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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3597_Библиотеки_им_академика_М_И_Перельмана
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Research Techniques
A-1
B-1 B-3 B-4
Figure 9-16 Images from optical coherent imaging system after drug-
eluting stent implantation. A-1, Optical coherence tomography (OCT ) image
immediately after stent implantation. Struts are visible with shadows at 4
o’clock and 6 o’clock positions. A-2, Magnified view of stent strut covered
by endothelium. B-1, Stent malapposed to vessel with evident struts at
distance from vessel wall at 3 o’clock to 6 o’clock positions. B-2, B-3, and
B- 4, Magnified sections of B-1 showing apposed and unopposed struts.
(From Kubo T, Imanishi T, Kitabata H, et al: Comparison of vascular response
after sirolimus-eluting stent implantation between patients with unstable
and stable angina pectoris: a serial optical coherence tomography study.
JACC Cardiovasc Imaging 1:475– 484, 2008.)
A-2
B-2
1350 nm) to produce high-resolution, in vivo, real-time images of coronary arteries. In this technique, a fiberoptic wire (0.019-inch diameter)
emits light and records reflection during rotation and pull back within
the artery. The glass fibers that transmit the light for imaging constitute
a fiberoptic array with a distal lens that serves to focus the transmitted
light. Advantages of OCT are high axial (12 to 18 µm) and lateral (20
to 90 µm) resolution in comparison to IVUS (150 to 300 µm) as well
as relatively faster pull back capability (20 to 40 mm/sec) with newergeneration systems. OCT requires a blood free zone, which can be
accomplished with either balloon occlusion and saline infusion or, in
systems with faster pull back, brief contrast bolus injections (~4 mL/
sec) (Fig. 9-16).
Current OCT systems allow tissue penetration of 1.5 to 3.5 mm
(versus 4 to 8 mm with IVUS). OCT can be used to identify and delineate thin fibrous caps, calcium, vessel dissection, and thrombus with
high resolution. For PCI patients, the high resolution of OCT also
allows detailed imaging of stent apposition and the degree of neointimal tissue coverage of stent struts (see Fig. 9-16). In fact, this technique
has yielded important new insight in this regard.
Angioscopy
Coronary angioscopy (Fig. 9-17), which allows direct visualization
of the internal surface of a vessel, provides information about the
pathology of coronary lesions and the pathophysiology of acute coronary syndromes. The coronary angioscope (Vecmova, Clinical Supply
Co., Gifu, Japan) uses a fiber optic core advanced through a delivery
catheter over a wire to the coronary artery. A soft atraumatic latex
balloon on the delivery catheter is inflated to occlude blood flow.
Blood is then cleared away from view with injection of 5 to 10 mL
saline. Angioscopy has been demonstrated to be safe and feasible in
human coronary arteries during cardiac catheterization. It provides a
full color, three-dimensional (3D) image of the coronary artery internal vessel surface and can be used to assess plaques that have ruptured or are involved with thrombus. The current generation of
angioscopes has excellent image resolution and increased flexibility,
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L
1 mm
T
U
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Typical fibrous
cap disruption
1 mm
Typical fibrous
cap erosion
1 mm
T
T
A
Figure 9 -17
A), angioscopy (column B), and gray-scale intravascular ultrasound (IVUS)
(column C). Top row shows typical fibrous cap disruption, middle row shows
fibrous cap erosion, and bottom row shows intraluminal thrombi. (From Kubo
T, Imanishi T, Takarada S, et al: Assessment of culprit lesion morphology in
acute myocardial infarction: ability of optical coherence tomography compared with intravascular ultrasound and coronary angioscopy. J Am Coll
Cardiol 50:933–939, 2007.)
1 mm
Corresponding optical coherence tomography (OCT) (column
WT
WT
RT
B
C
1 mm
Typical
intraluminal
thrombi
1 mm
allowing for better examination of complex and vulnerable lesions.
However, several limitations to performing angioscopy exist. Angioscopy can only visualize the surface of the vessel without imaging
below the very thin intima. Plaque composition can only be inferred
from the intensity of the yellow color. The yellow plaque is confirmed
indirectly by histology to be lipid-rich vulnerable plaque. Visualization
of proximal blood vessel segments is limited due to the need for a
sufficient landing zone beyond the left main artery for the occluding
balloon. Distal vessel segments are also not readily visualized. Finally,
balloon occlusion can lead to myocardial ischemia.
