Download PDF Article - JACC: Cardiovascular Imaging

758
Letters to the Editor
JACC: CARDIOVASCULAR IMAGING, VOL. 9, NO. 6, 2016
JUNE 2016:751–64
REFERENCES
1. Flachskampf FA, Biering-Sørensen T, Solomon SD, Duvernoy O, Bjerner T,
Smiseth OA. Cardiac imaging to evaluate left ventricular diastolic function.
J Am Coll Cardiol Img 2015;8:1071–93.
shortened apparent deceleration time of the fused
E-A signal. The authors raise the possibility that E-A
fusion is present in our example of restrictive transmitral filling (Figure 4 [1]). This example is from a
2. Chung CS, Kovács SJ. Consequences of increasing heart rate on deceleration
time, the velocity-time integral, and E/A. Am J Cardiol 2006;97:130–6.
40-year-old patient with uncontrolled hypertension,
3. Chung CS, Methawasin M, Nelson OL, et al. Titin based viscosity in ventricular physiology: an integrative investigation of PEVK-actin interactions.
a left ventricular ejection fraction of 30%. In general,
severe heart failure with pulmonary congestion, and
J Mol Cell Cardiol 2011;51:428–34.
at a heart rate of 100 beats/min, there may be E-A
4. Kilner PJ, Yang GZ, Wilkes AJ, Mohiaddin RH, Firmin DN, Yacoub MH.
fusion. In our case, however, this would imply that
Asymmetric redirection of flow through the heart. Nature 2000;404:
759–61.
the fused A-wave would occur before the end of the
5. Nagueh SF, Appleton CP, Gillebert TC, et al. Recommendations for the
evaluation of left ventricular diastolic function by echocardiography. J Am Soc
Echocardiogr 2009;22:107–33.
P-wave (Figure 1A, dashed blue line in the magnified
beat from our original recording), which seems unlikely. We agree that the bright small wave well after
the QRS duration is probably not the A-wave, but a
THE AUTHORS REPLY:
small A-wave is visible immediately after the P-wave
in the magnified beat (red arrow). We present an
additional recording (Figure 1B) from this patient
3 days earlier than the that reproduced in our article,
We thank Drs. Chung and Afonso for their interest
at a heart rate of 92 beats/min, again with a restrictive
and careful scrutiny of our article (1). We fully agree
transmitral pattern, where the A-wave in beats 2 and
that heart rate and the fusion of the transmitral dia-
5 is well recognizable and the E-wave deceleration
stolic E-wave and A-wave occurring at higher heart
time is 95 ms, similar to the deceleration time of
rates are an important concern in assessing left ven-
102 ms in Figure 4 in our paper (1). In the other beats
tricular diastolic function and find the example in
in Figure 1A, the A-wave is less well defined, but
Figure 1A of their letter, in particular regarding the
definitely not merged with the peak of the E-wave.
F I G U R E 1 Restrictive Transmitral Pulsed-Wave Doppler Profile
Magnification of the fourth beat from Figure 4 in our article (1). The E-wave ends before the end of the electrocardiographic P-wave
(blue lines), making E-A fusion unlikely. There is a small wave (red arrow) immediately after the E-wave and the electrocardiographic P-wave,
which is probably the real A-wave. (B) Transmitral profile of the patient in Figure 4 in our paper (1), obtained 48 h earlier at a slightly lower
heart rate (92 beats/min). A clear A-wave is visible in beats 2 and 5. The E-wave deceleration time is 95 ms, similar to the deceleration time
in Figure 4 of our paper. Peak E-wave velocity in both figures is w100 cm/s. bpm ¼ beats per minute.
