From the Department of Cardiology of the Thoraxcenter and Department of
Pathology (M.K.), Erasmus University Rotterdam, Netherlands.
Correspondence to Rob Krams, MD, PhD, Laboratory for Hemodynamics, Room Ee2322, Erasmus University Rotterdam, PO Box 1738, Dr Molewaterplein 30, 3000 DR Rotterdam, The Netherlands.
Methods and Results—End-diastolic septal wall
thickness was significantly increased in patients with HCM
(25.8±2.9 mm) in comparison with cardiac transplant recipients
(control subjects: 11.4±3.0 mm; P<0.05). Although
the diameter of the left anterior descending coronary artery
was similar in both groups (3.0±0.8 versus 3.0±0.5 mm,
P=NS), the coronary resistance reserve
(CRR=CRRbasal/CRRhyperemic), corrected
for extravascular compression (end-diastolic left
ventricular pressure), was reduced to 1.5±0.6 in HCM
(P<.05; control, 2.6±0.8). Arteriolar lumen (AL)
divided by wall area was lower in HCM (21±5% versus 30±4%;
P<.05), and capillary density tended to decrease (from
1824±424 to 1445±513 per mm2, P=.11)
in HCM. CRR was linearly related to normalized AL according to the
formula CRR=0.1 AL-0.45 (r=.57; P<.05).
Further analysis revealed that CRR, AL, and capillary density
were all linearly related to the degree of hypertrophy.
Conclusions—Decrements in CRR were related to changes of the
coronary microcirculation. Both the decrease in CRR and these
changes in the coronary microcirculation were related to the
degree of hypertrophy. All these factors might contribute
to the well-known occurrence of ischemia in this patient group.
Although the CFR is decreased in HCM, in accordance with the findings
of experimentally induced
hypertrophy,9 10 it is unknown at
present whether the decreased CFR is related to the abnormal
arterioles and whether a decrease in capillary density accompanies this
decrease in AL. To that end, we measured CFR in combination with a
quantitative analysis of AL, wall area and capillary density in
myocardial tissue obtained during surgery (HCM) and obtained from
endomyocardial biopsies (HTx).
Doppler Measurements
Quantitative Angiographic Measurements
Echocardiographic Measurements
Histological Measurements
End-diastolic septal wall thickness was significantly
increased in patients with HCM (25.8±2.9 mm) compared with
members of the control group (11.4±3.0 mm; P<.05).
All HCM patients had normal angiograms. The diameter of the LAD was
similar in both groups (3.0±0.8 versus 3.0±0.5 mm).
Coronary velocity during baseline conditions was higher for HCM
patients (34±11 versus 20±11 cm/s, P<.05), whereas
velocities during hyperemia were similar (49±20 versus 53±22
cm/s). As a consequence, the CFR was reduced from 2.6±0.8 in the
control group to 1.8±0.9 in the HCM group (P<.05).
Coronary resistance values, corrected for extravascular
compression (see above), were lower (3.7±2.1 versus 6.5±2.2
mm Hg · s · cm-1, P<.05) during
baseline conditions and were similar during hyperemia (2.6±1.5
versus 2.6±1.0, P=NS) in HCM. Consequently, the CRR was
lower (1.5±0.6 versus 2.6±0.8, P<.05) in HCM than in the
control group. Arteriolar wall area was similar (5720±2130 versus
7107±3544 µm2; P=NS), but
lumen area (1273±688 versus 2260±1165
µm2; P<.05) and diameters were
significantly lower (19.6±4.5 versus 25.9±4.3 µm;
P<.05) in HCM compared with control values. Consequently,
AL was lower in the HCM (21±5%) than in the control group (30±4%;
P<.05), and capillary density tended to decrease from
1824±424 to 1445±513 per square millimeter in HCM (P=.11).
In addition, both the CFR and the CRR were linearly related to AL
according to the formula CFR=0.1 AL-0.45 (r=.57;
P<.05) and CRR=0.07 AL+0.35 (r=.50;
P<.05; Fig 1A
A decreased capillary density has been measured in several animal
studies with experimentally induced secondary hypertrophy
and recently in humans with secondary
hypertrophy.12 13 Although
differences between the groups in capillary density did not reach
levels of statistical significance, there clearly was an inverse
relationship between capillary density and degree of
hypertrophy. Furthermore, the decrements in capillary
density and decrements of AL are related in HCM. These findings may
imply that the decreased AL induces periods of ischemia, which
results in increased angiogenesis. This angiogenesis normalizes the
decrements in capillary density. However, because we did not
analyze HCM myocardial tissue without hypertrophy,
we cannot exclude the possibility that the occurrence of changes in the
coronary microcirculation in HCM is a more independent
phenomenon and not directly related to the degree of
hypertrophy.6 7
In conclusion, septal hypertrophy is associated with
decrements in CFR and CRR in HCM patients. Arterioles of HCM patients
exhibited a smaller lumen at similar wall thickness, which correlated
well with decrements in CFR and CRR. These findings suggest that
abnormal arterioles might contribute to the perfusion abnormalities
found in these patients, resulting in recurrent myocardial
ischemia.
