Regional Differences in Aortic Geometry - JACC: Cardiovascular [PDF]

with a past history of EBV, CMR detected only fibrotic lesions, and the histology documented healed myocarditis, emphasi

0 downloads 6 Views 326KB Size

Recommend Stories


Regional differences in sports participation
Happiness doesn't result from what we get, but from what we give. Ben Carson

Regional differences in psychiatric disorders in Chile
Ask yourself: What would I be risking if I did some of the things that are outside of my comfort zone?

PDF Download Geometry in Figures
It always seems impossible until it is done. Nelson Mandela

[PDF] Diabetes in Cardiovascular Disease
Never let your sense of morals prevent you from doing what is right. Isaac Asimov

Sex Differences and Survival in Adults With Bicuspid Aortic Valves
Ask yourself: When was the last time I read a book that had a major influence on me? Next

Differences-in-Differences
What we think, what we become. Buddha

Regional Differences in Economic Impacts of Power Outages in Finland
Love only grows by sharing. You can only have more for yourself by giving it away to others. Brian

The JACC study
Sorrow prepares you for joy. It violently sweeps everything out of your house, so that new joy can find

Regional hydraulic geometry models for Queensland streams
You have to expect things of yourself before you can do them. Michael Jordan

Geometry Textbook [PDF]
5.1 Perpendiculars and Bisectors. 264. ▻ CONCEPT ..... Area of Polygons and Circles. CHAPTER STUDY GUIDE. 660. Angle Measures in Polygons. 661. Areas of Regular Polygons. 669. Perimeters and Areas of Similar Figures. 677. ▻ CONCEPT ..... In the c

Idea Transcript


562

Letters to the Editor

JACC: CARDIOVASCULAR IMAGING, VOL. 4, NO. 5, 2011 MAY 2011:561– 4

Figure 1. Cardiac Magnetic Resonance Image of a Patient with Positive LGE Area in the Inferior Wall and Matching Pathology Image of Active Myocarditis Epicardial late gadolinium enhanced area (LGE) in the inferior wall of left ventricle (left, arrow) and corresponding pathology image (right, arrows), indicative of active myocardial inflammation (hematoxylin-eosin, ⫻200).

with a past history of EBV, CMR detected only fibrotic lesions, and the histology documented healed myocarditis, emphasizing the complementary role of the 2 techniques in myocarditis assessment. EBV infection usually presents neurologically or hematologically, with no cardiac complications. Although it can lead to myocarditis in immunodepressed patients, it has been rarely attributed to myocarditis in immunocompetent patients. Myocardial viral genome evaluation in dilated cardiomyopathy showed a high prevalence of viruses in the myocardium (Parvo-B19 51.4%; Herpes virus 6 21.6%). However, the EBV genome was found in only 2% of patients (1). The interesting finding in our patients was that the typical signs and symptoms of EBV infection occurred simultaneously with cardiac symptoms. Fatal myocarditis has already been described as a rare complication during acute EBV infection, but not in healed myocarditis after EBV infection. According to our findings, EBV can provoke VT by both acute and chronic myocardial inflammation. This study has some limitations because: 1) only a small number of patients were examined; 2) children and patients with immunodeficiency and/or under immunosuppressive treatment prone to EBV infection were not included; and 3) only a short-term follow-up was performed. In conclusion, a common virus like EBV, usually known for extracardiac complications, can provoke VT both on an acute and a chronic basis. There is a complementary association between EMB and CMR in myocarditis evaluation. Sophie Mavrogeni, MD,* Konstantinos Spargias, MD, Costas Bratis, MD, Genovefa Kolovou, MD, Evangelia Papadopoulou, MD, Gregory Pavlides, MD *50 Esperou Street, 175-61 P. Faliro, Athens, Greece. E-mail: [email protected] doi:10.1016/j.jcmg.2010.11.022

REFERENCES

1. Ishikawa T, Zhu BL, Li DR, Zhao D, Maeda H. Epstein-Barr virus myocarditis as a cause of sudden death: two autopsy cases. Int J Legal Med 2005;119:231–5.

