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Article ; Online: Changing the view: Preventing pneumothorax during transvenous pacemaker implantation.

Loudon, Brodie L / Wong, Geoffrey R

Journal of cardiovascular electrophysiology

2024 Volume 35, Issue 3, Page(s) 438–439

MeSH term(s)	Humans ; Pneumothorax/etiology ; Pneumothorax/prevention & control ; Pacemaker, Artificial/adverse effects ; Defibrillators, Implantable ; Prosthesis Implantation ; Axillary Vein
Language	English
Publishing date	2024-02-01
Publishing country	United States
Document type	Editorial
ZDB-ID	1025989-2
ISSN	1540-8167 ; 1045-3873
ISSN (online)	1540-8167
ISSN	1045-3873
DOI	10.1111/jce.16198
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Article ; Online: Remote monitoring in heart failure.

Frenneaux, Michael P / Gollop, Nicholas D / Loudon, Brodie L / Parasuraman, Sathish

European heart journal. Quality of care & clinical outcomes

2015 Volume 1, Issue 2, Page(s) 45–46

Language	English
Publishing date	2015-11-01
Publishing country	England
Document type	Journal Article
ZDB-ID	2823451-0
ISSN	2058-1742 ; 2058-5225
ISSN (online)	2058-1742
ISSN	2058-5225
DOI	10.1093/ehjqcco/qcv018
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Article ; Online: Cardiac metabolism - A promising therapeutic target for heart failure.

Noordali, Hannah / Loudon, Brodie L / Frenneaux, Michael P / Madhani, Melanie

Pharmacology & therapeutics

2017 Volume 182, Page(s) 95–114

Abstract: Both heart failure with reduced ejection fraction (HFrEF) and with preserved ejection fraction (HFpEF) are associated with high morbidity and mortality. Although many established pharmacological interventions exist for HFrEF, hospitalization and death ... ...

Abstract	Both heart failure with reduced ejection fraction (HFrEF) and with preserved ejection fraction (HFpEF) are associated with high morbidity and mortality. Although many established pharmacological interventions exist for HFrEF, hospitalization and death rates remain high, and for those with HFpEF (approximately half of all heart failure patients), there are no effective therapies. Recently, the role of impaired cardiac energetic status in heart failure has gained increasing recognition with the identification of reduced capacity for both fatty acid and carbohydrate oxidation, impaired function of the electron transport chain, reduced capacity to transfer ATP to the cytosol, and inefficient utilization of the energy produced. These nodes in the genesis of cardiac energetic impairment provide potential therapeutic targets, and there is promising data from recent experimental and early-phase clinical studies evaluating modulators such as carnitine palmitoyltransferase 1 inhibitors, partial fatty acid oxidation inhibitors and mitochondrial-targeted antioxidants. Metabolic modulation may provide significant symptomatic and prognostic benefit for patients suffering from heart failure above and beyond guideline-directed therapy, but further clinical trials are needed.
MeSH term(s)	Energy Metabolism/drug effects ; Heart Failure/drug therapy ; Humans ; Molecular Targeted Therapy/methods ; Myocardium/metabolism
Language	English
Publishing date	2017-08-15
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	194735-7
ISSN	1879-016X ; 0163-7258
ISSN (online)	1879-016X
ISSN	0163-7258
DOI	10.1016/j.pharmthera.2017.08.001
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Article ; Online: Present and future pharmacotherapeutic agents in heart failure: an evolving paradigm.

Loudon, Brodie L / Noordali, Hannah / Gollop, Nicholas D / Frenneaux, Michael P / Madhani, Melanie

British journal of pharmacology

2016 Volume 173, Issue 12, Page(s) 1911–1924

Abstract: Many conditions culminate in heart failure (HF), a multi-organ systemic syndrome with an intrinsically poor prognosis. Pharmacotherapeutic agents that correct neurohormonal dysregulation and haemodynamic instability have occupied the forefront of ... ...