Near-Infrared Spectroscopy Coronary
Imaging System
Invasive imaging of the coronary artery with IVUS provides a detailed
anatomic quantitative description. VH can be produced by the analysis of RF backscatter signals applying Fourier transforms and statistical
validations for four tissue histologies. Color-coding the VH signals
permits identification of thin cap fibroatheroma as well as other more
stable plaque types (Fig. 9-18).
In a manner similar to VH, NIR wavelength light can be used to
detect cholesterol content in a vessel, another component intimately
associated with vulnerable coronary plaques. The NIR LipiScan catheter uses the basic principle of spectroscopy, a technique used by
chemists to identify molecules based on their distinct spectroscopic
signature. Using this principle, the catheter has a fiberoptic core
reflecting laser light at a specific wavelength trained at linoleic acid,
the major chemical constituent of cholesterol within plaques. The
fiberoptic core transmits NIR light and is used in a manner analogous
to an IVUS catheter. An automatic pull back device pulls the infrared
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A
Research Techniques
B
Figure 9-18
and attached cable to the automatic pull back interface device, which
transmits near-infrared (NIR) catheter signals into the console for analysis.
B, Close-up of LipiScan display screen showing low-cholesterol (red) and
high-cholesterol (yellow) content inside vessel. (Images reprinted with permission of Infraredx, Inc.)
A, LipiScan console with display screen, enclosed computer,
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catheter within the artery from distal to proximal during the scanning
for cholesterol. As the spectrum of light goes through the blood and
into the vessel wall, its reflection is collected and analyzed. Because
the vessel wall absorbs some of the spectra, the spectroscopic signature is a function of the light sent out and light returned (the difference
is the absorbed light). Cholesterol signal is designated as yellow and
nonlipid as red or black. No signal is white. The LipiScan console
performs several functions. In brief, it provides (1) NIR light source for
spectroscopy, (2) data-processing system that analyzes the signals
returned from the pull back interface, (3) user interface to the system,
(4) means of data storage, and (5) communication to the pull back
interface that drives the automated scanning of the LipiScan coronary
imaging catheter core. The console consists of the following major
components: laser and laser delivery system, computer system and
software, and power module.
This technique provides a “chemographic” map of cholesterol
deposits within the artery, displayed as if the artery had been laid open
and spread out from distal to proximal. The chemogram is based on
an algorithm that quantitates the likelihood of a lipid-core plaque in
any particular 2-mm block of vessel. The chemogram is color-coded,
with bright yellow indicating a greater than 90% likelihood of a lipidcore plaque and red indicating no evidence of lipid-core plaque. The
chemogram approach was validated in an autopsy study. The Food
and Drug Administration (FDA) has approved the LipiScan catheter
for the detection of lipid-core plaques. The risks and limitations of the
LipiScan catheter are similar to those of the IVUS catheter.
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Combined Hemodynamic and
Echocardiographic Modalities
Although cardiac catheterization provides gold-standard data regarding intracardiac pressures, essential data regarding chamber volumes
are lacking in commonly used catheter systems. Simultaneous 2D
echocardiography can provide volumetric data, in addition to tissue
Doppler imaging for characterization of ventricular motion. An advantage of echocardiography is the potential for continuous observation
of LV chamber size, geometr y, wall motion, and beat-to-beat changes
in flow during study interventions without additional radiation.
Some echocardiographic machines used for studies in the cardiac
catheterization laboratory can be modified to accept pressure and
other signals from the physiologic recorder (Figs. 9-19 and 9-20).
Specialized input amplifiers for echocardiographic machines are
available, facilitating the recording of pressures simultaneously with
echocardiographic parameters. Use of Doppler echocardiography
and simultaneous hemodynamics has advanced the understanding of
cardiac function and provides a means of examining questions previously unanswered with the use of other techniques.
Myocardial Metabolism
Measurement of Specialized Blood Products
Transmyocardial (proximal aorta/coronary ostium and CS) blood
sampling is used to study myocardial metabolism. Measurements of
pyruvate, lactate, and oxygen extraction are the most common outputs.