JACC: CARDIOVASCULAR IMAGING, VOL. 9, NO. 6, 2016
Letters to the Editor
JUNE 2016:751–64
We did not choose this recording as an example
clopidogrel, and unfractionated heparin and “spon-
because of the variability in the A-wave signal. Note
taneous” fibrinolysis should be considered among the
that E-wave peak velocities in the 2 recordings, at
possible explanations for the low number and/or size
100 beats/min and 92 beats/min, are both nearly
of the thrombi in these patients.
equal at w100 cm/s, different from the example of
They then cite our animal study that showed, by
E-A fusion in their letter, where the fused signal has a
scanning electron microscopy and arterial flow
substantially higher peak velocity than the nonfused
monitoring, that endothelial damage and thrombosis
E-wave. However, we agree that E-A fusion must be
can occur even in circumstances of partial arterial
considered in the recording in Figure 4 of our article
constriction (40% to 60% luminal diameter reduc-
and regret the ambiguity in the recording. We
tion), especially if superimposed on pre-existing
commend the authors of the letter for their clever and
arteriosclerosis (2). However, they did not mention a
instructive “detective work” in pointing this out.
critically important controlled finding of that study
that the hemodynamic forces at such sites of partial
Frank A. Flachskampf, MD, PhD*
Tor Biering-Sørensen, MD, PhD
Scott D. Solomon, MD
Olov Duvernoy, MD, PhD
Tomas Bjerner, MD, PhD
Otto A. Smiseth, MD, PhD
coronary constriction can be sufficiently severe
to exceed what has been calculated to be the “yield
stress” of the endothelial lining. This hemodynamically induced damage was found to range from
focal vacuolar injury to cellular fragmentation and
desquamation
*Uppsala Universitet
with
exposure
of
highly
throm-
bogenic subendothelial tissues. These animal studies
Institutionen för Medicinska Vetenskaper
suggested that coronary spasm may cause myocardial
Akademiska Sjukhuset
ischemia not just by total obstruction of the artery at
Ingång 40, Plan 5
the site of spasm, but also by endothelial damage
Uppsala 751 85
and thrombus formation that may occur at sites of
Sweden
spasm even, and perhaps particularly, when the
E-mail: frank.fl[email protected]
reduction in luminal diameter is insufficient to
http://dx.doi.org/10.1016/j.jcmg.2015.11.015
reduce the rate of distal coronary flow (2,3). Indeed,
Please note: The authors have reported that they have no relationships relevant
to the contents of this paper to disclose.
the endothelial damage, whether hemodynamically
REFERENCE
promote or exacerbate underlying atherosclerosis.
1. Flachskampf FA, Biering-Sørensen T, Solomon SD, Duvernoy O, Bjerner T,
Smiseth OA. Cardiac imaging to evaluate left ventricular diastolic function.
J Am Coll Cardiol Img 2015;8:1071–93.
graphy that blood flow at sites of coronary spasm was
or otherwise induced, would also be expected to
By showing with correlative quantitative angioreduced in only one-half of patients with angina
and in less than one-third of patients with acute
myocardial infarction, the study by Shin et al. (1)
Vasospastic Angina and Hemodynamic Injury
provides strong clinical support for the experimentally demonstrated role of hemodynamic forces in
In their study of optical coherence tomography
vascular damage and thrombosis in patients with
(OCT)-defined
vasospastic angina.
morphological
characteristics
of
coronary artery spasm sites in vasospastic angina,
Shin et al. (1) found thrombi at only 23 (29%) of 80
sites of spasm in patients with vasospastic angina and
in only one-half of patients with a diagnosis of acute
myocardial infarction. They reported a reduction in
coronary flow at only 40 (50%) of 80 sites of spasm in
patients with vasospastic angina and in only 31% of
patients with acute myocardial infarction.
The authors point out that it is thought that
thrombosis is the result of grossly reduced blood flow
secondary to critical vascular constriction and suggest that the lack of a correlation between frequency
of thrombus and clinical presentation in their study
may be related to the relatively small size of the
thrombi as seen on OCT. Triple therapy with aspirin,
S. David Gertz, MD, PhD*
Gideon Uretzky, MD
Lilach Gavish, PhD
Mervyn S. Gotsman, MD
*Institute for Medical Research
The Hebrew University–Hadassah Medical School
P.O. Box 12272
Jerusalem
Israel 91120
E-mail: [email protected]
http://dx.doi.org/10.1016/j.jcmg.2015.12.009
Please note: This work is supported in part by the Rosetrees Trust Fund of the
UK and The Brandman Foundation. The authors have reported that they have
no relationships relevant to the contents of this paper to disclose.
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