Abstract	Many conditions culminate in heart failure (HF), a multi-organ systemic syndrome with an intrinsically poor prognosis. Pharmacotherapeutic agents that correct neurohormonal dysregulation and haemodynamic instability have occupied the forefront of developments within the treatment of HF in the past. Indeed, multiple trials aimed to validate these agents in the 1980s and early 1990s, resulting in a large and robust evidence-base supporting their use clinically. An established treatment paradigm now exists for the treatment of HF with reduced ejection fraction (HFrEF), but there have been very few notable developments in recent years. HF remains a significant health concern with an increasing incidence as the population ages. We may indeed be entering the surgical era for HF treatment, but these therapies remain expensive and inaccessible to many. Newer pharmacotherapeutic agents are slowly emerging, many targeting alternative therapeutic pathways, but with mixed results. Metabolic modulation and manipulation of the nitrate/nitrite/nitric oxide pathway have shown promise and could provide the answers to fill the therapeutic gap between medical interventions and surgery, but further definitive trials are warranted. We review the significant evidence base behind the current medical treatments for HFrEF, the physiology of metabolic impairment in HF, and discuss two promising novel agents, perhexiline and nitrite.
MeSH term(s)	Cardiovascular Agents/therapeutic use ; Heart Failure/drug therapy ; Heart Failure/metabolism ; Humans ; Nitrites/therapeutic use ; Perhexiline/therapeutic use
Chemical Substances	Cardiovascular Agents ; Nitrites ; Perhexiline (KU65374X44)
Language	English
Publishing date	2016-05-06
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	80081-8
ISSN	1476-5381 ; 0007-1188
ISSN (online)	1476-5381
ISSN	0007-1188
DOI	10.1111/bph.13480
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Article ; Online: Biventricular pacemaker therapy improves exercise capacity in patients with non-obstructive hypertrophic cardiomyopathy via augmented diastolic filling on exercise.

Ahmed, Ibrar / Loudon, Brodie L / Abozguia, Khalid / Cameron, Donnie / Shivu, Ganesh N / Phan, Thanh T / Maher, Abdul / Stegemann, Berthold / Chow, Anthony / Marshall, Howard / Nightingale, Peter / Leyva, Francisco / Vassiliou, Vassilios S / McKenna, William J / Elliott, Perry / Frenneaux, Michael P

European journal of heart failure

2020 Volume 22, Issue 7, Page(s) 1263–1272

Abstract: Aims: Treatment options for patients with non-obstructive hypertrophic cardiomyopathy (HCM) are limited. We sought to determine whether biventricular (BiV) pacing improves exercise capacity in HCM patients, and whether this is via augmented diastolic ... ...

Abstract	Aims: Treatment options for patients with non-obstructive hypertrophic cardiomyopathy (HCM) are limited. We sought to determine whether biventricular (BiV) pacing improves exercise capacity in HCM patients, and whether this is via augmented diastolic filling. Methods and results: Thirty-one patients with symptomatic non-obstructive HCM were enrolled. Following device implantation, patients underwent detailed assessment of exercise diastolic filling using radionuclide ventriculography in BiV and sham pacing modes. Patients then entered an 8-month crossover study of BiV and sham pacing in random order, to assess the effect on exercise capacity [peak oxygen consumption (VO Conclusion: Symptomatic patients with non-obstructive HCM may benefit from BiV pacing via augmentation of diastolic filling on exercise rather than contractile improvement. This may be due to relief of diastolic ventricular interaction. Clinical trial registration: ClinicalTrials.gov NCT00504647.
MeSH term(s)	Cardiac Pacing, Artificial ; Cardiac Resynchronization Therapy Devices ; Cardiomyopathy, Hypertrophic/therapy ; Cross-Over Studies ; Diastole ; Exercise Tolerance ; Female ; Heart Failure/therapy ; Humans ; Male ; Middle Aged ; Pacemaker, Artificial ; Quality of Life ; Stroke Volume ; Ventricular Function, Left
Language	English
Publishing date	2020-01-23
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1483672-5
ISSN	1879-0844 ; 1388-9842
ISSN (online)	1879-0844
ISSN	1388-9842
DOI	10.1002/ejhf.1722
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Article: Assessment of pulmonary artery pressure by echocardiography-A comprehensive review.