The transmyocardial extraction of drugs after systemic delivery can
also be determined. Under normal circumstances, lactate is actively
taken up in the myocardium and converted to pyruvate for subsequent
oxidative metabolism, such that the gradient of lactate from CS to
artery is positive. With ischemia, this gradient is reversed, and lactate
accumulates in the CS blood.
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40 mm Hg
0 mm Hg
Figure 9-19 Simultaneous high-fidelity lef t ventricular (LV) pressure (0- to
40-mm Hg scale) superimposed on Doppler echocardiogram, showing peak
early (PE) and peak atrial (PA) filling waves of mitral valve inflow. Also superimposed is the dP/dt signal from LV pressure tracing and the electrocardiogram. These combined methods permit analysis of function that is not
available with a single technique. dP/dt, Derivative of pressure (dP) with
respect to time (dt).
LV pressure
PE PA
*
Doppler
.2 m/s
dP/dt
1 m/sec
**
Figure 9-20 Aor tic and left ventricular (LV) pressure superimposed on
Doppler aortic flow velocity showing aor tic stenosis and insufficiency characterized by the Doppler waveform. Aor tic stenosis is superimposed on the
systolic ejection gradient (**), and aor tic insufficiency can be observed over
the diastolic period with reversed diastolic velocity observed (*).
Specialized collection tubes for various substances and heparinized syringes for oxygen blood samples should be prepared in advance
so that the physician can pass the drawn blood quickly to the technicians for insertion into the collecting tubes. In addition to sample tube
preparation, ice, a centrifuge, or a series of dilutional tubes may be
required. These techniques are not complicated, but correct labeling
and anticipation of which samples will be obtained at which point in
the procedure reduce errors without unnecessarily prolonging the
study.
Coronary Sinus Catheterization
CS catheterization can be performed with a superior or inferior central
venous approach. The ostium of the CS is located inferior and
posterior to the tricuspid valve. Suitable for cannulation of the CS
are Amplatz left catheters or multipurpose coronary catheters. After
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careful insertion in the right atrium, the catheter is directed toward
the tricuspid valve and in a posterior direction. Gentle medial advancement with a 1- to 2-mL flush of contrast medium enables the physician
to know when the catheter has entered the CS. Ventricular ectopy
indicates contact with the right ventricular wall or septum, which is
corrected with withdrawal and advancement after slight rotation. The
CS catheter is usually positioned in the anteroposterior view, with the
catheter seen passing upward across the tricuspid valve and spine. In
the LAO position, the catheter appears to be coming directly in plane
toward the observer. In the RAO position, it should pass posterior and
away from the ventricular apex (i.e., not into the right ventricle). Care
should be taken not to cannulate the inferior cardiac vein and to avoid
perforation of the CS, right ventricle, or atrium. Historically, dedicated
CS thermodilution catheters were used to measure myocardial blood
flow to solve for myocardial oxygen consumptions using the Fick
method. However, these catheters are no longer available, and flow
may be best assessed using a Doppler flow wire in an epicardial
vessel.
High-Fidelity Micromanometers
Pressure data from standard fluid-filled catheter systems are sufficient
for most clinical hemodynamic studies but suffer from well-recognized
artifacts and suboptimal frequency-response to accurately assess
ventricular properties in research studies. When high-fidelity data are
required for hemodynamic assessment, micromanometer transducertipped catheter measurements are used. High-fidelity pressure
measurements are useful for studies of cardiac contractility, diastolic
relaxation, compliance, afterload reduction, and myocardial metabolism. High-fidelity pressures also may be combined with quantitative
volume measurements to examine chamber function. Volumetric data
can be acquired using ventricular angiography, simultaneous echocardiography, or in specialized centers, a conductance catheter system.
Assessment of Systolic Function
Contractility represents the ability of the myocardial muscle to shorten
or thicken against a load. Although ejection fraction (EF) is the most
common clinical assessment of contractility in practice, it is highly
dependent on ventricular afterload. For example, at the same level of
contractility, EF steeply declines as afterload increases. Robust measures of chamber contractility must account for both afterload and
preload.
