Download Is diastolic heart failure synonyms with heart failure with

Letters to the Editor
JACC Vol. 42, No. 7, 2003
October 1, 2003:1334–7
W.H. Wilson Tang, MD
Department of Cardiovascular Medicine
Cleveland Clinic Foundation
9500 Euclid Avenue
Desk F25
Cleveland, OH 44195
E-mail: [email protected]
Gary S. Francis, MD, FACC
Byron J. Hoogwerf, MD
James B. Young, MD, FACC
1335
promotes the investigative efforts that are long overdue for these
patients.
Kenneth M. Kessler, MD
University of Miami School of Medicine
Division of Cardiology
26 William Howard Drive
Glen Mills, PA 19342
E-mail: [email protected]
doi:10.1016/S0735-1097(03)00997-5
doi:10.1016/S0735-1097(03)00996-3
REFERENCES
REFERENCES
1. Tang WHW, Francis GS, Hoogwerf BJ, Young JB. Fluid retention
after initiation of thiazolidinedione therapy in diabetic patients with
established chronic heart failure. J Am Coll Cardiol 2003;41:1394 –8.
2. Larsen TM, Toubro S, Astrup A. PPARgamma agonists in the
treatment of type II diabetes: is increased fatness commensurate with
long-term efficacy? Int J Obes Relat Metab Disord 2003;27:147–61.
1. Zile MR. Heart failure with preserved ejection fraction: is this diastolic
heart failure? J Am Coll Cardiol 2003;41:1519 –22.
2. Echeverria HH, Bilsker MS, Myerburg RJ, Kessler KM. Congestive
heart failure: echocardiographic insights. Am J Med 1983;75:750 –5.
3. Hunt SA, Baker DW, Chin MH, et al. ACC/AHA guidelines for the
evaluation and management of chronic heart failure in the adult:
executive summary: a report of the American College of Cardiology/
American Heart Association Task Force on Practice Guidelines (Committee to Revise the 1995 Guidelines for the Evaluation and Management of Heart Failure). J Am Coll Cardiol 2001;38:2101–13.
Is Diastolic Heart Failure
Synonymous With Heart Failure
With Preserved Ejection Fraction?
REPLY
In his excellent Editorial Comment, Dr. Zile states that “heart
failure with a preserved ejection fraction” and “diastolic heart
failure” are synonymous (1). Respectfully, I must disagree. Not all
patients with diastolic heart failure have left ventricular hypertrophy. Therefore, the general applicability of the study cited supporting the equivalency of the two terms might be limited because
all patients in that study had echocardiographic evidence for left
ventricular hypertrophy, and diastolic dysfunction is generally
accepted to precede hypertrophy. In our early experience about
one-third of patients with heart failure with a preserved ejection
fraction had explanations for the signs and symptoms of failure
other than diastolic dysfunction, predominately right heart failure
due to pulmonary disease and regurgitant valvular heart disease (2).
The nonspecific nature of the symptoms of heart failure and
iatrogenic volume overload were also noted. It is unclear to what
extent stricter diagnostic criteria for heart failure would affect these
findings, and I believe that our initial criteria would still lead most
clinicians to the diagnosis of heart failure. Furthermore, a patient
with heart failure due to chronic, severe mitral regurgitation with
an ejection fraction of 40% or even 50% has predominately systolic,
not diastolic, heart failure. Therefore, I believe it is best to
conclude that patients with “diastolic heart failure” form a subgroup of patients with “heart failure with a preserved ejection
fraction.”
