greater individual predisposition to LV obstruction, or a different regional or global LV contractile response to dobutamine in patients with a history of ABS compared with control subjects.

Plasma brain natriuretic peptide concentrations in patients with valvular heart disease.

Objective Plasma brain natriuretic peptide (BNP) concentrations predict prognosis in patients with valvular heart disease (VHD), but it is unclear whether this directly relates to disease severity. We assessed the relationship between BNP and echocardiographic measures of disease severity in patients with VHD. Methods Plasma BNP concentrations were measured in patients with normal left ventricular (LV) systolic function and isolated VHD (mitral regurgitation (MR), n=33; aortic regurgitation (AR), n=39; aortic stenosis (AS), n=34; mitral stenosis (MS), n=30), and age-matched and sex-matched controls (n=39) immediately prior to exercise stress echocardiography. Results Compared with controls, patients with VHD had elevated plasma BNP concentrations (MR median 35 (IQR 23–52), AR 34 (22–45), AS 31 (22–60), MS 58 (34–90); controls 24 (16–33) pg/mL; p<0.01 for all). LV end diastolic volume index varied by valve lesion; (MR (mean 77±14), AR (91±28), AS (50±17), MS (43±11), controls (52±13) mL/m2; p<0.0001). There were no associations between LV volume and BNP. Left atrial (LA) area index varied (MR (18±4 cm2/m2), AR (12±2), AS (11±3), MS (19±6), controls (11±2); p<0.0001), but correlated with plasma BNP concentrations: MR (r=0.42, p=0.02), MS (r=0.86, p<0.0001), AR (r=0.53, p=0.001), AS (r=0.52, p=0.002). Higher plasma BNP concentrations were associated with increased pulmonary artery pressure and reduced exercise capacity. Despite adverse cardiac remodelling, 81 (60%) patients had a BNP concentration within the normal range. Conclusions Despite LV remodelling, plasma BNP concentrations are often normal in patients with VHD. Conversely, mild elevations of BNP occur with LA dilatation in the presence of normal LV. Plasma BNP concentrations should be interpreted with caution when assessing patients with VHD.

Morphology of congenital and acquired aortic valve disease by cardiovascular magnetic resonance imaging

Echocardiography is the principal non-invasive tool for initial evaluation and longitudinal monitoring of patients with significant valvular heart disease. However echocardiography can be limited by poor acoustic windows, and is dependent on the skill and experience of the sonographer. Cardiovascular magnetic resonance (CMR) can provide a comprehensive non-invasive assessment of valvular morphology, quantification of the severity of valvular dysfunction, determination of its aetiology, assessment of the consequences for the heart from the valve lesion including measurement of ventricular volumes and function, and evaluation of haemodynamic abnormalities. Additional information such as great vessel anatomy and the presence of coronary disease and myocardial scar can also be obtained from CMR. Aortic valve disease can manifest as aortic regurgitation, aortic stenosis or a mixture of both. Structural abnormalities of the valve (congenital or acquired) or disease of the aorta (structurally normal valve) can cause aortic valve disease. This review describes the role of CMR in evaluation of patients with aortic valve diseases, and illustrates the typical and distinguishing morphological features seen on CMR in a range of congenital and some common acquired aortic valve lesions. Although CMR can provide important information about the morphology of aortic valve, its full potential has yet to be realised, and further studies of clinical outcomes are needed before CMR data can be integrated into the management of patients with significant aortic valvular lesions.

Rationale and design of the myocardial microinjury and cardiac remodeling extension study in the sodium lowering in dialysate trial (Mac-SoLID study)

BackgroundThe Sodium Lowering in Dialysate (SoLID) trial is an ongoing a multi-center, prospective, randomised, single-blind (assessor), controlled, parallel assignment clinical trial, enrolling 96 home and self-care hemodialysis (HD) patients from 7 centers in New Zealand. The trial will evaluate the hypothesis that lower dialysate [Na+] during HD results in lower left ventricular (LV) mass. Since it’s inception, observational evidence has suggested increased mortality risk with lower dialysate [Na+], possibly due to exacerbation of intra-dialytic hypotension and subsequent myocardial micro-injury. The Myocardial Micro-injury and Cardiac Remodeling Extension Study in the Sodium Lowering In Dialysate Trial (Mac-SoLID study) aims to determine whether lower dialysate [Na+] results in (i) increased levels of high-sensitivity Troponin T (hsTnT), a well-established marker of intra-dialytic myocardial micro-injury in HD populations, and (ii) increased fixed LV segmental wall motion abnormalities, a marker of recurrent myocardial stunning and micro-injury, and (iii) detrimental changes in LV geometry due to maladaptive homeostatic mechanisms.Methods/designThe SoLID trial and the Mac-SoLID study are funded by the Health Research Council of New Zealand. Key exclusion criteria: patients who dialyse > 3.5 times per week, pre-dialysis serum sodium <135 mM, and maintenance haemodiafiltration. In addition, some medical conditions, treatments or participation in other dialysis trials that contraindicate the study intervention or confound its effects, will be exclusion criteria. The intervention and control groups will receive dialysate sodium 135 mM and 140 mM respectively, for 12 months. The primary outcome measure for the Mac-SOLID study is repeated measures of [hsTnT] at 0, 3, 6, 9, and 12 months. The secondary outcomes will be assessed using cardiac magnetic resonance imaging (MRI), and comprise LV segmental wall motion abnormality scores, LV mass to volume ratio and patterns of LV remodeling at 0 and 12 months.DiscussionThe Mac-SoLID study enhances and complements the SoLID trial. It tests whether potential gains in cardiovascular health (reduced LV mass) which low dialysate [Na+] is expected to deliver, are counteracted by deterioration in cardiovascular health through alternative mechanisms, namely repeated LV stunning and micro-injury.Trial registrationAustralian and New Zealand Clinical Trials Registry number: ACTRN12611000975998.