The peak rate of pressure increase during isovolumic contraction
(dP/dt
measured using a high-fidelity micromanometer, by taking the first
derivative of pressure (dP) with respect to time (dt). dP/dt
directly with preload, which limits its use during interventions that
alter chamber filling volume, but it is very useful in detecting acute
changes in chamber contractility where preload is relatively constant,
such as with acute administration of cardiac resynchronization
therapy. The preload sensitivity of dP/dt
ing to instantaneous pressure, and an advantage of this parameter is
the lack of a requirement for simultaneous volume assessment. dP/
dt
poor frequency response.
work index (SWI), preload-recruitable stroke work (PRSW), and endsystolic elastance (Ees; see Fig. 9-21). Stroke work is defined by the
area subtended by the pressure-volume loop, quantifying the hydraulic work performed by the LV with each beat. This is often estimated
, Fig. 9-21) is relatively afterload independent and readily
max
varies
max
can be mitigated by index-
max
should not be estimated from fluid-filled catheters given their
max
Other load-independent measures of contractility include stroke
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0.04 sec 0.2 sec
ECG
200 mm Hg
+dP/dt
Ao
0
Figure 9-21 High-fidelity, micromanometer-tipped hemodynamic tracings
of aortic and left ventricular (LV) pressures with dif ferentiated dP/dt signal
showing method of calculation of dP/dt. See text for details.
To compute dP/dt:
1. Slope height (SH): mm deflection from ramp over 80 msec
2. Derivative height (DH): mm deflection of square box of derivative
3. Compute K = (12.5 × SH)/DH
4. Scale factor P = mm paper deflection of 200 mm Hg
5. Compute dP/dt:
Peak dP/dt positive or negative deflection; normal value range: 1500 to
1800 mm Hg/sec. Ao, Aortic pressure; dP/dt, derivative of pressure (dP)
with respect to time (dt); ECG, electrocardiogram; P, paper height for 200
mm Hg; RA , right atrial pressure; Ramp, ramp from differentiator.
LV
–dP/dt
dP dt
RA
200
mm Hg
P
.08 sec
SH
DH
P
Ramp
K/ ( )=
in practice by the product of mean blood pressure and stroke volume.
Similar to dP/dt
, stroke work varies directly with preload, and divid-
max
ing by left ventricular end-diastolic volume (LVEDV) makes SWI a relatively load-independent ejection measure of inotropy.
Conductance catheter systems are required for measurement of
Ees and PRSW. These systems combine a high-fidelity pressure micromanometer with electrodes that measure the conductance of a small
voltage difference between the tip of the catheter and specified proximal electrodes. The conductance between these sites varies with
chamber volume, and after calibration, it provides real-time measures
of LV volume. Use of these methods requires specialized catheters and
analysis systems but provides accurate data regarding ventricular systolic and diastolic function.
Measurement of Diastolic Function
In routine diagnostic catheterization, an elevated left ventricular enddiastolic pressure (LVEDP) in a normally-sized heart is often assumed
to indicate a stiff ventricle from diastolic dysfunction. Although this
assumption may often be true, it must be remembered that increased
intrathoracic pressure, right-heart pressures, and pericardial restraint
may each contribute to observed increases in LVEDP, particularly in
patients with heart failure.
The gold-standard index of early diastolic relaxation is the time
constant tau (τ) of LV pressure decay, which can be readily obtained
during isovolumic relaxation (the time between aortic valve closure
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ESPVR
Slope = Ees
LV pressure
A
Figure 9-22 Ventricular contractility in the pressure-volume plane is
expressed by end -systolic elastance (Ees), defined by the slope and intercept
of the end-systolic pressure-volume relationship (ESPVR). A, Stroke work
performed by the ventricle is represented by the area of the pressure-volume
loop (shaded area). Indexing stroke work to preload (end- diastolic volume
[EDV]) provides a measure of contractility. The slope of the relationship
between stroke work and EDV (preload- recruitable stroke work [PRSW]) is
higher in normal hearts than in hearts of patients in systolic hear t failure.