Parasuraman, Sathish / Walker, Seamus / Loudon, Brodie L / Gollop, Nicholas D / Wilson, Andrew M / Lowery, Crystal / Frenneaux, Michael P

International journal of cardiology. Heart & vasculature

2016 Volume 12, Page(s) 45–51

Abstract: Pulmonary hypertension is a pathological haemodynamic condition defined as an increase in mean pulmonary arterial pressure ≥ 25 mmHg at rest, assessed using gold standard investigation by right heart catheterisation. Pulmonary hypertension could be a ... ...

Abstract	Pulmonary hypertension is a pathological haemodynamic condition defined as an increase in mean pulmonary arterial pressure ≥ 25 mmHg at rest, assessed using gold standard investigation by right heart catheterisation. Pulmonary hypertension could be a complication of cardiac or pulmonary disease, or a primary disorder of small pulmonary arteries. Elevated pulmonary pressure (PAP) is associated with increased mortality, irrespective of the aetiology. The gold standard for diagnosis is invasive right heart catheterisation, but this has its own inherent risks. In the past 30 years, immense technological improvements in echocardiography have increased its sensitivity for quantifying pulmonary artery pressure (PAP) and it is now recognised as a safe and readily available alternative to right heart catheterisation. In the future, scores combining various echo techniques can approach the gold standard in terms of sensitivity and accuracy, thereby reducing the need for repeated invasive assessments in these patients.
Language	English
Publishing date	2016-07-04
Publishing country	Ireland
Document type	Journal Article ; Review
ZDB-ID	2818464-6
ISSN	2352-9067
ISSN	2352-9067
DOI	10.1016/j.ijcha.2016.05.011
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Article ; Online: Inorganic nitrate and nitrite supplementation fails to improve skeletal muscle mitochondrial efficiency in mice and humans.

Ntessalen, Maria / Procter, Nathan E K / Schwarz, Konstantin / Loudon, Brodie L / Minnion, Magdalena / Fernandez, Bernadette O / Vassiliou, Vassilios S / Vauzour, David / Madhani, Melanie / Constantin-Teodosiu, Dumitru / Horowitz, John D / Feelisch, Martin / Dawson, Dana / Crichton, Paul G / Frenneaux, Michael P

The American journal of clinical nutrition

2019 Volume 111, Issue 1, Page(s) 79–89

Abstract: ... sodium chloride (1 g/L) in drinking water ad libitum for 7 d before killing. Skeletal muscle mitochondrial ...

Abstract	Background: Inorganic nitrate, abundant in leafy green vegetables and beetroot, is thought to have protective health benefits. Adherence to a Mediterranean diet reduces the incidence and severity of coronary artery disease, whereas supplementation with nitrate can improve submaximal exercise performance. Once ingested, oral commensal bacteria may reduce nitrate to nitrite, which may subsequently be reduced to nitric oxide during conditions of hypoxia and in the presence of "nitrite reductases" such as heme- and molybdenum-containing enzymes. Objective: We aimed to explore the putative effects of inorganic nitrate and nitrite on mitochondrial function in skeletal muscle. Methods: Mice were subjected to a nitrate/nitrite-depleted diet for 2 wk, then supplemented with sodium nitrate, sodium nitrite, or sodium chloride (1 g/L) in drinking water ad libitum for 7 d before killing. Skeletal muscle mitochondrial function and expression of uncoupling protein (UCP) 3, ADP/ATP carrier protein (AAC) 1 and AAC2, and pyruvate dehydrogenase (PDH) were assessed by respirometry and Western blotting. Studies were also undertaken in human skeletal muscle biopsies from a cohort of coronary artery bypass graft patients treated with either sodium nitrite (30-min infusion of 10 μmol/min) or vehicle [0.9% (wt:vol) saline] 24 h before surgery. Results: Neither sodium nitrate nor sodium nitrite supplementation altered mitochondrial coupling efficiency in murine skeletal muscle, and expression of UCP3, AAC1, or AAC2, and PDH phosphorylation status did not differ between the nitrite and saline groups. Similar results were observed in human samples. Conclusions: Sodium nitrite failed to improve mitochondrial metabolic efficiency, rendering this mechanism implausible for the purported exercise benefits of dietary nitrate supplementation. This trial was registered at clinicaltrials.gov as NCT04001283.
MeSH term(s)	Animals ; Cohort Studies ; Dietary Supplements/analysis ; Female ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; Mitochondria/drug effects ; Mitochondria/metabolism ; Muscle, Skeletal/drug effects ; Muscle, Skeletal/metabolism ; Nitrates/administration & dosage ; Nitric Oxide/metabolism ; Nitrites/administration & dosage ; Uncoupling Protein 3/genetics ; Uncoupling Protein 3/metabolism
Chemical Substances	Nitrates ; Nitrites ; Uncoupling Protein 3 ; Nitric Oxide (31C4KY9ESH)
Language	English
Publishing date	2019-09-30
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	280048-2
ISSN	1938-3207 ; 0002-9165
ISSN (online)	1938-3207
ISSN	0002-9165
DOI	10.1093/ajcn/nqz245
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Article ; Online: Diastolic Ventricular Interaction in Heart Failure With Preserved Ejection Fraction.

