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Article ; Online: Design and evaluation of a new consolidation exercise for students studying cardiac physiology: a digital escape room.

Horn, Margaux A

2022 Volume 47, Issue 1, Page(s) 82–92

Abstract: The current student body will, by and large, seek online resources to supplement their learning. However, resources that are freely available online vary in accuracy and quality, and the vast majority rely on passive learning. Therefore, there is a need ... ...

Abstract	The current student body will, by and large, seek online resources to supplement their learning. However, resources that are freely available online vary in accuracy and quality, and the vast majority rely on passive learning. Therefore, there is a need for interactive physiology teaching resources that facilitate application of knowledge, that can be accessed by students in their own time. The aim of this study was to design a digital escape room on the topic of cardiac arrhythmias and to evaluate this resource as a consolidation exercise to support learning and enjoyment of physiology. The digital escape room was designed as a series of interactive puzzles and created with a website page builder on a freely accessible WordPress site. To facilitate engagement, the escape room incorporated a countdown timer. Second-year medical students were invited to play the digital escape room remotely as a group exercise after delivery of the relevant teaching. Evaluation of the resource took place quantitatively with Google Analytics and Tag Manager software and qualitatively with a questionnaire (Microsoft Forms). Quantitative evaluation suggested that the puzzles were created across a range of difficulties but that most groups were able to complete the exercise and remained engaged throughout. Student feedback suggests that the format of the resource was rated positively, and most participants felt that the game helped to consolidate and apply their knowledge of cardiovascular physiology. Future studies will focus on examining whether the cardiovascular-themed digital escape room improves knowledge attainment among students studying physiology in higher education.
MeSH term(s)	Humans ; Problem-Based Learning ; Students, Medical ; Educational Measurement ; Surveys and Questionnaires ; Cardiovascular Physiological Phenomena
Language	English
Publishing date	2022-12-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	1024917-5
ISSN	1522-1229 ; 1043-4046
ISSN (online)	1522-1229
ISSN	1043-4046
DOI	10.1152/advan.00176.2022
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Article ; Online: Cardiac Physiology of Aging: Extracellular Considerations.

Horn, Margaux A

Comprehensive Physiology

2015 Volume 5, Issue 3, Page(s) 1069–1121

Abstract: Aging is a major risk factor for the development of cardiovascular disease, with the majority of affected patients being elderly. Progressive changes to myocardial structure and function occur with aging, often in concert with underlying pathologies. ... ...

Abstract	Aging is a major risk factor for the development of cardiovascular disease, with the majority of affected patients being elderly. Progressive changes to myocardial structure and function occur with aging, often in concert with underlying pathologies. However, whether chronological aging results in a remodeled "aged substrate" has yet to be established. In addition to myocyte contractility, myocardial performance relies heavily on the cardiac extracellular matrix (ECM), the roles of which are as dynamic as they are significant; including providing structural integrity, assisting in force transmission throughout the cardiac cycle and acting as a signaling medium for communication between cells and the extracellular environment. In the healthy heart, ECM homeostasis must be maintained, and matrix deposition is in balance with degradation. Consequently, alterations to, or misregulation of the cardiac ECM has been shown to occur in both aging and in pathological remodeling with disease. Mounting evidence suggests that age-induced matrix remodeling may occur at the level of ECM control; including collagen synthesis, deposition, maturation, and degradation. Furthermore, experimental studies using aged animal models not only suggest that the aged heart may respond differently to insult than the young, but the identification of key players specific to remodeling with age may hold future therapeutic potential for the treatment of cardiac dysfunction in the elderly. This review will focus on the role of the cardiac interstitium in the physiology of the aging myocardium, with particular emphasis on the implications to age-related remodeling in disease.
MeSH term(s)	Aging/metabolism ; Aging/physiology ; Animals ; Extracellular Matrix/metabolism ; Heart/growth & development ; Heart/physiology ; Homeostasis ; Humans ; Myocytes, Cardiac/metabolism
Language	English
Publishing date	2015-07-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ISSN	2040-4603
ISSN (online)	2040-4603
DOI	10.1002/cphy.c140063
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Article ; Online: Aging and the cardiac collagen matrix: Novel mediators of fibrotic remodelling.

Horn, Margaux A / Trafford, Andrew W

Journal of molecular and cellular cardiology

2015 Volume 93, Page(s) 175–185

Abstract: Cardiovascular disease is a leading cause of death worldwide and there is a pressing need for new therapeutic strategies to treat such conditions. The risk of developing cardiovascular disease increases dramatically with age, yet the majority of ... ...

