David H. MacIver

A new method for quantification of left ventricular systolic function using a corrected ejection fraction.

AIMSnLeft ventricular ejection fraction (EF) is a suboptimal measure of ventricular function. Recent mathematical modelling of left ventricular contraction has shown that the EF is determined by both myocardial shortening (strain) and by end-diastolic wall thickness. Increasing end-diastolic wall thickness resulted in augmented radial wall thickening. This may result in a significant overestimation of ventricular systolic function as assessed by the EF. This study proposes a new measure of ventricular systolic function, the corrected EF (EF(c)) to allow for the presence of concentric left ventricular hypertrophy (LVH).nnnMETHODS AND RESULTSnThe study uses a new two-layer, three-dimensional mathematical model of ventricular contraction. Changes in end-diastolic wall thickness in addition to long-axis and mid-wall circumferential strain were modelled. Iso-strain lines were obtained where myocardial shortening (strain) is constant; EF increases with increasing end-diastolic wall thickness. The corrected EF is determined by following the iso-strain lines to the equivalent EF in the absence of hypertrophy (e.g. 9 mm thickness). For example, an individual with a mean end-diastolic wall thickness of 20 mm and measured EF of 60% has a corrected EF (EF(c)) of 37%.nnnCONCLUSIONnThe study shows that the EF is determined by absolute wall thickening and provides a nomogram for comparing EF when LVH is present. The EF(c) is a potential new measure of left ventricular systolic function. Its possible role will need validating in mortality trials.

A general theory of acute and chronic heart failure.

Current concepts of heart failure propose multiple heterogeneous pathophysiological mechanisms. Recently a theoretical framework for understanding chronic heart failure was suggested. This paper develops this framework to include acute heart failure syndromes. We propose that all acute heart failure syndromes may be understood in terms of a relative fall in left ventricular stroke volume. The initial compensatory mechanism is frequently a tachycardia often resulting in a near normal cardiac output. In more severe forms a fall in cardiac output causes hypotension or cardiogenic shock. In chronic heart failure the stroke volume and cardiac output is returned to normal predominantly through ventricular remodeling or dilatation. Ejection fraction is simply the ratio of stroke volume and end-diastolic volume. The resting stroke volume is predetermined by the tissues needs; therefore, if the ejection fraction changes, the end-diastolic volume must change in a reciprocal manner. The potential role of the right heart in influencing the presentation of left heart disease is examined. We propose that acute pulmonary edema occurs when the right ventricular stroke volume exceeds left ventricular stroke volume leading to fluid accumulation in the alveoli. The possible role of the right heart in determining pulmonary hypertension and raised filling pressures in left-sided heart disease are discussed. Different clinical scenarios are presented to help clarify these proposed mechanisms and the clinical implications of these theories are discussed. Finally an alternative definition of heart failure is proposed.

An alternative approach to understanding the pathophysiological mechanisms of chronic heart failure

No single well established hypothesis for the mechanisms of heart failure currently exists. Those definitions that do exist are either not universally applicable or are not exclusive to heart failure. The pathogenesis of heart failure has been considered by some to be too complex to define with multiple pathophysiological processes being implicated. The many clinical and neurohumoral features of heart failure may be more dependent on the severity of the condition and its speed of onset rather than its etiology. This suggests a potential single common pathway or pathogenic mechanism in all forms of heart failure regardless of cause. This viewpoint uses the framework of myocardial mechanics and energetics to propose an alternative, simplified definition and unifying hypothesis for the pathogenesis of chronic heart failure. Chronic heart failure may be understood as follows. Cardiac output and stroke volume are determined by the tissues requirements; the ejection fraction is determined by both myocardial shortening and degree of end-diastolic wall thickness; the end-diastolic volume is determined by the requirement to normalize stroke volume. We will argue that chronic heart failure can be viewed as a condition where the dominant compensatory mechanism is through regulation of ventricular end-diastolic volume. Consequently, in conditions where there is a fall in tissue perfusion, stroke volume and tissue perfusion are returned toward normal predominantly via this feedback mechanism. It is important for researchers, clinicians and their patients that we strive for a comprehensive, inclusive and unambiguous unifying hypothesis for pathophysiological mechanisms of heart failure.