Parasuraman, Sathish K / Loudon, Brodie L / Lowery, Crystal / Cameron, Donnie / Singh, Satnam / Schwarz, Konstantin / Gollop, Nicholas D / Rudd, Amelia / McKiddie, Fergus / Phillips, Jim J / Prasad, Sanjay K / Wilson, Andrew M / Sen-Chowdhry, Srijita / Clark, Allan / Vassiliou, Vassilios S / Dawson, Dana K / Frenneaux, Michael P

Journal of the American Heart Association

2019 Volume 8, Issue 7, Page(s) e010114

Abstract: Background Exercise-induced pulmonary hypertension is common in heart failure with preserved ejection fraction ( HF p EF ). We hypothesized that this could result in pericardial constraint and diastolic ventricular interaction in some patients during ... ...

Abstract	Background Exercise-induced pulmonary hypertension is common in heart failure with preserved ejection fraction ( HF p EF ). We hypothesized that this could result in pericardial constraint and diastolic ventricular interaction in some patients during exercise. Methods and Results Contrast stress echocardiography was performed in 30 HF p EF patients, 17 hypertensive controls, and 17 normotensive controls (healthy). Cardiac volumes, and normalized radius of curvature ( NRC ) of the interventricular septum at end-diastole and end-systole, were measured at rest and peak-exercise, and compared between the groups. The septum was circular at rest in all 3 groups at end-diastole. At peak-exercise, end-systolic NRC increased to 1.47±0.05 ( P<0.001) in HF p EF patients, confirming development of pulmonary hypertension. End-diastolic NRC also increased to 1.54±0.07 ( P<0.001) in HF p EF patients, indicating septal flattening, and this correlated significantly with end-systolic NRC (ρ=0.51, P=0.007). In hypertensive controls and healthy controls, peak-exercise end-systolic NRC increased, but this was significantly less than observed in HF p EF patients ( HF p EF , P=0.02 versus hypertensive controls; P<0.001 versus healthy). There were also small, non-significant increases in end-diastolic NRC in both groups (hypertensive controls, +0.17±0.05, P=0.38; healthy, +0.06±0.03, P=0.93). In HF p EF patients, peak-exercise end-diastolic NRC also negatively correlated ( r=-0.40, P<0.05) with the change in left ventricular end-diastolic volume with exercise (ie, the Frank-Starling mechanism), and a trend was noted towards a negative correlation with change in stroke volume ( r=-0.36, P=0.08). Conclusions Exercise pulmonary hypertension causes substantial diastolic ventricular interaction on exercise in some patients with HF p EF , and this restriction to left ventricular filling by the right ventricle exacerbates the pre-existing impaired Frank-Starling response in these patients.
MeSH term(s)	Aged ; Analysis of Variance ; Cardiac Volume/physiology ; Case-Control Studies ; Echocardiography, Stress ; Exercise/physiology ; Female ; Heart Failure, Diastolic/physiopathology ; Humans ; Hypertension, Pulmonary/physiopathology ; Male ; Stroke Volume/physiology ; Ventricular Function, Left/physiology ; Ventricular Function, Right/physiology
Language	English
Publishing date	2019-03-29
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2653953-6
ISSN	2047-9980 ; 2047-9980
ISSN (online)	2047-9980
ISSN	2047-9980
DOI	10.1161/JAHA.118.010114
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Article ; Online: Osteoprotegerin and Myocardial Fibrosis in Patients with Aortic Stenosis.

