doi: 10.1161/CIRCULATIONAHA.105.559781
(Circulation. 2005;112:e135-e136.)
© 2005 American Heart Association, Inc.
Correspondence |
Letter Regarding Article by Lyseggen et al, "Myocardial Acceleration During Isovolumic Contraction: Relationship to Contractility"
Hospital for Sick Children, Toronto, Ontario, Canada
Skejby Hospital, Aarhus, Denmark
Kinderherz Praxis, Munich, Germany
We would like to commend Lyseggen et al for this detailed study1 and presentation of these fascinating data. The authors confirmed our findings that long-axis ventricular myocardial isovolumic acceleration showed good correlation with dP/dtmax, with positive inotropy induced by dobutamine infusion, and its relative preload resistance over a physiological range.2 We do, however, have some reservations regarding the authors’ interpretation of some of their other findings and the conclusions drawn from them.
There was a significant decrease in myocardial isovolumic acceleration (IVA) after volume loading, which caused an acute elevation in left ventricular end-diastolic pressure from a baseline of 5.9±1.3 mm Hg to a nonphysiological value of 19.0±2.2 mm Hg. First, few indexes of contractile performance could be expected to be resistant to loading change of this magnitude. Furthermore, in Figure 6, the linearity of IVA at more physiological changes in preload is demonstrated. This is in keeping with our conclusion that IVA "is unaffected by preload and afterload changes within a physiological range."
With ischemia lasting 1 to 2 minutes, the present study demonstrated changes in motion during the isovolumic contraction period, with marked initial lengthening resulting in a negative velocity spike and the disappearance of a positive IVA spike. The conclusion that IVA is unhelpful during ischemia is in contrast to earlier findings by the same group3 and those of others4 demonstrating the added benefit of examining myocardial motion in the isovolumic contraction period. Indeed, although referenced, the differing data in the present study are not discussed in relationship to the group’s own previously published data. We think, therefore, that it is premature to dismiss IVA as being unable to "reflect impaired myocardial function during ischemia."
Finally, the authors demonstrate maintenance of IVA, despite the lack of a preceding atrial systole. Analysis of the relationship between IVA and the phonocardiogram showed that the onset of IVA coincided with the onset of the low-frequency vibrations of the first heart sound. Most data support the hypothesis that these vibrations are caused by the onset of ventricular myocardial contraction.5 Because the high-frequency component of the first heart sound occurs late in the isovolumic period, it is not surprising that IVA shows no significant relationship to this event. Furthermore, the classic work of Rushmer clearly demonstrates active asynchronous contraction as the initial stage of long-axis ventricular shortening because it assumes a more spherical shape.6 The evidence, therefore, for Lyseggen et al concluding that IVA may be "related to late diastolic events" is not clear to us.
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References |
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 Top References References |
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1. Lyseggen E, Rabben SI, Skulstad H, Urheim S, Risøe C, Smiseth OA. Myocardial acceleration during isovolumic contraction: relationship to contractility. Circulation. 2005; 111: 1362–1369.
2. Vogel M, Cheung MM, Li J, Kristiansen SB, Schmidt MR, White PA, Sorensen K, Redington AN. Noninvasive assessment of left ventricular force-frequency relationships using tissue Doppler-derived isovolumic acceleration: validation in an animal model. Circulation. 2003; 107: 1647–1652.
3. Edvardsen T, Urheim S, Skulstad H, Steine K, Ihlen H, Smiseth OA. Quantification of left ventricular systolic function by tissue Doppler echocardiography: added value of measuring pre- and postejection velocities in ischemic myocardium. Circulation. 2002; 105: 2071–2077.
4. Penicka M, Bartunek J, Wijns W, De Wolf I, Heyndrickx GR, De Raedt H, Barbato E, De Bruyne B. Tissue doppler imaging predicts recovery of left ventricular function after recanalization of an occluded coronary artery. J Am Coll Cardiol. 2004; 43: 85–91.
5. Hada Y, Takenaka K, Ishimitsu T, Yamaguchi T, Amano K, Takahashi H, Takikawa R, Sakamoto T. Echophonocardiographic study of the initial low frequency component of the first heart sound. J Am Coll Cardiol. 1983; 2: 445–451.[Abstract]
6. Rushmer RF Initial phase of ventricular systole: asynchronous contraction. Am J Physiol. 1956; 184: 188–194.[Medline] [Order article via Infotrieve]
Institute for Surgical Research, Department of Cardiology, Rikshospitalet University Hospital, Oslo, Norway
We have read the comments by Cheung and colleagues about our article in Circulation1 with interest. The first comment addresses the question of load dependency. Although there may be only minor changes in myocardial isovolumic acceleration (IVA) within a physiological range of filling pressures (normal heart function), the important implication of IVA would be in patients with heart disease. End-diastolic pressures in the range of 15 to 20 mm Hg are not uncommon in patients with severe heart failure, and in our model, peak IVA was markedly reduced at this preload level. Furthermore, Figure 6 demonstrates no plateau in the relationship between physiological left ventricular end-diastolic pressure and IVA. In this representative example, there were moderate changes in IVA when changes in left ventricular end-diastolic pressure were induced within the physiological range (eg, between 6 and 12 mm Hg). Although the changes in left ventricular filling that were induced in our study were large and nonphysiological, the preload dependency of IVA should be noted and investigated further.
The second comment addresses the main finding of our study, which was the inability of peak IVA to reflect impaired regional myocardial function during ischemia. In severely ischemic dyskinetic myocardium, peak IVA did not change and therefore did not reflect regional contractility. Cheung et al refers to a previous study from our laboratory2 and comments that there may be inconsistency with the present study. On the contrary, the studies are entirely consistent because both showed a marked negative velocity component during IVC caused by systolic lengthening of the ischemic segment. Importantly, in the study by Edvardsen et al, there was no measure of IVA, and measurements were done at a time when systolic lengthening dominated the isovolumic velocities.
The last comment relates to the mechanisms of IVA. The main focus of the present study was not to define the etiology of IVA, but rather to investigate its relationship to regional contractility. We do agree, however, that the mechanisms behind IVA are most likely related to events during isovolumic contraction and not late diastole. The observation that IVA still existed after abolishment of atrial contraction is consistent with this notion. We do not dismiss the possibility that early contraction is important in determining IVA. The insensitivity to reflect regional ischemia, however, indicates involvement of other mechanisms, which are presently subjected to further investigation in our laboratory.
Response
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Disclosure
While doing work with the IVA study, Dr Rabben was the recipient of a 3-year postdoctoral fellowship from the Research Council of Norway. The followship ended in November 2003. Dr Rabben has since changed fields to medical image processing and currently works for GE Vingmed Ultrasound.
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TopReferencesReferences |
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1. Lyseggen E, Rabben SI, Skulstad H, Urheim S, Risøe C, Smiseth OA. Myocardial acceleration during isovolumic contraction: relationship to contractility. Circulation. 2005; 111: 1362–1369.
2. Edvardsen T, Urheim S, Skulstad H, Steine K, Ihlen H, Smiseth OA. Quantification of left ventricular systolic function by tissue Doppler echocardiography: added value of measuring pre- and postejection velocities in ischemic myocardium. Circulation. 2002; 105: 2071–2077.
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