Received August 22, 1997;
revision received October 30, 1997;
accepted October 31, 1997.
2.
Camici P, Chiriatti G, Lorenzoni R, Bellina RC, Gistri
R, Italiani G, Parodi O, Salvadori PA, Nista N, Papi L, L'Abbati A.
Coronary vasodilatation is impaired in both hypertrophied and
non-hypertrophied myocardium of patients with hypertrophic
cardiomyopathy: a study with nitrogen-13 ammonia
and positron emission tomography. J Am Coll Cardiol. 1991;17:879–886.[Abstract]
3.
Pasternac A, Noble J, Streulens Y, Elie R, Henschke C,
Bourassa M. Pathophysiology of chest pain in patients with
cardiomyopathies and normal coronary
arteries. Circulation. 1982;65:778–788.
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Nienaber CA, Gambhir SS, Vaghaiwalla F, Ratib O, Huang
S-G, Phelps ME, Schelbert HR. Regional myocardial blood flow and
glucose utilization in symptomatic patients with
hypertrophic cardiomyopathy.
Circulation. 1993;87:1580–1590.
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Toshima H, Maron BJ, eds. Hypertrophic
Cardiomyopathy.
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Press; 1988.
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Maron BJ, Wolfson JK, Epstein SE, Robert WC.
Intramural (`small vessel') coronary artery disease in
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7.
Tanaka M, Fuijiwara H, Onodera T, Wu DJ, Matsuda M,
Hamashima Y, Kawai C. Quantitative analysis of narrowing of
intramyocardial small arteries in normal heart, hypertensive hearts,
and hearts with hypertrophic cardiomyopathy.
Circulation. 1987;75:1130–1139.
8.
O'Gara PT, Bonow RO, Maron BJ, Damske BA, van Lingen
A, Bacharach SL, Larson SM, Epstein SE. Myocardial perfusion
abnormalities in patients with hypertrophic
cardiomyopathy: assessment with thallium-201
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9.
Spaan JAE, ed. Coronary Blood Flow:
Mechanics, Distribution, and Control. Developments in
Cardiovascular Medicine. Boston, Mass: Kluwer Academic
Publishers; 124; 1991.
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Marcus ML. The Coronary Circulation in
Health and Disease. New York, NY: McGraw-Hill Publishing Co; 1983.
11.
Serruys PW, di Mario C, Meneveau N, de Jaegere P,
Strikwerda S, de Feyter PJ, Emanuelsson H. Intracoronary
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© 1998 American Heart Association, Inc.
Brief Rapid Communications
Decreased Coronary Flow Reserve in Hypertrophic Cardiomyopathy Is Related to Remodeling of the Coronary Microcirculation
Abstract
Top
Abstract
Introduction
Methods
Results
Discussion
References
Background—Ischemia occurs
frequently in hypertrophic cardiomyopathy (HCM)
without evidence of epicardial stenosis. This study evaluates
the hypothesis that the occurrence of ischemia in HCM is
related to remodeling of the coronary microcirculation.
Key Words: cardiomyopathy • arteries • capillaries • ischemia
Introduction
Top
Abstract
Introduction
Methods
Results
Discussion
References
Anginal symptoms and
signs of ischemia occur frequently in patients with HCM without
detectable lesions of the major epicardial
arteries,1 2 3 4 5 suggesting that the presence of
ischemia is the result of abnormalities of the coronary
microcirculation. Indeed, postmortem analysis of HCM hearts
showed the existence of arterioles with abnormally thick
walls.6 7 Furthermore, in experimentally induced
hypertrophy, it has been shown that the hypertrophic
process is accompanied not only by decrements in CFR but also by
structural changes in the coronary microcirculation
(coronary remodeling), including a decreased capillary
density.8 9 10 The resulting increased diffusion
distances for oxygen and the disturbed perfusion of the capillary bed
have been forwarded as an explanation for
ischemia.8 9 10
Methods
Top
Abstract
Introduction
Methods
Results
Discussion
References
Subjects and Protocol
Studies were performed in a group of patients with hypertrophic
obstructive cardiomyopathy (HCM; n=10) who were
referred for cardiac catheterization. The control group
consisted of asymptomatic cardiac transplant recipients
(HTx group; n=8) undergoing follow-up coronary angiography
after transplantation. Informed consent was obtained from all patients.