Until a uniformly accepted and therapeutically meaningful
measure of diastolic dysfunction is defined, diastolic heart failure is
in many ways a diagnosis of exclusion. The value of initially using
the term “heart failure with preserved, or normal, ejection fraction”
underscores the need to define left ventricular function in virtually
all patients with heart failure (3) as well as the need to carefully
eliminate other cardiac and noncardiac possibilities from the
patient’s signs and symptoms. After eliminating other possibilities,
I agree that the term “diastolic heart failure” seems most appropriate, and I hope, as Dr. Zile does, that accepting the term
One of the first, if not the first, study to use the term “diastolic
heart failure” was by Dr. Kessler in 1988 (1). His report was truly
innovative and showed remarkable insight into a difficult clinical
problem. I enthusiastically agree with Dr. Kessler’s point of view
and I am grateful to receive his support. In his letter to the editor
of the JACC, he raises three important issues: 1) some patients with
diastolic heart failure do not have left ventricular (LV) hypertrophy; 2) the diagnosis of diastolic heart failure should exclude
patients with noncardiac (such as pulmonary disease) and other
cardiac (such as mitral stenosis, regurgitant valve disease) causes of
heart failure; and 3) left ventricular (LV) function must be
measured in every patient with heart failure.
In the study that Dr. Kessler refers to in his letter (2), only about
one-third of the patients had LV hypertrophy defined as LV mass
ⱖ125 g/m2. However, all patients had concentric hypertrophic
remodeling characterized by a decreased LV end diastolic
volume/mass ratio or LV end diastolic dimension/wall thickness
ratio or an increased relative wall thickness. I believe that a
majority of patients with diastolic heart failure in fact have
either concentric remodeling or some other evidence of myocardial or cardiac structural alterations such as an enlarged left
atrium. With or without concentric remodeling, if a patient
truly has objective signs and symptoms of heart failure and
noncardiac and other cardiac causes have been ruled out, then
heart failure with a normal ejection fraction (EF) is caused by
diastolic dysfunction and the appellation “diastolic heart failure”
should be applied.
Dr. Kessler correctly points out that in patients with primary
right heart failure (caused by chronic lung disease, pulmonic
stenosis, tricuspid regurgitation) or mitral stenosis or left-sided
regurgitant valvular disease, this can result in heart failure with a
normal EF. I am grateful that Dr. Kessler emphasized this point
because our previous publications (2,3) did not make it explicitly
clear that we had in fact excluded patients with noncardiac and
other cardiac causes of heart failure in this study patient cohort.
1336
Letters to the Editor
JACC Vol. 42, No. 7, 2003
October 1, 2003:1334–7
It is critical that LV function, both systolic and diastolic, be
measured in every patient with heart failure. The advent of tissue
Doppler (and other echo-Doppler techniques) has made it easier
and more practical to identify abnormalities in diastolic function.
Nonetheless, precise and comprehensive assessment of diastolic
function requires the use of invasive catheterization techniques.
However, if noncardiac and other cardiac causes of heart failure are
excluded, the remaining patients with heart failure and a normal
EF all have abnormalities of diastolic function making measurement of diastolic function confirmatory rather than a mandatory
component of diagnostic criteria.
Finally, I join Dr. Kessler in his enthusiastic use of the term
“diastolic heart failure” and renew my editorial plea: “Stop the
discrimination against the term diastolic heart failure.”
Michael R. Zile, MD
Cardiology/Medicine
Medical University of South Carolina
135 Rutledge Avenue
Suite 816
P.O. Box 250592
Charleston, SC 29425
E-mail: [email protected]
doi:10.1016/S0735-1097(03)00998-7
REFERENCES
1. Kessler KM. Heart failure with normal systolic function. Arch Intern
Med 1988;148:2109 –11.
2. Zile MR, Gaasch WH, Carroll JD, et al. Heart failure with a normal
ejection fraction. Is measurement of diastolic function necessary to make
the diagnosis of diastolic heart failure? Circulation 2001;104:779 –82.
3. Zile MR. Heart failure with preserved ejection fraction: is this diastolic
heart failure? J Am Coll Cardiol 2003;41:1519 –22.