B, Adrenergic stimulation with dobutamine increases this slope, indicative
of an increase in contractility. EF, Ejection fraction; ESV, end-systolic volume;
HF, heart failure; LV, left ventricular; SV, stroke volume. (Modified from
Borlaug BA, Kass DA: Invasive hemodynamic assessment in hear t failure.
Heart Fail Clin 5[2]:217–228, 2009.)
EF = SV/EDV
SV
ESV EDV
LV volume
Stroke work
(shaded)
Stroke work
B
Dobutamine
Normal
Systolic HF
LV volume (preload)
and mitral opening) using micromanometer catheters (Fig. 9-22). τ is
typically <
40 to 45 msec in a normal LV and is prolonged in patients
with heart failure, cardiomyopathy, or hypertensive heart disease. The
maximal rate of pressure drop (dP/dt
can be determined in a manner similar to that of dP/dt
) during isovolumic relaxation
min
, as another
max
measure of early relaxation. These indices should not be calculated
from fluid-filled pressure data.
The so-called passive stiffness of the LV is more difficult to
measure, because it requires simultaneous assessment of chamber
pressure and volume to plot the curvilinear end-diastolic pressurevolume relationship (EDPVR; Figs. 9-22 and 9-23). An EDPVR that is
shifted up and to the left indicates increased diastolic stiffness. The
EDPVR from a single heartbeat may differ markedly from the curve
measured at different preloads, and gold-standard measurement of the
EDPVR ideally requires measuring pressure and volume during diastasis (where transmitral flow is zero), under a number of different
preload states using a conductance catheter. This is usually performed
with an inferior vena cava (IVC) occlusion catheter and is only done
in highly specialized research protocols.
Exercise in the Catheterization
Laboratory
Heart failure may be broadly defined as an inability of the heart to
pump blood to the body commensurate with its metabolic needs or
to do so only with elevated filling pressures. However, in patients
without apparent volume overload (particularly with a normal EF), it
is often difficult to discern whether symptoms of dyspnea or fatigue
are due to cardiovascular pathologies or other mechanisms, such as
pulmonary disease, obesity, or deconditioning. Dynamic exercise can
discern cardiac versus noncardiac sources of symptom limitation.
Exercise evaluations help relate symptoms to hemodynamic changes
reflective of cardiac dysfunction and can point toward noncardiac
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Elevated LVEDP
Prolonged
LV pressure
relaxation
(↑τ)
A B
Figure 9-23 A, Kinetics of lef t ventricular (LV) relaxation are quantified by
rate of pressure decay during isovolumic relaxation (the period between
aortic valve closure and mitral valve opening). With prolonged relaxation
(increased time constant τ), LV pressure remains elevated longer in early
diastole. B, The gold standard for assessing diastolic LV compliance relies
on measuring curvilinear slope of the end -diastolic pressure -volume relationship (EDPVR). A steeper slope (dotted line), shif ted up and to the left, indicates decreased diastolic compliance compared with a normal EDPVR (curve
A). Elevated left ventricular end-diastolic pressure (LVEDP) may exist if the
ventricle is stiffer (curve B), overly filled with blood as in systolic heart failure
(curve D), or with enhanced external pressure as in pericardial constriction
(curve C). In most hear t failure patients, some combination of each of these
factors contributes. (Modified from Borlaug BA, Kass DA: Invasive hemody namic assessment in hear t failure. Heart Fail Clin 5[2]:217–228, 2009.)
Time LV volume
Normal LVEDP
LV pressure
A
C
D
B
causes of dyspnea when hemodynamic responses are normal. Exercise may be dynamic or isometric—the former being more representative of activities of daily life and the latter being more feasible to
perform in most catheterization laboratories.
In healthy young humans, upright exercise is associated with an
increase in LV preload (end-diastolic volume [EDV]) with no change
in LV filling pressure and decreases in end-systolic volume (ESV;
increase in contractility). Enhanced diastolic filling is achieved by
creation of a suction gradient during early diastole from LV apex to
base, favoring rapid filling. In patients with coronary artery disease or
heart failure, these reserve mechanisms may be insufficient to cope
with stress, and LV filling pressure then increases with exercise.