2. Abdel-Aty H, Boye P, Zagrosek A, et al. Diagnostic performance of cardiovascular magnetic resonance in patients with suspected acute myocarditis: comparison of different approaches. J Am Coll Cardiol 2005;45:1815–22. 3. Mahrholdt H, Wagner A, Deluigi C, et al. Presentation, patterns of myocardial damage and clinical course of viral myocarditis. Circulation 2006;114:1581–90. 4. Lorenz CH, Walker ES, Morgan VL, Klein SS, Graham TP Jr. Normal human right and left ventricular mass, systolic function, and gender differences by cine magnetic resonance imaging. J Cardiovasc Magn Reson 1999;1:7–21.

Regional Differences in Aortic Geometry Pathologic or Compensatory? We refer to the Hickson et al. (1) recent interesting report on regional differences in aortic stiffness. As they note, their results are in contrast to 3 other reports in the literature (2,3), including our own (4), raising themes that warrant further discussion. First, Hickson et al. (1) make a very important point, specifically, that aortic diameter is an important, but usually overlooked, influence on pulse wave velocity. This is particularly relevant since pulse wave velocity, despite being a surrogate marker, has become the noninvasive gold standard for assessment of arterial stiffness. Second, our study used cardiac magnetic resonance to calculate the local distensibility directly, not the pulse wave velocity, and found the predominant effect of aging was an increase in the difference between the distensibility of the ascending compared with that of the distal aorta. Both our own and Hickson et al.’s (1) report show that ageing appears to have its predominant absolute effect in the distal descending aorta, although in our cohorts, the greatest proportional change occurred in the proximal (elastic) aorta. Hickson et al. (1) are probably correct in that changes in aortic diameter tend to compensate for primary distensibility changes, and this may be responsible for their variant results. In this context, a serious dilemma remains as to whether distensibility (and possibly diameter changes per se) or the deranged

JACC: CARDIOVASCULAR IMAGING, VOL. 4, NO. 5, 2011

Letters to the Editor

563

MAY 2011:561– 4

hemodynamic effects mediated through pulse wave velocity is the important pathophysiological factor. Furthermore, the issue still remains whether this phenomenon acts either as a primary determinant of adverse outcomes or simply as a biomarker of systemic disease. The increase in ascending aortic diameter (decreasing pulse wave velocity) and increase in regional length (increasing transit time at a given pulse wave velocity) with very little change in other segments, as reported by Hickson et al. (1) (their Fig. 4), would have a significant effect on the relative timing of any reflected pressure wave within the cardiac cycle and therefore on central blood pressure. The net influence of these changes would be to delay return of any reflected wave; although these could be seen as compensatory changes, they apparently generally fail, as aging is associated with earlier (systolic) pressure augmentation. It therefore remains uncertain whether the established deleterious effect of aortic stiffening (age or disease related) is mediated by the effect of local changes in mechanics and geometry as has been suggested (5), secondary effects related to suboptimal hemodynamic coupling, or whether increased aortic stiffening is merely acting as a biomarker of a progressive systemic condition (e.g., ageing, atherosclerosis, arteriosclerosis). The influence of aortic diameter as opposed to wave reflection and pulse wave velocity in determining cardiovascular risk have been debated, and we would suggest that the most relevant issue is how these factors are related to central blood pressure. The work by Hickson et al. (1) offers further insight into these issues and, equally relevant, highlights the potential for cardiac magnetic resonance to individualize cardiovascular risk prediction and management. Adam J. Nelson, BMedSc, MBBS,* Matthew I. Worthley, MBBS, PhD,* James D. Cameron, MBBS, MD, MBE(Elec), MEngSc *Cardiovascular Investigation Unit, Royal Adelaide Hospital, North Terrace, Adelaide 5000, South Australia, Australia. E-mail: [email protected] doi:10.1016/j.jcmg.2011.02.006