Patients in the HCM group were symptomatic (NYHA class II
or III) despite ß-blockade therapy (n=5) or therapy with calcium
antagonists (n=5). These patients were considered
candidates for surgery (myotomy/myectomy). Medical therapy was
continued in both groups. Right heart catheterization
was performed with a 7F balloon-tipped flow-directed thermodilution
catheter. A 7F temporary pacemaker was positioned into the right
atrium. Left heart catheterization was carried out,
after which left ventricular angiography and
coronary arteriography were performed with standard techniques.
A 0.014-in Doppler guidewire with a floppy distal end
(Cardiometrics, Inc) was introduced through an 8F guiding catheter and
positioned at the midsegment of the LAD to measure Doppler flow
velocity at rest and after hyperemia. In both groups, hearts
were paced at a constant heart rate of 100 bpm to avoid
metabolic vasodilatation during determination of the CFR.
After optimization of the settings of the velocity signal and 3 to 5
minutes after intracoronary injection of a bolus of 2 to 3 mg
isosorbide dinitrate, baseline recordings of flow velocity and
perfusion pressure were collected and digitized at a sample rate of 125
Hz for off-line analysis. Maximal hyperemia was induced
by an intracoronary bolus injection of 18 µg
adenosine.10
The sample volume of the Doppler wire was positioned at a
distance of 5.2 mm from the transducer and was 
2.25 mm
wide. After power spectral analysis based on a fast Fourier
transform algorithm, the maximal Doppler shift (kHz) was
automatically tracked and converted to the instantaneous velocity
values (cm/s). CFR was defined as hyperemic divided by basal
velocity (Vcor). Coronary resistance was
defined as
(Pao-Ped)/Vcor,
where Pao is aortic pressure and
Ped is end diastolic pressure.
Ped was subtracted to account for increments in
extravascular compression. CRR was defined as the ratio of basal
divided by hyperemic resistance.
A validated on-line analysis system operating on digital
images (ACA-DCI, Philips11 ) was used during the
catheterization procedure. With this system, the
end-diastolic diameter of the LAD was determined in the
segment of the LAD in which the sample volume of the Doppler wire
was located.
Two-dimensional echocardiographic studies were
performed (HP Sonos 1500) with the heart being visualized from standard
cross-sectional planes while images were recorded on videotape
(VHS) for off-line analysis. Septal wall thickness was measured
in diastole from both the parasternal short-axis and
long-axis views. From the recordings on videotape,
representative stop-frames from the various
cross-sectional planes were acquired to determine septal wall thickness
with the aid of a computer and a dedicated software program. To obtain
an average for septal wall thickness, the various cross-sectional
planes were pooled. One patient from the control group was not
analyzed because of insufficient image quality. Thickness of
the septal wall for the HCM and the control groups was defined as the
degree of hypertrophy.
The myocardial tissues from the HCM group (n=9) and from the
control group (n=8) were obtained from surgical myectomy (left
ventricular septal tissue; weight, 0.3 to 1 g) and
myocardial biopsies (left ventricular septal tissue;
weight, 0.5 to 1 mg), respectively. During
catheterization, one HCM patient presented
without a subvalvular pressure gradient and was not operated
on. The tissue was fixed with paraldehyde and immersed in 10% buffered
formalin. van Gieson staining was used for identification and
analysis of intramyocardial small arteries. Arterioles were
identified on the basis of the appearance of a layer of media and
diameter <100 µm. Only arterioles with round cross sections and
without side branches were analyzed. Capillaries were
identified with specific antibodies (CD34) against
endothelium. Quantitative morphometric analysis
of the histological sections occurred with an
in-house–developed software program applied to a morphometric system
(Clemex Technology Inc) that calculated density of capillaries
(capillaries per square millimeter), taking tissue shrinkage into
account. Five cross sections per patient (1000 capillaries) were
analyzed. In addition, software was available that allowed us
to trace the arteriolar lumen-intima and adventitia-media borders,
which defined the lumen and wall thickness regions. The areas of these
regions were obtained from the number of pixels in the two regions.
