Publications by authors named "David H MacIver"

Background: Global longitudinal active strain energy density (GLASED) is an innovative method for assessing myocardial function and quantifies the work performed per unit volume of the left ventricular myocardium. The GLASED, measured using MRI, is the best prognostic marker currently available. This study aimed to evaluate the feasibility of measuring the GLASED using echocardiography and to investigate potential differences in the GLASED among athletes based on age and sex.

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Aims: Identifying the imaging method that best predicts all-cause mortality, cardiovascular adverse events, and heart failure risk is crucial for tailoring optimal management. Potential prognostic markers include left ventricular (LV) myocardial mass, ejection fraction, myocardial strain, stroke work, contraction fraction, pressure-strain product, and a new measurement called global longitudinal active strain density (GLASED). This study sought to compare the utility of 23 potential LV prognostic markers of structure and contractile function in a community-based cohort.

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Aims: This study compared commonly used methods for calculating left ventricular wall stress with the finite element analysis and evaluated different approaches to strain estimation. We sought to improve the accuracy of contractance estimation by developing a novel stress equation.

Background: Multiple methods for calculating LV contractile stress and strain exist.

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Aims: Myocardial contractility is poorly defined and difficult to compare between studies. Contractance or myocardial active strain energy density (MASED) measures the mechanical work done per unit volume (with units of kJ/m) by any cardiac tissue during contraction. Contractance is an ideal candidate for measuring contractile function as it combines information from both stress and strain.

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The left ventricular ejection fraction does not accurately predict exercise capacity or symptom severity and has a limited role in predicting prognosis in heart failure. A better method of assessing ventricular performance is needed to aid understanding of the pathophysiological mechanisms and guide management in conditions such as heart failure. In this study, we propose two novel measures to quantify myocardial performance, the global longitudinal active strain energy (GLASE) and its density (GLASED) and compare them to existing measures in normal and diseased left ventricles.

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Left ventricular ejection fraction (LVEF) has a limited role in predicting outlook in heart diseases including heart failure. We quantified the independent geometric factors that determine LVEF using cardiac MRI and sought to provide an improved measure of ventricular function by adjusting for such independent variables. A mathematical model was used to analyse the independent effects of structural variables and myocardial shortening on LVEF.

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The view that chronic heart failure was exclusively a disease of the heart dominated the cardiovascular literature until relatively recently. However, over the last 40 years it has increasingly come to be seen as a multisystem disease. Aside from changes in the sympathetic and parasympathetic nervous systems and the renin-angiotensin-aldosterone system, adaptations to the lungs, muscles and gastrointestinal tract have been clearly documented.

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Aims: The aims of this study were to establish the left ventricular (LV) phenotype in rugby football league (RFL) athletes and to mathematically model the association between LV size, strain (ɛ) and ejection fraction (EF).

Methods And Results: 139 male athletes underwent echocardiographic LV evaluation including ɛ imaging. Non-athletic males were used for comparison.

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Background: Immersion pulmonary edema is potentially a catastrophic condition; however, the pathophysiological mechanisms are ill-defined. This study assessed the individual and combined effects of exertion and negative pressure breathing on the cardiovascular system during the development of pulmonary edema in SCUBA divers.

Methods: Sixteen male professional SCUBA divers performed four SCUBA dives in a freshwater pool at 1 m depth while breathing air at either a positive or negative pressure both at rest or with exercise.

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Article Synopsis
  • There are two main ideas about how the heart's structure is organized: one is called the myocardial band, and the other is the myocardial mesh model.
  • New studies suggest that the mesh model is a better explanation for how the heart works.
  • This research shows that different medical imaging tools back up the mesh model and that the band model doesn't match what scientists have found.
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The concept of the 'unique myocardial band', which proposes that the ventricular myocardial cone is arranged like skeletal muscle, provides an attractive framework for understanding haemodynamics. The original idea was developed by Francisco Torrent-Guasp. Using boiled hearts and blunt dissection, Torrent-Guasp created a single band of ventricular myocardium extending from the pulmonary trunk to the aortic root, with the band thus constructed encircling both ventricular cavities.