Abstract	Cardiovascular disease is a leading cause of death worldwide and there is a pressing need for new therapeutic strategies to treat such conditions. The risk of developing cardiovascular disease increases dramatically with age, yet the majority of experimental research is executed using young animals. The cardiac extracellular matrix (ECM), consisting predominantly of fibrillar collagen, preserves myocardial integrity, provides a means of force transmission and supports myocyte geometry. Disruptions to the finely balanced control of collagen synthesis, post-synthetic deposition, post-translational modification and degradation may have detrimental effects on myocardial functionality. It is now well established that the aged heart is characterized by fibrotic remodelling, but the mechanisms responsible for this are incompletely understood. Furthermore, studies using aged animal models suggest that interstitial remodelling with disease may be age-dependent. Thus with the identification of new therapeutic strategies targeting fibrotic remodelling, it may be necessary to consider age-dependent mechanisms. In this review, we discuss remodelling of the cardiac collagen matrix as a function of age, whilst highlighting potential novel mediators of age-dependent fibrotic pathways.
MeSH term(s)	Aging/metabolism ; Animals ; Biomarkers ; Collagen/metabolism ; Extracellular Matrix/metabolism ; Fibrosis ; Humans ; Matrix Metalloproteinases/metabolism ; Myocardium/metabolism ; Myocardium/pathology ; Protein Processing, Post-Translational ; Tissue Inhibitor of Metalloproteinases/metabolism ; Ventricular Dysfunction/etiology ; Ventricular Dysfunction/metabolism ; Ventricular Dysfunction/pathology ; Ventricular Dysfunction/physiopathology ; Ventricular Remodeling
Chemical Substances	Biomarkers ; Tissue Inhibitor of Metalloproteinases ; Collagen (9007-34-5) ; Matrix Metalloproteinases (EC 3.4.24.-)
Language	English
Publishing date	2015-11-11
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	80157-4
ISSN	1095-8584 ; 0022-2828
ISSN (online)	1095-8584
ISSN	0022-2828
DOI	10.1016/j.yjmcc.2015.11.005
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Article ; Online: Temporal Development of Autonomic Dysfunction in Heart Failure: Effects of Age in an Ovine Rapid-pacing Model.

Horn, Margaux A / Bode, Elizabeth F / Borland, Samantha J / Kirkwood, Graeme J / Briston, Sarah J / Richards, Mark A / Dibb, Katharine M / Trafford, Andrew W

The journals of gerontology. Series A, Biological sciences and medical sciences

2015 Volume 71, Issue 12, Page(s) 1544–1552

Abstract: Heart failure (HF) is predominantly a disease of older adults and characterized by extensive sympatho-vagal imbalance leading to impaired reflex control of heart rate (HR). However, whether aging influences the development or extent of the autonomic ... ...

Abstract	Heart failure (HF) is predominantly a disease of older adults and characterized by extensive sympatho-vagal imbalance leading to impaired reflex control of heart rate (HR). However, whether aging influences the development or extent of the autonomic imbalance in HF remains unclear. To address this, we used an ovine model of aging with tachypacing-induced HF to determine whether aging affects the chronotropic and inotropic responses to autonomic stimulation and reduction in heart rate variability (HRV) in HF. We find that aging is associated with increased cardiac dimensions and reduced contractility before the onset of tachypacing, and these differences persist in HF. Additionally, the chronotropic response to β-adrenergic stimulation was markedly attenuated in HF, and this occurred more rapidly in aged animals. By measuring HR during sequential autonomic blockade, our data are consistent with a reduced parasympathetic control of resting HR in aging, with young HF animals having an attenuated sympathetic influence on HR. Time-domain analyses of HR show a reduction in HRV in both young and aged failing animals, although HRV is lowest in aged HF. In conclusion, aging is associated with altered autonomic control and β-adrenergic responsiveness of HR, and these are exacerbated with the development of HF.
MeSH term(s)	Acetylcholine/pharmacology ; Adrenergic beta-Antagonists/pharmacology ; Age Factors ; Animals ; Autonomic Nervous System/physiopathology ; Biomarkers/blood ; Cardiac Pacing, Artificial ; Disease Models, Animal ; Dobutamine/pharmacology ; Echocardiography ; Electrocardiography ; Enzyme-Linked Immunosorbent Assay ; Female ; Heart Failure/physiopathology ; Heart Rate/drug effects ; Heart Rate/physiology ; Hemodynamics ; Norepinephrine/blood ; Sheep, Domestic ; Time Factors
Chemical Substances	Adrenergic beta-Antagonists ; Biomarkers ; Dobutamine (3S12J47372) ; Acetylcholine (N9YNS0M02X) ; Norepinephrine (X4W3ENH1CV)
Language	English
Publishing date	2015-12-26
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1223643-3
ISSN	1758-535X ; 1079-5006
ISSN (online)	1758-535X
ISSN	1079-5006
DOI	10.1093/gerona/glv217
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Article ; Online: Perturbed atrial calcium handling in an ovine model of heart failure: potential roles for reductions in the L-type calcium current.