Is remodeling the dominant compensatory mechanism in both chronic heart failure with preserved and reduced left ventricular ejection fraction

The mechanisms of heart failure are ill understood with multiple, heterogeneous hypotheses proposed to describe the condition. This study examines the individual effects of left ventricular hypertrophy, long-axis shortening and the effect of left ventricular remodeling on ejection fraction, end-diastolic volume and stroke volume using a mathematical model of left ventricular contraction. Reducing long-axis shortening caused a decline in stroke volume independently of hypertrophy. Increasing concentric left ventricular hypertrophy resulted in an increase in ejection fraction secondary to augmented wall thickening. A decline in stroke volume occurred despite a preserved ejection fraction when concentric hypertrophy was present. Normalization of stroke volume by remodeling resulted in a marked increase in end-diastolic volume in the absence of hypertrophy and an end-diastolic volume similar to normal in the presence of concentric hypertrophy. The model predicts that the dominant compensatory mechanism in chronic heart failure is remodeling with normalization of stroke volume. Observational data cited supports this conclusion.

Assessment of the Helical Ventricular Myocardial Band Using Standard Echocardiography

In the discussion of their recent article, Hayabuchi and his colleagues acknowledge that the “helical myocardial band” remains controversial. In the accompanying editorial, Buckberg harbored no such doubts. Are the limited echocardiographic findings illustrated truly sufficient for Hayabuchi and his colleagues to conclude that there is a “helical ventricular myocardial band”? They refer to a model that Torrent-Guasp had carved out of the ventricular muscular mass by disrupting myriads of myocardial branches, suggesting moreover that this band is freely moveable on itself. The histological studies produced by Hort and Feneis, however, provided evidence that the ventricular cone does not have discrete origins and insertions of the cardiomyocytes as found in skeletal muscle. Pettigrew had demonstrated more than a century ago the multiple interleaving sheets of cardiomyocytes to be found within the cone. Lev and Simkins, cited by Buckberg, also had emphasized that the cone can be dissected at the whim of the prosector, as achieved by Torrent-Guasp when subjectively producing the preparations now modeled by Buckberg. Our investigations, cited by Hayabuchi and colleagues, endorse the works of Feneis and Hort. The histological findings show no obvious anatomical substrate, other than the obvious change in alignment of the aggregated chains of cardiomyocytes, to explain the echocardiographic feature emphasized by the Japanese workers. They certainly provide none that represent a substantial proportion of the width of the septum, as the echocardiograms seem to suggest. The echogenic band is seen in the equatorial and basal regions of each of the walls of the left ventricle when viewed from the apex. No such band is seen when the ventricular mass is viewed using the parasternal window. We suggest that the echogenic band represents an area of distinct myocyte orientation within the continuous mesh of the septum, where the reflected ultrasound is perpendicular to the dominant orientation of the cardiomyocytes, thus giving maximum intensity compared with the surrounding tissue. The echogenic band, when viewed from the apex, therefore, is likely to represent no more than the chains of cardiomyocytes located within the mid-wall of the ventricular cone which are aligned circumferentially. The concept of the helical ventricular myocardial band does not model the circumferential orientation in this region. There are further problems, however, with the concepts advanced by Buckberg, His inferences are based on imaging systems that measure only strain, as opposed to assessing the local development of force. The onset of shortening is not identical with the onset of contraction, so it is his mistake to interpret late shortening as delayed contraction. We have shown that within the ventricular cone, there are extended zones in which the myocardium contracts auxotonically, that is, the force increases during systole. The features of such auxotonic contraction are delayed onset, restricted shortening, and delayed termination.

A new understanding and definition of non-compaction cardiomyopathy using analysis of left ventricular wall mechanics and stresses

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The key role of the RV in the pathogenesis of acute pulmonary oedema

Dear Editor, nnThe article entitled ‘The pathophysiology of hypertensive acute heart failure’1 provides an excellent contemporary review of mechanisms involved in the development of acute pulmonary oedema (APO). We wish to highlight the potential important role of the RV in the pathogenesis of APO.2nnAPO is often thought to result from backward pressure where a disease of the LV causes the LV end-diastolic pressure (LVEDP) to rise, resulting in …