Normalized wall area is given by circular wall area/(lumen area+wall
area). This value was calculated for 10 arterioles per patient. Data
are presented as mean±SD. Regression analysis, ANOVA,
and t tests were performed with standard statistical
software (SPSS). A value of P<.05 was considered
significant.
Results
Top
Abstract
Introduction
Methods
Results
Discussion
References
The HTx recipients, who served as control subjects, had no cardiac
complaints, and all of them had normal coronary arteriograms.
The time interval of catheterization after
transplantation was 4±2 years. Medication of HTx patients at the time
of catheterization was immunosuppression (n=8)
Ca2+ antagonists (n=8), aspirin
(n=5), and dipyridamole (n=4). No member of the control
group had signs of rejection on the basis of the biopsies. Age
distributions between the HCM (45.5±14.6 years) and control (48.7±6.0
years) groups were similar. HCM patients were symptomatic
(NYHA class II or III), whereas all members of the control group were
symptom free (NYHA class I). HCM patients had a subvalvular
gradient of 88±31 mm Hg and a lower aortic pressure (103±14
versus 120±15 mm Hg, P<.05), a higher
end-diastolic left ventricular pressure (22±1
versus 12±6 mm Hg, P<.05), a lower cardiac index
(2.7±0.5 versus 3.5±0.7 L/m2,
P<.05), and a lower heart rate during baseline conditions
(70±13 versus 97±13 bpm, P<.05) than the control
group. 
). Further
analysis revealed that the degree of AL (AL=-0.85 Hyp+43.7;
r=.71; P<.05; Fig 1B), the CFR (CFR=-0.17
Hyp+5.9; r=.80; P<.05), the CRR (CRR=-1.2
Hyp+4.7; r=.7; P<.05; Fig 1C), and the capillary
density (CD=-51 Hyp+2750; r=.53; P<.05; Fig 1D)
were all inversely related to the degree of hypertrophy
(Hyp). In addition, a linear relationship between AL and capillary
density was measured (AL=42 CD+577; r=.54;
P<.05).
View larger version (14K):
[in a new window]
Figure 1. Relationship of CRR with AL (A), AL and degree of
hypertrophy (B), CRR and degree of hypertrophy
(C), and capillary density and degree of hypertrophy
(D).
Discussion
Top
Abstract
Introduction
Methods
Results
Discussion
References
In symptomatic patients with HCM without
evidence of a functional stenosis of the epicardial vessels,
decrements in CFR were detected, confirming earlier
studies.1 2 3 4 5 Similar decrements in CRR were
measured, implying that these findings could not be explained by
increments in extravascular compression.9 10
Abnormal arterioles with decreased lumen were detected in HCM patients,
suggesting that a structural change in the coronary
arterial vascular tree might be related to this finding.
Indeed, a positive relationship between both CFR and CRR and AL,
corrected for tissue shrinkage by normalization to the wall
area,7 was detected. Furthermore, an inverse
relationship was noted between AL and the degree of
hypertrophy, confirming earlier postmortem
studies.7 Because of this relationship, an
inverse relationship between CFR and the degree of
hypertrophy could be measured. Again, a similar
relationship was found between CRR and degree of
hypertrophy, implying that extravascular compressive forces
were not essential for these findings. In large-animal models of
pressure overload–induced left ventricular
hypertrophy, vascular medial hypertrophy has
been observed only when the coronary circulation was exposed to
high perfusion pressures. The present arteriolar abnormalities were
obtained at normal to low aortic pressures and might imply that
hypertrophy of the arterioles, in parallel to the
hypertrophy of the myocardium, is an
independent process.7
Selected Abbreviations and Acronyms
AL
=
normalized arteriolar lumen
CFR
=
coronary flow reserve
CRR
=
coronary resistance reserve
HCM
=
hypertrophic cardiomyopathy
HTx
=
cardiac transplant
LAD
=
left anterior descending coronary artery
References
Top
Abstract
Introduction
Methods
Results
Discussion
References
1.
O'Cannon RO, Schenke WH, Maron BJ, Tracy CM, Leon
MB, Brush JE, Rosing DR, Epstein SE. Differences in coronary
flow and myocardial metabolism at rest and during pacing
between patients with obstructive and patients with non-obstructive
hypertrophic cardiomyopathy. J Am Coll
Cardiol. 1987;10:53–62.[Abstract]
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