Clarke, Jessica D / Caldwell, Jessica L / Horn, Margaux A / Bode, Elizabeth F / Richards, Mark A / Hall, Mark C S / Graham, Helen K / Briston, Sarah J / Greensmith, David J / Eisner, David A / Dibb, Katharine M / Trafford, Andrew W

Journal of molecular and cellular cardiology

2014 Volume 79, Page(s) 169–179

Abstract: Heart failure (HF) is commonly associated with reduced cardiac output and an increased risk of atrial arrhythmias particularly during β-adrenergic stimulation. The aim of the present study was to determine how HF alters systolic Ca(2+) and the response ... ...

Abstract	Heart failure (HF) is commonly associated with reduced cardiac output and an increased risk of atrial arrhythmias particularly during β-adrenergic stimulation. The aim of the present study was to determine how HF alters systolic Ca(2+) and the response to β-adrenergic (β-AR) stimulation in atrial myocytes. HF was induced in sheep by ventricular tachypacing and changes in intracellular Ca(2+) concentration studied in single left atrial myocytes under voltage and current clamp conditions. The following were all reduced in HF atrial myocytes; Ca(2+) transient amplitude (by 46% in current clamped and 28% in voltage clamped cells), SR dependent rate of Ca(2+) removal (kSR, by 32%), L-type Ca(2+) current density (by 36%) and action potential duration (APD90 by 22%). However, in HF SR Ca(2+) content was increased (by 19%) when measured under voltage-clamp stimulation. Inhibiting the L-type Ca(2+) current (ICa-L) in control cells reproduced both the decrease in Ca(2+) transient amplitude and increase of SR Ca(2+) content observed in voltage-clamped HF cells. During β-AR stimulation Ca(2+) transient amplitude was the same in control and HF cells. However, ICa-L remained less in HF than control cells whilst SR Ca(2+) content was highest in HF cells during β-AR stimulation. The decrease in ICa-L that occurs in HF atrial myocytes appears to underpin the decreased Ca(2+) transient amplitude and increased SR Ca(2+) content observed in voltage-clamped cells.
MeSH term(s)	Action Potentials ; Animals ; Calcium/metabolism ; Calcium Channels, L-Type/metabolism ; Disease Models, Animal ; Female ; Heart Atria/metabolism ; Heart Atria/pathology ; Heart Failure/metabolism ; Heart Failure/pathology ; Homeostasis ; Intracellular Space/metabolism ; Ion Channel Gating ; Models, Biological ; Receptors, Adrenergic, beta/metabolism ; Sarcoplasmic Reticulum/metabolism ; Sarcoplasmic Reticulum Calcium-Transporting ATPases/metabolism ; Sheep ; Systole
Chemical Substances	Calcium Channels, L-Type ; Receptors, Adrenergic, beta ; Sarcoplasmic Reticulum Calcium-Transporting ATPases (EC 3.6.3.8) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2014-11-22
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80157-4
ISSN	1095-8584 ; 0022-2828
ISSN (online)	1095-8584
ISSN	0022-2828
DOI	10.1016/j.yjmcc.2014.11.017
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Article ; Online: Characterization of an extensive transverse tubular network in sheep atrial myocytes and its depletion in heart failure.

Dibb, Katharine M / Clarke, Jessica D / Horn, Margaux A / Richards, Mark A / Graham, Helen K / Eisner, David A / Trafford, Andrew W

Circulation. Heart failure

2009 Volume 2, Issue 5, Page(s) 482–489

Abstract: Background: In ventricular myocytes, the majority of structures that couple excitation to the systolic rise of Ca(2+) are located at the transverse tubular (t-tubule) membrane. In the failing ventricle, disorganization of t-tubules disrupts excitation ... ...