Loudon, Brodie L / Ntatsaki, Eleana / Newsome, Simon / Halliday, Brian / Lota, Amrit / Ali, Aamir / Malley, Tamir / Selvendran, Subothini / Aggarwal, Nikhil / Lam, Willis / Donovan, Jackie / Auger, Dominque / Raphael, Claire E / Flynn, Paul D / Pennell, Dudley J / Vassiliou, Vassilios S / Prasad, Sanjay K

Scientific reports

2018 Volume 8, Issue 1, Page(s) 14550

Abstract: ... fibrosis did not have higher levels of OPG compared to those without fibrosis (6.78 vs. 5.25 pmol/L, p = 0 ... 78 vs. 6.97 pmol/L, p = 0.27). However, OPG levels in patients with chronic myocardial infarction ...

Abstract	Left ventricular myocardial fibrosis in patients with aortic stenosis (AS) confers worse prognosis. Plasma osteoprotegerin (OPG), a cytokine from the TNF receptor family, correlates with the degree of valve calcification in AS, reflecting the activity of the tissue RANKL/RANK/OPG (receptor activator of nuclear factor κΒ ligand/RANK/osteoprotegerin) axis, and is associated with poorer outcomes in AS. Its association with myocardial fibrosis is unknown. We hypothesised that OPG levels would reflect the extent of myocardial fibrosis in AS. We included 110 consecutive patients with AS who had undergone late-gadolinium contrast enhanced cardiovascular magnetic resonance (LGE-CMR). Patients were characterised according to pattern of fibrosis (no fibrosis, midwall fibrosis, or chronic myocardial infarction fibrosis). Serum OPG was measured with ELISA and compared between groups defined by valve stenosis severity. Some 36 patients had no fibrosis, 38 had midwall fibrosis, and 36 had chronic infarction. Patients with midwall fibrosis did not have higher levels of OPG compared to those without fibrosis (6.78 vs. 5.25 pmol/L, p = 0.12). There was no difference between those with midwall or chronic myocardial infarction fibrosis (6.78 vs. 6.97 pmol/L, p = 0.27). However, OPG levels in patients with chronic myocardial infarction fibrosis were significantly higher than those without fibrosis (p = 0.005).
MeSH term(s)	Aged ; Aged, 80 and over ; Aortic Valve Stenosis/blood ; Aortic Valve Stenosis/complications ; Aortic Valve Stenosis/pathology ; Female ; Fibrosis ; Heart Ventricles/pathology ; Humans ; Male ; Middle Aged ; Myocardial Infarction/blood ; Myocardial Infarction/complications ; Myocardial Infarction/pathology ; Myocardium/pathology ; Osteoprotegerin/blood
Chemical Substances	Osteoprotegerin
Language	English
Publishing date	2018-09-28
Publishing country	England
Document type	Clinical Trial ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-018-32738-y
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Article ; Online: Nitrite circumvents platelet resistance to nitric oxide in patients with heart failure preserved ejection fraction and chronic atrial fibrillation.