17 Coronary angiography in a district general hospital

Introduction CTCA is now an established diagnostic tool in the evaluation of chest pain, and with the recently up-dated NICE CG95 guidelines its use is likely to increase nationally.1 We aimed to assess the demographics of our local patient cohort, protocol use, radiation dose and the accuracy and outcomes from our CT service. Methods Demographic and outcome data was collected for a 17 month period from Jul 2015–Nov 2016. The CTCA result was compared with the invasive angiogram in patients who had both investigations. Results 689 scans were performed with 95% for rule out of coronary artery disease. 8% of the scan protocols used were calcium scores only, 25% were prospectively ECG triggered spiral acquisition (FLASH), 60% prospective, 4% retrospective and 3% required more than 2 contrast scans. Mean BMI was?29±11 Kgm−2, median DLP 137 mGy*cm (IQR 87–230 mGy*cm), mean acquisition heart rate 61±21 bpm and median IV metoprolol dosage used was 8mg (IQR 0–20 mg). 98% of scans were diagnostic. 11% were referred on for angiography, 88% were recommended medical therapy and 1% were referred for MRI. There was 80% agreement with coronary angiography with 65% proceeding to intervention. 0% of patients who had a negative CTCA required subsequent intervention (before 15/11/16). Conclusion Our real-world data demonstrates that CTCA in a district general hospital is an accurate and effective way to rationalise investigations, particularly in the management of coronary artery disease.

089 Effect of circumferential and longitudinal strain on radial function: implications for regional vs global left ventricular function: Abstract 089 Table 1

Introduction Hypertrophic left ventricular disease occurs in numerous conditions including hypertension, aortic stenosis, hypertrophic cardiomyopathy, Fabry disease, amyloid and heart failure with a normal ejection fraction. Many clinical studies have showed the presence of abnormal longitudinal and circumferential left ventricular regional function (strain, strain rate, peak shortening velocities etc) in patients with concentric left ventricular hypertrophy. In addition, there is significantly reduced radial strain in many of these conditions despite the apparent normal radial ‘function’ and ejection fraction. In order to improve understanding of the relationship between strain and wall thickening, this study assesses the effect of left ventricular end-diastolic wall thickness and circumferential/longitudinal strain on radial strain and wall thickening. Methods The deformation characteristics of an isolated cube of myocardium 9×9×9u2005mm were assessed. The myocardial tissue was assumed to be a non-compressible elastomer. Circumferential (CS) and longitudinal strain (LS) were adjusted as follows, normal (–20%), moderately reduced (−15%) and severely reduced (–10%). The effect of changing end-diastolic wall thickness (EDWT) and LS/CS on radial strain (RS ie, relative wall thickening) and absolute wall thickening were calculated. Results Increasing end-diastolic wall thickness, with constant LS and CS, increased end-systolic wall thickness and absolute wall thickening but radial strain remained constant. When LS & CS were reduced, end-systolic wall thickness, RS and absolute thickening decreased. However, in the presence of an increase in end-diastolic wall thickness, absolute wall thickening remained normal despite a reduction in radial strain (see abstract 089 table 1) Abstract 089 Table 1 Normal peak stain −20% Abnormal peak stain −15% Abnormal peak stain −10% End-diastolic thickness (mm) 9 13 17 21 9 13 17 21 9 13 17 21 End-systolic thickness (mm) 14 20 27 33 13 19 25 31 13 18 24 29 Radial stain (%) 56 56 56 56 38 38 38 38 23 23 23 23 Absolute wall thickening (mm) 5.1 7.3 9.6 11.8 3.5 5.0 6.5 8.1 2.1 3.1 4.0 4.9 Conclusion LS & CS determine RS. However, absolute radial thickening is determined by both end-diastolic wall thickness and RS. Since, the external left ventricular circumference reduces by only 3% the absolute radial thickening determines most of the endocardial displacement and hence determines stroke volume. It is essential to differentiate between absolute and relative radial thickening when describing radial function. An increase in end-diastolic wall thickness with normal shortening must lead to an increased absolute thickening; in order for the absolute wall thickening to remain normal, myocardial shortening must be reduced. Myocardial strain has to be reduced proportionally to the degree of concentric hypertrophy otherwise the ejection fraction and stroke volume will be inappropriately increased. This study explains the geometric findings in hypertrophic heart disease regardless of the cause. A normal ejection fraction does not equate to normal deformation or even normal systolic function. The term ‘global systolic function’ is unhelpful, misleading and should be abandoned.