Abstract	Background: In ventricular myocytes, the majority of structures that couple excitation to the systolic rise of Ca(2+) are located at the transverse tubular (t-tubule) membrane. In the failing ventricle, disorganization of t-tubules disrupts excitation contraction coupling. The t-tubule membrane is virtually absent in the atria of small mammals resulting in spatiotemporally distinct profiles of intracellular Ca(2+) release on stimulation in atrial and ventricular cells. The aims of this study were to determine (i) whether atrial myocytes from a large mammal (sheep) possess t-tubules, (ii) whether these are functionally important, and (iii) whether they are disrupted in heart failure. Methods and results: Sheep left atrial myocytes were stained with di-4-ANEPPS. Nearly all control cells had an extensive t-tubule network resulting in each voxel in the cell being nearer to a membrane (sarcolemma or t-tubule) than would otherwise be the case. T-tubules decrease the distance of 50% of voxels from a membrane from 3.35 + or - 0.15 to 0.88 + or- 0.04 microm. During depolarization, intracellular Ca(2+) rises simultaneously at the cell periphery and center. In heart failure induced by rapid ventricular pacing, there was an almost complete loss of atrial t-tubules. The distance of 50% of voxels from a membrane increased to 2.04 + or - 0.08 microm, and there was a loss of early Ca(2+) release from the cell center. Conclusions: Sheep atrial myocytes possess a substantial t-tubule network that synchronizes the systolic Ca(2+) transient. In heart failure, this network is markedly disrupted. This may play an important role in changes of atrial function in heart failure.
MeSH term(s)	Animals ; Atrial Function, Left ; Calcium Signaling ; Cardiac Pacing, Artificial ; Disease Models, Animal ; Fluorescent Dyes ; Heart Atria/metabolism ; Heart Failure/metabolism ; Heart Failure/pathology ; Heart Failure/physiopathology ; Image Processing, Computer-Assisted ; Microscopy, Confocal ; Myocardial Contraction ; Myocytes, Cardiac/metabolism ; Myocytes, Cardiac/pathology ; Pyridinium Compounds ; Rats ; Sarcolemma/metabolism ; Sarcolemma/pathology ; Sheep ; Ventricular Function, Left
Chemical Substances	Fluorescent Dyes ; Pyridinium Compounds ; 1-(3-sulfonatopropyl)-4-(beta)(2-(di-n-butylamino)-6-naphthylvinyl)pyridinium betaine (90134-00-2)
Language	English
Publishing date	2009-07-29
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2429459-7
ISSN	1941-3297 ; 1941-3289
ISSN (online)	1941-3297
ISSN	1941-3289
DOI	10.1161/CIRCHEARTFAILURE.109.852228
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Article ; Online: Age-related divergent remodeling of the cardiac extracellular matrix in heart failure: collagen accumulation in the young and loss in the aged.

Horn, Margaux A / Graham, Helen K / Richards, Mark A / Clarke, Jessica D / Greensmith, David J / Briston, Sarah J / Hall, Mark C S / Dibb, Katharine M / Trafford, Andrew W

Journal of molecular and cellular cardiology

2012 Volume 53, Issue 1, Page(s) 82–90

Abstract: The incidence of heart failure (HF) increases with age. This study sought to determine whether aging exacerbates structural and functional remodeling of the myocardium in HF. HF was induced in young (~18 months) and aged sheep (>8 years) by right ... ...