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The evidence is increasing that left ventricular noncompaction cardiomyopathy as it is currently defined does not represent a failure of compaction of pre-existing trabecular myocardium found during embryonic development to form the compact component of the ventricular walls. Neither is there evidence of which we are aware to favour the notion that the entity is a return to a phenotype seen in cold-blooded animals. It is also known that when seen in adults, the presence of excessive ventricular trabeculations does not portend a poor prognosis when the ejection fraction is normal, with the risks of complications such as arrhythmia and stroke being rare in this setting.

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This study assessed the relation between altered cardiac function and the development of interstitial pulmonary edema in scuba divers. Fifteen healthy men performed a 30-minute scuba dive in open sea. They were instructed to fin for 30 minutes and were wearing wet suits.

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Hypertensive heart disease is often associated with a preserved left ventricular ejection fraction despite impaired myocardial shortening. The authors investigated this paradox in 55 hypertensive patients (52±13 years, 58% male) and 32 age- and sex-matched normotensive control patients (49±11 years, 56% male) who underwent cardiac magnetic resonance imaging at 1.5T.

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Background: The anatomical substrate for the mid-mural ventricular hyperechogenic zone remains uncertain, but it may represent no more than ultrasound reflected from cardiomyocytes orientated orthogonally to the ultrasonic beam. We sought to ascertain the relationship between the echogenic zone and the orientation of the cardiomyocytes.

Methods: We used 3D echocardiography, diffusion tensor imaging, and microcomputed tomography to analyze the location and orientation of cardiomyocytes within the echogenic zone.

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Pulmonary hypertension is usually related to obstruction of pulmonary blood flow at the level of the pulmonary arteries (eg, pulmonary embolus), pulmonary arterioles (idiopathic pulmonary hypertension), pulmonary veins (pulmonary venoocclusive disease) or mitral valve (mitral stenosis and regurgitation). Pulmonary hypertension is also observed in heart failure due to left ventricle myocardial diseases regardless of the ejection fraction. Pulmonary hypertension is often regarded as a passive response to the obstruction to pulmonary flow.

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We present three cases of thoracic aortic aneurysms caused by giant cell aortitis. Thoracic aortic aneurysms are common and usually related to hypertension, a bicuspid aortic valve or connective tissue diseases such as Marfan syndrome. Our report serves as a reminder that giant cell aortitis is an unusual yet very important cause of thoracic aortic aneurysm.

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The pathophysiological mechanisms underlying the clinical phenotype of sarcomeric hypertrophic cardiomyopathy are controversial. The development of cardiac hypertrophy in hypertension and aortic stenosis is usually described as a compensatory mechanism that normalizes wall stress. We suggest that an important abnormality in hypertrophic cardiomyopathy is reduced contractile stress (the force per unit area) generated by myocardial tissue secondary to abnormalities such as cardiomyocyte disarray.

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Aims: Atrial stunning, a loss of atrial mechanical contraction, can occur following a successful cardioversion. It is hypothesized that persistent atrial fibrillation-induced electrical remodeling (AFER) on atrial electrophysiology may be responsible for such impaired atrial mechanics. This simulation study aimed to investigate the effects of AFER on atrial electro-mechanics.

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Heart failure with preserved ejection fraction (HFpEF) accounts for about 50% of heart failure cases. It has features of incomplete relaxation and increased stiffness of the left ventricle. Studies from clinical electrophysiology and animal experiments have found that HFpEF is associated with impaired calcium homeostasis, ion channel remodeling and concentric left ventricle hypertrophy (LVH).

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Objectives: The purpose of this study was to determine the mathematical relationship between left ventricular ejection fraction and global myocardial strain. A reduction in myocardial strain would be expected to cause a fall in ejection fraction. However, there is abundant evidence that abnormalities of myocardial strain can occur with a normal ejection fraction.

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