REFERENCES

1. Hickson SS, Butlin M, Graves M, et al. The relationship of age with regional aortic stiffness and diameter. J Am Coll Cardiol Img 2010;3: 1247–55. 2. Redheuil A, Yu WC, Wu CO, et al. Reduced ascending aortic strain and distensibility: earliest manifestations of vascular aging in humans. Hypertension 2010;55:319 –26. 3. Rogers WJ, Hu YL, Coast D, et al. Age-associated changes in regional aortic pulse wave velocity. J Am Coll Cardiol 2001;38:1123–9. 4. Nelson AJ, Worthley SG, Cameron JD, et al. Cardiovascular magnetic resonance-derived aortic distensibility: validation and observed regional differences in the elderly. J Hypertens 2009;27:535– 42. 5. Dart AM, Kingwell BA, Gatzka CD, et al. Smaller aortic dimensions do not fully account for the greater pulse pressure in elderly female hypertensives. Hypertension 2008;51:1129 –34.

of the human aorta (1). We observed the greatest age-related difference in the aortic pulse wave velocity in the distal abdominal aorta, and the least in the aortic arch, suggesting that the distal aorta stiffened most with age. As we noted in our discussion, and as Dr. Nelson and colleagues reiterate, others have reported the converse, that is, that the ascending aorta stiffens most with age (2,3). No doubt, there are several explanations for these discrepant observations, not least the very small sample sizes reported by some authors (2,3), the use of differing techniques to estimate regional stiffness, methodological issues such as the use of nonsimultaneous, peripheral pressure when calculating distensibility/compliance (3), and technical issues such as inaccurate edge detection with cardiac magnetic resonance with varying sequences (4). Interestingly, a recent postmortem analysis of a relatively large collection of human aortae suggests that the abdominal aorta may indeed stiffen most with age (5). However, further carefully conducted studies employing large sample sizes, with prospective in vivo observations are required. We would agree with Dr. Nelson and colleagues that it is unclear how changes in aortic stiffness alter cardiovascular risk. However, we believe that changes in aortic pressure probably play an important role. Although the ascending aorta may stiffen less with age, changes in the stiffness of the first part of the aorta are likely to have a more profound effect on aortic pressure than do changes in the more distal parts. This is because most of the volume buffering (or windkessel effect) occurs in the first part of the aorta. Therefore, we hypothesized that dilation of the aorta helps to offset the detrimental effect of aortic stiffening on peak systolic pressure by increasing the capacitance of the aorta. Despite this potential protective effect, stiffening and dilation will still lead to a loss of elastic recoil and fall in diastolic pressure. Since coronary perfusion occurs mainly in diastole, such an effect is likely to be detrimental to the myocardium. Unfortunately, we did not assess the windkessel effect in our original study because of the limitation of the cardiac magnetic resonance technique we employed with respect to accurate edge detection, but this could be done with alternative approaches. Finally, we believe that determining which part of the aorta stiffens most with age remains an important question, because the structure of the aorta changes considerably along its length. Thus, we may have a better knowledge of the processes involved in age-related stiffening, or arteriosclerosis, if we can first define the region of the aorta this affects most, and then relate stiffness of the structural and biochemical changes at this and other locations, which some authors have already attempted to do. Ultimately, these data may help provide targets for future antiarteriosclerotic interventions.

Ian B. Wilkinson, DM,* Carmel M. McEniery, PhD Stacey S. Hickson, PhD

REPLY We thank Dr. Nelson and colleagues for their interest in our recent work concerning the effect of age on the biomechanical properties

*Addenbrooke’s Hospital, Clinical Pharmacology Unit, Hills Road, Cambridge CB2 0QQ, United Kingdom. E-mail: [email protected] doi:10.1016/j.jcmg.2011.03.005

Smile Life

When life gives you a hundred reasons to cry, show life that you have a thousand reasons to smile

Get in touch

© Copyright 2015 - 2024 PDFFOX.COM - All rights reserved.