Although the definition of abnormal LV filling pressure with exercise
has not been clearly agreed on, pulmonary capillary wedge pressures,
left atrial pressures (in the absence of mitral stenosis), or LVEDPs of
more than 25 mm Hg are considered by most to be elevated. The
upper limit of normal probably varies with age, because prior studies
of healthy elderly men without cardiovascular disease reported
increases in pulmonary capillar y wedge pressures during exercise to
17 ±
5 mm Hg in the absence of symptoms. Ideally, pressures are
reported at end-expiration, where there is equalization between intrathoracic and atmospheric pressure, but automated systems generally
use the mean of inspiration and expiration. The latter can disagree
substantially with end-expiratory values in patients with morbid
obesity or parenchymal lung disease, for which intrathoracic pressure
swings are dramatic.
During exercise, cardiac output (CO) should increase in tandem
with oxygen consumption. When oxygen delivery is insufficient to
meet metabolic needs, increased extraction occurs, such that the
arterial-venous difference increases and pulmonary artery saturation
drops. The Dexter index has been suggested as one method to quantify what constitutes a “normal” CO response to exercise, where the
predicted cardiac index (CI) is equal to 2.99 + 0.0059 × (measured
oxygen [O
] consumption index with exercise). This equation was
2
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derived from seven healthy volunteers studied by Dexter and colleagues. An abnormal CI response is present if the observed peak CI
is <80% of that predicted by the Dexter formula. A related scheme
relies on the “exercise factor”: for every 100-mL/min increase in oxygen
consumption with exercise, the CO should increase by at least 600 mL/
min; thus, the normal exercise factor is ≥6. Numerous studies since
those of Dexter have confirmed that the normal increase in CO relative
to oxygen consumption is 6:1. A limitation for many laboratories is that
this method requires simultaneous assessment of oxygen consumption, which is not available in many or most laboratories.
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Dynamic Physical Exercise
Exercise hemodynamics may be measured in supine or upright positions depending on equipment availability and vascular access. There
are a number of important differences between upright and supine
exercise.
1. Ventricular EDV, EDP, and stroke volume are lower at rest when
upright. Preload EDV is maximal at rest in the supine position and
does not increase further with exercise. In contrast, with upright
exercise, EDV does increase, with enhanced venous return.
2. Resting heart rate and diastolic arterial pressure are both higher
when upright, whereas pulmonary artery and intracardiac filling
pressures are lower.
3. Stroke volume increases 1.4-fold to twofold with maximal upright
exercise and tends to increase proportionally more compared with
supine because preload (EDV) starts from a lower rest level. Stroke
volume increases less with supine exercise.
4. Exercise pulmonary artery and wedge pressures and stroke volumes
are lower in the upright position, but the total exercise changes
(i.e., exercise–baseline) are similar between upright and supine
exercise.
The supine cycle ergometry exercise protocol used in the Mayo
Clinic Catheterization Laboratory is as follows:
1. Resting hemodynamic data recordings are obtained with the
patient supine and feet flat. A tight-fitting mask coupled to a metabolic cart with expiratory gas analyzer is used to measure ventilation, oxygen consumption, and carbon dioxide production. The
metabolic measurements allow quantification of exercise capacity
and CO by the Fick method.
2. Exercise begins at 20 Watts, followed by 10- to 20 -Watt increases
every 3 minutes until maximum tolerated workload. Heart rate is
recorded continuously; and pressures in the pulmonary artery,
wedge, and right atrium are recorded halfway through each stage.
We use a 7-F catheter introduced through a 9-F sheath, with the
side arm of the sheath transducing central venous right anterior
pressures continuously. If expired gas analysis is performed, the CO
may be determined by the Fick method. If oxygen consumption
cannot be measured, thermodilution CO should be used, because
the Fick method cannot be used during exercise without simultaneous gas analysis (oxygen consumption increases severalfold during
exercise). It is often difficult to obtain reproducible and accurate
thermodilution outputs during exercise. Patient-reported symptoms
of dyspnea and fatigue are quantified by Borg Scales at each stage.
3. When the patient is near maximum tolerated workload, based
either subjectively or on a respiratory quotient of >1.0, peak pressures are recorded with repeat assessment of CO.
4. Additional measures may be required based on the specifics of the
case (e.g., assessment of transvalvular gradients in mitral or aortic
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