Abstract	The incidence of heart failure (HF) increases with age. This study sought to determine whether aging exacerbates structural and functional remodeling of the myocardium in HF. HF was induced in young (~18 months) and aged sheep (>8 years) by right ventricular tachypacing. In non-paced animals, aging was associated with increased left ventricular (LV) end diastolic internal dimensions (EDID, P<0.001), reduced fractional shortening (P<0.01) and an increase in myocardial collagen content (P<0.01). HF increased EDID and reduced fractional shortening in both young and aged animals, although these changes were more pronounced in the aged (P<0.05). Age-associated differences in cardiac extracellular matrix (ECM) remodeling occurred in HF with collagen accumulation in young HF (P<0.001) and depletion in aged HF (P<0.05). MMP-2 activity increased in the aged control and young HF groups (P<0.05). Reduced tissue inhibitor of metalloproteinase (TIMP) expression (TIMPs 3 and 4, P<0.05) was present only in the aged HF group. Secreted protein acidic and rich in cysteine (SPARC) was increased in aged hearts compared to young controls (P<0.05) while serum procollagen type I C-pro peptide (PICP) was increased in both young failing (P<0.05) and aged failing (P<0.01) animals. In conclusion, collagen content of the cardiac ECM changes in both aging and HF although; whether collagen accumulation or depletion occurs depends on age. Changes in TIMP expression in aged failing hearts alongside augmented collagen synthesis in HF provide a potential mechanism for the age-dependent ECM remodeling. Aging should therefore be considered an important factor when elucidating cardiac disease mechanisms.
MeSH term(s)	Age Factors ; Animals ; Collagen/metabolism ; Disease Models, Animal ; Endomyocardial Fibrosis/metabolism ; Extracellular Matrix/metabolism ; Female ; Heart/physiopathology ; Heart Failure/metabolism ; Myocardial Contraction ; Myocardium/metabolism ; Sheep ; Tissue Inhibitor of Metalloproteinases/metabolism ; Ventricular Remodeling
Chemical Substances	Tissue Inhibitor of Metalloproteinases ; Collagen (9007-34-5)
Language	English
Publishing date	2012-03-30
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80157-4
ISSN	1095-8584 ; 0022-2828
ISSN (online)	1095-8584
ISSN	0022-2828
DOI	10.1016/j.yjmcc.2012.03.011
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Article ; Online: Impaired β-adrenergic responsiveness accentuates dysfunctional excitation-contraction coupling in an ovine model of tachypacing-induced heart failure.

Briston, Sarah J / Caldwell, Jessica L / Horn, Margaux A / Clarke, Jessica D / Richards, Mark A / Greensmith, David J / Graham, Helen K / Hall, Mark C S / Eisner, David A / Dibb, Katharine M / Trafford, Andrew W

The Journal of physiology

2011 Volume 589, Issue Pt 6, Page(s) 1367–1382

Abstract: Reduced inotropic responsiveness is characteristic of heart failure (HF). This study determined the cellular Ca2+ homeostatic and molecular mechanisms causing the blunted β-adrenergic (β-AR) response in HF.We induced HF by tachypacing in sheep; ... ...

Abstract	Reduced inotropic responsiveness is characteristic of heart failure (HF). This study determined the cellular Ca2+ homeostatic and molecular mechanisms causing the blunted β-adrenergic (β-AR) response in HF.We induced HF by tachypacing in sheep; intracellular Ca2+ concentration was measured in voltage-clamped ventricular myocytes. In HF, Ca2+ transient amplitude and peak L-type Ca2+ current (ICa-L) were reduced (to 70 ± 11% and 50 ± 3.7% of control, respectively, P <0.05) whereas sarcoplasmic reticulum (SR) Ca2+ content was unchanged. β-AR stimulation with isoprenaline (ISO) increased Ca2+ transient amplitude, ICa-L and SRCa2+ content in both cell types; however, the response of HF cells was markedly diminished (P <0.05).Western blotting revealed an increase in protein phosphatase levels (PP1, 158 ± 17% and PP2A, 188 ± 34% of control, P <0.05) and reduced phosphorylation of phospholamban in HF (Ser16, 30 ± 10% and Thr17, 41 ± 15% of control, P <0.05). The β-AR receptor kinase GRK-2 was also increased in HF (173 ± 38% of control, P <0.05). In HF, activation of adenylyl cyclase with forskolin rescued the Ca2+ transient, SR Ca2+ content and SR Ca2+ uptake rate to the same levels as control cells in ISO. In conclusion, the reduced responsiveness of the myocardium to β-AR agonists in HF probably arises as a consequence of impaired phosphorylation of key intracellular proteins responsible for regulating the SR Ca2+ content and therefore failure of the systolic Ca2+ transient to increase appropriately during β-AR stimulation.
MeSH term(s)	Animals ; Disease Models, Animal ; Excitation Contraction Coupling/physiology ; Female ; Heart Failure/etiology ; Heart Failure/physiopathology ; Myocardial Contraction/physiology ; Receptors, Adrenergic, beta/physiology ; Sheep ; Tachycardia, Ventricular/complications ; Tachycardia, Ventricular/physiopathology
Chemical Substances	Receptors, Adrenergic, beta
Language	English
Publishing date	2011-01-17
Publishing country	England
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3115-x
ISSN	1469-7793 ; 0022-3751
ISSN (online)	1469-7793
ISSN	0022-3751
DOI	10.1113/jphysiol.2010.203984
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