Milk of calcium pericardial effusion

A 50-year-old woman presented with progressive right heart failure. A chest x-ray showed a right-sided pleural effusion and pericardial calcification. Echocardiography revealed constrictive physiology with preserved biventricular systolic function. There was a small pericardial effusion with an echogenic pericardium. A non-contrast cardiac computed tomography (CT) revealed partial calcification of the visceral and parietal pericardium with a hyperdense pericardial effusion (Hounsfield units (HU) e 150) suggestive of “milk of calcium” pericardial effusion (Fig. 1A & B). Right heart catheterization confirmed constriction with late diastolic equalization of pressures in all cardiac chambers. A large amount of viscous muddy-coloured pericardial fluid (Fig. 1C) was identified during pericardiectomy. Analysis of the pericardial fluid using flame atomic absorption showed a very high calcium content

Multi-modality imaging in congenital aorto-right atrial tunnel

A 38-year-old woman presented with paroxysmal atrial fibrillation. Echocardiography ( Panel A ; see Supplementary data online, Movies S1 and S2 ) revealed a prominent left sinus of Valsalva with tortuous tubular structure seen superior to the atria adjacent to the intra-atrial septum and emptying into the superior aspect of the right atrium (RA). Computed tomography (CT) coronary angiogram ( Panels B – D ) and cardiac magnetic resonance (CMR) imaging ( Panels E – G ; see Supplementary data online, Movie S3 ) confirmed a tortuous, tubular structure arising from the left sinus of Valsalva taking a retroaortic course running adjacent to the RA aspect of the inter-atrial septum …

Computed Tomography in Prosthetic Aortic Graft Infections.

Prosthetic aortic grafts infection is associated with consider-able morbidity and mortality. Staphylococcus species are themost commonly implicated causative organisms. Computedtomography (CT) is the imaging modality of choice in theinvestigation of patients with suspected prosthetic aorticgraft infection, particularly in the assessment of abscessand pseudo-aneurysms associated with aortic graft infec-tions.WedescribetwocasesinwhichCTprovidesincremen-tal information about the complications associated withprosthetic aortic graft infection which is essential in guidingtreatment and management.Case 1: 45 year-old man with previous Bentall’s graft with25 mm St Jude valve conduit for bicuspid aortic valve anddilated aortic root presented with night sweats, weight loss,and rash. Transthoracic echocardiogram (Fig. 1A, video I)demonstrated a large pseudo-aneurysm anterior to the Ben-tall’s with free moving echogenic mass within likely consis-tent with vegetations. CT thoracic aorta (Fig. 1B-1D) showeda large complex pseudo-aneurysm anterior to the aortic rootand the main pulmonary artery with fistula origin at theright coronary artery anastomosis. He subsequently under-went redo Bentall’s procedure with 23 mm ATS bileafletmechanical valve and 30 mm Gelweave valsalva graft. Sur-gery confirmed a large pseudo-aneurysm arising from theaortic root with vegetations in the cavity. Propionibacteriumacnes was isolated and he was treated with six weeks ofintravenous benzyl penicillin followed by oral penicillinfor three months.Case 2: 19 year-old man with end-stage renal failure pre-sented with an aortic root abscess (Fig. 2A) secondary toMethicillin-resistant Staphylococcus aureus bacteraemia withthe presumed infection likely arising from right internaljugular tunnelled line for haemodialysis. He underwent anurgent homograft aortic root replacement in view of severeaorticincompetence(Fig.2B)and completeheartblock.Post-operative echocardiogram (Fig. 2C & 2D, videos II & III)showedalargeparavalvularechofreespaceposteromediallyand another anterolaterally consistent with pseudo-aneurysm. CT thoracic aorta (2E & 2F) demonstrated twopseudo-aneurysms arising from the left ventricular outflowtract. Redo aortic root replacement was performed but com-plicated by significant bleeding from the root despite multi-ple suturing, topical measures and packing, and eventuallyhe died.Keywords Computer tomography Echocardiogram Prosthetic aortic graft infections

Two Causes of Ventricular Tachycardia in a 26 Year-old Male

We present the case of a 26 year-old man who presented to hospital with monomorphic ventricular tachycardia (VT) at a rate of 170bpm after exercising on a treadmill. Multimodality imaging with transthoracic echocardiogram (TTE), cardiac magnetic resonance imaging (CMRI) and computed tomography coronary angiogram (CTCA) demonstrated two causes for ventricular tachycardia; hypertrophic cardiomyopathy (HCM) and an anomalous right coronary artery (RCA) arising from the left coronary sinus, with a potentially malignant interarterial course. Both conditions can be associated with sudden cardiac death (SCD). We discuss the management dilemmas in this unique patient.