Determination of the Natural
History of Aspirin Resistance Among
Stable Patients With Cardiovascular Disease
We read with interest the recent study by Gum et al. (1) regarding
aspirin resistance. Their results, in particular the focus on longterm follow-up, offer important information in the confusing but
clinically important area of aspirin resistance. They were able to
show that, by using standard light-transmittance aggregometry in
a population of patients already on aspirin therapy, the response to
two different platelet agonists could predict long-term outcome.
However, in these investigators’ original study of baseline aspirin
responsiveness in this identical patient population, a point-of-care
test, the platelet function analyzer (PFA)-100, was also used to
determine aspirin responsiveness along with light transmittance
aggregometry (2). In the first study, minimal correlation between
the two methods was found. It is unclear to us, though, why
long-term outcomes based on baseline aspirin responsiveness as
determined by the PFA-100 were not also included in their present
report. Clearly the routine determination of aspirin responsiveness
will depend upon the ability to measure it with a point-of-care
device. Therefore, whether or not the PFA-100 results correlated
with long-term clinical outcomes would have important implications regarding its utility in that role. The importance of this
question is highlighted in the editorial following the Gum et al. (3)
study as well as in a recent review of the topic, as both suggest that
the PFA-100 may be well suited for the routine determination of
aspirin resistance (3,4). However, this would likely not be the case
if PFA-100 results were found to not have any clinical relevance in
terms of future thrombotic events.
Steven R. Steinhubl
University of North Carolina
Division of Cardiology
CB #7075
Chapel Hill, NC 27599
E-mail: [email protected]
Jay S. Varinasi, MD
Lee Goldberg, MD
doi:10.1016/S0735-1097(03)00999-9
REFERENCES
1. Gum PA, Kottke-Marchant K, Welsh PA, White J, Topol EJ. A
prospective, blinded determination of the natural history of aspirin
resistance among stable patients with cardiovascular disease. J Am Coll
Cardiol 2003;41:961–5.
2. Gum PA, Kottke-Marchant K, Poggio ED, et al. Profile and prevalence
of aspirin resistance in patients with cardiovascular disease. Am J
Cardiol 2001;88:230 –5.
3. Eikelboom JW, Hankey G. Aspirin resistance: a new independent
predictor of vascular events. J Am Coll Cardiol 2003;41:966 –8.
4. McKee SA, Sane DC, Deliargyris EN. Aspirin resistance in cardiovascular disease: a review of prevalence, mechanisms, and clinical significance. Thromb Haemost 2002;88:711–5.
REPLY
We appreciate and share the interest of Dr. Varinasi and colleagues
in aspirin resistance and its clinical relevance. Previously, we
documented the profile and prevalence of aspirin resistance in
stable patients with cardiovascular disease (1). In this initial study,
we used both optical platelet aggregation, which we consider to be
the gold standard for the determination of platelet reactivity in the
presence of aspirin, and a rapid, whole-blood assay, the platelet
function analyzer (PFA)-100, to determine the prevalence of
aspirin resistance. The kappa statistic between these two methods
was 0.1 (95% confidence interval 0.045 to 0.246), indicating a poor
correlation between optical platelet aggregation and the PFA-100
in detection of aspirin resistance.
In our more recently published work (2), we reported an
increased risk of death, myocardial infarction (MI), or stroke
associated with aspirin resistance as determined by optical platelet
aggregation. In analysis, long-term outcomes (death/MI/stroke)
were not related to aspirin resistance status as determined by the
PFA-100 (12.9% aspirin sensitive vs. 15.1% aspirin resistant, p ⫽
0.4). These findings seem to indicate that the PFA-100 is not as
specific a test as compared to optical platelet aggregation for
determining clinically relevant aspirin resistance. In fact, this
supposition may be supported by the poor kappa statistic between
the two tests. However, prior to categorically drawing this conclusion, one must acknowledge the real possibility of a type II error.
Although there may be no statistical association between the
PFA-100 and clinical outcomes in our investigation, a real association may have been missed by the small sample size of our study.