Borgognone, Alessandra / Shantsila, Eduard / Worrall, Sophie M / Prompunt, Eakkapote / Loka, Thomas / Loudon, Brodie L / Chimen, Myriam / Ed Rainger, G / Lord, Janet M / Turner, Ashley / Nightingale, Peter / Feelisch, Martin / Kirchhof, Paulus / Lip, Gregory Y H / Watson, Steve P / Frenneaux, Michael P / Madhani, Melanie

Cardiovascular research

2018 Volume 114, Issue 10, Page(s) 1313–1323

Abstract: Aims: Heart failure (HF) is a pro-thrombotic state. Both platelet and vascular responses to nitric oxide (NO) donors are impaired in HF patients with reduced ejection fraction (HFrEF) compared with healthy volunteers (HVs) due to scavenging of NO, and ... ...

Abstract	Aims: Heart failure (HF) is a pro-thrombotic state. Both platelet and vascular responses to nitric oxide (NO) donors are impaired in HF patients with reduced ejection fraction (HFrEF) compared with healthy volunteers (HVs) due to scavenging of NO, and possibly also reduced activity of the principal NO sensor, soluble guanylate cyclase (sGC), limiting the therapeutic potential of NO donors as anti-aggregatory agents. Previous studies have shown that nitrite inhibits platelet activation presumptively after its reduction to NO, but the mechanism(s) involved remain poorly characterized. Our aim was to compare the effects of nitrite on platelet function in HV vs. HF patients with preserved ejection fraction (HFpEF) and chronic atrial fibrillation (HFpEF-AF), vs. patients with chronic AF without HF, and to assess whether these effects occur independent of the interaction with other formed elements of blood. Methods and results: Platelet responses to nitrite and the NO donor sodium nitroprusside (SNP) were compared in age-matched HV controls (n = 12), HFpEF-AF patients (n = 29), and chronic AF patients (n = 8). Anti-aggregatory effects of nitrite in the presence of NO scavengers/sGC inhibitor were determined and vasodilator-stimulated phosphoprotein (VASP) phosphorylation was assessed using western blotting. In HV and chronic AF, both nitrite and SNP inhibited platelet aggregation in a concentration-dependent manner. Inhibition of platelet aggregation by the NO donor SNP was impaired in HFpEF-AF patients compared with healthy and chronic AF individuals, but there was no impairment of the anti-aggregatory effects of nitrite. Nitrite circumvented platelet NO resistance independently of other blood cells by directly activating sGC and phosphorylating VASP. Conclusion: We here show for the first time that HFpEF-AF (but not chronic AF without HF) is associated with marked impairment of platelet NO responses due to sGC dysfunction and nitrite circumvents the 'platelet NO resistance' phenomenon in human HFpEF, at least partly, by acting as a direct sGC activator independent of NO.
MeSH term(s)	Aged ; Aged, 80 and over ; Atrial Fibrillation/blood ; Atrial Fibrillation/diagnosis ; Atrial Fibrillation/physiopathology ; Blood Platelets/drug effects ; Blood Platelets/metabolism ; Case-Control Studies ; Cell Adhesion Molecules/blood ; Chronic Disease ; Drug Resistance/drug effects ; Female ; Heart Failure/blood ; Heart Failure/diagnosis ; Heart Failure/physiopathology ; Humans ; Male ; Microfilament Proteins/blood ; Nitric Oxide/blood ; Nitric Oxide Donors/metabolism ; Nitric Oxide Donors/pharmacology ; Nitroprusside/metabolism ; Nitroprusside/pharmacology ; Phosphoproteins/blood ; Phosphorylation ; Random Allocation ; Sodium Nitrite/pharmacology ; Soluble Guanylyl Cyclase/blood ; Stroke Volume ; Ventricular Function, Left
Chemical Substances	Cell Adhesion Molecules ; Microfilament Proteins ; Nitric Oxide Donors ; Phosphoproteins ; vasodilator-stimulated phosphoprotein ; Nitroprusside (169D1260KM) ; Nitric Oxide (31C4KY9ESH) ; Soluble Guanylyl Cyclase (EC 4.6.1.2) ; Sodium Nitrite (M0KG633D4F)
Language	English
Publishing date	2018-04-16
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80340-6
ISSN	1755-3245 ; 0008-6363
ISSN (online)	1755-3245
ISSN	0008-6363
DOI	10.1093/cvr/cvy087
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